AnthonyColpo

Dumbest Email of the Week

Anthony Colpo — Mon, 06 Sep 2010 09:44:13 +0000

Note: This post contains strong language. Please close this page immediately if you are a minor or easily offended.

I’m hoping this won’t become a regular feature, as I’ve deliberately structured the image and content of my sites to discourage lazy, dogmatic, fad-loving Internet users of questionable intelligence. And judging by the drastically reduced volume of hate mail I receive (especially from demented low-carbers), the strategy seems to be working nicely. Unfortunately, the occasional lunatic still slips through the cracks. Below are the emails of one such correspondent to which, probably against my better judgment, I took the time to reply. I did, however, terminate the conversation after my second reply due to the increasingly hostile and pointless nature of the correspondent’s emails, adding the individual’s email address to my spam filter.

Whilst this individual is clearly beyond help, the rest of us can learn a lot from analyzing his/her distorted mindset. Read on to find out why rejecting the currently fashionable politically correct “victim” mentality could be the best thing you ever do.

Reader “R. Celentano” writes:

Hello Anthony,

Just wanted to give you some feedback about an article you wrote about HcG. First off, since you are selling YOUR own product for weight loss (and financial gain), WHY should I trust your research? And your article was offensive – I believe your words were “fat lazy asses”, referring to us who are challenged by obesity. Trying to get people to buy your book by subjecting them to ridicule probably does not work very well. How about a bit more charitable approach. I’ll bet you would sell more books. Not to me, however. Sincerely, R. Celentano

Anthony replies:

“First off, since you are selling YOUR own product for weight loss (and financial gain), WHY should I trust your research?”

Well gee, you could actually check the references I cite in support of my contentions and discover for yourself that I’m telling the truth. I’m not asking anyone to blindly trust what I say, and I repeatedly encourage people to check the science I cite for themselves. But I guess it’s too much for you to get off your fat lazy ass and do that.

“Challenged by obesity”? Give me a break…there are scores of people with real physical challenges, like paraplegia, who still find it within themselves to keep in shape. These folks have lost limbs yet still get into the gym instead of looking for the easy way out – so what’s your excuse? Too weak willed to resist that box of choc chip cookies that shouldn’t even be in your pantry in the first place?

Poor diddums.

Mate, it says on the front page of my website that anthonycolpo.com is not for the lazy. Please take note and stop wasting my time.

“R. Celentano” replies:

Hey, You obviously know NOTHING about food addiction – or other addictions such as alcohol, sex, money, porn, etc. If you did, you would certainly not say the “fat lazy ass” comment. You are boorish and uninformed and rude and I could go on but you clearly are not worth it. I am sorry that you chose the profession you did. I actually weigh 147 pounds but have struggled to get there – exercise being a life saver. I STILL resent your attitude, Mate. YOU are boorish.

Anthony replies:

C’mon Sunshine, tell me how you really feel!

Mate, you are a politically correct pansy who needs to harden the hell up.

If you want pity, you’ve definitely come to the wrong place. I’ve got all the time in the world for people who are genuinely prepared to put in an honest effort on a consistent basis to get themselves into shape – and absolutely none for those with a victim mentality looking for the easy, effortless way out. I don’t care how fat or what shape people are in when they come to me, if they can show me they’re prepared to buckle down and work, then they have my time.

Call me a “boor” if it makes you feel better, but this “boor” has helped a lot more fat people lose serious amounts of weight than your self-righteous, whining, politically correct do-gooder self could ever do in ten lifetimes. The kind of PC nonsense spouted by yourself is water off a duck’s back to me. I’ve been a certified trainer for almost 20 years now, and in that time I’ve helped more people get in shape than I care to remember. They did it, not by pissing and moaning about their food/porn/booze/sex “addiction”, but by taking the bull by the horns and committing to eating right and training regularly.

As for your “addiction” BS… grow up! This is the real world, not Oprah. Regrettably, the word “addiction” has been hijacked by politically correct apologists like yourself to be used in place of “extreme lack of discipline”. When you’ve seen someone violently shaking and writhing in the midst of drug withdrawal, when you’ve had friends so devastated by heroin that it wrecked their homes, drove their parents to divorce, and ultimately killed them…then, and only then, you can talk to me about addiction. Food addiction? Give me a fucking break. When someone can’t resist the urge to shove another Twinkie down their already overfed Western gob, that’s not addiction – that’s sloth. When they would rather watch TV than go outside for a ride or head to the gym, that’s not addiction – that’s plain laziness.

I’ve trained way too many people who were prepared to get out of bed that extra hour earlier in order to train, who wanted a lean healthy body much more than they wanted that extra slice of cheesecake, who were prepared to turn off the idiot box so they could prepare their next day’s meals so they wouldn’t be tempted by the crap in the office vending machines or work canteen…I’ve dealt with way too many of these folks to have even the slightest amount of sympathy for those who piss and moan about how getting in shape is “all too hard”, or how they’ve “tried everything”. In almost every instance, these folks have not adhered for any meaningful length of time to a scientifically backed strategy that involves a sensible and sustainable caloric deficit, such as that outlined in The Fat Loss Bible.

You think you’re taunting me when you gloat that you won’t buy my book, but the joke’s on you. The reality is that I’ve sold thousands of copies of The Fat Loss Bible and have had scores of people write to tell me how the book has allowed them to decisively cut through all the confusing BS, to finally lose weight and get in the best shape of their lives. I’ve had people in their 40s and 50s telling me how they’re now leaner than they were in their teens and twenties, and others excitedly gushing about how members of the opposite sex are suddenly starting to take notice of them. Unlike you, they don’t need to whack off to Internet porn or get drunk to approach women, or engage in whatever other vices you partake in and rationalize away as “addictions”. The The Fat Loss Bible, I’m proud to say, has produced a lot of very happy readers. That you will never be one of them is your loss, not mine.

You think you’re sticking up for the interests of overweight people, but people like you are actually their worst enemy. From you they will get counterproductive rationalizations that merely reinforce their victim mentality and keep them stuck in a rut. From me, they get results.

Now once again, stop wasting my time. You clearly have nothing intelligent to say and I’m certainly not going to pander to your victim mentality. Go join a fat acceptance forum or something…

Anthony’s further comments:

I was going to let this exchange rest after my last reply, but similar to the emails from Neil F-S I recently commented on, Celentano’s correspondence reveals a rather obnoxious brand of self-righteous stupidity that warrants further analysis. Unfortunately, self-appointed PC police like Celentano are everywhere, and they seem to believe they have some God-given mandate to tell the rest of us how to think, talk and act. Maybe that wouldn’t be so bad if they truly were fountains of wisdom and maturity, but the reality is that PC stormtroopers like Mr/Ms Celentano are so full of scheisen they can’t think straight to save their own lives, let alone ours.

Gordon Ramsey becomes an international celebrity after replacing 95% of his vocabulary with the F-word, while people like Simon Cowell and Paula Abdul enjoy lucrative careers and achieve hit ratings for American Idol by mercilessly ridiculing hopeful young contestants (in at least one instance, to the point of suicide)…but Celentano gets all bent out of shape because I tell overweight people tempted by scams like HCG to instead get off their “fat lazy asses” and commit to sensible nutrition and regular exercise?

What a joke.

I think now’s a highly appropriate moment to post one of my all-time favourite comedy videos, from fellow Aussie comedian Ronnie Johns:

The catchcry is “Harden the F**k Up, Australia”, but of course the message applies equally to America, from whom we inherited all this politically correct claptrap.

Thanks to increasing automation that has all but removed the need for physical activity and the widespread availability of calorie-dense foods, affluent Western societies have become increasingly complacent, overfed, lazy and fat. We’ve also become so full of shit that when someone has the temerity to suggest we’ve become lazy and fat, we get our XXXL knickers in a knot, spit our dummies and throw a super-sized politically correct tantrum.

Or at least folks like Celentano do.

Where exactly does all this PC bullshit end? What about us genetically ungifted ectomorphs who have to fight tooth and nail to put on even an ounce of muscle, who nonchalantly refer to ourselves as “skinny bastards”? What about all the folks who have successfully lost weight that proudly refer to themselves as FFBs (“Former Fat Bastards”)? Are we all being “rude”, “boorish” and “offensive” – to ourselves?!

My advice to Celentano (and all folks like him/her) is to take off your pink chiffon, give it back to the dainty little ballerina you stole it from, then brew yourself a nice extra-strength cup of Harden-The-Fuck-Up® – and drink it straight. While you’re at it, try lightening up and developing a sense of humour, along with a sense of perspective. There are infinite scams, injustices, and evils taking place in the world on a daily basis, yet you specifically take time out to antagonize someone who’s encouraging overweight people to do something positive about their condition, rather than continuing to fall for every half-baked weight loss scam that comes along.

Nice one.

I know it’s fashionable in this day and age to be an overly sensitive wuss and to wear one’s vices like some kind of badge of honour, but there comes a point in life where you have to pull your gonads out of the freezer, look in the mirror, and say to yourself:

“You know what? I’m sick of this shit. I’m sick of feeling like crap and looking like a body double for Moby Dick. Today – not tomorrow, but today – is the first day of my journey towards my new lean, healthy body. A body that I can actually be proud of instead of always covering up with oversized apparel that could provide shelter to third world villages. This journey will have its ups and downs, but screw it, I’m a grown adult with the capacity for self-control and discipline and I’m going to bloody well start using it.

During this journey, I’m going to start using that omega-3- and cholesterol-rich lump of grey matter that’s been lying dormant inside my skull. When some sleazy low-carb guru tells me I can magically start burning an extra 600 calories per day by remaining on my fat ass and simply cutting carbs out of my diet, or when some bloke who’s had numerous FTC indictments for false advertising tells me the “secret cure” for obesity is a fertility drug, I’m not going to succumb to the perennial human desire for the easy way out. Instead, I’m going to engage my rational faculties and realize these people are full of shit. I’m going to lose weight the time-proven way: with a nutrient-rich diet that provides a sufficient and sensible calorie deficit, and with good old sweat-inducing physical activity on a daily basis. I’m not going to do this for 3 weeks, get pissed off because I don’t yet look like Brooke Burke/Georges St-Pierre, then give up and piss and moan for the rest of my life that “diets don’t work” or that exercise is useless. I realize it took me a lot longer than that to get to the state I’m in, and it’s going to take a lot longer to get back down to my ideal body fat percentage. That’s OK, because Rome wasn’t built in a day and I plan to be around for a long, long time.

And I’m not going to piss and moan about having to do daily exercise, because it wasn’t that long ago in history that most people spent the greater part of their day engaged in physical labour, sometimes of a dangerous back-breaking nature. As such, I really don’t think it’s a huge ask for me to take one or two hours out of my sedentary life each day and give my body the physical stimulation it desperately needs. Instead of lying in front of the idiot box each night like a comatose lump of lard, I’m going to place the interests of my body above those of the commercial networks and their advertisers. Desperate Housewives, NCIS, and CSI Miami/New York/Las Vegas/Los Angeles/Smithfield Plains will just have to get by without me.

And when jealous co-workers, friends, and even family members feel threatened and start attacking my healthy new habits, in the form of feigned concern or snide remarks thinly disguised as humour, I’m not going to buckle and give in just to fit in with the rest of the mediocre and deeply insecure crowd. If my healthy new habits make the slothful and cellulite-laden feel uneasy, screw ‘em. When they keep offering me crappy foods or extra servings that I – and they – know full well I shouldn’t have, I won’t let my willpower collapse like a Dow Jones meltdown. I’ll simply say one magic little word – “NO” – over and over until they get the message. Either that, or I’ll pretend to suffer from a rare genetic condition involving unpredictable spastic movements and launch the creamcake all over their new sofa setting. Bet they don’t offer me any more food after that…

Yep, today is the day I turn my life around and start proving to myself that I’m not like every other spineless, soft-assed, limp-dicked, instant gratification-seeking consumerist automaton who thinks the purpose of life is to acquire more and more shit they don’t need, and are happy to watch their health and body go to hell in the process.”

As you’ve probably figured by now, people like Mr/Ms Celentano have a snowball’s chance in hell of infecting me with their nampy-pamby, politically correct, victim mentality. In fact, after having known people with real addictions, and having seen people battle truly debilitating conditions, I find Celentano’s attitude to be quite repugnant and insulting. Food addiction? Yeah sure, if you have a genuine genetic disorder like the rare Prader-Willi syndrome.

Folks like Celentano can come up with all the rationalizations they want, but after two decade’s worth of training people I can assert the following with 100% confidence: The human body does not listen to excuses. You might not like it, but that’s the truth, Ruth. No-one ever subverted the laws of nature and the need for a caloric deficit to induce weight loss by wanking on about addictions/gut microbes/fat-depositing aliens. Sorry folks, but I’m not in the business of bullshitting people. If you’re hoping I’m going to one day pull a Kevin Trudeau and offer some magical quick-fix weight loss “cure” comprised of HCG, micro-filtered ethyl-ester red chilli pepper extract, and a special blend of metabolism-boosting South Australian Free-Range Grass Clippings, you’ve definitely come to the wrong place. If you can’t deal with this, hey, no problemo. Just click the little cross at the very top right hand corner of your browser and…presto!…no more Colpo and his annoying habit of telling the truth! You can remain content in your misery, without people like me correctly pointing out that self-responsibility and the shunning of idiotic and fraudulent fads are paramount for achieving a lean, healthy, athletic body.

Ciao,

Anthony.

“Political correctness is tyranny with manners.”
Charlton Heston

“Political Correctness: A doctrine which holds forth the proposition that it is entirely possible to pick up a turd by the clean end.”
Unknown

—

Anthony Colpo is an independent researcher, physical conditioning specialist, and author of the groundbreaking books The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

Being a Health ‘Expert’ is a Health Hazard

Anthony Colpo — Thu, 02 Sep 2010 02:50:24 +0000

Below is a fascinating article about the very poor longevity track record of famous health ‘experts’ and diet ‘gurus’. From what I have been able to gather by Googling around, the article was penned in 2000 by John MacGregor, a fellow Aussie. MacGregor wrote the piece as the first of a series for a local newspaper (I haven’t been able to ascertain which paper, or if it was in fact ever published). It’s worth noting the article was written a few years before the controversy-filled passing of low-carbohydrate author Dr. Robert Atkins, one of the most famous diet ‘gurus’ in history. Atkins, as many of you will remember, died after slipping on an icy New York footpath. He spent nine days in a coma before dying on April 17, 2003 aged 72. A year earlier, Atkins had suffered cardiac arrest due to cardiomyopathy, which he reportedly developed after a viral infection in 2000.

Other recent developments include:

The heart attack death of K. Dun Gifford, who promoted the Mediterranean diet, at 71;
Michio Kushi, macrobiotic advocate and author of The Cancer Prevention Diet, suffering colon cancer at 81. He is still alive, but his wife died of cervical cancer at 78.
The death of Roy Walford in 2004 at age 79. The longevity researcher and author died of respiratory failure as a complication of amyotrophic lateral sclerosis (commonly known as Lou Gehrig’s Disease). Walford’s books included Maximum Life Span and The 120-Year Diet.
The death of Robert E. Kowalski from a pulmonary aneurysm in 2007, aged 65. Kowalski wrote several best-selling books, including The 8-Week Cholesterol Cure, The 8-Week Cholesterol Cure Cookbook, Cholesterol & Children, 8 Steps to a Healthy Heart (a guide to recovery from heart attack and bypass surgery), The Type II Diabetes Diet Book, and The Blood Pressure Cure: 8 Weeks to Lower Blood Pressure Without Prescription Drugs. Kowalski developed his programs after enduring a major heart attack and multiple-bypass surgery at age 35.

Enjoy the article – and please don’t ever refer to me as a “diet guru”; “Anthony” works just fine. And before I get any hate emails from blindly loyal followers of the figures mentioned in this article, let me make it perfectly clear the purpose of this post is not to ridicule; instead, it is to remind people that celebrity diet and health ‘gurus’ are fallible human beings just like the rest of us. Their exalted status is usually the result, not of superior knowledge, but clever promotion, timely PR and the eternal gullibility of folks looking for the next ‘hot’ diet and health strategy. People should really have a good, long, hard think about their tendency to sheepishly worship diet ‘experts’. Someone might have a great publicity agent, a supportive publisher that knows a great gimmick when they see one, a good relationship with journalists and be a darling of the media, but that’s no guarantee they know what they’re talking about.

As for why diet and health gurus tend to be riddled with poor health and premature mortality, my suspicion is that many of these folks (and their followers) get so caught up in whatever novel angle they are pushing (carbohydrate restriction, fat restriction, permanent calorie restriction, high-dose supplements, juice fasting, etc, etc) that they lose sight of the bigger picture. And the bigger picture, judging by the habits of long lived societies, is a diet and lifestyle that encompasses predominantly nutrient-rich whole foods, avoidance of both caloric overconsumption and underconsumption (the former leads to obesity and chronic disease, the latter results in malnutrition), and a lifestyle marked by temperance, regular physical activity, sufficient sound sleep, a supportive social circle, low stress and/or superior stress coping mechanisms. I’ve known several barely literate elderly Italians who lived well into their 90s and beyond. None of them ever wrote a diet book; heck, none of them would have had a clue what terms like ‘ketosis’ or ‘macrobiotic’ meant. They regularly ate bread and pasta (made from white flour) – and lived a lot longer than Dr. Robert Atkins. They also regularly cooked with olive oil, butter and lard – and outlived vocal low-fat author Nathan Pritikin by decades. They did so because they lived their life largely in accordance with the requirements I described earlier. Focusing on one or two novel health factors while ignoring the rest of the aforementioned critical requirements is a sure-fire recipe for ill health and shortened lifespan.

It is also apparent that some of these ‘experts’ had deluded themselves into believing their brand of diet or health gimmick excused their other lifestyle indiscretions (I’ve personally met more than a few people like this). Let that be a warning to you; if you think that eating low-carb negates the need for regular exercise, or that taking high dose supplements allows you to smoke, drink, and party hardy til the wee hours, or that your visits to the gym negate the effects of a junk diet, chances are one day you’ll receive a very rude shock.

Health ‘Experts’ and Longevity Article

by John MacGregor

Despite claiming to hold the secrets to superb health and long life, famous diet gurus and health experts fare very poorly in the longevity stakes, as John MacGregor explains.

Dr Paavo Airola was once the best-known health expert in the United States. His books were international best-sellers. In 1983 Dr Airola offered to publish a health book I had written in the US.

We corresponded to this end for some time. But then he stopped writing. Weeks went by, then months. Eventually I assumed that Dr Airola had got cold feet.

Little did I realise how cold. Ultimately a letter arrived from his office.

America’s most acclaimed longevity specialist – author of How To Get Well and How to Keep Slim, Healthy and Young With Juice Fasting – had died of a stroke at 64. This was more than a decade short of 74.5, the average age of male mortality.

Paavo Airola had opened the batting for an epidemic of premature death among longevity experts.

Next cab off the rank, in 1985, was Nathan Pritikin – who suicided as leukemia overtook him, at 69. Australian health writer Ross Horne, a friend of Pritikin’s, says he would have lived years longer had he only embraced ‘Man’s natural diet’, fruitarianism.

T.C. Fry – leader of the Natural Hygiene movement in the US – did exactly this, when ill-health hit him in his late sixties. He even died a fruitarian: at the age of 70, of a pulmonary embolism.

Longevity experts seem to expire earlier than everyone except rock stars – who leave us, according to a recent US survey, on average at 36.9 years.

But rock stars can have dangerous lifestyles. (Of the 317 surveyed, 40 died of drug overdose, 36 suicided, 22 died in plane accidents, and 18 were murdered.) Longevity experts should have no such excuse.

So how to explain this epidemic? Was exercise the missing ingredient? Probably not: most of these people at least walked a lot. Paavo Airola was a jogger.

So, too, was Jim Fixx. Indeed Fixx founded the jogging cult in the USA, with his 1977 Complete Book of Running. One chapter is a scorching repudiation of a Playboy article titled Jogging Can Kill You.

In 1984 Jim Fixx was felled by a heart attack as he jogged through the streets near his home. He was 52.

Should Fixx have read up on the world famous brothers, Drs William and Evan Shute, who proclaimed that heart disease could be prevented with Vitamin E?

Maybe not. In 1981, whilst continuing to lecture on the prevention of heart disease with Vitamin E, Dr William Shute developed heart disease, and died after a bypass operation. Dr Evan Shute pre-deceased him by a short period.

The author JI Rodale – founder of Prevention magazine – had a more comprehensive answer to the problem of heart disease, and other illnesses. He preached a spectrum of minerals and vitamins, and an organic diet. I asked American raw food writer Bob Avery how Rodale’s story ended:

“He died of a heart attack during taping of the Dick Cavett TV talk show, shortly after he had completed his interview. He was 72. During the interview he stated his intention to live to 100. The talk show host thought he had dozed off in his chair.”

George Ohsawa, inventor of Macrobiotics (“the way of long life”) had a more comprehensive approach still: embodying spiritual as well as nutritional values. He expired of lung cancer at 73.

Adelle Davis sold ten million copies of Let’s Eat Right and a string of other best-sellers through the 1960s and 1970s. Davis came from the ‘high protein’ generation which preceded today’s high carbohydrate orthodoxy. She used to say she had never seen anyone die of cancer who drank a quart of milk a day, as she did.

Adelle Davis died of cancer in 1974, aged 70. The average age of female mortality is 81.

A serious high protein aficionado was author Vilhjalmur Stephansson, who ate an all-meat diet. He developed serious cardiovascular disease [Anthony's note: Stephansson died of a stroke at 82].

Britain’s Sir Francis Chichester, lone sailor and fitness book author, died of spinal cancer in 1972, aged 70. American health author Dr Stuart Berger, who advocated vitamins, minerals and exercise, died of a heart attack at 40.

A few longevity experts did live long lives. (Paul Bragg, 95. Dr Norman Walker, 108-117, depending on whom you believe). [Anthony's note: Bragg's true birth date is controversial, while several Internet sources cite Walker's true age of passing as 99] But most did not even make the average for their gender – let alone the ton. And most made large amounts of money from telling us how to prolong our lives.

So what killed them? Perhaps the high-carbohydrate diet helped dispatch some. (As we shall see next week, this orthodoxy is now coming into question). Others, like Paavo Airola, had health traumas early in life. But that’s not an excuse for the pattern. (The SAD eaters whose deaths make up the averages were exposed to a comparable range of stresses.)

And there were, of course, those who just did not follow their own rules.

I asked veteran American health writer Ric Lambart about Adelle Davis:

“She simply led a very self-destructive life. She did some of the very same things she urged others not to do: smoke and drink… In fact, when I first met her, it was Paavo who introduced us, and he had to locate her in a busy hotel – so he went right to the bar, where she was engaged nurturing a drink that was clearly not some sort of fruit drink.”

Ric also had something to say about that least considered factor contributing to early death: chronic stress. Herbert Shelton – the first doyen (before TC Fry) of the Natural Hygiene movement in the US – was perennially hounded by the medical establishment. Shelton “…never got out from behind the “eight ball,” stress-wise… He was constantly overworked and engaged in extreme legal warfare. The medical establishment over here did all they could at every turn to put him out of business and in prison.”

But there was also the fact that Shelton “apparently did not consume a natural diet himself.”

Ric Lambart also knew TC Fry:

“Terry Fry…was under unrelenting stress and never got out of one legal battle or confrontation before he was engaged in a new one. He spread much good information, though, so should be considered as one of those who contributed some good gospel to the Alternative Health field. He burned his candle at both ends, so, almost predictably, passed away prematurely.”

Most of the above pundits condemned ‘crackpot’ and ‘fad’ diets (that is, diets other than their own). To be fair, some of them undoubtedly contributed a piece or two to the slow-forming jigsaw of health. (Even getting people to think about nutrition in the 1950s and 1960s was an achievement.)

Collectively, however, their premature exits cast a humbling shadow over our present certainties. Are dietary principles as transient as those of (say) political correctness?

Perhaps these mournful departures should make us more modest in our assessment of our own understanding. And less fevered in our judgement of those who differ from us.

In the coming weeks we’ll look at a range of exciting new ideas in health. Hopefully they will give you some ‘Eureka moments’, as they did me.

But it would be good to remember that no-one has a monopoly on knowledge. Many who have have thought themselves to be on the one true path have found out otherwise in their final hours.

—

Anthony Colpo is a distinctly non-guruish independent researcher, physical conditioning specialist, and author of the groundbreaking books The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Breaking News: Men Like Big Breasts

Anthony Colpo — Fri, 27 Aug 2010 02:20:41 +0000

Every now and then, I take time out from researching critical topics such as health, athletic performance and longevity to tackle the issues that really matter. And so do French researchers, judging by some research recently sent my way.

Nicolas Gueguen and his assistants from the Universite´ de Bretagne-Sud in France, pondered an issue that has troubled great minds for millennia: Do men really have an evolutionary hard-wired preference for well-endowed women, or is this just a baseless myth promulgated by the folks who produce beer commercials and Snap-On® calendars?

Being the meticulous professionals they were, they didn’t rely on hearsay, the dubious claims of self-proclaimed ‘breast gurus’, or the opinions of clueless Internet forum participants. Instead, Gueguen and his helpers did what any good research group would do: they headed out into the field to test the hypothesis under controlled conditions.

Wonder Bra Works Wonders at the Bar

In the first experiment, a 20-year-old female sat in a nightclub located in an area popular with young tourists. She was selected for the experiment because male students rated her physical attractiveness as “average“ and because she usually wore an ‘‘A’’ cup bra, the smallest cup size in France. This allowed researchers to create three different experimental conditions by modifying the size of her bra cup: “A” cup, ‘‘B’’ cup (average cup size in France) and a ‘‘C’’ cup (bigger than average cup size).

Except for the type of bra used, the 20-year-old decoy wore the same clothes: a pair of neat jeans, light-coloured sneakers and a white figure-hugging sweatshirt that highlighted her bust.

The young lady was instructed to sit in the nightclub by herself for an hour and to not make eye contact with any of the guys. An inconspicuous observer watched her and noted the number of men who approached her. Whenever a man made contact with her, she told him she was waiting for her boyfriend, a strategy which previous research had shown to be an effective method for immediately ending the interaction.

In the second experiment, the same girl wearing the same clothes and bras sat with a drink at a table outside a bar in the same part of town. Again, she was instructed to stay in the same place for an hour while an inconspicuous observer noted the number of men who approached her. If a man approached, she was instructed to feed the poor bloke the same “I’m waiting for my boyfriend” line.

So what did the results of this epic study find?

In the first experiment, 13 guys approached the girl when she was wearing an A cup and 19 approached when she sported a B cup. When she donned the C cup, the number of approaches jumped markedly; 44 blokes hoping for a little holiday action went over to talk to her.

In the second experiment, 5, 9 and 16 guys approached her in the A, B, and C cup conditions, respectively.

And yes, the results were statistically significant.

Hey Honey, Going My Way?

In another experiment, the same girl stood by the side of a road and held her thumb out in the universal hitchhiking gesture. Hitchhiking is legal in France and, according to one previous study, 78% of French people have hitchhiked (they must be a very trusting lot in France). To help guard against any hairy situations, a male observer hid 30 meters from where the girl stood; his assistance was not required during the experiment (replicating this study in the USA or Australia would likely demand armed SWAT officers and high speed pursuit vehicles, and their assistance probably would be required).

Anyway, each time 100 cars had passed, the girl changed her bra size. Two observers sat in a car 500 meters behind counting the number of motorists that stopped. Because the “I’m waiting for my boyfriend” line wouldn’t have made much sense in this scenario, the girl instead told the motorists she was conducting an experiment on hitchhiking and thanked them for their help.

When the results were tallied, 14.92% and 17.79% of passing motorists stopped to offer a lift when the girl was wearing the A and B cup bras, respectively. When she wore the C cup bra, 24% of passing motorists pulled over to offer a ride. The difference between the A and C bras was statistically significant. The extra ride offers all came from men; altering bra cup size made no difference in the number of female motorists who pulled over.

Researchers found bigger cup size greatly increased hitchhiking success rate

Other methods didn’t work so well.

Don’t Blame Men, it’s in their Genes

These are hardly the first studies to indicate a male preference for larger breasts, although they are the first, to this author’s knowledge, to test this preference in the field in such a controlled manner. Previous research has found men value physical attractiveness more than women (for all you sneering, politically correct, anti-male types, it’s worth remembering women don’t score so well on the shallowness scale either, with financial prospects and social status of potential male suitors receiving similarly high priority. Yep, evolution has seen to it that both males and females have evolved to be exceedingly superficial…).

From an evolutionary perspective, the male is under pressure to disseminate his genes. Men may have thus evolved to seek partners that maximize their chances of gene transmission, in the same way that females appear to have evolved with a preference for partners with higher status to maximize the survival and replication prospects of both themselves and their offspring. The researchers postulate that large breasts attract males at a subconscious level because they are considered a highly feminine trait and perceived as a sign of fertility.

Nobel Prize, Please

So there you have it – proof that scientists are not all a bunch of socially inept nerds holed up in laboratories studying the fibre composition of insect wings. Some researchers really are toiling away in a heroic effort to uncover the truths that monumentally impact the future destiny of the human species.

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Additional reading
For those fascinated by the topic of human attraction and mate selection, Ricardo Carvalho has compiled an extensive list of studies at his Canibais e Reis blog, many with free full text access. You can access the studies, including the full texts of the studies cited in this article, here.

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References

Gueguen N. Women’s bust size and men’s courtship solicitation. Body Image. 2007 Dec; 4 (4): 386-390.

Guéguen N. Bust size and hitchhiking: a field study. Perceptual and Motor Skills, 2007 Dec; 105 (3 Pt 2): 1294-1298.

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Using Caffeine to Boost Athletic Performance

Anthony Colpo — Mon, 23 Aug 2010 03:37:17 +0000

(Almost) Everything You Need To Know About Caffeine and Sports Performance

Caffeine is one of humankind’s oldest drugs – and the most widely used. While coffee consumption is not believed to have begun in earnest until the 15th century, researchers believe caffeine itself may have been consumed as early as 700,000 years ago. Prehistoric humans got their caffeine fix, not by firing up their Mr Coffee® espresso machines, but by chewing on the seeds, leaves and bark of caffeine-containing plants.

Some 90% of adults in the United States consume caffeine daily, in the form of coffee, tea, soda, and energy drinks. US adults ingest an average of 3 mg/kg (225 mg for a 75 kg person) of caffeine daily.

One of the reasons caffeine-containing beverages and foods have enjoyed such enduring popularity is because of caffeine’s stimulant effects. These properties have not gone unnoticed by the athletic community, and caffeine has enjoyed a long history of use as an ergogenic aid.

Despite this long history, confusion reigns when it comes to caffeine and sports performance. How much caffeine is necessary to produce performance-enhancing effects? Exactly when should you take caffeine to enjoy a performance boost? Do the ergogenic effects of caffeine diminish with regular use? Will caffeine boost your maximum strength, or only your endurance?

I recently sat down and poured through some interesting studies and reviews on the topic of caffeine and athletic performance and figured I’d share the key findings with my readers. Before I do that though, there’s something we need to clear up.

Coffee versus Caffeine

While coffee and caffeine have become nearly synonymous in common parlance, it goes without saying the two are not the same thing. Caffeine (1,3,7-trimethylxanthine) is just one of many compounds found in coffee. Most of the research examining the effects of caffeine on sports performance has employed isolated caffeine in the form of anhydrous caffeine capsules; caffeine gums, gels, and caffeine-containing energy drinks have also been studied. Despite its universal consumption, few studies have examined the ergogenic effect of actual coffee.

Whether coffee offers the same ergogenic benefits as caffeine is a point of contention. I was in Borders the other day browsing through a popular US bodybuilding magazine when I came across an article flatly inisting coffee offered none of the ergogenic benefit imparted by caffeine. The author’s evidence for this claim appeared to be a single Canadian study published in 1998. Let’s take a look at this study, then the other studies involving coffee and athletic performance.

Is Coffee an Ergogenic Dud?

Graham et al from University of Guelph in Ontario, Canada, compared the effects of coffee versus caffeine in a double-blind fashion in nine young adults who were active endurance runners[1]. On five separate occasions, the subjects consume either a placebo capsule with water, a caffeine capsule with water, decaffeinated coffee, decaffeinated with added caffeine, or regular coffee.

In all three caffeine trials, the caffeine dose was 4.45 mg/kg body weight (i.e., 334 mg for a 75 kg person) and the volume of liquid was identical. One hour after consuming the caffeine/coffee/placebo, the subjects jumped on a treadmill and ran at 85% of maximal oxygen consumption (VO2max) until voluntary exhaustion. The subjects were instructed to abstain from all caffeine-containing foods and beverages for 48 hours prior to each treadmill trial, to prepare as they would for an athletic competition (i.e., well rested, consuming a high-carbohydrate diet) and to prepare for each trial in an identical fashion.

Plasma concentrations of caffeine and paraxanthine (the major metabolite of caffeine) were similar in all three caffeine trials 60 minutes prior to, at the start of, and at the completion of exercise. Despite this, only ingestion of the caffeine capsules resulted in a significant increase in time-to-exhaustion (7.5-10 minutes compared with with the other four trials). There was no difference in time-to-exhaustion between the placebo, decaf, decaf+caffeine capsule, and regular coffee trials. These observations led the researchers to speculate that one or more of the numeorus compounds found in coffee may counter the ergogenic effect of caffeine.

However, the findings of Graham et al have not been replicated by other researchers.

McLellan and Bell, for example, took thirteen physically active subjects and had them consume on separate occasions:

Decaf coffee + placebo capsule
Decaf + caffeine capsule
Coffee (1.1 mg/kg caffeine) + caffeine capsule (5 mg/kg)
Coffee + caffeine caspule (3 mg/kg)
Coffee + caffeine capsule (7 mg/kg)
Colored water + caffeine capsule (5 mg/kg)

The subjects consumed the beverages 90 minutes prior to exercise testing. The capsules were consumed 30 minutes after the beverages, 60 minutes prior to the tests. The study was performed in double-blind fashion. Times to exhaustion were significantly greater for all trials with caffeine versus placebo. Mean exercise times (in minutes) were, in the same order as above:

21.7
29.0
27.8
25.1
26.4
26.8

McLellan and Bell, in other words, found no inhibitory effect of coffee on the performance-enhancing action of caffeine[2].

Nor did Wiles et al, who examined the effect of coffee on 1500 meter treadmill running. On separate occasions, eighteen male athletes were given 3 grams of coffee (containing approximately 150-200mg caffeine) or 3 grams of decaf 60 minutes prior to three different exercise trials[3]. These trials tested the following outcomes:

Time taken to complete a 1500 m run;
The speed at which athletes completed a 1-minute ‘finishing burst’ at the end of a high-intensity run;
Respiratory factors, perceived exertion and blood lactate levels during a high intensity 1500-m run.

The results showed that ingestion of caffeinated coffee decreased the time taken to run 1500 m, increased the speed of the ‘finishing burst’, and increased VO2 during the high-intensity 1500-m run. The average mean time to complete the run was 4.2 s faster following the ingestion of caffeinated coffee, with 14 of the 18 subjects experiencing faster mean times after the ingestion of caffeinated coffee. All ten of the subjects performing the second trial recorded faster speeds (mean speed increase = 0.6 km/h) during the final minute of their run after ingesting caffeinated coffee. In the third test, all six participating subjects produced a higher mean VO2 during the caffeinated coffee runs.

The celebrated exercise physiologist David Costill and co-workers also examined this issue way back in the 1970s[4]. They took nine competitive cyclists (two females and seven males) into the lab, and made them ride until exhaustion on a bicycle ergometer at 80% of VO2 max. One trial was performed an hour after ingesting decaf coffee, the other was performed one hour after consuming coffee containing 330 mg of caffeine. After taking the caffeinated coffee, the subjects were able to perform an average of 90.2 minutes of cycling as compared to an average of 75.5 minutes in the decaf trial.

The results of Graham et al, therefore, appear to be an anamoly. One posited explanation is that coffee beans from different regions and producers may vary widely in their content of non-caffeine components, and that the coffee used in the Canadian study may have featured an unusually large amount of substance/s with the potential to impair the actions of caffeine. In cell culture studies, de Paulis et al found certain derivatives of chlorogenic acid produced during the roasting of coffee interfered with the binding of caffeine to adenosine receptors. When high doses of these compounds were given to mice, the poor little buggers subsequently exhibited less activity and movement when placed in an open field box [5]. In earlier research, Tse isolated a cholinergic compound from both regular and decaffeinated coffee, purified it, and observed that injecting it into rats produced an abrupt decrease in blood pressure and heart rate[6].

Exactly what this all means in humans is unclear. Three of the four studies I could find examining regular coffee have found a performing enhancing effect. However, if you are using caffeine to boost performance before an important competitive event, and want to maximize the chances of experiencing such an ergogenic effect, the use of caffeine (i.e. NoDoz) rather than coffee would be wise.

Caffeine Study Results: Wide Variability

Another important point to keep in mind as we review the ergogenic effects of caffeine on performance is that research results in this area are subject to annoyingly wide variation, which makes it difficult to impart blanket recommendations.

For example, the research in its entirety supports ergogenic caffeine doses of 3-6 mg/kg, with dosages of 9 mg/kg typically showing no extra benefit. In fact, in some users the latter amount may impair performance due to negative effects such as confusion, light-headedness and an impaired ability to concentrate. But on an individual level, responses can vary widely. A study by the aforementioned University of Guelph team examined 3, 6 and 9 mg/kg doses of caffeine in non-users, low-users and regular consumers of caffeine and found no relationship between habitual use and effective dosage. The subjects, all well-trained distance runners, were instructed to abstain from caffeine for 48 hours prior to running to exhaustion at 85% VO2max.

Overall, the best results were seen with doses of 3-6 mg/kg, with 9 mg/kg delivering a lower mean improvement that was not statistically significant from placebo. However, these were the mean results of the group as a whole; individually, the data were not so clear cut. Two subjects, both caffeine users, had their best result with 9 mg/kg of caffeine, whereas three subjects actually ran longer with placebo than with 9 mg/kg of caffeine. The heaviest caffeine user had his longest run after 3 mg/kg of caffeine but the two nonusers in the study exhibited the greatest endurance with 6 mg/kg of caffeine. One subject had been previously tested in the same laboratory and had run a whopping 25.2 minutes longer with 9 mg/kg of caffeine than with placebo. Two years later he ran 21.15 min longer at the same power output. Some subjects, especially the lightest users and nonusers, complained of mental confusion and an inability to focus with the highest dose[7]. Given the results on this and numerous other studies, most folks should stick with doses of 3-6 mg/kg.

Several factors could contribute to the wide variation in caffeine/athletic performance research results, which we will discuss later. Those interested in using caffeine as an ergogenic aid are advised to read what follows remembering that it is a generalized summary, consult the cited research, then experiment with caffeine in their training to arrive at a protocol that works for them on contest day.

I would also like to emphasize that the information that follows is intended for healthy adults only. Athletic children and teenagers should focus on developing healthy nutrition habits (namely, a diet primarily of nutrient- and antioxidant-rich whole foods containing sufficient calories, protein, carbohydrates, essential fatty acids and appropriate non- stimulant supplements) and developing the skills and physical and psychological qualities necessary for optimal performance in their chosen sport.

Caffeine and Endurance

The first review I’ll summarize was published in the January 2009 issue of Journal of Strength and Conditioning Research[8]. Ganio et al sought to determine the effect of caffeine on sports endurance performance. Rather than gather up every single study they could find, they specifically sought out studies involving time trial formats rather than time-to- exhaustion tests. Many studies involving caffeine and endurance involved subjects given caffeine or a placebo then instructed to perform at a set pace or %VO2max for as long as possible. While this kind of test can indeed help to identify ergogenic effects, it bears little resemblance to real life sport activities, most of which are conducted over a set distance or within a set time frame. Ganio and colleagues, therefore, scoured the literature for studies examining the effect of caffeine on time-trial endurance (equal to or greater than 5 minutes). Their literature search revealed 21 eligible studies containing 33 trials.

Thirty of the 33 trials showed positive improvements in performance with caffeine, but only 15 were statistically significant (p 0.05 or less). The mean improvement in performance with caffeine ingestion was 3.2%; however, this improvement was highly variable between studies (-0.3 to +17.3%), possibly due to such factors as ingestion timing, ingestion mode, and subject habituation. The largest mean improvement (4.4%) was observed in studies involving stationary cycling, but again this may have been due to the much larger number of studies employing this mode of exercise compared to running, rowing, skiing and swimming.

The ingestion of caffeine was similarly ergogenic regardless of whether it was ingested around 60 minutes before or during exercise. The mean improvement was slightly greater when caffeine was ingested both before and during exercise (4.3%) compared with only before exercise (2.3%), but again this may be attributable to a greater number of trials examining the latter condition and/or wide variability.

The amount of caffeine commonly shown to improve endurance performance is between 3 and 6 mg/kg body mass; these amounts are equally effective when combined with a carbohydrate/electrolyte solution or water. Performance improvements with caffeine are maximized with amounts up to 6 mg/kg and are not generally improved with 9 mg/kg.

Early research suggested that the ergogenic effect of caffeine was due to increased fat oxidation and subsequent sparing of muscle glycogen. However, more recent research suggests that caffeine affects endurance performance largely through its antagonist effect on adenosine receptors in the brain. Acting through this mechanism, caffeine may modulate central fatigue and influence ratings of perceived exertion, perceived pain, and levels of vigor, all of which may lead to performance improvements. Caffeine is able to cross the blood-brain barrier and is a powerful antagonist of adenosine receptors in the central nervous system. As a result, caffeine counteracts the inhibitory effects of adenosine on neuroexcitability, neurotransmitter release, and arousal.

Chronic caffeine consumption in animal models results in upregulation of the number and an increase in the affinity of adenosine receptors within the central nervous system. This may result in an increased amount of caffeine needed to have the same antagonist activity on the receptors (termed ‘‘caffeine habituation’’). It is possible that the varied degree of improvements observed between studies may be attributable to lack of control over subject habituation.

The ergogenic effects of caffeine may be more pronounced in those who do not or rarely consume caffeine, whilst habitual users may require stronger doses to get an ergogenic effect. Bell and McLellan compared the effect of 5 mg/kg caffeine at 1, 3 and 6 hours prior to rides to exhaustion (in all the trials, Gatorade was also consumed 1 hour prior) and found that increases were greater for caffeine non-users (<50 mg caffeine per day) vs. users (>300 mg caffeine per day). Furthermore, the effect of caffeine in the nonusers was still evident 6 hours after ingestion of the drug, whereas in the users this was not the case[9].

It is not known how many days an endurance athlete should abstain from caffeine to maximize its ergogenic effects. Animal studies show increases in adenosine receptor number and affinity are maximized in seven days. Therefore, researchers recommend athletes abstain from caffeine ingestion for at least 7 days before competition. This should allow forwithdrawal symptoms (which may negatively affect performance) to subside and allow sufficient time for adenosine receptor downregulation to occur.

Caffeine in Power, Strength and Team Sports

The ergogenic effect of caffeine on endurance performance is well-known and widely accepted, but whether caffeine benefits power and strength-type activities is another story. While caffeine routinely enhances time-to-exhaustion and time trial performance in bouts lasting over 5 minutes, a performance-enhancing effect on shorter duration activities, or on repeated intermittent sprint activities is more elusive.

Does Caffeine Boost Strength?

If you’re hoping a couple of pre-workout espressos will help you set a new PR on the bench or squat, you’re bound to be disappointed. Yours truly found three studies examining the effect of caffeine on 1RM during dynamic weight training (the kind you and I perform in the gym with free weights and plate-loaded machines, as opposed to aeronautical-looking EMG-equipped laboratory apparatus).

Astorino and Rohman tested the effect of caffeine (6 mg/kg, 60 minutes prior to exercise) on one-repetition maximum in the bench press and leg press. The subjects were resistance trained men with a mean daily coffee consumption of 110 mg. No difference in bench press or leg press 1RM strength was observed; eleven men lifted at least 10 kg more weight with caffeine, yet 8 lifted more with placebo, and 3 showed no difference between treatments[10].

Beck et al found that a supplement containing numerous ingredients (guarana, green/black tea extract, various herbs, vitamin C, B vitamins, cinnamon) including caffeine at a dose of 2.4 mg/kg taken 60 minutes preexercise increased bench press 1RM by a mean 2.1 kg in men regularly participating in strength training. However, no change was observed in leg extension 1RM nor mean and peak power from the Wingate test. Two minutes after testing for their 1RM on the bench and leg extension, each subject performed a set to failure with 80% of their 1RM. Caffeine had no effect on the total volume of weight lifted (80%RM x repetitions achieved) in the leg extension, but resulted in a small and statistically non- significant 5% increase in bench press total volume[11].

While the tiny 2.5 kg increase in bench press 1RM met the mathematical criteria for “significance”, seasoned lifters would hardly consider a 2.5 kg gain significant; natural strength can easily vary from day to day by this amount. Furthermore, the study design precludes embracing these results as proof of caffeine’s ergogenic effect. Because of their short duration, it is feasible (and common) for caffeine studies to be performed in “crossover” fashion, i.e. each subject undergoes placebo and caffeine treatments on separate occasions. This study, however, used a protocol in which all subjects underwent initial testing, then 48 hours later were randomized to either a placebo or caffeine group. Hence, the 2.5 kg gain in the bench press could easily have been due to a “learning” effect in some individuals from having performed a 1RM in the bench only 2 days earlier.

When the same researchers later tested a similar supplement, this time using a crossover protocol (so that all subjects were tested in both the placebo and caffeine conditions), they found no differences in bench press 1RM (nor running time to exhaustion)[12]. For some reason, the researchers used untrained subjects in their second study, introducing a new variable (lack of regular training) that may or may not have confounded the results. Nevertheless, the evidence for any claim that caffeine may increase maximal strength must be considered extremely weak.

Caffeine may however increase performance in later bouts of higher intensity activities. To address this issue, Astorino et al recently reviewed caffeine studies involving resistance training, team sports (which often feature intermittent bursts of intense activity) and power-based activities[13].

Eleven of 17 eligible studies revealed significant improvements in team sports exercise and power-based sports with caffeine, but the effects were more common in elite athletes who did not regularly ingest caffeine. Mean improvement in these studies was 6.5%.

As for resistance training, six of 11 studies revealed significant caffeine-induced improvements, usually in the form of increased number of repetitions or higher EMG-measured torque.

Caffeine dosages used in the positive studies ranged from 110 mg to 7mg/kg body weight.

Again, there was considerable variability across studies, suggesting only some individuals may experience improved performance with acute caffeine intake.

One potential explanation for the equivocal data regarding caffeine’s ability to alter high-intensity exercise may be differences in subjects’ training status. Of the studies revealing a significant improvement in short-term high-intensity exercise performance, many included trained athletes and not untrained, recreationally active, or weight training college students. It is likely that athletes have greater motivation to perform fatiguing exercise and can provide more consistent performance day-to-day , which may reduce variability and thus increase statistical power. In some studies, subjects were low-caffeine consumers (<100 mg per day) which may have potentiated the ergogenic effect of the drug compared with subjects tolerant to the effects of caffeine.

Also, most of the research with caffeine is conducted in free-living subjects who are instructed to refrain from caffeine for a set period prior to the start of the experiment and to maintain their usual dietary and lifestyle habits prior to each experimental trial. However, as the subjects are not living in a closely monitored ward situation, their exact compliance with these requirements is not known.

An additional explanation is that genetic variation may at least partially explain differences between individuals in their response to caffeine. Research suggests that variations in genotype may alter caffeine metabolism and possibly the magnitude of performance in response to caffeine. Caffeine is metabolized in the liver by cytochrome P450 1A2, which shows marked variation between individuals. A single substitution in the gene causes some persons to be “slow” caffeine metabolizers, whereas those who are homozygous for the allele metabolize caffeine more rapidly. The elucidation of exactly what influence genetic factors have upon the individual performance response to caffeine requires further research.

Further Considerations for the Athlete

Caffeine Abstinence Before Competition

As a strategy, if the athlete decides to stop consuming caffeine before competition to optimize its benefits during competition, he or she should reduce caffeine consumption at least 1 week before competition to be completely free from withdrawal effects. To avoid negative effects on training, the dose should be gradually reduced over 3 or 4 days, instead of quitting abruptly. Resuming caffeine on the day of competition will again provide the desired ergogenic effects, as it would for a nonuser.

Caffeine Effects and Hydration Status

The common belief that a diuretic effect of caffeine leads to dehydration and causes impaired athletic performance has been disproved by numerous studies[14]. A recent study examined body fluid, temperature regulation or electrolyte indices during twelve days of controlled caffeine ingestion (3 mg/kg caffeine daily for the first 6 days, and either 0, 3 or 6 mg/kg on days 7-12). On day 12, the subjects walked for 90 minutes on a 5% gradient in 37.7C heat. No changes were noted in the aforementioned indices[15,16].

Caffeine and Post-Workout Recovery

A recent study by researchers at RMIT University over the border in my old home Victoria, examined the effect of consuming caffeine, not pre-workout, but post-workout[17]. The aim of the study was to see what effect this had on glycogen replenishment after exhaustive exercise. On the evening prior to the experiment, seven endurance-trained cyclists and triathletes performed high intensity intermittent cycling and then consumed a low-carbohydrate meal to induce a glycogen-depleted state. The following morning subjects reported back to the lab and rode until volitional fatigue.

Upon completion of this ride subjects consumed either carbohydrate or the same amount of carbohydrate plus caffeine during four hours of passive recovery. A total of 4 g/kg of carbohydrate was consumed within 5 minutes of stopping exercise and again after 60, 120 and 180 minutes. During the caffeine trial, the same carbohydrate ingestion regimen was followed along with a total of 8 mg/kg caffeine administered in two equal doses immediately post exercise and after 2 hours of recovery. Muscle biopsies and blood samples were taken at regular intervals throughout recovery. Muscle glycogen levels were similar at exhaustion and increased by a similar amount (~80%) after 1 h of recovery. After 4 hours of recovery, however, the carbohydrate + caffeine treatment resulted in higher glycogen accumulation (313 vs. 234 mmol.kg-1 d.w., P<0.001). The overall hourly rate of re-synthesis for the 4 hour recovery period was 66% higher with the caffeine treatment.

So should you start chugging down coffee and NoDoz after glycogen-depleting exercise? That depends on how sensitive you are to caffeine, and whether you prefer to spend your evenings sleeping soundly or staring wide-eyed at the ceiling. According to the researchers, several of the athletes in the study reported difficulty sleeping the night after the trial, hardly surprising seeing they’d consumed the equivalent of 5-6 cups of strong coffee. Several of the others, however, fell asleep during the recovery period and reported no adverse effects. As one of the researchers noted, the next logical step is to repeat the study using a lower dosage of caffeine and see if enhanced glycogen resynthesis still occurs[18].

Unless you are going to be performing a second bout of intense exercise later in the day, my advice would be to reserve caffeine for pre-event use (and peri- in the case of longer events).

Caffeine and Creatine

Creatine has become one of the most popular supplements among strength athletes and recreational weight trainers. In early studies showing ergogenic effects of creatine, the powdered creatine was often mixed into warm drinks such as tea (which contains caffeine, albeit at much lower amounts than coffee) to increase solubility. So it was rather surprising when a couple of subsequent papers claimed caffeine impaired the absorption/actions of creatine.

The first of these studies was published in 1996[19]. Nine recreationally active males were studied before and after 6 days of placebo, creatine (0.5 g/kg daily), or the same dose of creatine plus caffeine (5 mg/kg daily). The subjects were then tested on an isokinetic leg extension dynamometer; testing consisted of three consecutive maximal isometric contractions and three interval bouts of 90, 80, and 50 maximal voluntary contractions performed with a rest interval of 2 minutes between bouts.

Muscle ATP concentration remained constant over the three experimental conditions, while creatine and creatine + caffeine increased muscle phosphocreatine concentration by 4-6%. Dynamic torque production was increased by 10-23% by creatine but was not changed by creatine + caffeine. Torque improvement during creatine was most prominent immediately after the 2-minute rest between the exercise bouts. According to the researchers, who initially expected that caffeine would enhance the effects of creatine, “The data show that [creatine] supplementation elevates muscle [phosphocreatine] concentration and markedly improves performance during intense intermittent exercise. This ergogenic effect, however, is completely eliminated by caffeine intake.”

In order to understand why caffeine would impair the effect of creatine supplementation, the researchers conducted another study[20]. Ten students were assigned in random crossover fashion to five experimental protocols, each lasting 8 days and separated by a washout period of 5 weeks (muscle creatine levels return to baseline around 4-5 weeks after cessation of supplementation). Exercise tests were performed before and after creatine supplementation (4 × 5 g/daily for 4 days), short-term caffeine intake (5 mg/kg daily for 3 days), creatine supplementation + short-term caffeine intake, acute caffeine intake (5 mg/kg) or placebo.

Maximal torque, contraction time from 0.25 to 0.75 of maximal torque, and relaxation time from 0.75 to 0.25 of maximal torque were measured during an exercise test consisting of 30 intermittent quadriceps contractions (2 seconds stimulation, 2 seconds rest) induced by electrical stimulation. Compared with placebo, creatine shortened relaxation time by 5%; in contrast, caffeine increased relaxation time by 10%. When caffeine was combined with creatine, relaxation time increased by 7%.

Skeletal muscle relaxation after a contraction is initiated by a reduction in sarcoplasmic calcium ion concentrations, and the researchers speculated that caffeine may interfere with this process in a detrimental manner. Relaxation time increases as a muscle fatigues, and in this study caffeine amplified the effect of fatigue on relaxation time. As the researchers point out, theoretically muscle relaxation rate is important to power production during sprint-type exercise. During fast repetitive concentric muscle contractions, recovery time from the previous contraction is critical to maximal force output during the next contraction.

However, this study involved subjects whose muscles were wired up and given electrical stimulation to induce contraction. Neither this nor the previous study measured power output or performance during a “real life” activity such as cycling, running, or dynamic weight lifting. If these results held, then performance in subsequent bouts of maximal sprint exercise would be expected to be impaired by caffeine. While one oft-quoted study did indeed show a statistically significant reduction (7%) in peak power output on the last of 4 x 30 second “Wingate” sprints following caffeine ingestion[21], numerous other studies involving Wingate protocols have shown no difference; some have even found benefit.

Vanakoski et al studied seven trained athletes in a randomized, placebo-controlled, double-blind crossover fashion[22]. The treatments were: placebo, a single oral dose (7 mg/kg) of caffeine, repeated oral doses (3 x 100 mg/kg daily) of creatine for 3 days, or the combination of caffeine and creatine before physical exercise. Supplement administration was followed 70 minutes later by 3 repetitive 1-minute exercise bouts on a stationary bike at maximal speed. This was followed by 45 minutes of cycling at a constant speed and workload. Neither creatine nor caffeine, alone or in combination, improved maximal pedaling speed, maintenance of maximal speed or total work output during the 1 -minute bouts, when compared with placebo.

Contrasting results were obtained by British researchers who had fourteen trained male subjects perform treadmill running to exhaustion at an exercise intensity equivalent to 125% VO2max. Three trials were performed, one before 6 days of creatine loading (0.3 g/kg daily), and two further trials after the loading period. One hour before the post-loading trials, caffeine (5 mg/kg daily) or placebo was ingested in cross-over, double-blind fashion. The mean time to exhaustion was significantly longer in the caffeine trial (222.1 seconds) than both baseline (200.8 s) and placebo (198.3 s) trials[23].

It’s probably safe to assume that the vast majority of individuals taking creatine are doing so, not for performance enhancement, but for aesthetic bodybuilding purposes. The aforementioned studies were of short duration and tell us nothing about what sort of muscle gain or body composition changes may occur with longer term creatine use.

One study, from the University of Oklahoma, did run for a longer duration, but it involved a supplement containing, not just caffeine and creatine, but several other ingredients[24]. It also did not examine the effects of creatine and caffeine separately. This single-blinded, placebo-controlled study examined the effects of a pre-workout supplement known as Game Time® or placebo combined with three weeks of high-intensity interval training (HIIT) on aerobic and anaerobic running performance, training volume, and body composition[23].

Twenty-four moderately-trained recreational athletes were assigned to either Game Time® (which contains Cordyceps sinensis, Arginine AKG, Kre-Alkalyn, Citrulline AKG, Eleutherococcus senticosus, Taurine, Leucine, Rhodiola Rosea, Sodium Chloride, Valine, Isoleucine, Caffeine, Whey Protein Concentrate) or placebo. The supplement/placebo powders were consumed thirty minutes prior to all testing and training sessions. Training comprised of a three-week HIIT program three days per week, and testing was conducted before and after the training. Each training session consisted of five sets of two-minute running bouts with one minute of rest between each bout.

Both the Game Time® and placebo groups demonstrated significant increases in VO2max from pre- to post-training resulting in a 10.3% and 2.9% improvement, respectively. Critical velocity (maximal running velocity that can be maintained for an extended period of time using only aerobic energy stores) increased for the supplement group by 2.9%, but remained unchanged in the placebo group. Anaerobic running capacity increased for the placebo group by 22.9% and for the Game Time® group by 10.6%. Training volume was 11.6% higher for the supplement versus placebo group. As for body composition changes, bodyfat decreased from 19.3% to 16.1% for the Game Time group and decreased from 18.0% to 16.8% in the placebo group. Lean body mass increased from 54.2 kg to 55.4 kg for the Game Time® group and decreased from 52.9 kg to 52.4 kg in the placebo group (p = 0.694).

Again, it must be noted that this study involved numerous other ingredients and did not separately examine the effects of caffeine and creatine. Also, Game Time® contains 100 mg of caffeine, a much lower dose than what is typically used for ergogenic purposes.

While commentators on both sides of the fence of confidently assert that caffeine “does/does not/does too!” impair the actions of creatine, the research so far is equivocal. More research is required to determine for sure if, and under what conditions, caffeine anatagonizes the actions of creatine.

Summary of Key Points

The amount of caffeine commonly shown to improve endurance performance is between 3 and 6 mg per kg of body weight; these amounts are equally effective when combined with a carbohydrate/electrolyte solution or water.
Acute ingestion should occur around 60 minutes before and, if practical, during competition.
Given the available evidence, endurance athletes should abstain from caffeine use at least 7 days before competition to maximize its ergogenic effect.
Because some individuals react differently to caffeine than others, it is recommended athletes try caffeine while training before using it in competition. In the midst of an important race is not the ideal time to discover that caffeine upsets your stomach or gives you a sudden overwhelming urge to empty the contents of your nethermost regions.
Caffeine research consistently shows improvement in endurance performance. Improvements in team sports and power-type activities are much more erratic. Based on current research, caffeine does not appear to increase maximal strength in weight lifting exercises.

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References

Graham TE, et al. Metabolic and exercise endurance effects of coffee and caffeine ingestion. Journal of Applied Physiology, 1998; 85 (3): 883–889.
McLellan, TM and Bell, DG. The impact of prior coffee consumption on the subsequent ergogenic effect of anhydrous caffeine. International Journal of Sport Nutrition and Exercise Metabolism, 2004; 14: 698–708.
Wiles JD, et al. Effect of caffeinated coffee on running speed, respiratory factors, blood lactate and perceived exertion during 1500-m treadmill running. British Journal of Sports Medicine, 1992; 26: 116-120.
Costill DL, et al. Effects of caffeine ingestion on metabolism and exercise performance. Medicine and Science in Sports and Exercise, 1978 Fall; 10 (3): 155-158.
de Paulis T, et al. Dicinnamoylquinides in roasted coffee inhibit the human adenosine transporter. European Journal of Pharmacology, 2002 May 10; 442 (3): 215-223.
Tse SY. Cholinomimetic compound distinct from caffeine contained in coffee. II: Muscarinic actions. Journal of Pharmaceutical Sciences, 1992 May; 81 (5): 449-452.
Graham TE, Spriet LL. Metabolic, catecholamine, and exercise performance responses to various doses of caffeine. Journal of Applied Physiology, 1995; 78 (3): 867-874.
Ganio MS, et al. Effect of caffeine on sport-specific endurance performance: a systematic review. Journal of Strength and Conditioning Research, 2009; 23 (1): 315–324.
Bell DG, McLellan TM. Exercise endurance 1, 3, and 6 h after caffeine ingestion in caffeine users and nonusers. Journal of Applied Physiology, 2002; 93: 1227–1234.
Astorino TA, Rohmann RL. Effect of caffeine ingestion on one-repetition maximum muscular strength. European Journal of Applied Physiology, 2008; 102: 127–132.
Beck TW, et al. The acute effects of a caffeine-containing supplement on strength, muscular endurance, and anaerobic capabilities. Journal of Strength and Conditioning Research, 2006; 20 (3): 506–510.
Beck TW, et al. The acute effects of a caffeine-containing supplement on bench press strength and time to running exhaustion. Journal of Strength and Conditioning Research, 2006; 22 (5): 1654–1658.
Astorino, TA and Roberson, DW. Efficacy of acute caffeine ingestion for short-term high-intensity exercise performance: A systematic review. Journal of Strength and Conditioning Research, 2010; 24 (1): 257–265.
Sokmen B, et al. Caffeine use in sports: considerations for the athlete. Journal of Strength and Conditioning Research, 2008; 22 (3): 978–986.
Roti MW, et al. Thermoregulatory responses to exercise in the heat: chronic caffeine intake has no effect. Aviation, Space Space, and Environmental Medicne, 2006; 77: 124–129. http://www.simplyfit.com/RS.Thermoregulation.and.Caffeine.pdf
Armstrong LE, et al. Fluid, electrolyte and renal indices of hydration during eleven days of controlled caffeine consumption. International Journal of Sport Nutrition and Exercise Metabolism, 2005; 15: 252-265. http://www.sportsnutritionworkshop.com/Files/32.SPNT.pdf
Pedersen DJ, et al. High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is coingested with caffeine. Journal of Applied Physiology, 2008 Jul; 105 (1): 7-13.
Post-Exercise Caffeine Helps Muscles Refuel. ScienceDaily, July 2, 2008. http://www.sciencedaily.com/releases/2008/07/080701083456.htm
Vandenberghe K, et al. Caffeine counteracts the ergogenic action of muscle creatine loading. J Appl Physiol. 1996 Feb; 80 (2): 452-457.
Hespel P, et al. Opposite actions of caffeine and creatine on muscle relaxation time in humans. J Appl Physiol, 2002; 92: 513–518.
Greer F, et al. Caffeine, performance, and metabolism during repeated Wingate exercise tests. Journal of Applied Physiology, 1998; 85: 1502–1508.
Vanakoski J, et al. Creatine and caffeine in anaerobic and aerobic exercise: effects on physical performance and pharmacokinetic considerations. Int J Clin Pharmacol Ther. 1998 May; 36 (5): 258-62.
Doherty M, et al. Caffeine is ergogenic after supplementation of oral creatine monohydrate. Med Sci Sports Exerc, 2002; 34: 1785–1792.
Smith AE, et al. The effects of a pre-workout supplement containing caffeine, creatine, and amino acids during three weeks of high-intensity exercise on aerobic and anaerobic performance. Journal of the International Society of Sports Nutrition, Feb 15, 2010; 7: 10.

Cycling and Bone Health: Why Cyclists MUST Lift Weights

Anthony Colpo — Sun, 08 Aug 2010 06:38:06 +0000

Ah, cycling – the world’s second most enjoyable activity (if you’re wondering what the first is, this website probably isn’t for you).

There’s something inherently novel and extremely gratifying about being your own engine. Few things match the sense of solitude and tranquility that comes from rolling through beautiful hills, the immense satisfaction of conquering a steep climb, and the sheer exhilaration of howling through corners at 70 km/h on tires barely an inch wide.

Up until recently, I believed there was only one thing preventing cycling from being a truly perfect endeavor: motorists. Regrettably, transport infrastructure in Western countries has been built almost entirely around internal combustion-powered vehicles, with little forethought given to alternative and far more environmentally-friendly forms of transport such as bicycles (to find out how and why this was allowed to happen, I highly recommend Edwin Black’s Internal Combustion). As such, cyclists are typically forced to share the same patch of asphalt as speeding 1800-kilogram missiles, some piloted by individuals with atrocious driving habits and highly questionable mental health.

Lunatics in wayward tin-tops are not the only health hazard to cyclists; the constant pressure on a rider’s reproductive bits, and an associated increased risk of impotence and testicular cancer, attracted scientific and medical scrutiny several years back. Thankfully, anatomically designed saddles that keep your southerly wares healthy are now widely available. But cyclists aren’t out of the woods yet – scientists have discovered another potential health risk associated with cycling.

A bunch of road cyclists led by some guy called Lance.

Cycling and Reduced Bone Density

Andrew Coggan, a senior scientist and exercise physiologist at Washington University in St. Louis, had been cycling one to two hours a day for about 15 years when he crashed in 1989. Coggan suffered a hip fracture during the fall, an injury common in senior citizens. However, Coggan was only 30 years old at the time of his mishap.

“And I recall prior to that,” he says, “when I’d be chatting with a group of cyclists, I’d be taking note of the fact that everybody had scars from things like broken arms and broken collarbones.”[1]

“Sometimes athletes in their late 20s and early 30s will come in for a femur or a hip fracture, and they’ll be surprised because the fall was really not that bad,” says Dr. Max Testa, a sports medicine physician at the Orthopedic Specialty Hospital in Salt Lake City who routinely treats elite cyclists. “But we’ll look at the X-rays and see that there is some osteopenia [lower-than-normal bone density] there.”[1]

As it turns out, the primary culprit is a factor long considered a positive of cycling. It’s a low-impact sport that puts little mechanical load on the bones. That’s great if you have joint problems, but it’s the weight-bearing nature of exercise that stimulates bones to become denser. That’s why weightlifters have far denser and stronger bones than normal folk, while low bone mineral densities are often observed in swimmers and long distance runners[2-5].

Ride Your Butt to the Gym, Pronto!

A study published in 2008 comparing bone mineral density (BMD) in recreational cyclists and runners uncovered some rather disconcerting findings. When people of think of strong healthy bones, runners are often the last group that come to mind; long distance runners have long been considered poster boys for the emaciating effects of excessive endurance exercise. But in this study, the cyclists fared even worse:

The cyclists had significantly lower BMD of the whole body and spine than the runners, despite having similar age, weight, body mass index, body composition, hormonal status, current activity level, and nutrient intakes.
63% of the cyclists had osteopenia of the spine or hip, compared with 19% of the runners.
Cyclists were 7 times more likely to have osteopenia of the spine than runners, controlling for age, body weight, and bone-loading history.

Now that sucks. The researchers concluded that “bone-loading activity should be sustained during adulthood to maintain bone mass”[6]. In other words, get your multi-coloured Lycra-clad butt into the gym and do some weight-bearing activity. Squats (back squats, front squats, jump squats) and deadlifts (conventional, stiff-leg, one-leg) should form the core of your lower body weight regimen. And don’t forget upper body work: bench pressing, rowing, pulldowns, power cleans and snatches, and overhead pressing.

Numerous other studies have also found that, although highly trained and physically fit, serious cyclists frequently exhibit low bone density and may be at high risk for developing osteoporosis with advancing age[7,8].

Even riders at the very top of the sport aren’t immune. In a 1994 paper, German researchers reported BMD measurements in internationally top-ranked weight lifters, boxers, and cyclists. All the cyclists were professionals and some were Tour de France participants. The measurements were carried out by dual-energy X-ray absorptiometry (DEXA) and the results compared with twenty-one age-matched male controls. The BMD of the weight lifters was greater than the controls by a hefty 24% on the anterior-posterior (AP) view and 23% on the lateral view, while difference in BMD between the boxers and the controls was +17% on the AP view and and +19% on the lateral view. But in all the endurance cyclists, the BMD of the lumbar spine was – gulp – 10% and 8% lower in the AP view and lateral view, respectively[9]. Unlike the weightlifters and boxers, the road cyclists performed almost pure endurance training, covering distances of 3,000-10,000 km in low and middle gears during the pre-competition period.

Road vs Track vs Mountain

The BMD risk appears specific to road cyclists. A 2002 paper in Bone journal found that mountain bikers had significantly higher BMD than road cyclists, possibly due to the higher impact nature of their activity[10].

A 2002 study found mountain bikers had significantly higher bone density than road cyclists.
Even when they rode in high heels.

Another study comparing sprint- and distance-trained masters track cyclists found greater lower leg bone strength in the former, and to a lesser degree in the latter, compared with sedentary controls[11]. Sprint cycling is, by its very nature, a more explosive and forceful activity; track sprinters also tend to much more appreciative of the significant benefits of weight training.

The mighty pins of British track cycling champ Chris Hoy. Something tells me his BMD is just fine.

The Bottom Line

Road cycling does wonders for your lungs and muscular endurance, but its effect on bones leaves a lot to be desired. If, like yours truly, you’re a road cycling addict then be sure to set aside some time for weight training. You don’t have to become a gym rat and compromise your training on the bike; 3 whole-body sessions a week, lasting 45-60 minutes, utilizing the basic compound lifts mentioned above will do wonders for your strength and BMD.

—

References

1. Stein J. Cyclists at risk for bone loss. LA Times, February 16, 2009.
http://articles.latimes.com/2009/feb/16/health/he-cycling162. Frost HM. Why do marathon runners have less bone than weight lifters? A vital-biomechanical view and explanation. Bone, Mar 1997; 20 (3): 183-189.
3. Karlsson MK, et al. Bone mineral density in weight lifters. Calcified Tissue International, 1993; 52 (3): 212-215.
4. Mudd LM, et al. Bone mineral density in collegiate female athletes: comparisons among sports. Journal of Athletic Training, 2007 Jul-Sep; 42 (3): 403-408.
5. Magkos F, et al. The bone response to non-weight-bearing exercise is sport-, site-, and sex-specific. Clinical Journal of Sport Medicine, Mar 2007; 17 (2): 123-128.
6. Rector RS, et al. Participation in road cycling vs running is associated with lower bone mineral density in men. Metabolism, Feb 2008; 57 (2): 226-232.
7. Campion F, et al. Bone status in professional cyclists. International Journal of Sports Medicine, Jul 2010; 31 (7): 511-515.
8. Nichols JF, et al. Low bone mineral density in highly trained male master cyclists. Osteoporosis International, Aug 2003; 14 (8): 644-649.
9. Sabo D, et al. Bone quality in the lumbar spine in high-performance athletes. European Spine Journal, 1996; 5 (4): 258–263.
10. Warner SE, et al. Bone mineral density of competitive male mountain and road cyclists. Bone, Jan 2002; 30 (1): 281-286.
11. Wilks DC, et al. Forearm and tibial bone measures of distance- and sprint-trained master cyclists. Medicine and Science in Sports and Exercise, Mar 2009; 41 (3): 566-573.

Reader Mail: HCG Diet, The Great Eades Smackdown, and More!

Anthony Colpo — Wed, 04 Aug 2010 06:31:04 +0000

HCG for Fat Loss: The Potential Side Effects “They” Don’t Want You to Know About

Hi Anthony,

Your article on the HCG scam was very well written (though I am not surprised because your other books are also really well written). At this point in time, in the Portland, OR area, there is a HCG clinic opening every month and no one is really questioning the safety or efficacy of these weight “loss” centers.

Beyond the obvious problems with sustainable weight loss and very low calorie diets, I wonder about the long-term effects of HCG’s immunity lowering properties. This is a hormone that DOES effect the immune system. The most problematic effect of HCG immune action is lowering a person’s T-cell activity. T-cells are involved in identifying and eradicating cancer. Have you read anything or seen any studies on supplemental HCG and immunity? I tried to find some, but they are all regarding short term use.

Anthony replies:

Hi GR,

thanks for the email and the positive feedback. My purpose in writing the HCG article was merely to show that the weight loss claims were a scam, and that any wonderful weight loss advantage claimed by its proponents/users was entirely due to the placebo effect. As such, I didn’t really delve into the side effect issue; however, there are indeed a number of possible side effects that can arise from use of HCG.

Unwanted Pregnancy

The first and most obvious one, given that HCG is used as a fertility drug, is unwanted pregnancy. As a weight loss strategy, pregnancy blows.

Gynecomastia

The second most obvious one is gynecomastia, affectionately known as “gyno” or “bitch tit” among bodybuilders. For those who are unfamiliar with this condition, it refers to the development of breast-like growth around the male nipple area. High levels of testosterone from exogenous sources or as a result of T-boosting drugs such as HCG increase the rate of aromatization, ie, the conversion of testosterone to estrogen. That’s why geared bodybuilders have developed such a fondness for anti-estrogen preparations over the years – and why gyno has been observed in men treated with HCG for low sperm counts[1-3].

Serious cases of gyno require surgery to remove the unwanted growth. It should be pointed out that while Simeons’ weight loss protocol used 125 IU HCG six days a week, men treated with HCG for sperm issues are usually administered larger doses less frequently (2-3 x week). As the bodybuilding experience has shown, some guys are far more prone to gyno than others; some blokes can take truckloads of gear and remain unaffected, while others start rummaging through their junk mail for brassiere catalogues at relatively low dosages. Whether or not a guy will develop gyno as a result of manipulating his hormone levels with preparations like HCG is a bit of a crap shoot. The possibility that the Simeons’ HCG protocol could help blokes get in touch with their more feminine side cannot be dismissed, especially in males with a tendency for excessive aromatization or naturally high estrogen levels.

Immune effects

During pregnancy, a women’s immune system undergoes changes to allow the development of a fetus containing foreign (paternal) antigens. HCG is one of a number of hormones with immunosuppressive effects that helps to avoid a “transplant rejection” reaction in the womb[4,5].

HCG has been shown to be immunosuppressive in animals and in vitro studies with human blood suggest it could have the same effect in otherwise healthy humans[6]. What this all means in terms of real life susceptibility to bacterial and viral infections among HCG users remains, to the best of my knowledge, unknown.

Nonetheless, if one insists on using HCG (or must use it for legitimate medical reasons) then avoidance of people who sniffle, cough, and rub their genitals would probably be a great idea. Even better would be to re-read my HCG article and wake up to the fact that the HCG fad is just a big overhyped and overpriced placebo wank.

Cancer

HCG and its metabolites are also produced in abundant amounts by cancer cells to assure adequate supplies of oxygen and nutrition to tumours, by stimulating blood vessel growth[7].

The ability of HCG and its variants to impede white blood cells is critical not only for embryo survival, but helps tumours to grow and spread without being attacked by the patient’s normal immune response to disease.

Many scientific studies have implicated HCG and its variants in causing or worsening cancer. In fact, a number of Biotech companies have studied the use of HCG-suppressing preparations as anti-cancer agents:

http://www.cancerbacteria.com/trial.html#current

HCG isn’t just a wank – it’s a potentially harmful wank

Much of the current success of HCG’s recent comeback appears to be predicated on the laughable claim that HCG is a highly effective, super cool “underground” weight loss agent that has been deliberately suppressed by governments and drug companies. Like yours truly, Ralph W. Moss (author of The Cancer Industry) is hardly a big fan of the FDA, but finds himself agreeing with them when they warn people away from using HCG for weight loss. Moss has also written a piece on HCG and its potential dangers, and warns:

“hCG can cause considerable fluid retention, making it potentially dangerous for people with cardiac or kidney problems, asthma, epilepsy or migraine. Men taking hCG may develop a distressing condition called gynecomastia – enlargement of the male breasts. There have also been a number of reports in the medical literature describing the development of testicular cancer in young men taking hCG, and although a definite causative link has not been clearly established, there is legitimate cause for concern. There is also some evidence that there is an increased risk of ovarian cancer in women treated with hCG for infertility.”

Moss concludes:

“HCG may yet turn out to hold important clues concerning cancer’s ability to evade the body’s immune system, but as method of controlling one’s weight it is potentially dangerous. I would avoid it until further studies are done to establish its safety and effectiveness.”

Folks, find yourself a more effective and less risky way to lose weight – HCG is just another stupid and potentially dangerous fad.

The HCG Diet Does Too Work Because…I Say So

You are very narrow minded. HCG does work and you can take that from someone who has lost 75 pounds which I could not do with any amount of exercise and calorie counting. You really should check with the many who are successful.. It seems to be sweeping the nation and a lot of people are losing weight and when they do they will not need to communicate with guys like you or even with a lot of doctors because they will be healthier. Shame on you for being so critical and like I said narrow minded.

Violet F.

Anthony replies:

Dear Violet,

congratulations on successfully using the PLACEBO effect to lose weight.

As for your “narrow minded” accusation, how precious – I’m not the one who refuses to acknowledge the overwhelming evidence that HCG is a scam, and that your results could have been replicated by placebo injections.

Good luck to you,

Regards,

Anthony further replies:

I’ve contemplated Violet’s email some more, and you know what – she’s right! Shame on me for telling the truth about HCG – how narrow-minded of me! I need to, you know, loosen up my ethics a little, embrace the latest fad that’s “sweeping the nation”, tell people what they want to hear no matter how fallacious it is, and open up a whole new world to myself. One filled with Lamborghinis, jacuzzis, Dom Perignon, and high-priced lawyers to fight off FTC and ACCC lawsuits. So to all you out there who steadfastly refuse to acknowledge the HCG hoopla is nonsense and that any weight loss benefits derived from HCG injections/oral solutions/scented enemas are purely placebo in nature, I am pleased to announce the following special offer!

Ladies and gentlemen, for a mere $599.99 I’ll express ship a month’s supply of saline solution, uh, I mean “HCG”, complete with your very own numbered set of limited edition Kevin Trudeau syringes! That’s right folks, only $599.99! Don’t miss this outstanding opportunity to get shafted – send your credit card details right away to:

i.am.a.gullible.dimwit.who.believes.the.most.asburd.bullshit@overpricedplacebos.com

And for those too stupid to acknowledge the overwhelming evidence that low-carb metabolic advantage dogma (MAD) is a fraud, stay tuned for next week’s fantastic offer – a Special Limited Edition Picture Ketostix set featuring such lovable low-carb icons as Dr. Fatkins, Dr. Sleaze, Captain Good Calories/Bad Calories, and more! Now every morning you can pee on your favourite low-carb guru and watch their face turn purple! Don’t miss out – coming soon at OverpricedPlacebos.com!

The Great Eades Smackdown, 2010

Due to an exceedingly busy schedule and an all-consuming interstate move, it’s been a long time since I’ve posted a reader mail segment. The Great Eades Smackdown, 2010 Part 1 and Part 2 articles from earlier this year drew a flood of supportive email; rather than reprint all the “Anthony, you da man! You killed him!”-type replies (which believe me, I appreciate ) I’ve included a few of the more informative replies that help shed further light on the MAD issue. There was only one hostile response received, which I’ve reprinted further down the page along with my comments.

A Black Swan … Or Fooled By Randomness?

Anthony,

Something you didn’t mention is that Eades’ black swan analogy simply doesn’t work when dealing with results which are subject to statistical error.

Repeat an experiment 100 times and you expect 5 “positive” results even where there’s no underlying difference.

Obviously quite different to finding 5 actual “black swans” – hence a totally inappropriate analogy.

Anyway, good work as ever with your reply.

Regards,

SR.

Anthony replies:

Hey SR,

Good point, and this is why research results must be able to be successfully replicated by other researchers before being embraced as ‘proof’ of anything.

However, as we have seen with our MAD friends, a lot of people will happily jump on any finding that can be remotely interpreted as supportive. They’ll trumpet the results far and wide, loudly proclaiming “case closed!” and “we were right all along!”

If one really cares about the truth, rather than just supporting their own personal dogmatic beliefs, science just doesn’t work that way. Science is not marketing or public relations – it’s a search for the facts, not the juicy bits one can use to support their own beliefs and agenda

All these people are really demonstrating is their own woefully dogmatic, myopic, ignorant (and in some instances, thoroughly dishonest and corrupt) mindset.

Cheers,

Anthony.

The First and Second Laws of Reality Evasion

Hi Anthony,

I saw an interview with Dr Liebel on a BBC Horizon programme

http://www.youtube.com/watch?v=T5liKz1X-Tw&feature=related (from 8 minutes)

and looked him up. His work does seem to be very rigorous and it is the first time I have been made aware of significant variations in the metabolisms of thin and fat people, although I had wondered how the metabolism of a fat person might compare to that of a normally thin person after they had lost weight.

Dr Liebel does seem a bit fatalisic in his conclusions though. Sure, it will be harder for these people – but tens of thousands of individuals (if not millions) with similar genes managed to control their weight and live happy, productive lives in decades gone by (albeit in a slightly different environment).

With regards to your ongoing dispute with Dr Eades, I might be able to make a small contribution (although I do wonder why you bother with these people – it seems a bit like trying to debate creationists).

Firstly, as a graduate chemist, and a teacher of advanced level chemistry for many years, I am familiar with the laws of thermodynamics. What staggers me after looking up some of the aricles by the likes of Eades and Feinman is the way they seem to use these laws out of context in ways that could only baffle the non-specialist and obscure the real argument. Dr Feinman is a Biochemist, not a chemist, and he admits he doesn’t understand thermodynamics. He is right that the 2nd law is about the dispersal of energy, but there is absolutely no need to bring it into the debate. His use of the Gibbs free energy equation cycle in his paper is actually an application of Hess’s Law, which is derived from the 1st law about the conservation of energy. (Interestingly, young-earth creationists also like to use inappropriate arguments about the second law to support their crazy views).

As I understand it, the situation is this:

The metabolism of fats, proteins and carbohydrates in the body follow different biochemical pathways, which have varying degrees of efficiency, and result in slightly different values of useable energy than might be expected from a calorimeter in a laboratory experiment. Few people seem to dispute this, including yourself.

Tightly controlled experimental evidence shows that differences in available energy are not very significant and do not offer much in the way of a metabolic advantage for weight loss. This seems to be the area of dispute and it seems to me this should be settled by an analysis and evaluation of rigorous experiments and observations, rather than lengthy discussions about the laws of nature; especially when those involved in the discussion are not specialists in the field. You may be interested to know that BBC Horizon reported on a study using identical twins in a metabolic chamber to investigate this:

http://www.youtube.com/watch?v=vKfNEO75rKc&NR=1 (near the end of the video, but the whole programme is interesting and also looks at a study where the calorific intake of people on various diets, including Atkins, were analysed).

I also read in a book called Fat Wars, by Ellen Ruppel Shell, that storing carbohydrate as body fat requires 15 – 20% of calories eaten whereas fat only 3% of calories eaten. I’m not sure where she got the figures from, but this article also supports the idea that ingested fat is more efficiently stored as body fat than carbs:

http://www.fao.org/docrep/W8079E/w8079e0m.htm.

This could mean that any slight ‘advantage’ in metabolism is offset by a ‘disadvantage’ in storage.

The food combining dieters also claim a similar metabolic advantage to the low carbers, this study debunks that:

http://news.bbc.co.uk/1/hi/health/703030.stm

There’s also an interesting video here showing how people often under-report calorie intake:

http://www.youtube.com/watch?v=1Kq3aheebGY

Regards

Joe

Anthony replies:

Hi Joe,

in the original edition of The Fat Loss Bible I also cite the Laws of Thermodynamics, but I will be removing all mention of them from the coming update because, quite simply, it’s a moot point. Tightly controlled clinical trials serving the subjects isocaloric diets of varying macronutrient content have repeatedly failed to find any fat loss advantage for low-carbohydrate diets. Citing the Laws of Thermodynamics simply allows the promoters of fallacious metabolic advantage dogma (MAD) to ignore these highly uncomfortable results and instead opt for the “baffle them with bullshit” approach. That is, to drone on in a manner that sounds highly technical and impressive to the uninitiated layman, but is really a pseudoscientific smokescreen designed to deflect attention from the fact that tightly controlled trial results do not support their contentions and in fact flatly contradict them.

I won’t play that game.

If someone claims a metabolic advantage exists, the onus is on them to provide tightly controlled clinical data showing as much. As we have seen, this evidence simply does not exist – there is not a single tightly controlled study in existence showing greater fat loss on an isocaloric low-carb diet.

It’s a bit like the guy who watches the UFC on TV and says, “I would have weaved to the right, done a spinning roundhouse kick, launched into a flying knee, come down with an elbow to his forehead, then dumped him on his ass…man!”

Sure thing mate… now try jumping in the cage and show us all how it’s done. When we throw aside all the theoretical MAD wanking, and throw the theory into the clinical ring to fend for itself, it gets its butt kicked every time.

I’d seen the BBC documentary several years ago, like many BBC productions it’s a good one devoid of sensationalism and laden with a healthy dose of good old common sense. As the narrator states:

“Don’t blame your metabolism, just count your calories – even of healthy foods. It may be hard to accept, but if you’re overweight, you have simply eaten more than your body needs and it’s stored the excess as fat”

Amen.

Selective Citation + Does Calorie Restriction Lower Your Metabolism?

Anthony,

It’s strange that those who trumpet about science won’t listen to science when it contradicts their opinions or beliefs. One thing I’d like to know and maybe you can help. Does a significantly calorie reduced or restricted diet put the body into “starvation mode” and result in a lower resting metabolic rate. I’ve heard this many times but have seen no references to actual studies that support this factoid. If you’ve written about this I’d appreciate it if you could send a link, and if not, just your ideas on the subject.

All the Best,

George.

Anthony replies:

Hi George,

It’s a common trait in the diet and health arenas; those who promote a certain viewpoint loudly beat their chest about their utmost respect for the scientific method and often go to great lengths to denigrate their opponents for using sloppy science – but then turn around and embrace shoddy science themselves when it supports their viewpoint.

Both the low-fat and low-carb movements have this pious and self-serving hypocrisy honed to a fine art. Each accuses the other of intellectual dishonesty, poor scientific analysis, and often outright corruption. Each will mercilessly pick apart any evidence cited by the opposing side, highlighting even the most minute possible flaws, but will then embrace with open arms even the most absurd and shabbily conducted research when it supports their own beliefs.

I’ve said it many times before, and I’ll no doubt repeat it many times before my time on this planet is through, but dogmatists of all stripes have one unifying characteristic in common: confirmation bias. When it comes to assessing what constitutes good and bad evidence, these folks abide by two very simple rules:

“Bad evidence: that which conflicts with what we want to believe, no matter tightly controlled and professionally conducted!

Good evidence: that which supports what we want to believe, no matter poorly controlled and unprofessionally conducted!”

Hence, we have low-fat, anti-cholesterol advocates ignoring the legions of non-supportive studies and citing such nonsense as the LRC Trial and T. Colin Campbell’s The China Study. Meanwhile, low-carbers ignore the overwhelming majority of tightly controlled ward studies showing their beloved metabolic advantage theory to be bollocks and instead cite such poorly controlled slop as the Rabast and Kekwick and Pawan studies.

What a farce. To any intelligent and impartial outside observer, the whole game is readily transparent. Unfortunately, a lot of people are easily sucked in by this tomfoolery.

To answer your question about calorie restriction and metabolic rate, yes, your metabolic rate will slow down in response to calorie restriction. The degree of slowdown will correspond to the degree of calorie restriction. In most people, this is only temporary and metabolism perks right back up again when a higher caloric intake is resumed.

The exception is the minority of folks who experience permanent reductions in metabolic rate due to excessive bouts of severe calorie restriction. Such behaviour depletes the body of critical nutrients, exhausts the adrenal glands, and leaves your physiology in a permanent state of slowdown in response to what it originally perceived as a severe stress (this state can be reversed but it requires numerous tests and takes a lot of effort and diligence).

This is why I caution against severe caloric restriction, and why I always urge those wanting to shed fat to increase their activity levels. Unlike caloric restriction, increased activity actually increases your daily calorie burn. In fact, when people take up a sport in a competitive and serious recreational manner, their caloric intake often increases, yet they lose weight.

Why?

Because their increased calorie burn is outpacing their newly increased calorie intake.

I’ve written about the topic of metabolic rate reductions in The Fat Loss Bible, complete with references.

Hope that helps,

Cheers,

Anthony.

Of Mice and Metabolism

Dear Anthony,

The mice on the keto diet ate the same number of calories but were thinner than the chow-fed mice:

Kennedy AR, et al. A high-fat, ketogenic diet induces a unique metabolic state in mice. Am J Physiol Endocrinol Metab, 2007; 292: E1724–E1739.
http://ajpendo.physiology.org/cgi/content/full/292/6/E1724

Can’t spot the flaw!

All the best,

JC.

Anthony replies:

Hey JC,

The flaw sticks out like Andrew Dice Clay at a feminist convention – the mice fed the keto diet experienced an increase in energy expenditure. As human studies repeatedly show, and as discussed in Part 1 of The Smackdown, this never happens in humans.

I keep pointing out repeatedly that rodents and humans have markedly different physiology, and that to get a reliable picture of what happens to humans you have to look at studies with…humans. I’m really not sure why MAD shills have such a hard time with this simple fact.

Actually, I tell a lie. I know full well why they avoid human studies – they show MAD to be complete bollocks.

Furthermore, despite the obvious differences between rodents and humans, this increased metabolism and weight loss is not seen in all rodent studies. True to their usual form, low-carb advocates simply ignore the studies that don’t support their hypothesis.

Here’s a study by the same researchers that failed to find any increased metabolism or weight loss in ob/ob (specially bred obesity-prone) mice:

Badman MK, et al. A very low carbohydrate ketogenic diet improves glucose tolerance in ob/ob mice independently of weight loss. American Journal of Physiology. Endocrinology and Metabolism, November 1, 2009; 297 (5): E1197-E1204.
http://ajpendo.physiology.org/cgi/content/short/297/5/E1197

Here’s a further sampling of non-supportive studies using calorie-matched and ad libitum-fed rodents:

Cheng CM, et al. A Ketogenic Diet Increases Brain Insulin-Like Growth Factor Receptor and Glucose Transporter Gene Expression. Endocrinology, 2003; 144 (6): 2676–2682.
http://endo.endojournals.org/cgi/reprint/144/6/2676.pdf

Ribeiro LC, et al. Ketogenic diet-fed rats have increased fat mass and phosphoenolpyruvate carboxykinase activity. Molecular Nutrition & Food Research, 2008; 52 (11): 1365-1371.
http://www3.interscience.wiley.com/journal/120847631/abstract

Murphy P, et al. The Antidepressant Properties of the Ketogenic Diet. Biological Psychiatry, 2004;56: 981–983.
http://www.freewebs.com/stopped_our_statins/Diet%20-%20Ketogenic%20-%20Antidepressant%20Properties.pdf

Todorova MT, et al. The Ketogenic Diet Inhibits Epileptogenesis in EL Mice: A Genetic Model for Idiopathic Epilepsy. Epilepsia, 2000; 41 (8): 933-940.
http://www3.interscience.wiley.com/cgi-bin/fulltext/119003648/PDFSTART

So even when it comes to utterly irrelevant animal studies, the low-carb mob still need to selectively cite studies using certain strains of mice to support their case. It must be tough living on the lunatic fringe…

Cheers mate,

Anthony.

“The best health advice I have ever read!”

Dear Anthony,

Your summary of what it takes to achieve and maintain weight loss is the single best explanation I have ever read, and I have read lots.

I will keep this information in front of me every day so I will stay on the right track.

Now I am looking for the single best exercises to rebuild bone density. I am thinking of racewalking, elliptical and, of course, resistance training. I should be able to focus on that now that you have explained why people can achieve their health goals on a variety of eating plans. I guess our bodies are capable of being sustained on whatever we throw at them as long as it is good whole foods within the correct calorie range for our activity level.

Thanks again for your work. You are my hero.

The best health advice I have ever read! [from Part 2 of The Smackdown]:

“The future of weight loss belongs to those who understand that a calorie deficit achieved by exercise and/or calorie restriction is the key to weight loss, and that there are numerous dietary routes to this goal. Despite what low-carb dogmatists wish to believe, many people successfully lose weight on high- and moderate-carbohydrate diets. Whatever diet one chooses to follow should be based on the diet that is most appropriate for their personal preferences, health requirements, lifestyle and convenience considerations, and activity levels. Cultural factors also need to be considered here (try telling overweight Japanese they should stop eating rice or obese older Italians to avoid pasta…good luck with that!). Wherever possible, this choice should be made in conjunction with information disseminated by non-partisan commentators with a scientific orientation, not blatantly biased diet shills whose primary concerns are PR and profits.

My prediction is that the very low-carb and low-fat paradigms will continue to fall by the wayside, as people continue to gravitate toward the middle ground, where fresh meats and produce and low-glycemic, evolutionary-correct carbohydrate sources abound.”

Carolyn T

Anthony replies:

Hi Carolyn,

thanks so much for your email, it is extremely gratifying when people read my work and ‘get it’, like you obviously do.

“The best health advice I have ever read!”

Judging by reader feedback, that passage has really struck a chord. I think a lot of people are getting sick of the partisan behaviour so prevalent in the diet industry: low-fat vs low-carb vs Paleo vs vegetarian vs vegan vs fruitarian vs raw foodists vs food combing vs…zzzz…zzzz…zzzz…

It’s a bit like listening to arguments about Republicans vs Democrats (they’re both rotten to the core) or religious people going on about how there’s only one God and one true faith which, of course, just happens to be the one they believe in.

The truth is, humans can survive and thrive on a wide variety of dietary patterns, and the proof for that is basically the entire history of the Homo sapiens species. We’ve penetrated every corner of the globe and have successfully lived off a wide variety of game and fresh produce, and a wide range of macronutrient ratios. Contrary to the low-carb dogma, the most long-lived societies eat significant amounts of carbohydrates. And contrary to the vegetarian propagandists, meat has formed an important part of the human diet for millions of years, supplying nutrients that are either absent or found in low amounts among plant foods (iron, zinc, B-vitamins, carnitine, carnosine, creatine, taurine, preformed vitamin A, long chain omega-3 fats, etc, etc).

The unifying theme seems to be a diet of whole fresh nutrient-dense foods, minimal to non-existent intake of highly processed foods, regular physical activity, and a caloric intake closely matched to one’s energy expenditure. Large long term deficits lead to under/malnutrition, long term surpluses lead to overweight and obesity.

“Thanks again for your work. You are my hero.”

No worries and…I’m blushing LOL

Thanks again,

Anthony.

Anthony, You’re a Bad, Bad Man! Or Maybe Not…

Anthony,

I have read both of your books and am am [SIC] envious of your knowledge and talent.

However, what is your problem?

You could spend your time pursuing those that are telling the world to eat more and more carbohydrates and basically killing millions of people. There are few people with your intellect.

Instead, you waste it on this petulant project with Dr Eades.

If I had your ability I would not be squandering it on this silly attack on Dr Eades that you seem to think everyone is so interested in. We’re not Anthony. We don’t care. You win. Happy now?

Can’t you see that all you are doing is alienating the very people who are (were) your readers.

There is no ‘Eades’ people versus ‘Colpo’ people, the same people that buy his books are buying your books. We are all on the same side fighting against the ‘Low Fat Dogma’ tsunami that spills forth every day.

You are obviously a very angry man. Do you think your father would be proud of this latest effort?

I don’t think so.

And Part 2, won’t even bother reading it.

Neil F-S.

Anthony replies:

I don’t have a problem Neil, except with people who publicly slander me. If you think I’m going to lie down while people publicly piss on me, you’re sadly mistaken.

What would my father think? He would be damn proud that his son sticks up for what is right.

As for your claim that people are not interested in this “Colpo vs Eades” thing, speak for yourself. The interest in Part 1 was so overwhelming I had to upgrade my web hosting plan after receiving a notice from my hosting service that I was about to exceed my monthly traffic limit.

“You are obviously a very angry man”.

To be honest, I’m feeling pretty damn pleased with life these days.

“And Part 2, won’t even bother reading it.”

Neil, do yourself a favour and unsubscribe from my newsletter. You clearly aren’t the type of person I’m trying to reach.

The following email was received from Neil F-S just over 2 weeks later:

Hi Anthony,

Perhaps you are right.

http://www.thebsdetective.com/2009/10/bullshitter-of-day-oct-7th-gary-taubes.html

Regards,

Neil.

Anthony’s comment:

I was going to let Neil’s second email pass without comment, but there is something I find especially troubling about people like Neil.

No, it’s not the rampant idiocy of a person who wails on about how evil it was to post Part 2 of The Smackdown – then acknowledges he hasn’t even read it.

Nor is it the laughable hypocrisy of someone who is so easily irritated and angered accusing moi of being an “angry man”.

Nor the hypocrisy of chastising me for this “petulant project” – I’m betting that Neil never sent a similarly furious chastisement to our buddy Eades even though it was the latter who, entirely of his own volition, chose to restart this rather tiresome war with his February 8 “dismemberment”.

Nor is it the pathetically transparent attempt at piety and righteousness when Neil cites my father. I’m not sure what my late father has to do with any of this, but I will give Neil the following advice: You can get away with saying almost anything over the Internet these days, but if you meet the target of your misguided vitriol in person be real careful about invoking their parents in support of your argument.

Nor is it Neil’s brainless attempt to place me in the same basket as his fellow carb-phobic basket-cases, although I would like to make something clear in regards to this point: I am not anti-carb, and am not on the “same side” as all those dogmatic dimwits who believe that carbohydrates are satanic. Mate, I love carbohydrates – they are the undisputed champions at fueling glycogen-dependent activity and, besides, they taste bloody good. Just because sedentary Western society has binged on sugar- and flour-laden crap for the last few decades and munched and slobbered its way into epidemic levels of obesity and diabetes, doesn’t mean we have to become carb-phobic morons. There’s a huge difference between your typical supermarket and vending machine carbs, and the wholesome carbohydrate foods that humans evolved on. In nearly twenty years as a certified fitness trainer, I’ve yet to meet a single person who became fat on sweet potatoes and pomegranates

So Neil, you and your fellow carb-phobes need to get it into your glucose-depleted craniums that I’m not on some driven mission to convince people to eat more or less carbs. If you are a highly active individual, there’s a good chance I’m going to tell you to eat more carbs, because there are way too many serious exercisers out there who’ve been swayed by nonsensical low-carb dogma, trying to fuel an athlete’s lifestyle on diets more suitable for sedentary housewives. These diets were never designed to fuel high level physical activity. On the other hand, if you are a sedentary person with low or essentially non-existent activity levels, than there’s a good chance I’ll recommend reducing your carbohydrate intake (albeit never to ketogenic levels). After all, exactly what justifies a high carbohydrate intake in a person who does bugger all activity? Exactly what huge glycogen replenishment needs do you have when the most exhausting things you do are watch TV and type angry self-contradictory emails?

But I’m digressing…

None of the above is what really irks me about people like Neil. The Internet has more nuts than the bulk section at Woolworths, and I’ve witnessed all manner of bizarre behaviour on the web over the years. After a while, it gets a little jading.

What really troubles me about people like Neil is that they are complete sheep, and that there are so many of these sheep-like automatons in circulation.

Case in point: Neil sends an email unleashing a bucket of angry hogwash, scolding me for having the temerity to expose the low-carb movement’s reigning Grandmaster of BS.

A couple of weeks later, however, he sends a sheepish (no pun intended) email telling me that I may be right.

What inspired this 180 degree turn in sentiment? Did Neil sit down and retrieve all the references I cited in support of my argument, and carefully read through them for himself, one by one? Did he check the tabulated data in these papers and realize I was telling the truth? Was it then that he realized that I may have been right all along and that Eades’ arguments were nonsense?

Nope.

Neil believes I may be right simply because he discovered another Internet commentator agreeing with me on the MAD issue. This, of course, hasn’t convinced Neil totally – as his use of the word “perhaps” indicates, he’s not 100% sure if I’m right yet. Neil probably needs another 5 or 6 like-minded commentators before he’ll be totally convinced. If they are particularly prosaic, well-known, or have a really cool looking website then that number may be reduced to 2 or 3. But the bottom line is that, like most people, Neil cannot think for himself, has no idea how to analyze the actual evidence, and so is heavily influenced by other people’s opinions. Neil is no doubt spitting his Atkins Advantage Bar all over his keyboard right now and getting ready to launch into another angry diatribe that invokes my late Dad, Grandfathers, Grandmothers, and the rest of my family tree.

However, Neil shouldn’t take this personally. The tendency to follow the crowd and seek consensus from those around us is an almost universal human trait. As Mark Twain said, “We are discreet sheep; we wait to see how the drove is going, and then go with the drove.”

While people love to kid themselves about what wonderfully unique and independent individuals they are (“Look at my arm band tattoo – what a rebel I am!”), the truth is that humans place an inordinate emphasis on what others think. Researchers have shown that people are more likely to be swayed by a statement if: 1) many other people believe it, and/or 2) an influential person/s believes it. People will even change their mind on a belief to conform to what the majority or influential figures believe. This phenomenon is known in the field of psychology as “social proof”.

The phenomenon of social proof is exploited by advertisers, governments, confidence tricksters (yes, I know the line between the aforementioned is often very blurry) and guys who are good with women (or so I’ve heard, hehe). Social proof is why television producers insert laugh tracks into comedy sitcoms; the fact that other people are already laughing makes us more likely to laugh also.

Heck, if you really need convincing of how incredibly powerful social proof is, just take a look at Mick Jagger. In the real world, guys who look like Jagger tend not to have very active sex lives, unless they make regular trips to Thailand. But put a guy in a chart-topping rock band, and the picture changes dramatically. Women screamed, swooned, fainted, and threw their panties skyward when Jagger stepped on stage; had he not been so famous, they probably would’ve just screamed.

And you wonder why your son spends so much time jamming in the garage instead of doing his homework?

That folks, is the power of social proof.

Social proof is an evolutionary programmed trait. In other words, it is so prevalent in humans because at some point in our history it conferred a survival advantage. Observation of hunter-gatherer societies shows that many of their members are exceptionally knowledgeable about their surroundings (witness the amazing feats of Aboriginal trackers). So when everybody in the tribe expressed fear of eating a certain plant, there was probably a good reason. In this environment, ignoring the tribe and being an independent-thinking maverick might have meant succumbing to fatal poisoning.

And our inordinate emphasis on the opinions of famous, popular and authoritative figures? The leaders and wise men of a tribe likely earned their reputations for a reason ; experience, not clever advertising or PR campaigns, established they really were more knowledgeable, smarter, and physically adept than the rest of the tribe. Listening to them again would have conferred a survival advantage.

Hunter-gatherers also learned to respect what the rest of the tribe thought because being cast out from the tribe would have placed one at greatly increased vulnerability to starvation and predation.

So 100,000 years ago, caring so much about what others thought and did was actually a positive trait that conferred a very real survival advantage.

Of course, our society has become infinitely more complex since the Paleolithic. What were once protective traits have now become potential liabilities that can readily be exploited by the more cunning and unscrupulous members of our society.

These traits have become serious impediments to knowledge acquisition. Instead of a wise elder explaining why we should avoid a certain toxic plant, we now have legions of bullshitting diet ‘gurus’ all preaching contradictory theories. Folks, don’t look to the tribe for some sort of consensus on which of these gurus is right, because your fellow tribesfolk are every bit as clueless. Today’s hot diet sensation is tomorrow’s failed fad; millions of people can all be wrong – and routinely are!

The only way you’ll ever truly begin to make sense of all the conflicting ‘scientific’ claims is to check the science for yourself with a clear and unbiased mind. Unfortunately, most people will never do this (by the way, cutting and pasting an abstract from Pubmed onto an Internet forum and pretending to discuss its meaning with a bunch of other shills who’ve also never read the full text is not scientific analysis – it’s a wank).

I am right on the MAD issue, not because the majority agree with me (and for the record, outside of the myopic little world of low-carbia the overwhelming majority of non-Atkins-funded scientists do agree that MAD is false). I’m right because my argument is validated by over seven decades’ worth of tightly controlled trials that have completely failed to demonstrate greater fat loss on isocaloric low-carb diets.

I’m not sure whether Neil laughs along with mediocre sitcoms or whether he has ever swooned over Mick Jagger, but he is a classic example of the influence of social proof. It was only after he read a short article by someone else agreeing with my stance on MAD that his high blood pressure returned to normal and that he began to consider that I may in fact be correct. I’m not sure exactly how many supporting opinions Neil needs before he finally feels safe in concluding that MAD is bollocks, and to be quite honest, I don’t care.

I just wish people like Neil would realize my website simply isn’t for them. This is not a place where dogmatists can come and feel warmly comforted as I piss in their ear with selectively cited research and reassuring anecdotes about how wonderful their chosen beliefs are. There is no one dietary paradigm that is right for everybody. As I alluded to earlier, the eating patterns best for a serious road cyclist, a 185-lb bodybuilder looking to crack the 200-lb barrier, and a sedentary housewife with suboptimal glycemic control are going to be very different.

A lot of people are utterly incapable of realizing this – they really seem to believe there is only one right way, and adopt a religious approach to nutrition. If that’s you, then take a hike. Seriously. I can’t stand dogmatists, and I find it particularly offensive that certain people expect me to be one, just so I don’t offend their tender and myopic sensibilities. So if you’re one of these self-labeling dolts that explicitly classifies yourself as a “low-carber”, a “vegan”, a “raw Paleo” dieter, or whatever, do yourself a favour and tune out from my site (be sure to read this article before you depart). It is too rational, objective, and impartial for you. This is a website for athletically-inclined people who want to look, feel and perform at their best, and couldn’t give a rat’s rectum about dogma. If, as Neil fears, that alienates certain of my readers – i.e. those masochistic sods from the low-carb movement who for reasons unknown keep reading my work even though it so clearly causes them much grief and consternation – then, great! I can’t work out for the life of me why these lard-asses come to my site in the first place…

Until next time, ciao!

—

References

1.    Schopohl J. Pulsatile gonadotrophin releasing hormone versus gonadotrophin treatment of hypothalamic hypogonadism in males. Human Reproduction, 1993; 8 (Suppl.2): 175-179.
2.    Burgues S, et al. Subcutaneous self-administration of highly purified follicle stimulating hormone and human chorionic gonadotrophin for the treatment of male hypogonadotrophic hypogonadism. Human Reproduction, 1997; 12 (5): 980–986.
3.    Klatskin G, Munson PL. Experimental Production of Gynecomastia with Chorionic Gonadotropin. Yale Journal of Biological Medicine, June, 1952; 24 (6): 474–497.
4.    Shirshev SV. Effect of chorionic gonadotropin on the formation of the secondary immune response. Bulletin of Experimental Biology and Medicine. October, 1993; 116 (4): 1245-1247.
5.    Bartocci A, et al. Immunosuppressive activity of human chorionic gonadotrophin preparations in vivo: Evidence for gonadal dependence. Cellular Immunology. December 1983; 82 (2): 334-342.
6.    Adock EW, et al. Human Chorionic Gonadotropin: Its Possible Role in Maternal Lymphocyte Suppression. Science, Aug. 31, 1973; 181 (4102); 845-847.
Tsampalas M, et al. Human chorionic gonadotropin: A hormone with immunological and angiogenic properties. Journal of Reproductive Immunology, 2010; 85: 93–98.

HCG for Fat Loss: The Potential Side Effects “They” Don’t Want You to Know About

Hi Anthony,

Your article on the HCG scam was very well written (though I am not surprised because your other books are also really well written). At this point in time, in the Portland, OR area, there is a HCG clinic opening every month and no one is really questioning the safety or efficacy of these weight “loss” centers.

Hi GR,

Unwanted Pregnancy

The first and most obvious one, given that HCG is used as a fertility drug, is unwanted pregnancy. As a weight loss strategy, pregnancy blows.

Gynecomastia

Immune effects

HCG has been shown to be immunosuppressive in animals and in vitro studies with human blood suggest it could have the same effect in otherwise healthy humans[6]. What this all means in terms of real life susceptibility to bacterial and viral infections among HCG users remains, to the best of my knowledge, unknown.

Cancer

HCG and its metabolites are also produced in abundant amounts by cancer cells to assure adequate supplies of oxygen and nutrition to tumours, by stimulating blood vessel growth[7].

http://www.cancerbacteria.com/trial.html#current

HCG isn’t just a wank – it’s a potentially harmful wank

Moss concludes:

Folks, find yourself a more effective and less risky way to lose weight – HCG is just another stupid and potentially dangerous fad.

The HCG Diet Does Too Work Because…I Say So

Violet F.

Anthony replies:

Dear Violet,

congratulations on successfully using the PLACEBO effect to lose weight.

Good luck to you,

Regards,

Anthony further replies:

I’ve contemplated Violet’s email some more, and you know what – she’s right! Shame on me for telling the truth about HCG – how narrow-minded of me! I need to, you know, loosen up my ethics a little, embrace the latest fad that’s “sweeping the nation”, tell people what they want to hear no matter how fallacious it is, and open up a whole new world to myself. One filled with Lamborghinis, jacuzzis, Dom Perignon, and high-priced lawyers to fight off FTC and ACCC lawsuits. So to all you out there who steadfastly refuse to acknowledge the HCG hoopla is a wank and that any weight loss benefits derived from HCG injections/oral solutions/scented enemas are purely placebo in nature, I am pleased to announce the following special offer!

i.am.a.gullible.dimwit.who.believes.the.most.asburd.bullshit@overpricedplacebos.com

The Great Eades Smackdown, 2010

Due to an exceedingly busy schedule and an all-consuming interstate move, it’s been a long time since I’ve posted a reader mail segment. “The Great Eades Smackdown, 2010” Part 1 and Part 2 articles from earlier this year drew a flood of supportive email; rather than reprint all the “Anthony, you da man! You killed him!”-type replies (which believe me, I appreciate J ) I’ve included a few of the more interesting and expansive replies. There was only one hostile response received, which I’ve reprinted further down the page along with my comments.

A Black Swan … Or Fooled By Randomness?

Anthony,

Something you didn’t mention is that Eades’ black swan analogy simply doesn’t work when dealing with results which are subject to statistical error.

Repeat an experiment 100 times and you expect 5 “positive” results even where there’s no underlying difference.

Obviously quite different to finding 5 actual “black swans” – hence a totally inappropriate analogy.

Anyway, good work as ever with your reply.

Regards,

SR.

Hey SR,

Good point, and this is why research results must be able to be successfully replicated by other researchers before being embraced as “proof” of anything.

All these people are really demonstrating is their own woefully dogmatic, myopic, ignorant (and in some instances, thoroughly dishonest and corrupt) mindset.

Cheers,

Anthony.

The First and Second Laws of Reality Evasion

Hi Anthony,

I saw an interview with Dr Liebel on a BBC Horizon programme

http://www.youtube.com/watch?v=T5liKz1X-Tw&feature=related (from 8 minutes)

As I understand it, the situation is this:

I also read in a book called Fat Wars, by Ellen Ruppel Shell, that storing carbohydrate as body fat requires 15 – 20% of calories eaten whereas fat only 3% of calories eaten. I’m not sure where she got the figures from, but this article also supports the idea that ingested fat is more efficiently stored as body fat than carbs:

http://www.fao.org/docrep/W8079E/w8079e0m.htm.

This could mean that any slight ‘advantage’ in metabolism is offset by a ‘disadvantage’ in storage.

The food combining dieters also claim a similar metabolic advantage to the low carbers, this study debunks that:

http://news.bbc.co.uk/1/hi/health/703030.stm

There’s also an interesting video here showing how people often under-report calorie intake:

http://www.youtube.com/watch?v=1Kq3aheebGY

Regards

Joe

Hi Joe,

in the original edition of The Fat loss Bible I also cite the Laws of Thermodynamics, but I will be removing all mention of them from the coming update because, quite simply, it’s a moot point. Tightly controlled clinical trials serving the subjects isocaloric diets of varying macronutrient content have repeatedly failed to find any fat loss advantage for low-carbohydrate diets. Citing the Laws of Thermodynamics simply allows the promoters of fallacious metabolic advantage dogma (MAD) to ignore these highly uncomfortable results and instead opt for the “baffle them with bullshit” approach. That is, to drone on in a manner that sounds highly technical and impressive to the uninitiated layman, but is really a pseudoscientific smokescreen designed to deflect attention from the fact that tightly controlled trial results do not support their contentions and in fact flatly contradict it.

I won’t play that game.

I’d seen the BBC documentary several years ago, like many BBC productions it’s a good one devoid of sensationalism and laden with a healthy dose of good old common sense. As the narrator states:

Amen.

Selective Citation + Does Calorie Restriction Lower Your Metabolism?

Anthony,

All the Best,

George.

Hi George,

“Bad evidence: that which conflicts with what we want to believe, no matter tightly controlled and professionally conducted!

Good evidence: that which supports what we want to believe, no matter poorly controlled and unprofessionally conducted!”

What a farce. To any intelligent and impartial outside observer, the whole game is readily transparent. Unfortunately, a lot of people are easily sucked in by this tomfoolery.

Why?

Because their increased calorie burn is outpacing their newly increased calorie intake.

I’ve written about the topic of metabolic rate reductions in The Fat Loss Bible, complete with references.

Hope that helps,

Cheers,

Anthony.

Of Mice and Metabolism

Dear Anthony,

The mice on the keto diet ate the same number of calories but were thinner than the chow-fed mice:

Kennedy AR, et al. A high-fat, ketogenic diet induces a unique metabolic state in mice. Am J Physiol Endocrinol Metab, 2007; 292: E1724–E1739.
http://ajpendo.physiology.org/cgi/content/full/292/6/E1724

Can’t spot the flaw!

All the best,

JC.

Hey JC,

The flaw sticks out like Andrew Dice Clay at a feminist convention – the mice fed the keto diet experienced an increase in energy expenditure. As human studies repeatedly show, and as discussed in part 1 of The Smackdown, this never happens in humans.

Actually, I tell a lie. I know full well why they avoid human studies – they show MAD to be complete bollocks.

Cheng CM, et al. A Ketogenic Diet Increases Brain Insulin-Like Growth Factor Receptor and Glucose Transporter Gene Expression. Endocrinology, 2003; 144 (6): 2676–2682.
http://endo.endojournals.org/cgi/reprint/144/6/2676.pdf

Kinzig KP, Taylor RJ. Maintenance on a ketogenic diet: voluntary exercise, adiposity and neuroendocrine effects. International Journal of Obesity, 2009; 33: 824–830.

Ribeiro LC, et al. Ketogenic diet-fed rats have increased fat mass and phosphoenolpyruvate carboxykinase activity. Molecular Nutrition & Food Research, 2008; 52 (11): 1365-1371.
http://www3.interscience.wiley.com/journal/120847631/abstract

Murphy P, et al. The Antidepressant Properties of the Ketogenic Diet. Biological Psychiatry, 2004;56: 981–983.
http://www.freewebs.com/stopped_our_statins/Diet%20-%20Ketogenic%20-%20Antidepressant%20Properties.pdf

Todorova MT, et al. The Ketogenic Diet Inhibits Epileptogenesis in EL Mice: A Genetic Model for Idiopathic Epilepsy. Epilepsia, 2000; 41 (8): 933-940.
http://www3.interscience.wiley.com/cgi-bin/fulltext/119003648/PDFSTART

So even when it comes to utterly irrelevant animal studies, the low-carb mob still need to selectively cite studies using specially bred mice to support their case. Times must be real tough on the lunatic fringe…

Cheers mate,

Anthony.

“The best health advice I have ever read!”

Dear Anthony,

Your summary of what it takes to achieve and maintain weight loss is the single best explanation I have ever read, and I have read lots.

I will keep this information in front of me every day so I will stay on the right track.

Thanks again for your work. You are my hero.

The best health advice I have ever read! [from Part 2 of The Smackdown]:

Carolyn T

Hi Carolyn,

thanks so much for your email, it is extremely gratifying when people read my work and ‘get it’, like you obviously do.

“The best health advice I have ever read!”

“Thanks again for your work. You are my hero.”

No worries and…I’m blushing LOL

Thanks again,

Anthony.

Anthony, You’re a Bad, Bad Man! Or Maybe Not…

Anthony,

I have read both of your books and am am [SIC] envious of your knowledge and talent.

However, what is your problem?

You could spend your time pursuing those that are telling the world to eat more and more carbohydrates and basically killing millions of people. There are few people with your intellect.

Instead, you waste it on this petulant project with Dr Eades.

If I had your ability I would not be squandering it on this silly attack on Dr Eades that you seem to think everyone is so interested in. We’re not Anthony. We don’t care. You win. Happy now?

Can’t you see that all you are doing is alienating the very people who are (were) your readers.

You are obviously a very angry man. Do you think your father would be proud of this latest effort?

I don’t think so.

And Part 2, won’t even bother reading it.

Neil F-S.

Anthony’s reply:

I don’t have a problem Neil, except with people who publicly slander me. If you think I’m going to lie down while people publicly piss on me, you’re sadly mistaken.

What would my father think? He would be damn proud that his son sticks up for what is right.

“You are obviously a very angry man”.

To be honest, I’m feeling pretty damn pleased with life these days.

“And Part 2, won’t even bother reading it.”

Neil, do yourself a favour and unsubscribe from my newsletter. You clearly aren’t the type of person I’m trying to reach.

The following email was received from Neil F-S just over 2 weeks later:

Hi Anthony,

Perhaps you are right.

http://www.thebsdetective.com/2009/10/bullshitter-of-day-oct-7th-gary-taubes.html

Regards,

Neil.

Anthony’s comment:

I was going to let Neil’s second email pass without comment, but there is something I find especially troubling about people like Neil.

No, it’s not the rampant idiocy of a person who wails on about how evil it was to post Part 2 of The Smackdown – then acknowledges he hasn’t even read it.

Nor is it the laughable hypocrisy of someone who is so easily irritated and angered accusing moi of being an “angry man”.

Nor is it Neil’s brainless attempt to place me in the same basket as his fellow carb-phobic basket-cases, although I would like to make something clear in regards to this point: I am not anti-carb, and am not on the “same side” as all those dogmatic dimwits who believe that carbohydrates are satanic. Mate, I love carbohydrates – they are the undisputed champions at fuelling glycogen-dependent activity and, besides, they taste bloody good. Just because sedentary Western society has binged on sugar- and flour-laden crap for the last few decades and munched and slobbered its way into epidemic levels of obesity and diabetes, doesn’t mean we have to become carb-phobic morons. There’s a huge difference between your typical supermarket and vending machine carbs, and the wholesome carbohydrate foods that humans evolved on. In nearly twenty years as a certified fitness trainer, I’ve yet to meet a single person who became fat on sweet potatoes and pomegranates

So Neil, you and your fellow carb-phobes need to get it into your glucose-depleted craniums that I’m not on some driven mission to convince people to eat more or less carbs. If you are a highly active individual, there’s a good chance I’m going to tell you to eat more carbs, because there are way too many serious exercisers out there who’ve been swayed by nonsensical low-carb dogma, trying to fuel an athlete’s lifestyle on diets more suitable for sedentary housewives. These diets were never designed to fuel high level physical activity. On the other hand, if you are a sedentary person with low or essentially non-existent activity levels, than there’s a good chance I’ll recommend reducing your carbohydrate intake (albeit never to ketogenic levels). After all, exactly what justifies a high-carbohydrate intake in a person who does bugger all activity? Exactly what huge glycogen replenishment needs do you have when the most exhausting things you do are watch TV and type angry self-contradictory emails?

But I’m digressing…

What really troubles me about people like Neil is that they are complete sheep, and that there are so many of these sheep-like automatons in circulation.

Case in point: Neil sends an email unleashing a bucket of angry hogwash, scolding me for having the temerity to expose the low-carb movement’s reigning Grandmaster of BS.

A couple of weeks later, however, he sends a sheepish (no pun intended) email telling me that I may be right.

Nope.

Neil believes I may be right simply because he discovered another Internet commentator agreeing with me on the MAD issue. This, of course, hasn’t convinced Neil totally – as his use of the word “perhaps” indicates, he’s not 100% sure if I’m right yet. Neil probably needs another 5 or 6 like-minded commentators before he’ll be totally convinced. If they are particularly prosaic, well-known, or have a really cool looking website then that number may be reduced to 2 or 3. But the bottom line is that, like most people, Neil cannot think for himself, has no idea how to analyse the actual evidence, and so is heavily influenced by other people’s opinions. Neil is no doubt spitting his Atkins Advantage Bar all over his keyboard right now and getting ready to launch into another angry diatribe that invokes my late Dad, Grandfathers, Grandmothers, and the rest of my family tree.

And you wonder why your son spends so much time jamming in the garage instead of doing his homework?

That folks, is the power of social proof.

Hunter-gatherers also learned to respect what the rest of the tribe thought because being cast out from the tribe would have placed one at greatly increased vulnerability to starvation and predation.

So 100,000 years ago, caring so much about what others thought and did was actually a positive trait that conferred a very real survival advantage.

A lot of people are utterly incapable of realizing this – they really seem to believe there is only one right way, and adopt a religious approach to nutrition. If that’s you, then take a hike. Seriously. I can’t stand dogmatists, and I find it particularly offensive that certain people expect me to be one, just so I don’t offend their tender and myopic sensibilities. So if you’re one of these self-labelling dolts that explicitly classifies yourself as a “low-carber”, a “vegan”, a “raw Paleo” dieter, or whatever, do yourself a favour and tune out from my site (be sure to read this article before you depart). It is too rational, objective, and impartial for you. This is a website for athletically-inclined people who want to look, feel and perform at their best, and couldn’t give a rat’s rectum about dogma. If, as Neil fears, that alienates certain of my readers – ie those masochistic sods from the low-carb movement who for reasons unknown keep reading my work even though it so clearly causes them much grief and consternation – then, great! I can’t work out for the life of me why these lard-asses come to my site in the first place…

Boosting Growth Hormone with Diet & Training: Fact or Fiction? Part 2

Anthony Colpo — Wed, 04 Aug 2010 06:04:52 +0000

Do Low-Carb Diets Boost Growth Hormone Levels?

In Part 1, we examined the claim that training-induced spikes in growth hormone (GH) increase muscle growth and strength. Despite the sanctity of this myth among large sections of the bodybuilding and strength training communities, it is false. As numerous studies have shown, manipulating workouts specifically for the purpose of boosting GH does not accelerate hypertrophy or strength gains. If you missed Part 1, you can read it here.

This week we’ll take a close look at the oft-repeated claim that low-carbohydrate diets increase GH levels. Dump the carbs, and a lifetime of accelerated fat-burning, heightened energy, bigger muscles, taut supple skin, and all the other wonderful benefits that come with optimal GH levels are yours for the taking. Or so the spin goes…

Like so much of the alleged “science” that emanates from the low-carbohydrate arena, it’s complete nonsense.

The low-carb camp, just like the low-fat movement it takes so much delight in deriding, has a special knack for taking isolated findings, adding a large helping of wishful thinking, then making huge leaps of faith to arrive at conclusions that bolster their own dogma. Their cherished ‘insulin’ theory of fat loss is a classic example. Short-term experiments show that administration of insulin can temporarily suppress fatty acid oxidation. This, claim the low-carbers, is proof that endogenous insulin suppresses actual body fat loss and that carbohydrates (generally the most insulinogenic of macronutrients) are fattening.

However, clinical trials have shown that differences in glycemic status do not affect weight loss, and tightly controlled metabolic ward trials show no difference in fat loss between isocaloric high- and low-carbohydrate diets, even when carbohydrate levels are reduced to zero. This is an inconvenient finding for those who promote and subscribe to low-carb diets, so they simply ignore it or contrive the most ludicrous rationalizations in an attempt to explain it away (this is discussed in detail in Chapter 1 of The Fat Loss Bible, and you can freely enjoy my merciless destruction of an especially duplicitous low-carb guru and his fraudulent “metabolic advantage” claims here and here).

Someone Forgot to Tell Contador Carbs Will Make Him Fat

You’d be hard pressed to find a group that eats more carbohydrate on a daily basis than professional road cyclists. Researchers who monitored world class roadies during the Tour de France found they consumed a whopping 6600 to 7800 calories and 12-13 grams of carbohydrate per kilogram of bodyweight (a hefty 780–910 grams for a 65 kg rider) daily. Despite consuming massive amounts of carbohydrate and enough calories to fatten a small truck, the cyclists barely managed to maintain their weight during the three-week event[1]. Why? Because they were riding several hours a day, burning calories faster than politicians spend your tax money.

Calorie balance, not carbohydrate intake or insulin output, is king when it comes to weight status. The insulin theory sounds great in low-carb books and Internet forums, but in reality it’s a dud.

And so it is with the ‘low-carb-diets-increase-GH’ theory. This myth is predicated on the observation that experimental episodes of hypoglycemia (low blood sugar) can be accompanied by increased GH output. But that’s only part of the story. Here’s what the low-carb hucksters aren’t telling you: When researchers induce this state, they first give their subjects a large dose of glucose that causes initial hyperglycemia (high blood sugar), followed a few hours later by hypoglycemia. The initial hyperglycemia is accompanied by suppressed GH levels, but three to five hours after the initial bolus of glucose, the subsequent hypoglycemia of these subjects is accompanied by a rise in GH[2].

Researchers postulate that the initial inhibitory effect of glucose on GH release may be due to stimulation of hypothalamic somatostatin release, which suppresses serum GH for the first 1-3 hours. This reduced GH release results in an increase in the pituitary stores of GH. When somatostatin release eventually declines, endogenous growth hormone-releasing hormone (GHRH) secretion is activated in response, and available pituitary stores of GH are released, leading to a rebound increase in serum GH levels[3].

Deliberately bouncing your blood sugar levels to extreme high and then low levels completely contravenes prevailing low-carb dogma, which places a premium on minimal insulin release and Spartan carbohydrate consumption. Nonetheless, low-carb commentators are happy to embrace the connection between hypoglycemia and increased GH release – they just, you know, kinda sorta leave out the bit about what researchers do to induce this hypoglycemic state in the first place.

Furthermore, prolonged hypoglycemia, irrespective of whether it is accompanied by increased GH release, is not a good thing. Unless of course, you think it’s cool to suffer lethargy, brain fog, shakiness, dizziness, adrenal dysfunction, and an increased risk of premature cardiovascular and all-cause death. If you are experiencing wild fluctuations in blood glucose and/or extended periods in a hypoglycemic state, then you need to improve your diet and lifestyle pronto.

Clearly, the theoretical basis for the ‘low-carb-increases-GH’ claim comes from some pretty dodgy extrapolation of studies involving experimentally-induced hypoglycemia. But what about studies examining actual GH output on low-carb versus higher-carb diets? Have they been conducted, and if so, do they support any claim for low-carb-induced GH elevations?

Let’s find out…

GH: High- vs Low-Carb

Canadian researchers evaluated glycemic and GH responses in eight obese women during a weight maintenance control period (using a 44% carbohydrate diet), and after 1 and 3 weeks of a 750 cal/day 1% carbohydrate diet. Plasma insulin and glucose concentrations fell by 50% and 16%, respectively. Rather than increase, fasting GH concentrations decreased from 3.4 to 1.6 ng/ml, although the difference was not statistically significant[4].

Volek et al examined the effect of a low-carbohydrate diet delivering a mean 46 grams of carbohydrate per day on body composition and hormonal responses in normal weight young men[5]. The researchers did not measure GH levels but during the six-week study there were no significant changes in glucagons, testosterone, SHBG, cortisol, or insulin-like growth factor-1 (IGF-I). Like GH, IGF-1 is an anabolic hormone; it is produced in the liver in response to stimulation by GH.

Much ado has been made about the small fat loss and increase in lean mass among the subjects who ate the low-carb diet in this study. However, despite the widely known fact that exercise (especially resistance training) can have a significant impact on body composition, no attempt was made to standardize activity levels. The subjects were merely told to maintain their current activity levels during the study. According to the researchers:

“Subjects were moderately active performing a variety of different aerobic and weight-training routines, but none were competitive athletes. In the carbohydrate-restricted diet group, 1 subject was sedentary, 5 performed regular aerobic exercise (2 to 4 times/wk for 20 to 60 minutes), and 6 performed a combination of aerobic exercise (3 to 5 times/wk for 15 to 90 minutes) and resistance exercise (2 to 6 times/wk for 45 to 120 minutes).”

No description of activity levels in the low-protein/high-carbohydrate group was provided.

Activity was not the only factor that wasn’t standardized. The subjects in the low-carb group also increased their protein intake by 56%, something that has been shown to cause a repartitioning effect favoring increased lean mass and greater fat loss, especially in exercising subjects. Carbohydrate restriction itself has not been shown to favor such changes; in fact, as I explain in The Fat Loss Bible, carbohydrate restriction typically produces unfavorable changes in markers of anabolism/catabolismsuch as decreased BCAA absorption and decreased nitrogen retention. So if the favorable body composition changes in this study were diet-induced, it was likely due to increased protein intake.

Harber et al studied eight young, healthy volunteers who ate a high-carb (60% carbohydrate, 30% fat, 10% protein) for two days, followed immediately by 7 days of an isocaloric low-carb (5% carbohydrate, 60% fat, 35% protein) diet. There was no change in GH secretion (mean GH 2.09 vs 1.54 2.09 µg/l and basal GH 0.41 vs 0.49 µg/l before and after the low-carb diet, respectively). Total plasma IGF-I concentrations did not change, free IGF-I decreased by approximately 30%, but muscle IGF-I doubled. Protein synthesis increased, but so too did protein breakdown. Not surprisingly, there was no measurable change in fat free mass during the study[6].

Nuttall et al examined twelve type 2 diabetic subjects (10 males, two females) who consumed 2 weight-maintaining diets in random order: 1) 15% protein, 30% fat, 55% carbohydrate; 2) 30% protein, 30% fat, 40% carbohydrate. Each diet was followed for 5 weeks. It should be pointed out that the latter diet, containing an average 223 grams of carbs per day, was not a low-carb diet[7]. Why I have still included it in this analysis will become apparent in a moment.

The mean fasting GH concentration after the 55% carbohydrate diet was 0.15 ng/ml compared to 0.32 on the 40% carbohydrate diet; this difference was not statistically significant. The mean IGF-I concentration also was increased when the subjects ingested the 40% carbohydrate diet (149 vs. 205 ng/ml). The 30% protein/40% carbohydrate diet resulted in a 39% increase in 24-hour free cortisol, which just failed to reach statistical significance (P 0.06).

A later study by the same researchers compared a 5-week diet of 20% carbohydrate/30% protein/50% fat with one containing 55% carbohydrate/15% protein/30% fat in Type 2 diabetic men[8]. The slightly greater decline in GH on the low-carbohydrate diet was not statistically significant. There was a significantly greater rise in serum IGF-1 from 115 to 161 ng/ml.

In a third study by the same researchers, eight Type 2 diabetic men consumed a weight-maintaining diet consisting of 30% protein, 40% fat, and 30% carbohydrate for 5 weeks. During the low-carb diet, GH levels rose from 0.2 to 0.5 ng/ml but the difference was not statistically significant. Fasting plasma total IGF-1 once again rose from 118 to 158 ng/ml, a statistically significant difference. Free cortisol was increased, although the difference was not statistically significant[9].

It’s worth noting that in the four aforementioned studies, the elevated muscle/blood levels of IGF-1 occurred on diets that were not only low in carbohydrate but 200-350 percent higher in protein. That this rise in IGF-1 was a result of increased protein and not carbohydrate restriction is reinforced by the fact it was observed whether the diets contained 5, 20, 30, or 40% carbohydrate. If it’s increased anabolism you’re after, a high-protein/moderate- to high-carbohydrate diet remains a better bet than a high-protein/low-carbohydrate diet. In the latter, the anabolic effect of the extra protein will potentially be negated by reduced levels of carbohydrate and hence insulin.

At Last, Some Supportive Studies?

The only studies I could find showing greater GH levels during low-carbohydrate diets were three trials involving exercise. Before low-carb advocates start peeing their pants in ketotic delight, let’s take a closer look at these findings.

Low-Carb and Exercise: Boosts GH but Kills Performance

The first of these studies was conducted by Langfort et al at the Polish Academy of Sciences[10]. They took healthy young men and made them ride on a stationary cycle, incrementally increasing the intensity until they reached exhaustion. The load was increased 40 watts at a time, with each load lasting 3 minutes interspersed by 1 minute’s rest. On one occasion, the performed the test after 3 days of a 20% protein, 30% fat, 50% carbohydrate diet; on the other occasion, the test was performed after 3 days of a 45% protein, 50% fat, 5% carbohydrate diet.

The authors reported that, after 3 days of the low-carbohydrate diet resting concentrations of GH were significantly higher but concentrations of testosterone were significantly lower (actual values not provided in the paper).

During exercise, the maximal mean wattage achieved after both diets was 262. Again, exact figures were not provided for GH output; in a style more akin to older papers, the GH and testosterone data are plotted on very rudimentary graphs in which it is impossible to determine the exact values, but running a ruler across from the scale to the plots gives approximate peak wattage GH values of 97 and 77 mU.l¹ in the low- and high-carbohydrate groups, respectively. This difference was not statistically significant.

Using the same method to ascertain testosterone levels at peak wattage yields approximate testosterone values of 24 and 29 nmol.l¹ in the low- and high-carbohydrate groups, respectively. This difference did reach statistical significance.

So here’s a study that reported higher resting GH levels as a result of low-carb eating. Should we get excited?

Hardly.

The diets only lasted 3 days each. It is well known that the body adapts to radical changes in diet by making short-term adjustments, and during this temporary adjustment phase blood values of certain markers can show significant change before eventually returning to baseline. Given that other studies have repeatedly failed to confirm increases in resting GH over the longer term, it’s likely this study is a demonstration of this phenomenon in action.

Furthermore, this study involved not only a reduced carbohydrate intake but also a more than doubling of protein intake during the low-carb diet. Italian researchers have reported increases in GH during high-protein, high-carbohydrate diets[11] (and refer back to the 30% protein/40% carb diet study by Nuttal et al above), although other researchers have failed to confirm this finding. The finding of reduced testosterone in the low-carb group may also have been a function of the high-protein intake, with the literature showing a more consistent association between high protein levels and reduced testosterone (something worthy of further elaboration in a future article – stay tuned).

Danish researchers examined the effect of four days of 13% protein/77% fat and a 13% protein/77% carbohydrate diets in 7 healthy men[12]. There were two zero-carbohydrate periods and one high-carb period; the diets were followed in crossover fashion with seventeen days in between each diet period. At the start of each period, the subjects performed 45 minutes of glycogen-depleting exercise at 80% VO2max. At the end of each diet phase, the subjects exercised to exhaustion at 70% VO2max.

Resting GH levels rose higher after both zero-carb diet periods, from 1.0 to 3.8 mU/l and 2.0 to 5.2 mU/l (exact figures for high-carbohydrate diet not supplied). Levels of the thyroid hormone T3 declined significantly only after the zero-carb diets.

During exercise, GH rose significantly higher on the zero-carb diet. This was in no way a reflection of improved anabolism or energy levels; in fact, it was quite the opposite. The total time the subjects could sustain on a treadmill was slashed by a whopping 40-45% after the zero-carb phases. Not only did the subjects reach exhaustion sooner after the zero-carb diets, but they felt a whole lot worse when they got there; after the zero-carb phase, subjects reported symptoms of hypoglycemia that included weakness, irritability, mental confusion, nausea, hunger, cold sweating and disturbed co-ordination. GH levels were higher during exercise after the low-carb phase, but so too were levels of other fuel mobilizing hormones such as epinephrine, glucagon, and cortisol. The increase in GH signified, not a supercharged body awash with performance-enhancing anabolic hormones, but one struggling to mobilize extra glucose and fatty acid in the face of insufficient muscle glycogen[12,13].

Bogardus et al placed eight untrained obese females on one of two 830-kcal/d diets: carbohydrate-containing: 35% protein, 29% fat, 36%, or carbohydrate-restricted: 35% protein, 64% fat, 1% carbohydrate[14]. The diets were followed for six weeks. There was no difference in resting GH concentrations between the groups, but GH levels during exercise were higher in the 1% carb group. Again, this was little cause for celebration but rather a reflection of a struggling biochemical physiology. Pre-exercise thigh muscle glycogen did not change significantly in the 36% carb group, but plummeted 49% in the 1% carb group after only 1 week, and by 51% after 6 weeks. This rapid drop in glycogen was accompanied by similarly disastrous exercise outcomes: endurance at approximately 75% VO2max on a stationary bike decreased by a whopping 50% in the 1% carb group, while no change was seen in the 36% carb group.

Post-Workout Carbs and GH

As I review extensively in The Fat Loss Bible, the significant benefits of post-workout carbohydrate supplementation have been clearly established in the literature. They include a doubling in the post-exercise rate of glycogen re-synthesis, a huge help to those engaged in daily sessions of glycogen-depleting exercise. And while weight-training is not generally as glycogen-depleting as activities such as MMA, boxing, track and road cycling, and sprinting, bodybuilders can still benefit from both the extra calories and the enhanced insulin release and hence increased muscle protein synthesis afforded by post-workout carbohydrates.

Certain low-carb gurus, however, would have you forgo these important benefits because they believe post-exercise carbohydrates suppress GH release. These jokers would have us shun the very real and tangible improvements in post-workout recovery afforded by carbohydrates for fear they may suppress GH release.

This ass-backwards line of thinking reminds me of the old joke:

Q. Why are Pentecostal preachers so violently opposed to premarital sex?

A. Because it could lead to dancing.

When someone claims a certain training or dietary strategy will increase/suppress GH during/after training, your response should be an utterly indifferent “so what?” As explained in Part 1, temporary spikes in GH have no anabolic effect. Heck, even daily recombinant GH injections fail to add muscle in healthy young men.

Furthermore, post-workout carbs do not suppress GH release. A number of clinical trials has shown that consuming carbs immediately after training either has no effect on GH or actually increases it[15-18].

Another Low-Carb Myth Dissected, Dismembered and Dis-troyed

The low-carb movement thrives on promoting pseudoscientific hogwash, and the low-carb-boosts-GH dogma is no exception.

Study after study has repeatedly failed to find any significant increase in baseline GH secretion as a result of carbohydrate restriction – with the sole exception of short 3 and 4-day studies where the difference could easily be explained by transient homeostatic changes. Longer studies have failed to confirm this finding. The only consistent rise in GH reported in the literature for low-carb diets occurs during exercise. As explained in Part 1, manipulating training to produce greater spikes in GH has no favorable effect on muscle or strength gains. In the case of very low-carb dieting, it gets worse – higher peri-exercise GH levels are typically accompanied by performance-killing declines in muscle glycogen and large reductions in endurance.

When chasing optimal health, fitness, and performance, you have to focus on your end goals. You need to decide what’s more important – chasing transient spikes in GH, or smashing your previous best times and exploding through previous plateaus in the weight room? Once you can answer this simple question, then everything else promptly falls in to proper perspective. You need to manipulate your diet and training to produce tangible changes in truly relevant factors such as strength, power, agility, and endurance. Study after study shows that, if you’re a serious exerciser after optimal fitness and performance, a low-carbohydrate diet is not the way to do it.

—

References

1. Saris WH, et al. Study on food intake and energy expenditure during extreme sustained exercise: the Tour de France. International Journal of Sports Medicine, 1989; 10 (suppl 1): S26–S31.

2. Roth J, et al. Hypoglycemia: a potent stimulus to secretion of growth hormone. Science, May 31, 1963; 140: 987-988.

3. Giustina A, Veldhuis JD. Pathophysiology of the neuroregulation of growth hormone secretion in experimental animals and the human. Endocrine Reviews, Dec, 1998; 19 (6): 717-797.

4. Reid D, Rasio E. Glucose utilization and nitrogen balance in the obese on a protein-lipid hypocaloric diet. Canadian Journal of Physiology and Pharmacology, Mar, 1982; 60 (3): 319-323.

5. Volek JS, et al. Body composition and hormonal responses to a carbohydrate-restricted diet. Metabolism. 2002 Jul; 51 (7): 864-870.

6. Harber MP, et al. Effects of dietary carbohydrate restriction with high protein intake on protein metabolism and the somatotropic axis. Journal of Clinical Endocrinology & Metabolism, Sep 2005; 90 (9): 5175-5181.

http://jcem.endojournals.org/cgi/reprint/90/9/5175

7. Nuttall FQ, et al. The Metabolic Response of Subjects with Type 2 Diabetes to a High-Protein, Weight-Maintenance Diet. Journal of Clinical Endocrinology & Metabolism, 2003; 88 (8): 3577-3583.

8. Nuttall FQ, Gannon MC. The metabolic response to a high-protein, low-carbohydrate diet in men with type 2 diabetes mellitus. Metabolism, Feb, 2006; 55 (2): 243-251.

9. Nuttall FQ, et al. Metabolic effect of a LoBAG30 diet in men with type 2 diabetes. American Journal of Physiology – Endocrinology and Metabolism, 2006; 291: E786–E791.

10. Langfort JL, et al. The effect of low-carbohydrate diet on the pattern of hormonal changes during incremental, graded exercise in young men. International Journal of Sport Nutrition and Exercise Metabolism, Jun, 2001; 11 (2): 248-257.

11. Sellini M, et al. [Behavior of basal values and circadian rhythm of ACTH, cortisol, PRL and GH in a high-protein diet]. Bollettino della Società Italiana di Biologia Sperimentale, May 15, 1981; 57 (9): 963-969.

12. Johannessen A, et al. Prolactin, Growth Hormone, Thyrotropin, 3,5,3′-Triiodothyronine, and Thyroxine Responses to Exercise after Fat- and Carbohydrate-Enriched Diet. Journal of Clinical Endocrinology & Metabolism, 1981: 52 (1): 56-61.

13. Galbo H, et al. The effect of different diets and of insulin on the hormonal response to prolonged exercise. Acta Physiologica Scandinavica, Sep, 1979; 107 (1): 19-32.

14. Bogardus C, et al. Comparison of carbohydrate-containing and carbohydrate-restricted hypocaloric diets in the treatment of obesity. Endurance and metabolic fuel homeostasis during strenuous exercise. Journal of Clinical Investigation, 1981; 68 (2): 399-404.

15. Williams AG, et al. Effects of resistance exercise volume and nutritional supplementation on anabolic and catabolic hormones. European Journal of Applied Physiology, Feb 2002; 86 (4): 315-321.

16. Koeslag JH, et al. The effects of alanine, glucose and starch ingestion on the ketosis produced by exercise and by starvation. Journal of Physiology, Apr 1982; 325: 363-376.

17. Kraemer WJ, et al. Hormonal responses to consecutive days of heavy-resistance exercise with or without nutritional supplementation. Journal of Applied Physiology, Oct 1998; 85 (4): 1544-1555.

http://jap.physiology.org/cgi/content/full/85/4/1544

18. Chandler RM, et al. Dietary supplements affect the anabolic hormones after weight-training exercise. Journal of Applied Physiology, Feb 1994; 76 (2): 839-845.

How to Become an Easily-Brainwashed Sucker in 5 easy steps!

Anthony Colpo — Tue, 03 Aug 2010 22:54:20 +0000

(The following article was originally posted on the Internet January 17, 2005).

What is the scarcest commodity on planet Earth right now? Oil? Gas? Clean water? Unpolluted air?

If you nodded “yes” to any of the above, you’re not even close. The scarcest commodity on this planet right now is the ability to think in a rational, critical, logical, and independent manner.

If you want to be among the world’s great mass of unthinkers whose ignorance and gullibility allows the incompetent, the unscrupulous, and the corrupt to run amok, then be sure to live by the following five tips!

1. Fail to verify information for yourself

Perhaps the most important characteristic of the Easily-Brainwashed Sucker is a blind reliance on second-hand information. This is information derived from external sources, such as newspapers, magazines, Internet sites, popular books, television, family members, neighbors, work mates, and so on.

You would think that, when contemplating information whose accuracy could have a profound impact on one’s continued well-being–for example, the decision to change one’s diet, take a prescription medicine, make a large financial commitment, or support a nation’s entry into war–one would make an exerted effort to verify the reliability of that information as best as possible.

Most people, however, put more effort into combing their hair than they do analyzing the validity of potentially life-altering information. It is nothing short of startling how many of us will make major life decisions based on information that is little more than hearsay.

Unwilling or unaware of how to check out the facts for ourselves, many of us assume that because: something is in print; reported in the media; widely believed by others, or; has been disseminated to us by some apparently respectable source, it must be true.

The situation is worsened when such folks are presented with a multitude of differing opinions or viewpoints. “There’s so much conflicting information out there,” they complain, “you don’t know who to believe”. Many folks simply bury any rising sense of confusion by going along with majority opinion or the opinion of whoever appears to be the most highly decorated or popular commentator. Others will simply believe the version of events that ‘seems’, ‘feels’ or ‘sounds’ right to them.

If someone says that studies have proven “beyond all doubt” that eating saturated fats is harmful, do you ask to see those studies before vowing to surgically trim all the fat from any piece of meat that ever passes your lips? Or do you simply believe them? When vegetarian activists claim that avoiding meat will make you live longer, do you ask whether any studies exist that actually show this to be true? Or do you believe their emotionally based anti-meat scare mongering and proceed to delete the most nutrient dense food ever known from your diet? When the leader of your country announces that he is about to support war on a country that is allegedly harboring weapons of mass destruction, but cannot provide anything that even remotely resembles evidence, do you smell a rat? Or do you join the frenzied masses and demand that we send our young men and women off to kill and be killed, to fight in a war that will inevitably result in the annihilation of thousands of innocent civilians?

There is a widespread phenomenon that I like to refer to as the “They Syndrome”. This is when people say things like “They say that low-carbohydrate diets are bad for you” or “They reckon ACME shares are a pretty good buy at the moment” or “They said in this morning’s paper that Osama Bin Laden is hiding in Outer Mongolia”.

Who the hell is “they”?

“They” is typically a vague and often completely unidentifiable and unverifiable source floating somewhere out “there”. For the Easily-Brainwashed Sucker, that’s as good a source as any!

2. Believe that because something is widely held as fact, it must be true

Humans typically find great solace in being part of the crowd. As Mark Twain once wrote, “We are discreet sheep; we wait to see how the drove is going, and then go with the drove.”

Being part of the crowd provides a sense of comfort and belonging. It can also have an incredibly powerful mind-dulling effect, one that is strongly antithetical to logical and independent thought. As anyone who has ever watched a mob riot or stock market panic can attest, even highly intelligent and respectable individuals quickly come unglued when caught up in the mass-hysteria of crowds. In chaotic events like these, being part of the crowd can rouse people into acting in the most irrational and self-destructive manner.

During less stormy times, being part of the crowd lulls people into believing that if everybody believes something, it must be true. After all, why would so many people believe something if it wasn’t? Never mind that, not too far back in history, the overwhelming majority of people believed that the world was flat; never mind that that the increasingly concentrated ownership of mass media outlets makes the spreading of misinformation easier than ever before.

Nope, never you mind these things at all; if you want to be an Easily-Brainwashed Sucker, you need to think like the rest of the crowd. In fact, if you’re a really good member of the flock, you’ll make a point of vigorously ridiculing those obnoxious black sheep who dare to speak their own minds–regardless of whether or not they may actually be speaking the truth!

Baaa!

3. Practice blind obedience to authority

Some especially gullible members of our society believe that if something is proclaimed by a large organization that is considered an ‘authority’ in its field, then it must be factual.

I have actually read arguments in support of the anti-cholesterol, anti-fat hypothesis that went something like this:

“Do you really think that respectable authorities like the Government, the American Heart Association, the American Medical Association, the American Dietetic Association, the Food and Drug Administration, the National Institutes of Health, the USDA, the American Diabetes Association, yaada, yaada, yaada, are all mistaken when they tell us that saturated fat and cholesterol are harmful?”

Such a stance is known as the ‘appeal to authority’, and if you ever come across anyone who uses it, rest assured you are dealing with a first-class moron.

This line of argument assumes that when a group of fallible human individuals become part of a large and so-called ‘respected’ organization, then suddenly, almost as if by magic, they collectively become wonderfully impartial and infallible.

Reality suggests otherwise. Most of these oft-quoted organizations have extensive financial ties to food and/or drug manufacturers that stand to benefit from official support of the lipid hypothesis.

The American Heart Association, for example, has several hundred products bearing its famous ‘heart-check’ logo. It is estimated that the AHA earned over two million dollars from its certification program in 2002(1). Among the so-called ‘heart-healthy’ foods that can be found on the AHA heart-check list are(2):

* General Mills Cheerios, Cocoa Puffs, Cookie Crisp, Corn Chex, and Count Chocula;
* Healthy Choice Low Fat Ice Creams;
* Chocolate Moose Milk Chocolate Drinks;
* Malt-O-Meal Frosted Mini Spooners, Honey Graham Squares, and Honey Nut Toasty O’s;
* Kellogg’s Frosted Mini-Wheats Big Bite;
* Kellogg’s Nutri-Grain Cereal Bars;
* Pop-Secret 94% Fat Free Butter Microwave Premium Popcorn.

Sugar-laden, highly processed garbage, you say? Well, don’t expect the AHA to concur, so long as the giant health organization continues to receive up to $7,500 per product per year to endorse such foodstuffs! The AHA has also received funding from cholesterol-lowering drug manufacturers like Merck, Pfizer, Astra-Zeneca, and Bristol-Myers-Squibb.

The American Dietetic Association (ADA) issues ‘fact sheets’ providing information on various nutrition and health topics; most of these are underwritten by companies whose products are discussed in the fact sheets. Manufacturers that have given at least $100,000 towards the production of these sheets include Coca-Cola, Kellogg, Kraft Foods, Weight Watchers International, Campbell Soup, National Dairy Council, Nestle USA, General Mills, Monsanto, Nabisco, Procter and Gamble, Ross Products, Wyeth-Ayerst Labs, and Uncle Ben’s(1).

The Los Angeles Times revealed in late 2003 that hundreds of National Institutes of Health employees had been accepting consulting fees from biotech and pharmaceutical companies at least since November 1995. Over 500 agency employees had engaged in paid consulting arrangements with 1,515 outside employers since 1999. Some of these contracts involved such major cholesterol-lowering drug manufacturers including Pfizer, Wyeth Pharmaceuticals, and AstraZeneca(3-5).

The Food and Drug Administration (FDA) is the massive government agency that decides which new drugs will be allowed into the market, when a drug should be pulled from sale because of safety concerns, and whether specific health claims can be made for individual food products and supplements.

In September 2000, USA Today reported that fifty-four percent–more than half–of the experts hired to advise the FDA on the safety and effectiveness of medicines have financial relationships with drug manufacturers that will be helped or hurt by their decisions. Some of these advisors had helped a pharmaceutical company develop a medicine then served on an FDA advisory committee that judged the drug!(6)

The close financial ties between these ‘impartial’ and ‘respected’ organizations and large companies that benefit greatly from the low-fat, low-cholesterol paradigm may explain why the are reluctant to come to the only conclusion one can come to after a thorough review of the relevant literature: namely, that this paradigm is utter garbage.

It was government meddling in the nutrition arena that allowed the low-fat, high-carbohydrate theory to really kick off in America and, by default, the rest of the Western world. Along with the AHA, the U.S. Government’s National Heart, Lung, and Blood Institute (a division of the NIH) was a key player in winning acceptance for the anti-cholesterol hypothesis, while the USDA’s geometric nutritional absurdity, the ‘Food Guide Pyramid’, influenced millions of folks into believing that a high-carbohydrate grain-based diet was the epitome of healthy eating. The end result of this scientifically baseless stupidity is the unprecedented levels of obesity and type 2 diabetes we now see around us.

If you want to be an Easily-Brainwashed Sucker, believe with all your might that governmental and private authorities are competent, benevolent and bipartisan folks that are always acting in your best interests. When they screw up in spectacular fashion, blame it on the weather!

4. Place great emphasis on formal credentials

If someone has presented a plausible and intriguing argument, then that argument should be assessed on its own merits, not on the glowing qualifications–or lack thereof–of its author.

When the Easily-Brainwashed Sucker reads or hears something that he is not sure about, does he jump on the Internet or drive down to his local library in an effort to obtain first-hand the data that would help him ascertain the validity of this information? Hell no! That would be too much work and would cut into valuable TV time!

The Easily-Brainwashed Sucker is too lazy to expend the effort required to verify the facts. Instead, he relies on the opinion of people who might have already done this for him; people with lots of fancy initials after their names. After all, you have to pretty smart and have spent a lot of time at university to have all those titles, right?

Some pretty wise individuals do indeed emerge from the university system–as do an incredibly large number of unthinking twits who couldn’t tell a donut from a hemorrhoid cushion.

To illustrate my point, let me again cite the case of two of modern medicine’s favorite whipping boys: saturated fat and cholesterol. Four decades’ worth of clinical trials have completely failed to show that dietary saturated fat restriction or dietary cholesterol-lowering can reduce CHD mortality(7). Of the 23 long-term prospective studies that examined the relationship between dietary fat and CHD, you could count those that found even desperately weak associations between saturated fat and CHD on one hand–with a couple of fingers missing (8-30). Even statin drugs, the alleged saviors of the lipid hypothesis, don’t even work by cholesterol-lowering; these drugs are now well known to exert a host of biochemical effects beyond mere cholesterol-lowering (effects that were not exerted by their largely ineffective cholesterol-lowering predecessors, the fibrates), and clinical trials have repeatedly shown a dissociation between the mortality benefit of statins and the level of LDL cholesterol-lowering they induce.

Despite a complete lack of corroborating evidence, however, ‘highly-educated’ researchers the world over still believe that saturated fat and cholesterol cause heart disease!

Extensive education does not in any way impart a monopoly on intelligence or the ability to think critically. In fact, it often does just the opposite. Modern education is aimed overwhelmingly at inculcating students with rigid, often outdated, and sometimes downright erroneous curricula.

This last century has seen an increasing reliance by universities on funding from ‘benevolent’ foundations, the largest of which are little more than tax-exempt mechanisms for extending the influence of their wealthy corporate creators. In more recent decades, there has also been a dramatic increase in direct corporate sponsorship of universities. If you believe that these financial ‘gifts’ have come with no strings attached, you would be well advised to read the disturbing revelations in Foundations: Their Power and Influence by Rene Wormser, a member of the Reece Committee that conducted a congressional investigation of tax-exempt foundations in the early fifties. The Reece Committee discovered that foundations frequently used their financial power to determine the curriculum and research conducted at the universities they sponsored.

And when you are done with Wormser’s book, be sure to read Unhealthy Charities: Hazardous to Your Health and Wealth by James T. Bennett and Thomas J. Dilorenzo. You will learn how health charities such as The American Heart Association and the American Cancer Society spend much time and money on things that have nothing to do with research and aid to disease victims–like crying poor and pleading for donations when they are in fact hoarding hundreds of millions in money, real estate, cars, stocks & bonds, paying their top staff 6-figure salaries, holding ‘conferences’ at luxurious hotels, and enlisting government support to drive out smaller competing charities in order to ensure that their monopolistic reign continues unchallenged.

You may also like to consider the findings of a recent review published in the Journal of the American Medical Association, in which researchers analyzed data encompassing a total of 1,140 original studies that had addressed the association between industry sponsorship and research outcome. When the results of all these studies were pooled, they showed that industry-sponsored research was 3.6 times more likely to produce favorable findings than studies with no financial ties to the industry. The study also found that: “Approximately one fourth of investigators have industry affiliations, and roughly two thirds of academic institutions hold equity in start-ups that sponsor research performed at the same institutions.”(31)

If you want to be an Easily-Brainwashed Sucker, however, please do not consider the information provided by these commentators–you might just learn that our education system has many flaws. This will mean that you’ll have to get up off your weak-willed butt and start thinking and researching for yourself! Such a scenario is clearly unacceptable–no self-respecting Easily-Brainwashed Sucker would be caught dead engaged in such a frivolous activity as the independent and uncompromising pursuit of truth!

5. Be swayed by the ad hominem attack

One sure-fire sign of intellectual bankruptcy is reliance on the ad hominem attack. This is when someone seeks to discredit another person’s argument, not by rationally and systematically addressing the key points of that person’s argument, but by instead attacking that person’s personal character. To call someone unqualified, uneducated, disreputable, or a conspiracy nut, or to claim that they are a pug-ugly loser whose mother engages in the paid distribution of sexual favors, while failing to intelligently refute their arguments, is akin to placing a huge flashing sign above one’s head–one that screams “I cannot intelligently refute this person’s argument to save my life, so I am trying to divert attention to his alleged character flaws instead!” To maintain a robust Brainwashed Sucker state, ignore this warning sign no matter how brightly it flashes!

Ignorance is Bliss

Follow the tips in this article and you will be a welcome and easily-manipulated member of the worldwide family of Easily-Brainwashed Suckers, a group whose membership is in no way restricted by geographic, racial, cultural, gender, socioeconomic, or professional barriers!

—

References

1. Center for Science in the Public Interest. Lift the Veil report: Professional associations, charities, and industry front groups. Available online:
http://www.cspinet.org/new/pdf/lift_the_veil_guts_fnl.pdf (accessed August 18, 2004).

2. American Heart Association. Current Heart-Check mark products. Available online: http://216.185.112.90/productlist.aspx (accessed August 18, 2004).

3. Mondics C. Charges of ethical misbehavior stagger U.S. health agency. San Diego Tribune, Jun 1, 2004. Available online: http://www.signonsandiego.com/uniontrib/20040601/news_1n1nih.html
(accessed June 9, 2004).

4. Willman D. U.S. Scientists’ Deals With Drug Firms Under Review. Los Angeles Times, Dec 29, 2003.

5. Willman D. NIH Directors No Longer Drug Firm Consultants. Los Angeles Times, Jan 23, 2004.

6. Cauchon D. FDA Advisers Tied to Industry. USA Today, Sept. 25, 2000.

7. Corr LA, Oliver MF. The low fat/low cholesterol diet is ineffective. European Heart Journal, 1997; 18: 18-22.

8. Paul O, et al. A longitudinal study of coronary heart disease. Circulation, Jul 1963; 28: 20-31.

9. Gordon T. The Framingham Diet Study: diet and the regulation of serum cholesterol. In: The Framingham Study: An Epidemiological Investigation of Cardiovascular Disease, Section 24. U.S. Government Printing Office, Washington, D.C., 1970.

10. Medalie JH, et al. Five-year myocardial infarction incidence. II. Association of single variables to age and birthplace. J Chronic Dis, Jun, 1973; 26 (6): 325-349.

11. Morris JN, et al. Diet and heart: a postscript. British Medical Journal, 1977; 2: 1307-1314.

12. Yano K, et al. Dietary intake and the risk of coronary heart disease in Japanese men living in Hawaii. American Journal of Clinical Nutrition, Jul, 1978; 31: 1270-1279.

13. Garcia-Palmieri MR, et al. Relationship of dietary intake to subsequent coronary heart disease incidence: The Puerto Rico Heart Health Program. American Journal of Clinical Nutrition, Aug, 1980; 33 (8): 1818-1827.

14. Gordon T, et al. Diet and its relation to coronary heart disease in three populations. Circulation, Mar, 1981; 63; 500-515.

15. Shekelle RB, et al. Diet, serum cholesterol, and death from coronary heart disease: the Western Electric Study. New England Journal of Medicine, 1981; 304: 65-70.

16. McGee DL, et al. Ten-year incidence of coronary heart disease in the Honolulu Heart Program: relationship to nutrient intake. American Journal of Epidemiology, 1984; 119: 667-676.

17. Kromhout D, de Lezenne Coulander C. Diet, prevalence and 10-year mortality from coronary heart disease in 871 middle-aged men: the Zutphen Study. American Journal of Epidemiology, 1984; 119: 733-741.

18. Kushi LH, et al. Diet and 20-year mortality from coronary heart disease: the Ireland-Boston Diet-Heart Study. New England Journal of Medicine, 1985; 312: 811-818.

19. Lapidus L, et al. Dietary habits in relation to incidence of cardiovascular disease and death in women: a 12-year follow-up of participants in the population study of women in Gothenburg, Sweden. American Journal of Clinical Nutrition, Oct, 1986; 44 (4): 444-448.

20. Khaw KT, Barrett-Connor E. Dietary fiber and reduced ischemic heart disease mortality rates in men and women: a 12-year prospective study. American Journal of Epidemiology, Dec, 1987; 126 (6): 1093-1102.

21. Farchi G, et al. Diet and 20-y mortality in two rural population groups of middle-aged men in Italy. American Journal of Clinical Nutrition, Nov, 1989; 50 (5): 1095-1103.

22. Posner BM, et al. Dietary lipid predictors of coronary heart disease in men: the Framingham Study. Archives of Internal Medicine, 1991; 151: 1181-1187.

23. Dolecek TA. Epidemiological evidence of relationships between dietary polyunsaturated fatty acids and mortality in the multiple risk factor intervention trial. Proc Soc Exp Biol Med, Jun, 1992; 200 (2): 177-182.

24. Fehily AM, et al. Diet and incident ischaemic heart disease: the Caerphilly Study. British Journal of Nutrition, 1993; 69: 303-314.

25. Goldbourt U, et al. Factors predictive of long-term coronary heart disease mortality among 10,059 male Israeli civil servants and municipal employees: a 23-year mortality follow-up in the Israeli Ischemic Heart Disease Study. Cardiology, 1993; 82: 100-121.

26. Esrey KL, et al. Relationship between dietary intake and coronary heart disease mortality: Lipid Research Clinics Prevalence Follow-Up Study. Journal of Clinical Epidemiology, Feb, 1996; 49 (2): 211-216.

27. Ascherio A, et al. Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United States. British Medical Journal, 1996; 313: 84-90.

28. Pietinen P, et al. Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men: the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. American Journal of Epidemiology, 1997;145: 876-887.

29. Hu FB, et al. Dietary fat intake and the risk of coronary heart disease in women. New England Journal of Medicine, Nov 20, 1997; 337 (21): 1491-1499.

30. Tanasescu M, et al. Dietary fat and cholesterol and the risk of cardiovascular disease among women with type 2 diabetes. American Journal of Clinical Nutrition, Jun, 2004; 79: 999-1005.

31. Bekelman JE, et al. Scope and impact of financial conflicts of interest in biomedical research: a systematic review. Journal of the American Medical Association, Jan 22-29, 2003; 289 (4): 454-465.

The HCG Diet – Just Another Scam

Anthony Colpo — Fri, 23 Jul 2010 05:56:01 +0000

One of the latest fads to sweep the fat loss arena is the “HCG Diet”. HCG stands for human chorionic gonadotropin, a hormone used in fertility treatments and found naturally in the bodies of pregnant women to ensure the developing foetus receives enough calories. Most bodybuilders will instantly recognize the HCG pseudonym; pharmaceutically enhanced male lifters have long used HCG injections “post cycle” to kick start their natural production of testosterone, which typically shuts down during a steroid cycle.

Which raises the obvious question: why on earth would anyone use this stuff in an attempt to lose weight?

Pregnant Women and Indian “Fat Boys”

The idea of employing HCG for weight loss first occurred to one Dr ATW Simeons back in the 1930s. After studying pregnant women and treating “fat boys” in India with HCG who didn’t lose weight yet allegedly reduced their hip circumference, Simeons came to the conclusion that HCG was an effective fat ‘mobilizing’ agent. He believed the observed change in body shape “could only be explained by a movement of fat away from abnormal deposits on the hips, and if that were so there was just a chance that while such fat was in transition it might be available to the body as fuel”. This, he surmised, would make it possible “to keep a “fat boy” on a severely restricted diet without a feeling of hunger, in spite of a rapid loss of weight.”[1].

Over the next 20 years, Simeons reportedly placed hundreds of his patients on a strict weight-loss regimen: a daily shot of HCG and two daily meals consisting of 100 grams of lean meat, some leafy vegetables, fruit and a piece of crispbread, for a total of no more than 500 calories a day.

In 1954, he claimed in the Lancet patients following the regimen for 40 days lost 20 to 30 pounds, and that 70% of them maintained their weight loss after going off the diet[2].

Other doctors began placing their own patients on Simeons’ regimen and claimed similar successes. The use of HCG for weight loss spread and during the seventies, weight loss clinics using HCG flourished. Of course, a lot of dodgey things flourished in the 70s (ELO and bell bottom jeans, anyone?).

When the veracity of the HCG weight loss claims was put to the test in tightly controlled trials, the results painted an entirely different picture. Sure, significant weight losses were often observed on the Simeon regimen – but in most instances, identical weight losses were also observed in those eating the same diet but receiving a placebo. Any spectacular weight loss seen with the Simeons regimen was due to the extremely low calorie diet employed, not HCG.

After a string of failed trials and a series of statements from medical and health organizations discouraging the use of HCG for weight loss, its use gradually fell out of favour. In 1976, the Federal Trade Commission issued an order “requiring five independent California weight reduction clinic operators [including two Simeons companies], among other things to cease failing to make conspicuous disclosure statements in advertising, and to potential purchasers that drugs used in weight reducing programs have not been approved by the Food and Drug Administration as safe and effective for weight control; drugs do not cause more attractive redistribution of weight; and treatment required adherence to a 500 calorie daily diet.”[3]

However, after a long hiatus, the HCG weight loss claims are back. For this we can thank none other than infomercial king Kevin Trudeau.

The Ineffective Weight Loss Treatment ‘They’ Don’t Want You to Know About!

Trudeau’s 2007 book, The Weight Loss Cure They Don’t Want You to Know About, claims that “an absolute cure for obesity was discovered almost fifty years ago” but was “suppressed” by the AMA, the FDA, and “other medical establishments throughout the world.” Trudeau further claims that until now, “this miracle weight loss breakthrough has been hidden from the public so that drug companies can make billions of dollars selling their expensive drug treatments and surgical procedures for obesity.” The alleged “cure” consists of HCG injections plus a long list of do’s and don’ts [4].

Rest assured, I need little convincing that governments, businesses and influential ‘non-profit’ organizations routinely feed us misinformation on health (and just about everything else) in order to further their own dubious agendas. But Trudeau’s claim that the “miracle” weight loss effects of HCG (not a natural supplement but a pharmaceutical drug, remember) have been suppressed by governments and pharmaceutical companies is utter garbage. The truth is that the fat loss effects of HCG are far from miraculous – as we shall discuss shortly.

In 2007, the FTC charged Kevin Trudeau with violating a court order by misrepresenting the contents of the book [5]. In infomercials, Trudeau falsely claimed that the book’s weight-loss plan is easy to do (it’s not), can be done at home (well, I guess it can, if you can find a doctor or black market source for genuine HCG and are comfortable giving yourself the shots), and ultimately allows readers to eat whatever they want (gee, where have we heard that one before?).

Previous FTC action had led to a court order banning Trudeau from using infomercials to sell any product, service, or program except for books and other publications. The order specified he not misrepresent the content of the books. In 2008, the Court ruled that Trudeau had violated the previous order and ordered him to pay more than $37 million. Trudeau’s previous claims to fame include being sued by the FTC for claiming that a coral calcium product he sold cured cancer.

Clearly, anything promoted by Kevin Trudeau should be regarded with the utmost suspicion. But human hope, gullibility and sheer stupidity spring eternal. So let’s take a look at the evidence (or lack of it) for HCG. What exactly did the clinical trials show?

HCG on Trial

The earliest published trial examining the effect of HCG on weight loss was conducted by Dr Stuart Carne[6]. The British physician had been using Simeon’s protocol on overweight patients since 1959 with mixed results. It had become clear to Carne that strict adherence to the 500-calorie diet was essential for the plan to deliver results similar to those reported by Simeon. In order to determine whether HCG played any real role in the weight loss, or whether the extremely low calorie diet alone was responsible, he conducted two trials.

In the first, two groups of patients were given either HCG (125 IU daily, as prescribed by Simeons) or placebo injections containing a saline solution. According to Carne, both substances were presented to him in identical vials as a powder to be reconstituted, and numbered in random order. He did not know which contained HCG and which contained the placebo until the trial was over. In no case was a vial prepared for one patient and used for another. After six weeks, there was no significant difference in weight loss (21 versus 19 pounds in the HCG and placebo groups, respectively).

In the second trial patients were randomly selected to undergo the diet plus daily saline injections or the diet alone. And this is where things got interesting. After six weeks, there was a statistically significant greater weight loss in the group receiving saline placebo injections (22.4 versus 17.7 pounds in the placebo injection + diet versus diet only groups, respectively). Weekly weight loss was greater during the entire six week period with the placebo injections. The patients receiving the saline injection also gushed on about how much easier it was to follow the diet and how much more energy they had when compared to their previous attempts to follow very low calorie diets.

Is there something “miraculous” about injectable saline that causes accelerated weight loss and increased energy levels?

Of course not. The real reason for the greater weight loss is hardly out-of-this-world. As Carne explained, the subjects receiving injections “not only had to come to my surgery six days every week, but they were also weighed by me on my scales every day. Failure to lose weight from one day to the next or even worse, the slightest gain in weight, led to a careful review by me of their previous day’s diet. As one patient (a – schoolmistress) said to me: ” You know, Doctor, every time I look at a piece of food I think of what is going to happen when I get on your scales tomorrow morning.” On the other hand, those on the diet alone had only to report to me twice a week to be weighed. We might presume that when they were tempted by food they may have said to themselves: “Never mind if I do eat it, I can always make up for it in the next couple of days.”

But what about the reports of diminished lethargy and increased energy that allow people to adhere to a normally intolerable intake of only 500 calories per day? Carne elucidated the real factor: “It would be a boon to those who are overweight to have some drug that would enable them to lose weight safely without having to fight their appetite urges. C.G. is not an answer, nor does it seem appreciably to increase their weight loss if they do adhere to a very rigid 500-calorie diet. On the other hand, those on the diet alone constantly complained of feeling tired or weak. The patients on either C.G. or the inert placebo were keen to tell me how much benefit they got from the injections and how previously they had failed to keep to any diet they had tried (for obesity is usually a chronic disease and we rarely see a patient who has not tried other methods of shedding their excess weight).”

In other words, the true value of the HCG and saline shots was their placebo effect. Tell someone to follow a 500-calorie diet and they’ll struggle to stick to it. But the moment you start sticking needles into people’s posteriors, they start to believe they are receiving some high-tech, super-effective fat loss agent. Buoyed by this knowledge, their mental outlook changes to such a positive degree they truly believe the treatment is favourably affecting their physiology.

The placebo effect, my friends, is very real. And it has made a lot of dietary and medical charlatans very, very rich over the years.

More Trials Debunk HCG For Weight Loss

We could write off HCG from Carne’s results alone, but numerous other investigators have also examined the Simeon regimen. Let’s see what they found.

In 1963, Dr. LS Craig treated twenty obese female clinic outpatients for a forty-day period with a 550-calorie diet similar to Simeon’s and a daily injection of either chorionic gonadotropin or a placebo solution, administered in double-blind fashion[7].

All but one of the women lost weight during the treatment period. A weight gain of 2 pounds occurred in one woman who was treated with chorionic gonadotropin. The difference in loss of weight in the treated women and in the control subjects was insignificant. The average loss at the end of the treatment period was 6.5 pounds in the treated women and 8.8 pounds in the control subjects. Maximum loss in a treated subject was 23 pounds and in a control subject 17 pounds.

Among the fourteen women who agreed to have their body measurements taken before and after treatment, circumference of waist, hips or axillary area of the HCG and control subjects did not vary significantly.

Craig noted “the losses were small and not uniform, suggesting varied adherence to the diet. The basal metabolic rate was increased in four treated patients and two control subjects. These changes could not be correlated with weight loss, apparent adherence to diet or protein-bound iodine levels.”

Capt. Barry W. Frank, MC, from the U. S. Army Hospital, Medical Service, Fort Carson, Colorado studied obese men and women given HCG or placebo[8]. Thrice weekly the subjects received an injection of either 200 mg HCG or placebo. The diet prescribed was an exchange-type diet consisting of 85 g of protein, 31 g of fat, 133 g carbohydrate and approximately 1,030 calories.

HCG devotees have criticised Frank for his use of a 1,030 calorie diet instead of Simeons’ 500-calorie regimen. Frank deliberately chose the higher calorie intake to make the adherence to the diet easier for his subjects. Furthermore, 1,000 calories per day is still a very low calorie intake for most people – only the smallest sedentary female would fail to achieve a calorie deficit on such a low energy intake. If HCG was the miraculous “fat mobilizing” and satiating agent that is was purported to be, then it should have produced significantly greater fat loss at any degree of weight loss-inducing caloric restriction.

But it didn’t.

The mean weight loss of the group treated with the hormone was 12.3 pounds and of the control group 11.5 pounds. There were no significant differences in weight loss, body girth measurements, or subjective symptoms of hunger.

Finally, Some Scientific Support?

The next two trials to be published both claimed to have found greater weight losses on patients treated with HCG. The first of these was reported by London doctor Philip Lebon, who assigned obese patients to Simeons’ 500-calorie diet and either HCG or placebo injections[9]. Some of the patients received as many as 3 courses of treatment. Of those who underwent only one course of treatment, Lebon reports that patients given HCG lost 13.0 pounds, compared to 9.6 pounds.

While HCG proponents would no doubt embrace this supportive study, it is problematic for several reasons:

In his paper, Lebon did not discuss randomization procedures, for the highly probable reason there were none. Scanning through the list of patients reveals several instances of identical surnames within the HCG and placebo groups, indicating that patients were manually and non-randomly assigned to the groups, in some instances on the basis of familial relationship.

The paper is poorly reported, with age information missing for forty percent of the patients.
Although data for 47 patients are originally presented in the HCG vs placebo trial, only 24 are considered in the final results.

The length of treatment varied widely among patients, ranging from four to 40 days.
The difference in weight loss is wholly explained by extreme differences in ‘outliers’. The 24 patients whose results were considered were divided into four groups based on the degree of weight loss: “very good” (18 lbs or more), “good” (14-18 lbs), “fair” (10-14 lbs), and “poor” (less than 10 lbs).In both groups, there were 2 patients in the “good” category and 5 and 7 patients in the “fair” category in the HCG and placebo groups, respectively. The majority of patients fell into these two middle categories, and there was little difference between them. However, there were five patients from the HCG group in the “very good” category, but none from the placebo group. Meanwhile, in the “poor” category, there were three from the placebo group but none from the HCG group. Are these differences in the outlier groups a genuine artifact of the HCG treatment – or purely due to chance? If larger studies of higher quality fail to confirm these results, then we have our answer

No offense to Lebon, who for all I know may have been a wonderfully upstanding citizen and conscientious practitioner, but both his trial and published paper were of highly questionable quality.

Asher and Harper to the Rescue?

The remaining supportive study was conducted by two doctors, one of which used HCG in his own practice to treat obese patients. Claiming that most of the previous non-supportive studies used protocols not exactly identical to those used by Simeon, they set out to correct this alleged discrepancy in their own double blind trial.

Asher and Harper compared twenty female patients on 500- to 550-calorie diets receiving daily injections of 125 IU of human chorionic gonadotrophin (HCG) with 20 female patients on isocaloric diets receiving placebo injections[10]. Patients in both groups were instructed to return for daily injections 6 days each week for a total of 36 injections (unless desired weight was achieved prior to this). The HCG group lost significantly more mean weight, had a significantly greater mean weight loss per injection, and lost a significantly greater mean percentage of their starting weight. The mean weight loss in the HCG group was 19.96 pounds and 11.05 pounds in the placebo group. The percentage of affirmative daily patient responses indicating “little or no hunger” and “feeling good to excellent” was also significantly greater in the HCG group than in the placebo group.

So at last, confirmation that HCG really does work for fat loss, right?

Not so fast.

Again, one of the critical tests of validity for research findings is that they are able to be replicated by other researchers. If you claim a certain finding in your research, but other scientists fail to replicate those results no matter how hard they try, then your findings are untenable.

So, seeking to replicate these results, researchers from the Letterman Army Medical Research Center in San Francisco randomized women to either HCG or placebo[11]. They recruited slightly more patients, of similar age, starting weight and height, than Asher and Harper. Each patient was given the same diet (the one prescribed in the Asher-Harper study), was weighed daily Monday through Saturday and was counselled by one of the investigators who administered the injections. Laboratory studies were performed at the time of initial physical examinations and at the end of the study. Twenty of 25 in the HCG and 21 of 26 patients in the placebo groups completed 28 injections. There was no statistically significant difference between the two groups in number of injections received, weight loss, percent of weight loss, hip and waist circumference, weight loss per injection, or in hunger ratings.

Thus, Asher and Harper’s results were not replicated. One of the authors (Harper) had a vested financial and professional interest in the Simeons protocol, as he used it in his own practise. However, both Asher and Harper adamantly maintain that a strict double blind protocol was adhered to at all times during the study. Let’s give them the benefit of the doubt and see if anything else may have affected the results.

Reading through the Asher and Harper paper, we learn that of the forty patients starting the study, 17 of 20 in the HCG group and 13 of 20 in the placebo group completed 30 or more injections. This would suggest a greater lack of compliance, for reasons unknown, in the placebo group. The authors acknowledged this but believed that an appetite-suppressing effect of HCG was responsible. However, other researchers have continually failed to detect this mystical appetite suppressing effect.

We also learn that the patients followed their regimens for different lengths of time, and not all received their injections in the intended manner. Patients were to return to the office six days each week for 36 injections “unless the desired weight was achieved prior to this”. According to the authors: “The majority of these missed injections were for legal misses, i.e., holidays (the study was done between August and February and holiday injections were not required). In addition…some patients did not receive shots during the time of heavy menstrual flow and a few of the misses occurred because of trips and for other “excused” reasons.”[12]

The authors deny any of this could significantly have affected the results, but nonetheless the picture quickly begins to emerge that compliance and control in this study was less than optimal.

While Asher and Harper’s patients received 36 injections over a variable number of days (exact information not published), all of the Letterman study participants received 28 injections over a 32-day period.

Another significant difference between the two studies is that all the patients in the Letterman study “had the added reinforcement to comply by peer pressure as they all reported daily to the clinic at the same time and developed a certain “group spirit” which the Asher-Harper patients did not have.” Whether this any extra motivation from this camaraderie overrode any appetite suppressing effect HCG, or whether the alleged appetite suppressing effects of HCG are simply a myth, could not be discerned from this study. What we do know is that was a more strictly conducted endeavour that completely failed to replicate the results of Asher and Harper.

Lebon 1966 and Asher and Harper 1973 are the only two published and allegedly double blind trials that have reported positive results for HCG. Both feature problematic methodology and both have been disproved by many more trials of higher quality.

Interestingly, Asher and Harper briefly mention in their paper an earlier trial they had performed that failed to find any weight loss benefit for HCG. This study was never published.

HCG Continues its Downward Slide into Weight Loss Purgatory

In the largest trial examining HCG for weight loss, two hundred two patients participated in a double-blind randomized crossover study of HCG vs placebo[13]. “Crossover” means that all subjects in the study receive both HCG and placebo during alternate and randomly assigned periods. Serial measurements were made of weight, skin-fold thickness, dropout rates, reasons for dropping out, and patient subjective response. There was no statistically significant difference in any of these measures between those receiving HCG vs placebo during any phase of this study.

Greenway and Bray randomized forty women to receive injections of either HCG or placebo 6 days a week for 6 weeks[14]. As well as weight loss and subjective rating of hunger, the researchers measured the circumference of the mid-thigh, chest, hip and upper arm. Weight loss was identical between the two groups, and there were also no differences in hunger nor localized body measurements.

Miller and Schneiderman performed a double blind crossover trial of HCG vs placebo and observed no significant differences in weight loss, mood, hunger, and no apparent difference in adherence to diet compared to placebo[15]. In contrast, a significant difference was found in the ability of subjects to lose weight in the first four weeks of the study in contrast with the second four weeks, no matter which agent was used.

In a double-blind, placebo-controlled study by Bosch et al, the effects of HCG on weight loss were compared with placebo injections[16]. Forty obese women (body mass index greater than 30 kg/m2) were placed on the same diet supplying 1200 calories per day and received daily injections of saline or HCG, 6 days a week for 6 weeks. A psychological profile, hunger level, body circumferences, a fasting blood sample and food records were obtained at the start and end of the study, while body weight was measured weekly. Subjects receiving HCG injections showed no advantages over those on placebo in respect of any of the variables recorded. The researchers concluded “there is no rationale for the use of HCG injections in the treatment of obesity.”

After a nine-day control period, six hospitalized obese women were placed on 500 calorie diets and were given 125 IU of human chorionic gonadotropin (HCG) intramuscularly daily for 30 days[17]. Another five obese women consumed identical diets but received placebo injections. Mean weight loss in the two groups was almost identical, and there were no differences in reduction of triceps skinfold thickness or circumferential body measurements of the chest, waist, hips, and thighs. Patterns of change of a variety of plasma and urine substrates, electrolytes, and hormones were similar in the two groups and consistent with semistarvation and weight loss.

A 1996 meta-analysis examining eight uncontrolled and 16 controlled clinical trials of HCG for weight loss concluded “there is no scientific evidence that HCG is effective in the treatment of obesity; it does not bring about weight-loss or fat-redistribution, nor does it reduce hunger or induce a feeling of well-being.”[18]

The Oral HCG and Obesity Website

If you run a Google search for “HCG Diet”, one of the first results to show will be for “The oral hCG (Human Choriogonadotropin) and obesity website” run by a Daniel Belluscio M.D. from Argentina. Of the oral HCG regimen, Belluscio’s website claims: “This reliable and effective method for obesity management has been validated by the appropriate Double-Blind studies”. When one clicks on the provided hyperlink to view these studies, they are taken to a page http://www.hcgobesity.org/hcg1.htm featuring a single unpublished, non-peer reviewed report of a study allegedly conducted by Belluscio and two other doctors.

In this study, the volunteers drank their HCG instead of being injected with it. There were two HCG groups receiving a low and higher dose, and a placebo group.

The abstract states “Female obese volunteers participating in a double blind study, and submitted to the administration of an oral presentation of hCG (Human Choriogonadotropin) plus a VLCD (Very Low Calorie Diet), decreased specific body circumferences and skinfold thickness from conspicuous body areas more efficiently than Placebo+VLCD -treated subjects.”

As one proceeds to read through the body of the study, one is confronted with a poorly written mountain of statistical gobbledegook that a skeptical mind would strongly suspect is designed to downplay the fact that HCG failed to achieve statistically significant differences in the overwhelming majority of body composition measures.

Close inspection of these results shows that the study in no way “validated” oral HCG as a “reliable and effective method for obesity management”. If anything, the results show oral HCG is basically a waste of time and money, and that one would be far better served using proven superior fat loss methods with an established track record.

The doctors claimed that “our results indicate that specific [skinfolds] are highly responsive to hCG pharmacological intervention (upper and lower umbilical)…The greater response was obtained in those regions where the corresponding circumference assessments resulted in nearly significant or significant decreases through the trial period”.

In other words, there was no greater weight loss http://www.hcgobesity.org/images/figure1abc.gif in the HCG groups, and no significant difference in changes of any body composition measure except for a mere two skinfold measures in the upper and lower umbilical areas of the stomach.

Belluscio et al also claim, “hCG-treated volunteers (G1+G2) showed a trend to improvement of inter-personal contacts and mood control when confronting upsetting or conflicting situations.” When researchers claim a “trend” towards a certain finding, it means there was no statistically significant finding. In a larger study with similar findings, the “trend” may reach statistical significance; of course, if that larger study was ever performed, the finding may not be replicated at all.

Sorry folks, but if I’m going to start injecting myself with fertility medications in the hope of getting shredded, I’m going to need far more convincing evidence than a badly written, unpublished, non-peer reviewed Internet “study” that failed to demonstrate clinically meaningful differences between the HCG and placebo groups.

HCG: Humanity’s Chronic Gullibility

I guess it’s too much to ask for people to get off their fat lazy asses and do some regular sweat-inducing physical activity on a regular basis and adopt sensible, healthy eating habits for the long term. Nope, such a boring non-gimmicky approach lacks the instant gratification factor that appeals to Homo televisionis and its increasingly stunted attention span. It also requires such distinctly unfashionable attributes like discipline, common sense, patience, and the cessation of acting like a helpless victim. As such, people remain prey to even the most idiotic weight loss fads – as the HCG hoopla shows, even fertility drugs are fair game as Generation XXL waddles on in search of the next magic weight loss bullet.

Despite its clinically demonstrated inefficacy, interest in HCG as a weight loss agent continues to grow. According to the LA Times, “more and more online companies are promising to supply the injections. The shots can come at a significant cost: Online prices range from $30 to more than $600 for a month’s supply. And they have side effects. Simeons noted that his female patients often became pregnant while on the shots, and today, in fact, HCG is approved by the Food and Drug Administration as a fertility treatment.”[19]

Other companies are getting around the legal ramifications of selling real HCG by offering oral “homeopathic” HCG. In other words, a product that effectively contains no HCG.

A fool and his money…

—

References

1. Simeons ATW. Pounds and Inches : a new approach to obesity. Private printing, 1974

http://www.hcgmedical.com/simeons/index.html

2. Simeons ATW. The action of chorionic gonadotropin in the obese. Lancet, 1954; II: 946-947.

http://www.ftc.gov/os/decisions/docs/vol87/FTC_VOLUME_DECISION_87_%28JANUARY_-_JUNE_1976%29PAGES_1184-1278.pdf

4. Trudeau K. The Weight Loss Cure They Don’t Want You to Know About. Alliance Publishing, 2007.

5. FTC: Marketer Kevin Trudeau violated prior court order. FTC news release, Sept 14, 2007.

http://www.ftc.gov/opa/2007/09/trudeau.shtm

6. Carne S. The action of chorionic gonadotropin in the obese. Lancet , 1961; II: 1282-1284.

7. Craig LS. Chorionic gonadotrophin in the treatment of obese women. American Journal of Clinical Nutrition, 1963; 12: 230–234.

http://www.ajcn.org/cgi/reprint/12/3/230

8. Frank BW. The use of chorionic gonadotrophin hormone in the treatment of obesity. A double-blind study. American Journal of Clinical Nutrition, 1964; 14:133–136.

http://www.ajcn.org/cgi/reprint/14/3/133.pdf

9. Lebon P. Treatment of overweight patients with chorionic gonadotrophin: follow-up study. Journal of the American Geriatric Society, 1966; 14: 116–125.

10. Asher WL, Harper HW. Effect of human chorionic gonadotropin on weight loss, hunger and feeling of well-being. American Journal of Clinical Nutrition, 1973; 26: 211-218.

http://www.ajcn.org/cgi/reprint/26/2/211

11. Stein MR and others. Ineffectiveness of human chorionic gonadotrophin in weight reduction: a double-blind study. American Journal of Clinical Nutrition, 1976; 29: 940–948.

http://www.ajcn.org/cgi/reprint/29/9/940.pdf

12. Asher WL, Harper HW. Human chorionic gonadotropin treatment for obesity: a rebuttal. American Journal of Clinical Nutrition, May 1974; 27: 450-455.

http://www.ajcn.org/cgi/reprint/27/5/450.pdf

13. Young RL, et al. Chorionic gonadotropin in weight control. A double-blind crossover study. JAMA, Nov 29, 1976; 236 (22): 2495-2497.

http://www.ncbi.nlm.nih.gov/pubmed/792477

14. Greenway FL, Bray GA. Human Chorionic Gonadotrophin (HCG) in the treatment of obesity: a critical assessment of the Simeons method. West Journal of Medicine, 1977; 127: 461–463.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1237915/pdf/westjmed00268-0035.pdf

15. Miller R, Schneiderman LJ. A clinical study of the use of human chorionic gonadotrophin in weight reduction. Journal of Family Practice 4:445–448, 1977.

http://www.ncbi.nlm.nih.gov/pubmed/321723?dopt=Abstract

16. Bosch B, et al. Human chorionic gonadotrophin and weight loss. A double-blind, placebo-controlled trial. South African Medical Journal, 1990 Feb 17; 77 (4): 185-189.

http://www.ncbi.nlm.nih.gov/pubmed/2405506?dopt=Abstract

17. Shetty KR, Kalkhoff RK. Human chorionic gonadotrophin (HCG) treatment of obesity. Archives of Internal Medicine, 1977; 137: 151-155.

http://archinte.ama-assn.org/cgi/content/abstract/137/2/151

18. Lijesen GK, et al. The effect of human chorionic gonadotropin (HCG) in the treatment of obesity by means of the Simeons therapy: a criteria-based meta-analysis. British Journal of Clinical Pharamacology, 1995; 40: 237-243. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1365103/pdf/brjclinpharm00004-0042.pdf

19. Conis E. HCG diet was largely discredited long ago. LA Times, November 02, 2009.
http://articles.latimes.com/print/2009/nov/02/health/he-nutrition2

1. Simeons ATW. Pounds and Inches : a new approach to obesity. Private printing, 1974 http://www.hcgmedical.com/simeons/index.html

2. Simeons ATW. The action of chorionic gonadotropin in the obese. Lancet, 1954; II: 946-947.

3. In the matter of Simeon Management Corporation et al. Order, opinion etc., in regard to alleged violation of Secs. 5 and 12 of the Federal Trade Commission Act. Docket 8996. Complaint, Oct 15, 1974. Final Order April 29, 1976. http://www.ftc.gov/os/decisions/docs/vol87/FTC_VOLUME_DECISION_87_%28JANUARY_-_JUNE_1976%29PAGES_1184-1278.pdf

4. Trudeau K. The Weight Loss Cure They Don’t Want You to Know About. Alliance Publishing, 2007.

5. FTC: Marketer Kevin Trudeau violated prior court order. FTC news release, Sept 14, 2007. http://www.ftc.gov/opa/2007/09/trudeau.shtm

6. Carne S. The action of chorionic gonadotropin in the obese. Lancet , 1961; II: 1282-1284.

7. Craig LS. Chorionic gonadotrophin in the treatment of obese women. American Journal of Clinical Nutrition, 1963; 12: 230–234. http://www.ajcn.org/cgi/reprint/12/3/230

8. Frank BW. The use of chorionic gonadotrophin hormone in the treatment of obesity. A double-blind study. American Journal of Clinical Nutrition, 1964; 14:133–136. http://www.ajcn.org/cgi/reprint/14/3/133.pdf

9. Lebon P. Treatment of overweight patients with chorionic gonadotrophin: follow-up study. Journal of the American Geriatric Society, 1966; 14: 116–125.

10. Asher WL, Harper HW. Effect of human chorionic gonadotropin on weight loss, hunger and feeling of well-being. American Journal of Clinical Nutrition, 1973; 26: 211-218. http://www.ajcn.org/cgi/reprint/26/2/211

11. Stein MR and others. Ineffectiveness of human chorionic gonadotrophin in weight reduction: a double-blind study. American Journal of Clinical Nutrition, 1976; 29: 940–948. http://www.ajcn.org/cgi/reprint/29/9/940.pdf

12. Asher WL, Harper HW. Human chorionic gonadotropin treatment for obesity: a rebuttal. American Journal of Clinical Nutrition, May 1974; 27: 450-455. http://www.ajcn.org/cgi/reprint/27/5/450.pdf

13. Young RL, et al. Chorionic gonadotropin in weight control. A double-blind crossover study. JAMA, Nov 29, 1976; 236 (22): 2495-2497. http://www.ncbi.nlm.nih.gov/pubmed/792477

14. Greenway FL, Bray GA. Human Chorionic Gonadotrophin (HCG) in the treatment of obesity: a critical assessment of the Simeons method. West Journal of Medicine, 1977; 127: 461–463. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1237915/pdf/westjmed00268-0035.pdf

15. Miller R, Schneiderman LJ. A clinical study of the use of human chorionic gonadotrophin in weight reduction. Journal of Family Practice 4:445–448, 1977. http://www.ncbi.nlm.nih.gov/pubmed/321723?dopt=Abstract

16. Bosch B, et al. Human chorionic gonadotrophin and weight loss. A double-blind, placebo-controlled trial. South African Medical Journal, 1990 Feb 17; 77 (4): 185-189. http://www.ncbi.nlm.nih.gov/pubmed/2405506?dopt=Abstract

17. Shetty KR, Kalkhoff RK. Human chorionic gonadotrophin (HCG) treatment of obesity. Archives of Internal Medicine, 1977; 137: 151-155. http://archinte.ama-assn.org/cgi/content/abstract/137/2/151

19. Conis E. HCG diet was largely discredited long ago. LA Times, November 02, 2009. http://articles.latimes.com/print/2009/nov/02/health/he-nutrition2

Boosting Growth Hormone with Diet & Training: Fact or Fiction? Part 1

Anthony Colpo — Wed, 21 Jul 2010 04:56:12 +0000

Do post-workout spikes in GH (and testosterone, IGF-1) increase muscle growth?

An ongoing obsession of bodybuilders and strength athletes is boosting growth hormone (GH) levels. This preoccupation extends back to the 1980s when, inspired by the infamous “Life Extension” duo Durk Pearson and Sandy Shaw, bodybuilders gulped down ungodly amounts of the GH-spiking amino acid l-arginine (and, in some instances, l-ornithine) in the hope of experiencing steroid-like muscle growth.

It didn’t work. These amino acids failed to produce the promised anabolic effects and, like so many highly-hyped muscle-building supplements, eventually fell by the wayside (and, like so many highly-hyped nutrition fads, were recently resurrected and marketed to a new generation of suckers, um, pardon me, customers too young to remember the fad’s original failure. In this case, arginine and ornithine have recently been doing the rounds in the form of largely useless pre-workout “nitric oxide boosters”).

In recent times, strength athletes have tried manipulating both their workouts and diets in an attempt to increase GH levels. The two best-known training methods for boosting GH are inclusion of compound multi-joint leg exercises such as squats and the use of short rest periods between sets (60 seconds or less).

As for diet, some strength athletes have been convinced by promoters of low-carbohydrate diets that these regimens will produce marked increases in GH. We’ll discuss the evidence, or complete lack of it, for this contention in Part 2. Today, we’ll take a critical look at the belief that workout-induced spikes of GH and other anabolic hormones result in greater muscle size and strength gains.

Squatting for Upper Body Growth?

Weight training folklore has long held that performing heavy lower body exercises such as squats results in extra muscle growth, not just in your legs but in your upper body as well. According to this theory, by regularly performing heavy squats your chest, shoulder, latissimus and arm exercises will produce more muscle growth than they otherwise would. The reason for this extra muscle growth, so the story goes, is that squats cause your body to pump out greater amounts of GH.

A lot of folks in the Iron Game regard the squats-boost-GH-boosts-upper-body-muscle-growth theory as a sacred tenet, and can readily regale you with tales of how their best whole-body muscle gains were made whilst regularly performing gut-busting squat sessions.

Others think the squat-upper body growth theory is a load of bollocks and maintain they’ve never noticed any difference in upper body growth as a result of regular squatting.

So who’s right?

Gone in Sixty Seconds

The fact that short rest periods (60s or less) produce greater GH spikes than longer rest periods between sets is not in dispute – it has been shown time and time again in controlled studies. Science has also clearly demonstrated that performing heavy leg workouts results in a far greater GH spike than performing workouts comprised solely of exercises for small muscle groups such as the upper arm muscles.

The real question is, do the brief growth hormone spikes that occur in conjunction with weight training workouts actually help to increase muscle growth or strength?

In 2001, a study was published in which 16 young untrained males were assigned to an arm-only training group, or a leg plus arm training group[1]. The study lasted nine weeks, and hormonal responses were tested during the first and last training sessions.

During this time, no difference was seen in resting hormone concentrations between the two groups. However, during the first training session plasma testosterone as well as plasma cortisol increased significantly in the leg+arm training group but not the arm-only group. Plasma GH rose in all exercise tests, except during the last test in the leg+arm group group. However, plasma GH was significantly higher in leg+arm training group than the arm-only group in the first training session.

At the end of the study, isometric (static) arm strength increased to a significantly greater degree in the leg+arm group. This finding is often used as ‘proof’ that training-induced GH and testosterone spikes have a positive effect on training outcomes. However, the leg+arm group started the study with significantly lower isometric arm strength, so this may have been the real factor behind their greater improvement. The fact that there was no difference between the two groups in functional strength gains adds further credence to this contention.

More Recent Research

In 2009, West et al published a study showing marked spikes in GH, testosterone, and IGF-1 after an arm+leg training workout. When the same subjects performed an arm-only workout, no such spikes in these hormones were seen. To see if the acute elevation of anabolic hormones was stimulating greater arm muscle growth in the arm+leg group, the researchers performed muscle biopsies four hours after both workouts. To further boost muscle protein synthesis, twenty-five grams of whey protein was given to the subjects post-workout on both occasions. No differences in muscle protein synthesis were observed between the two workout conditions[2].

These results indicate that acute training-induced hormone spikes have no anabolic effect during the post-workout recovery period.

But West et al didn’t stop there – they wanted to see what happened over the longer term. In a subsequent study, they took twelve healthy young men and studied the effects of training-induced hormone spikes on arm growth over a 15-week period[3]. Instead of dividing the lads into two groups, the researchers had them train their arms on separate days during the study. One day, their arm workout was followed by leg training. On the other day, they performed the arm workout only.

In weeks 1–6, the subjects trained each arm three times over 2 weeks, allowing 72 hours between the arm+leg and arm-only workouts. This format was used to ensure that enhanced post-workout muscle protein synthesis, which can be elevated in the untrained state for around forty-eight hours, occurred exclusively on the background of basal hormone concentrations after the arm-only workout and was not influenced by the hormonal spike from the arm+leg workout.

The researchers had previously shown that regular weight training shortens the duration (i.e. <28 hours) for which muscle protein synthesis is elevated after exercise, so in weeks 7–15, an extra training session was added to enhance the training stimulus. This meant each arm was now being trained twice per week with at least 48 hours between workouts.

Participants consumed eighteen grams of whey protein immediately before exercise and 18 grams at 90 minutes after all arm workouts to support maximal rates of muscle protein synthesis both in the absence and presence of elevated hormone concentrations. This procedure also helped to reduce variability of and standardize the nutritional environment surrounding the training sessions.

The workouts in the arm-only group consisted of bicep curls performed with one arm only. Three to four sets of 8–12 repetitions at a load around 95% of the subjects’ 10-repetition maximum (RM) were performed, such that voluntary failure occurred during the final set.

The same bicep curl routine was performed by the arm+leg group, but was then immediately followed by five sets of 10 repetitions of leg press and three sets of 12 repetitions of leg extension/leg curl “supersets” (1 set of each exercise, back-to-back, with no rest between sets) at around 90% of 10 RM. Between-set rest intervals for arm and leg exercises were 120 and 60 seconds, respectively. Participants followed a progressive training protocol, increasing the amount of weight lifted as their strength increased. Each training session was supervised individually, and compliance across 56 sessions (28 per arm) was 96%.

There was no elevation in serum growth hormone (GH), insulin-like growth factor (IGF-1), or testosterone after the arm-only protocol but significant elevations in these hormones immediately and 15 and 30 minutes after the leg+arm protocol. This significant difference in hormonal output was seen at both the start and end of the study.

So, once again, heavy leg training and short rest periods produced markedly higher post-workout hormone levels. But did this have any positive effect on muscle growth or strength increases?

Nope.

At the end of the study, there were no significant differences in any of the measured hypertrophy or strength variables. The cross sectional area (CSA) of type I muscle fiber increased 9% and 11%, type II muscle fiber CSA increased 21% and 24%, and elbow flexor CSA increased by 12% and 10% in in the arm-only and arm+leg groups, respectively.

Isometric strength increased by an average 20% and 19% in the arm and arm+leg groups, respectively. Similarly, 1 RM increased 23% and 25%, and 10 RM increased 46% and 47%.

More Research Debunks the GH-Spike Theory

de Souza et al, from the Metropolitan University of Santos in Brazil, compared the effect on strength and hypertrophy of eight weeks’ weight training using constant rest intervals and decreasing rest intervals between sets[4]. Twenty young men recreationally trained in strength training were randomly assigned to 2 groups. During the first two weeks of training, 3 sets of 10-12 repetition maximum with 2-minute rest intervals between sets and exercises were performed by both groups.

During the next six weeks of training, one group continued using 2 minutes rest between sets and exercises (4 sets of 8-10RM),while the other used rest intervals that gradually declined from 2 minutes to 30 seconds as the remaining 6 weeks progressed (4 sets of 8-10RM).

Total training volume (load × repetitions) of the bench press and squat were significantly lower for the decreasing rest interval group compared to the constant interval group (bench press 9.4% and squat 13.9% lower).

No significant differences were shown between the constant and decreasing rest interval groups for muscle cross sectional area (arm 13.8 vs. 14.5%, thigh 16.6 vs. 16.3%, respectively), 1RM (bench press 28 vs. 37%, squat 34 vs. 34%, respectively), and isokinetic peak torque.

de Salles et al randomly assigned thirty-six recreationally trained men to 1 minute, 3 minutes or 5 minute rest intervals[5]. Each group performed the same resistance training program for sixteen weeks. Four workouts were performed each week with the target rep ranges (4-6 RM and 8-10 RM) alternated every other workout.

The total training volume performed by the 3- and 5-minute groups was significantly greater for the bench press and leg press over the 16-weeks. Despite similar baseline bench press strength, the final results in this lift were 92.5 versus 98.2 kg in the 1- and 5-minute groups, respectively. For the leg press, the final scores were 276.7, 305.and 321.7 kg in the 1-, 3-, and 5-minute groups, respectively. Muscle hypertrophy was not measured in this study.

Robinson et al assigned thirty-three strength trained men into 3 equal groups[6]. All used the same set, rep and exercise scheme except that rest periods varied according to group (30, 90 and 180 seconds). Training was performed four days per week for 5 weeks. At the start and conclusion of the study the following variable were measured:

1 RM squat
vertical jump height
performance during intermittent stationary bicycle sprint exercise (peak power, average peak power across 15 sprints, average power during each sprint, total work during each sprint and average total work of 15 sprints)
Body mass and composition

One rep maximum in the squat increased by 3kg, 7 kg and 9 kg in the 30, 60, and 180-second groups, respectively. Vertical jump ability did not improve significantly in any group. No significant difference in cycle sprinting outcomes was observed. No significant differences in body weight, skinfold or girth measurements were seen between the groups.

Western Australia researchers also examined the effect of manipulating rest period length on cycling sprint performance[7]. This study varied from most in that it involved female subjects and used higher rep ranges (15-20 RM) during the 5-week training regimen.

The eighteen active females were matched according to leg strength and repeated-sprint ability and randomly allocated to one of two groups; one group performed weight 3 days a week with 20-second rest intervals between sets, the other used 80-second rest intervals. Repeated-sprint ability (5 x 6-second maximal cycle sprints) improved to a greater degree after training with 20-second rest intervals (12.5% vs 5.4%) while greater increases in 3 RM squat strength occurred after training with 80-second rest intervals (45.9% versus 19.6%). There were no changes in body composition or weight for either group following training.

Buresh et al compared 60 and 150 second rest periods on changes in hormone response, strength, arm and thigh cross-sectional area and body composition during a 10-week training period[8]. Twelve untrained males trained four times per week and were instructed to consume 1.7 grams of protein per kilogram of body weight during the study.

One potential flaw of this study is that, unlike most other similar studies, the subjects conducted the majority of their workouts unsupervised. In other words, there were no researchers or trainers to ensure that the subjects adhered to the prescribed rest intervals; as anyone who has trained on both short and long rest interval routines, the former often require far greater discipline. Getting back under the bar after a mere minute’s rest, while you are still puffing like a locomotive from your previous set, requires a certain level of internal fortitude. One may reasonably question whether a group of subjects with no previous weight training involvement possessed this requisite level of fortitude. However, training logs maintained by both groups indicated shorter workout duration in the 60-second rest group, as would be expected due to their shorter rest intervals.

In week 1, postexercise plasma testosterone and cortisone levels were greater in the 60-second group, but no differences were seen in GH levels. At weeks 5 and 10, there were no differences in hormone levels. Arm cross sectional area increased significantly more with 150-second than with 60-second rest periods. There were no differences in strength increases.

Training in Tokyo

Japanese researchers measured acute changes in serum GH after 3 types of knee extension routines:

“hypertrophy-type”
“strength-type” (S-type),
“combi-type”

The male subjects aged 20–23 years had a minimum of several months’ weight training experience, but they had not taken part in any regular training program for at least 6 months prior to the beginning of the study[9].

In the hypertrophy-type routine, eight of the subjects performed nine sets of leg extension at 80–40% of 1RM. The session was divided into three parts with 3 sets each, and the rest periods between sets and parts were 30 seconds and 3 minutes, respectively. In each part, the percentage of 1RM was gradually lowered set-by-set.

The strength-type routine consisted of five sets at 90% of 1RM with 3-minute rest periods between sets.

In the combi-type regimen, subjects completed a routine identical to the strength-type protocol, but with an additional set of exercise of 50% of 1RM after the last set, with a 30-second rest period (similar to the final “back-off” set concept that used to be popular with bodybuilders back in the 80s).

GH concentrations were significantly higher after the hypertrophy-type regimen (419.8 ng·ml-1) than after combi-type (221.5 ng·ml-1) and strength-type (56.1 ng·ml-1) regimens.

To ascertain whether this made any difference to long-term weight training outcomes, the researchers then got sixteen subjects to perform leg press and leg extension exercises twice per week. During the first 6 weeks, all subjects used the hypertrophy-type regimen to gain muscular size (in this phase, the hypertrophy protocol consisted of two parts of 3 sets). During a subsequent four week strength phase, they were divided into two groups performing combi-type and strength-type regimens.

No significant changes were observed in body mass or percentage of body fat at any time points over the training period. Cross sectional thigh muscle area significantly increased in both groups during the hypertrophy phase. During the subsequent strength phase, CSA showed a further increase in the combination group but not the strength group but the difference was not statistically significant.

Muscular endurance assessed by work volume performed in the knee extension exercises improved significantly in both groups during the hypertrophy phase but showed a further increase during the strength phase only in the combination group (18.8 vs 24.7%).

1RM increased similarly during the first six weeks in both groups, but rose by significantly higher during the subsequent strength phase in the combination group (14.7%) than in the strength group (9.3%).

So in the final four weeks, a routine associated with higher GH output did result in statistically significant greater gains in 1RM and muscular endurance. Given the evidence so far, it’s probably safe to assume that these improvements had little to do with GH release but rather the neuromuscular and metabolic effects of the extra high-rep set. The light weight used in this set would have allowed a more explosive lifting action, possibly assisting in power and force development during performance of heavy lifts (explosive lifting with light weights is now a mainstay of many powerlifting routines). Meanwhile, the high repetition range of the extra set would have allowed for greater improvements in muscular endurance than the routine comprised only of low rep sets.

Another ‘Bro-Science’ Myth Busted

While certain training strategies can spike post workout release of GH (and testosterone and IGF-1), there is no evidence to show that these spikes in any way enhance muscle growth or strength gains.

Many weight trainers, having become especially enamored with the hormone-spiking theory, will have a hard time accepting this finding. However, when one considers the broader research findings, it makes perfect sense. Daily injections of recombinant growth hormone fail to add lean muscle to young men[10], so it’s hardly surprising that short-lived post-workout spikes in GH fail to do the same. Testosterone injections do indeed pack plenty of muscle onto a young buck’s frame, but only after raising blood levels of the mighty T to far higher levels than would ever be seen as a result of training-induced manipulations[11]. Interestingly, it’s well-known among the juicing fraternity that while GH injections often amplify the muscle-building effects of exogenous testosterone and anabolic steroids, used alone they have little effect on muscle hypertrophy.

While a minimum level of natural testosterone production is necessary for growth, and suppression of this production impairs the response to strength training[12], any short-lived spike achieved after training does not appear to exert a meaningful impact over and above that exerted by endogenous testosterone levels.

The mechanisms behind increases in exercise-induced hormones are unclear but, as West et al point out, are more likely related to metabolic stress and/or fuel mobilization rather than muscle anabolism. For example, strenuous regimens involving reduced rest times impede intra-workout recovery and result in greater lactate accumulation, which in turn appears to trigger greater GH output.

What Does This Mean For You?

Should you stop doing squats and discard short rest periods to the scrap heap of training history?

Hell no.

Irrespective of their effects on GH, squats are one of the most highly productive exercises a strength athlete could possibly perform. Not only do they provide a high degree of stimulation to the thigh, gluteus and lower back musculature, but they force a myriad of other muscles to assist in stabilizing the torso and fixing the loaded barbell in place on the lifter’s back or clavicles (in the case of front squats). Furthermore, the hip control learned during squatting is invaluable when instructing trainees in proper performance of many other lifts, especially the Olympic lifts and their variants. These training effects simply cannot be mimicked by using squat alternatives such as the leg press or machine hack squat.

As for short rest periods, I have witnessed some rather spectacular hypertrophy and strength gains in trainees performing routines with rest periods as low as 30 seconds. If this seems counter-intuitive in light of the evidence just presented, let me emphasize some important points:

With the exception of the Japanese study which used an extra high-rep set, the studies discussed above invariably prescribed the same number of sets and reps. In the long rest groups, where greater recovery between sets occurred, this allowed a higher weight to be used during subsequent sets, because the load on the bar often had to be reduced to maintain the desired rep range in the short-rest groups. This means that total volume (in terms of total greater poundage), a critical factor in strength and hypertrophy outcomes, was significantly greater during the longer rest routines. However, perhaps the greatest value of using short rest periods is that they will allow more sets, and hence greater total volume, to be performed during a given time frame. If your weight training sessions last 40-60 minutes, you’ll fit many more sets in when using short rest periods.
The impressive gains I have witnessed during short rest protocols were made in the context of programs that interspersed lower- and higher-volume phases, a highly effective technique for eliciting hypertrophy and strength gains and routinely used by elite weightlifting teams. The short-rest periods were used during the high volume phases for the reason just discussed above.

Also, I’ve observed that as a trainee adapts to using short rest periods, there is often little to no drop in weight on many exercises when working in the 5-6 rep range, while drops in weight are still necessary when using > 8 reps, no doubt due to the different primary energy pathways employed by these divergent rep ranges.

So keep squatting, and strongly consider interspersing training phases employing short rest periods with those using longer rest periods. Also be aware that there’s a way to minimize the reduction in weight that occurs during short-rest routines: performing exercises for different bodyparts back-to-back. This allows you to maintain a high volume of work during your training sessions (and a high calorie burn, which is especially helpful when trying to create a calorie deficit for fat loss).

Few studies have looked at this strategy; a recent study by researchers from the University of Ballarat in Victoria, Australia compared the acute effects of performing paired set versus traditional set training over 3 consecutive sets on volume load and electromyographic (EMG) activity of the pectoralis major, anterior deltoid, latissimus dorsi, and trapezius muscles[12]. There was no difference between volume load or EMG activity of the four monitored muscles was not different for the 2 conditions. However, the average rest between sets was 4 minutes in the traditional sets group, and 2 minutes in the paired set group, which is far longer than what I’ve successfully employed with myself and others (typically 10 – 30 seconds).

The paired set approach is a viable way to increase workout efficiency by greatly increasing volume without increasing the duration of your workouts. Caution should be exercised when using the paired set (or “superset”) approach with little or no rest – exercises requiring a high level of concentration and co-ordination, such as the Olympic lifts, are best performed in the traditional straight set manner, with sufficient rest periods to allow the performance of subsequent sets with minimal fatigue in order to maintain optimal technique. High demand exercises like squats and deadlifts are also probably best performed in straight set fashion.

Conclusion

Don’t waste your time chasing GH spikes during and after your workouts. The evidence overwhelmingly indicates that workout-induced hormone spikes have no effect on muscle growth and strength gains. Focus instead on optimizing far more important training variables such as volume, frequency and exercise selection.

Stay tuned for part 2, where we’ll destroy another laughable low-carb myth, that of wonderfully high GH output as a result of carbohydrate restriction.

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References

Hansen S, et al. The effect of short-term strength training on human skeletal muscle: the importance of physiologically elevated hormone levels. Scandinavian Journal of Medicine & Science in Sports, 2001; 11: 347–354.

West DW, et al. Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men. Journal of Physiology, 2009; 587: 5239–5247.
http://jp.physoc.org/content/587/21/5239.full.pdf+html

West DW, et al. Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors. Journal of Applied Physiology, 2010 Jan; 108 (1): 60-67.
http://jap.physiology.org/cgi/content/full/108/1/60

de Souza TP Jr, et al. Comparison between constant and decreasing rest intervals: influence on maximal strength and hypertrophy. Journal of Strength & Conditioning Research, Jul, 2010; 24 (7): 1843-1850.

de Salles BF, et al. Strength increases in upper and lower body are larger with longer inter-set rest intervals in trained men. Journal of Science and Medicine in Sport, 2010 Jul; 13 (4): 429-433.

Robinson JM, et al. Effects of different weight training exercise-rest intervals on strength, power and high intensity exercise. Journal of Strength & Conditioning Research,1995; 9: 216-221.

Hill-Haas S, et al. Effects of rest interval during high-repetition resistance training on strength, aerobic fitness, and repeated-sprint ability. J Sports Sci. 2007 Apr; 25 (6): 619-28.

Buresh R, et al. The effect of resistive exercise rest interval on hormonal response, strength, and hypertrophy with training. Journal of Strength & Conditioning Research, 2009 Jan; 23 (1):62-71.

Goto K, et al. Muscular adaptations to combinations of high and low intensity resistance exercises.Journal of Strength & Conditioning Research, 2004; 18: 730-737.

Yarasheski KE, et al. Effect of growth hormone and resistance exercise on muscle growth in young men. Am J Physiol Endocrinol Metab, 1992; 262: E261–E267.
http://ajpendo.physiology.org/cgi/reprint/262/3/E261?ijkey=52412d739c04b9f120ffe4bce648bcc0b184935c

Bhasin S, et al. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med, 1996; 335: 1–7.
http://content.nejm.org/cgi/reprint/335/1/1.pdf?ijkey=58de964f45a998acc7eb83f9d6f777a8efd54922

Kvorning T, et al. Suppression of endogenous testosterone production attenuates the response to strength training: a randomized, placebo-controlled, and blinded intervention study. Am J Physiol Endocrinol Metab, 2006; 291: E1325–E1332.
http://ajpendo.physiology.org/cgi/reprint/291/6/E1325?ijkey=f4686a7d641507dc9e11c406c533a8fff0eb92ab

Robbins DW, et al. Physical performance and electromyographic responses to an acute bout of paired set strength training versus traditional strength training. Journal of Strength & Conditioning Research, 2010 May; 24 (5): 1237-1245.