Vegetarian Diets Reduce Heart Disease? Nonsense!
Mar 2013 23
Print Friendly

Several readers have asked me about a study published back in January claiming to show vegetarians have a 32% lower risk of cardiovascular disease than meat eaters. I’ve only just had a chance to sit down, read through the study, and digest the results.

My conclusion, in short: It’s a load of cobblers.

The study in question is the massive EPIC-Oxford study, from which sources who should know better are claiming “Vegetarianism Can Reduce Risk of Heart Disease by Up to a Third“!

Holy asparagus.

Before you fall for this kind of nonsense, there’s a few things about this study you should know.

Real Science versus Pretend Science

Firstly, it was not a clinical trial that took a large group of people and randomly assigned them to either a vegetarian or meat-containing diet then followed them for a specified period of time, and found the vegetarian group had a 32% lower risk of CVD. Instead, it was a study that falls into the category of epidemiology, a field of research which without question constitutes the most useless and bullshit-filled arena in all of the modern health sciences.

If that sounds harsh…it isn’t. I could be far more scathing, considering the immeasurable damage caused by the modern infatuation with epidemiology and the associated and widespread idiocy that insists on accepting its statistical associations as physiological fact, despite the fact that one of the most basic rules of science is association does not equal causation.

So what exactly is epidemiology, I hear some of you asking?

Nutritional epidemiology is where researchers study populations for relationships between dietary factors and certain diseases. There are several types of epidemiological studies, including cross-cultural or ecological ones, which compare the relationships between diet and disease among different countries. This is the least reliable form of epidemiology, as you are often comparing the proverbial apples with oranges. For example, do you think, just maybe, there might be other factors aside from diet affecting heart disease risk in a country undergoing major political, economic and/or social upheaval, when compared to peaceful, affluent countries?

If you answered “no” to that question, then rejoice, for a secure and lucrative career as a money-wasting epidemiologist who fills journals with useless papers that come to utterly unfounded conclusions awaits you!

For the rest of you whose brains remain intact, the obvious answer to the above question is yes. Average stress levels in countries experiencing upheaval tend to be higher, and stress is a major contributor to heart disease (take a look at Eastern Europe, for example). Other factors such as cigarette smoking, differences in medical diagnosis, and excessive Vodka consumption (if you think I’m joking, take a look at Eastern Europe again) may also differ greatly from that experienced by someone living in a peaceful country.

Cross-cultural epidemiology, by the way, is the very kind that gave us the idiotic and highly destructive cholesterol theory of heart disease. Thanks to Ancel Keys and the obsession with cholesterol and saturated fat spawned by his fraudulent epidemiology, modern medicine is still nowhere near to finding a cure for heart disease, and its preventive efforts revolve around toxic statin drugs of negligible efficacy. It’s an absolute disgrace, and for that we have epidemiology to thank.

Eat the Red Ones Last

So why not recruit people in the same country, and follow them instead, you ask? Well, someone just a little bit smarter than Ancel Keys once asked the same thing, and the phenomenon of prospective cohort studies was born. This is where you take a bunch of folks who live in the same country (preferably in the same area of that country) and follow them for a given period of time. You tally up the amount of people who succumbed to whatever disease you are studying, then examine their dietary habits to see if any relationships consistently stand out. For example, if heart attack victims in the large mid-Western town of Dumpsterville tended to eat more red M&Ms but healthy people tended to eat more of the yellow ones, and you had the one-dimensional mind that seems to predominate among modern epidemiologists, you would conclude that red M&Ms cause heart disease, while yellow M&Ms prevent heart disease. Easy!

If that sounds absolutely ridiculous to you, then congratulations – you’re well on your way to grasping the field of nutritional epidemiology!

The reality is that the above hypothetical study could never prove jack about jack. There could be a million reasons why people who ate more red M&Ms suffered more heart disease. Perhaps these people had more aggressive temperaments or handled stress poorly, perhaps they came from lower-socioeconomic backgrounds, perhaps they smoked more, drank more and consumed more recreational drugs, perhaps they had a higher rate of childhood undernutrition, perhaps they were more likely to be overweight, perhaps they spent less time out in the sun and hence had lower blood levels of vitamin D…the list of potential confounders goes on and on.

And on.

Multivariate Self-Flagellation

Sometimes epidemiologists attempt to ‘adjust’ for these confounders in a process typically known as multivariate analysis, but this is merely mathematical maneuvering that attempts to do after the fact what real studies (i.e. randomized clinical trials) do right from the outset. RCTs minimize the effect of confounding factors right from the word go; before the study has even started, the participants in an RCT have been randomly assigned to the treatment and control groups. This means that each group is likely to have the same average age and a similar number of males, females, overweight subjects, smokers, drinkers, drug takers, sun worshippers, exercisers, and supplement users. Randomization isn’t perfect; sometimes the role of chance dictates that a group in a study is burdened with a higher number of smokers, as happened in the LA Veterans study that compared high-saturate and polyunsaturate-rich diets.

Most of the time though, randomization works remarkably well, as anyone who has ever spent any meaningful amount of time poring through the baseline characteristic tables of published RCTs can attest.

There’s one other important benefit of randomization: It ensures that each group is also more likely to have an even distribution of factors that contribute to heart disease that we don’t know about, or that researchers typically overlook. This is especially pertinent because epidemiologists often fail to include factors in their multivariate analyses that we already do know to contribute to heart disease. For example, nutritional epidemiology studies examining heart disease rarely, if ever, inquire about – let alone adjust for – bodily iron stores, psychosocial stress, sunlight/vitamin D levels, and use of recreational drugs aside from alcohol – even though all the aforementioned have a significant volume of evidence linking them to heart disease.

RCTs minimize the effect of these confounders on the end result by maximizing the likelihood that treatment and control groups are evenly weighted with subjects sporting these characteristics. That way we can be pretty confident that if the treatment group in an RCT enjoyed a significantly lower rate of heart disease, it was in fact due to the treatment and not some unforeseen confounder that was more prevalent in one group.

Epdemiology, in contrast, makes no such effort whatsoever. Instead, epidemiologists fire up their calculators after the study has finished and attempt to weed out the influence of whatever select list of confounding factors they have compiled. There’s an astronomical difference between running a few calculations on paper and actually going back in time and physically removing all important non-dietary differences from the participants of an epidemiological study. And at any rate, the second option is impossible.

Epidemiology has its legitimate uses, but the fact remains it is a vastly inferior and often totally inadequate mode of research for studying relationships between diet and disease. It’s a sad, sad testament to the woeful state of nutritional science when so many researchers and so-called ‘experts’ hold epidemiology in the same esteem as data from randomized controlled clinical trials, when the typically inaccurate and confounder-prone data of the former cannot even begin to compare with the far more reliable data of the latter.

So, to reiterate, the EPIC-Oxford study is an epidemiological study. Which means that right from the outset it blows compared to properly conducted RCTs, and that it is not equipped to detect anything other than statistical associations. And I will repeat: The first rule of good science is that association does not equal causation. Sadly, the first rule of epidemiology these days seems to be association equals causation, baby!

So being an epidemiological study, those of you who subscribe to good science rather than pseudoscientific bollocks might expect it to have more than a few flaws.

Your expectations will be met quite lavishly.

vegetarians-side-dishes-demotivationalAn Epic Omission

The authors mention early on in the paper that arecent analysis of the European Prospective Investigation into Cancer and Nutrition (EPIC)–Oxford cohort also showed a 17% lower risk (albeit nonsignificant) of fatal IHD in vegetarians than in nonvegetarians”.

In other words, the authors had already dredged the EPIC-Oxford data for CHD (essentially the same thing as IHD, if you’re wondering) relationships and were only able to come up with a non-significant relationship between vegetarianism and reduced CHD death. So they had another go, this time using a combined endpoint of non-fatal and fatal CHD. Combining endpoints is always a handy method for achieving statistical significance when your original sole endpoint failed to do so.

Before we discuss the results that ensued, it’s also worth mentioning something that the authors avoided mentioning: The previous EPIC-Oxford analysis they refer to found no overall mortality advantage to vegetarians whatsoever. Fish eaters and vegetarians had slightly lower rates of coronary heart disease than meat eaters, but higher rates of stroke. Total cancer incidence was significantly lower among fish eaters and borderline significantly lower among vegetarians than among meat eaters. In stark contrast to prevailing anti-meat dogma, the risk of colorectal cancer was significantly higher among vegetarians. For all causes of death combined, mortality in fish eaters was non-significantly lower than in meat eaters, while mortality in vegetarians was non-significantly higher.

Yet that study got relatively little attention – I certainly don’t recall “Vegetarian Diet Sucks for Improving Lifespan!” splashed across headlines all around the world. Why didn’t the EPIC-Oxford authors make a big ballyhoo about the distinctly uninspiring results of their 2008 paper which, if we are to take this epidemiology gig seriously, indicated that vegetarianism will do absolutely bugger all to extend life? Improved health and longevity is a big selling point of the vegetarian shills, yet here is the largest ever study on the subject showing otherwise. Why ignore the overall mortality result (not to mention the association between vegetarianism and higher stroke and colorectal cancer risk, the latter of which we are incessantly told is promoted by meat consumption) and instead make a big circus solely out of the CHD results, when most people really don’t fancy escaping CHD only to get struck down by some other form of premature death?

Well, if I wanted to play devil’s advocate, I could surmise that maybe some of the authors of this study had strong vegetarian leanings and therefore had a strong subconscious motivation to validate their beliefs.

I can’t speak for all the authors, but the paper itself mentions that one of the authors, Timothy J. Key is a member of the UK Vegetarian Society, which describes itself as “an educational charity working to support, represent and increase the number of vegetarians in the UK”. No other such affiliations are disclosed, yet a quick Google search reveals that one of his co-authors, Paul Appleby, is a member of the International Vegetarian Union, “an international non profit organization whose purpose is to promote vegetarianism”.

How sweet.

So at least 2 of the authors of this study belong to organizations whose stated goal is to convince more people to become vegetarians. Personally, I couldn’t give a rat’s rectum about furthering the vegetarian cause, especially if that cause is based on myth and pseudoscience. I just want at the facts, and the facts are that this study is severely lacking on several counts.

Pssst…Wanna Join a Study?

The EPIC-Oxford study began back in the early 90s and “aimed to recruit participants with a wide range of diets and targeted vegetarians and vegans as well as the UK general population.” Between 1993 and 1999, 57,446 men and women aged >20 were recruited to take part in the study and completed a baseline questionnaire.

The EPIC-Oxford participants were recruited through general practices in Oxfordshire, Buckinghamshire, and Greater Manchester and by post with the aim of attracting health-conscious people living throughout the UK. Participants were excluded from the analysis if they were over 90 years at recruitment, had no follow-up, had a prevalent registered or self-reported malignant cancer, were of unknown smoking category or unknown diet group, had unreliable nutrient data, or had a self-reported history of heart attack, stroke, or angina at baseline, which left a total of 46,694 participants available for the  analysis we are discussing today.

Along with answering questions about their education and socioeconomic status, smoking and exercise habits, oral contraceptive and hormone use (if female), and health history, participants also completed a food-frequency questionnaire that estimated the intake of 130 different food items over the past 12 months.

Participants were asked whether they ate any meat, fish, eggs, or dairy products and were categorized as nonvegetarians if they ate any meat or fish, and as vegetarians if they did not eat meat and fish. Time of adherence to a vegetarian diet was calculated by subtracting the age at which the participant last ate meat or fish from their age at the time of recruitment.

Around the time of recruitment, blood samples and blood pressure readings were also requested, and provided by 19,103 participants. Despite the numerous differences we could expect to find between the blood of meat eaters and vegetarians, the only thing examined was serum concentrations of lipids and apolipoproteins.

Take special note of all this folks: The subjects completed a single questionnaire at the start of the study, asking about diet and a limited number of confounding factors. A single blood pressure measurement was taken, and blood samples were obtained from less than half the participants, and then checked for an extremely limited number of markers. We’ll get back to how this could affect the results in a moment.

The Baseline Data

A look at the baseline data reveals a few interesting discrepancies.

It’s no big secret that CVD incidence is associated with age. The older you are, the more likely you are to suffer a stroke, heart attack or angina. Now, if this were a well-conducted RCT, randomization would usually ensure that the non-vegetarian and vegetarian groups had a similar mean age. But of course, this was an epidemiological study that contained no such safeguard. In both the male and female cohorts of the study, vegetarians on average were 8 years younger than their non-vegetarian counterparts. So the vegetarians had a rather significant advantage in terms of an average younger age.

Non-vegetarians had a slightly higher consumption of alcohol, but the study data tells us nothing about the actual pattern of alcohol consumption (i.e. did the non-vegetarians also engage in more binge-drinking, which also increases the risk of CVD?)

Non-vegetarian males were more likely to have ever smoked, and were more likely to be current smokers. Smoking habits were fairly similar between the two female groups, with the exception of a higher number of heavy smokers in the non-vegetarian female group. Needless to say, smoking is a pretty substantial risk factor for CVD, and the vegetarian cohort enjoyed a slight advantage in this respect.

Being male is also a pretty significant risk factor for CVD, and it’s interesting that this study was heavily weighted in favour of females; less than a quarter of the study participants were male. Given that most heart attack victims are male, especially at the average age of the participants in this study, it is not unreasonable to question the validity of generalizing whatever results were obtained from the study to both females and males.

Body mass index (BMI) was slightly but not significantly lower in vegetarians.

Slightly more of the non-vegetarians described themselves as “inactive” (around 4% in absolute numbers), and a similar proportion of the vegetarians described themselves as “active”, but no information is given about the type and total volume of exercise performed by each group. So the vegetarians also appear to have a slight advantage in terms of higher activity levels, which are also protective against CVD.

Interestingly, vegetarians were more likely to have higher educational status but more likely to be poor…hmmm, damn the cost of organic soy grits these days!

Non-vegetarians were more likely to have diabetes, were twice as likely to have hypertension, and significantly more likely to have been receiving long-term medical treatment.

Now why would this be?

There is no tightly controlled RCT in existence showing that animal foods cause diabetes or hypertension or predispose one to developing a higher rate of long-term medical problems. Yes, there is plenty of epidemiological slop claiming otherwise, but when these findings are subject to the bright light of randomized clinical scrutiny, they fall flat in a heap.

The real answer is simple: Vegetarians tend to be health conscious people, and engage in a number of activities aside from dietary change in order to improve their health. And that was indeed the case in the EPIC-Oxford study, where vegetarians were less likely to smoke and more likely to exercise. They were also significantly younger, which in itself proffered a significant CVD advantage.

Another thing worth mentioning: After 5 years, the researchers asked how many of the vegetarian participants were still following their meat-free way of life. They also asked the non-vegetarians if they had become vegetarians.

At 5 years, 10.6% of the male and 16.3% of the female vegetarians had abandoned their meatless ways, while only 2.8% and 2.6% of male and female meat eaters had switched to the herbivorous camp.

This was the only time the participants were asked about adherence to their original diets, yet mean follow-up in this study was 11.6 years! So how do we know exactly how many vegetarians remained that way by the time the final data were tallied up?

We don’t.

Personally, as a person who prefers his science to be of the randomized, controlled variety, this study has already lost me – it has more holes than a Swiss cheese factory, and the groups are too dissimilar in baseline factors for me to even begin to care about the results. However, I belong to a species known as Homo sapiens whose members believe in all manner of weird shit, including the notion that a food group (meat) that formed a staple of our diet for some 2.4 million years and enabled us to survive in often inhospitable conditions and outlive countless other species that went extinct (okay, we helped put more than a few of those species out of commission along the way but that was because we were vigorously hunting them for their meat..duh!) is somehow bad for us.

?!

And so here I am on a Saturday morning typing up this dissection which points out the bleeding obvious when really I should be out walking my dog, watching him sniff then pee against tree after tree, marveling at the seemingly limitless holding capacity of the canine bladder and wondering just why dogs have such a fascination for each other’s urinary output. Don’t laugh, if you own a dog then I know full well you’ve wondered the exact same thing. Sorry Ramone, I promise we’ll go for an extra long walk later, OK champion? I might even walk you past the university and let you eat an epidemiologist or two.

JUST KIDDING! I would never feed my dog such poor quality fare.

Um, anyway, back to the merde at hand…oops…I meant matter at hand. Truly.

After tallying up the data, and ‘adjusting’ for age, smoking, alcohol, physical activity, educational level, affluence level (and use of oral contraceptives or hormone therapy for menopause in women), the researchers claimed that after total follow-up of 517,960 person-years “Vegetarians had a 32% lower risk of IHD”.

Further adjustment for BMI reduced this number to 28%, but interestingly it’s the 32% number that seems to have made it’s way into all the press releases.

What would have been a far more accurate conclusion – albeit far less exciting for the Internationally United Promoters of Vegetarian Propaganda – is something like the following:

“Nominating one’s self as “vegetarian” at the start of the study was, after adjustment for a very limited number of confounding factors, statistically associated with a lower incidence of the combined endpoint of fatal and non-fatal CHD.”

Good science forbids us from claiming vegetarian diets lower CHD risk, because it is clear from this study that the vegetarians came into the study with several advantages, including younger age, lower smoking levels, and a lower incidence of long-term health problems that cannot reasonably and logically be blamed upon meat consumption.

Yes, we tried adjusting the results for several confounders, but this was an after-the-fact mathematical exercise that could never even begin to replicate the equalizing effects of randomization garnered in RCTs. Also, the number of confounders we considered was only a small sampling of the total number of potential factors affecting CHD and even those factors were anlaysed in the crudest sense possible (i.e., no consideration of drinking patterns or type or volume of exercise).

While a number of us are vegetarian ourselves, we are magnificently impartial individuals who place ethics and ruthlessly objective scientific scrutiny above any emotional attachment we may have to vegetarianism, and therefore would never ever be so crass as to claim that ‘Vegetarian Diets Reduce Heart Disease by 32%!’. The relative risk reduction found in our study was nothing more than a statistical association and does not even begin to infer causality. Before one could even begin to claim a causal association, the RR found in our study would need to be confirmed in the controlled, randomized clinical trial setting in which two similar diets varying only in their inclusion of meat (non-vegetarian group) or an isocaloric non-meat substitute (vegetarian group) were consumed for several years. This way, one would truly be comparing the effect of meat-containing and non-meat containing diets, with minimal or no interference from other unrelated dietary and lifestyle factors.”

Yeah, it’s a little more wordy, but gives a far more truthful picture of what really went on.

vegans-carnivore-demotivational-poster
Out of Sight, Out of Mind

In the discussion section of the paper, the authors discuss the results of other epidemiological studies that appear to support their results, but nowhere do they discuss the complete lack of RCT evidence confirming a cardiovascular benefit for vegetarian diets.

Heck, they don’t even discuss the epidemiological evidence that contradicts their “Vegetarianism is Heart Healthy!” thesis.

Let’s take a look at another recent epidemiological study of similar size that examined the relationship of meat intake to CHD, stroke, and total CVD incidence. This study is interesting because it involves a population incessantly cited by the anti-meat/anti-cholesterol/anti-saturate/anti-everything tasty crowd – the Japanese.

The study was conducted by researchers from universities all around the country that gave us sushi, Nissan GTRs, Kazushi Sakuraba, and shy, demure girls who often turn out to be anything but shy and demure when you…uh, never mind, where was I…oh yeah, the big Japanese epidemiological study.

Yes, as part of the Japan Collaborative Cohort Study (JACC Study), researchers conducted a prospective cohort study of 51,683 Japanese (20,466 men and 31,217 women) aged 40-79 years living in all of Japan. Similar to EPIC-Oxford, a food frequency questionnaire was administered at baseline. The questionnaire included questions about consumption of meat, including beef, pork, poultry, liver and processed meat. Five choices were presented for each item with regard to consumption habits: rarely, 1–2 days a month, 1 –2 days a week, 3 –4 days a week and almost daily.

During 820,076 person-years of follow-up for 51,683 persons, the JACC researchers documented 537 deaths due to ischemic heart disease, 1209 due to stroke and 2685 total cardiovascular deaths.

For men, there were no associations between total meat consumption and age-adjusted mortality from stroke or total CVD. However, when one looks at the CHD data in isolation, as the EPIC-Oxford researchers chose to do for their latest analysis, there was an inverse trend with mortality from CHD. In other words, as meat consumption increased, CHD mortality decreased. After multivariable adjustment, the relative risk reduction for the highest versus lowest quintile of total meat consumption was 34% and remained statistically singificant.

For women, total meat consumption was not associated with mortality CHD or total CVD in either age-adjusted or multivariable models. Although there was an inverse trend with mortality from stroke in the age-adjusted model, the association was no longer statistically significant after multivariate analysis.

The inverse association with CHD was similarly observed for red and processed meat consumption among men, while no association existed for any subtype of meat consumption among women(Nagao 2012).

In other words, an even larger study than the EPIC-Oxford, in terms of both number of participants and person follow-up years, and conducted by researchers who to the best of my knowledge do not belong to any organizations dedicated to to furthering the vegetarian cause, found completely opposite results.

You see how this vegetarian promotion gig works, folks?

It’s a bit like choosing an outfit before a big date. You pick the clothes that flatter your physique and hide its flaws. If you’re female, you wear a wonder-bra, look in the mirror and frown, then stuff a few tissues either side of your fledgling cleavage to perk things up a little, until you’re confident that the object of your affections will see something that really isn’t there. If you’re a bloke, you douse yourself with poncey-sounding colognes to give the impression you’re a dapper dude who always smells like a subtle but enticingly masculine blend of wooded musk and cinnamon.

The whole point of this carry-on, of course, is to hide your numerous flaws and present only the side of yourself you wish for your target to see, in the hope of forming the most favourable possible impression.

Yep, sometimes researchers are a lot like dodgey pick-up artists. They have an end game, and often aren’t above engaging in illusory shenanigans to get to home base.

Show Me the RCTs!

I’ve talked a lot about RCTs, so the next question that begs asking is: Have any RCTs been conducted comparing omnivorous diets with vegetarian diets that ran long enough to establish a body count?

Despite the exuberant claims made by vegetarians, none of the long term dietary intervention RCTs examining the effect of diet on CHD incidence and mortality involved vegetarian diets.

There was a small trial that has been the subject of incessant vegetarian shilling, but a close examination of its results reveals a very different story to the hooplah. I’m talking, of course, about the Lifestyle Diet Heart Trial headed by one Dean Ornish.

Ornish has built a pretty lucrative career off the back of this trial, claiming his program has been “proven to reverse heart disease.”

The reality is that Ornish’s program has been shown to do no such thing.

Ornish’s program actually involves several interventions aside from the omission of meat. Participants are counseled to exercise, engage in stress reduction activities, and to cut all the refined and heavily processed crap from their diets. All these factors on their own could have an impact on CHD risk, but despite these confounding factors Ornish routinely cites his intervention as proof of the efficacy of meat-free and low-fat diets.

But just how effective is his program, anyway?

After one year of follow-up in the Lifestyle trial the researchers reported 82% of those in the experimental group experienced regression of arterial plaque, compared to only 42% of those in the control group. The experimental group subjects also experienced significantly less chest pain. But these factors could easily be due to exercise and stress reduction(Ornish 1990).

In 1998, the Journal of the American Medical Association published the five-year follow-up data for the Lifestyle Heart Trial. While the experimental group experienced a significantly reduced overall incidence of cardiac events (a classification that included angioplasty, bypass surgery, heart attack, and hospitalization for any cardiac cause), the treatment group actually experienced one more death than the control group (two people in the intervention group died compared to one person in the control group).

According to Ornish, one of the treatment group deaths was in a participant who had stopped following the intervention. Another intervention subject reportedly got a little too enthusiastic whilst exercising, exceeding his prescribed target heart rate with fatal consequences.

So maybe Lady Luck wasn’t looking out for Ornish in the first Lifestyle Trial. Maybe she was trying to send him some kind of message, like, “Oi! Yeah, you with the white coat and bean sprout sandwich! How about running a larger and longer trial before making all these dodgey claims?!?”

I’m not sure if this is what actually transpired, but at any rate Ornish did actually launch another trial. And I’m sure by now you know why few people have ever heard of the follow-up trial.

Yessirree, it was a certified fizzer.

The Multicenter Lifestyle Demonstration Project sought to apply the intervention in Ornish’s original trial to a larger group of patients recruited from clinics across the U.S.(Ornish 1998). Practitioners from eight medical centers around the country were trained in all aspects of the Lifestyle program, which they proceeded to administer to patients with coronary artery disease. The study was not a randomized, controlled trial; instead, outcomes in the 194 patients who completed the intervention were compared with 139 patients who did not take part in the Lifestyle program but had recently undergone revascularization procedures.

After three years, there were no significant differences in cardiac event rates nor mortality between patients in the intervention and control groups. The number of cardiac events per patient year of follow-up when comparing the experimental group with the control group was as follows: 0.012 versus 0.012 for myocardial infarction, 0.014 versus 0.006 for stroke, 0.006 versus 0.012 for non-cardiac deaths, and 0.014 versus 0.012 for cardiac deaths (none of the differences were statistically significant)(Ornish 1998).

This is despite the fact that the Lifestyle participants received dedicated counseling, lost weight and improved their exercise tolerance. No corresponding data were given for the control group, but given the absence of the intense counseling afforded to the intervention group, it is unlikely that the former would have experienced such changes – a contention supported by the original Lifestyle trial.

In his 1998 paper reporting on the MCLP results, though, Ornish writes as if these uninspiring results were a great success. His reasoning is that his program is cheaper than revascularization, yet produced similar coronary event and mortality rates. Because 150 of his 194 patients avoided revascularization (44 still had to be wheeled into the operating theater during the 3-year study), Ornish’s selling point in the paper is that his program is a cheaper alternative to revascularization.

That all sounds great, but if you’ve read The Great Cholesterol Con you’ll know that when revascularization is put to the test in RCTs, it has repeatedly failed to show any mortality advantage and some studies have actually shown a slight disadvantage, when compared to patients receiving standard non-invasive medical care. So, in effect, Ornish’s 1998 paper is boasting that his program is no more effective but at least cheaper than another largely ineffective option.

Woohoo…

Where the Tofu Hits the Road

So looking at the epidemiological data and the meager clinical data, we see absolutely no reduction in overall mortality among vegetarians, even when the vegetarian participants are afforded important baseline or peri-trial advantages. Despite the fact that most of these epidemiological studies show vegetarians to be slimmer, more active and less likely to smoke than omnivores, they enjoy no overall mortality advantage. Logically, this would indicate that something about the vegetarian diet counteracts lower levels of smoking, overweight, and inactivity to such a degree that mortality remains as high as that seen among omnivores with generally unhealthier lifestyles. It’s no secret that vegetarians (and especially vegans) are more likely to be deficient in B12, a critically important vitamin whose importance still isn’t fully appreciated by many medical and layfolk alike. Vegetarians, by avoiding fish, deprive themselves of long-chain omega-3 fatty acids, which have been shown in large clinical trials to reduce CHD mortality. Blood sampling often shows vegetarians to have higher blood levels of the omega-6 fat linoleic acid; a high blood n-6:n-3 ratio does not bode well for future CVD risk.

Meat is also rich in numerous critical nutrients such as creatine, carnosine, carnitine and taurine, all of which are either absent or found in negligible amounts in plants, and all of which are found in lower average amounts in vegetarians. Taurine has shown promise in helping patients with chronic heart failure, although studies to date have been small, short and scarce. Not so with carnitine, which has been shown by Italian researchers to reduce mortality from both heart failure and CHD. Creatine has also shown promise in patients with congestive heart failure and has even been shown in at least one trial to raise intelligence in vegetarians (no, I’m not kidding).

Carnosine, meanwhile, is a potent inhibitor of anti-glycosylation end products (aptly named AGEs), meaning it prevents the forming of protein-sugar cross-links in your body that quite literally cause you to age faster. No surprise then, that these same studies show that vegetarians have higher blood levels of AGEs.

AGEs, by the way, are a big reason why diabetics age much faster and suffer higher rates of just about every known health ailment, including CHD.

(References for all the above nutrient information can be found at the end of this article)

To turn around and claim in the face of all this contradictory evidence that vegetarian diets reduce heart disease is so stupid it defies comprehension.

Such a thesis can only be maintained by citing data from supportive confounder-prone epidemiological studies, and completely ignoring the non-supportive and often completely contradictory body of clinical evidence.

Suffice to say for now that the claimed heart-healthiness of vegetarianism is a complete and utter sham. The next time I find a few spare moments to knock out an article, I’ll discuss the kind of diet that has been shown to dramatically reduce CHD and overall mortality in randomized controlled clinical trials.

Here’s a clue: It contains meat.

Yep, that’s all I’m giving you for now :)

Until next time, adios amigos!

 

 

 

 

 

 

 

Disclosure Statement: The author of this article (in non-third person terms, that would be me, Anthony) has absolutely no relationship, financial or otherwise, with the meat, dairy, or egg industries. The author does, however, make a point of enjoying a bloody good steak on a very regular basis.

References:

Nagao M, et al. Meat consumption in relation to mortality from cardiovascular disease among Japanese men and women. European Journal of Clinical Nutrition, Jun, 2012; 66 (6): 687-693.

Ornish D, et al. Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial. Lancet, Jul 21, 1990; 336 (8708): 129-133.

Ornish D, et al. Intensive Lifestyle Changes For Reversal of Coronary Heart Disease. Journal of the American Medical Association, Dec 16, 1998; 280 (23): 2001-2007.

Ornish D, et al. Avoiding Revascularization with Lifestyle Changes: The Multicenter Lifestyle Demonstration Project. American Journal of Cardiology, Nov 26, 1998; 82 (10B): 72T-76T.

Antony AC. Vegetarianism and vitamin B-12 (cobalamin) deficiency. American Journal of Clinical Nutrition, 2003; 78: 3-6.

Chan KM, Decker EA. Endogenous skeletal muscle antioxidants. Critical Reviews in Food Science and Nutrition, 1994; 34 (4): 403-26.

Hipkiss AR. Carnosine. a protective, anti-ageing peptide? International Journal of Biochemistry & Cell Biology, 1998; 30: S63-868.

Price DL, et al. Chelating Activity of Advanced Glycation End-product Inhibitors. Journal of Biological Chemistry, 2001; 276 (52): 48967-48972.

Davini P, et al. Controlled study on L-carnitine therapeutic efficacy in post-infarction. Drugs Under Experimental and Clinical Research, 1992; 18: 355-365.

Sebekova K, et al. Plasma levels of advanced glycation end products in healthy, long-term vegetarians and subjects on a western mixed diet. European Journal of Nutrition, Dec, 2001; 40 (6): 275-281.

Rizos I. Three-year survival of patients with heart failure caused by dilated cardiomyopathy and L-carnitine administration. American Heart Journal, Feb, 2000; 139 (2, Pt 3): S120-123.

Iliceto S, et al. Effects of L-carnitine administration on left ventricular remodeling after acute anterior myocardial infarction: the L-Carnitine Ecocardiografia Digitalizzata Infarto Miocardico (CEDIM) Trial. Journal of the American College Of Cardiology, Aug, 1995; 26 (2): 380-387.

Kreider RB. Effects of creatine supplementation on performance and training adaptations. Molecular and Cellular Biochemistry, Feb, 2003; 244 (1-2): 89-94.

Andrews R, et al. The effect of dietary creatine supplementation on skeletal muscle metabolism in congestive heart failure. European Heart Journal, Apr, 1998; 19 (4): 617-622.

Gordon A, et al. Creatine supplementation in chronic heart failure increases skeletal muscle creatine phosphate and muscle performance. Cardiovascular Research,Sep, 1995; 30 (3): 413-418.

Lukaszuk JM, et al. Effect of creatine supplementation and a lacto-ovo-vegetarian diet on muscle creatine concentration. International Journal of Sport Nutrition & Exercise Metabolism, Sept, 2002; 12 (3): 336-348.

Harris RC, et al. Absorption of creatine supplied as a drink, in meat or in solid form. Journal of Sports Sciences, Feb, 2002; 20 (2): 147-151.

Laidlow SA, et al. The taurine content of common foodstuffs. Journal of Parenteral Enteral Nutrition, Mar-Apr, 1990; 14 (2): 183-188.

Pasantes-Morales H, et al. Taurine content in foods. Nutrition Reports International, 1989; 40: 793-801.

Schaffer SW, et al. Interaction between the actions of taurine and angiotensin II. Amino Acids, 2000; 18 (4): 305-318.

Azuma J, et al. Therapeutic effect of taurine in congestive heart failure: a double-blind crossover trial. Clinical Cardiology, May, 1985; 8 (5): 276-282.

Azuma J, et al. Double-blind randomized crossover trial of taurine in congestive heart failure. Current Therapeutic Research, Clinical and Experimental, 1983; 34 (4): 543-57.

Beyranvand MR, et al. Effect of taurine supplementation on exercise capacity of patients with heart failure. Journal of Cardiology, May, 2011; 57 (3): 333-337.

Laidlaw SA, et al. Plasma and urine taurine levels in vegans. American Journal of Clinical Nutrition, 1988; 47: 660-663.

Pasantes-Morales H, et al. Taurine content in breast milk of Mexican women from urban and rural areas. Archives of Medical Research, Spring, 1995; 26 (1): 47-52.

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

Copyright © Anthony Colpo.

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.

Be Sociable, Share!