“Look at me, I have a PhD!” Janet Brill, and the framed piece of paper she believes makes her an omnipotent fountain of dietary wisdom, even when she clearly has no idea what she’s talking about.
Just thought I would pass along what some "expert" had to say about you. I was trying to have a discussion with this person (Dr Janet Brill) about grains and other things. I had mentioned your post "Whole Grain Scam" as one source of information. Here is what she said:
“Looks like you and I respectfully disagree. Despite the wealth of scientific references you cited above (some valid, others not so much), I can tell you that with two master's degrees and a PhD later--having studied nutrition science, health and fitness for many decades--that the bulk of the scientific evidence supports my views regarding the health benefits of whole grains and my criticism of the Zone and Paleo diets.
I can also tell you with 100% confidence that Anthony Colpo is not a nutrition scientist and needs to hit the books. In fact, his views are completely out in left field, unsubstantiated by sound science and could potentially cost human lives if his advice regarding cholesterol were to be followed. He wrote the book "The Cholesterol Con," which competes with my bestselling book, "Cholesterol DOWN" (mine, of course, sells much better 🙂
Bottom line: a nutrient dense, plant-based diet rich in whole foods including whole grains, fresh fruit, vegetables, olive oil, legumes, nuts, fish and fat-free dairy is the optimal eating plan for good health and wellness.
Best, Dr. J”
I did respond briefly to her less-than-positive comments about you:
Seeing that you felt it was necessary to be completely dismissive and disparaging of Mr Colpo's writings (really an ad hominem argument) instead of sticking to discussing the evidence that I offered or even the evidence that Mr Colpo used in his argument, I felt that I should offer a short reply.
Your points about Mr Colpo are disappointing but not surprising. He can certainly defend himself, but I will say a couple of things…
First, the validity of a person's argument does not rest solely on whether they have a lot of formal credentials or not. Lay people can read, understand and write about research very well, although it is not very common.
Second, have you read his grain article? If so, did he misrepresent the evidence (about 50 studies) that he used to support his argument? If so, where did he go wrong?
Third, have you read Mr Colpo's cholesterol book? I have and I would say that it was well written. It is certainly your prerogative to disagree with his conclusions, but it should not be because he didn't support his arguments with logical and often thorough explanations of the relevant topics regarding cholesterol and copious citations to the medical literature (I would say he did "hit the books")
Forth, I am glad that you have sold a lot of your cholesterol book, apparently more than Mr Colpo, but that in no way validates your viewpoint. I am sure you would agree that there are many nutrition books on the market that have sold huge quantities, but that would not stop you from dismissing them as rubbish, as you should.
Fifth, there are a number of other people with plenty of academic credentials who have "hit the books" that also feel that the lipid hypothesis is a weak argument for explaining the development of cardiovascular disease.
Anyway, the whole cholesterol thing is for another day.
J further writes:
Here is the latest comment from Dr. Brill (below), she actually said something this time. I am going to read it tonight and start formulating a response, would be glad to get some input from you if you have the time.
Here are some references and a short piece I wrote on whole grains and the prevention of heart disease (the leading cause of death in this country).
5 good reasons why you should eat whole grains:
1. Boost total antioxidant capacity and curb LDL oxidation
Getting in at least three servings of whole grains daily will raise your blood’s total antioxidant capacity (TAC) because whole grains are virtual antioxidant factories, housing a nice amount of vitamin E, the mineral selenium, and the polyphenol phenolic acids ferulic acid and caffeic acid.
Most people are unaware that whole grains possess strong disease-fighting antioxidant activity. In fact, the average antioxidant activity of whole grains is actually greater than most fruits and vegetables. Remember, the antioxidants and other phytochemicals are most concentrated in the bran and the germ of the kernel—so make sure you’re eating the whole oat or grain, not its refined counterpart. If you miss out on any part of the grain—the bran, for example—you could miss out on as much as 98% of those TAC-enhancing antioxidants.
A last note on TAC: remember to eat your grains throughout the day, in order to maintain a high level of antioxidants in your bloodstream and build up your antioxidant defense system.
2. Stabilize vulnerable plaque by lowering LDL cholesterol
Eating whole grains, especially oats and barley, will make a significant dent in your LDL cholesterol, reducing it an average of 14 mg/dL for oats and 10 mg/dL for barley. The American Heart Association recommends all Americans get their LDL cholesterol down to under 100 mg/dL to help them prevent heart disease—the leading cause of death among American men and women. For those individuals with coronary artery disease, lowering LDL cholesterol is extremely important for stabilizing vulnerable plaque—the type that cause most heart attacks.
3. Prevent and treat high blood pressure
Eating whole grains can slash your risk of developing high blood pressure, another factor that significantly increases your risk of having a heart attack. That’s the news from the most recent results of the ongoing Health Professionals Follow-Up Study, begun in 1986, where over 51,000 male health professionals continue to provide health data and detailed dietary information at four-year intervals. This particular subset followed 33,000 men, without high blood pressure at the onset, for eighteen years, where their diet and lifestyle habits as well as health status were tracked. According to Harvard researchers, the men who had the highest intake of whole grains (bran in particular), estimated at 46 grams of whole grains per day, had a 19 percent reduced risk of developing high blood pressure compared to those men eating just 3 grams of whole grains a day.
If you already have high blood pressure, the simple act of swapping brown rice for white, 100 percent whole grain bread for white bread and barley for refined grains can lower your blood pressure a statistically measurable amount after just five weeks.
4. Prevent and treat metabolic syndrome and type 2 diabetes
Eating whole-grain will lessen your risk of contracting metabolic syndrome—the constellation of metabolic disturbances that predisposes you to developing type 2 diabetes and accelerates atherosclerosis. If you have already been diagnosed with metabolic syndrome, take heart in knowing that eating whole grains will improve your blood sugar metabolism and can delay or prevent the progression of metabolic syndrome to type 2 diabetes.
Whole grains, and especially whole grains containing a large cache of the LDL-draining soluble fiber beta-glucan (found in high concentration in oats, barley, and rye), are particularly helpful in treating blood sugar abnormalities. It is the gel-forming property of the soluble type of fiber in the intestines that is responsible for regulating your circulating blood sugar level. Beta-glucan is beneficial for controlling blood sugar because it acts like a sponge, entrapping carbohydrates and thereby delaying their release from the stomach into the intestines as well as slowing the absorption of carbohydrates into the bloodstream.
Insulin resistance is the body’s inability to control its blood sugar level with a normal level of insulin, and an early step in the development of type 2 diabetes. Whole grains can make insulin-resistant muscles, well, less resistant. In 2003, the results of a study examining the relationship between wholegrain intake and the development of metabolic disorders and diabetes was published in the American Journal of Clinical Nutrition. Whole-grain eaters were found to have a lower fasting insulin blood concentration (termed “improved insulin sensitivity”) when compared to those individuals who subsisted on mostly refined grains. Thus, the researchers concluded that whole grains have an “insulinsensitizing” method of action in the body.
WHOLE-GRAIN- MEDITERRANEAN DIET STAVES OFF NEED FOR DRUGS IN NEW DIABETICS
Italian research published in 2009 involving over 200 newly diagnosed subjects with type 2 diabetes compared a traditional American Heart Association low-fat diet with a whole-grain-rich, moderate carbohydrate Mediterranean diet. After four years, the subjects on the Mediterranean diet lost more weight and needed less medication to treat their diabetes. Only 44 percent of the participants who stuck with the Mediterranean diet required blood-sugar-lowering medication compared to 70 percent of people on the low-fat diet. According to the researchers, the whole-grain-rich Mediterranean diet was clearly the superior dietary treatment for type 2 diabetics. What did the diet consist of? Carbohydrate intake was mostly in the form of whole grains, nuts, fruits, and vegetables, capped at up to 50 percent of daily calories. Compared to the low-fat diet, it included fewer carbs and a much larger amount of the “healthy” fat, olive oil (used as the subjects’ main fat).
Source: Katherine Esposito et. al., “Effects of a Mediterranean-style diet on the need for antihyperglycemic drug therapy in patients with newly diagnosed type 2 diabetes: a randomized trial,” Annals of Internal Medicine 151, no. 5 (2009): 306–314.
Eating whole grains can have a dramatic effect on your odds of actually developing type 2 diabetes, a disease you want to aggressively prevent or manage because 75 percent of diabetics will die from heart disease. Findings from a meta-analysis of six studies examining the relationship between whole-grain consumption and the development of type 2 diabetes found that for each two-serving-per-day increment in whole-grain intake, risk of type 2 diabetes dropped 21 percent.
5. Control your weight and prevent obesity
Filling your plate with whole grains will help you to control your weight, which is important because being overweight or obese are independent risk factors for heart disease. In another subset of the Health Professionals Follow-Up Study, a group of just over 27,000 healthy men at the onset was followed for eight years to examine the potential association between whole-grain intake and long-term weight gain.
The researchers calculated each subject’s whole-grain intake (in grams) per day. It was shown that those who ate the most whole grains were leaner at the end of the eight-year reporting period. Specifically, weight gain was reduced by approximately 2.5 pounds for each 40 g/day increment in whole-grain intake—the amount equal to about two slices of 100 percent whole-grain bread. The researchers concluded that the high fiber and high water content of whole grains lessened weight gain by promoting satiety. Whole-grain foods also contain fewer calories than the equivalent weight of a refined grain.
1. I. Flight and P. Clifton, “Cereal grains and legumes in the prevention of coronary heart disease and stroke: a review of the literature,” European Journal of Clinical Nutrition 60 (2006): 1145–1159.
2. Philip B. Mellen et al., “Whole grain intake and cardiovascular disease: a meta-analysis,” Nutrition, Metabolism & Cardiovascular Diseases 18 (2008): 283–290.
3. Arja T. Erkkilä et al., “Cereal fiber and whole-grain intake are associated with reduced progression of coronary-artery atherosclerosis in postmenopausal women with coronary artery disease,” American Heart Journal 150 (2005): 94–101.
4. Lin Nie et al., “Avenanthramide, a polphenol from oats, inhibits vascular smooth muscle cell proliferation and enhances nitric oxide,” Atherosclerosis 186 (2006): 260–266.
5. Judith Hallfrisch and Kay M. Behall, “Mechanisms of the effects of grains on insulin and glucose responses,” Journal of the American College of Nutrition 19, no. 3 (2000): 320S–325S.
6. Mark A. Pereira et al., “Dietary fiber and risk of coronary heart disease: a pooled analysis of cohort studies,” Archives of Internal Medicine 164 (2004): 370–376.
7. Institute of Medicine, “Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids,” The National Academies Press, September 2002, http://www.iom.edu/Object.File/Master/4/154/MACRO8pgFINAL.pdf.
8. International Food Information Council Foundation, “Whole Grains Fact Sheet,” http://www.ific.org/publications/factsheets/wholegrainsfs.cfm.
9. Joanne L Slavin et al., “Plausible mechanisms for the protectiveness of whole grains,” American Journal of Clinical Nutrition 70 (1999): 459S–463S.
10. U.S. Department of Health & Human Services, “FDA Health Claim Notification for Whole-Grain Foods, http://www.fda.gov/Food/LabelingNutrition/LabelClaims/FDAModernizationActFDAMAClaims/ucm 073639.htm.
11. Harold E. Miller et al., “Antioxidant content of whole-grain breakfast cereals, fruits and vegetables,” Journal of the American College of Nutrition 19 (2000): 312S–319S.
12. Claudine Manach et al., “Polyphenols: food sources and bioavailability,” American Journal of Clinical Nutrition 79, no. 5 (2004): 727–747.
13. Ripple Talati et al., “The effects of barley-derived soluble fiber on serum lipids,” Annals of Family Medicine 7 (2009): 157–163.
14. Alan J. Flint et al., “Whole-grains and incident hypertension in men,” American Journal of Clinical Nutrition 90 (2009): 493–498.
15. Kay M. Behall et al., “Whole-grain diets reduce blood pressure in mildly hypercholesterolemic
First of all J, thanks for your kind defence of my writings, I much appreciate it.
If I was to reply to every screwball that badmouths me on the Internet, I’d have little time for anything else - but I can’t let Janet Brill’s comments pass. Hey, we’re all entitled to our own differing points of view, but when someone who clearly has no idea what she’s talking about - and who profits from the dissemination of misleading nonsense - accuses me of being out in left field and endangering people’s lives, then that’s a wee bit rich for my liking.
I might not have any formal tertiary qualifications in nutrition or medicine, and Brill might have two master's degrees and a PhD, and she might have sold more books so far, but that’s not going to help her today. You see, I have something that Brill, despite all her years of studying and thousands of dollars spent on “higher” education, sadly lacks. Namely, a sharp, reasoning, analytical brain that refuses to be suckered in by widely accepted but scientifically untenable dogma.
By the way, “Doctor” Janet Brill, it should be pointed out, is not a medical doctor but a certified personal trainer, a “wellness coach” (whatever the hell that is), and a dietician; one that recommends soy protein, phytosterol-enhanced margarines, and Metamucil as prophylactics against CHD, despite the fact that no controlled clinical trial has ever found any of these agents to reduce CHD morbidity or mortality.
Our uber-smug pseudo-doctor writes of yours truly:
“In fact, his views are completely out in left field, unsubstantiated by sound science and could potentially cost human lives if his advice regarding cholesterol were to be followed. He wrote the book "The Cholesterol Con," which competes with my bestselling book, "Cholesterol DOWN" (mine, of course, sells much better :-)”
What a wanker.
Let’s take a closer look at Brill’s “best-selling” book, Cholesterol Down. According to the blurb at Amazon:
“Take Control of Your Cholesterol— Without Drugs
If you are one of the nearly 100 million Americans struggling with high cholesterol, then Dr. Janet Brill offers you a revolutionary new plan for taking control of your health—without the risks of statin drugs. With Dr. Brill’s breakthrough Cholesterol Down Plan, you simply add nine “miracle foods” to your regular diet and thirty minutes of walking to your daily routine. That’s all. This straightforward and easy-to-follow program can lower your LDL (“bad”) cholesterol by as much as 47 percent in just four weeks.
Cholesterol Down explains Dr. Brill’s ten-point plan as well as the science behind it. You’ll learn how each miracle food affects LDL cholesterol and how the foods work together for maximum effect, as well as:
• How eating whole grains helps reduce LDL cholesterol in your bloodstream
• Why antioxidants keep plaque from building up in your arteries
• How certain steps change the structure of LDL cholesterol particles (and why it’s best for them to be large and fluffy)
• Why walking just thirty minutes a day lowers “bad” cholesterol and cuts dangerous belly fat
With everything you need to stay focused on the plan, including a daily checklist, a six-month chart for racking LDL cholesterol changes, tools for assessing your risk level for cardiovascular disease, sample weekly menus, and even heart-healthy recipes, Cholesterol Down is the safe and effective alternative or complement to statin drugs.”
What a load of unscientific rubbish.
You know, if I wanted to take the Janet Brill Pissing Contest approach to scientific discussion, I could point out she has never published a peer reviewed paper, only a rubbish-filled popular format book that totally misleads people about the role of LDL cholesterol in CHD while trotting out the usual “miracle food” hyperbole.
In contrast, my 2005 peer-reviewed paper from the Journal of American Physicians and Surgeons explains in detail just why the LDL theory of heart disease is completely false. You can access the full text right here for free. While you do that, let me beat my chest, shake what my Momma gave me, and pull out a measuring tape to see how far I just peed! Woo-hoo! 7 foot, 11 inches - beat that, Janet!
Here are a few of the untenable contradictions to the LDL 'bad cholesterol' theory that I would dearly love the self-aggrandizing Brill to coherently explain:
If LDL cholesterol causes atherosclerosis, logic dictates that there should be a strong correlation between blood levels of LDL cholesterol, extent of atherosclerosis, and CHD mortality. But as I explain in the JPANDS paper, no tightly controlled clinical trial has ever conclusively demonstrated that LDL cholesterol reductions can prevent cardiovascular disease or increase longevity.
In the large GISSI-Prevenzione trial in Italy, the mortality benefits of omega-3-rich fish oil appeared early on in the study as did an increase in LDL cholesterol levels. Mean LDL levels in the subjects given fish oil rose from 136 mg/dL at baseline to 150 mg/dL after 6 months, before gradually returning to initial levels at 42 months. A similar pattern was observed in the control group. This extended period of elevated LDL levels did not prevent the fish-oil patients from experiencing significantly more favourable cardiovascular and mortality outcomes.
Bottom line. NO difference in LDL levels between the two groups, but lower mortality in the fish oil subjects.
Scientific Reality: 1, Janet Brill: 0.
In the Lyon Diet Heart Study, an experimental group advised to increase consumption of root vegetables, green vegetables, fish, fruit, and omega-3 fatty acids also experienced greatly improved cardiovascular and survival outcomes. The study was originally intended to follow the patients for 4 years, but death rates diverged so dramatically early on that researchers decided it would be unethical to continue, and called an end to the trial. After an average follow-up of 27 months, the all-cause death rate of the control group was more than twice that of the experimental group.
One little-publicized finding from this well-known trial was that the total and LDL cholesterol levels of the treatment and control groups were virtually identical throughout the study. Those in the treatment group, however, did show significantly higher blood levels of omega-3 fatty acids and antioxidants.
Again, NO difference in LDL levels, but lower mortality in the antioxidant- and n-3-enhanced intervention group.
Scientific Reality: 2, Janet Brill: 0.
Von Shacky et al, in a 2-year double-blind trial in patients with CHD, found that daily fish-oil supplementation increased the incidence of atherosclerotic regression, and decreased the loss in minimal luminal diameter, as assessed by quantitative coronary angiography. Fish-oil recipients also experienced fewer cardiovascular events. That’s because their LDL levels went down to a greater degree, right? Nope. LDL cholesterol levels tended to be greater in the fish-oil group.
Scientific Reality: 3, Janet Brill: 0.
Hecht et al compared patients given aggressive LDL cholesterol-lowering treatment (statins plus niaicin) with those receiving less aggressive treatment (statins alone). Despite greater LDL reductions in the former group, there were no differences in calcified plaque progression as detected by electron beam tomography. The authors concluded: “.. with respect to LDL cholesterol lowering, ‘lower is better’ is not supported by changes in calcified plaque progression.””[Hecht]
Scientific Reality: 4, Janet Brill: 0.
In the Scottish Aortic Stenosis and Lipid Lowering Trial, patients with calcific aortic stenosis were randomly assigned to receive either 80 mg of Lipitor (atorvastatin) daily or placebo. After 25 months, serum LDL concentrations remained at an average 130 mg/dL in the placebo group but fell significantly to 63 mg mg/dL in the atorvastatin group. Despite the fact that LDL levels were reduced by more than half in the atorvastatin subjects, there was no difference in aortic-jet velocity or progression in aortic-valve calcification between the treatment or placebo groups[Cowell].
Scientific Reality: 5, Janet Brill: 0.
Hmmm, not looking too good, Janet!
And need I mention the lack of association between LDL and CHD morbidity and mortality in large epidemiological studies like the Women’s Health Study?
Among the 28,000-plus participants of the WHS, 46% of first cardiovascular events occurred in women with LDL cholesterol levels less than 130 mg/dL - the ‘desirable’ target for primary prevention set by the National Cholesterol Education Program (NCEP).
As we saw in Brill’s rambling whole grain article, she’s happy to cite Italian research when it suits her to do so. But for some strange reason she never mentioned the GISSI study, nor does she mention the Cardiovascular Study in the Elderly (CASTEL), which followed up 3120 elderly Northern Italians for 12 years. Prevalence of heart disease was 66.4% in men and 45.9% in women, despite the fact that women had slightly higher serum concentrations of total cholesterol (5.9 vs 5.4 mmol/L; 228 vs 208 mg/dL) and LDL (3.6 vs 3.4 mmol/L; 139 vs 131 mg/dL). Someone obviously forgot to tell these elderly Italian ladies they were supposed to be dying at a slightly higher rate than their male paesani.
The risk of total mortality in women, and fatal heart failure in both sexes, decreased with higher LDL. For total mortality in men, and cardiovascular mortality in women and men, the relationship with LDL was U-shaped (meaning increased risk was seen at the higher and lower ends of the LDL spectrum)[Tikhonoff].
I guess my Italian forebears are just a stubborn, feisty bunch that refuse to conform to all this "colesterolo Americano merde", right? Using their zen-like powers of acuity, learned from passing Buddhist monks and honed from years of meditating in the Italian Alps, they simply willed themselves to live longer despite their rising LDL levels!
Uh, yeah, right.
The more likely explanation is that LDL cholesterol has bugger all causative association with heart disease. Any association between high LDL and increased CHD mortality is likely due to the fact that cholesterol is an antioxidant and a cellular repair substrate (look it up, Janet) and therefore used to repair damaged arteries. As people grow older and this process becomes impaired, the statistical association between total and LDL cholesterol and CHD, which folks like Brill mistake as causative, begins to disintegrate.
In elderly Dutch folks aged 85 or older and followed up for 4 years, all-cause mortality was higher in those with low cholesterol (163-195 mg/dl) than those whose cholesterol was in the intermediate and high categories (208-280 mg/dl). Similar results were seen for LDL – those in the lowest LDL category (94-116 mg/dl) had a higher risk of overall mortality than those in the intermediate and high categories (132-196 mg/dl). The leading cause of death was cardiovascular disease, with similar mortality risks in all tertiles of LDL cholesterol level. The researchers found that both low LDL cholesterol and low HDL cholesterol concentrations were associated with an increased mortality risk of infection: 2.7 and 2.4, respectively[Weverling-Rijnsburger AW]. This is not a trivial finding; with their comparatively weaker immune systems, elderly folks are more susceptible to infections than the rest of us. So that I don’t go off on a time-consuming tangent, I highly recommend interested readers consult Dr. Uffe Ravnskov’s 2003 Quarterly Journal of Medicine paper titled “High cholesterol may protect against infections and atherosclerosis”, which you can access for free right here:
In this paper, Ravnskov discusses the abundant evidence showing LDL cholesterol exerts potent anti-microbial effects.
Uffe Ravnskov: This bloke doesn’t swagger around, swinging his schlong and boasting about how many books he’s sold. He just diligently pumps out paper after paper detailing uncomfortable contradictions to the lipid hypothesis that the medical mainstream would prefer to ignore.You really should read them, Janet.
Back to the lack of association between LDL and mortality in the elderly: In a study of almost 6,000 US citizens aged 65 or over, total and LDL cholesterol had no relationship with CHD or total mortality (crude rates of these events were actually notably higher in the lowest cholesterol and LDL categories, but the difference disappeared after adjustment for age, sex, diabetes mellitus, smoking status, cardiovascular disease, and systolic blood pressure)[Psaty].
Now, folks like Janet Brill might be inclined to dismiss the elderly as some kind of inconsequential aberration to the LDL hypothesis. Trouble with that line of wantonly wishful and selective thinking is that the overwhelming majority of cardiovascular morbidity and mortality occurs in...the elderly.
What about heart attack patients? Do they provide some kind of salvation for the LDL theory? Surely those sporting lower LDL levels fare better than those with higher levels, right?
Researchers from the Henry Ford Heart and Vascular Institute, Detroit, examined the relationship between admission LDL levels and long-term outcomes in patients with non-ST segment elevation heart attack. This is a form of heart attack in which the artery in question is only partially blocked, in contrast to the more severe form of ST segment elevation myocardial infarction where the artery is totally blocked and far more heart muscle damage occurs.
After 3 years, patients with admission LDL of 105 mg/dL or less had over double the all-cause mortality than patients with LDL greater than 105 mg/dL (14.8% vs. 7.1%, p = 0.005). The higher all-cause mortality persisted even after adjustment for confounding variables[Al-Mallah].
In other words, in heart attack patients presenting to the emergency ward with higher levels of LDL - the very substance that folks like Brill would have us believe is their most fearsome enemy - survival was significantly higher.
By the way, this is hardly the only study to find that acute coronary syndrome patients with higher cholesterol levels are more likely to survive[Boersma][ Wang].
So what folks like Brill would evidently have us believe is that LDL, a perfectly natural, healthy and downright essential substance found inside every human body, is in fact a deadly toxin that should be pounded down to absurdly low levels – but suddenly becomes harmless or even beneficial in women, elderly folks and heart attack patients! Hang on – aren’t women, elderly folks and heart attack victims human beings too? If LDL is toxic for CHD-free non-elderly blokes, why wouldn’t it be toxic for these other groups also? The elderly, especially, are more susceptible to physiological and biochemical insults, so if LDL was so toxic then the relationship between LDL and increased mortality should in fact be much more readily apparent in them.
Or maybe the LDL cholesterol theory is just a complete and utter farce.
Dr Janet Brill’s book excitedly wanks on about how you can lower your LDL cholesterol by up to 47%, but why would you want to? Why would you want to halve it, in the process denying your cells an important substrate, and potentially imparting yourself with a higher death risk? Leave that nonsense to folks like Janet Brill. If she earnestly believes this anti-cholesterol nonsense, despite the overwhelming volume of contradictory literature, then let her practice it. If you truly value your life, then you really need to start viewing the cholesterol hypothesis for the idiotic sham that it is.
Lowering LDL isn’t going to help you reduce your oxidized LDL cholesterol levels, either. The degree of LDL oxidation is a function of your antioxidant status, not your blood LDL levels.
In animal studies, administration of antioxidant drugs like probucol impairs LDL oxidation and arterial plaque formation, even when there is no change in blood cholesterol levels. In fact, administration of the antioxidant butylated hydroxytoluene (BHT) significantly reduces the degree of atherosclerosis in the aorta of rabbits, even though it raises LDL cholesterol levels[Sasahara][Tangirala][Carew TE][Daugherty][Bjorkhem].
Of course, human data is much more relevant to humans than research with furry little critters. So let's take a look at that.
Among elderly Belgians, higher levels of oxidized LDL were accompanied by a significantly increased risk of heart attack, regardless of total LDL levels[Holvoet][Holvoet].
In 1997 Swedish researchers published a comparison of CHD risk factors among men from Vilnius in Lithuania and Linkoping in Sweden. These two groups were selected because the former had a four-fold higher death rate from CHD than the latter. Very little difference in traditional risk factors existed between the two groups, except that the men from CHD-prone Vilnius had lower total and LDL cholesterol levels.
According to folks like Brill, the lower total and LDL cholesterol of the Lithuanian men should have placed them at reduced risk of heart disease. But reality often veers markedly from the politically correct garbage folks like Brill subscribe to. When the researchers probed further, they discovered that the men from Vilnius had significantly higher concentrations of oxidized LDL. They also displayed significantly lower blood levels of diet-derived antioxidants such as beta carotene, lycopene, and gamma tocopherol (a form of vitamin E). So while the Lithuanian men had lower LDL levels, they were more prone to the formation of oxidized LDL owing to what appeared to be a poorer intake of antioxidant-rich foods[Kristenson].
In Japanese patients undergoing surgery to remove plaque from their carotid arteries, blood levels of oxidized LDL were significantly higher than those measured in healthy controls. Advanced carotid plaques removed from these patients showed far higher levels of oxidized LDL than neighbouring sections of artery that were disease-free. Elevated oxidized LDL was also associated with an increased susceptibility of plaque rupture. However, there was no association between oxidized LDL concentrations and total LDL levels[Nishi].
A mere nine days of atorvastatin administration (20 mg/day) was shown to significantly decrease platelet levels of oxidized LDL. These changes were observed before any noteworthy drop in LDL cholesterol was evident[Albert]. In patients randomly assigned to receive 10 mg of pravastatin or 20 mg of fluvastatin for 12 weeks, significant reductions in oxidized LDL occurred in both groups. The reduction was significantly higher in the fluvastatin group than in the pravastatin group (47.5% vs 25.2%, respectively). Reductions in total and LDL cholesterol, however, did not differ between the two groups[Yasunari].
I will reiterate once more: Oxidized LDL levels have nothing to do with your blood LDL levels. If you want to reduce the amount of free radical damage to your LDL cholesterol, you need to forget the counter-productive cholesterol-lowering wank and focus instead on fortifying your antioxidant status (you can do that by reducing your bodily iron burden, eating antioxidant-rich plant foods, teas and spices, and judicious supplementation. All of which are discussed in my book The Great Cholesterol Con, which reportedly hasn't sold as many copies as Brill's Cholesterol Down, but hey, the Ramones didn't sell as many records as the Spice Girls, either).
Quantity vs Quality: British teeny-boppers The Spice Girls (top) sold way more records than punk rock legends Ramones (bottom). If you earnestly believe this means the Spice Girls made better music, then I strongly urge you to take up skydiving – without a parachute.
Ladies and gentlemen, you can listen to the published clinical data, or you can listen to people like Janet Brill, who simply soak up via passive osmosis the anti-cholesterol garbage they’ve been taught at school. Brill has never stopped to question this garbage, because she earnestly believes that everything taught at university is rock solid fact. Having obtained a PhD, she now believes she is an omnipotent fountain of dietary and health knowledge, when in reality her writings are a quagmire of ignorance and misinformation.
The Whole Grain Scam, Part 7,395
Clearly, “Dr” Brill has no clue about LDL, but what about whole-grains? Is it true that they improve antioxidant status, fight diabetes, and lower CHD risk, as Brill claims?
Not bloody likely.
Most of the studies Brill cites in support of whole grains are epidemiological studies. These are not controlled clinical trials but population studies where the researchers ask study participants what they eat, then follow them for a specified period of time to see who got fat, sick or died. If you’re thinking this is a pretty shaky way to determine the value of something like whole grains, you’re right. For starters, long running epidemiological studies rely on self-reported food intakes. During a ten-year period, a participant typically only has to submit a handful of 24-hour diet recalls or food questionnaires asking what they ate over the last few days. It doesn’t take a genius to work out how this kind of data acquisition could result in less than sterling data; inaccurate recall and questionable estimation of serving sizes could completely throw the results out.
The other huge confounding factor with the epidemiological whole grain studies is that it’s a well-known fact health conscious people tend to believe the whole-grain hype and therefore eat more whole grains. So when you see a study claiming whole grains are associated with a superior health outcome, was this a result of the whole grains, or the fact that whole grain consumers tend to exercise more, smoke less, and follow numerous other healthy practices? There is simply no way of answering this question honestly from epidemiological studies.
A much more reliable way to answer this question is to conduct a randomized controlled clinical trial. We take a group of regular people, randomly assign some of them to consume whole grains, the remainder to eat refined grains, then follow them over a given time frame and see who fares best.
We can also take the same individuals, and instead of dividing them into 2 parallel groups, we can actually subject each person to an identical period of time on each diet. Such a study is known as a “crossover” trial, and bears the distinct advantage of eliminating the possibility that, despite randomization, group differences influenced the outcome of the trial.
Guess what? There have been numerous such trials conducted, and there are no prizes for guessing why Brill ignores them; they clearly show her whole grain dogma to be a load of false and potentially harmful nonsense.
As I mentioned earlier, Brill does cite one clinical trial in support of whole grains: the Esposito et al study. But this study involved not just increased whole grain consumption, but also "nuts, fruits, and vegetables, capped at up to 50 percent of daily calories. Compared to the low-fat diet, it included fewer carbs and a much larger amount of the “healthy” fat, olive oil".
In other words, it involved several interventions at once. How do we know if whole grains contributed to the positive outcome? That’s easy – we look at studies that examined increased whole grain consumption in isolation. When we do that, the rosy picture Brill paints for whole grains suddenly begins to look a whole lot different.
Whole Grains on Trial
We hear it all the time: Eat more whole-grains, they’re good for you! They increase your intake of healthy nutrients, they lower blood sugar, they fight cancer, they protect you from heart disease, blah, blah, blah!
They do no such thing.
I’ve discussed ad nauseum, in my books and on this site, the fact that whole cereal grains have a far higher concentration of undesirable anti-nutrients. Even grain-centric researchers acknowledge the presence of these anti-nutrients, but they of course play down the potential adverse health effects of these substances.
Don’t you do the same.
To find out why not, we’ll first look at the short term studies examining health markers, then we’ll take a look at the long term studies that actually gathered mortality data.
For some time now, I’ve been encouraging readers to opt for white rice instead of brown. Contrary to what you’ve been told, white rice is healthier. I think I can hear Janet choking on her tofu as she reads this, but it’s the plain truth.
As far back as 1949, researchers from the University of Ceylon in Colombo found feeding brown rice to healthy male medical students for three weeks worsened their calcium and magnesium status, even though their intake of these nutrients was higher than when they ate white rice. Three of the subjects were fed brown rice diet for an extended period of 18 weeks, and their calcium and magnesium balances began to improve, suggesting an adaptation to their lowered absorption of these important minerals. That this adaptation was not sufficient was suggested by the data for week 19 of the experiment, when the reintroduction of white rice diet was accompanied by an immediate increase in the amounts of calcium and magnesium retained[Cullumbine]. A 1960 paper by Indian researchers reported similar findings for calcium and warned "the exclusive consumption of brown rice in diets containing marginal or submarginal amounts of calcium is not to be recommended as it may produce negative calcium balances."[Rama Rao]
Japanese researchers fed low protein (0.5g/kg bodyweight) diets to healthy males; white rice was consumed for the first 14 days, then brown rice was eaten for the next 8 days. Not surprisingly, nitrogen balance was negative on both diets, but fell to a greater extent on the brown rice diet[Miyoshi].
Conventional dieticians claim the higher fibre count of brown rice is better for maintaining healthy blood sugar levels. That’s also nonsense. White and brown versions of the same rice variety return almost identical scores when subject to GI testing. The GI of white Doongara rice, for example, is 64; the corresponding score for brown Doongara rice is 66. Both versions also have virtually identical insulin index scores.
The GI of rice is largely determined by its amylose levels, not its fibre content. The varying amylose content of different rice varieties is why this grain shows such a wide range of scores on the GI charts, with high amylose varieties sporting significantly lower GI scores. Long grain rice strains have higher amylose contents than their short grain cousins, so wherever possible opt for long grain rices like Basmati and Doongara, as they tend to have lower GI scores than instant, converted and short-grain varieties[Williams][Miller]. Jasmine is an exception to the rule as it sports a higher GI despite its long grain status.
A recent clinical trial from China further puts lie to the claim brown rice has some sort of anti-diabetic effect. Researchers randomly assigned 202 middle-aged adults with diabetes or a high risk for diabetes to consume either white or brown rice ad libitum for 16 weeks. No differences were noted in BMI, waist circumference, glycated hemoglobin, blood glucose or insulin concentrations between the two groups[Zhang].
Unless you exclusively eat rice grown and watered under strict organic growing conditions, it is true that you may get a little something extra from brown rice. Unfortunately, that something extra happens to be a Group 1 carcinogen. You see, vitamins, minerals, amino acids and trace elements are not the only things plants absorb from the soil and water in which they grow. Toxic metals like arsenic also find their way into plants; analyses of hundreds of varieties of white and brown rice have found the latter to contain higher levels of arsenic than white rice[Meharg][Zavala]. The higher concentration of arsenic in brown rice is attributed to the fact it still retains its outer layers; rice bran is an especially rich source of arsenic[Sun].
(For further information on how to dramatically lower the arsenic content of the rice you eat, please refer to the info at the end of this article)
What About Whole Wheat?
As with rice, there exists absolutely no evidence in real live humans to support the incessant claims that whole wheat is healthier than its refined counterpart.
Brill claims that whole grains improve antioxidant status, but does not give a single verifiable citation. She really should check out the paper by Jenkins et al, who gave type 2 diabetics a low-wheat fibre diet and a high-wheat fibre diet containing bran-rich bread and breakfast cereal for three months each. Free radical damage of LDL cholesterol increased during the high-wheat fibre phase[Jenkins].
In a University of Minnesota experiment, healthy young males and females followed a refined grain diet, or a diet in which refined grains were replaced by whole grain and whole meal products in random order. Despite its higher content of the antioxidant nutrients vitamin B6, folate, selenium, zinc, magnesium and cysteine, the whole grain diet produced no improvement whatsoever in blood antioxidant capacity, nor in urinary markers of antioxidant status[Enright].
When Brill tells you that whole-grains improve your antioxidant status, she's either lying or simply is not aware of the relevant research showing otherwise. Neither possibility instils me with much confidence in the accuracy of her writings.
Fruit and Veggies Kick Whole Grain Ass!
Compare the pathetic inability of whole grains to improve antioxidant status with that of nutritionally superior fruit and vegetables. When young and older adult subjects doubled their usual intake of fruit and vegetables from five to 10 servings daily, substantial increases in blood antioxidant capacity were seen after 15 days[Cao]. In a Danish study, healthy males and females who consumed an extra 600 grams of fruit and vegetables daily for 25 days experienced reductions in lipoprotein oxidation and increases in the activity of glutathione peroxidase, an enzyme in the body that is a powerful scavenger of free radicals[Dragsted].
But back to the mineral-excreting effects of whole-grains: A 1976 paper reported a tightly controlled metabolic ward study in Iran in which two men at 2 different diets for 20 days each. During the first 20 days, more than 50% of their energy intake was provided by white bread. During the second 20-day period, the white bread was replaced with Bazari, a traditional whole grain bread. Apart from the different breads, the experimental diets contained identical amounts of cheese, milk, mutton, fruits and vegetables, beans, rice, turnips, oils, tea/water, and sugar.
Zinc balance was positive during the white bread diet, but became negative during the Bazari period. Increased faecal excretion was responsible for the change. Calcium balance also declined in both men during the Bazari period, despite moderately increased calcium intakes. The high content of magnesium in the bread led to a nearly doubled intake during its consumption compared with white bread. However, magnesium excretion in faeces increased to a still greater extent while that in urine also rose substantially. Moderately negative magnesium balances resulted while Bazari was being consumed[Reinhold].
Some readers might object that these results, and those of the abovementioned rice experiments, wouldn’t apply to well fed Westerners eating whole grains and also consuming plenty of magnesium, zinc and calcium. But as I’ve also discussed ad nauseum, marginal intakes of zinc and magnesium are quite common in the West. NHANES data show that mean magnesium intake in the US for example, is actually below the RDA. In other words, insufficient magnesium intake is the norm, not the exception. Given that magnesium is a critical mineral for cardiovascular, muscular and neurological function, should we really embrace foods that actively impair its absorption? Ditto with zinc – given its importance in immune and reproductive health, is it really wise to recommend foods that antagonize its uptake in the body? Why are Western health 'experts' encouraging us to emulate aspects of Third World diets that researchers in the Third World have long since identified as problematic?
The Real Nitty Gritty – Longer Term Trials
The numerous nutritional shortcomings of whole-grains may help explain why the only randomized clinical trial to have ever examined the hypothesis that wheat fibre can reduce CHD actually found a small increase in coronary and overall mortality[Burr]. You read that right; the DART trial, the only trial to put the “grain fiber = heart healthy” to the test, found it was a complete flop in preventing CHD or overall mortality.
Protection from cancer is another claim frequently made for high-fibre cereal foods; colon cancer in particular, we are repeatedly told, would be dramatically reduced if only we would all eat more whole-grains. While confounder-prone epidemiological studies backing this notion are easy to find, none of the numerous randomized controlled intervention trials conducted in this area support the possibility that high cereal fibre intakes prevent the progression of colon cancer[Asano]. In fact, some of these trials noted worse outcomes in the treatment groups. In the four-year Polyp Prevention Trial, colorectal cancer was diagnosed in 10 subjects from the high fibre group, and only 4 from the low-fibre group. Even after excluding those diagnosed within the first year of the study, the results were similarly unfavourable; four cases in the intervention group as compared to 2 in the control group. Polyp recurrence was virtually identical between the two groups[Schatzkin].
In the three-year double-blind Phoenix Colon Cancer Prevention trial, there was a significantly higher proportion of subjects with three or more recurring polyps in the high-fibre group. Seven cases of colon cancer were reported in the high-fibre group, but only 2 in the low-fibre group. Those who have abandoned cereal grains and relished the subsequent improvements in gastrointestinal function would not be at all surprised to learn that the incidence of nausea, abdominal pain, diarrhea, constipation, intestinal gas, and abdominal bloating was significantly higher among those receiving the high-wheat fibre diet[Alberts].
Scientific reality: Um, I’ve lost count; Janet Brill: 0
Sorry Janet, but you really need to start hitting the books. When it comes to whole-grains, you are so far out in left field it just isn’t funny. The clinical evidence simply does not support your whole grain hyperbole. About the only demonstrable results to be gained from eating whole grains instead of refined is a greater likelihood of adverse gastrointestinal effects and a potential increase in your risk of colorectal cancer and cardiovascular disease mortality.
Thanks, but no thanks.
The Mediterranean Diet that Never Was
There’s one more thing that I really need to get off my chest, and that’s this absurd belief that the Mediterranean diet was and is based around whole grains. This myth is peddled by such ‘esteemed’ sources as the Oldways Preservation & Exchange Trust, the Harvard School of Public Health and the World Health Organization.
Like so much of mainstream 'wisdom', it’s bollocks.
I grew up in an Italian-Australian household, and spent a lot of time in other Italian-Australian households, and can tell you without a shadow of a doubt that whole-grains are about as Italian as cricket, NASCAR, and chicken vindaloo.
It’s true that Italy enjoys a lower rate of heart disease than countries such as the USA, UK, and Australia, but this has absolutely nothing to do with whole grain consumption. Italians make, and have traditionally made, their bread, pasta, pizza and biscotti from WHITE flour. Their seafood risotto is made using WHITE rice. The first time my parents, who grew up in post-war Italy, ate wholemeal pasta was here in Australia when they were almost 50, and that was only because their eldest son – who shall remain nameless, yessirree – fell victim to the reigning low-fat propaganda and bought some home from the supermarket. I still vividly remember the old boy’s considered appraisal after taking his first few mouthfuls:
“What is this shit?!”
Yep, they love their whole grains, the Italians!
Ditto with the French, who have the lowest CHD rates in all of Europe, and make their breads and baguettes from WHITE flour.
And need I mention the Japanese, whose diet is comprised heavily of WHITE rice and who have even lower rates of CHD than the Mediterraneans?
If you really want to know what the Mediterraneans (and the Asians) eat, ask Mediterraneans and Asians, not researchers and book authors from the US, UK or Australia. The latter view everything through their own biased lenses and have the annoying tendency to create revisionist portrayals of other cultures' diets that conform to the anti-cholesterol, whole grain dogma they've been so heavily inculcated with.
Milia, an 82-year old maternal relative, describes how Italians in pre-, peri and post-war Calabria, in southern Italy used to prepare their grains: Corn and wheat were grown by villagers, taken to a local water mill, where the kernel was separated from the husk. The villagers returned home with their newly milled grain and proceeded to feed the bran - the portion of the grain that researchers in distant Anglo countries hold in God-like awe - to their animals. Keep in mind that economic conditions in southern Italy at the time were quite poor and that the residents were thrifty people who didn't waste anything - yet they still went to the trouble of milling their grain and relegating the outer husk for use as animal feed. There probably wasn't a single nutrition PhD in the entire Calabrian region, yet these folks were intuitively far more knowledgeable about grains than today's batch of 'educated', self-assured yet largely clueless dieticians.
In closing J, I can tell you with 100% confidence that Dr Janet Brill is totally incapable of accurately representing the science on either whole grains or cholesterol, and really needs to hit the journals. In fact, her views are completely out in left field, unsubstantiated by sound science and could potentially cost human lives if her advice regarding cholesterol and whole grains were to be followed. She wrote the book Cholesterol Down, which she believes competes with my book, The Great Cholesterol Con, but the truth is, they’re not even in the same league (mine, of course, is filled with verifiable facts while hers is replete with unsubstantiated garbage 🙂
To be fair, despite her general cluelessness, Brill manages to get a few things right. Her advice to eat fruit and vegetables is sound, as is her advice to do regular exercise. But you can find this out in my books, minus the misleading whole grain and anti-cholesterol BS.
The real problem, and the very real danger, with people like Janet Brill, is that their incessant blathering about cholesterol distracts people from doing the things that really matter: maintaining youthful bodily iron stores (EXTREMELY IMPORTANT), avoiding psychosocial stress, getting regular exercise that is progressively graduated in its duration and intensity, maintaining optimal glycemic control, eating a nutrient dense diet and employing judicious nutritional supplementation to ensure optimal intakes of key heart-healthy nutrients like magnesium, long chain n-3 fats, co-enzyme Q10, etc.
Now, where did I leave the tape measure?
(To view Janet Brill's reply to this article, click here)
Addendum: Avoiding Arsenic in Rice
Numerous analyses of the arsenic content of rice have been published, and the results consistently show that Californian varieties contain lower levels of arsenic than rice grown in the southern US states of Arkansas, Louisiana, Mississippi and Texas. Previous arsenic-based pesticide use on cotton fields now being used for rice production is believed to be the culprit[Williams]. Internationally, rice from Europe (Italy, Spain, France) also shows comparatively high arsenic levels[Zavala][ Meharg].
What, if any, effect this has on human health is still a relatively understudied area, but I’d personally prefer to err on the side of caution. Along with avoiding brown rice (for reasons discussed above), I’d avoid rice from high-arsenic sources, and to further reduce arsenic content I’d use a high water:rice volume when cooking. A 2009 study found that a 6:1 water:rice ratio (i.e. using 6 cups of water to 1 cup of rice) removed 45% of arsenic in long-grain rice. The rice was boiled to eating texture and the remaining water discarded. Steaming was less consistent in reducing arsenic content, while low volume water cooking (2.5:1 water:rice ratio, boiled to dryness] failed to remove arsenic. Rinsing the rice prior to cooking produced a fourteen percent reduction in arsenic content, but the effect was only observed in basmati rice. The rinsing method employed was to place 100 grams of rice in 600 millilitres of distilled and deionised water, and agitate the mixture routinely for 3 minutes. The water was then drained, and the process repeated once more with a fresh batch of water[Raab]. An Indian study using similar water:rice ratios during cooking found similar results, but that a more extensive washing procedure (rinsing the rice 5-6 times until the discarded water became clear) removed 28% of arsenic[Sengupta].
Hecht HS, Harman SM. Relation of aggressiveness of lipid-lowering treatment to changes in calcified plaque burden by electron beam tomography. 2003; 92: 334-336.
Cowell SJ, Newby DE, Prescott RJ, et al. A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis. 2005; 352: 2389-2397.
Tikhonoff V, et al. Low-Density Lipoprotein Cholesterol and Mortality in Older People. J Am Geriatr Soc. 2005; 53 (12): 2159-2164.
Weverling-Rijnsburger AW, et al. High-density vs low-density lipoprotein cholesterol as the risk factor for coronary artery disease and stroke in old age. Arch Intern Med. 2003 Jul 14; 163 (13): 1549-1554.
Psaty BM, et al. The Association Between Lipid Levels and the Risks of Incident Myocardial Infarction, Stroke, and Total Mortality: The Cardiovascular Health Study. J Am Geriatr Soc, 2004; 52: 1639–1647.
Al-Mallah MH, et al. Low admission LDL-cholesterol is associated with increased 3-year all-cause mortality in patients with non ST segment elevation myocardial infarction. Cardiology Journal, 2009; 16 (3): 227–233.
Boersma E, et al. Predictors of outcome in patients with acute coronary syndromes without persistent ST-segment elevation. Results from an international trial of 9461 patients. The PURSUIT Investigators. Circulation, 2000; 101 (22): 2557–2567.
Wang TY, et al. Hypercholesterolemia Paradox in Relation to Mortality in Acute Coronary Syndrome. Clinical Cardiology, 2009 Sep; 32 (9): E22-28.
Sasahara M, et al. Inhibition of hypercholesterolemia-induced atherosclerosis in the nonhuman primate by probucol, I: is extent of atherosclerosis related to resistance of LDL to oxidation? 1994;94:155-164.
Tangirala RK, et al. Effect of the antioxidant N,N’-diphenyl 1,4-phenylenediamine (DPPD) on atherosclerosis in apo E-deficient mice 1995;15:1625-1630.
Carew TE, et al. Antiatherogenic effect of probucol unrelated to its hypocholesterolemic effect: evidence that antioxidants in vivo can selectively inhibit low density lipoprotein degradation in macrophage-rich fatty streaks and slow the progression of atherosclerosis in the Watanabe-heritable hyperlipidemic rabbit. 1987;84:7725-7729.
Daugherty A, Zweifel BS, Schonfeld G. Probucol attenuates the development of aortic atherosclerosis in cholesterol-fed rabbits. 1989;98:612-618.
Bjorkhem I, Henriksson-Freyschuss A, Breuer O, et al. The antioxidant butylated hydroxytoluene protects against atherosclerosis. 1991; 11: 15-22.
Holvoet P, et al. The metabolic syndrome, circulating oxidized LDL, and risk of myocardial infarction in well functioning elderly people in the Health, Aging, and Body Composition Cohort. 2004; 53:1068-1073.
Holvoet P, et al. Association of high coronary heart disease risk status with circulating oxidized LDL in the well-functioning elderly: Findings from the Health, Aging, and Body Composition Study. 2003; 23: 1444-1448.
Kristenson M, et al. Antioxidant state and mortality from coronary heart disease in Lithuanian and Swedish men: concomitant cross sectional study of men aged 50. 1997; 314: 629-633.
Nishi K, et al. Oxidized LDL in carotid plaques and plasma associates with plaque instability. Arterioscler Thromb Vasc Biol, 2002; 22: 1649-1654.
Albert MA, Danielson E, Rifai N, et al. Effect of statin therapy on C-reactive protein levels: the Pravastatin Inflammation/CRP Evaluation (PRINCE): randomized trial and cohort study. JAMA, 2001;286:64-70.
Yasunari K, Maedi K, Minami M, Yosikawa J. HMG-CoA reductase inhibitors prevent migration of human coronary smooth muscle cells through suppression of increase in oxidative stress. Arterioscler Thromb Vasc Biol, 2001;21:937-942.
Cullumbine H, et al. Mineral Metabolism on Rice Diets. British Journal of Nutrition, 1950; 4: 101-111.
Rama Rao G, et al. The Effect of the Degree Of Polishing of Rice on Nitrogen and Mineral Metabolism in Human Subjects. Cereal Chemistry, Jan-Feb, 1960; 37 (1): 71-78.
Miyoshi H, et al. Effects of brown rice on apparent digestibility and balance of nutrients in young men on low protein diets. Journal of Nutritional Science and Vitaminology, 1987; 33: 207-218.
Williams VR, et al. Rice Starch, Varietal Differences in Amylose Content of Rice Starch. Journal of Agricultural and Food Chemistry, 1958; 6 (1): 47–48.
Miller JB, et al. Rice: a high or low glycemic food? American Journal of Clinical Nutrition, 1992; 56: 1034-1036.
Zhang G, et al. Substituting white rice with brown rice for 16 weeks does not substantially affect metabolic risk factors in middle-aged Chinese men and women with diabetes or a high risk for diabetes. Journal of Nutrition, Sep, 2011; 141 (9): 1685-1690.
Meharg AA, et al. Speciation and localization of arsenic in white and brown rice grains. Environmental Science & Technology, Feb 15, 2008; 42(4): 1051-1057.
Zavala YJ, Duxbury JM. Arsenic in rice: I. Estimating normal levels of total arsenic in rice grain. Environmental Science & Technology, May 15, 2008; 42 (10): 3856-3860.
Sun GX, et al. Inorganic Arsenic in Rice Bran and Its Products Are an Order of Magnitude Higher than in Bulk Grain. Environmental Science & Technology, 2008; 42 (19): 7542–7546.
Jenkins DJ, et al. Effect of wheat bran on glycemic control and risk factors for cardiovascular disease in type 2 diabetes. Diabetes Care, Sep, 2002; 25 (9): 1522-1528.
Enright L, Slavin J. No effect of 14 day consumption of whole grain diet compared to refined grain diet on antioxidant measures in healthy, young subjects: a pilot study. Nutrition Journal, Mar 19, 2010; 9: 12.
Cao G, et al. Increases in human plasma antioxidant capacity after consumption of controlled diets high in fruit and vegetables. American Journal of Clinical Nutrition, 1998; 68: 1081-1087.
Dragsted LO, et al. The 6-a-day study: effects of fruit and vegetables on markers of oxidative stress and antioxidative defense in healthy nonsmokers. American Journal of Clinical Nutrition, 2004; 79: 1060-1072.
Reinhold JG, et al. Decreased Absorption of Calcium, Magnesium, Zinc and Phosphorus by Humans due to Increased Fiber and Phosphorus Consumption as Wheat Bread. Journal of Nutrition, 1976; 106: 493-503.
Burr ML, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet, 1989; 2: 757-761.
Asano T, McLeod RS. Dietary fibre for the prevention of colorectal adenomas and carcinomas (Cochrane Review). In: The Cochrane Library, Issue 2, 2002. Oxford.
Schatzkin A, et al. Lack of effect of a low-fat, high-fiber diet on the recurrence of colorectal adenomas. New England Journal of Medicine, Apr 20, 2000; 342 (16): 1149-1155.
Alberts DS, et al. Lack of effect of a high fiber cereal supplement on the recurrence of colorectal adenomas. New England Journal of Medicine, Apr. 20, 2000; 342 (16): 1156-1162.
Williams PN, et al. Market Basket Survey Shows Elevated Levels of As in South Central U.S. Processed Rice Compared to California: Consequences for Human Dietary Exposure. Environmental Science & Technology, 2007; 41: 2178-2183.
Zavala YJ, Duxbury JM. Arsenic in rice: I. Estimating normal levels of total arsenic in rice grain. Environmental Science & Technology, May 15, 2008; 42 (10): 3856-3860.
Meharg AA, et al. Geographical variation in total and inorganic arsenic content of polished (white) rice. Environmental Science & Technology, Mar 1, 2009; 43 (5): 1612-1617.
Raab A, et al. Cooking rice in a high water to rice ratio reduces inorganic arsenic content. Journal of Environmental Monitoring, 2009; 11: 41-44.
Sengupta MK, et al. Arsenic burden of cooked rice: traditional and modern methods. Food Chemical Toxicology, 2006; 44: 1823-1829.
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.