Tuesday, October 9, 2012

Animal flesh is a good source of vitamin B12?

Perhaps not.

According to the Framingham Offspring Study, 39 percent of people aged 26 to 83 years, primarily flesh-eaters, have low B12 levels.  Since vegans form less than one percent of the population, this study indicates that B12 deficiency plagues nearly 40 percent of people who eat animal products.

B12 Deficiency May Be More Widespread Than Thought / August 2, 2000 / News from the USDA Agricultural Research Service

In this study, consumption of supplements and fortified foods (i.e. foods with the supplement added) markedly reduced the risk of low serum B12 levels:

"The researchers also expected to find some connection between dietary intake and plasma levels, even though other studies found no association. And they did find a connection. Supplement use dropped the percentage of volunteers in the danger zone--plasma B12 below 185 pmol/L--from 20 percent to 8. Eating fortified cereals five or more times a week or being among the highest third for dairy intake reduced, by nearly half, the percentage of volunteers in that zone--from 23 and 24 percent, respectively, to 12 and 13 percent."
This report does not make it clear whether or how the researchers sorted the effect of supplements and fortified foods from the effects of dairy.  I predict that since people commonly pour cow milk over their fortified cereals, and that people who consume more milk tend also to be more likely to use fortified cereals and supplements, because these behaviors would characterize people who have conventional health consciousness. If so, high dairy intake would strongly correlate with intake of supplements and fortified cereals, making it very difficult to separate the effects of these three potential B12 sources.  

However,  the research found no relationship between flesh intake and plasma B12 levels.

"Oddly, the researchers found no association between plasma B12 levels and meat, poultry, and fish intake, even though these foods supply the bulk of B12 in the diet. “It’s not because people aren’t eating enough meat,” Tucker said. "The vitamin isn’t getting absorbed.”"

Well, apparently the vitamin is getting absorbed from supplements, fortified foods, or dairy.  Tucker seems to have presented evidence to make this statement more correct: "The vitamin isn't getting absorbed from meat, fish, or poultry."

Got Vitamin B12?  Source.

Regarding dairy, a cup of milk supplies 0.9 mcg of B12, and an ounce of cheese supplies about  0.5 mcg.  In comparison, one serving of Kellogg's All Bran cereal provides 5.8 mcg of B12 (more than twice the RDA).  One-half cup of All Bran provides about 10 times the amount of B12 found in one-half cup of milk or one ounce of cheese.  Most people will eat more than one-half cup of All Bran in one sitting (it only provides 80 calories), probably more like one- and one-half or two cups (17.4 to 23.2 mcg of B12).  Three-quarters of a cup of General Mills Cocoa Puffs provides 1.5 mcg of B12, three times what is found in one-half cup of milk used to top it.  Again, three-quarters cup of Cocoa Puffs only provides about 100 kcal; I think most kids would consume two to three of those servings, providing 3.0 to 4.5 mcg of B12.   I would guess that odds favor that a person who eats milk, cheese, and fortified cereal will probably get a larger dose of B12 from the cereal than from the milk products. 

Now take a look at supplements.  Bayer's One-A-Day for Women contains 6 mcg of B12, and the One-A-Day for men contains a whopping 18 mcg.   A woman would have to consume more than six cups of milk, or 12 ounces of cheese to get the same B12 intake as found in her One-A-Day for Women; and a man would have to consume more than 18 cups of milk and 36 ounces of cheese to get the B12 in his One-A-Day.

So these Tufts University researchers have found some evidence suggesting that animal flesh does not reliably constitute a good source of B12, and that among omnivores, the people who consume B12 supplements or fortified foods have the best B12 status.

Seems we have to say goodbye to these ideas:

Eating flesh reliably prevents B12 deficiency. -- False

Only vegans get B12 deficiency. -- False

Since only microbes produce vitamin B12,  I guess modern antibiotic hygiene and agricultural practices, which have reduced the number of B12-producing bacteria in our soils, water, and general environment, have caused this epidemic of vitamin B12 insufficiency.

Vegan or flesh-eater, this research suggests you probably need to get your B12 from microbes by taking a B12 supplement or eating B12 fortified foods, which provide microbial-source B12 in adequate quantities.


David Despain said...

Vitamin B12 absorption is somewhat complex. In flesh, as you say, B12 is bound to protein and it must be released through action of stomach acid. Then, the B12 can finally be complexed with intrinsic factor secreted by the stomach cells. The complex can then travel to the small intestine where it can be absorbed. So, while flesh contains plenty of B12, it may be that some folks might lack intrinsic factor or, as with older folks, may lack sufficient production of hydrochloric acid to release B12 or allow it to bind to intrinsic factor. Anyway, this may explain why getting B12 from a supplement or fortified foods may be easier than flesh.

screennamerequired said...

Oysters and clams are a great source. It's pretty hard to argue against the occasional consumption of oysters. I'm not big on the taste but I do occasionally enjoy them fresh and lightly steamed.

Jozef Varhaník said...

This is starting to get soo funny with each post. So you suggest that foods fortified with synthetic cyano+cobalamin with it's poor bioavailabilty compared to cobalamin bound to "natural" sources is the way to go? B12 absorbtion from animals is around 60%, 25% for cyanoB12. Also if you are worried by your B12 status eat a pig's liver once a week. 100 grams/134kcals of it has 26mcg B12. "Created by mother nature", not in bacterial fermentation wats and then thrown into charcoal so it adds cyanide to itself that has to be cleared out of your system. But I guess you already know that and and a lot more, you just no longer wish to do/recommend it. I can only wonder why.

Jimmy Gee said...

I guess I would ask "what is low?" (and please don't quote an RDA / RDI etc...- rhetorical question). And again is the purported "low" related to eating or not eating meat at all - who's to say. Framingham is reporting a number, but did they explain their assessment of that finding?

Don said...


All B12 in the world is produced/synthesized by microbes, including that found in pig's liver.

The B12 in supplements is not man-made, it is microbe-made, just like the B12 in flesh foods.

Bacterial fermentation is part of "mother nature." None of these bacteria are man made either. We just cultivate them, the same way we cultivate plants and animals. The same way we cultivate yeasts in making, for example, alcohol, which we also cultivate in vats.

You say that B12 from supplements has a low bioavailability compared to that in flesh, but one of the points of this study was that it found evidence indicating just the opposite.

Which suggests that something in animal products reduces the availability of B12.

The amount of cyanide (2% of the weight, or 20 micrograms cyanide in a 1 mg cyanocobalamin tab) is far less than ingested in many natural foods.

I don't know many people who relish the idea of eating a pig's liver. Among readers of AOL Food, a poll found that liver is the most hated food.


I would imagine that if humans were naturally adapted to eating animal flesh, there would be an almost universal and natural (not learned) liking for eating animal guts, as we find in wild carnivores and omnivores. In my mind, the fact that so many hate and feel revulsion at even the thought of eating liver and other viscera suggests many humans are psychophysically poorly adapted to eating animals.

anand srivastava said...

If the real food is not giving the numbers that the supplements are giving, I would think something is wrong with our understanding of the problem.

We wouldn't have survived if we needed supplements during evolution.

The Humane Hominid said...

Sure we would have, Anand. Nature is full of supplements. Why else do you think all animals eat dirt, visit salt licks, drink "contaminated" water, and so forth?

Also, nutrient deficiency of some sort is pretty much a baseline condition of most wild animals. All evolution "cares" about is whether they make it to reproductive age. It doesn't give a damn about their health otherwise.

Charles Grashow said...


White rice can be a “safe” starch

I don’t think it’s necessary to completely eliminate rice from the diet. The EPA’s 5 ppb per day limit on arsenic is probably what we should shoot for in our diets, in light of current evidence. Many of the white rice products tested had fairly low levels of arsenic, and in the context of a few servings a week for an adult, it’s probably not an issue. As for very young children and infants, I don’t recommend serving them rice products in general, so they shouldn’t be exposed to arsenic from rice anyway. Pregnant women may want to be cautious about their rice intake, and minimize their exposure to arsenic to protect their developing fetus; finding another safe starch to replace rice during pregnancy would be wise.

So if you choose to purchase white rice, buy a brand made in California like Lundberg; their California White Basmati Rice has only 1.3 to 1.6 ppb arsenic per serving (1/4 cup uncooked), well below the safe limit. In addition, rinsing the rice before cooking and boiling it in a high water-to-rice ratio can help reduce the arsenic content significantly. So if you want to keep white rice as a part of your diet, I recommend looking for a safe brand like Lundberg and rinsing the rice thoroughly before cooking in a large quantity of water; this should be adequate to make rice a safe food to eat in moderation.

Brown rice: Not a health food!

Brown rice, on the other hand, has significantly more arsenic than white rice and should be avoided or consumed rarely. Some of the brown rice brands tested contained at least 50% more than the safe limit per serving, and a few even had nearly double the safe limit. (PDF with complete details of test results) Note that some of the worst offenders for arsenic are made from brown rice: processed rice products like brown rice syrup, brown rice pasta, rice cakes and brown rice crisps. These processed products are commonly consumed by those following a “healthy” whole grain rich or gluten-free diet, but they clearly pose a significant risk of arsenic overexposure, especially if a person eats more than one serving per day. Obviously, brown rice is not a food that should be a dietary staple, or even eaten on a regular basis.


Cooking rice in a high water to rice ratio reduces inorganic arsenic content


Jimmy Gee said...


Define nutrient deficiency.

This is another area of research that is based more upon biological plausibility than actual experimental evidence. Admittedly, creating an experiment (RCT) that purposely induces deficiency in order to test this deficiency's effect on human health would never (nor should it ever) be done. However, many people live well beyond reproductive years with vitality without meticulously monitoring for deficiency, so I doubt the relevance of purported minimum requirements.

Charles Grashow said...


Most books, articles, and web sites on diet and nutrition, especially those on "alternative" diets, are written by folks who, although quite possibly sincere, could not pass an 8th grade science quiz, or add 1/2 + 1/3. Thus, they generally are full of nonsense, errors of fact, faulty (or no) logic, unsupported rumors, innumeracy, errors copied from other credibility-challenged sources, or the unsupported belief systems of various fad-diet microcultures.

Worse, most orthodox nutritional texts tout the orthodox party line, conceptually sponsored by the USDA, which is nothing more than a trade organization of the agricultural/meat/dairy/grain industries. The "scientists" supporting the Big Four Food Group mythical paradigm, although they may have some limited expertise in a narrow, restricted field, are so ill-educated in the broader sense as to actually believe that animal flesh, milk, eggs, and grains are useful 'foods' for our frugivorous ape species when there is not one iota of scientifically credible evidence supporting these traditional, profit-oriented beliefs.

That humans are indeed frugivorous apes is evidenced by the fact that the "genetic distance" between chimpanzees and humans is only a scant 1.6%, and clearly, that difference is expressed in the physical differences, not in inherent digestive and systemic biochemistry.

In fact, all scientific evidence, not unsupported opinion, refutes these dogmatic beliefs in the Big Four Food Groups. Yes, even "scientists" have been so conditioned by their life-long cultural dietary programming, starting at birth, that they have totally lost their objectivity in this most fundamental concept of human diet

This is a very interesting site

Charles Grashow said...


Then Dr. Gofman asked people about their health and diet. He learned that having high LDL or high triglycerides correlated with an increased risk of heart disease, high HDL correlated with a low risk of heart disease, and that the two profiles responded entirely differently to foods in the diet. (He also learned that cholesterol could be packaged either tightly clustered or loosely assembled within LDL; measuring it did little to reflect this risk.) Saturated fat raised LDL, while carbohydrates raised triglycerides, ultimately lowering HDL. (Dr. Gofman even recognized that LDL was made up of subtypes, although the meaning of the diversity was unclear at first.) It was groundbreaking work, but too advanced for the movement it ultimately spawned. With so few analytical ultracentrifuges available, researchers began using cheaper methods of counting lipoproteins, methods now offered during routine physicals. One form of cholesterol became "good," the other "bad."

Dr. Krauss was working part-time in Dr. Gofman's old lab and flipping through some data cards when he noticed a correlation that would change everything. As he combed through a recently completed study of 80 men and 54 women in Modesto, California, Dr. Krauss noticed that the people with low HDL tended to have high LDL. But not just any LDL was elevated; only the smaller forms observable to Dr. Gofman's analytical ultracentrifuge.

"I started studying these readouts, and what popped out were some amazingly strong inverse correlations," he says, still amazed at his good fortune. "It was just sitting there in the data." Dr. Krauss had found that small, dense LDL particles were the evil twin of good cholesterol. HDL and small LDL tended to move at the same time, he discovered, but in opposite directions. If your smaller forms of LDL were high, your HDL was low; if your smaller forms of LDL were low, your HDL was high. Whether one was the cause and the other was the effect was unclear, but given the newly discovered importance of HDL, the importance of smaller forms of LDL was now real.

Charles Grashow said...

This created a practical problem. Lumping all forms of LDL cholesterol together, as labs currently do when they count it in your basic blood draw, tells us little about how much of that LDL is small and how much is large. "Everyone doesn't necessarily have the same amount of very small LDL in their LDL," Dr. Krauss explains. Some people have mostly large LDL, a group Dr. Krauss would describe as "pattern A," while others have mostly small LDL (and usually, low HDL and high triglycerides), a group Dr. Krauss would label "pattern B." The second group has an increased risk of heart disease (a finding suggested again this year through the use of ion mobility). Large LDL, on the other hand — and large LDL is usually the majority of the LDL that shows up in a standard blood profile — is mostly benign.

Dr. Krauss discovered that while a diet high in saturated fat from dairy products would indeed make your LDL levels rise, "saturated fat intake results in an increase of larger LDL rather than smaller LDL particles," as he wrote in an American Journal of Clinical Nutrition review he co-authored in 2006. A diet heavy in full-fat cheese and butter — but not overloaded in calories — triggered the relatively harmless health profile described as pattern A. (Having demonstrated the benign consequences for cholesterol from consuming dairy fat, he is currently conducting studies to find out if the same holds true for diets high in saturated fat from beef.)

Not only is dairy fat unlikely to increase heart-disease risk, Dr. Krauss and others have learned, but reducing saturated fat in a way that increases carbohydrates in a diet can shift a person's LDL profile from safe to dangerous. That's pretty much what happens whenever some well-meaning person with "high LDL" starts eating "low-fat" frozen dinners filled out with corn-derived additives, all the while engaging in the customary ravaging of a basket filled with dinner rolls.

Healthy Longevity said...

Krauss RM has disclosed receiving grants from: Dairy Management Inc, the National Cattleman's Beef Association, Robert and Veronica Atkins Foundation

Nevertheless, here are the findings from one of the latest papers Krauss co-authored:

Effects of dietary saturated fat on LDL subclasses and apolipoprotein CIII in men.
Conclusions: Taken together with previous observations, these findings suggest that, at least in the context of a lower CHO high beef protein diet, HSF [high saturated fat] intake may increase CVD risk by metabolic processes that involve apoCIII.

Here is a rebuttal to one of Krauss’s most well-known papers:

Diet-heart: a problematic revisit

Here are findings from systematic reviews regarding LDL subfractions and risk of cardiovascular disease:

Systematic review: association of low-density lipoprotein subfractions with cardiovascular outcomes.
CONCLUSION: Higher LDL particle number has been associated with cardiovascular disease incidence, but studies have not determined whether any measures of LDL subfractions add incremental benefit to traditional risk factor assessment. Routine use of clinically available LDL subfraction tests to estimate cardiovascular disease risk is premature.

Clinical utility of inflammatory markers and advanced lipoprotein testing: Advice from an expert panel of lipid specialists
Studies have linked large LDL particles to atherosclerosis in nonhuman primates, in patients with familial hypercholesterolemia (who have an elevated concentration of predominantly large LDL particles), in participants of the population-based MESA study, in normolipidemic men with CHD, and among patients after MI in the Cholesterol And Recurrent Events (CARE) study.

Many studies document links between small dense LDL particles and atherosclerotic CVD. However, these statistical associations between small, dense LDL and CV outcomes are either significantly attenuated or abolished when the analyses are adjusted for the overall number of circulating LDL particles (LDL -P) either by adjustment for Apo B levels or by adjustment for nuclear magnetic resonance–derived LDL- P.

All lipoprotein particles in the LDL fraction are atherogenic, independent of size. LDL particles become trapped in the arterial wall and are internalized by macrophages through scavenger receptors on the macrophage surf ace, resulting in foam cell formation, activation of these foam cells and expansion of the inflammatory response.

The NLA Biomarkers Expert Panel was unable to identify any patient subgroups in which LDL subfractionation is recommended.

Healthy Longevity said...

Here are findings from reviews that demonstrate that LDL concentration is a causal risk factor for coronary heart disease and all-cause mortality:

Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis
The meta-regression analysis included 108 randomised trials involving 299 310 participants at risk of cardiovascular events. All analyses that adjusted for changes in low density lipoprotein cholesterol showed no association between treatment induced change in high density lipoprotein cholesterol and risk ratios for coronary heart disease deaths, coronary heart disease events, or total deaths. With all trials included, change in high density lipoprotein cholesterol explained almost no variability (<1%) in any of the outcomes. The change in the quotient of low density lipoprotein cholesterol and high density lipoprotein cholesterol did not explain more of the variability in any of the outcomes than did the change in low density lipoprotein cholesterol alone. For a 10 mg/dl (0.26 mmol/l) reduction in low density lipoprotein cholesterol, the relative risk reduction was 7.2% (95% confidence interval 3.1% to 11%; P=0.001) for coronary heart disease deaths, 7.1% (4.5% to 9.8%; P<0.001) for coronary heart disease events, and 4.4% (1.6% to 7.2%; P=0.002) for total deaths, when adjusted for change in high density lipoprotein cholesterol and drug class.

To take into account non-lipid effects of specific drugs (such as potential pro-thrombotic effects of hormone therapy), we included a categorical variable of drug class in the meta-regression model and did a meta-regression analysis stratified by drug class. We used R2 to measure the proportion of the variability in the log risk ratio of an outcome explained by the statistical model.

Similarly, we found no association between change in triglycerides and risk of coronary heart disease events whenever the model included an adjustment for the change in low density lipoprotein cholesterol (data available from the authors). Change in low density lipoprotein cholesterol, however, remained a significant predictor in a multivariable model adjusting for change in high density lipoprotein cholesterol, change in triglycerides, and class of intervention, with a 7.4% (4.4% to 10.4%; P <0.001) relative risk reduction for coronary heart disease events.

A Mendelian Randomized Controlled Trial of Long Term Reduction in Low-Density Lipoprotein Cholesterol Beginning Early in Life

Number of participants in meta-analysis = 1,003,207

Prolonged exposure to lower LDL-C beginning early in life associated with 3-fold greater clinical benefit for each unit lower LDL than treatment with a statin started later in life (Mean age at randomization in statin trials: 63 years; p = 0.00000000000000000843)

Absence of Heterogeneity: Suggests the effect of each of included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL-C, rather than through some other pleiotropic effect.

The increased clinical benefit associated with lowering LDL-C beginning early in life appears to be independent of the mechanism by which LDL-C is lowered. Diet and exercise are probably as effective as other therapies at reducing the risk of CHD (per unit reduction in LDL-C)

Charles Grashow said...


Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis

Results: After adjustment for demographics, lifestyle, and dietary confounders, a higher intake of dairy SF was associated with lower CVD risk [HR (95% CI) for +5 g/d and +5% of energy from dairy
SF: 0.79 (0.68, 0.92) and 0.62 (0.47, 0.82), respectively]. In contrast, a higher intake of meat SF was associated with greater CVD
risk [HR (95% CI) for +5 g/d and a +5% of energy from meat SF: 1.26 (1.02, 1.54) and 1.48 (0.98, 2.23), respectively]. The substitution
of 2% of energy from meat SF with energy from dairy SF was associated with a 25% lower CVD risk [HR (95% CI): 0.75 (0.63, 0.91)]. No associations were observed between plant or butter SF and CVD risk, but ranges of intakes were narrow.



Charles Grashow said...


Re your NIH study

https://intermountainheartcenter.com/wp content/uploads/2012/04/2011LipidEvaluation.pdf

Dr. Davidson has received research grants from Abbott
Laboratories, Daiichi Sankyo, GlaxoSmithKline, Merck &
Co. and Roche. Dr. Davidson has received consulting fees
from Abbott Laboratories, Aegerion Pharmaceuticals, Amgen,
AstraZeneca, Atherotech Inc., Daiichi Sankyo, DTC
MD, Esperion, GlaxoSmithKline, Intelligent Medical Decisions,
Kinemed, LipoScience, Merck & Co, Novo Nordisk,
Roche, Sanofi-Aventis, Synarc, Takeda Pharmaceuticals,
and Vindico Medical Education. Dr. Davidson has received
honoraria related to speaking from Abbott Laboratories,
GlaxoSmithKline and Merck & Co. Dr. Davidson has
served on the Board of Directors of DTC MD, Omthera,
Professional Evaluation Inc., and Sonogene.
Dr. Ballantyne has received research grants from Abbott
Laboratories, AstraZeneca, Bristol-Myers Squibb, dia-
Dexus Inc., GlaxoSmithKline, Kowa Pharmaceuticals,
Merck & Co., Novartis Pharmaceuticals, Roche, Sanofi-
Synthelabo, and Takeda Pharmaceuticals. Dr. Ballantyne
has received consulting fees from Abbott Laboratories, Adnexus,
Amylin Pharmaceuticals, AstraZeneca, Bristol
Myers-Squibb, Esperion, Genentech, GlaxoSmithKline,
Idera Pharmaceuticals, Kowa Pharmaceuticals, Merck &
Co., Novartis Pharmaceuticals,Omthera, Resverlogix, Roche,
Sanofi-Synthelabo, and Takeda Pharmaceuticals. Dr. Ballantyne
has received honoraria related to speaking from Abbott
Laboratories, AstraZeneca, GlaxoSmithKline, Merck & Co.,
Sanofi-Synthelabo, and Takeda Pharmaceuticals.
Dr. Jacobson has received consulting fees from Abbott
Laboratories, Amarin Pharmaceuticals, AstraZeneca,
GlaxoSmithKline and Merck & Co.
Dr. Bittner has received research grants from Abbott
Laboratories, National Institutes of Health, Spirocor,
Roche, GlaxoSmithKline, Gilead, and Pfizer Inc

Charles Grashow said...

Dr. Braun has received honoraria related to speaking
from the American Heart Association and the Preventive
Cardiovascular Nurses Association. Dr. Braun has received
salary support from the National Institutes of Health.
Dr. Alan S. Brown has received honoraria related to
speaking from Abbott Laboratories, Forest Laboratories
and Daiichi Sankyo.
Dr. W. Virgil Brown has received consulting fees from
Abbott Laboratories, Amgen, Anthera, Genzyme, Pfizer
Inc., LipoScience, and Merck & Co. Dr. W. Virgil Brown
has received honoraria related to speaking from Abbott
Laboratories, LipoScience, and Merck & Co.
Dr. Cromwell has received consulting fees from Isis
Pharmaceuticals, LabCorp, and Health Diagnostics Laboratory.
Dr. Cromwell has received research grants from Isis
Pharmaceuticals. Dr. Cromwell has received honoraria related
to speaking from Abbott Laboratories, LipoScience,
Merck & Co., and Merck Schering Plough.
Dr. Goldberg has received research grants from Abbott
Laboratories, GlaxoSmithKline and Roche. Dr. Goldberg
has received consulting fees from GlaxoSmithKline, Daiichi
Sankyo, and Pfizer Inc. Dr. Goldberg has received honoraria
related to speaking from Daiichi Sankyo,
GlaxoSmithKline, and Merck & Co.
Dr. McKenney has no relevant disclosures.
Dr. Remaley has received research grants from Alpha-
Core Pharmaceuticals, Kinemed, and VirxSys Inc.
Dr. Sniderman has received research grants from Astra-
Zeneca. A. D. S. has received honoraria related to speaking
from Merck & Co.
Dr. Toth has received consulting fees from Abbott Laboratories,
AstraZeneca, GlaxoSmithKline, Kowa Pharmaceuticals,
Pfizer Inc., and Merck & Co. Dr. Toth has
received honoraria related to speaking from Abbott Laboratories,
AstraZeneca, Boehringer Ingelheim, Glaxo-
SmithKline, Pfizer Inc., Merck & Co., and Takeda
Dr. Tsimikas has received consulting fees from ISIS,
Merck & Co., Genzyme/Sanofi and Quest. Dr. Tsimikas
has received honoraria related to speaking from Merck &
Co. Dr. Tsimikas has received research grants from Merck
& Co. and Pfizer Inc. Dr. Tsimikas has received equity interest
from Atherotope.
Dr. Ziajka has received honoraria related to speaking
from Abbott Laboratories, AstraZeneca and Merck & Co.
Dr. Ziajka has received research grants from Genzyme.
Dr. Maki has received research grants from Abbott
Laboratories, Amarin Pharmaceuticals, Atherotech, Bio-
Sante Pharmaceuticals, Cargill, Coca-Cola, Dairy Research
Institute, Fermenich, GlaxoSmithKline, Kao Corporation,
Kellogg Co., Monsanto, National Starch/Corn Products,
Ocean Spray, Omthera, PepsiCo, Pharmavite, Shaklee,
Solae, Trygg Pharmaceuticals and Welch’s. Dr. Maki has
received consulting fees from Abbott Laboratories, Cargill,
Dairy Research Institute, General Mills, GlaxoSmithKline,
Omthera, PepsiCo, Pharmavite and Trygg Pharmaceuticals.
Dr. Maki has received salary support from Biofortis.

Dr. Dicklin has received research grants from Abbott
Laboratories, Amarin Pharmaceuticals, Atherotech, Bio-
Sante Pharmaceuticals, Cargill, Coca-Cola, Dairy Research
Institute, Fermenich, GlaxoSmithKline, Kao Corporation,
Kellogg Co., Monsanto, National Starch/Corn Products,
Ocean Spray, Omthera, PepsiCo, Pharmavite, Shaklee,
Solae, Trygg Pharmaceuticals and Welch’s. Dr. Dicklin
has received consulting fees from Abbott Laboratories,
Dairy Research Institute, General Mills, GlaxoSmithKline,
Omthera, PepsiCo, Pharmavite, and Trygg Pharmaceuticals.
Dr. Dicklin has received salary support from Biofortis

We thank Biofortis-Provident Clinical Research for
writing and editorial assistance

Charles Grashow said...



2003 - 2005 Associate Principal Scientist
Kraft Foods
Glenview, Illinois

2000 - 2003 Senior Research Scientist
Kraft Foods
Glenview, Illinois

1998 - 2000 Research Scientist
Kraft Foods
Glenview, Illinois

Talk about conflicts of interest

Healthy Longevity said...

I am not suggesting that Krauss’s conclusion are faulty and misleading entirely on the basis that he receives grants from the livestock industry, but because a large amount of data demonstrates that this is the case. His conflicts of interest may merely explain why he has chosen to take this stance to downplay the detrimental effects of certain foods.

Here are the conclusions from the expert panel from the NIH in 1984, before the panel was financially influenced by the statin industry:
Elevated blood cholesterol level is a major cause of coronary artery disease. It has been established beyond a reasonable doubt that lowering definitely elevated blood cholesterol levels (specifically blood levels of low-density lipoprotein cholesterol) will reduce the risk of heart attacks due to coronary heart disease

The recent expert panel agreed that other measurements of lipids including LDL-P and Apo B are useful biomarkers to predict CVD risk, and therefore would see little reason why they would not agree that measuring LDL subfractions is a useful biomarker if the scientific literature demonstarted that large LDL particles are not a risk factor for CVD, which is clearly not the case.

Individuals who have familial hypercholesterolemia have elevated concentrations of predominantly large LDL particles, and it is well established that their elevated levels of LDL increase their risk of coronary heart disease. The work of Michael S. Brown and Joseph L. Goldstein who were awarded a Nobel Prize for their research on the metabolism of LDL cholesterol was primarily based around individuals with familial hypercholestemia.

In regards to your study on differences in CVD risk for saturated fat from dairy and red meat, as the authors mentioned, this could be largely explained due to the higher content of sodium and dietary heme in red meat which was not adjusted for in this study. In the higher quality Nurses’ Health Study which included a much larger number of participants and used higher quality dietary measurement methods, indeed replacing red meat with high fat dairy decreased the risk of coronary heart disease, but replacement with other foods low in saturated fat decreased risk to a much larger degree.

Charles Grashow said...

@ Healthy Longevity

I think I need to do more research as to the relationship between heme iron in red meat and heart disease

Possibly it's not the saturated fat that causes the problem

If prehistoric man bled a large amount from insect bites, wounds, etc. and that's why we evolved to store iron so efficiently perhaps that's the problem with red meat

This needs further exploring

Your thoughts

fitnesswayne.com said...

So what is a good source of B12 for those of us who follow paleo and don't eat cereal or milk?

The Humane Hominid said...

@Charles: If prehistoric man bled a large amount from insect bites, wounds, etc. and that's why we evolved to store iron so efficiently perhaps that's the problem with red meat

This needs further exploring

Your thoughts

What makes you think this is a specifically-human adaptation, as opposed to a vertebrate one?

Not all traits are adaptations. Most are just inheritances that get passed on as baggage or useful tools.

I'd be surprised if the basic mechanism of heme iron homeostasis weren't ancestral to nearly all animal life.

Charles Grashow said...

The Humane Hominid said...

I'd be surprised if the basic mechanism of heme iron homeostasis weren't ancestral to nearly all animal life.

My question remains - is the "problem" with red meat the saturated fat or the heme iron buildup or some combination of the two

Healthy Longevity said...


In regards to iron intake from animal sources, Don created a very informative post regarding this topic a year ago:

One of the problems is that humans cannot regulate heme iron and therefore it will be absorbed even if iron levels are already high causing iron overload. On the other hand, humans are able to regulate non-heme iron which helps to avoid this problem. Dr. Greger provided a number of references regarding this topic in his video found below:

Here is a new meta-analysis regarding heme iron, body iron stores and risk of type 2 diabetes:

Dietary iron intake, body iron stores, and the risk of type 2 diabetes: a systematic review and meta-analysis.
Conclusion: Higher heme iron intake and increased body iron stores were significantly associated with a greater risk of T2DM. Dietary total iron, non-heme iron, or supplemental iron intakes were not significantly associated with T2DM risk.

Evidence from controlled feeding experiments have established that heme iron from meat increases the production of NOCs (N-nitroso compounds) in the digestive tract to concentrations similar to that found in cigarette smoke, which in-turn promotes the formation of cancerous DNA adducts in the human digestive tract.

This data suggests that humans have not evolved to efficiently digest heme iron to the extent that it will not increase the risk of developing fatal diseases after the end of the reproduction cycle at which evolutionary pressure/selection pressure would do little to prevent.

In regards to saturated fat:

Saturated fat and heart disease
First, the notion that there exists such a thing as “the effect of saturated fat” is flawed. A lower intake of saturated fat implies an increased intake of some other source of calories to maintain caloric balance. Different substitutions for saturated fat have different effects on risk of coronary heart disease (CHD) and need to be discussed separately.

Evidence strongly suggests that it is a combination of nutrients, such as but not limited to heme, saturated fat, ruminant trans-fat, dietary cholesterol, and methionine and the lack of dietary fiber, phytochemicals and antioxidants that increases the risk of chronic disease when meat is chosen in favour of whole-plant foods.

Charles Grashow said...


Atherosclerosis. 2012 Aug 24. pii: S0021-9150(12)00522-9. doi: 10.1016/j.atherosclerosis.2012.08.002. [Epub ahead of print]

Statins use and coronary artery plaque composition: Results from the International Multicenter CONFIRM Registry.

Nakazato R, Gransar H, Berman DS, Cheng VY, Lin FY, Achenbach S, Al-Mallah M, Budoff MJ, Cademartiri F, Callister TQ, Chang HJ, Cury RC, Chinnaiyan K, Chow BJ, Delago A, Hadamitzky M, Hausleiter J, Kaufmann P, Maffei E, Raff G, Shaw LJ, Villines TC, Dunning A, Feuchtner G, Kim YJ, Leipsic J, Min JK.


Cedars-Sinai Heart Institute and Department of Imaging, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: Ryo.Nakazato@cshs.org.



The effect of statins on coronary artery plaque features beyond stenosis severity is not known. Coronary CT angiography (CCTA) is a novel non-invasive method that permits direct visualization of coronary atherosclerotic features, including plaque composition. We evaluated the association of statin use to coronary plaque composition type in patients without known coronary artery disease (CAD) undergoing CCTA.


From consecutive individuals, we identified 6673 individuals (2413 on statin therapy and 4260 not on statin therapy) with no known CAD and available statin use status. We studied the relationship between statin use and the presence and extent of specific plaque composition types, which was graded as non-calcified (NCP), mixed (MP), or calcified (CP) plaque.


The mean age was 59 ± 11 (55% male). Compared to the individuals not taking statins, those taking statins had higher prevalence of risk factors and obstructive CAD. In multivariable analyses, statin use was associated with increased the presence of MP [odds ratio (OR) 1.46, 95% confidence interval (CI) 1.27-1.68), p < 0.001] and CP (OR 1.54, 95% CI 1.36-1.74, p < 0.001), but not NCP (OR 1.11, 95% CI 0.96-1.29, p = 0.1). Further, in multivariable analyses, statin use was associated with increasing numbers of coronary segments possessing MP (OR 1.52, 95% CI 1.34-1.73, p < 0.001) and CP (OR 1.52, 95% CI 1.36-1.70, p < 0.001), but not coronary segments with NCP (OR 1.09, 95% CI 0.94-1.25, p = 0.2).


Statin use is associated with an increased prevalence and extent of coronary plaques possessing calcium. The longitudinal effect of statins on coronary plaque composition warrants further investigation.

Charles Grashow said...

@Healthy Longevity

So - saturated fat from plant sources (coconut, avocado, durian, etc.) is just as bad as saturated fat from meat?


Healthy Longevity said...

As I mentioned in my last comment, there are a lot of differences between whole plant foods, including those high in fat and meat other than saturated fat content. Avocadoes are not that high in SFA and also have a high MUFA/SFA ratio which may be important. It would be recommended to limit intake of plant foods high in SFA, especially in the form of refined oils which are low in health promoting nutrients found in primarily in whole plant foods such as fiber.

A recent cross-country analysis found that palm oil was associated with an increased risk of ischemic heart disease.

Peter said...
This comment has been removed by the author.
Peter said...


LOL! Having a good grasp of your intetions, don’t you think it’s perfectly natural that those who are in statin medication have the most plaque in their arteries? As cholesterol denialists and creationists would say: "correlation does not equal causation". Second, calcium-dense plaques are the most mild form of plaque, the lipid-dense plaque are the real nightmare. Statins have an ability to stabilize the plaque and change its composure from lipid-dense to more calcium-dense form.

What would be the biological mechanism which would cause HMG-CoA reductase inhibitors to produce more plaque in the artery? Now, don't spam to a next copypaste, but instead think about this question and give your elaborate answer. Given the amount of manipulation and confusion you constantly attempt to create, I think you you owe this one for us.

Peter said...


view this picture:


You can see that Rosuvastatin produced significant changes to the plaque composure. Altering its constitution from more lipid-dense to more fibrous as well slightly more calcified. Lipid-dense plaques are the most rupture prone. Calcified and fibrous plaques more stabil and safer. Moreover, pay attention that Rosuvastatin not only produced changes in the plaque form but significantly reduced its size as well.

Early intervention with rosuvastatin decreases the lipid components of the plaque in acute coronary syndrome: analysis using integrated backscatter IVUS (ELAN study).

I find it weird that the creationist -fringe online neglect these findings. The take-home message is that low LDL does a lot of good things for us.

Charles Grashow said...

Latest blood test results


Total Cholesterol - 242 mg/dL
LDL-C (Direct Measure) - 118 mg/dL
HDL-C - 76 mg/dL
Triglycerides - 41 mg/dL
Apoliprotein B - 104 mg/dL