Category Archives: Omega-3 and Omega-6 Fats - Page 2

Omega-3 Fats, Angiogenesis, and Cancer: Part I

In the book we discuss the issue of omega-3 toxicity (pp 56-58, 71-72), why it is most dangerous when omega-3 fats are combined with alcohol or fructose, and why fish oil capsules are particularly dangerous (see Fish, Not Fish Oil Capsules, June 16, 2010).

We recommend eating about 1 pound per week of omega-3 rich marine fish, like salmon, sardines, or herring, but taking no omega-3 supplements. This amount is sufficient to optimize the tissue omega-6 to omega-3 ratio for cardiovascular health, and is not so great as to raise great risks of toxicity. We also recommend avoiding mixing omega-3 fats with sugar or alcohol – a point I reiterated in last week’s post (How to Raise HDL, April 20, 2011):

Drink alcoholic beverages – but only when consuming meals low in polyunsaturated fats. Drink up when you eat beef, but be cautious when the entrée is salmon.

Some new papers have recently come out on the subject of omega-3 toxicity, and may lead some in the Paleo community, possibly including us, to reconsider our advice about omega-3 fats.

High Omega-3 Intakes in the Paleo Community

Our 1 pound fish per week recommendation works out to about 1.5 g omega-3 fats per day. But some Paleo authorities recommend much higher intakes.

Various emailers and commenters have mentioned Robb Wolf’s recommendations. Beth summarized Robb’s advice:

Robb Wolf promotes a short period of hefty omega 3 supplementation for unhealthy folks — on the order of 1g/10lbs of body weight per day.

Which would work out to 18 g/day for me, about 12-fold more than we recommend. Of course, if this is only for a short period, it may not be a big deal. However, I know from emails that some people take large doses continuously. Here’s one of my emailers:

Supplements are 10g of fishoil – 3.5g of epa/dha …

Bit surprised about [recommendation to reduce] the Fish oil, since i’m on the very low end of what other people are recommending, for fat loss as well, ie. robb wolf, poliquin etc.

The Whole9 folks host a Robb Wolf fish oil calculator which recommends that a 180-pound man take 4.5 g EPA+DHA per day. Depending on whether it is accompanied by other omega-3 fats in fish oil, this could be anywhere from 3 to 10 times our recommended intake, and is in line with what my emailer was taking.

Some Known Consequences of Omega-3 Excess

What are the likely consequences of omega-3 toxicity?

The obvious dangers are those related to oxidative stress from lipid peroxidation. The concern with omega-3 fats is not direct toxicity, but toxicity from their oxidation products. Omega-3 fats have a lot of fragile carbon double bonds which are easily oxidized: EPA has 5 double bonds and DHA 6. These are therefore among the most fragile lipids in the human body.

We would expect such problems to show up primarily in the liver and in the nervous system, where EPA and DHA levels are highest.

Indeed, they do. In mice, high dietary omega-3, in conjunction with alcohol or sugar, induces fatty liver disease. [1] In pregnant rats, excessive doses of omega-3 fats cause offspring to have shortened life span and neural degeneration. The authors concluded, “both over- and under-supplementation with omega-3 FA can harm offspring development.” [2]

However, there are associations of high omega-3 intake with disease in other tissues. In particular, emerging work is linking high omega-3 intake to diseases of pathological angiogenesis.

Angiogenesis is the creation of new blood vessels in mature tissue. (Vasculogenesis is the creation of vessels in a developing embryo.) It is a normal part of wound healing, but over a dozen diseases feature inappropriate angiogenesis.

Omega-3 Intake Is Usually Anti-Angiogenic

Before I go further, let me emphasize that nothing I am saying here repudiates the idea that it is desirable to bring tissue omega-6 and omega-3 fats into proper balance.

There are many studies showing that when tissue omega-6 to omega-3 ratios are too high, as on the standard American diet (SAD), additional omega-3 DHA and EPA can improve the omega-6 to omega-3 balance, reduce inflammatory signaling, and through reduced inflammation exercise an anti-angiogenic effect.

The mechanisms linking the anti-angiogenic effects of omega-3 to a condition of omega-6 excess are fairly well understood. Here is one description of the mechanism:

Here, we demonstrate that omega-6 PUFAs stimulate and omega-3 PUFAs inhibit major proangiogenic processes in human endothelial cells, including the induction of angiopoietin-2 (Ang2) and matrix metalloprotease-9, endothelial invasion, and tube formation, that are usually activated by the major omega-6 PUFA arachidonic acid. The cyclooxygenase (COX)-mediated conversion of PUFAs to prostanoid derivatives participated in modulation of the expression of Ang2. Thus, the omega-6 PUFA-derived prostaglandin E2 augmented, whereas the omega-3 PUFA-derived prostaglandin E3 suppressed the induction of Ang2 by growth factors. Our findings are consistent with the suggestion that PUFAs undergo biotransformation by COX-2 to lipid mediators that modulate tumor angiogenesis, which provides new insight into the beneficial effects of omega-3 PUFAs. [3]

So the question at issue is not whether omega-6 and omega-3 balance needs to be achieved. Rather, two points are at issue:

(a)  At what level of polyunsaturated (and omega-3) fat intake should balance be achieved – high or low?

(b)  Does overshooting toward an omega-3 excess generate significant or insignificant dangers?

If omega-3 toxicity is significant, then it will be important to achieve balance at low intakes of both omega-6 and omega-3, and to be careful to avoid overshooting to an omega-3 excess.

New Paper: DHA Linked to Cancer Progression

A new paper, just published yesterday, from “the largest study ever to examine the association of dietary fats and prostate cancer risk” has linked blood DHA levels to cancer risk. Specifically:

Docosahexaenoic acid was positively associated with high-grade disease (quartile 4 vs. 1: odds ratio (OR) = 2.50, 95% confidence interval (CI): 1.34, 4.65) … [4]

This is a large effect: the highest quartile had 2.5-fold higher risk than the lowest-quartile.

That it was the omega-3 DHA specifically, and not polyunsaturated fats generally, that caused the problem, is supported by the fact that (note: edited to correct error in original post – PJ) omega-6 linoleic acid had no effect, and 18:1 and 18:2 trans-fats which are mostly obtained from partially hydrogenated vegetable oils were associated with protection against cancer:

TFA 18:1 and TFA 18:2 were linearly and inversely associated with risk of high-grade prostate cancer (quartile 4 vs. 1: TFA 18:1, OR = 0.55, 95% CI: 0.30, 0.98; TFA 18:2, OR = 0.48, 95% CI: 0.27, 0.84). [4]

People in the top trans-fat quartile had only half the risk of people in the lowest omega-6 quartile. This makes it looks like omega-6-derived trans-fats were protective.

This result conflicts with the idea that the only influence of omega-3 fats is through regulation of inflammation; if so the anti-inflammatory omega-3 would have suppressed cancer. As lead study author Theodore Brasky said in the press release:

“We were stunned to see these results and we spent a lot of time making sure the analyses were correct,” said Brasky, a postdoctoral research fellow in the Hutchinson Center’s Cancer Prevention Program. “Our findings turn what we know — or rather what we think we know — about diet, inflammation and the development of prostate cancer on its head and shine a light on the complexity of studying the association between nutrition and the risk of various chronic diseases.”

Angiogenesis A Possible Pathway

Angiogenesis is very important for cancer progression. Cancers need to form angiogenic vessels if the tumor is to be able to grow beyond about 0.5 mm (0.02 inch) in diameter.

Indeed, angiogenesis seems to be a controlling factor for cancer mortality risk. It is believed that 50% of adults over age 40, and 100% of adults over age 70, have microscopic cancers. However, most tumors never develop an ability to induce angiogenesis and thus the tumors never grow beyond 0.5 mm and cause no observable disease.

Dietary factors that promote angiogenesis favor cancer progression, and anti-angiogenic factors tend to prevent cancer progression. Diet seems to be crucial for cancer prevention. Here is a TED video by Dr. William Li discussing the link between angiogenesis, dietary influences upon angiogenesis, and cancer.


So far, we’ve set the stage. On Thursday I’ll discuss a mechanism by which excessive DHA intake may promote angiogenesis. If this mechanism is important, then excessive fish oil or DHA supplementation may act as a major cancer-promoting food.

UPDATE: The next post in this series: Omega-3s, Angiogenesis and Cancer: Part II


[1] Nanji AA et al. Dietary saturated fatty acids: a novel treatment for alcoholic liver disease. Gastroenterology. 1995 Aug;109(2):547-54.

[2] Church MW et al. Excess omega-3 fatty acid consumption by mothers during pregnancy and lactation caused shorter life span and abnormal ABRs in old adult offspring. Neurotoxicol Teratol. 2010 March – April;32(2):171-181.

[3] Szymczak M et al. Modulation of angiogenesis by omega-3 polyunsaturated fatty acids is mediated by cyclooxygenases. Blood. 2008 Apr 1;111(7):3514-21.

[4] Brasky TM et al. Serum Phospholipid Fatty Acids and Prostate Cancer Risk: Results From the Prostate Cancer Prevention Trial. Am. J. Epidemiol. April 24, 2011 DOI: 10.1093/aje/kwr027 (Will be at

Answer Day: What Causes High LDL on Low-Carb Paleo?

First, thank you to everyone who commented on the quiz. I enjoyed reading your thoughts.

Is High LDL Something to Worry About?

Perhaps this ought to be the first question. Jack Kronk says “I don’t believe that high LDL is necessarily a problem” and Poisonguy writes “Treat the symptoms, Larry, not the numbers.” Poisonguy’s comment assumes that the LDL number is not a symptom of trouble. Is it?

I think so. It helps to know a little about the biology of cholesterol and of blood vessels.

When cells in culture plates are separated from their neighbors and need to move, they make a lot of cholesterol and transport it to their membranes. When cells find good neighbors and settle down, they stop producing cholesterol.

The same thing happens in the body. Any time there is a wound or injury that needs to be healed, cholesterol production gets jacked up.

When people have widespread vascular injuries, cholesterol is produced in large quantities by cells lining blood vessels. Now, to repair injuries cells have to coordinate their functions. Endothelial cells are the coordinators of vascular repair: they direct other cell types, like smooth muscle cells and fibroblasts, in the healing of vascular injuries.

To heal vascular injuries, these cells not only need more cholesterol for movement; they also need to multiply. It turns out that LDL, which carries cholesterol, also causes vascular cells to reproduce (“mitogenesis”):

The best-characterized function of LDLs is to deliver cholesterol to cells. They may, however, have functions in addition to transporting cholesterol. For example, they seem to produce a mitogenic effect on endothelial cells, smooth muscle cells, and fibroblasts, and induce growth-factor production, chemotaxis, cell proliferation, and cytotoxicity (3). Moreover, an increase of LDL plasma concentration, which is observed during the development of atherosclerosis, can activate various mitogen-activated protein kinase (MAPK) pathways …

We also show … LDL-induced fibroblast spreading … [1]

If endothelial cells are the coordinators of vascular repair, and LDL particles their messengers to fibroblasts and smooth muscle cells, then ECs should be able to generate LDL particles locally. Guess what:  ECs make a lipase whose main effect is to decrease HDL levels but can also convert VLDL and IDL particles into LDL particles and remove fat from LDL particles to make them into small, dense LDL:

Endothelial lipase (EL) has recently been identified as a new member of the triglyceride lipase gene family. EL shares a relatively high degree of homology with lipoprotein lipase and hepatic lipase …

In vitro, EL has hydrolyzed phospholipids in chylomicrons, very low density lipoprotein (VLDL), intermediate density lipoprotein and LDL. [2]

Immune cells, of course, are essential for wound healing and they should be attracted to any site of vascular injury. It turns out that immune cells have LDL receptors and these receptors may help them congregate at sites of vascular injury. [3]

I don’t want to exaggerate the state of the literature here:  this is a surprisingly poorly investigated area. But I believe these things:

1.      Cholesterol and LDL particles are part of the vascular wound repair process.

2.      Very high LDL levels are a marker of widespread vascular injury.

Now this is not the “lipid hypothesis.” Compare the two views:

  • The lipid hypothesis:  LDL cholesterol causes vascular injury.
  • My view:  LDL cholesterol is the ambulance crew that arrives at the scene of the crime to help the victims. The lipid hypothesis is the view that ambulance drivers should be arrested for homicide because they are commonly found at murder scenes.

So, to Poisonguy, on my view high LDL numbers are a symptom of vascular injury and are a cause for concern.

Big-Picture View of the Cause of High LDL

So, on a micro-level, I think vascular damage causes high LDL. But what causes vascular damage?

Here I notice a striking difference in commenters’ perspectives and mine. I tend to take a big-picture, top-down view of biology. There are three basic causes of nearly all pathologies:

1.      Toxins, usually food toxins.

2.      Malnutrition.

3.      Pathogens.

The whole organization of our book is dictated by this view. It is organized in four Steps. Step One is about re-orienting people’s views of macronutrients away from high-grain, fat-phobic, vegetable-oil-rich diets toward diets rich in animal fats. The other steps are about removing the causes of disease:

1.      Step Two is “Eat Paleo, Not Toxic” – remove food toxins.

2.      Step Three is “Be Well Nourished” – eliminate malnutrition.

3.      Step Four is “Heal and Prevent Disease” – address pathogens by enhancing immunity and, where appropriate, taking advantage of antibiotic therapies.

So when someone offers a pathology, any pathology, my first question is: Which cause is behind this, and which step do they need to focus on?

In Larry’s case, he had been eating low-carb Paleo for years. So toxins were not a problem.

Pathogens might be a problem – after all, he’s 64, and everybody collects chronic infections which tend to grow increasingly severe with age – but Larry hadn’t reported any other symptoms. More to the point, low-carb Paleo diets typically enhance immunity, yet Larry had fine LDL numbers before adopting low-carb Paleo and then his LDL got worse. So it wouldn’t be infectious in origin unless his diet had suppressed immunity through malnutrition – in which case the first step would be to address the malnutrition.

Step Three, malnutrition, was the only logical answer. The conversion to Paleo removes a lot of foods from the diet and could easily have removed the primary sources of some micronutrients.

So I was immediately convinced, just from the time-course of the pathology, that the cause was malnutrition.

Micronutrient Deficiencies are Very Common

In the book (Step Three) we explain why nearly everyone is deficient in micronutrients. The problems are most severe for minerals:  water treatment removes minerals from water, and mineral depletion of soil by industrial agriculture leads to mineral deficiencies in farmed plants and grain-fed animals.

This is why our “essential supplements” include a multimineral supplement plus additional quantities of five minerals – magnesium, copper, chromium, iodine, and selenium. Vitamins get a lot of attention, but minerals are where the big health gains are.

Copper Deficiency and LDL

Some micronutrient deficiencies are known to cause elevated LDL.

Readers of our book know that copper causes vascular disease; blog readers may be more familiar with an excellent post by Stephan, “Copper and Cardiovascular Disease”, discussing evidence that copper deficiency causes cardiovascular disease. As I’ve just argued that cardiovascular disease causes high LDL, it shouldn’t be a surprise that copper deficiency also causes hypercholesterolemia:

Copper and iron are essential nutrients in human physiology as their importance is linked to their role as cofactors of many redox enzymes involved in a wide range of biological processes, as well as in oxygen and electron transport. Mild dietary deficiencies of both metals … may cause long-term deleterious effects in cardiovascular system and alterations in lipid metabolism (3)….

Several studies showed a clear correlation among copper deficiency and dyslipidemia. The main alterations concern higher plasma CL and triglyceride (TG) concentrations, increased VLDL-LDL to HDL lipoproteins ratio, and the shape alteration of HDL lipoproteins.  [4]

The essentiality of copper (Cu) in humans is demonstrated by various clinical features associated with deficiency, such as anaemia, hypercholesterolaemia and bone malformations. [5]

Over the last couple of decades, dietary copper deficiency has been shown to cause a variety of metabolic changes, including hypercholesterolemia, hypertriglyceridemia, hypertension, and glucose intolerance. [6]

Copper deficiency is, I believe, the single most likely cause of elevated LDL on low-carb Paleo diets. The solution is to eat beef liver or supplement.

So, was my advice to Larry to supplement copper?  Yes, but that was not my only advice.

Other Micronutrient Deficiencies and Elevated LDL

Another common micronutrient deficiency that causes elevated LDL cholesterol is choline deficiency that is NOT accompanied by methionine deficiency. That is discussed in my post “Choline Deficiency and Plant Oil Induced Diabetes”:

Choline deficiency (CD) by itself induces metabolic syndrome (indicated by insulin resistance and elevated serum triglycerides and cholesterol) and obesity.

A combined methionine and choline deficiency (MCD) actually causes weight loss and reduces serum triglycerides and cholesterol …

I quote both these effects because it illustrates the complexity of nutrition. A deficiency of a micronutrient can present with totally different symptoms depending on the status of other micronutrients.

Julianne had a really nice comment, unfortunately caught in the spam filter for a while, with a number of links. She mentions vitamin C deficiency and, with other commenters, noted the link between hypothyroidism and elevated LDL. As one cause of hypothyroidism is iodine or selenium deficiency, this is another pathway by which mineral deficiencies can elevate LDL.

UPDATE: Mike Gruber reduced his LDL by 200 mg/dl by supplementing iodine. Clearly iodine can have big effects!

Other commenters brought up fish oil. They may be interested to know that fish oil not only balances omega-6 to modulate inflammatory pathways, it also suppresses endothelial lipase and thus moderates the LDL-raising and HDL-lowering effect of vascular damage:

On the other hand, physical exercise and fish oil (a rich source of eicosapentaenoic acid and docosahexaenoic acid) suppress the activity of EL and this, in turn, enhances the plasma concentrations of HDL cholesterol. [7]

Whether this effect is always desirable is a topic for another day.

My December Advice to Larry

So what was my December advice to Larry?

It was simple. In adopting a low-carb Paleo diet, he had implemented Steps One and Two of our book. My advice was to implement Step Three (“Be well nourished”) by taking our recommended supplements. Eating egg yolks and beef liver for copper and choline is a good idea too.

Just to cover all bases, I advised to include most of our “therapeutic supplements” as well as all the “essential supplements.”

Since December, Larry has been taking all the recommended supplements and eating 5 ounces per week of beef liver. As I noted yesterday, Larry’s LDL decreased from 295 mg/dl to 213 mg/dl, HDL rose from 74 mg/dl to 92 mg/dl, and triglycerides fell from 102 to 76 mg/dl since he started Step Three. This is all consistent with a healthier vasculature and reduced production of endothelial lipase.


Some people think there is something wrong with a diet if supplements are recommended. They believe that a well-designed diet should provide sufficient nutrition from food alone, and that if supplements are advised then the diet must be flawed.

I think this is quite mistaken. The reality is that Paleolithic man was often mildly malnourished, and modern man – due to the absence of minerals from treated water and agriculturally produced food, and the reduced diversity and higher caloric density of our foods – is severely malnourished compared to Paleolithic man.

We recommend eating a micronutrient-rich diet, including nourishing foods like egg yolks, liver, bone broth soups, seaweed, fermented vegetables, and so forth. But I think it’s only prudent to acknowledge and compensate for the widespread nutrient depletion that is so prevalent today. Even when nutrient-rich food is regularly eaten, micronutrient deficiencies are still possible.

Eating Paleo-style is not enough to guarantee perfect health. Luckily, supplementation of the key nutrients that we need for health and that are often missing from foods will often get us the rest of the way.


[1] Dobreva I et al. LDLs induce fibroblast spreading independently of the LDL receptor via activation of the p38 MAPK pathway. J Lipid Res. 2003 Dec;44(12):2382-90.

[2] Paradis ME, Lamarche B. Endothelial lipase: its role in cardiovascular disease. Can J Cardiol. 2006 Feb;22 Suppl B:31B-34B.

[3] Giulian D et al. The role of mononuclear phagocytes in wound healing after traumatic injury to adult mammalian brain. J Neurosci. 1989 Dec;9(12):4416-29.

[4] Tosco A et al. Molecular bases of copper and iron deficiency-associated dyslipidemia: a microarray analysis of the rat intestinal transcriptome. Genes Nutr. 2010 Mar;5(1):1-8.

[5] Harvey LJ, McArdle HJ. Biomarkers of copper status: a brief update. Br J Nutr. 2008 Jun;99 Suppl 3:S10-3.

[6] Aliabadi H. A deleterious interaction between copper deficiency and sugar ingestion may be the missing link in heart disease. Med Hypotheses. 2008;70(6):1163-6.

[7] Das UN. Long-chain polyunsaturated fatty acids, endothelial lipase and atherosclerosis. Prostaglandins Leukot Essent Fatty Acids. 2005 Mar;72(3):173-9.

Why We Get Fat: Food Toxins

Erich asked about the link between omega-6 fats and obesity. It’s a good question and also a good way to introduce the first step of the Perfect Health Diet weight loss program:  removal of toxic foods from the diet.

Vegetable Oils With Fructose or Alcohol

These toxic foods are particularly dangerous in combination. We discuss this mix of toxins in the book (pp 56-59).

If you feed lab animals high doses of polyunsaturated fat (either omega-6 or omega-3 will do) along with high doses of either fructose or alcohol, then fatty liver disease develops along with metabolic syndrome. Metabolic syndrome is a major risk factor for obesity, and it’s not very difficult to induce obesity on these diets.

Both sugar and vegetable oils are individually risks for obesity:

  • Stephan did a nice post a few years back, “Vegetable Oil and Weight Gain,” discussing a couple of studies showing that both rats and humans get fatter the more polyunsaturated fat they eat.
  • Dr. Richard Johnson and colleagues did a review of the evidence for sugar (fructose) as a cause of obesity in the American Journal of Clinical Nutrition a few years ago. [1]

What the animal studies show us is that when fructose and vegetable oils are consumed together, they multiply each other’s obesity-inducing effects.

Here are a few pictures illustrating the correlation between polyunsaturated fat consumption, fructose consumption, and obesity.

Here is the Johnson et al chart showing historical fructose consumption in the UK and US [1]:

Here is Stephan’s chart showing historical polyunsaturated fat consumption in the US:

And here are obesity rates in the US:

Cereal Grains

It’s a common observation that the toxic grains, especially wheat, can produce a potbelly or “beer belly.” Rice doesn’t seem to do that.

There is epidemiological evidence for this effect. Here, for instance, is obesity prevalence by country from the World Health Organization Global Infobase:

Note the low obesity prevalence in the rice eating countries of China, India, Japan, Indonesia, and southeast Asia; and in sub-Saharan Africa, where a diversity of starch sources are eaten, including manioc/cassava, sorghum, millet, rice, maize, and wheat. The highest obesity prevalence is found in wheat-eating countries.

This correlation persists within countries. In the China Study, the correlation of wheat consumption with BMI was 56%, whereas the correlation of total calorie intake with BMI was only 13%. (Since total calorie intake is correlated with muscle mass, total calorie intake may be completely uncorrelated with fat mass. It’s not how much you eat, but how much wheat!)

Similar outcomes occur in mice. I can’t find any mouse studies comparing wheat to rice, but I did find one comparing wheat to rye [4]. Wheat was far more obesity-inducing than rye:

Body fat percentage was 20.2% in the wheat group, 13.7% in the rye group; fasting insulin was 126 pM in the wheat group, 90 pM in the rye group; and fasting cholesterol, triglycerides, and free fatty acids were higher in the wheat group.

In short:  wheat made mice fatter, more insulin resistant, and more dyslipidemic than rye.

Just for fun here’s a picture comparing fat tissue in the rye (left) versus wheat (right) fed mice:

I believe that rice would have done even better than rye, but I was unable to find a paper directly comparing rice vs wheat or rye.

Why We Get Fat

This brings me to a point of difference with Gary Taubes. Although glucose is toxic in high doses, the body has an extensive machinery for disposing of excess glucose. As we discussed in our last post, all tissues of the body participate in glucose disposal. Dietary glucose is not likely to do much damage unless the body’s glucose-disposal machinery has been damaged by other toxins first.

Obesity is caused not by carb calories per se, but by natural plant toxins. Plants, not carbs, make you fat!

It’s possible, by the way, that differing toxicities among grains could be responsible for epidemiological evidence favoring “whole grains” over “refined grains.” In America, products made with refined grains are usually 100% wheat; but products made with whole grains are often of mixed origin (“7 grain bread”). Since wheat is the most obesity-inducing grain, dilution of wheat content may be masking the toxicity of whole grains.


Certain toxic foods seem to be very effective at causing obesity:  vegetable oils, fructose, and wheat. Along with malnourishment (for instance, by choline deficiency) and infectious disease, food toxins are why we get fat.

The first step in any weight loss effort, therefore, ought to be removal of these toxic foods from the diet. Removing these toxins may not cure obesity; but without this step a cure is unlikely.


[1] Johnson RJ et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr. 2007 Oct;86(4):899-906.

[2] Andersson U et al. Metabolic effects of whole grain wheat and whole grain rye in the C57BL/6J mouse. Nutrition. 2010 Feb;26(2):230-9.

Are the Boston Red Sox Malnourished?

Last Thursday’s post was mainly concerned with Abby’s bone injury that refused to heal. I noted that four nutrients – vitamins C, D, and K2, and magnesium – were essential for bone health, and that deficiencies could have contributed both to Abby’s injury and her slow healing.

Today’s post is about another group of people who frequently break their bones and don’t heal well:  the Boston Red Sox.

Injury-Prone Sox

Those who follow baseball may know that a promising 2010 Red Sox season was sabotaged by a rash of broken bones:

  • Centerfielder Jacoby Ellsbury missed 144 games with hairline fractures in four ribs; they failed to heal properly and re-fractured months after the initial injury.
  • Second baseman Dustin Pedroia missed all but two games after breaking his foot June 25.
  • Catcher Victor Martinez missed a month with a broken thumb.
  • Backup catcher Jason Varitek played just five games after breaking his foot on July 2.

There were muscle and joint injuries too, but let’s stick to bones.

Is it possible the Red Sox players are suffering from micronutrient deficiencies?

The Red Sox Hire a Dietitian

A few years ago the Red Sox hired a professional dietitian to advise their players: Tara Mardigan of the Dana-Farber Cancer Institute.

Ms Mardigan is a lovely woman, a marathoner and former gymnast, with a charming personality that shines through in radio interviews. She obtained her position with the Red Sox after meeting Red Sox president Larry Lucchino at a charity breakfast.

But what is her diet advice, and which players are taking it? I found a hint about the latter question in an interview in the student newspaper at Tufts University’s Friedman School of Nutrition Science, where Ms Mardigan studied:

I stopped working full-time at Dana-Farber to accommodate working with the Red Sox, and luckily they have a great relationship with the team so I was able to reduce my hours.  I also work with the Red Sox’s minor league teams, the Lowell Spinners, Pawtucket Red Sox, and Portland Sea Dogs. This is where I really make changes.  I work with young guys who are interesting in learning about how nutrition can improve their performance.  They are hungry to get to the big leagues. It’s great to see them move up into the major league, and then become someone like Jacoby Ellsbury (Left Field/Center Field) who is now well-versed in nutrition.

Uh oh! Jacoby Ellsbury, who managed only 18 games in 2010, whose bones break on incidental contact and whose hairline fractures won’t heal in six months, is the dietitian’s prize pupil?

The Dietitian Advises Avoiding Supplements

The Friedman School interview didn’t tell us much about Ms. Mardigan’s dietary recommendations, other than that she opposes most nutritional supplements:

I try to get them to choose food before supplements, and only supplements when necessary. Athletes are vulnerable and think [supplements] are well made and well regulated, and they are shocked when they find out they are not.

Those who have read our book know that we have a chapter titled “Why Moderns are Malnourished” which explains why modern agriculturally-produced foods and treated water don’t provide enough micronutrients, and why supplements are needed to optimize health.

Among the micronutrients for which supplementation is most needed are vitamin K2 and magnesium – two crucial nutrients for bone health.

What Is Her Diet Advice?

To get an idea of what diet she might be recommending, I looked at the Dana-Farber nutrition team web site, and was surprised to see this graphic illustration of their “Optimal Diet plan for cancer survivors”:

Yikes! No fats, and no mention of healthy plant foods like starchy tubers. A quarter of the diet is toxic grains and the protein may be derived from toxic legumes. It looks like roughly 70% of calories come from carbs and 25% from protein.

Later in the page they suggest such omega-6-rich oils as soybean oil, canola oil, flaxseed oil, wheat germ oil, and walnuts – all eliminated on the Perfect Health Diet.

It seems Ms Mardigan has recommended a similar diet to the Red Sox. From the Dana-Farber site:

On staff with the club since January 2006, she attends most home games to meet with players and make sure grilled chicken, steamed vegetables, and other healthful options are available in the team dining room.

Vegetables and lean protein, just like the Dana Farber diet. Another clue from this interview:

“My diet is very restricted right now, but Tara has been wonderful at helping me figure out what I can eat, like certain thick-skinned fruits and soy products,” says Anne Forgit, a leukemia patient and recent bone marrow transplant recipient.

Soy products. As readers of our book know, this is a highly toxic food.

Ms Mardigan does have a personal home page. The only clues I found there to her diet advice reside on her “Resources” page, where she recommends Michael Pollan’s In Defense of Food and  Dr. Walter Willett’s Eat, Drink, and Be Healthy. Pollan is a journalism professor who has made a career attacking industrial agriculture, and has likened the Atkins diet to an eating disorder. He seems to avoid specific diet advice, but it looks like he favors grains and omega-6-rich plant fats over animal fats. Dr. Willett is mentioned in our book, where we object to his opposition to coconut oil and saturated fat. He is a promoter of polyunsaturated fat and whole grain consumption.

If this is what Ms Mardigan is recommending to the Red Sox, it’s no wonder their bones are breaking:

  • Grains are toxic to bones. Wheat, oats, and other grains induce rickets, a softening of the bones that leads to frequent fractures. (This is discussed extensively in our book, and has been known since Mellanby’s original experimental investigations into rickets in dogs [1].)
  • Omega-6 polyunsaturated fats reduce bone mineral density. [2]

The Missing Nutrients

So the Red Sox players are being recommended a diet that is highly toxic to bones. But what about the key bone nutrients?  Are they lacking in those as well?

The answer is almost certainly yes. The fat-soluble nutrients are critical to bone remodeling, and it seems the Red Sox diet is completely lacking in vitamin K2.  Plant sources of vitamin K1 aren’t sufficient for bones, and animal sources of K2 seem to be excluded from the Red Sox diet.

Bone fracture rates are very strongly dependent on vitamin K2 levels. Most people are deficient, and supplementation with K2 reduces risk of vertebral fractures by 60%, hip fractures by 77%, and non-vertebral fractures by a remarkable 81%. [3]

If that happens on ordinary diets, the reduction in fracture rates would probably be even more remarkable on a K2-empty diet like the one that has been recommended to the Red Sox.


If a biomedical scientist were asked to contrive a diet that maximized the likelihood of bone fractures, the advice would be:

  1. Eat lots of grains to induce rickets.
  2. Eat vegetable oils and non-tropical fatty plants to reduce bone mineral density.
  3. Avoid animal and dairy fats to deprive the body of fat-soluble vitamins needed for bone mineralization, such as vitamin K2.
  4. Do not take nutritional supplements, in order to maintain a deficiency of bone nutrients.

It seems that this is precisely the advice that is being given to the Red Sox and their minor league players.

This year’s broken bones cost the Red Sox a chance at a World Series. The player who followed this diet advice most rigorously, Jacoby Ellsbury, lost a full season to bone fractures, and his injury history could cost him millions when he becomes a free agent next year.

As a lifelong Red Sox fan, I beseech the team to reconsider their diet advice.


[1] Mellanby E. (March 15 1919) An experimental investigation on rickets. The Lancet 193(4985):407-412. Reprinted in Nutrition. 1989 Mar-Apr; 5(2): 81-6; discussion 87.

[2] Watkins BA et al. Dietary ratio of n-6/n-3 PUFAs and docosahexaenoic acid: actions on bone mineral and serum biomarkers in ovariectomized rats. J Nutr Biochem. 2006 Apr;17(4):282-9. Watkins BA et al. Dietary ratio of (n-6)/(n-3) polyunsaturated fatty acids alters the fatty acid composition of bone compartments and biomarkers of bone formation in rats. J Nutr. 2000 Sep;130(9):2274-84.

[3] Cockayne S et al. Vitamin K and the prevention of fractures: systematic review and meta-analysis of randomized controlled trials. Arch Intern Med. 2006 Jun 26;166(12):1256-61.