Category Archives: Cancer

The Case of the Killer Protein

Earlier this week a paper was released to much fanfare, claiming that diets with over 20% of energy as animal protein might be as life-threatening as smoking.

  • The Huffington Post said, “Atkins aficionados, Paleo enthusiasts, and Dukan devotees, you may want to reconsider what’s on your plate. While high-protein diets have been all the rage over the last few years for their waist-whittling goodness, a new study says they could be as bad for you as smoking.”
  • Scientific American said “People who eat a high-protein diet during middle age are more likely to die of cancer than those who eat less protein, a new study finds.”
  • NPR said, “Americans who ate a diet rich in animal protein during middle age were significantly more likely to die from cancer and other causes.” They added, “In an age when advocates of the Paleo Diet and other low-carb eating plans such as Atkins talk up the virtues of protein because of its satiating effects, expect plenty of people to be skeptical of the new findings.” A sound prognostication!

Ray, Alex, Navy87Guy, Kat, Sam, and others asked for my thoughts.

What the Researchers Did

The article appeared in Cell Metabolism, a high-impact journal which likes long complex papers reporting years of work. [1] A common strategy for getting into such journals is to piece together a great variety of work into one article, weaving a narrative theme to unite them. That’s what this article did, using the theme “high protein diets may shorten lifespan” to link several relatively disconnected projects.

The NHANES Findings

The work that generated most of the buzz was an analysis of data from the National Health and Nutrition Examination Survey (NHANES). They looked at a group of 6,381 NHANES respondents and found, “Respondents aged 50–65 reporting high protein intake had a 75% increase in overall mortality and a 4-fold increase in cancer death risk during the following 18 years. These associations were either abolished or attenuated if the proteins were plant derived.”

Here’s their Figure 1:

Longo et al Figure 1

Two oddities in this result raise red flags:

  • First, protein appears harmful at age 50, neutral at age 65, and beneficial at age 80. This reversal of effects is incompatible with most mechanisms by which protein could affect aging or disease risk. In animal studies, we see the opposite: protein restriction extends maximum lifespan, which means that at high ages, mortality is lower, but increases risk of early death, which means that in middle age mortality is higher.
  • Second, they report that the effect was specific to animal protein: “[W]hen the percent calories from animal protein was controlled for, the association between total protein and all-cause or cancer mortality was eliminated or significantly reduced, respectively, suggesting animal proteins are responsible for a significant portion of these relationships. When we controlled for the effect of plant-based protein, there was no change in the association between protein intake and mortality, indicating that high levels of animal proteins promote mortality.” Yet, plant and animal proteins are biologically similar.

These two oddities strongly suggest that the appearance of negative health outcomes from protein is due to confounding factors – behaviors or foods associated with animal protein consumption in middle age, rather than effects caused by the protein itself.

When we look at how the analysis was performed, we find more reasons to doubt that protein is at fault. All of this data was found using a model which adjusted for the following covariates:

Model 1 (baseline model): Adjusted for age, sex, race/ethnicity, education, waist circumference, smoking, chronic conditions (diabetes, cancer, myocardial infarction), trying to lose weight in the last year, diet changed in the last year, reported intake representative of typical diet, and total calories.

Adjustment for a host of health-related conditions – waist circumference, diabetes, cancer, myocardian infarction, and even total calories which is effectively a proxy for obesity – can radically distort results, and even transform effects from positive to negative. I’ve discussed this issue previously in The Case of the Killer Vitamins.

In practice, many factors are highly correlated. The variables being studied – protein intake, waist circumference, total calorie intake, and others – are beset by the problem of collinearity. Attempting multiple regression analysis on collinear variables can generate very peculiar results. The more the number of adjustment factors grows, the more strange things tend to happen to data.

If they wanted us to understand whether their results are trustworthy, authors would present raw data, and then a sensitivity analysis that shows how introducing each covariate individually affects the results, then showing how including combinations of two covariates affects the results, and so forth. This would help us judge how robust the results are to alternative methods of analysis.

Of course, authors do not do this. Instead, they ask us to trust the analysis they have chosen to present – which is only one of billions they could have done. (This study adjusted for 13 covariates. The NHANES survey may have gathered data on, say, 40 variables. There are 40 choose 13, or 12 billion, possible multivariate regression analyses that could be performed using 13 covariates on this data set. Each of the 12 billion analyses would generate different outcomes.)

Are the authors trustworthy? Unfortunately, most academics today are not. Career and funding pressures are severe, and by and large those who are good at gaming the funding and publishing processes have triumphed professionally over careful, diligent truth seekers. It is much easier to construct a narrative that will garner attention and publicity and interest, than to carefully exclude non-robust results and publish only those results that are solidly supported.

Frankly, I give little credence to their NHANES analysis. And, judging by comments in the press, other epidemiologists don’t seem to give it much credence either. From the NPR article:

But could eating meat and cheese really be as bad for you as smoking, as the university news release describing the new Cell Metabolism paper suggested?

Well, that may be an exaggeration, according to Dr. Frank Hu, a researcher at the Harvard School of Public Health who studies the links between health, diet and lifestyle.

“The harmful effects of smoking on cancer and mortality are well-established to be substantial, while the harmful effects of red meat consumption are modest in comparison,” Hu wrote to us in an email.

The Mouse Experiments

So let’s turn to the next part of the study, the mouse experiments:

Eighteen-week-old male C57BL/6 mice were fed continuously for 39 days with experimental, isocaloric diets designed to provide either a high (18%) or a low (4%–7%) amount of calories derived from protein …

The low protein diets are really starvation diets, in terms of protein intake. The reason the low protein diets were sometimes 4% and sometimes 7% was because mice will often lose weight on 4% protein diets due to starvation (in the paper’s experiments on BALB/c mice, “the mice had to be switched from a 4% to a 7% kcal from protein diet within the first week in order to prevent weight loss.”). Animal control officers do not allow experiments to continue if the mice are obviously starving.

[B]oth groups were implanted subcutaneously with 20,000 syngeneic murine melanoma cells (B16).

This is an unusually small number of cells. Typically, cancer researchers implant a million cells to create a syngeneic tumor. Presumably they used this small number of cells in order to ensure that some mice would not develop tumors during the 39 day experiment. As it happened, this was a lucky (canny?) choice of cell quantity: while 10 of 10 mice on the high-protein diet developed tumors during the experiment, only 9 of 10 mice on the low-protein diet did. If they had used more cells, all mice on both diets would have developed tumors; if they had used fewer cells, some mice on the high protein diet would have failed to develop tumors. Either way, the results would appear less damning for the high protein diet.

The outcomes:

Longo et al Figure 3
Due to the small number of cells injected, it takes at least two weeks before tumors are detectable in size (normally they would be visible in ten days). They seem to be similar in size at about two weeks after implantation.

However, when the tumors reach larger sizes, growth is impaired on the low protein diets. A mouse weighs 20 grams, and a 2000 mm3 tumor weighs 2 grams, or 10% of body weight – equivalent to a 15-pound tumor in humans. Growing a tumor of this size requires building a large amount of tissue — blood vessels, extracellular matrix, and more. The ability to construct new tissue is constrained on a protein-starved diet, so it’s not surprising that tumor growth is slower when the tumor is large and protein is severely restricted.

Animal protocols generally require that mice be sacrificed when tumors reach 2000 mm3. Extrapolating the tumor growth curves, it looks like the mice in experiment (B) would be sacrificed 5 weeks after implantation on the high protein diet, or 8 weeks after implantation on the low protein diet; in experiment (G), mice on the high protein diet would be sacrificed about 9 weeks after implantation, while mice on low protein diets would have been sacrificed about 11 weeks after implantation.

In other words, tumors still kill you, just a bit more slowly if you are starving yourself.

It’s important to note a couple of things. First, the word “starving” is appropriate. 4% to 7% protein intakes are starvation levels for mice. In a nice blog post closely relevant to this topic, Chris Masterjohn notes that a 5% protein intake completely stunts the growth of young rats:

Chris rhetorically asks: “How many of us would deliberately feed a two-year old a diet that would cause them to stop growing altogether?”

Second, as Chris also points out in the same post, such low protein intakes actually make cancer more likely in the context of exposure to mutagens. For instance, aflatoxin exposure leads to cancer (or pre-cancerous neoplasms) much more frequently in rats on low-protein diets than in rats on high-protein diets:

In this experiment, there were two diets, 5% protein and 20% protein, and two diet periods, one during exposure to aflatoxin and one afterward. Rats exposed to aflatoxin while on a 5% protein diet were far more likely to develop neoplasms than rats exposed to aflatoxin on a higher protein diet. That is, the “20-5” rats had far fewer cancers than the “5-5” rats, and the “20-20” rats had far fewer cancers than the “5-20” rats. High protein for the win!

However, once the rats had neoplasms, the tumors grew more slowly on the low-protein diet. Just as the new study found.

So, if your goal is to avoid getting cancer, it is better to eat adequate protein. If you already have cancer, or if researchers have injected you with highly metastatic melanoma cells, you can buy yourself slightly slower tumor growth by starving yourself of protein. In laboratory mice, this extends lifespan a few weeks because they are not allowed to die from cancer, but are sacrificed when tumors reach a specific size. In humans, however, cancer death commonly follows from cachexia, or wasting of lean tissue. A low protein diet might promote cachexia and accelerate cancer death in humans. It is not possible to infer from this study that there would be a clinical benefit to a low protein diet in human cancer patients.

Other Negative Effects of Low-Protein Diets

The study noted a significant negative effect of low protein diets in older mice. While young mice (18 weeks, equivalent to young adults) lost only a few percent of body weight on the starvation low protein diets, elderly mice (2 years old) wasted away on low protein diets. The data:

Longo et al Figure 4

Both young and old mice managed to gain a bit of weight on the high protein diets, and both young and old mice lost weight on the low protein diets. The weight loss was much more severe in elderly than young mice.

Considering that wasting away commonly precedes death in the elderly, this is not a good sign for the low protein diets. The authors themselves argue that this is consistent with the NHANES finding that high protein diets become beneficial after age 65: “old but not young mice on a low protein diet lost 10% of their weight by day 15, in agreement with the effect of aging on turning the beneficial effects of protein restriction on mortality into negative effects.”

However, while I think it is clear that the dramatic weight loss in the elderly mice fed low protein is harmful, it is far from clear that the slight weight loss of the younger mice was harmless. Though they maintained their weight better than elderly mice, they may have been starving as well. To actually support the NHANES survey, the researchers should have maintained the mice on low or high protein diets for several years, and seen which group lived longer. They did not do this.

If they had, I speculate that the high protein mice would have lived longer.


This is a study in the line of T. Colin Campbell and other vegetarians who have tried to show that animal protein promotes cancer and mortality. These studies are unconvincing. They simply do not prove the conclusions they purport to draw.

The Perfect Health Diet takes a middle ground in regard to protein: We recommend eating about 15% protein, and argue that both high protein and low protein diets are likely to be harmful; high protein diets by accelerating aging or by making protein available to gut bacteria for fermentation, producing a less beneficial gut flora and generating nitrogenous toxins; low protein diets by starving the body of a key nutrient needed to maintain bodily functions, especially liver, kidney, and immune function.

Nothing in this study persuades me that those recommendations need revision.


[1] Levine ME et al. Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population. Cell Metabolism 19, 407–417, March 4, 2014.

Circus, Swim, and Nails: Three Cancer Stories

Last weekend we want to see Cavalia Odysséo, a circus of horses, acrobats, and aerialists. It is a magnificent show.

Our trip to the circus began, in a way, many months ago. In March 2012, I got an email that began, “My mother has terminal cancer.”

PHD and Laurette Charron’s Cancer

The email was from Michel Charron, an aerialist with Cavalia Odysséo. Here is what he wrote:

I rushed home from Miami … to New Brunswick, Canada, to see what I could do for Mom.  The doctors say there is nothing they can do for her now….  The doctors have already decided that she is dead, and that there is nothing to be done but to keep her as comfortable as possible to the end.

She has cancer of the liver and of the colon.  They have found lesions on her lungs, which they believe are also cancerous….

When I arrived ten days ago, my mother was totally unrecognizable.  She was taking six pain pills a day, had no tone in her facial expressions, could not pronounce the letter ‘s’ properly, had severely restricted mobility, as well as difficulty concentrating and following regular conversation….

We are all alone here and would greatly appreciate some friendly advice.

I gave my cancer suggestions. The gist of my dietary advice for cancer can be found in these two posts: An Anti-Cancer Diet, September 28, 2011, and Toward an Anti-Cancer Diet, September 15, 2011. Extracellular matrix is very important, so soups and stews with connective tissue are important. Good, balanced nutrition is crucial; many nutrient deficiencies, excesses, and imbalances promote cancer. Lifestyle is very important too: circadian rhythm entrainment may be the single most important factor determining cancer prognosis.

I didn’t hear from Michel for seventeen months. Last Friday, Michel sent another email:

I contacted you last year regarding my mother, Laurette, who was diagnosed with generalized cancer and given very little time to live.  You proved a light in very, very dark times.  My mother not only lived nine months longer than predicted, but the quality of her life improved dramatically.  Thank you for that.

Cancer is a terrible disease, and had Laurette’s cancer been caught earlier there would have been hope of recovery, but Michel was grateful for the extra time he had with his mom. She got off most of her prescription medications, dropping from 22 drugs to 5, and became physically and mentally able to enjoy what remained of her life. Michel and Laurette were able to spend time together, share their love for each other, and say farewell.

It happens that Cavalia Odysséo is playing in Boston right now, and Michel invited us to the show. If you ever have a chance, it is well worth a trip. The horses – there are 63 horses in the show – are a pleasure to watch; the scenery is magnificent; and the performers superb. This trailer will give you an idea of the show:

Here is the circus tent:

cavalia 01

Michel invited us back stage after the show. Here we are with some of the performers – Michel is holding our book:

cavalia 03

With Michel and his wife and co-performer Tomoko:

cavalia 03b

Some of the horses, exhausted by the show, turn their backs to visitors:

cavalia 02

And here I am getting a lesson in aerialism from Michel:

cavalia 04

Thank you, Michel! It was a magical night.

The Big Swim

If you’ve read the jacket of our book, you’ll know that Court Wing, head trainer at CrossFit NYC, says in his blurb, “One of my best friends was on the diet while undergoing chemo and his bloodwork numbers were so good that they would have been considered average … for a person without cancer.”

I haven’t yet told the story of Court’s friend, D. Kirk MacLeod. Kirk discovered he had cancer when his colon ruptured in August 2010. He’s had multiple surgeries and chemotherapies since.

Kirk has now done something remarkable. On August 4, he swam the Northumberland Strait between New Brunswick and Prince Edward Island – an 11 mile swim. He wrote beforehand:

I really do feel like I am accomplishing the impossible… I have gone from less than 160 pounds, weak and worn from chemotherapy before Christmas (less than I weighed in high school!) and two major surgeries in February and March…to 185 pounds, fit, strong and ready to swim over 14 kilometres on Sunday, August 4th!!! I started slowly training at the beginning of June!

In July I started training “hard” under the guidance of Court Wing (my Crossfit coach from Crossfit NYC) and Max Wunderle (my swim coach of TriMax Fitness). I also had invaluable eating advice from Paul Jaminet (The Perfect Health Diet). Their help and direction has been phenomenal – I couldn’t have done it without them!

After the swim, Kirk wrote:

It was brilliant… It was hard as hell…and it was an accomplishment I never imagined….

I finished in 6 hours and 25 minutes. We figure I swam about 17 km … maybe more.

I was only cleared to train at the end of May and started training in June…I began at zero. I couldn’t even do basic exercises with weights. I wasn’t a swimmer. I had never trained in swimming.

It’s an incredible story and an incredible accomplishment. Here’s Kirk:

cavalia 05

Kirk did his “Big Swim” to benefit the Brigadoon Children’s Camp Society, a charity for chronically ill kids. If you’d like to reward his hard work, donate here through Canada Helps.

Cancer and Nailbiting

Reports from other cancer patients suggest that cancer therapies are much less toxic when patients are eating PHD. Here, for example, is Bill Rafter:

About 6 months ago I learned that I had metastatic prostate cancer. The treatment recommended was hormone therapy and targeted radiation…. The effects are a total suppression of sexual drive, hot flashes similar to those experienced by menopausal women, and the feeling that one is an old, old man…. I found the last one particularly brutal, and questioned whether I wanted treatment at all.

A friend gave me a good book on cancer, recommending an all-out approach rather than the sequential attempts favored by most oncologists. Nutrition was a major part of the approach. I then trolled my friends for books on nutrition and one commented that PHD was the best he had ever read. I am overwhelmed by what it has done for me.

After reading PHD, I immediately adopted the recommendations in full, with the exception of fasting. I then went thru 44 radiation treatments, and never felt fatigue, a common symptom. No more old man feelings, and no thoughts of quitting treatment. Hot flashes are completely gone, which really puzzles the oncologists. Everyone wants to know what stopped the hot flashes.

Of course breezing through therapy is not the same as recovering, but it is a good start. If therapies have fewer side effects, higher doses can be utilized, and treatments might be more effective.

Bill continued:

But that’s not all. Ever since grade school I have been a nailbiter. I knew the habit was caused by a chemical imbalance, rather than behavioral, but could never figure out what. But since adopting PHD, my fingernails have grown to the extent that filing them is annoying. That makes me wonder that if PHD brought my system into balance, how many other imbalanced people could also benefit.

I think a lot of people can benefit from PHD. Similar to Bill’s case, it’s rare for only one health condition to improve when diet and lifestyle are improved. Usually all or nearly all health problems improve. This suggests that poor diet and lifestyle are contributors to many diseases.

Invitation to Perfect Health Retreats

A few recent events have increased my interest in how PHD, or ancestral diet and lifestyle generally, affect cancer:

  • Shou-Ching and I have recently been asked to assist in developing the dietary and lifestyle advice for a cancer clinical trial.
  • Our Perfect Health Retreats provide a fairly controlled environment where we might be able to see and measure the effect of PHD on cancer patients. Michel told us that when he put his mother on PHD, he saw notable improvements after two weeks. So a thirty day program may be long enough to generate observable results.
  • The launch of the Journal of Evolution and Health gives a scholarly forum for communicating observations and exploring hypotheses.

As readers know, my mother died of cancer, so this is of special interest to me. I suspect that diet and lifestyle have a much bigger impact on cancer than most realize. There is shockingly little research underway into this aspect of cancer management.

To gain more insight into how diet and lifestyle may affect cancer outcomes, I’d like to invite cancer patients to come to our Perfect Health Retreats. Perfect Health Retreats are not a medical program, there is no medical treatment or advice available – just great food, an environment designed for optimal healthfulness, and an educational program teaching how to live for optimal health. So the program will not be suitable for severely ill patients.

If you’re interested in participating, please contact me at 617-576-1753 or, or Whitney Ross Gray at 910-763-8530 or

Omega-3 Fats and Cancer

On Wednesday a new paper reported that higher levels of long-chain omega-3 fats (EPA, DPA, and DHA) in blood are associated with a 43% increased risk of prostate cancer and a 71% increased risk of aggressive prostate cancer. [1] This built on earlier work by the same group. [2] In a press release, the authors stated:

“We’ve shown once again that use of nutritional supplements may be harmful,” said Alan Kristal, Dr.P.H., the paper’s senior author …

“[W]e have confirmed that marine omega-3 fatty acids play a role in prostate cancer occurrence,” said corresponding author Theodore Brasky, Ph.D.

They sound confident! Is there anything to it, and should it affect our dietary advice?

Mechanisms Linking Omega-3 Fats to Cancer

In our book and on this blog, we’ve already discussed two mechanisms linking excessive omega-3 intake to cancer risk.

First, there is the issue of lipid peroxidation. Of all fatty acids, long-chain omega-3 fats are the most readily peroxidized:

PUFA relative peroxidizability

Peroxidation of PUFA generates highly toxic compounds, such as aldehydes, which mutate DNA and turn proteins into advanced lipoxidation end products (ALEs). [3, 4] These lipid peroxidation products have been implicated as causal factors in cancer. [5]

Second, oxidation products of DHA promote angiogenesis – the creation of new blood vessels to feed tumors. These products make cancers grow rapidly. I’ve blogged about this (DHA and Angiogenesis: The Bottom Line, May 4, 2011; Omega-3s, Angiogenesis and Cancer: Part II, April 29, 2011; Omega-3 Fats, Angiogenesis, and Cancer: Part I, April 26, 2011).

So there are known mechanisms by which the long omega-3s in fish oil may promote cancer.

The Brasky et al Papers

The new study by Brasky et al measured omega-3 fat levels in plasma phospholipids. Thus, it doesn’t measure any omega-3s in cells, only omega-3s in serum particles like LDL, HDL, and VLDL; and even in those particles it excludes omega-3 fats found in triglycerides.

This is a very different biomarker than the Omega-3 Index of William Harris, which looks at the omega-3 phospholipids in red blood cell membranes. [6] This biomarker might behave quite differently than the Omega-3 Index.

The study measured plasma phospholipid omega-3s in a group of people, then followed them for 6 years or so to see who developed cancer. Here are the group averages [1]:

Brasky 2013 Table 2

Statistically the most reliable data is in the no cancer vs total cancer comparison. There we find that subjects who went on to develop prostate cancer averaged 3% more DHA and 4% more EPA+DPA+DHA in plasma phospholipids than those who didn’t develop cancer.

Does This Variation Reflect Dietary Intake?

Chris Kresser kindly sent a link to an analysis of the study published at LecturePad by William Harris: “Omega-3 Fatty Acids and Risk for Prostate Cancer.” Harris tells us how to translate the plasma numbers to the corresponding Omega-3 Index numbers:

Based on experiments in our lab, the lowest quartile would correspond to an HS-Omega-3 Index of <3.16% and the highest to an Index of >4.77%).

Even the top quartile of the Brasky et al subjects had quite low omega-3 levels:

In Framingham, the mean Omega-3 Index of participants who were not taking fish oil supplements was 5.2% and for those taking supplements, it was 7.5% [7]. Both of these numbers are considerably higher than the values reported by Braskey et al., even in their highest quartile.

The trial asked its participants not to take supplements, and it looks like they drew a study population whose fish intake was much lower than that of Framingham, Massachusetts, residents.

If dietary omega-3 intake was low in all subjects and varied only slightly among participants, how do we know that this biomarker is related in any way to dietary intake? There could be other factors – genetics, oxidative environment, omega-6 fat intake, antioxidant intake, changes in the proportions of VLDL, LDL, and HDL, to name a few – that affect this biomarker.

Does High Dietary Intake Lead to More Cancer?

If high dietary intake of omega-3s caused more cancer, we would expect cultures that consume lots of fish oil to have higher prostate cancer rates. But epidemiological studies have found that high omega-3 intakes seem to be associated with low cancer rates. For instance, the Japanese eat eight times more omega-3 fatty acids than Americans and their blood levels are twice as high, yet the prostate cancer rates are only one-sixth the American rate.

Of course, there are many confounders in epidemiological studies. Harris helpfully provides a summary of clinical trials in which fish oil was provided as part of the study and cancer outcomes measured:

Harris reply to Brasky 2013

Although none of these studies produced a statistically significant link between omega-3 intake and cancer, incidence of cancer diagnosis or death was increased in every one of the clinical trials except the GISSI-Heart Failure study and perhaps the Origin study. A meta-analysis might find a small cancer promoting effect of omega-3s.

UPDATE: Vladimir Heiskanen points me to an interesting paper in which the effect of dietary fatty acids on cancer metastasis was examined. Colon carcinoma cells were injected into the portal vein (which leads from intestine to liver) of rats and 3 weeks later rats were sacrificed and their livers were examined for metastases. The rats were on three diets — low-fat, high omega-6 (safflower oil), high omega-3 (fish oil). The results:

At 3 weeks after tumor transplantation, the fish oil diet and the safflower oil diet had induced, respectively, 10- and 4-fold more metastases (number) and over 1000- and 500-fold more metastases (size) than were found in the livers of rats on the low-fat diet. [7]

I wish they’d used a saturated fat or monounsaturated fat diet, rather than a low-fat diet, as the control, as this would have clarified that polyunsaturates specifically promote metastasis; in the study the rats’ food was mixed with fish oil or safflower oil, greatly increasing the fat fraction and decreasing the carbohydrate, protein, and micronutrient fractions, so the control diet deviates in many respects from the high-PUFA diets. However, the results are consistent with the idea that fish oil is more cancer-promoting than the less peroxidizable safflower oil, perhaps because of the unique pro-angiogenic effects of DHA products.


There might be biological contexts in which omega-3 fats promote cancer.

This doesn’t mean we should refrain from eating omega-3 fats. Cardiovascular disease causes more deaths than cancer, and omega-3 fats are protective against CVD.

However, I think these studies support the PHD advice:

  • Eat enough oily marine fish to achieve omega-6 and omega-3 balance;
  • Minimize omega-6 intake so that omega-6 and omega-3 balance is achieved at the lowest possible intake of polyunsaturated fats.

All nutrients can be eaten in excess, and omega-3 fats surely fall into this category. The right amount of oily fish is probably about one to two meals per week.


[1] Brasky TM et al. Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial. J Natl Cancer Inst. 2013 Jul 10. [Epub ahead of print]

[2] Brasky TM et al. Serum phospholipid fatty acids and prostate cancer risk: results from the prostate cancer prevention trial. Am J Epidemiol. 2011 Jun 15;173(12):1429-39.

[3] Hulbert AJ et al. Life and death: metabolic rate, membrane composition, and life span of animals. Physiological Reviews 2007 Oct;87(4):1175–213,

[4] Hulbert AJ. Metabolism and longevity: is there a role for membrane fatty acids? Integretive and Comparative Biology 2010 Nov;50(5):808–17,

[5] Nair U, Bartsch H, Nair J. Lipid peroxidation-induced DNA damage in cancer-prone inflammatory diseases: a review of published adduct types and levels in humans. Free Radic Biol Med. 2007 Oct 15;43(8):1109-20.

[6] Harris WS, Von Schacky C. The Omega-3 Index: a new risk factor for death from coronary heart disease? Prev Med. 2004 Jul;39(1):212-20.

[7] Griffini P et al. Dietary omega-3 polyunsaturated fatty acids promote colon carcinoma metastasis in rat liver. Cancer Res. 1998 Aug 1;58(15):3312-9.

Pork: Did Leviticus 11:7 Have It Right?

If we were to rank popular meats by their healthfulness, the order would be (1) fish and shellfish, (2) ruminants (beef, lamb, goat), and (3) birds (duck, chicken, turkey). In last place would be pork.

Given the iconic place of bacon in the Paleo movement, it’s worth exploring the evidence against pork.  George Henderson has given us a great place to start:  “Nanji and Bridges identified possible problems with pork plus moderate alcohol in 1985 and other researchers have confirmed the pattern since.”

Pork Consumption and Liver Cirrhosis

Pork consumption has a strong epidemiological association with cirrhosis of the liver. Startlingly, pork may be even more strongly associated with alcoholic cirrhosis than alcohol itself!

The evidence was summarized by Francis Bridges in a recent (2009) paper [1], building on earlier work by Nanji and French [2]. A relation between pork consumption and cirrhosis of the liver is apparent across countries and has been consistently maintained for at least 40 years.

Here is the correlation between pork consumption and mortality from liver cirrhosis in 2003 [1]:

The correlation coefficient of 0.83 is extremely high – rarely seen in epidemiology. Correlation coefficients range from -1.0 to 1.0, and a coefficient of 1.0 would indicate that cirrhosis mortality was strictly proportional to pork consumption. The very low p-value confirms the statistical association.

Here is the relation between alcohol consumption and mortality from liver cirrhosis:

The correlation coefficient is lower than for pork consumption.

In epidemiological studies, beef, lamb, and pork are often grouped together as “red meat.” However, this may conceal differences between pork and the ruminant meats. Bridges found that beef actually appeared protective against cirrhosis:

In the present study using 2003 data, a significant negative association between dietary beef and rates of cirrhosis mortality was found…. [D]ietary beef may be a protective factor regarding the pathogenesis of alcoholic cirrhosis. [1]

This would be consistent with considerable evidence, discussed in our book (pp 57-58), showing that saturated fat is protective against liver disease, while polyunsaturated fat causes it. Epidemiological data confirms that saturated fat is protective; here is Bridges again [1]:

[A]nalysis of data from 17 countries indicated that diets high in cholesterol and saturated fat protected (i.e., inversely correlated) against alcoholic cirrhosis while polyunsaturated fats promoted (positively correlated) cirrhosis [8].

Beef is high in saturated fat, low in polyunsaturated fat. Pork is relatively high in polyunsaturated fat.

If the fat composition is playing a role, perhaps it is not that surprising that pork is more strongly related to cirrhosis than alcohol.

Either fructose or alcohol can react with polyunsaturated fat to produce liver disease. Sugar consumption, for example in soft drinks, may be just as likely to combine with pork to cause a cirrhotic liver as alcohol. But no other common dietary component can substitute for the role of polyunsaturated fat in causing liver disease.

Here Nanji and French summarize the correlation of pork with liver disease even in the absence of alcohol:

In countries with low alcohol consumption, no correlation was obtained between alcohol consumption and cirrhosis. However, a significant correlation was obtained between cirrhosis and pork. A similar relationship was seen in the ten Canadian provinces, where there was no correlation between cirrhosis mortality and alcohol consumption, but a significant correlation was obtained with pork. [2]

But fat composition is hardly likely to be the sole issue with pork. Most polyunsaturated fats in modern diets are derived from vegetable oils, not pork. It seems that there must be something else in pork besides polyunsaturated fat that is causing liver disease.

Pork and Liver Cancer

We would expect that if pork can cause liver cirrhosis it will also promote liver cancer, since injured and inflamed tissues are more likely to become cancerous.

Indeed, there is an association between pork consumption and the primary liver cancer, hepatocellular carcinoma. Nanji and French [3] write:

The authors investigated the possibility that dietary fat, meat, beef, and pork consumption might be factors that would, in addition to alcohol, correlate with mortality from hepatocellular carcinoma (HCC) in different countries….

The correlation between HCC and alcohol was 0.40 (p < 0.05); that with pork consumption was also 0.40 (p < 0.05). There was no correlation with total fat meat, beef, and cigarette and tobacco consumption.

Here is the raw data by country:

Another way of looking at the data is based on countries with low and high incidence of HCC. Countries with high incidence of HCC eat more pork and drink more alcohol, but actually eat less animal fat:

Pork and Multiple Sclerosis

Nanji and Norad [4] looked for other diseases that correlate with pork consumption, and hit upon multiple sclerosis. The connection is remarkable:

A significant correlation was obtained between prevalence of multiple sclerosis and … pork consumption (r = 0.87, p less than 0.001). There was no significant correlation with beef consumption. [4]

As noted earlier, a correlation coefficient of 0.87 is extremely high, and a p-value below 0.001 also shows a very strong relationship. MS is much more likely to befall pork eaters. Such a strong correlation makes it look like pork, or something found in pork, is the cause of MS.

Nanji and Norad further note that beef, the “other red meat,” is not associated with MS:

The correlation between pork consumption and MS prevalence was highly significant. Also, of major significance was the absence of a significant correlation between MS prevalence and beef consumption. This is consistent with the observations that MS is rare in countries where pork is forbidden by religious customs (e.g. Middle East) and has a low prevalence in countries where beef consumption far exceeds pork consumption (e.g. Brazil, Australia). [4]

The correlation between pork and MS may be seen here:

Lauer [5] verified the pork-MS link, but found it to be characteristic of processed pork:

When … quantitative data are taken into account, and a combined factor “smoked meat” or “smoked pork” is formed, the association is very high throughout. This factor is also compatible with the high risk of multiple sclerosis in Scotland and particularly in the Orkney and Shetland Islands and with the only transitorily high incidence in the Faroe Islands [6], whereas coffee can hardly explain both epidemiological features.

Arguments for the biological plausibility of some agents occurring in smoked and cured meat (in particular nitrophenol haptens and their protein conjugates) have been put forward [7]. There appears at present to be no plausibility for the factor “margarine”, which was also not compatible with the temporal pattern of multiple sclerosis in the Faroe Islands. [6]


There are remarkably strong correlations between pork consumption and liver disease, liver cancer, and multiple sclerosis.

What can be behind those relationships? The relatively high omega-6 fat content of pork may be a contributing factor, but it can’t be the whole story. It seems there is something else in pork that makes pork consumption risky.

What is it about pork that is so dangerous, and what does it mean for our dietary advice? That will be the topic of my next post.

Related Posts

Posts in this series:


[1] Bridges FS. Relationship between dietary beef, fat, and pork and alcoholic cirrhosis. Int J Environ Res Public Health. 2009 Sep;6(9):2417-25.

[2] Nanji AA, French SW. Relationship between pork consumption and cirrhosis.  Lancet. 1985 Mar 23;1(8430):681-3.

[3] Nanji AA, French SW. Hepatocellular carcinoma. Relationship to wine and pork consumption. Cancer. 1985 Dec 1;56(11):2711-2.

[4] Nanji AA, Narod S. Multiple sclerosis, latitude and dietary fat: is pork the missing link?  Med Hypotheses. 1986 Jul;20(3):279-82.

[5] Lauer K. The food pattern in geographical relation to the risk of multiple sclerosis in the Mediterranean and Near East region. J Epidemiol Community Health. 1991 Sep;45(3):251-2.

[6] Lauer K. Dietary changes in relation to multiple sclerosis in the Faroe Islands: an evaluation of literary sources. Neuroepidemiology. 1989;8(4):200-6.

[7] Lauer K. Environmental nitrophenols and autoimmunity. Mol Immunol. 1990 Jul;27(7):697-8.

[8] Nanji AA, French SW. Dietary factors and alcoholic cirrhosis. Alcohol Clin Exp Res. 1986 Jun;10(3):271-3.

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