Monthly Archives: February 2012 - Page 2

The Trouble with Pork, Part 2

Posted by on February 15, 2012 76 comments

So it looks like pork consumption is correlated with cirrhosis of the liver, liver cancer, and multiple sclerosis (Pork: Did Leviticus 11:7 Have It Right?, Feb 8, 2011). Why?

There are a number of potential dangers from pork, and to give each due consideration will require two posts. I’ll look at a few candidates today, and save my top candidate for Thursday.

Omega-6 Fats

Omega-6 fats are a health villain: Excess omega-6 contributes to general inflammation, fatty liver disease, metabolic syndrome, obesity, and impaired immune function.

And pork can be a major source of omega-6 fats. Nutritiondata.com lists the omega-6 fraction of lard at 11%. But the omega-6 fraction can be highly variable, depending on the pig’s diet. Chris Masterjohn recently reported that the lard used in the “high-fat” research diet was 32% polyunsaturated, nearly all of it omega-6:

The graph shows the difference between the actual fatty acid profile as determined by direct analysis of the lard and the previously reported fatty acid profile, which had been estimated using the USDA database.  We can see that the actual fatty acid profile is much higher in PUFAs, at the expense of both saturated and monounsaturated fats.  In fact, the company had originally estimated the diet to provide 17 percent of its fat as PUFA, but now estimates it to provide a whopping 32 percent!

Chris further reported that feeding the pigs a pasture and acorns diet would reduce lard PUFA levels to 8.7%, and feeding them a Pacific Islander PHD-for-pigs diet of coconut, fish, and sweet potatoes would reduce lard PUFA levels to 3%.

So the omega-6 content can cover a 10-fold range, 3% to 32%, with the highest omega-6 content in corn- and wheat-fed pigs who have been caged for fattening. Corn oil and wheat germ oil are 90% PUFA, and caging prevents exercise and thus inhibits the disposal of excess PUFA. Caging is a common practice in industrial food production; here is a picture of sows in gestation crates:

And here are some Chinese pigs in shipping cages for transport to market:

The Wall Street Journal reported Monday that McDonald’s, following Chipotle, has asked its pork suppliers to stop using gestation stalls, and the largest US hog producer, Smithfield Farms, has begun a 10-year plan to move pigs from small stalls into roomier “group housing systems.” So perhaps the omega-6 content of commercial pork will come down.

How much omega-6 are people actually getting from pork? In the Bridges database, the range in pork consumption across countries was 2 to 80 kg/yr, or 5 to 200 g/day. If this is from industrially raised pigs whose fat is 30% omega-6, then this works out to 0.25% to 10% of energy as omega-6 fats from pork. In most countries, pork is either the primary source of omega-6 fats or the second source after vegetable oils.

Moral of the story: If you’re going to eat a lot of pork, there are real benefits to finding a source of naturally raised pigs fed a healthy diet.

Aside: On a similar diet, human adipose tissue develops almost identical omega-6 levels to pig lard. The Finnish Mental Hospital Study [1] [2] [3], discussed in our book on pages 63-65, showed that on a normal dairy-rich hospital diet human adipose tissue is less than 10% omega-6, but on a soybean oil rich diet adipose tissue becomes 32% omega-6.

American diets have traversed this range in recent decades. Here is a plot of subcutaneous fat omega-6 levels from Stephan Guyenet:

But can omega-6 fats explain the remarkable correlation between pork consumption and liver cirrhosis mortality, hepatocellular carcinoma, and multiple sclerosis?

Polyunsaturated fats are usually a factor in liver diseases. As we discuss in the book (pp 57-58), polyunsaturated fats – either omega-6 or omega-3 – combined with alcohol or fructose are a recipe for fatty liver disease and metabolic syndrome, especially if micronutrient deficiencies figure in the mix. Two of the studies cited in the book:

  • Mice fed 27.5% of calories as alcohol developed severe liver disease and metabolic syndrome when given a corn oil diet (rich in omega-6), but no disease at all when given a cocoa butter diet (low in omega-6). (The first line of this paper reads, “The protective effect of dietary saturated fatty acids against the development of alcoholic liver disease has long been known”.) [4]
  • Scientists induced liver disease in mice by feeding alcohol plus corn oil.  They then substituted a saturated-fat rich mix based on beef tallow and coconut oil for 20%, 45%, and 67% of the corn oil. The more saturated fat, the healthier the liver. [5]

George Henderson, who got us started on this series, links to more papers connecting omega-6 fats to liver cirrhosis.

So: Pork can be a major source of omega-6 fats; and omega-6 fats are a cause of liver cirrhosis.

However, there are several reasons for thinking that omega-6 fats cannot be the primary reason pork raises mortality from our three diseases.

First, vegetable oil consumption seems to be largely uncorrelated with the pork-associated diseases. If omega-6 fats were the primary cause then vegetable oils should have been as strongly correlated as pork. Yet there are plenty of cases of high vegetable oil and low pork consumption (eg Israel), or low vegetable oil and high pork consumption. Disease rates track pork consumption only.

Second, high intake of omega-6 fats causes a mild elevation of risk for a wide range of diseases, much like obesity (which high omega-6 intake causes). Yet pork is associated with extreme elevation of three diseases, and little association with other diseases – not at all the pattern we would expect for omega-6 fats.

Overall, I think we can say that omega-6 fats are probably a contributing factor in liver disease and liver cancer, possibly in multiple sclerosis, but they are unlikely to be the primary factor in the high correlation between pork consumption and liver cirrhosis mortality, liver cancer mortality, and multiple sclerosis.

Processed Meat Toxins

In many countries, most pork consumption is in the form of processed meats. In the United States, about two-thirds of pork is processed. Here is a table (hat tip: Mary Lewis):

Smoked ham is 28% of US pork consumption, sausage is 13%, bacon 6%, processed lunchmeat 6%, and other forms of processed pork another 10%. Among fresh pork cuts, pork chops lead with 11% of US consumption.

In epidemiological studies, processed meat consumption is often associated with poor health. The strongest association is for colorectal cancer [6] and other cancers of the digestive tract, liver, and prostate.

The main types of processing are curing and smoking. Smoking introduces to the meat smoke toxins such as phenols, aldehydes, and polycyclic aromatic hydrocarbons. Curing uses salt, sugar, and nitrite, and while these are fairly benign on their own, various toxins can be formed from them, notably glycation products from the sugar and “N-nitroso compounds” such as nitrosamines from the nitrite.

Some people have concerns about the salt in processed pork. MScott provided evidence that the salt could promote peroxidation of omega-6 fats. Vladimir Heiskanen sent me a link to a blog post arguing that upsetting the sodium-potassium balance could be important:

Dr. Kublina also stressed that people must understand the massive impact that processing has on foods. She cites, for example, that 100 g of unprocessed pork contains 61 mg of sodium and 340 mg of potassium, but turning this into ham alters that ratio significantly, to yield a whopping 921 mg of sodium and, to boot, reduces the potassium content to 240 mg.

On the other hand, john linked to a paper showing that bacon protected against colon cancer, probably due to its salt content. Personally, I think salt is quite healthy, even at the levels contained in bacon, as long as one drinks water and eats vegetables for potassium.

Of all the toxins in processed pork, the most plausible causal agent for our three diseases are the N-nitroso compounds. These compounds are highly abundant in processed pork:

N-nitroso content of food items ranged from <0.01?g/100 g. to 142 ?g/100 g and the richest sources were sausage, smoked meats, bacon, and luncheon meats. [7]

The most common N-nitroso compound in pork products is N-nitrosodimethylamine (NDMA), followed by N-nitrosopiperidine (NPIP), N-nitrosodiethylamine (NDEA), N-nitrosopyrrolidine (NPYR), N-nitrosomorpholine, and N-nitrosothiazolidine (NTHZ).

Nitrosamine levels are increased by high-temperature cooking: “Frying of bacon and cured, smoked pork bellies led to substantially increased levels of NPYR.” [8] In general, high-temperature cooking of meats is a bad idea, as it can generate mutagenic and carcinogenic compounds even in fresh meat. [9]

N-nitroso compounds are known causal agents for liver cancer. Scientists commonly use N-nitrosodiethylamine (NDEA) to induce hepatocellular carcinoma in rats (669 citations, eg [10]). In primates, N-nitroso compounds specifically cause cancers of the liver:

Conversely, all except two of the N-nitroso compounds were carcinogenic. Diethylnitrosamine (DENA) was the most potent and predictable hepatocarcinogen in cynomolgus, rhesus, and African green monkeys. [11]

A Finnish study found an increased risk of colorectal cancer with exposure to N-nitrosodimethylamine (NDMA) from smoked and salted meats, mainly fish and pork [12]. In China, intake of N-nitroso compounds correlates with the incidence of esophageal cancer. [13]

So it seems like we have a likely causal agent here linking pork to liver cancer.

But not so fast!

Although N-nitroso compounds undoubtedly can cause liver cancer, there is a big obstacle to attributing the correlation of human liver cancer with pork consumption to the N-nitroso compounds in processed pork. This is that human liver cancer rates seem to be more strongly related to consumption of fresh pork than processed pork.

I’ve seen several studies showing this, and none showing the reverse. Here’s an example: “A prospective study of red and processed meat intake in relation to cancer risk” [14]. Remember, red meat includes pork, and pork is the most dangerous red meat; processed meat is mainly processed pork.

Here is the hazard ratio of various cancers for the top quintile versus bottom quintile of red meat intake:

Liver cancer has the highest hazard ratio, 1.61.

Here are the hazard ratios for processed meat:

.

Liver cancer is eleventh most likely among the cancers, and the hazard is insignificant.

Here’s another study, an analysis of colorectal cancer rates in the European Prospective Investigation into Cancer (EPIC), which also supports the idea that (a) pork is worse than beef and (b) fresh pork is worse than processed pork:

In analyses of subgroups of red meats, colorectal cancer risk was statistically significantly associated with intake of pork (for highest versus lowest intake, HR = 1.18, 95% CI = 0.95 to 1.48, Ptrend = .02) and lamb (HR = 1.22, 95% CI = 0.96 to 1.55, Ptrend = .03) but not with beef/veal (HR = 1.03, 95% CI = 0.86 to 1.24, Ptrend = .76). In analyses in which intake of each meat was mutually adjusted for intake of the other meats, only the trend for increased colorectal cancer risk with increased pork intake remained statistically significant (Ptrend = .03). Intakes of ham (for highest versus lowest intake, HR = 1.12, 95% CI = 0.90 to 1.37, Ptrend = .44), of bacon (HR = 0.96, 95% CI = 0.79 to 1.17, Ptrend = .34), and of other processed meats (mainly sausages) (HR = 1.05, 95% CI = 0.84 to 1.32, Ptrend =.22) were not independently related to colorectal cancer risk. [15]

Beef is harmless, lamb is not statistically significant after adjustment for pork intake, but pork was harmful in all analyses. However, processed pork had lower hazard ratios than fresh pork, and bacon even appeared protective!

Before I conclude this post, let me present one more fact. This is that fiber consumption is protective against pork-induced cancer. Here is representative data, from [15]:

Look at panel B: With high fiber intake there is essentially no additional cancer risk; but if fiber intake is low, then pork consumption is much more effective at elevating cancer rates.

Conclusion

So let’s add up the evidence and see where it leads:

  • First, the only potentially dangerous component of fresh natural pork, omega-6 fats, can’t account for the data.
  • Second, processed pork, which has other dangerous compounds like N-nitroso compounds, actually appears safer than fresh pork.
  • Third, fiber is protective against pork dangers.

To me these suggest that an infectious pathogen is the cause we are looking for.

Consider: Traditional methods of processing pork, such as salting, smoking, and curing, are antimicrobial. They were developed to help preserve pork from pathogens. So if processed pork is less risky than fresh pork, we should look for a pathogen that is reduced in number by processing.

If a pathogen is the cause, then it makes sense that fiber would be protective. Fiber increases gut bacterial populations. Gut bacteria get “first crack” at food and release proteases and other compounds that can kill pathogens. Also, a large gut bacterial population makes for a vigilant immune system at the gut barrier, making it more likely that pathogens will fail to enter the body. The gut flora are a valuable part of the gut’s immune defenses.

In my next post I’ll look at the pathogens that can infect both pigs and humans, and see (1) if there is a likely candidate for the association of pork consumption with liver cirrhosis, liver cancer, and multiple sclerosis, and (2) how we can best protect ourselves against this threat.

Related Posts

Posts in this series:

References

[1] Miettinen M et al. Effect of cholesterol-lowering diet on mortality from coronary heart-disease and other causes. A twelve-year clinical trial in men and women. Lancet. 1972 Oct 21;2(7782):835-8. http://pmid.us/4116551.

[2] Turpeinen O et al. Dietary prevention of coronary heart disease: the Finnish Mental Hospital Study. Int J Epidemiol. 1979 Jun;8(2):99-118. http://pmid.us/393644.

[3] Miettinen M et al. Dietary prevention of coronary heart disease in women: the Finnish mental hospital study. Int J Epidemiol. 1983 Mar;12(1):17-25. http://pmid.us/6840954.

[4] You M et al. Role of adiponectin in the protective action of dietary saturated fat against alcoholic fatty liver in mice. Hepatology. 2005 Sep;42(3):568-77. http://pmid.us/16108051.

[5] Ronis MJ et al. Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition. J Nutr. 2004 Apr;134(4):904-12. http://pmid.us/15051845.

[6] Santarelli RL et al. Processed meat and colorectal cancer: a review of epidemiologic and experimental evidence. Nutr Cancer. 2008;60(2):131-44. http://pmid.us/18444144.

[7] Stuff JE et al. Construction of an N-nitroso database for assessing dietary intake. J Food Compost Anal. 2009 Dec 1;22(Suppl 1):S42-S47. http://pmid.us/20161416.

[8] Ellen G et al. N-nitrosamines and residual nitrite in cured meats from the Dutch market. Z Lebensm Unters Forsch. 1986 Jan;182(1):14-8.  http://pmid.us/3953157.

[9] Sinha R. An epidemiologic approach to studying heterocyclic amines. Mutat Res. 2002 Sep 30;506-507:197-204. http://pmid.us/12351159.

[10] Peto R et al. Effects on 4080 rats of chronic ingestion of N-nitrosodiethylamine or N-nitrosodimethylamine: a detailed dose-response study. Cancer Res. 1991 Dec 1;51(23 Pt 2):6415-51. http://pmid.us/1933906.

[11] Thorgeirsson UP et al. Tumor incidence in a chemical carcinogenesis study of nonhuman primates. Regul Toxicol Pharmacol. 1994 Apr;19(2):130-51. http://pmid.us/8041912.

[12] Knekt P et al. Risk of colorectal and other gastro-intestinal cancers after exposure to nitrate, nitrite and N-nitroso compounds: a follow-up study. Int J Cancer. 1999 Mar 15;80(6):852-6. http://pmid.us/10074917.

[13] Lin K et al. Dietary exposure and urinary excretion of total N-nitroso compounds, nitrosamino acids and volatile nitrosamine in inhabitants of high- and low-risk areas for esophageal cancer in southern China. Int J Cancer. 2002 Nov 20;102(3):207-11. http://pmid.us/12397637.

[14] Cross AJ et al. A prospective study of red and processed meat intake in relation to cancer risk. PLoS Med. 2007 Dec;4(12):e325. http://pmid.us/18076279.

[15] Norat T et al. Meat, fish, and colorectal cancer risk: the European Prospective Investigation into cancer and nutrition. J Natl Cancer Inst. 2005 Jun 15;97(12):906-16. http://pmid.us/15956652.

Around the Web; Happy Valentine’s Day!

Posted by on February 14, 2012 19 comments

Happy Valentine’s Day, everyone!

[1] Paleo Summit: Sean Croxton is about to launch his “Paleo Summit”. It features multimedia interviews with 23 speakers, including myself. It’s a mini-Ancestral Health Symposium, but without the travel. Check it out!

[2] Dan’s Plan: I’ve agreed to become a scientific advisor to Dan’s Plan.

Dan’s Plan is a promising young startup founded by Dan Pardi, one of the rising stars of the ancestral health community. Dan’s Plan is pioneering “Quantified Paleo,” the use of Quantified Self tools to help members adopt an ancestral lifestyle and to support self-experimentation and group experimentation that can solve health problems.

Dan’s Plan provides content modules in three areas: Eat, Sleep, Move. “Eat” is about diet, of course; “Move” about fitness; and “Sleep” about lifestyle generally – how do you support healthy circadian rhythms?  We’ll be contributing Perfect Health Diet-based content, such as meal plans, to the “Eat” section.

One of the things that has me excited about Dan’s Plan is the potential for us to do science together as a community. Quantified Self tools make it easy to record data and upload them to a database. Suppose Dan’s Plan ends up with content modules for a half dozen different diets. The Dan’s Plan database may be able to track results for every diet, charting out weight loss results, quit rates, and other data for the community. Is it normal to gain a few pounds at the start of the diet? All kinds of questions can be answered with this kind of data, and we can more effectively find out what really works.

I’ll have more to say about Dan’s Plan and what we’ll be doing with them later. For now, I’d just like to encourage anyone who’s curious to become a member. Membership in Dan’s Plan is free.

[3] Other news: I had a very fun interview last week with Andy Oudman and Pam Killeen of 1290 AM CJBK, London, Ontario. Pam is associated with the Weston A Price Foundation and will be speaking at this year’s Wise Traditions conference; Andy is the most popular radio host in London and extremely entertaining. Thanks, Pam and Andy!

Also, Constantin Gonzalez has published a German language review of our book. (English-language translation)  Constantin also produced a German-language version of our food plate. Thanks Constantin!

[4] Music to Read By: These are the Valentine’s dreams you will savor:

[5] Cute Animals:

Via Jasmyn Campbell.

[6] Interesting recent items:

Steph is ready for a bright, shining world.

The Atlantic has a great story on a topic we’ve discussed previously: Toxoplasma gondii infections alter behavior. One claim: Toxo may kill as many people as malaria, a million people per year, when you account for its induction of reckless behavior.

Via John Hawks, malaria kills twice as many people as previously thought. They were only counting deaths from acute infection, but chronic infection kills too.

But it’s not all bad news: T. gondii makes you have car accidents, but soil bacteria puts you in a good mood.

Did biological warfare win the Stalingrad campaign?

Mark Sisson discusses the “Asian Paradox”: how can Asians eat rice in the “insidious weight gain” calorie region, and not gain weight?

Ann Marie Michaels, aka Cheeseslave, explains why she ditched low carb. Barry Cripps of Paleo Diet News also benefited from increasing carbs. Julianne Taylor disputes the “carbs can kill” meme.

Matt Metzgar reviews our book; he wants us to go higher carb. Joanne Eglash gives us a mention in examiner.com.

Speaking of reviews, I reviewed Richard Nikoley’s new book on Amazon. I think it’s an excellent introduction to “Paleo 1.0”.

New research may explain why the zebra got its stripes. Revisions may be necessary to this book.

Monsanto is coming out with genetically engineered omega-3 producing soybeans.

FoodSnipps has recipes for Perfect Health Dieters. Mike Skiff is starting a 30-day experiment. JD Moyer discusses the benefits of intermittent fasting, with a link to us.

Dennis Mangan wonders: What’s behind the obesity epidemic in pets?

Bruce Charlton argues for electroconvulsive therapy, nicotine patches, and caffeine against Parkinson’s.

Congratulations, Razib!

The Flavorists have triumphed: the many flavors of Chinese potato chip.

Mayonnaise is even more dangerous than I thought. (Via Rantburg.)

Stephan Guyenet wonders if smoking delayed the obesity epidemic by keeping people in the 1950s and 1960s lean. I wonder if smoking epigenetically modified the children, promoting obesity in the next generation.

J Stanton sends me a link: pork is good for – stanching nosebleeds?

Visiting social web sites relaxes the heart.

Dr Briffa shares a picture of a man who injected insulin in his belly repeatedly.

Finally, Chicago magazine has an article on Dr Mercola. I thought his history was interesting:

At first, he was a traditional drug-prescribing doctor…. “I thought drugs were the answer,” he says with a shrug.

That changed in the early 1990s, when conventional treatments failed to help a young patient with recalcitrant diarrhea. Flummoxed, Mercola found a possible answer in a book called The Yeast Connection. After he tried the all-natural protocol the book recommended, he says, “the kid had a miraculous recovery.”

Over the next several years, Mercola began networking with a number of like-minded physicians “who were getting pretty good results with nontraditional therapies.” He grew increasingly skeptical of traditional medicine and interested in treatments designed, he says, to “treat the whole person” rather than just symptoms….

In 1997, as a way to share what he had found that would be “useful and helpful,” he started Mercola.com. It proved a hit.

[7] Bonus animal: We all need a hug now and then:


Via Godvine.com.

[8] Comments:

Sofie recommends fasting for avoidance of jet lag.

Connie Warner tells about an unexpected food contaminant: “I remember hearing from an FDA food safety chemist that he wouldn’t eat shrimp because the rat urine from the ship rats wouldn’t wash out of the shrimp.”

Josh Almanza on Facebook presents evidence white rice is better than brown rice.

[9] Honorable mention: An article about us appeared in the February edition of Healthy Cells magazine: “What’s For Dinner?” by Sandra Bender, BSN, PhD, on pp 8-9:

My husband and I chose the Perfect Health Diet after cancer treatment because we feel healthier than on the plant-based diet, we enjoy the food – and my long-lived grandparents ate this. Daily, we eat about four ounces meat, four ounces fish, ¾ cup cooked rice or potatoes, eggs, cheese, and whole fermented milk (kefir), lots of vegetables, and fruit for dessert, all organic. We eat fat with meat and dairy, butter, gravy, or coconut sauces on everything. Once a day we have a half-ounce dark chocolate, an anti-cancer antioxidant. Yummy! After eating this way for two years, my cholesterol and triglycerides are excellent and inflammation markers and insulin are low. My omega 3:6 is balanced.

[10] Not the Weekly Video: Max Ehrmann’s “Desiderata”:

Desiderata from R Smittenaar on Vimeo.

[11] Shou-Ching’s Photo Art:

[12] Weekly video: Dr Thomas Tartaron lectures on Ötzi the Iceman. Interesting aspects: Ötzi had Lyme disease and intestinal whipworm parasites; he had atherosclerosis and calcified coronary arteries despite a “healthy” (but grain-rich) diet and plenty of exercise.

Via Dienikes.

Chopped Liver Paté

Posted by on February 11, 2012 96 comments

Leila left us a recipe for liver paté:

This is my new (ok, only) favorite way to eat liver …

Today I had some for dinner on rice crackers – yum!… It took about 15 minutes to make, not counting the soaking time.

We tried it last weekend for the Super Bowl, and it was excellent.

Ingredients

We would recommend beef or lamb liver (not pork liver – see the upcoming conclusion to the pork series) from a naturally pastured and fed animal. Chicken liver is also good, but again should be from a healthy naturally raised animal. We don’t normally insist on grassfed for most cuts, but it’s worth insisting on grassfed when you eat liver. The liver is a detoxification organ and unhealthy animals can easily have livers that are rich in toxins and inflammatory molecules.

Supporting that judgment, we have found that grassfed beef livers have a noticeably better taste than conventional livers. Fortunately, organ meats are inexpensive even from organic farmers. We typically pay $4.99 per pound for grassfed beef liver. (Here is the price list of a Massachusetts farm we’ve bought from recently).

Leila’s trick is to soak the liver in milk beforehand, which helps remove things like blood that may contribute to a bad taste.

Here are our ingredients:

This was 1/2 lb (225 g) of liver. This is an appropriate amount of beef liver for two people to eat in a week. The liver has been sliced into pieces 1 cm (1/2 inch) thick, and is soaking in milk. Other ingredients are an onion and boiled egg; 4 tbsp butter plus a similar amount of coconut oil; and cilantro. Leila used kimchi in place of the cilantro, for a spicier flavor.

Preparation

After soaking the liver for an hour or so in milk, discard the milk. Brown the liver slices in the butter, cooking 3-4 minutes per side on relatively low heat:

Remove the liver when it has been browned on all sides and add diced onion.

Then put everything – the cooked liver, cooked onion, cooking fluids from the pot, boiled egg, coconut oil, and cilantro – into a blender and purée. The result:

Serve with rice crackers:

Conclusion

This still has a bit of a liver taste, but tastes really good to us. There’s room to experiment with ingredients; Leila writes:

I’ll probably use more kimchee next time to make it a bit spicier, and more onion.

We recommend consuming in the range 1/4 to 1/2 lb (100 to 200 g) ruminant (beef, lamb, or goat) liver per week for copper, vitamin A, phospholipids, and other nutrients. This eliminates any need for copper supplementation, and provides a great bounty of other nutrients.

If you eat more than ½ lb (200 g) per week of ruminant liver, copper toxicity becomes a real danger. If you intend to eat liver in larger quantities, switch to chicken liver once your ruminant liver intake gets above 150 g or so in a week. Finally, we recommend avoiding pork liver, for reasons we’ll get to in the next (or next two) science posts.

Pork: Did Leviticus 11:7 Have It Right?

Posted by on February 8, 2012 143 comments

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]

Conclusion

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:

References

[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. http://pmid.us/19826553.

[2] Nanji AA, French SW. Relationship between pork consumption and cirrhosis.  Lancet. 1985 Mar 23;1(8430):681-3. http://pmid.us/2858627.

[3] Nanji AA, French SW. Hepatocellular carcinoma. Relationship to wine and pork consumption. Cancer. 1985 Dec 1;56(11):2711-2. http://pmid.us/2996744.

[4] Nanji AA, Narod S. Multiple sclerosis, latitude and dietary fat: is pork the missing link?  Med Hypotheses. 1986 Jul;20(3):279-82. http://pmid.us/3638477.

[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. http://pmid.us/1757770.

[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. http://pmid.us/2755551.

[7] Lauer K. Environmental nitrophenols and autoimmunity. Mol Immunol. 1990 Jul;27(7):697-8. http://pmid.us/2395440.

[8] Nanji AA, French SW. Dietary factors and alcoholic cirrhosis. Alcohol Clin Exp Res. 1986 Jun;10(3):271-3. http://pmid.us/3526949.