Around the Web; Paleo Summit Edition

Posted by on February 25, 2012 30 comments

Thank you to all readers who have helped out on the Q&A thread! I have been exceedingly busy and am still behind on some important obligations, so it is difficult to find time to answer questions. But I do intend to respond to everyone’s questions. I’m grateful to those readers who are sharing their knowledge to help others.

[1] Paleo Summit starts tonight:

Sean Croxton’s Paleo Summit begins at midnight tonight with presentations by Mark Sisson and Diane Sanfilippo. Presentations are free for 24 hours, when a new set of presentations appears. The summit will continue until interviews with 23 speakers, including myself, have appeared.

There is a Summit Upgrade package of videos, audio files, transcripts, and bonuses that will go on sale Tuesday.

It’s a mini-Ancestral Health Symposium, but without the travel. I understand that 14,000 people have already registered. Check it out!

[2] Music to read by: The Seekers perform “I’ll Never Find Another You” in 1993:

Judith Durham’s voice is as lovely as ever, and she looks fantastic. Compare how she looked in the 1960s:

Nowadays when I see someone who’s aged gracefully I wonder what her diet is like.

[3] Raw Milk Debate: I was privileged to attend a recent debate over raw milk at Harvard Law School (site of the upcoming Ancestral Health Symposium), featuring Sally Fallon Morell of the Weston A Price Foundation and three others, two on each side. All of the panelists were great and the debate was excellent. And it’s available on video:

[4] Interesting posts this week:

I was in New York for a business trip on Thursday and was able to stop by at CrossFit NYC to talk to some of their members. John Durant was there and mentioned my ranking of the different meats in his Friday post.

Good news for Court Wing, head trainer and co-owner at CrossFit NYC: walking speed is a good indicator of future lifespan.

The Daily Mail wonders why today’s women are developing gray hair in their 20s. Michael A Smith wonders whether tyrosine can reverse it.

The New York Times reports on a study showing that the aging eye blocks blue light, so that the elderly need more sunlight and blue light to maintain their circadian rhythms and health.

Chris Kresser asks: Is chlorine in shower water making you sick?

Huffington Post reports that BPA’s Obesity And Diabetes Link Strengthened By New Study.

Gregory Cochran: Doctors aren’t innovators and don’t generate new knowledge.

J Stanton informs that some Japanese with yeast infections get drunk from rice; in extreme instances blood ethanol concentrations may reach fatal levels of 80 mg/dl or almost 1% blood alcohol concentration.

Seth Roberts explains what Richard Bernstein taught the world.

ScienceDaily reports that Vitamin D up to a serum 25(OH)D level of 50 ng/ml helps reduce inflammation.

Fight Aging! reports that stem cell transplantation extends lifespan in mice.

Bix reports that glycogen in the brain is increased by exercise.

Prof Dr Andro says that slower weight loss works better. We argued that in our book also. Focus on health first, weight second, and you’ll lose weight more successfully.

Peter Janiszewski reports that food reward is self-regulating: The more you eat something, the less you like it.

Julianne Taylor has lost an inch from her waist and improved her Raynaud’s. Paleo Pepper has benefited from adding carbs to her diet: “Since adding carbohydrates to my diet– call me crazy– I’ve been less sickly.  The acne scars on my face heal much more quickly than they used to.  Most importantly, my breasts and hips have gotten larger, and my thighs a bit I guess, but my stomach has stayed flat flat flat.  How nice is that?”

Greatist.com has released an infographic, The Ultimate Guide to Eating Paleo.

Coming soon: Test-tube meat.

Via Newmark’s Door, “How Cancer Drugs Make Cancer Worse and Kill Patients.”

In North Carolina, a child’s homemade lunch was seized and the child forced to buy chicken nuggets because her lunch didn’t comply with Federal guidelines.

In a post relevant to my conversation with the Peat-atarians, Stephan Guyenet asks whether fructose sugar can cause obesity. His answer:

[H]igh-sugar diets don’t necessarily produce body fat accumulation in humans, and they can even allow body fat loss under some circumstances, but are there situations where sugar can cause fat accumulation?  The answer is an emphatic yes….

[E]xcessive consumption of refined sugar can promote elements of the metabolic syndrome, and this is due specifically to its fructose content.

Fortunately, Stephan projects that US sugar consumption won’t reach 100% of calories until 2606.

Good news for pet lovers: Cats can serve as blood glucose monitors.

[5] Cute animals:

Via Aravindan Balasubramanian.

[6] The competition is heating up: Hitler has decided to start a Paleo blog:

(Via Stabby.)

[7] How the brain ages: A fascinating plot at Marginal Revolution:

[8] Not the Weekly Video: I hope this Chinese candy artist is using safe sugars!

[9] Shou-Ching’s Photo Art:

[10] Weekly video: We might as well wrap up the pork series with evidence that pigs will eat almost anything:

± I.M.F. ± from PlusqueMinusque on Vimeo.

Via Naked Capitalism

The Trouble With Pork, Part 3: Pathogens

Posted by on February 22, 2012 147 comments

We started this series with a look at remarkably strong correlations between pork consumption and liver cirrhosis mortality, liver cancer, and multiple sclerosis (Pork: Did Leviticus 11:7 Have It Right?, Feb 8, 2012). In Part 2, we looked at omega-6 fats in industrial pork meat and toxins in processed pork products as possible causes (The Trouble with Pork, Part 2, Feb 15, 2012).

That second post left us with several clues that some pathogen (or pathogens) that (a) infects both pigs and humans and (b) can be transmitted from pigs to humans via the eating of pork, is responsible for the disease associations. These clues include:

  1. The risk is higher for fresh pork than processed pork. Processed pork is generally cured or smoked, both steps that are anti-microbial.
  2. Eating fiber, which increases gut bacterial populations and enhances immune vigilance of the gut, is protective.
  3. The disease risk is specifically associated with two organs – the central nervous system (multiple sclerosis) and the liver (cirrhosis, hepatocellular carcinoma). Pathogens are more likely than other pork components to have tissue specificity.

Our mission today is to try to track down the pathogen(s), and figure out how to minimize risk of infection.

Pigs And Zoonotic Infections

Scientists studying xenotransplantation – the transplantation of animal organs into a person to replace a failing organ – have had the best luck with pig organs. Pigs are easier to work with than primates, not dramatically different in size than humans, and their organs are less likely to provoke rejection than those of other mammals. This suggests a similarity of biology between pigs and humans.

But biological similarity has its downsides. A large number of pathogens can infect both pigs and humans. More than any other animal, pigs pass pathogens to humans.

Indeed, investigators have been surprised at how frequently pathogens pass back and forth. According to a new study (discussed at Aetiology) of the evolutionary history of methicillin-resistant Staphylococcus aureus (MRSA), S. aureus was passed to pigs by their human caretakers. In pigs, which are routinely given antibiotics by industrial food producers, S. aureus picked up resistance genes to tetracyclines and methicillins. The resulting antibiotic-resistant ST398 strain was passed back to humans.

Wikipedia lists some of the pathogens that flourish in both pigs and humans and can infect humans who eat infected pork, usually undercooked pork:

Although all of these pathogens are potential concerns, I do not see strong specific links between the above pathogens and our three pork-associated diseases – liver cirrhosis, liver cancer, and multiple sclerosis.

However, there is another pathogen capable of infecting humans from pork that is a strong candidate: hepatitis E virus (HEV).

Hepatitis E

Hepatitis E was first observed in a 1955 outbreak in New Delhi, India. It generally produces an acute disease that lasts for several weeks; most victims recover with few symptoms, but in a few this acute illness progresses into a severe liver disease that can be fatal. About 2% of all infections lead to death from this acute liver disease; death rates are higher in pregnant women.

Hepatitis E seems to have evolved in the last millennium: There are four known genotypes, all of which infect humans and two of which infect pigs, and their common ancestor dates to 536 to 1344 years ago. [1] However, the pig-infecting genotypes 3 and 4 of Hepatitis E underwent a notable population expansion in the twentieth century, during which there has been “an extensive genetic divergence of HEV strains and high prevalence of HEV infections in many parts of the world.” [2]

The human-only genotypes of Hepatitis E are transmitted by fecal contamination of drinking water and are prevalent only in developing countries with poor sanitation; but the pig-and-human genotypes are transmitted primarily through pork consumption:

[G]enotypes 3 and 4 are associated with sporadic disease attributable to exposure to body fluids of infected swine [8] and ingestion of food products from pigs, boars and deer [11], [16], [18]. [1]

Hepatitis E seems to be most prevalent in Asia, the Middle East, and Africa:

Hepatitis E is the most important or the second most important cause of acute clinical hepatitis in adults throughout Asia, the Middle East and Africa. [8]

However, it has been spreading to Europe and the Americas:

HEV was rarely identified in industrialized countries, and the few reported cases of infection were usually in someone who had recently traveled to an endemic region. In the past few years this pattern has changed, as cases of endemic or autochthonous hepatitis E have been diagnosed with increasing frequency in individuals who have not traveled abroad….

Cases have been reported with increasing regularity throughout Western Europe, as well as in some Eastern European countries. [7]

The genotypes that coinfect humans and pigs may have originated in East Asia:

All but one genotype 4 sequence originated either from China or Japan…. [T]he genotype 3 sequences were divided into 3.1 and 3.2 clades … [A]lthough 87.5% of the clade 3.1 variants were from Asia and 60% of the clade 3.2 variants were from Europe (Table S1), these clades were found to have similar histories (Fig. 6). [1]

Historically, China and Japan did not raise cattle for food and pigs have been the major source of meat. Even today in southern China, pigs are often kept in the yards of homes, and close contact between pigs and humans facilitates zoonotic transmission.

At pig farms, Hepatitis E virus seems to spread readily. A Japanese study reported:

[O]ur estimates imply that more than 95% of pigs are infected before the age of 150 days. [3]

Presumably this is due to fecal-oral transmission among pigs in close quarters. At French farms, 65% of pigs were found to be hepatitis E infected at age 90 days. [4]

Transmission to Humans Via Pork

Can humans get infected by eating pork products? It now seems clear that the answer is yes.

A French study found that the genotype distribution of hepatitis E infecting humans is identical to the genotype distribution in pigs at slaughterhouses:

Frequent zoonotic transmission of hepatitis E virus (HEV) has been suspected, but data supporting the animal origin of autochthonous cases are still sparse. We assessed the genetic identity of HEV strains found in humans and swine during an 18-month period in France. HEV sequences identified in patients with autochthonous hepatitis E infection (n = 106) were compared with sequences amplified from swine livers collected in slaughterhouses (n = 43). Phylogenetic analysis showed the same proportions of subtypes 3f (73.8%), 3c (13.4%), and 3e (4.7%) in human and swine populations. Furthermore, similarity of >99% was found between HEV sequences of human and swine origins. These results indicate that consumption of some pork products, such as raw liver, is a major source of exposure for autochthonous HEV infection. [5]

As hepatitis E concentrates in the liver in both pigs and humans, swine livers were the natural place to test for hepatitis E presence, and probably the riskiest part of the pig to eat.

Further evidence that hepatitis E in pigs can infect humans was found in another French study. The researchers reasoned that sausage made from pig liver would be a likely vector for hepatitis E transmission to humans, especially a form of smoked pig liver sausage traditionally eaten raw – figatellu. Their findings:

Acute or recent HEV infection, defined by detection of anti-HEV immunoglobulin M antibodies and/or HEV RNA, was observed in 7 of 13 individuals who ate raw figatellu and 0 of 5 individuals who did not eat raw figatellu (P=.041). Moreover, HEV RNA of genotype 3 was recovered from 7 of 12 figatelli purchased in supermarkets, and statistically significant genetic links were found between these sequences and those recovered from patients who ate raw figatellu….

Our findings strongly support the hypothesis of HEV infection through ingestion of raw figatellu. [6]

The titer of hepatitis E viruses in the supermarket sausage reached as high as a million copies per slice. [6] This data suggests that a majority of figatellu in French supermarkets carries hepatitis E virus, and that a majority of people who eat figatellu acquire hepatitis E infections.

Contact with pigs can also lead to transmission; swine workers have an elevated prevalence of antibodies to HEV in the United States. [7]

Does Cooking Inactivate the Viruses?

What level of cooking is needed to inactivate the virus?

It is difficult to prove that any particular cooking or processing method renders HEV non-infectious:

How safe are these products? The question is difficult to answer because HEV grows poorly in cell culture, and in vivo testing of viability requires nonstandard laboratory animals—nonhuman primates or pigs for genotypes 3 and 4. [7]

Since scientists don’t have the funding or facilities to see if feeding cooked, cured, or smoked pork to primates or pigs gives them hepatitis E, they have no way of verifying that cooked, cured, or smoked pork is free of HEV.

In test tube experiments, HEV was still viable and infectious after cooking for 1 hour at 56°C, the temperature of rare to medium-cooked meat. [9] About 80% of viruses were inactivated after an hour at 60°C, and an hour at 70°C probably eliminates the viruses.

The implication is that thorough cooking would destroy HEV, but that some HEV will survive in rare to medium cooked pork, with liver likely having the greatest viral titer. [9] “However, much pork is consumed that has not had even that degree of cooking.” [7]

One way to reduce the risk of infection is to avoid the pig tissues that have the highest viral titers:

HEV can be found in the liver, blood, and intestinal tract, which are all consumed in one form or another and often together, such as in sausages. [7]

So: to avoid HEV infection, it’s best to avoid pork liver, intestines, or blood, or products made from them such as sausage; other cuts should be carefully rinsed of all blood and then cooked thoroughly to a temperature of at least 70°C. Simmering in near-boiling water for an hour should be sufficient.

The most dangerous pork product is likely to be sausage, which often uses pork liver meat, and traditionally uses pig intestines as the casing. It may also contain traces of pig blood. Pig blood pudding, a traditional Chinese dish, should also be avoided.

Links to Pork-Associated Liver Diseases

Hepatitis E was discovered as a cause of acute liver disease. But what about chronic diseases like alcoholic cirrhosis and liver cancer? Is there really evidence linking it to these diseases?

First, studies of organ-transplant recipients who contracted hepatitis E from their donors have shown that HEV seems to establish chronic infections in at least 58% of infected persons. [10] When anti-HEV antibodies exist, generally active viral RNA is present too. [12] So the virus is persistent.

Hepatitis B and C viruses are known causes of alcoholic liver cirrhosis. What about HEV? There have been few studies, but those that exist suggest it is likely:

  • A child developed cirrhosis after a bone marrow transplant due to a swine-derived form of hepatitis E. [11]
  • A Spanish study found a strong association between HEV and cirrhosis in people infected with HIV: “Liver cirrhosis was the only factor independently associated with the presence of anti-HEV, which was documented in 23% of patients with cirrhosis and 6% of patients without cirrhosis (P?=?0.002; odds ratio 5.77). HEV RNA was detected in three seropositive patients (14%), two of whom had liver cirrhosis.” [12]
  • HEV seems to be a common cause of cirrhosis in Egypt. [13]

Hepatitis B and hepatitis C viruses are known causes of hepatocellular carcinoma. What about HEV? If there were few studies linking HEV to cirrhosis, there are even fewer investigating its relationship to HCC.

I did find one Chinese study showing that HEV infection greatly elevated the association of aflatoxin with HCC. (Aflatoxin, a fungal toxin that damages the liver, is a known risk factor for HCC.) [14]

Epidemiology is also suggestive. I mentioned earlier that the pork-transmitted genotypes of HEV have only recently appeared in the Americas. If HEV is responsible for alcoholic cirrhosis, hepatocellular carcinoma (HCC), or multiple sclerosis, then we should be seeing the incidence of those diseases increase. In fact, that is true for HCC:

In the U.S., incidence rates of HCC in both men and women have increased steadily during the past three decades. The reasons for this steady increase remain unknown. [15]

What About Multiple Sclerosis?

There have been no studies searching for a specific link between HEV and multiple sclerosis.

However, it may be worth reviewing what some mouse models tell us about the potential for a hepatitis virus to cause MS. MS is an infectious or autoimmune disease:

MS is felt to be most likely either due to an aberrant immune response or a pathogen, or possibly a combination of the two, and the animal models available reflect these two possible pathogeneses. [16]

Regular readers will know that I believe MS is infectious in origin. There are three animal models for MS. One of them (“experimental allergic encephalomyelitis” or EAE) involves immunizing mice with myelin or myelin proteins so that they develop antibodies to their own myelin; the other two involve infecting mice with viruses:

Two viruses, Theiler’s murine encephalomyelitis virus and murine hepatitis virus, are used to induce infectious models of the disease. [16]

The murine hepatitis virus (MHV) model is suggestive: it supports the idea that a virus that causes hepatitis may also cause MS. Some strains of MHV are neurotropic, infecting both the liver and central nervous system, and it is these that most readily produce an MS-like disease. [17]

If a hepatitis virus is causing MS in humans, we would expect MS patients to have high rates of liver disease. Indeed, there is a correlation.

MS patients are 3.7-fold more likely to have elevated ALT and 2.2-fold more likely to have elevated AST – both liver enzymes associated with liver disease. Also, elevated ALT and AST are associated with the more severe relapsing-remitting form of MS. [18]

A few perhaps insignificant links: Patients with systemic sclerosis, who are about 5-fold more likely to develop MS than others, are also at high risk for liver disease. [19] In the 1980s, doctors began observing MS patients with cases of primary biliary cirrhosis severe enough to require liver transplantation. [20]

Other Pig-Human Pathogens and MS

Pork can carry many pathogens; perhaps hepatitis E virus is not the MS-causing pathogen.

I don’t see obvious candidates however. Perhaps herpes viruses would be most likely. One of the human pathogens likely to be causal for MS is Epstein-Barr virus, also known as human herpes virus 4 (HHV-4). It causes mononucleosis but establishes persistent infections and is associated with a number of diseases, including lymphomas, MS, lupus, and rheumatoid arthritis.

Human herpes viruses may be able to establish infections in pigs. [21] And there are porcine herpes viruses that are closely related to Epstein-Barr virus. [22]

Conclusion

There is a strong association between pork consumption and liver cirrhosis mortality, liver cancer, and multiple sclerosis.

It seems likely that the association, if it is real, is mediated by a pathogen. The most likely pathogen in the case of the liver diseases is hepatitis E virus. In MS, the pathogen remains unknown, but is likely to be a virus.

Hepatitis E virus is not destroyed by casual cooking, smoking, or curing. It appears that meat must  reach temperatures of 70ºC (160ºF) before viruses are inactivated; and it is possible that meat must remain at that temperature for some time, perhaps as long as an hour. Rare or medium cooked pork could contain active viruses.

Hepatitis E viruses are most abundant in liver, intestine, and blood. Pork products containing these parts, such as sausage, may be best avoided.

Meat from parts of the pig with low viral titers, such as pork ribs or pork bellies, are likely to be safe to eat as long as they are well cooked. Be sure to wash the meat of all blood before cooking, and to cook thoroughly.

Related Posts

Posts in this series:

References

[1] Purdy MA, Khudyakov YE. Evolutionary history and population dynamics of hepatitis E virus. PLoS One. 2010 Dec 17;5(12):e14376. http://pmid.us/21203540.

[2] Purdy MA, Khudyakov YE. The molecular epidemiology of hepatitis E virus infection. Virus Res. 2011 Oct;161(1):31-9. http://pmid.us/21600939.

[3] Satou K, Nishiura H. Transmission dynamics of hepatitis E among swine: potential impact upon human infection. BMC Vet Res. 2007 May 10;3:9. http://pmid.us/17493260.

[4] Kaba M et al. Frequent transmission of hepatitis E virus among piglets in farms in Southern France. J Med Virol. 2009 Oct;81(10):1750-9. http://pmid.us/19697419.

[5] Bouquet J et al. Close similarity between sequences of hepatitis E virus recovered from humans and swine, France, 2008-2009. Emerg Infect Dis. 2011 Nov;17(11):2018-25. http://pmid.us/22099089.

[6] Colson P et al. Pig liver sausage as a source of hepatitis E virus transmission to humans. J Infect Dis. 2010 Sep 15;202(6):825-34. http://pmid.us/20695796.

[7] Purcell RH, Emerson SU. Hidden danger: the raw facts about hepatitis E virus. J Infect Dis. 2010 Sep 15;202(6):819-21. http://pmid.us/20695795.

[8] Purcell RH, Emerson SU. Hepatitis E: an emerging awareness of an old disease. J Hepatol. 2008 Mar;48(3):494-503. http://pmid.us/18192058.

[9] Emerson SU et al. Thermal stability of hepatitis E virus. J Infect Dis. 2005 Sep 1;192(5):930-3. http://pmid.us/16088844.

[10] Legrand-Abravanel F et al. Characteristics of autochthonous hepatitis E virus infection in solid-organ transplant recipients in France. J Infect Dis. 2010 Sep 15;202(6):835-44. http://pmid.us/20695798.

[11] Halac U et al. Cirrhosis due to Chronic Hepatitis E Infection in a Child Post-Bone Marrow Transplant. J Pediatr. 2012 Feb 15. [Epub ahead of print] http://pmid.us/22341950.

[12] Jardi R et al. HIV, HEV and cirrhosis: evidence of a possible link from eastern Spain. HIV Med. 2012 Jan 18. http://pmid.us/22257075.

[13] El Sayed Zaki M, Othman W. Role of hepatitis E infection in acute on chronic liver failure in Egyptian patients. Liver Int. 2011 Aug;31(7):1001-5. http://pmid.us/21733089.

[14] Tao P et al. Associated factors in modulating aflatoxin B1-albumin adduct level in three Chinese populations. Dig Dis Sci. 2005 Mar;50(3):525-32. http://pmid.us/15810636.

[15] Yuan JM et al. Synergism of alcohol, diabetes, and viral hepatitis on the risk of hepatocellular carcinoma in blacks and whites in the U.S. Cancer. 2004 Sep 1;101(5):1009-17. http://pmid.us/15329910.

[16] Pachner AR. Experimental models of multiple sclerosis. Curr Opin Neurol. 2011 Jun;24(3):291-9. http://pmid.us/21519255.

[17] Carbajal KS et al. Surgical transplantation of mouse neural stem cells into the spinal cords of mice infected with neurotropic mouse hepatitis virus. J Vis Exp. 2011 Jul 10;(53). http://pmid.us/21775959.

[18] Tremlett H et al. Liver test abnormalities in multiple sclerosis: findings from placebo-treated patients. Neurology. 2006 Oct 10;67(7):1291-3. http://pmid.us/17030771.

[19] Robinson D Jr et al. Systemic sclerosis prevalence and comorbidities in the US, 2001-2002.  Curr Med Res Opin. 2008 Apr;24(4):1157-66. http://pmid.us/18430269.

[20] A patient with primary biliary cirrhosis and multiple sclerosis. Am J Med. 1992 Apr;92(4):433-6. http://pmid.us/1558090.

[21] Kim JH et al. Infection of porcine cells with human herpesviruses. Transplant Proc. 2010 Jul-Aug;42(6):2134-7. http://pmid.us/20692426.

[22] Doucette K et al. Gene expression of porcine lymphotrophic herpesvirus-1 in miniature Swine with posttransplant lymphoproliferative disorder. Transplantation. 2007 Jan 15;83(1):87-90. http://pmid.us/17220799.

Tom Kha Shrimp and Scallop (Thai Soup)

Posted by on February 19, 2012 22 comments

We recommend making bone broths regularly, for the minerals and collagen extracted from the bone and joint tissue. The broths can be drunk as a beverage, used in cooking (eg in making rice), and used as the base for soups, curries, and stews.

We make broth most Saturdays, and use it throughout the week. For an example of how to make broth, see Bone Broth Revisited; and Pumpkin Soup, Oct 3, 2011. The nature of the broth depends on the type of bones you get. Marrow bones create a fattier broth; bones with joint tissue attached create a collagen-rich gelatin; bare bones create a mineral-rich watery broth. If you start with marrow and joint bones, then the first broth will have all the fat, the first and second will have a lot of collagen, and later batches will become progressively more watery.

Since broth itself has a mild taste, it can be the foundation for a great diversity of soups. Once you have broth, most soups can be made very quickly – often in 10 minutes.

Tom Kha Gai, or chicken galangal soup, is a classic dish of Thai cuisine. It’s always made with coconut milk and usually lemongrass (which has a mild citrus flavor) and some kind of spicy flavor.

Of course, there’s no need to use chicken, and we generally prefer seafood, ruminant meats, eggs, and even duck to chicken. In today’s recipe, we used shrimp and scallops as our meats.

Ingredients

We used coconut milk, bone broth (not shown), shrimp, scallops, cilantro (coriander leaves), lemongrass, lime juice, fish sauce (not shown), mushrooms, and in the small bowl on the right, a homemade chili paste, galangal root, and sliced Serrano or Jalapeno chili peppers.

Preparation

Place equal parts coconut milk and bone broth in a pot; add lemongrass, sliced galangal, lime juice, and 1 tbsp fish sauce:

You won’t eat the lemongrass, so it’s best to slice it in long diagonal strips that are easy to find and remove from the finished soup. Don’t cut it too small.

Bring the soup to a simmer for 5 minutes and add the remaining ingredients. Mushrooms, chili paste, and peppers:

Simmer another 5 minutes, and add shrimp and thin-sliced scallops:

The shrimp and scallops only need 2-3 minutes, so it’s almost done. Add cilantro:

It only takes a few minutes until everything is cooked, and it’s ready to serve:

Conclusion

Many variations are possible to alter the taste. Chili powder can be substituted for the paste, and ginger root for galangal. The lime juice can be used for the citrus flavor in place of lemongrass. Add more fish sauce for a saltier taste, or more lime juice for sourness.

Tom Kha Gai has always been one of our favorite soups, and it’s very easy to make. It’s even better with scallops and shrimp!

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.