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:
- The risk is higher for fresh pork than processed pork. Processed pork is generally cured or smoked, both steps that are anti-microbial.
- Eating fiber, which increases gut bacterial populations and enhances immune vigilance of the gut, is protective.
- 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:
- Pork tapeworm, Taenia solium, not only causes a parasitic infection of the intestines (the worm is typically 2 to 3 meters long) but also the larvae can infect the brain and muscles, causing the disease Cysticercosis which is a common cause of seizures.
- The roundworm Trichinella spiralis causes trichinosis. As in tapeworm infections, the mature worms are largely confined to the intestines where symptoms include nausea, heartburn, dyspepsia, diarrhea, and eosinophilia but larvae can migrate through the body, producing edema, muscle pain, fever, and weakness. The greatest danger is if the larvae reach the brain, where they can cause “serious neurological deficits (such as ataxia or respiratory paralysis), and even death.” Death results from a rare form of stroke, myocarditis, encephalitis, or pneumonia.
- Other helminths including pinworms and hookworms, and ascarid worms. [14]
- Listeria monocytogenes [24].
- E. coli, Salmonella, and Staphylococcus aureus [25].
- Yersinia enterocolitica, which causes gastroenteritis, is nearly always transmitted through pork.[28]
- Brucella spp., the bacteria which cause brucellosis or undulant fever.
- Various viruses, including porcine herpesvirus, rotavirus, parvovirus, and circovirus. Some influenza viruses, such as the famous “swine flu,” have been known to be transmitted from pigs to humans. SARS is an example of a coronavirus which was transmitted from pigs to humans. PERVS (porcine endogenous retroviruses) may also be infectious in humans; of three subgroups of infectious PERVs (PERV-A, PERV-B, and PERV-C), PERV-A and PERV-B have been shown to infect human cells in culture. [24][26]
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:
- Pork: Did Leviticus 11:7 Have It Right?, Feb 8, 2012
- The Trouble with Pork, Part 2, Feb 15, 2012
- The Trouble With Pork, Part 3: Pathogens, Feb 22, 2012.
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.
via this link:
On the persistence of HEV; the examples of persistence you cited seemed to involve either HIV or transplants, with the common theme of immunosupression (malnutrition could account for this in the Egtptian example?). Hep E seems to be an acute (non-persistent) infection like Hep A in immune-normal cases.
However the damage resulting this kind of insult can result in lasting inflammation if other factors, such as alcohol and/or high PUFA are also promoting inflammation.
This is what many of the PUFA liver studies look at; the effect of fats on the resolution or otherwise of liver inflammation caused by a single insult (drug or transection).
Also studies on the antifibrotic effects of retinol, niacinamide, colchicine, etc use this model.
So the question is really whether we should vaccinate children against HEV? http://www.ncbi.nlm.nih.gov/pubmed/17329696
But of course you’d not only be vaccinating them against Hep E, you’d be adding three (or 12? there are 4 genotypes) more vaccines (and their adjuvants) to an already overloaded schedule. The experiment cited lasted a median 804 days; it does not show that childhood vaccination confers protection many years`later; there are enough vaccines already that fail to protect when they are needed (why would the B cells always keep making antibodies against an old threat, when multiple novel vaccinations are subjecting them to fresh alarms? Might not this repeated “bait and switch” induce some degree of immune tolerance to the earlier antigens, which after all were not associated with the kind of “self” cell damage that keeps immune cells alert after real infections?).
There would not even be the protection of “herd immunity” from partial or temporary efficacy of a Hep E virus, because the virus can incubate in animals.
I am not an anti-vaccinationist, instead I think there are valuable vaccines, useless vaccines, and dangerous vaccines (as with any medical products), and that there is no will at present to use the advances of modern immunology – a science that has probably expanded more than any other in the last 2 or so decades – to distinguish between them or improve them. Once a vaccine is introduced, it is very hard to remove it from the schedule just because it turned out to be far less effective than originally thought, partly because development of alternatives would have ceased with its acceptance, but mainly for emotional and political reasons.
Vaccines are an example of politicized drugs, drugs which are sold and paid for by government decree. It is harder to repeal bad decisions through the marketplace, which is where the initial overvaluation of drugs is usually corrected.
Well said George.
Solution to the problem of pork, DON’T EAT IT! Why take the chance. It’s like putting a bullet in the chamber of a revolver, pointing it at your head and pulling the trigger. NO, it’s like putting 4 bullets in a six shot revolver, pointing it at your head and pulling the trigger. Maybe 5 bullets and for some 6.
Don’t be stupid, don’t eat pork.
Paul: Great to hear that you can achieve good health with just fish and eggs! I’m going to try that approach and see how it goes. I don’t have access to quality meat and don’t like handling/cooking meat anyway. Besides, there are too many other good things to eat! Again, many, many thanks for all you both do – I am very grateful!
Dan: Yes, I agree. It’s not worth the risk.
Lamb – hydatids
Beef – mad cow disease
Grains – coeliac and allergies, phytates
Legumes – FODMAPS, allergens, phytates
Fruit – FODMAPS, fructose, pesticides
Honey – botulism, fructose, galactose
Dairy – BCM7, galactose, immunoglobulins
Shellfish – vibrio (very bad news if you have hemochromatosis)
Fish – thiaminase, mercury
Greens – pesticides, oxalate
Water – giardia, cholera, chlorine, prozac, contraceptives
just about everything has lectins.
Just about anything you eat that’s nutritious might have your number on it IF
– you don’t prepare it appropriately – cooking or pickling
– you don’t look after your health or nutrition in general
– food production standards in your part of the world have slipped
Keep an eye on those three things and you should be ok.
Except that pig meat and shellfish have the added danger of being condemned by God. Avoiding them should be more important than how they are cooked and handled.
If you wish to avoid the wrath of the Levitican God, you must obey many more regulations than just the ban on pork and shellfish.
This is a hard God to please, but He does seem to know a thing or two about food.
And, of course, a piece of pork that you cook properly yourself might be less deadly than a chicken salad, or even a cucumber salad, that you buy ready-made.
I’m not going to worry about the odd bacon rasher or pork rib, but I’m even less convinced than I was before that a pork-based diet, a la Optimum Health, is the best way to eat.
Remember that low-carb doctors in Banting’s day thought pork was a carbohydrate (because it’s sweet). Maybe they had an intuitive insight they could only express symbolically.
Hello,
I wondered if anything in your series on Pork would suggest that we should not make broth/stock from pork trotters, bones etc..
I would like to make a Tonkatsu broth to use for soup/noodle dishes etc… and I am concerned whether I should be making pork broth etc.
Hi BigRob,
In general bone marrow is less exposed to pathogens than blood. I would rinse the bones thoroughly before cooking and then cook them thoroughly, making sure the internal temperature in the marrow is high. The pot should be covered so that any parts of the bone not submerged in water are exposed to steam.
PS – Shou-Ching recommends that you simmer at very low heat for 1 hour, then discard the water, then return the bones to the pot with fresh water and some salt and bring to a boil. While it is simmering the second time, scrape the bone marrow out of the bones with chopsticks so that it separates from the bones and floats in the water. After 3-4 hours, you have a nice fatty/marrow-rich broth.
Thank you, in general Tonkatsu broth for noodles is cooked for 6 to 8 hours and the bones are pre-rinsed and rinsed again once the bones and trotters have come to a boil. Thank you
Hi Paul,
How about marrow in the form of gelatin powder? I use it for fruit jello because I don’t make broth as often as I should. Of course it isn’t cooked for hours like real broth but just dissolved in boiling water, but do you think the processing of the powder should take care of pathogens?
When I first started buying gelatin, I was deciding between pork and beef versions, but felt whatever risk would be from mad cow disease because we don’t know where they take the marrow from. Would you still say that pork gelatin is safer than beef gelatin, or should I really just make broth more often? Thanks!
Hi SC,
I like the natural broth. I think beef gelatin is pretty safe, there are very few cases of mad cow disease and the infectious agents are in the brain and nerves, not the skin or joints where gelatin comes from. Pork gelatin ought to be very safe too but I think beef gelatin should be even safer.
Eat pork and you could have worms in your brain, like this woman, watch the video:
http://www.youtube.com/watch?v=sJCh7bR1Nf0
Pork, the deadly meat.
Paul, what I started doing is smoking my pork for an hour or so and then finishing with a pressure cooker for about 30 min.
I think that should take care of the bugs. What do you think?
thanks!
http://faculty.ccbcmd.edu/courses/bio141/labmanua/lab19/lab19.html
“a. Moist heat
Moist heat is generally more effective than dry heat for killing microorganisms because of its ability to penetrate microbial cells. Moist heat kills microorganisms by denaturing their proteins (causes proteins and enzymes to lose their three-dimensional functional shape). It also may melt lipids in cytoplasmic membranes.
1. Autoclaving
Autoclaving employs steam under pressure. Water normally boils at 100°C; however, when put under pressure, water boils at a higher temperature. During autoclaving, the materials to be sterilized are placed under 15 pounds per square inch of pressure in a pressure-cooker type of apparatus. When placed under 15 pounds of pressure, the boiling point of water is raised to 121°C, a temperature sufficient to kill bacterial endospores.
The time the material is left in the autoclave varies with the nature and amount of material being sterilized. Given sufficient time (generally 15-45 minutes), autoclaving is cidal for both vegetative organisms and endospores, and is the most common method of sterilization for materials not damaged by heat.”
Hi James,
Yes, that should work. It’s the internal temperature of the meat that matters, if it goes high enough then the germs will be killed.
Hey, Dr Mercola has picked up this series!
“As reported by Dr. Paul Jaminet, a trained astrophysicist and his wife Shou-Ching, a Harvard biomedical scientist, who together authored the book Perfect Health Diet”
http://articles.mercola.com/sites/articles/archive/2012/03/01/pork-consumption-prohibitions.aspx?e_cid=20120301_DNL_art_3
Here is some evidence that carnosine from meat is good for the liver and inhibits parasites:
Comp Biochem Physiol B Biochem Mol Biol. 2002 Mar;131(3):535-42.
Effects of carnosine on bilharzial infestation in hamsters: biochemical and histochemical studies.
Soliman KM, Abdel Aziz M, Nassar YH, Abdel-Sattar S, El-Ansary A.
SourceDepartment of Biochemistry, Faculty of Medicine, Cairo University, Cairo, Egypt. solimank2002@yahoo.com
Abstract
We tested the ability of carnosine to improve some liver disorders induced by Schistosoma mansoni parasite in hamsters (Mesocricetus auratus). Results indicate that parasitic infestation induced elevation in serum alkaline phosphatase, gamma-glutamyl transferase, aspartate aminotransferase and procollagen III peptide as a marker of liver fibrosis. Administration of carnosine (10 mg/day) for 15 days either concurrent with infection, 2 and 4 weeks post-infestation was effective in reducing differential worm burden. It was also effective in renormalizing blood glucose level depending on the time course. The most evident effect of carnosine was on serum procollagen III peptide level, which was lowered in infested groups treated with carnosine. Histopathological studies confirmed the potential use of carnosine for intervention in schistosomiasis.
PMID: 11959036 [PubMed – indexed for MEDLINE]
J Egypt Soc Parasitol. 2000 Aug;30(2):455-68.
Effect of carnosine administration on certain metabolic parameters in bilharzial infected hamsters.
Soliman KM, el-Ansary AK, Mohamed AM.
SourceDepartment of Biochemistry, Faculty of Medicine, Cairo University, Egypt.
Abstract
This study was designed to test the ability of carnosine to cure the metabolic disturbances induced by Schistosoma mansoni parasite. Results indicate that parasitic infection caused elevation of liver weight/body weight of S. mansoni infected hamsters, induced lipid peroxidation and reduced glycogen level. Moreover, the adenylate energy charge (AEC), ATP/ADP and ATP/AMP concentration ratios were markedly lower in infected hamsters. Administration of carnosine (10 mg/day) for 15 days either concurrent with infection, 2 and 4 weeks post exposure was effective in reducing worm burden and egg count only when given at the time of infection. It was also effective in renormalizing most of the measured parameters confirming the glycogen repletion, the antioxidant and AEC correcting actions of carnosine.
PMID: 10946508 [PubMed – indexed for MEDLINE]
Comp Biochem Physiol B Biochem Mol Biol. 2001 May;129(1):157-64.
Effect of carnosine administration on metabolic parameters in bilharzia-infected hamsters.
Soliman K, El-Ansary A, Mohamed AM.
SourceBiochemistry Department, Faculty of Medicine, Cairo University, Cairo, Egypt. solimank2002@yahoo.com
Abstract
Carnosine is a naturally occurring dipeptide (beta-alanyl-L-histidine) found in muscles, brain and other tissues. This study was designed to test the ability of carnosine to offset metabolic disturbances induced by Schistosoma mansoni parasitism. Results indicate that parasitic infection caused elevation of liver weight/body weight in S. mansoni-infected hamsters, induced lipid peroxidation and reduced glycogen levels. Moreover, adenylate energy charge (AEC) and ATP/ADP and ATP/AMP concentration ratios were markedly lower in infected hamsters. Administration of carnosine (10 mg/day) for 15 days concurrent with infection effectively reduced worm burden and egg count. Administration of carnosine 2 and 4 weeks post-exposure only partially ameliorated the S. mansoni effects on metabolism. Carnosine treatment also normalized most of the parameters measured, including glycogen repletion, the antioxidant status and AEC. These finding support the use of carnosine for possible intervention in schistosomiasis.
Thank you for posting all this. I haven’t eaten pork in over 20 years, and this reinforces my willingness to avoid it.
Now, I just need to find a glucosamine/chondroitin/msm supplement that is pork free!
Hi Paul,
Ned Kock claimed to have info that “exonerates pork” (http://perfecthealthdiet.com/?p=5569#comment-55122)
I was just curious your take on it and if it alters your view at all?
http://healthcorrelator.blogspot.com/2012/02/does-pork-consumption-cause-cirrhosis.html
Thanks!
Mark
Hi Mark,
I found it to be good analysis, but a little tangential to the issues I was exploring. Pork consumption is indeed positively related to lifespan, but that’s true of all animal food consumption. Yet, as the recent Harvard study shows, when you go down to individuals you can generate a negative association for pork … the “ecological fallacy” shows that the national and individual correlations can be opposite … but even at the individual level the result is highly dependent on how data is aggregated and what adjustment factors are included in regression analysis. So it’s still hard to say the results of observational studies, even with data at the individual level and acquired prospectively, are decisive.
I was looking at specific correlations with cirrhosis mortality and hepatocellular carcinoma mortality, and trying to find an explanatory mechanism. I don’t think Ned’s analysis excludes pork as a carrier of Hep E virus and HEV as a potential cause of those health problems.
So, is it clear that we should exclude pork from the diet? No, and in that sense Ned helps exonerate it. Pork may have dangers, but every food can potentially increase the incidence of certain diseases. On the other hand, the HEV evidence does show that pork liver and blood and intestines are particularly dangerous, and that cooking is probably very important. That’s useful info.
He’s saying that obesity is the risk factor for cirrhosis. This is true of NAFLD, but I do not believe it is true for alcoholic cirrhosis, nor does it seem to be true for HCV-related cirrhosis. I see cases of both from time to time, never in really obese people and often in the underweight. Total calorie intake over 2,000 kC per diem (FOOD calories, not booze) is said to be protective against alcoholic liver disease, drinking instead of eating is bad news for the liver – pretty much the opposite of NAFLD.
Note that alcohol can cause reductive stress – when NADH is too high and there is not enough NAD+ for oxidation.
Choline can protect against reductive stress by donating a methyl group to create methane (CH3 + H+ = CH4) which is dispersed out of the cell.
“Pathways of Alcohol Metabolism
Alcohol is broken down (i.e., metabolized) in the liver primarily through two pathways: the alcohol dehydrogenase (ADH) pathway and the microsomal ethanol–oxidizing system (MEOS). In people who consume alcohol at moderate levels and/or only occasionally, most of the alcohol is broken down by ADH, an enzyme found in the fluid that fills the cell (i.e., the cytosol). ADH converts alcohol (chemically known as ethanol) to acetaldehyde, a toxic and highly reactive molecule. During this reaction, hydrogen is removed from the alcohol and transferred to a molecule called nicotinamide adenine dinucleotide (NAD), converting it to reduced NAD (NADH). As described in the main article, NADH participates in numerous other metabolic reactions, passing on the hydrogen to other compounds, and excess cellular NADH levels have harmful effects on those cells.”
http://pubs.niaaa.nih.gov/publications/arh27-3/220-231.htm
A Person’s Nutrition Affects Liver Function
Malnutrition, regardless of its causes, can lead to liver damage and impaired liver function. For example, children in underdeveloped countries whose diets do not contain enough protein can develop a disease called kwashiorkor. One symptom of this disorder is the accumulation of fat in the liver, a condition known as fatty liver. Studies performed during and after World War II indicated that severe malnutrition also could lead to liver injury in adults. However, in these cases other factors, including exposure to certain toxins or parasites that are prevalent in war–ravaged or underdeveloped countries, may have exacerbated the relationship between liver injury and poor nutrition.
Because malnutrition also is common in alcoholics, clinicians initially thought that malnutrition, rather than alcohol itself, was responsible for alcohol–induced liver injury. Over the past 40 years, however, a more balanced view has evolved. Studies in humans, primates, and rodents have established that alcohol can cause liver damage even in well–nourished people (Lieber 1992). Moreover, controlled studies using hospitalized participants have demonstrated that even subjects receiving an enriched diet could develop fatty liver if the carbohydrates in the diet were replaced with alcohol. Finally, epidemiological analyses have found a close correlation between per capita alcohol consumption and the likelihood of cirrhosis, indicating that alcohol itself contributes to liver disease.
It is becoming clear that nutritional effects and the toxic effects of alcohol often are intertwined at the biochemical level. For example, alcohol induces the MEOS to break down alcohol, but this breakdown also leads to the previously mentioned waste of energy observed in alcoholics who replace carbohydrates in their diet with alcohol. Similarly, alcohol promotes the breakdown of nutrients such as vitamin A, of which alcoholics may already consume too little with their diet.
“For example, alcohol induces the MEOS to break down alcohol, but this breakdown also leads to the previously mentioned waste of energy observed in alcoholics who replace carbohydrates in their diet with alcohol.”
A waste of energy (the alcohol going through MEOS is not supplying acetyl-CoA) is not conducive to obesity.
Also, liver disease impairs fat absorption.
Here is another angle on choline; I think what might be going on here is not that unsaturated phospholipids are antioxidants, but that they are antireductants, that is, they are proton buffers (like cardiolipin, which is also an unsaturated phospholipid, found in mitochondria).
They are decreasing the excessive reduction of NAD+ by soaking up some of the H+ produced by alcohol dehydrogenase.
Both the whole molecule (as buffer) and any choline released from it (methyl donation) can soak up protons.
Cardiolipin as proton buffer:
During the oxidative phosphorylation process catalyzed by Complex IV, large quantities of protons are transferred from one side of the membrane to another side causing a large pH change. CL is suggested to function as a proton trap within the mitochondrial membranes, thereby strictly localizing the proton pool and minimizing the changes in pH in the mitochondrial intermembrane space.
This function is due to CL’s unique structure. As stated above, CL can trap a proton within the bicyclic structure while carrying a negative charge. Thus, this bicyclic structure can serve as an electron buffer pool to release or absorb protons to maintain the pH near the membranes.[7]
http://en.wikipedia.org/wiki/Cardiolipin
PPC.
One of the harmful consequences of alcohol breakdown by the MEOS is the formation of ROS, which among other effects can cause lipid peroxidation. Not all fat molecules, however, are equally sensitive to peroxidation. For example, polyunsaturated fats are more susceptible than monounsaturated or saturated fats. With fat molecules containing additional phosphate groups (phospholipids), however, the opposite may occur—polyunsaturated phospholipids may be particularly resistant to peroxidation. This hypothesis is supported by studies evaluating the effects of the compound polyenylphosphatidylcholine (PPC) in animal models. In these studies, PPC, which is a mixture of molecules known as phosphatidylcholines (extracted from soybeans), prevented lipid peroxidation (Aleynik et al. 1997) and attenuated the associated liver injury in rats that had been treated with hepatic toxins (Ma et al. 1996). Furthermore, PPC decreased oxidative stress (Lieber et al. 1997) and prevented the development of alcohol–induced cirrhosis in baboons (Lieber et al. 1994). Clinical trials currently are being conducted to test the effectiveness of PPC in the treatment of alcoholic liver disease.
http://pubs.niaaa.nih.gov/publications/arh27-3/220-231.htm
What about pancreatic enzymes from freeze-dried porcine pancreas? Specifically Dr. Ron’s New Zealand pigs product. I wonder if viruses could be in those?
Hi Janelle,
I don’t know. Do they purify the enzymes, or do they include pig tissue?
No it says six capsules provide the equivalant of one ounce of fresh raw whole organic pancreas taken from grassfed inspected animals.
Hi Janelle,
There’s probably some risk, but I don’t know how high it is.
How paranoid can you get,im surprised any of you take the chance of getting out of bed. What enjoyment can you get out of eating if your worrying what’s in it.A well balanced common sense diet is sufficient
If we stressing over food, it isn’t helping much. But being a incredulous jerk surely contributes to ill-health.
“A well balanced common sense diet is sufficient”
Define “well balanced”, define “common sense”.
Why is there always some one that has to sink to personal insults and stupid comments.
Please try to keep your comments factual
Most people these days surely know what a well balanced common sense diet is, its rammed down our throats all the time from the media.
But I suppose anyone who is not well balance or does not have any common sense would have difficulty in defining it.
Alan, it looks like you started the name-calling with “paranoid.” Please relax and be courteous.
I accidentally stumbled on this site and cant think of another suitable word.
All of us are paranoid about one thing or another and wouldn’t consider the comment being an insult, derogatory or rude.
However most people would think calling someone a incredulous jerk would be crossing the line a bit.
Wel-balanced is typical code language for “everything in moderation”. Including grains, fructose, legumes. Is that your take, Alan, for well-balanced?
Incredulous means doubtful, calling folks paranoid generally means you doubt their reasons for concern. Would you care to contribute why you believe Mr. Jaminet’s research in this post is over-wrought worry making?
Coming to this thread with the insult “im surprised any of you take the chance of getting out of bed” is very much a jerk thing to say to anyone you don’t know. Did you have an invisible smiley when you typed it that would put that statement in a more humorous tone? If so, I apologize for reading your comment as straight and serious.
I have no idea what grains, fructose or legumes are. Your definition of paranoid is different from Wikipedia ie paranoid is a thought process believed to be heavily influenced by anxiety or fear, often to the point of irrationality and delusion.
Incredulous means unwilling to admit or accept what is offered as true.
I’m sure if I delved into it deep enough and analysed the air we breath I could find a reason to live in a oxygen tent
or, you might find a reason to support your city’s efforts to clean up air pollution, which I don’t think anyone doubts is a cause of disease.
http://en.wikipedia.org/wiki/Air_pollution
Whole cultures avoid pork and I don’t believe this is associated with a greater rate of paranoia, though I could be wrong.
On the other hand, perhaps assuming that everyone who criticises a dietary blog actually has an interest in diet is a little bit paranoid, when they could just be an opinionated rubbernecker.
This is pretty interesting stuff and ultimately, in a house where I have Psoriasis and my wife has Multiple Sclerosis so we are hitting a 2 for 2 autoimmune disease average we are certainly going to drop pork.
We have recently been eating a fair bit of pork after going more fully Paleo after a detour into Veganism but where I am comfortable with grass fed beef I am not really happy with pasteured pork and most of our bacon was just standard supermarket fair so… the omega 6 and now these issues mean it is out.
“Tis better to have had bacon and lost it than never to have had bacon at all.”
Looks like we can have the occasional bit of streaky bacon from the pork belly of pastured animals anyhow, just have to cook it super crispy and make it a treat for birthdays and christmas.
I am off home to mourn bacon some more.
Love the quoted line Marcus! +1
I am still hung up on Leviticus 11:7. Folks in those days didn’t have a clue about viruses. But consider this: It is probably best to not eat the meat of animals that have similar immune systems as humans, like pigs and monkeys. Especially if the pigs are treated and fed poorly, they just become reservoirs of degenerate diseases waiting to jump to human beings.
Here’s a new article on Hep E in domestic pigs:
http://hepatitiscresearchandnewsupdates.blogspot.co.nz/2012/10/human-hepatitis-threat-present-in.html#.UGy_I5jA8sc
Considering the oral-fecal connection, it is interesting that, from what I have read, pigs are very fastidious in their natural evacuation habits. They identify a specific area in their environment and scrupulously use it as their ‘toilet’, avoiding contaminating the rest of their territory.
Hi Paul,
I don’t eat much pork because I prefer meat rare cooked but do use natural Armour Thyroid which is made from pig thyroid glands. Any thoughts as to whether or not this is risky from a pathogen point of view?
Hi Adrienne,
Good question. I don’t know how they process their thyroid extracts so I can’t say.
A quick Google search turned up somebody who blames Armour thyroid for a kidney infection: http://forums.bettermedicine.com/showthread.php/9671-armour-thyroid-caused-kidney-infection
Here’s an article: http://www.realthyroidhelp.com/forums/viewtopic.php?f=2&t=3448&start=0
I couldn’t find anything in Pubmed. It doesn’t seem to be on the radar of endocrinologists as an issue.