Meat diet reduces risk of pancreatic cancer
Although it didn’t come right out and say it in those words, a large study of 81,922 people published in the current issue of Gastroenterology shows data indicating that a meat diet protects against the development of pancreatic cancer. The researchers looked at consumption of methionine – a stand-in for meat – verses pancreatic cancer. The subjects consuming the most methionine developed pancreatic cancer at less than half the rates of those with the lowest methionine consumption. And these findings followed a dose-response curve meaning that as methionine intake went up, pancreatic cancer went down in all the groups studied, providing even more strength to the correlation.
This study uses data extracted from a couple of large, country-wide Swedish studies: the Swedish Mammography Cohort and the Cohort of Swedish Men. In 1997 researchers gave Food Frequency Questionnaires to men born between the years 1914 and 1948 and to women born between 1918 and 1952 asking them to recall their average dietary consumption over the previous year. Recently researchers from the Karolinski Institute in Stockholm pored through this data and eliminated anyone who reported bizarrely high or low caloric intakes and anyone with cancer. They evaluated the 81,922 people who made the cut for methionine and vitamin B6 intake. They then checked to see how many of these subjects had developed pancreatic cancer over the intervening 7.2 years and correlated these cases with quartiles of methionine and vitamin B6 consumption. It turns out that there isn’t a correlation with vitamin B6, but there is a significant correlation with methionine consumption.
Men who consumed the most methionine had under a third the cases of pancreatic cancer as compared to those who are the least. Women with the highest methionine intake had about half the pancreatic cancer rate as those with the lowest intakes. Men and women eating the most methionine, considered together, had only 44 percent of the rate of pancreatic cancer as compared to men and women with the least dietary intake.
There are a couple of interesting things of note about this study. First, my usual disclaimer: I hate data gathered from Food Frequency Questionnaires because it’s not the most reliable. But, because it is so much less expensive compared to other methods of obtaining data, almost everyone any more uses it, so we have to live with it.
The most interesting thing I found was that only one line in the study talked about what kinds of foods contain a lot of methionine. Buried in the discussion section is this line:
Foods rich in methionine include fish, poultry, meat, legumes, and dairy products.
I don’t know why they put legumes in there because there is no comparison in terms of methionine content between fish, poultry, meat and dairy products and legumes. If you look at a list of all the foods containing methionine, you’ll find the foods at the top of the list are all meats of one sort or another. I ran a search on methionine levels in 100 grams (about 3 1/2 ounces) of various foods and found that poultry contains about 1000 mgs/100 grams, beef, depending on the cut, about 950 mgs/100 grams, fish about the same (although smoked salmon could go as high as 1800 mgs/100 grams). Cheeses run about 850-950 mg/100 grams. (The only thing on the list above meat, fish, poultry and dairy products is dried seaweed at 1150 mgs/100 grams, but when was the last time you ate 31/2 ounces of dried seaweed.) When you get to legumes on the list you find that soybeans are first at about 450 mg/100 grams followed by all kinds of other beans in the 350-250 mg/100 gram range. It’s pretty obvious that meat provides the most bang for the methionine buck. To get the same amount of methionine that you would get in one 12 ounce steak you would have to eat almost 2 1/2 cans of beans.
I’m sure the authors didn’t make much of the sources of methionine for reasons of nutritional politics. No one wants to be responsible for telling people to eat meat, God forbid.
Another intriguing sentence buried in the paper without comment is this one:
We also considered adjustment for other potential confounders, including physical activity, aspirin use, vitamin supplement use, and intakes of alcohol, red meat, coffee and tea; however, because adjustment for these variables did not alter the risk estimates, they were not included in the final multivariate analysis.
In other words, we were sure that we would find that exercise, aspirin, and vitamins would decrease the risk and that alcohol, red meat, coffee and tea would increase the risk. But since they didn’t, we ignored them. With this one sentence we can see the bias of the researchers. Why even look at red meat unless you suspect it as a culprit?
Why would methionine (and by extension, meat) reduce the risk of pancreatic or any other cancer?
According to the authors of the study, methionine’s ability to act as a methyl donor is their best guess. WARNING: DO NOT READ THE FOLLOWING PARAGRAPH UNLESS YOU WANT TO GO BRAIN DEAD. I’ll interpret it after.
Biological plausibility for a relation between methyl group–deficient diets and risk of pancreatic cancer includes a high, specific requirement for methyl group donors the pancreas contains high levels of folate derivates, including 5-methyltetrahydrofolate, which is the product of the reaction catalyzed by 5,10-methylenetetrahydrofolate reductase (MTHFR). 5-Methyltetrahydrofolate serves as the methyl group donor for the remethylation of homocysteine to methionine, thereby ensuring the provision of S-adenosylmethionine necessary for biologic methylation reactions, including DNA methylation. Aberrant DNA methylation patterns may contribute to carcinogenesis, possibly by influencing genomic stability, gene expression, and the susceptibility of genes to muations. Animals fed diets deficient in methyl group donors (methionine and choline) have altered pancreatic acinar cell differentiation and impaired exocrine function of the pancreas. Furthermore, animals treated with ethionine, an inhibitor of cellular methylation reactions, develop acute pancreatitis. Supplementation with dietary methionine has also been shown to suppress the development of pancreatic cancer in the postinitiation phase of pancreatic carcinogenesis in hamsters. A possible role of reduced methyl group availability in pancreatic carcinogenesis is further supported by recent findings from 2 case-control studies showing that a functional polymorphism of the MTHFR gene, C677T, modified the risk of pancreatic cancer. The 2 studies reported that individuals carrying the MTHFR 677TT (variant) genotype, which is associated with decreased enzyme activity, lower plasma folate levels, and elevated plasma homocysteine levels, had a statistically significant approximately 2- to 5-fold higher risk of pancreatic cancer compared with individuals with the 677CC genotype. Another case-control study found no relation between the MTHFR C677T polymorphism and risk of pancreatic cancer. However, separate analyses in the same study showed that pancreatic cancers with reduced MTHFR function due to loss of an MTHFR allele had more DNA hypomethylation and more chromosomal deletions.
What does it all mean?
To understand it you need to understand the process called methylation. Methylation is the addition of a methyl group to another molecule. A methyl group is a carbon with three hydrogen atoms attached to it. Simplistic as this process of attaching a methyl group to another molecule seems, without it there would be no life.
Let’s look at a few examples.
Methylation regulates the fluidity of our cell membranes. The cell membrane needs to be rigid enough to provide support for the cell but at the same time fluid enough so that the receptors and other proteins in the membrane communicate with other cells and with hormones circulating throughout the body. With age, the fluidity of the cell membrane decreases, hindering these processes. The insulin resistance that comes with aging is thought to be in some measure due to the decrease in membrane fluidity and the resulting loss of function of the insulin receptor. The fatty substances making up the cell membrane are called phospholipids. Methylation of these phospholipids increases the fluidity of the membrane.
Methylation helps move fat out of the liver. A consequence of insulin resistance and hyperinsulinemia is an accumulation of fat in the liver, which, if not dealt with, can lead to inflammation, fibrosis, cirrhosis and even liver cancer. Providing plenty of methyl groups helps mobilize this fat.
Each cell in each of our bodies has all the genetic material necessary to produce all the tissues in the body. But liver cells produce more liver cells, lung cells produce other lung cells, stomach cells produce more stomach cells, etc. You wouldn’t want your liver to be producing skin cells, or even worse, your skin growing a liver. Yet skin cells have all the DNA to make liver just as liver has all the DNA to make skin or any other tissue in the body. What activates the DNA in the liver to make liver cells and suppresses the DNA that makes everything else? DNA methylation. Methyl groups on DNA regulate the expression of the genes.
As you might imagine proper methylation is essential for the growth of an embryo. As the cells in the growing embryo divide and multiply, methylation helps them along by determining what cells differentiate into what in order to have a healthy infant.
Methylation basically gives the cells a memory of who they are so that liver cells always produce other liver cells and skin cells more skin cells and so on. Sometimes, however, if the process of methylation breaks down, these cells can lose their ‘memory’ of who they are and start producing cancerous cells instead of the cells they should be producing.
Methionine is the body’s super methylating agent. It acts as a methyl donor, providing a methyl group as needed. It also acts as a team player along with other substances to transport methyl groups from one molecule to another. Methionine comes from the diet, but it can also be produced from homocysteine.
Elevated levels of homocysteine are thought to be a risk factor for cardiovascular disease. If we have plenty of folate, vitamin B12, and vitamin B6 we can easily convert homocysteine into methionine, which is why doctors always recommend folic acid, vitamin B12 and vitamin B6 to treat elevated levels of homocysteine. Although theoretically these substances will reduce homocysteine by converting it to methionine, in my experience and from what I’ve read in the medical literature, vitamin b12 does most of the heavy lifting in this process.
A number of studies have shown that, in general, vegetarians tend to have higher homocysteine levels than do non-vegetarians. Vegetarians get plenty of folic acid, which is found in fruits and vegetables and they get plenty of vitamin B6. What they’re lacking is vitamin B12, found only in foods of animal origin. Based on this fact alone, the case can be made that vitamin B12 is essential in converting homocysteine to methionine.
When one eats meat, one gets plenty of vitamin B12 and plenty of methionine. Homocysteine stays low as the vitamin B12 drives its conversion to methionine, providing even more methylating power.
The densely written paragraph that I quoted from the article makes the case that the cancer-fighting properties of the high methionine diet come about because of the increase in methylating potential the additional methionine brings. I agree, but I think there is another reason as well.
Methionine is a sulfur-containing amino acid. The immune system relies on a steady supple of sulfur to keep it humming along, and sulfur only comes in on sulfur-containing amino acids. Carbs and fats have no sulfur, only oxygens, carbons, and hydrogens. A steady supply of sulfur-containing amino acids is essential to proper immune function. Foods of animal origin are the primary sources of these amino acids, which is another reason vegetarians seem to be afflicted with more than their share of colds and other illnesses. The immune system, in addition to warding off bacterial and viral infections, is constantly on the prowl for cells that have – thanks to problems with methylation – converted into cancer cells. A properly functioning, vigilant, immune system attacks cancer cells and wipes them out before they have a chance to divide and become an actual cancer.
Methionine, then, by methylation and by immune enhancement should decrease the incidence of not just pancreatic cancer but other cancers as well. And methionine is found in meat. So, meat consumption should decrease the incidence of cancer because it supplies a large load of methionine. Why didn’t they just say so in the article. Nutritional correctness, I suppose.
I, however, am far from ‘nutritionally correct,’ so I will say it.
EAT MEAT–PREVENT CANCER!