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Okay, his first name is not Val. I added that. Whatever I can do to squeeze in an 80’s movie photo, damnit I’m willing to do it! He was a “real genius.”

Let’s focus more on McCully. It’s an Irish name. It’s St. Patrick’s Day. Pretty awesome huh? Yeah I know.

What’s the difference between Mick Jagger and an Irish farmer? Mick Jagger says ?Hey you, get off of my cloud. An Irish farmer says, ?Hey McCloud, get offa my ewe!

Okay, serious faces now everyone. Thinking caps?

Kilmer McCully was one of ‘those? good scientists who challenged the status quo about heart disease. Instead of merely looking at the hypothesis that saturated fat raises cholesterol and then cholesterol jumps into coronary arteries because it has nothing better to do ? meanwhile nodding his head, repeating the word ‘statin? in a catatonic state, and drooling all over his desk?

?Kilmer McCully did what a real scientist does, which is challenge a theory with more loopholes and contradictions than one can even begin to imagine (and was of course ostracized and cast into scientist purgatory for his heretical findings). Contradictions like, I don’t know, the fact that Australian Aboriginal men have low cholesterol (average less than 190 mg/dl), perfect blood pressure (average 125/77), a BMI of 23.2, and 5,000% more heart disease than butter-lovin? and higher cholesterol-havin? French women (that’s 50 times more for you non-mathorexics).

McCully noticed that there was no connection between cholesterol and heart disease, so he actually did do some real scientific work and found something that did play a role in heart disease ? elevated levels of homocysteine.

Homocysteine is a type of cysteine found in milk. But not just any milk. Specifically, Harvey Milk. It’s a joke, relax. I’m not going to eat junk food and start shooting people. I’m very sensitive to the gay community. I cried watching Milk and cried even harder watching Brokeback Mountain while the guy in front of me laughed and said ?anus? every time they said the name ?Ennis.

Homocysteine is a by-product of methionine metabolism. The amino acid methionine is supposed to be converted to homocysteine and then into cysteine. However, this conversion requires an abundance of three key nutrients: folic acid, B6, and B12 ? as well as adequate thyroid. Without those factors, homocysteine levels rise, predispose one to heart disease, cause inflammation, and accelerate the aging process.

But McCully was a real scientist with the ability to think intelligently, so I’m sure he didn’t realize the?role of thyroid in any of this?

?For many years deficiency of thyroid hormone secretion has been known to predispose to arteriosclerotic heart disease. In persons with a serious deficiency of thyroid hormone, the ability of the cells of the body to use oxygen is impaired. The basal metabolic rate is slowed in hypothyroidism, and the liver begins to make increased quantities of cholesterol and triglycerides. As a result the cholesterol and lipoprotein levels become elevated, and the risk of coronary heart disease increases? Subtle or marginal deficiencies of thyroid hormone, detected by measuring basal metabolic rate, are found to be widespread in populations with a high risk of arteriosclerotic heart disease.

Hmmm, sound familiar?? You can read about the importance of’thyroid and metabolism in health and?disease in how to RAISE YOUR METABOLISM.

But the important lesson here from a dietary perspective is pretty simple, and something that many would agree upon to at least some degree. And that would be that eating a diet with an excess of methionine and a bunch of B-vitamin depleted foods with it is a bad combination. This basic idea is not something new. Researchers noted long before the discovery of homocysteine that food is not metabolized correctly when B-vitamin intake is inadequate?

Robert McCarrison, while studying deficiency of various B-vitamins noted?

??in the absence of vitamins or in their inadequate supply, neither proteins nor fats nor carbohydrates nor [minerals] are properly utilized; some are largely wasted, while others yield products harmful to the organism.

While Roger J. Williams pointed towards a similar conclusion. This pretty much says it all?

?A large amount of information, based upon carefully controlled scientific experiments, indicated very strongly that vitamin B6 is another key nutrient which is often present in inadequate amounts in the cellular environment of those whose arteriosclerosis is extreme. Experiments with monkeys have yielded clear-cut results. When they are rendered vitamin B6 deficient, they develop arteriosclerosis rapidly. When monkeys are fed diets supplemented with vitamin B6, they have much lower levels of cholesterol in the blood than when these diets are not supplemented. The animals on the supplemented diet eat much more food than the others, and since their diet contains cholesterol, they get far more cholesterol into their bodies. This does not matter, however; the extra vitamin B6 they get allows them to dispose of the surplus, with the result that their cholesterol blood levels are not as high as in those animals that consume less cholesterol.


?High or low amounts of fats or carbohydrates are not atherogenic providing supportive nutrients, specifically pyridoxine (vitamin B6), are present. But if pyridoxine is not adequately provided, regardless of the relative amounts of fat or carbohydrate, the diet will be atherogenic.

Of course the joker in all of this is that just eating nutritious foods rich in say, B-12, isn’t necessarily going to give you high levels of vitamin B-12. The human body unfortunately is much more complex. But it certainly won’t hurt to eat vitamin-rich foods in preference to white stuff ? especially white sugar and high-fructose corn syrup which, unlike fortified flour and ?enriched? rice, contains absolutely no nutrients whatsoever ? real or synthetic.

But the concept is simple nonetheless. In the straightforward words of McCully?

?The dietary factors that determine whether blood homocysteine levels are elevated are the total methionine content of the dietary protein and the content of vitamins B6, B12 and folic acid in the diet.

McCully isn’t a big fan of fats either really, as they do nothing to offset the methionine content of the typical Western diet because they contain virtually no B-vitamins just like refined carbohydrates. Of course, I’ve pointed out many times that your typical American eats up to 50% of calories from refined carbohydrates and another 35% or so from fats, leaving little room for food containing water soluble vitamins.

One solution to this is of course to, as a general rule, consume less methionine-rich animal protein. Methionine restriction in mice, not surprisingly, has shown tremendous life extension. Ray Peat, another real scientist, has postulated that many of the longevity-enhancing effects of calorie restriction have nothing to do with the amount of energy ingested, but more to do with the total quantity of methionine and other amino acids in a similar pro-aging class. And as I’ve argued before over the controversial findings in The China Study in the past, it should be no surprise that animal protein increases health risks when added to the diet of people eating more than half of their calories from refined carbohydrates like rice and noodles.

Methionine is needed in substantial quantities during the growth period of life when we are adding lots of new lean tissue. Perhaps this is why methionine content is so high in say, eggs. Methionine all goes to the muscles and organs where it is concentrated. So, as a general rule, eating muscles and organs naturally lends itself towards a much higher total methionine intake, although not all meats are created equal.

But, as we reach adulthood and no longer have such a high requirement for total protein or methionine, in a conversation about a general ?ideal? diet (and such generalizations should never be made for something so individual as a person’s immediate nutritional needs ? a major mistake the government makes is not just their dietary recommendations alone, but the fact that they MAKE BROAD, SWEEPING DIETARY RECOMMENDATIONS in the first place), there would be no harm in eating ?mostly plants? with plenty of methionine-free gelatin-rich broths in lieu of giant T-bones or perpetuating the newfound American infatuation with lean chicken breast.

There’s no reason to fear methionine of course. You need some, and when you are going to eat some animal foods it’s probably best to get after the most nutritious of the bunch, such as B-vitamin superhero organ meats (I have pate in my fridge, which also protects against nitrate deficiency!), whole eggs, shellfish, and dairy products ? particularly cheese which contains a lower concentration of the ?bad? amino acids? that part is in the whey that bodybuilders and Mercola are consuming in outrageous quantities. Same thing with egg whites vs. the yolks.

And well, you already know how I feel about eating a lot of refined carbohydrates. What I like about McCully’s theory is that it is much more congruent with the observation in all cultures of a widespread health demise occurring when each society was introduced to refined carbohydrates for the first time, with or without other dietary and lifestyle factors.

Anyway I’m outta here. All this health food talk on St. Patty’s Day is filling my mind with visions of ice-cold Guinness. Here are some other McCully quotes to make your head hurt. No wonder so few people caught on to his theory. He wrote it in language that only a PHD already tied to the cholesterol theory could possibly understand. The final quote about unifying the respiratory, oncogene, and genetic theories of cancer is particularly painful, but interesting nonetheless?

?Current thinking about how homocysteine causes plaques in the arteries theorizes that a buildup of homocycsteine in the body leads to overproduction of a highly reactive form of homocysteine that causes LDL to become aggregated. This reactive form, homocysteine thiolactone, is made from methionine in the liver by an enzyme that participates in the protein formation and by other less well-understood processes. The LDL-homocysteine thiolactone aggregates are released into the blood from the liver. Then these aggregates are taken up by macrophages of the artery wall, many of which are derived from wandering monocytes of blood, to form foam cells of early arteriosclerotic plaques. These foam cells degrade the LDL-homocysteine thiolactone aggregates and release fat and cholesterol into developing plaques. The foam cells also release homocycsteine thiolactone into surrounding cells of the artery wall, affecting the way cells handle oxygen. As a result, highly reactive oxygen radicals accumulate within cells, damaging the lining cells of arteries, promoting blood clot formation and stimulating growth of arterial muscle cells which form fibrous tissue, mucoid matrix and degenerative elastic tissue.

The homocysteine theory explains why populations that consume foods of animal origin with abundant methionine and foods that are highly processed, refined and preserved with depletion of B vitamins are susceptible to arteriosclerosis.

p. 86

?Another very interesting feature observed in cell cultures from children with homocystinuria is the distinctive pattern of growth, which resembles the pattern of growth of cancer cells in culture. Furthermore, the muscle cells of arteries grow in a similar pattern in early arteriosclerotic plaques. As explained in Chapter 2, the 19th century German pathologist Rudolf Virchow likened the increased numbers of muscle cells in atheromas to tumors of the blood vessels. In some way, abnormal homocysteine productions induces cells to lose control of growth processes, causing growth of muscle cells in arteriosclerotic plaques. Recent experiments have shown that homocysteine damages cultured endothelial cells and increases the growth of smooth muscle cells. These effects on the cells of artery walls explain in a general way the early phases of production of arteriosclerotic plaques.

p. 96

?The origin of arteriosclerosis is now understood to be a toxic effect of a by-product of protein breakdown, the amino acid homocysteine. The importance of fats and sugars in the genesis of the disease is now understood to be related to loss of vitamins B6 and folic acid through processing, refining and preservation of foods, creating an imbalance between the abundant methionine of foods of animal origin and the amount of these essential vitamins necessary to prevent a buildup of homocysteine in the body.

p. 213

?In summary, the discoveries of the role of homocysteine thiolactone, thioretinamide, thioretinaco and thioco in malignant cells offer a new way to unite the respiration, genetic and oncogene theories of the induction of cancer. The loss of thioretinaco ozonide from cell membranes leads to the abnormal respiration of mitochondria in malignant cells, with secondary accumulation of reactive oxygen radicals. The loss of thioretinaco also allows excessive synthesis of homocysteine thiolactone from the methionine, causing aggregation and altered activation of nucleoproteins, abnormalities of cellular membranes, altered immunological recognition and increased growth potential through increased activation of oncogenes and increased formation of thioco.