Why Ray Recommends Eating Lots Of Calcium

[Elvie]

@Giraffe - for some reason I think that you'll enjoy it, I don't know exactly why but I guess that the presentation has some of your style..

--
For the angels that are not willing to watch the whole thing, skip to 7:42.
And for those that were interested, open that Youtube channel, it has many relevant presentations related to vit D. For example, Michael Holick's Q&A session about sun and supplements (audio gets better).

Thank you very much. I always learn something new from your posts!

 

[Amazoniac]

Thank you very much. I always learn something new from your posts!

!

 

[Amazoniac]

Calcium and Magnesium: Requirements, Health Benefits, Supplement info

"To help boost calcium levels in individuals with chronically low calcium absorption, supplementing Vitamin B5 (pantothenic acid) can be helpful in inhibiting the antagonistic action of phosphorus (if high)"

"Contrary to the claims of uninformed sources, Low Stomach Acid does not pose a problem with calcium absorption, as even patients with no acid production (achlorhydria) are able to absorb calcium regardless of whether it comes in the form of calcium citrate, calcium carbonate, or milk.
However low stomach acid affects the proper utilization of calcium, frequently resulting in calcium being deposited into soft tissue instead of bone, which as mentioned, increases the risk for developing arthritis, spurs, bone loss, cerebral and cardiovascular calcification, as well as other physical and mental disorders."

 

[Amazoniac]

William F. Koch Research Site

The position of calcium as an essential in the consideration of the diet in every disease, and especially in cancer, cannot be doubted. The cell bodies of cancer cells do not stain well in hemotoxylin, and other specific stains for calcium show that the protoplasm is very poor in calcium.

It is practically absent in fact. This should be true since the action of the synthetic carcinogenic agents is first of all marked by a loss of 50% of the calcium and iron content in the cells acted upon even before they have be come fully malignant. When they have become malignant, the rest of the calcium, iron and lipoid are lost. Calcium is certainly necessary to cellular oxidation, and cancer cells have lost their functional oxidation mechanism together with the calcium, in becoming anaplastic. One can see that the two factors work together. But calcium is necessary in another sense, just as it is needed for the coagulation of blood or the digestive clotting of milk, where it forms respectively fibrin and calcium caseinate. This, however, is a passive use of calcium and is due to the acids formed in the digestive process which combine the calcium as to form complex salts. In our October 30, 1920 article in the New York Medical Record, we demonstrated this use of calcium as essential to the process of removing effect material as dead cancer cells or coagulated blood, which of course must be digested and absorbed by organization. This is seen as the in-growth of fine capillaries in the microphotographs. The fact that Arginase will bring about similar calcification changes as reported by Irons, shows that the cancer cells are undergoing a physiological absorption and thus that so far as the process had progressed, a physiological involution was induced. Loss of an essential amino acid, in this way, could certainly be lethal. These observations again emphasize the essential role of calcium in the oxidation mechanism.

CALCIUM IMPORTANT

The cleavage of Arginine to guanidine and ornithin by Arginase brings up the action of the guanidin that is liberated within the cells themselves. We reported in the same paper that the blood underwent anti-mortem coagulation when guanidin was present in toxic quantities. Thus the coagulation of the cancer cells could be a lethal result of guanidine activity. The liver extract carrying the Arginase also contains the “Tissue Thrombin” we have reported as an impurity. The calcium deposition would again be the very necessary part of the first phase of digestion of the effected tissue; therefore, in any event, the place of calcium in the diet is therefore demonstrated here again. However, the action of any ferment introduced into the system or into a tissue in more than normal amounts, calls for the production of an anti-ferment. So as a treatment proposition, the end results of Arginase would be worse than if it had never been used.

This is especially true since the recovery process only removes a minor part of the tumor cells; the others having a chance to develop antiarginase soon prevent any action of the ferment. The many experimental means of destroying cancer in mice or rats have never proved valuable clinically for this reason. It must be concluded; therefore, that the calcium is needed to keep the tissues from going malignant and to eliminate cancer cells as fast as they die. When it is not supplied, the autolystic process is held up and over growths of angioblastic tissue for the purpose of removing the dead cancer cells will continue being formed, producing tumors as large as, or maybe larger than the original growth but all in vain. The production of such vascular tumors is very depleting to nutrient material. The patient shows loss of strength and weight, together with the increase in the size of the tumor, and an interference to function may be serious through pressure. This gives the picture of progress of the disease when the real situation is basically a deficiency in calcium, while the disease cause has actually been removed, and if calcium were supplied properly, all would go well.

CALCIUM PROTECTS AGAINST ACTION OF TOXINS

There is another function of calcium besides playing a part in the oxidation mechanism of function and in the digestion of dead tissue material for its elimination. This other function is the protection against the action of the toxins. It is of two types. In the first place, the calcium tends to preserve a state of dispersion of water in the lipoid phase within the cell protoplasm. Water-soluble substances of toxic nature do not readily enter through the lipoid membrane that has formed by diffusion of fat to the surface of the cell. The lipoids form a wall of protection. Through the action of carcinogens, the tissue cells while becoming cancer cells, demonstrate a lipoid in water phase and lose their lipoid content and hence, whatever lipoid traces may remain are also found in a water phase. Thus water-soluble substances, be they food or toxins, find easy entrance and the cell is readily stimulated or further poisoned. For this reason, cancer cells are more readily killed than normal cells, and likewise, they multiply more rapidly and are more dangerous to the rest of the body. The supply of calcium in good quantity offers them something they cannot use, but may help them anchor lipoid material and reverse their dispersion to a water in lipoid phase. The monovalent cations of sodium antagonize this protective action of calcium. Hence, the diet should take this fact into consideration by feeding less sodium while giving more calcium. Hydrochloric acid is needed to fix the calcium and should be prescribed regularly in the usual way.​

 

[Travis]

CALCIUM IMPORTANT
The cleavage of Arginine to guanidine and ornithin by Arginase brings up the action of the guanidin that is liberated within the cells themselves. We reported in the same paper that the blood underwent anti-mortem coagulation when guanidin was present in toxic quantities. Thus the coagulation of the cancer cells could be a lethal result of guanidine activity. The liver extract carrying the Arginase also contains the “Tissue Thrombin” we have reported as an impurity. The calcium deposition would again be the very necessary part of the first phase of digestion of the effected tissue; therefore, in any event, the place of calcium in the diet is therefore demonstrated here again. However, the action of any ferment introduced into the system or into a tissue in more than normal amounts, calls for the production of an anti-ferment. So as a treatment proposition, the end results of Arginase would be worse than if it had never been used.

This is good, but his words seem a bit quaint. Ignoring his lack of the terminal "e" in ornithine, there is a more serious dilemma. Arginine is thought to become ornithine and urea, not guinidine, by the action of arginase. Perhaps we can assume that guinidine was synonymous with urea back then.

click to embiggen

But regardless of whether or not urea or guinidine is formed by the action of arginase, this would be impossible in the presence of high methylglyoxal concentrations. Here is why:

It is well-known that methylglyoxal forms an imidizole ring on contact with methylglyoxal. This has been proven. Below is a brief representation of the event:

More detailed ones can be drawn. A similar image can be seen here, but it's given an improper name that doesn't account for the methyl group.

• Chumsae, Chris, et al. "Arginine modifications by methylglyoxal: discovery in a recombinant monoclonal antibody and contribution to acidic species." Analytical chemistry 85.23 (2013).

It's probably best called 5-methyl-4-imidazolon-2-yl ornithine, or 5-methyl-4-imidazolone when talking about the ring itself. It's called MG-H1 for short. These are the names that Thornally uses, and he has been publishing articles on methylglyoxal since the early 80s. He has designed a powerful glyoxylase I inhibitor and has published extensive reviews on the glyoxylase system. I don't think anyone knows more about methyglyoxal than Paul Thornally.

• Westwood, M. E., et al. "Methylglyoxal-modified arginine residues—a signal for receptor-mediated endocytosis and degradation of proteins by monocytic THP-1 cells." Biochimica et Biophysica Acta (BBA)-Molecular Cell Research 1356.1 (1997): 84-94.

So obviously, urea (or guanidine) cannot form from arginine in the presence of high methylglyoxal concentrations. The chemical species has transformed. Methylglyoxal can, of course, also react with free urea. This was shown as far back as 1927 by Seekles.

• Seekles, L. "The action of methylglyoxal on urea." Recueil des Travaux Chimiques des Pays-Bas 46.2 (1927): 77-84.

The action of methylglyoxal on urea might be expected to form 5-Methyl-2,4-imidazolidinedione, or 5-methylhydantoin. There is little data on this compound although the similar allantoin is a normal component of urine.

Here is an image of a few arginine–glyoxal products. Methylglyoxal mops-up nitrogen groups and many things can be formed. Two methylglyoxal's can form a pyrimidine ring. Interesting things may come of this:*

These authors believe that part of the endogenous uric acid may arise through synthesis from carbohydrates. They observed that carbohydrate-rich fatpoor diets cause a greater excretion of uric acid than do fat-rich carbohydrate-poor diets, even though the protein content and calorific value of the food are maintained constant. Umeda suggests that uric acid may arise from a condensation of urea with an intermediary product of carbohydrate metabolism, perhaps lactic acid. ―Rose

Methylglyoxal is a product of carbohydrate metabolism. It's concentrations are kept in-check throught the two enzymes glyoxylase I and glyoxylase II. First, methylglyoxal reacts with glutathione at the sulfhydryl. This is then slightly-modified by glyoxylase I and glyoxylase II does the rest: regenerating glutathione and forming lactic acid.

If Umeda suggests that uric acid can be formed from urea lactic acid, then he probably wouldn't mind the suggestion that it could be made by methylglyoxal—having the same amount of carbons yet more reactive. I don't think that lactic acid is a good candidate for uric acid formation. Armand Quick reports that the ingestion of lactic acid depresses uric acid excretion (Table I) while the ingestion of glucose raises it.†

You would certainly expect a fair amount of interplay between arginine, urea, and methylglyoxal. It's easy to see how methylglyoxal can turn-off cancer by transforming the some molecular growth factors, such as nitric oxide and polyamines, into more inert molecules such as substituted allantoins and pyrimidines. Or is it the other way around? . . . where these nitrogen compounds lower methylglyoxal and it's this that causes growth? I suspect the former. The glyoxylase system could be an endogenous recycling mechanism for amines, an another way in which the cell regulates growth.

Thornally has published a massive article on the glyoxylase system.‡ He has even shown that the methylglyoxal–arginine controls a nuclear transcription factor in the manner of a post-translational mechanism.§ An arginine side-chain in the sensitive DNA-binding domain is methylgloxylated, causing a shift in gene transcription.

Our studies demonstrate for the first time that methylglyoxal causes post-translational modification of a coregulator protein and that this modification affects gene expression. The extent of this modification reflects the net effect of a variety of intracellular processes, including metabolic flux and reactive oxygen formation, and may thus function as a new integrating signal to coordinately regulate distinct patterns of gene expression. ―Thornally

*Rose, William C. "The influence of food ingestion upon endogenous purine metabolism. I." Journal of Biological Chemistry 48.2 (1921): 563-573.
†Quick, Armand J. "The relationship between chemical structure and physiological response III. Factors influencing the excretion of uric acid." Journal of Biological Chemistry 98.1 (1932): 157-169.
‡Thornalley, Paul J. "The glyoxalase system in health and disease." Molecular aspects of medicine 14.4 (1993): 287-371.
§Yao, Dachun, et al. "High glucose increases angiopoietin-2 transcription in microvascular endothelial cells through methylglyoxal modification of mSin3A." Journal of Biological Chemistry 282.42 (2007): 31038-31045.

 

[jitsmonkey]

I am severely lactose intolerant. The small amounts in Lactaid (99% Lactose free) and in medications cause a stubborn spread of acne across my face.
additional Lactase enzymes don't help
I get even worse acne from eggshsell calcium and calcium carbonate.
Does anyone know another way?

How much Vitamin A and D are you getting>
I'd bet good money if you substantially increase your A dosage (and commensurate D) you'll tolerate the Lactaid milk and calcium
with no problem and no acne.

 

[jitsmonkey]

I have acne and vitamin A does zero in helping it so it isn't as easy as that

How much A have you taken?

 

[EIRE24]

How much A have you taken?

I have eaten loads of liver, beef liver to be exact which always makes me very naeseous. Also have taken 100'000 IU's of retinil without improvement. Why?

 

[Peater Piper]

Methylglyoxal is a product of carbohydrate metabolism. It's concentrations are kept in-check throught the two enzymes glyoxylase I and glyoxylase II. First, methylglyoxal reacts with glutathione at the sulfhydryl. This is then slightly-modified by glyoxylase I and glyoxylase II does the rest: regenerating glutathione and forming lactic acid.

That's not strictly the case, is it, or are you only looking at its formation through the carbohydrate pathway? Chris Masterjohn speaks of acetone being converted to methyglyoxal through CYP2E1, and acetone is formed through the burning of ketones. Ketogenic diets can lead to very high levels of methylglyoxal.

 

[Travis]

That's not strictly the case, is it,

No; you're right. I never said that it was a product of carbohydrate metabolism exclusively. It can be formed with the glycerol backbone of triglycerides as well as through the amino acid threonine—a little-known pathway. The enzyme threonine dehydrogenase in the liver turns it into aminoacetone, which is then converted into methylglyoxal through various deaminiation pathways including monoamine oxidase. I've read a few studies indicating that threonine creates aminoacetone in the blood, and a few other separate ones showing aminoacetone becoming methylglyoxal. I was really excited, but I hadn't found one that had directly linked threonine with methylglyoxal within the same study until weeks later when I stumbled upon this:

• MURATA, Kousaku, et al. "Metabolism of 2‐oxoaldehydes in yeasts." The FEBS Journal 157.2 (1986): 297-301.

It's a free full-text link. You can see how threonine upregulates glyoxylase I and glyoxylase II enzymes to deal with the extra methylglyoxal formed. You would expect this to raise the internal steady-state methylglyoxal concentration, but this is hard to measure—it's reactive and William Koch had written about his difficulties is preparing his glyoxylides. It spontaneously bonds with arginine and glutathione, with glutathione being regenerated by glyoxylase II—lactic acid being the other product.

You would expect threonine to be a methylglyoxal prodrug. Consuming threonine with an all-natural glyoxylase I inhibitor—like baicalin, lapachol, or hinokitiol—would amplify the effect even further. This is way better than consuming methylglyoxal directly, since it's constantly being recycled into lactic acid at a quick rate.

The interaction between methylglyoxal and amines appear to be a powerful intracellular system controlling growth. This idea is strengthened by the endorsement of William Koch and Szent-Györgi, and it even ties into the Warburg Effect through lactic acid. The enzymes glyoxylase I & II are often found upregulated in cancer; and many studies have shown this. High glyoxylase activity means both low methylglyoxal concentrations and high lactic acid.

 

[CoconutEffect]

How much Vitamin A and D are you getting>
I'd bet good money if you substantially increase your A dosage (and commensurate D) you'll tolerate the Lactaid milk and calcium
with no problem and no acne.

Hey - to save money I’ve been eating large amounts of liver a day for a few weeks, no improvement in terms of acne, but thanks for the suggestion.

Lactose —> sebum —> white heads

no stomach distress though, very strange.

 

[EIRE24]

Hey - to save money I’ve been eating large amounts of liver a day for a few weeks, no improvement in terms of acne, but thanks for the suggestion.

Lactose —> sebum —> white heads

no stomach distress though, very strange.

What kind of liver is it? Beef, lamb, chicken?

You notice that any lactose causes sebum for you? I think I notice the same thing.

 

[Travis]

I don't think it's lactose. I think its the androgens in dairy working directly on the nuclear androgen receptor upregulating a suite of sebum-producing genes. This is the classic effect of androgens on the skin. They also cause hair growth in certain areas like the beard, and are thought to paradoxically cause hair-loss of the scalp (but this is not true; it's really the cortisol and aldosterone working through the mineralcorticoid receptor.

 

[Frankdee20]

I have eaten loads of liver, beef liver to be exact which always makes me very naeseous. Also have taken 100'000 IU's of retinil without improvement. Why?

You can seriously throw off D with all that A

 

[Dave Clark]

Too much liver, too much iron.

 

[Amazoniac]

I don't think it's lactose. I think its the androgens in dairy working directly on the nuclear androgen receptor upregulating a suite of sebum-producing genes. This is the classic effect of androgens on the skin. They also cause hair growth in certain areas like the beard, and are thought to paradoxically cause hair-loss of the scalp (but this is not true; it's really the cortisol and aldosterone working through the mineralcorticoid receptor.

What about a proper adaptation from regular consumption? Can you desensitize to them? Acne usually appears during stress, when you're not being able to provide what it takes to adapt.

 

[Frankdee20]

Too much liver, too much iron.

Yes, but shouldn't the high copper and zinc balance out the iron in liver ? It's ridiculously high in copper

 

[Dave Clark]

Yes, but shouldn't the high copper and zinc balance out the iron in liver ? It's ridiculously high in copper

Or end up making you both high in copper and iron! I get why the people here want to eat liver, etc., but I personally think we shouldn't go overboard, because of the high iron, copper, etc. I enjoy liver once and awhile, but I don't make it my main food for vitamin A, just because it is so high in iron. Being a heme iron, it's not like you can drink a glass of wine with it to bind it up, the iron is still going to get absorbed. However, I know some here wouldn't approve, but using IP-6 can help solve that problem. Anyway, I think it is easier and more accurate to balance with supplements than food, vis a vis the vitamin A, etc., since we can't really tell exactly how much of anything is in a particular food that we eat, it's all an educated guess!

 

[Travis]

What about a proper adaptation from regular consumption? Can you desensitize to them? Acne usually appears during stress, when you're not being able to provide what it takes to adapt.

In vitro, androgens create sebum like nothing else. Acne is characterized by sebum with more wax esters than triglycerides, raising the melting point and created clogs. There is a physical basis for this and it's the wax/oil ratio of the sebum.

Bodybuilders know this. Anyone can take a few minutes to cruise the bodybuilding forums and for verification of this. The steroids that bodybuilder's use are mostly all androgens. There has been many good articles written on this.

And there are interesting DNA microarray and Western blot studies that can show you exactly which genes are upregulated in the skin in response to androgens.

• Barrault, Christine, et al. "Androgens induce sebaceous differentiation in sebocyte cells expressing a stable functional androgen receptor." The Journal of steroid biochemistry and molecular biology 152 (2015): 34-44.

Sebum itself has a specific composition with 30–50% triglycerides, 15–30% fatty acids, 26–30% wax esters, 12–20% squalene and less than 10% cholesterol and cholesterol esters [35]. [...] Thin layer chromatography/phosphorimaging shows, among other effects, a strong increase of triglycerides, free fatty acids and wax esters and a decrease of cholesterol esters in DHT-treated cultures (mostly visible at 7 days; Fig. 3C). Squalene which is not clearly detected under these conditions should migrate just above the cholesterol ester band. ―Barrault

Thin layer chromatogram showing squalene, cholesterol, wax esters, tryglycerides, and free fatty acids.

It took seven days. This implies a gene-shift of the cell, which had also been shown. Many enzymes were upregulated, and many downregulated. This is not an isolated finding and you will find the same thing in articles going back decades.

Here is a review article with a free full-text link:

• Kurokawa, Ichiro, et al. "New developments in our understanding of acne pathogenesis and treatment." Experimental dermatology 18.10 (2009): 821-832.

The reason that you can ingest some dairy and not get acne is probably based on dose, first and foremost, and sex hormone-binding globulin in the blood. This varies between person and person and some people can bind more androgens than others.

It's tempting to think that stress hormones could displace androgens from sex hormone-binding globulin in the blood, similar to how niacin can displace serotonin from the platelets and how linoleic acid can displace tryptophan from serum albumin–where high-stress cortisone release leads to high free androgens through Fernstrom-like kinetics, raising it's bioavailability and leading to acne one week later.

Androgens are probably why African Americans have less acne–they drink less milk, on average. Many Americans of African descent avoid dairy for genetic reasons, not having evolved the machinery to properly metabolize lactose. The Chinese, the ones in China, don't consume much dairy. And the only time I get acne is after I eat cheese and I'm fairly-certain that it's the androgens.

Now this is a common meme, but I think some are skeptical for mainly these reasons:

• It doesn't occur immediately
• It persists after stopping dairy
  
• It only happens with some people

I've said what I think about the last idea, but the lack of temporal association can be explained by the slow cellular response–this is a genetic event: Upon ligand binding the androgen receptor migrates into the nucleus and upregulates certain enzymes. This is the on-switch; the off-switch takes weeks. Acne does disappear after a few weeks of not eating androgens, in me anyway, and I have seen this happen multiple times–like clockwork.

Perhaps you can offset the androgens in dairy with progesterone?–I'm not sure. This is a Peat-friendly hormone and many people here use it.

I could probably get away with eating some dairy, but I find cheese actually addictive. It is simply impossible for me to eat just some once-in-a-while. I have to either eat a lot or none at all.

 

[Frankdee20]

Or end up making you both high in copper and iron! I get why the people here want to eat liver, etc., but I personally think we shouldn't go overboard, because of the high iron, copper, etc. I enjoy liver once and awhile, but I don't make it my main food for vitamin A, just because it is so high in iron. Being a heme iron, it's not like you can drink a glass of wine with it to bind it up, the iron is still going to get absorbed. However, I know some here wouldn't approve, but using IP-6 can help solve that problem. Anyway, I think it is easier and more accurate to balance with supplements than food, vis a vis the vitamin A, etc., since we can't really tell exactly how much of anything is in a particular food that we eat, it's all an educated guess!

True, that's why I donate blood every 8 weeks. I'm also AB + so I'm helping out 1 in 26 people, lol