Vitamin E, Anabolic / Catatoxic Steroids, Egg Yolks Stop Soft Tissue Calcification And (maybe) Even

haidut

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A great series of studies performed in the 1960s, with Hans Selye spearheading most of the investigations. It is amazing how much was known about human disease and aging, and how much of that knowledge has been so thoroughly forgotten to the point that doctors nowadays have never even heard of the term "catatoxic". One of most important topics the studies below cover is the fact that soft tissue calcification can be triggered by a variety of endogenous and environmental agents, many of which are considered beneficial by mainstream medicine and billions are spent every year promoting their use. As the study below states, some of those well-known (back in the 1960s, that is) endogenous agents triggerring soft-tissue calcification (calciphylaxis) include estrogen, serotonin and parathyroid hormone (PTH) - those same agents that pharma companies and public health authorities spent billions on advertising for every year.

[1] Prevention by calciphylaxis of the progeria-like syndrome induced by chronic dihydrotachysterol overdosage. - PubMed - NCBI

"...Calciphylaxis enables the organism to deposit calcium selectively in certain areas. Thus, following pretreatment with parathyroid hormone or dihydrotachysterol (DHT), various calciphylactic challengers (egg white, metals, serotonin, etc.) can induce selective calcification-often with inflammation, sclerosis, necrosis or degeneration--in the skin, muscles, cardiovascular system, pancreas, salivary glands, or uterus."

[2] Protection by catatoxic steroids against dihydrotachysterol intoxication. - PubMed - NCBI

"...Subsequently, it was noted that removal of the testis also increases the arterial calcification (Monckeberg’s sclerosis), and the loss of body weight induced in male rats by intoxication with dihydrotachysterol (DHT). These observations led to the suspicion that some, not further identified, “testicular factor” exerts a prophylactic action in these conditions[3] and soon afterwards it could be shown that this anti-DHT effect can be duplicated by methyltestosterone and abolished by estradiol."

However, as the series of studies in this post shows, the issue of calcification runs much deeper. This soft-tissue calcification (calciphylaxis) is actually a primary sign of a number of conditions involving premature aging (e.g. progeria), and in fact quite possibly the process of systemic human aging as well. Moreover, evidence exists that this calciphylaxis is not just a sign but the very cause of aging in humans. As such, agents such as estrogen, serotonin, PTH, heavy metals, etc can be considered as primary causes of aging and its associated pathology, and any agents capable of reversing this calciphylaxis (hereby called anacalciphylactic agents) can be thought of as general anti-aging substances. Note the description below and the image extracted from [1] above comparing an animal with calciphyalxis with one whose calciphylaxis has been blocked / reversed by (methyl) testosterone. The aged (calciphylactic) rat in section A is strikingly reminiscent of the appearance of an old human being.

[3] Effect of anabolic hormones and ferric dextran upon the progeria-like syndrome produced by dihydrotachysterol. - PubMed - NCBI

"...It is a well known fact that the calcium avidity of soft tissues increases with advancing age. In elderly patients, gross calcification often occurs in the cardiovascular system, cartilaginous structures, tendons, periarticular tissues and cataracts; furthermore, calcareous concretions tend to appear in the pineal gland, prostate, or the urinary passages [1]. Apart from such macroscopically visible calcium deposits there is a gradual increase in the chemically detectable calcium content of various organs in old individuals throughout the animal kingdom [2]. This tendency towards soft-tissue calcification also manifests itself in patients with premature senility as it occurs in the Hutchinson-Gilford syndrome, or progeria. Here, atrophy with wrinkling of the skin and calcifying arteriosclerosis of the Monckeberg type are combined with a shortened life span [3, 4, 5]. Although many investigators believe that this type of calcinosis is a secondary result of “decreased tissue vitality”, others maintain that an increase in the tissue calcium concentration may actually be the cause of the changes characteristic of senility [2]".

calciphylaxis_aging_progeria.png

So, what (if anything) can be done about this process of accelerated aging and "natural" human aging in general? Well, one of the studies above already hints at a solution. Namely, preserving gonadal function retards the aging process and soft-tissue calcification. The studies below demonstrate that a high dose (but commonly used by athletes) dosage of (methyl) testosterone can completely prevent these "aging" changes induced by calciphylaxis agent(s). In other words, (methyl) testosterone is an anacalciphylaxis agent. As demonstrated by [2] above, other catatoxic / anabolic steroids including oxandrolone, norbolethone, ethylestrenol, spironolactone, etc can also fully prevent the calciphylaxis / aging. The dosage of (methyl) testosterone used was equivalent to a human dose of 1.5 mg/kg daily, and the treatment lasted for 30 days. Such a dose of anabolic steroid is indeed high but it happens to be the standard dose for bodybuilders during a cycle - i.e. 100mg - 150mg of testosterone daily. Now, it is well-known that such high doses of anabolic steroids increase the risk of serious side effects. The good news is that a much lower dose (HED of 0.15 mg/kg daily) also had a protective effect but could not fully block the calciphylaxis. The even better news is according to [5] and [6] below a hefty dose of vitamin E (alpha-tocopherol acetate) was also able to fully block the calciphylaxis. Now, the dose of vitamin E used in that study was also quite high - an HED of about 4g-5g daily. However, the study used alpha-tocopheryl acetate, which is known to be only about 30% - 50% as effective as alpha-tocopherol. So, if one used pure alpha-tocopherol then a dose of 2g -2.5g daily should suffice. This is still a high dose but it has been used clinically in the 20th century for a variety if estrogen-related issues, especially by the Shute brothers. Perhaps just as importantly, study [7] below demonstrates that vitamin E protects from the side effects of high-dose anabolic steroids, which makes a combination of vitamin E + testosterone a rather good combination for blocking / reversing systemic soft-tissue calcification and possibly retarding the whole aging process. Unfortunately, there was no anacalciphylaxis synergy between vitamin E and testosterone, so the combined usage is aimed at reducing the steroid's side effects and not increasing the anacalciphylaxis. If one is too concerned about those side effects, then one can use vitamin E only, which even at the hefty multi-gram daily doses has few serious side effects in humans, with the possible exception of increased bleeding risk, which can easily be controlled by taking some vitamin K a few hours before/after the vitamin E regimen. It just so happens that vitamin K (10mg+ daily dose) is also a anacalciphylaxis agent [8], and together with vitamin E should make a great non-steroidal therapy for soft-tissue calcification and maybe aging in general. And if a person is really averse to using either a high dose anabolic steroid or vitamin E, the studies provide yet another alternative - eating egg yolks. Yes, the studies demonstrate that a HED of 1 g/kg egg yolk was highly effective as anacalciphylaxis agent when administered orally. However, please keep in mind the quote above from [1], which demonstrated that egg white is a potential calciphylaxis agent. So, if one decides to go the (delicious) route of egg yolks, please make sure only the yolks are consumed and not the whole eggs.

Finally, a few small but hopefully important observations. First, note that none of studies with vitamin E refer to it as an "antioxidant" - something mainstream medicine has spent billions to try to convince the public about. All of the studies in this post refer to vitamin E as an "anti-sterility vitamin", as Peat himself also mentioned quite a few times. This gives a clue to the possible mechanism of action for the benefit of vitamin E and (methyl) testosterone. Namely, opposition to estrogen. The anti-sterility effects of vitamin E are well-known to be linked to the powerful anti-estrogenic effects of this vitamin. Testosterone and its various synthetic derivatives including the methylated-varieties, is also a known estrogen antagonist. Estrogen is a potent calciphylaxis agent, as the quote from [2] clearly states. This raises the possibility that other anti-estrogenic agents such as progesterone (P4) should also work. However, study [2] did test P4 and did not find it to be effective. Maybe higher doses are needed for P4 to exert anacalciphylaxis effects. However, in corroboration of the role of serotonin as a calciphylaxis agent, the serotonin antagonist cyproheptadine has already been shown to prevent/reverse soft-tissue calcification. In addition, anti-serotonin chemicals have been shown to increase lifespan, which matches perfectly with the claims of the studies in this thread that anacalciphylaxis agents such as serotonin antagonists should have anti-aging effects.

[4] A progeria-like syndrome produced by dihydrotachysterol and its prevention by methyltestosterone and ferric dextran. - PubMed - NCBI

"...It has been known for more than thirty years that in the fetal or in the newborn rat, intoxication with an impure vitamin-D preparation (irradiated ergosterol) produces a kind of osteoporosis with spontaneous fractures, intense catabolism and loss of skin elasticity (2, 3), whereas in older rats, it tends to produce calcification in various soft tissues, especially in the arteries, heart and kidneys (3, 4). More recently, it was shown that a syndrome reminiscent of progeria can be produced by chronic overdosage with small doses of dihydrotachysterol (DHT) and that all the manifold manifestations of this experimental disease are inhibited when tissue calcification is prevented by simultaneous treatment with ferric dextran (Fe-Dex) (5), methyltestosterone (6) or 17 -ethyl-19-nortestosterone (7)."

"...During the five days preceding the initiation of DHT treatment, the animals of all groups gained weight approximately at the same rate and showed no evident clinical manifestations of disease, except for a slight brownish discoloration of the skin (indicative of mild hemosiderosis) in the group treated with ferric dextran. Accordingly, the body-weight curves in Graph I follow a virtually identical course until the first day of DHT treatment. However, after this the growth of the rats receiving DHT alone soon fell behind that of the other groups, and beginning on the fifth day it declined rapidly, until at the end of the observation period it returned to the starting level. On the other hand, the rats treated with DHT + methyltestosterone continued to grow just as rapidly as the controls. Indeed, their final weight was slightly (though not significantly) above that of the untreated controls. Eventually the body weight of these rats was more than twice that of the rats given DHT alone. We may well speak of a complete abolition of the DHT-induced catabolism."

[5] FURTHER STUDIES ON ANACALCIPHYLAXIS. - PubMed - NCBI

"...Calciphylaxis is a reaction through which the organism can send calcium selectively to certain organs; on the other hand, anacalciphylaxis (calciphylactic desensitization or reverse calciphylaxis) can prevent the formation of pathologic soft-tissue calcification (1). The mechanism through which calciphylaxis and its variant, anacalciphylaxis, exert these seemingly opposite effects is not yet well known. It appears however that, in calciphylaxis, sensitization with a systemic calcifying agent (e.g., vitamin-D derivatives) followed by the local application of a challenger (e.g., metallic compounds) to a limited tissue region, attracts calcium and causes massive mineralization of the part challenged. Conversely, in anacalciphylaxis, the challenger is diffusely distributed throughout the organism; thereby it induces a generalized avidity of tissues for calcium, phosphate or mineralizable organic matrix. Presumably, anacalciphylaxis prevents the massive mineralization of any one part, through competition for the available extraskeletal calcium which, being widely disseminated, is readily metabolized. It has long been known that an increased tendency toward soft-tissue calcification (particularly of the arteries, cartilages and the crystalline lens) is characteristic of senility."

"... For example, Fe-Dex proved to be more effective by the intraperitoneal than the subcutaneous route, whereas egg yolk was more potent when given orally rather than intravenously. Yet, even intravenous injection of egg yolk, the least effective among the procedures listed, permitted a statistically highly significant body-weight gain as compared with the controls given DHT alone (P < 0.01)....Egg yolk is also a potent calciphylactic challenger, hence its prophylactic action could depend upon a similar phenomenon, i.e., the deviation of calcium by diffusely distributed yolk corpuscles."

"...The growth inhibitory action of calciphylaxis (Group 10) was significantly counteracted by Fe-Dex, methyltestosterone and vitamin E (Groups 11-13). Here again, the anabolic effect was usually associated with a diminution in the cardiovascular and renal calcinosis as well as in the osseous changes, although methyltestosterone was least effective in these latter respects despite its potent growth-promoting action."

[6] EFFECT OF VITAMIN E AND METHYLTESTOSTERONE UPON THE PROGERIA-LIKE SYNDROME PRODUCED BY DIHYDROTACHYSTEROL. - PubMed - NCBI

"...Recently, we observed that vitamin E (d-atocopheryl acetate) can prevent the development of various forms of calcinosis normally induced in dihydrotachysterol-sensitized rats by the administration of certain calciphylactic challengers.[5]"

"...The present observations indicate that vitamin E also acts as a dihydnotachystenol antagonist, but-at least under our experimental conditions-its effect is not enhanced by the androgen. Among many agents tested, so far we have been able to find only the following three which can antagonize the production by dihydrotachysterol of the progenia-like syndrome: (1) fernic dextran, a calciphylactic challenger commonly used in clinical medicine to stimulate hemopoesis ; (2) methyltestosterone, an anabolic androgen ; and (3) d-a-tocopheryl acetate (an antistenility vitamin)."

[7] http://www.jofamericanscience.org/journals/am-sci/am130417/03_31829jas130417_24_36.pdf
[8] Calciphylaxis in a dialysis patient successfully treated with high-dose vitamin K supplementation
 

BRMarshall

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Thanks for this fine specimen of a post, one among many of the great data dump today from your blog, haidut.me/ , on to the Ray Peat Forum for discussion...Yes these post do need to be discussed.

This particular post I found fascinating and did go reference a recent podcast you were in, though I forgot which one, were you said that as regards the number of eggs yolks to have this effect would be like 4 per day if I recall....
 

shine

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This particular post I found fascinating and did go reference a recent podcast you were in, though I forgot which one, were you said that as regards the number of eggs yolks to have this effect would be like 4 per day if I recall....

He said 4-5 in the podcast. :thumbsup:

26:06

 

Gone Peating

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Would not be a good idea to eat 4 egg yolks grown under modern conditions tho right? Only if fed a non soy diet?
 

Tenacity

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I find that I can eat three yolks per day and still be under the 4g PUFA threshold on a low fat diet.
 

Regina

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A great series of studies performed in the 1960s, with Hans Selye spearheading most of the investigations. It is amazing how much was known about human disease and aging, and how much of that knowledge has been so thoroughly forgotten to the point that doctors nowadays have never even heard of the term "catatoxic". One of most important topics the studies below cover is the fact that soft tissue calcification can be triggered by a variety of endogenous and environmental agents, many of which are considered beneficial by mainstream medicine and billions are spent every year promoting their use. As the study below states, some of those well-known (back in the 1960s, that is) endogenous agents triggerring soft-tissue calcification (calciphylaxis) include estrogen, serotonin and parathyroid hormone (PTH) - those same agents that pharma companies and public health authorities spent billions on advertising for every year.

[1] Prevention by calciphylaxis of the progeria-like syndrome induced by chronic dihydrotachysterol overdosage. - PubMed - NCBI

"...Calciphylaxis enables the organism to deposit calcium selectively in certain areas. Thus, following pretreatment with parathyroid hormone or dihydrotachysterol (DHT), various calciphylactic challengers (egg white, metals, serotonin, etc.) can induce selective calcification-often with inflammation, sclerosis, necrosis or degeneration--in the skin, muscles, cardiovascular system, pancreas, salivary glands, or uterus."

[2] Protection by catatoxic steroids against dihydrotachysterol intoxication. - PubMed - NCBI

"...Subsequently, it was noted that removal of the testis also increases the arterial calcification (Monckeberg’s sclerosis), and the loss of body weight induced in male rats by intoxication with dihydrotachysterol (DHT). These observations led to the suspicion that some, not further identified, “testicular factor” exerts a prophylactic action in these conditions[3] and soon afterwards it could be shown that this anti-DHT effect can be duplicated by methyltestosterone and abolished by estradiol."

However, as the series of studies in this post shows, the issue of calcification runs much deeper. This soft-tissue calcification (calciphylaxis) is actually a primary sign of a number of conditions involving premature aging (e.g. progeria), and in fact quite possibly the process of systemic human aging as well. Moreover, evidence exists that this calciphylaxis is not just a sign but the very cause of aging in humans. As such, agents such as estrogen, serotonin, PTH, heavy metals, etc can be considered as primary causes of aging and its associated pathology, and any agents capable of reversing this calciphylaxis (hereby called anacalciphylactic agents) can be thought of as general anti-aging substances. Note the description below and the image extracted from [1] above comparing an animal with calciphyalxis with one whose calciphylaxis has been blocked / reversed by (methyl) testosterone. The aged (calciphylactic) rat in section A is strikingly reminiscent of the appearance of an old human being.

[3] Effect of anabolic hormones and ferric dextran upon the progeria-like syndrome produced by dihydrotachysterol. - PubMed - NCBI

"...It is a well known fact that the calcium avidity of soft tissues increases with advancing age. In elderly patients, gross calcification often occurs in the cardiovascular system, cartilaginous structures, tendons, periarticular tissues and cataracts; furthermore, calcareous concretions tend to appear in the pineal gland, prostate, or the urinary passages [1]. Apart from such macroscopically visible calcium deposits there is a gradual increase in the chemically detectable calcium content of various organs in old individuals throughout the animal kingdom [2]. This tendency towards soft-tissue calcification also manifests itself in patients with premature senility as it occurs in the Hutchinson-Gilford syndrome, or progeria. Here, atrophy with wrinkling of the skin and calcifying arteriosclerosis of the Monckeberg type are combined with a shortened life span [3, 4, 5]. Although many investigators believe that this type of calcinosis is a secondary result of “decreased tissue vitality”, others maintain that an increase in the tissue calcium concentration may actually be the cause of the changes characteristic of senility [2]".

View attachment 16341

So, what (if anything) can be done about this process of accelerated aging and "natural" human aging in general? Well, one of the studies above already hints at a solution. Namely, preserving gonadal function retards the aging process and soft-tissue calcification. The studies below demonstrate that a high dose (but commonly used by athletes) dosage of (methyl) testosterone can completely prevent these "aging" changes induced by calciphylaxis agent(s). In other words, (methyl) testosterone is an anacalciphylaxis agent. As demonstrated by [2] above, other catatoxic / anabolic steroids including oxandrolone, norbolethone, ethylestrenol, spironolactone, etc can also fully prevent the calciphylaxis / aging. The dosage of (methyl) testosterone used was equivalent to a human dose of 1.5 mg/kg daily, and the treatment lasted for 30 days. Such a dose of anabolic steroid is indeed high but it happens to be the standard dose for bodybuilders during a cycle - i.e. 100mg - 150mg of testosterone daily. Now, it is well-known that such high doses of anabolic steroids increase the risk of serious side effects. The good news is that a much lower dose (HED of 0.15 mg/kg daily) also had a protective effect but could not fully block the calciphylaxis. The even better news is according to [5] and [6] below a hefty dose of vitamin E (alpha-tocopherol acetate) was also able to fully block the calciphylaxis. Now, the dose of vitamin E used in that study was also quite high - an HED of about 4g-5g daily. However, the study used alpha-tocopheryl acetate, which is known to be only about 30% - 50% as effective as alpha-tocopherol. So, if one used pure alpha-tocopherol then a dose of 2g -2.5g daily should suffice. This is still a high dose but it has been used clinically in the 20th century for a variety if estrogen-related issues, especially by the Shute brothers. Perhaps just as importantly, study [7] below demonstrates that vitamin E protects from the side effects of high-dose anabolic steroids, which makes a combination of vitamin E + testosterone a rather good combination for blocking / reversing systemic soft-tissue calcification and possibly retarding the whole aging process. Unfortunately, there was no anacalciphylaxis synergy between vitamin E and testosterone, so the combined usage is aimed at reducing the steroid's side effects and not increasing the anacalciphylaxis. If one is too concerned about those side effects, then one can use vitamin E only, which even at the hefty multi-gram daily doses has few serious side effects in humans, with the possible exception of increased bleeding risk, which can easily be controlled by taking some vitamin K a few hours before/after the vitamin E regimen. It just so happens that vitamin K (10mg+ daily dose) is also a anacalciphylaxis agent [8], and together with vitamin E should make a great non-steroidal therapy for soft-tissue calcification and maybe aging in general. And if a person is really averse to using either a high dose anabolic steroid or vitamin E, the studies provide yet another alternative - eating egg yolks. Yes, the studies demonstrate that a HED of 1 g/kg egg yolk was highly effective as anacalciphylaxis agent when administered orally. However, please keep in mind the quote above from [1], which demonstrated that egg white is a potential calciphylaxis agent. So, if one decides to go the (delicious) route of egg yolks, please make sure only the yolks are consumed and not the whole eggs.

Finally, a few small but hopefully important observations. First, note that none of studies with vitamin E refer to it as an "antioxidant" - something mainstream medicine has spent billions to try to convince the public about. All of the studies in this post refer to vitamin E as an "anti-sterility vitamin", as Peat himself also mentioned quite a few times. This gives a clue to the possible mechanism of action for the benefit of vitamin E and (methyl) testosterone. Namely, opposition to estrogen. The anti-sterility effects of vitamin E are well-known to be linked to the powerful anti-estrogenic effects of this vitamin. Testosterone and its various synthetic derivatives including the methylated-varieties, is also a known estrogen antagonist. Estrogen is a potent calciphylaxis agent, as the quote from [2] clearly states. This raises the possibility that other anti-estrogenic agents such as progesterone (P4) should also work. However, study [2] did test P4 and did not find it to be effective. Maybe higher doses are needed for P4 to exert anacalciphylaxis effects. However, in corroboration of the role of serotonin as a calciphylaxis agent, the serotonin antagonist cyproheptadine has already been shown to prevent/reverse soft-tissue calcification. In addition, anti-serotonin chemicals have been shown to increase lifespan, which matches perfectly with the claims of the studies in this thread that anacalciphylaxis agents such as serotonin antagonists should have anti-aging effects.

[4] A progeria-like syndrome produced by dihydrotachysterol and its prevention by methyltestosterone and ferric dextran. - PubMed - NCBI

"...It has been known for more than thirty years that in the fetal or in the newborn rat, intoxication with an impure vitamin-D preparation (irradiated ergosterol) produces a kind of osteoporosis with spontaneous fractures, intense catabolism and loss of skin elasticity (2, 3), whereas in older rats, it tends to produce calcification in various soft tissues, especially in the arteries, heart and kidneys (3, 4). More recently, it was shown that a syndrome reminiscent of progeria can be produced by chronic overdosage with small doses of dihydrotachysterol (DHT) and that all the manifold manifestations of this experimental disease are inhibited when tissue calcification is prevented by simultaneous treatment with ferric dextran (Fe-Dex) (5), methyltestosterone (6) or 17 -ethyl-19-nortestosterone (7)."

"...During the five days preceding the initiation of DHT treatment, the animals of all groups gained weight approximately at the same rate and showed no evident clinical manifestations of disease, except for a slight brownish discoloration of the skin (indicative of mild hemosiderosis) in the group treated with ferric dextran. Accordingly, the body-weight curves in Graph I follow a virtually identical course until the first day of DHT treatment. However, after this the growth of the rats receiving DHT alone soon fell behind that of the other groups, and beginning on the fifth day it declined rapidly, until at the end of the observation period it returned to the starting level. On the other hand, the rats treated with DHT + methyltestosterone continued to grow just as rapidly as the controls. Indeed, their final weight was slightly (though not significantly) above that of the untreated controls. Eventually the body weight of these rats was more than twice that of the rats given DHT alone. We may well speak of a complete abolition of the DHT-induced catabolism."

[5] FURTHER STUDIES ON ANACALCIPHYLAXIS. - PubMed - NCBI

"...Calciphylaxis is a reaction through which the organism can send calcium selectively to certain organs; on the other hand, anacalciphylaxis (calciphylactic desensitization or reverse calciphylaxis) can prevent the formation of pathologic soft-tissue calcification (1). The mechanism through which calciphylaxis and its variant, anacalciphylaxis, exert these seemingly opposite effects is not yet well known. It appears however that, in calciphylaxis, sensitization with a systemic calcifying agent (e.g., vitamin-D derivatives) followed by the local application of a challenger (e.g., metallic compounds) to a limited tissue region, attracts calcium and causes massive mineralization of the part challenged. Conversely, in anacalciphylaxis, the challenger is diffusely distributed throughout the organism; thereby it induces a generalized avidity of tissues for calcium, phosphate or mineralizable organic matrix. Presumably, anacalciphylaxis prevents the massive mineralization of any one part, through competition for the available extraskeletal calcium which, being widely disseminated, is readily metabolized. It has long been known that an increased tendency toward soft-tissue calcification (particularly of the arteries, cartilages and the crystalline lens) is characteristic of senility."

"... For example, Fe-Dex proved to be more effective by the intraperitoneal than the subcutaneous route, whereas egg yolk was more potent when given orally rather than intravenously. Yet, even intravenous injection of egg yolk, the least effective among the procedures listed, permitted a statistically highly significant body-weight gain as compared with the controls given DHT alone (P < 0.01)....Egg yolk is also a potent calciphylactic challenger, hence its prophylactic action could depend upon a similar phenomenon, i.e., the deviation of calcium by diffusely distributed yolk corpuscles."

"...The growth inhibitory action of calciphylaxis (Group 10) was significantly counteracted by Fe-Dex, methyltestosterone and vitamin E (Groups 11-13). Here again, the anabolic effect was usually associated with a diminution in the cardiovascular and renal calcinosis as well as in the osseous changes, although methyltestosterone was least effective in these latter respects despite its potent growth-promoting action."

[6] EFFECT OF VITAMIN E AND METHYLTESTOSTERONE UPON THE PROGERIA-LIKE SYNDROME PRODUCED BY DIHYDROTACHYSTEROL. - PubMed - NCBI

"...Recently, we observed that vitamin E (d-atocopheryl acetate) can prevent the development of various forms of calcinosis normally induced in dihydrotachysterol-sensitized rats by the administration of certain calciphylactic challengers.[5]"

"...The present observations indicate that vitamin E also acts as a dihydnotachystenol antagonist, but-at least under our experimental conditions-its effect is not enhanced by the androgen. Among many agents tested, so far we have been able to find only the following three which can antagonize the production by dihydrotachysterol of the progenia-like syndrome: (1) fernic dextran, a calciphylactic challenger commonly used in clinical medicine to stimulate hemopoesis ; (2) methyltestosterone, an anabolic androgen ; and (3) d-a-tocopheryl acetate (an antistenility vitamin)."

[7] http://www.jofamericanscience.org/journals/am-sci/am130417/03_31829jas130417_24_36.pdf
[8] Calciphylaxis in a dialysis patient successfully treated with high-dose vitamin K supplementation
Fabulous post! :bouquet::bouquet::clapping::clapping:
Tocovit+Estroban+Progestene+Cypro+4 egg yolks+Kuinone. +Cortinon+Androsterone enough? to mimic results with no access to T or DHT.
 

tankasnowgod

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Joined
Jan 25, 2014
Messages
5,063
As such, agents such as estrogen, serotonin, PTH, heavy metals, etc can be considered as primary causes of aging and its associated pathology, and any agents capable of reversing this calciphylaxis (hereby called anacalciphylactic agents) can be thought of as general anti-aging substances. Note the description below and the image extracted from [1] above comparing an animal with calciphyalxis with one whose calciphylaxis has been blocked / reversed by (methyl) testosterone. The aged (calciphylactic) rat in section A is strikingly reminiscent of the appearance of an old human being.

The Rat in section A does remind me a lot of an old human being. It also reminds me of another class of human being.... modern bodybuilders. Many have the extremely pronounced veins that the first rat does, and often very poor quality skin as well. Sometimes, they almost look like they are going to burst, skin stretched tight over muscles, veins, even vital organs. Of course, diets and regimens can vary greatly, but huge doses of steriods (that often aromatise into estrogen) and egg whites feature very prominently.

The Classic Bodybuilders looked very different, certainly muscular and well developed, but they often looked very young as well. Steve Reeves and Vince Gironda are good examples, and looked more like prime human specimens than freak shows.
 

BRMarshall

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Messages
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The Rat in section A does remind me a lot of an old human being. It also reminds me of another class of human being.... modern bodybuilders. Many have the extremely pronounced veins that the first rat does, and often very poor quality skin as well. Sometimes, they almost look like they are going to burst, skin stretched tight over muscles, veins, even vital organs. Of course, diets and regimens can vary greatly, but huge doses of steriods (that often aromatise into estrogen) and egg whites feature very prominently.

The Classic Bodybuilders looked very different, certainly muscular and well developed, but they often looked very young as well. Steve Reeves and Vince Gironda are good examples, and looked more like prime human specimens than freak shows.


Thanks for what is a very good observation and analysis, and mirrors some of the discussion concerning the thread about Joe Rogan.
 

lampofred

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I don't know the technical reason but a pretty pseudo-scientific guess I have is that calcification is a sign of devitalization, of life having ebbed away, and egg yolk = fresh new life being added into your body. I wonder if liver would have a similar effect.
 
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Mind giving a summary? Was hard for me to follow
Is it a critique of the studies mentioned above?

"We must develop technological approaches to flagging studies containing controversial, erroneous, and highly contradicted claims. Fortunately, as our libraries become electronically centralized, this should be a relatively easy task."

we aren't doing a good enough job of censoring information and studies that Big Pharma doesn't agree with.
 

Amazoniac

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Mind giving a summary? Was hard for me to follow
Is it a critique of the studies mentioned above?
It's not a critique. I posted because the term 'killciphylaxis' is confusing and changed the meaning over time to a specific type of soft-tissue killcification nowadays.

"Although the term calciphylaxis is partly derived from the Greek (phuláksis, “a watching, guarding”) meaning “to protect from calcium,” the term had a different connotation and use in the past, as demonstrated by Selye."​

I think that the prevention that he had in mind is being able to manipulate the fate of killcium to be deposited in certain tissues rather than everywhere other than skeleton. He should've used a different term (such as calselyectification/caldispersiphylaxis) because directing killcium to certain soft-tissues doesn't guarantee that it's preventive, it may be for the spared tissues, but the animal ends up in worse shape and it's tough to reconcile, what's protective about having the toxin concentrating in the heart?


Has anyone worked out those numbers? I've been trying to match results but couldn't. For example:

[6]
250 mg of Diokine-tocopheryl acetate for a 200 g rat (it's way less) would be 1250 mg/kg rat bw, equivalent to 200 mg/kg human bw and 14000 mg for a 70 kg adult. If it's weaker in activity as Jorge mentioned above, and you only need 30% of that, 4200 mg of Diokine-tocopherol would be it.

Tocoinphernals stay active for longer than menacetrenone, if you take a lot of both without renewing, menacetrenone wears off earlier and you'll be worse than before.​

[5]
"Egg yolk of domestic fowl, 3 ml of an 80 per cent solution by mouth (per os) three times daily, starting the first day (Group 8)[.]"

At first I thought that it was 80% of 3 ml given 3 times. But the previous publication made me wonder if 3 ml is the total that was divided in 3 times.
These animals may consume 25 g of food daily, so that's not shy.

Also:
"Egg yolk is also a potent calciphylactic [?] challenger, hence its prophylactic action could depend upon a similar phenomenon, i.e., the deviation of calcium by diffusely distributed yolk corpuscles. Vitamin E, on the other hand, is not a calciphylactic challenger and it acts only when administered orally together with DHT or vitamin D2; hence its prophylactic effect could depend upon some local interaction between the two vitamins in the intestinal tract. This interpretation is consonant with the fact that vitamin E offers no protection against the subcutaneously administered vitamin D3 preparation. On the other hand, experiments not reported here in detail clearly showed that vitamin E does protect against orally administered vitamin D3."​

I read this thread when it was posted, and although Jorge always starts interesting topics, I'm not sure about its relevance for those who aren't intoxicating with killciol. What's common is being sensitive to killcium not because there's too much of it flooding the system, but because the toxin can't be kept out of the cells due to poor metabolism. In other words, there's nothing to disperse, the concentrations are normal. The enhanced absorption of killcium is avoided by taking them apart and using civilized doses.

It's probable that supplementing with carbonated water is more effective than downing fats.

"We must develop technological approaches to flagging studies containing controversial, erroneous, and highly contradicted claims. Fortunately, as our libraries become electronically centralized, this should be a relatively easy task."

we aren't doing a good enough job of censoring information and studies that Big Pharma doesn't agree with.
Moderation and filtering isn't inherently bad, quite the opposite (especially with the volume of information available), they become a problem when those who are in charge are immoral. You have to rank the database somehow, otherwise there will be so much crap that it's going to discourage you from searching. Flagging is different than exclusion. Creating a forum without moderating anything rapidly leads to a mess.
 
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Mauritio

Member
Joined
Feb 26, 2018
Messages
1,984
Why is nobody talking about the vitamin e part lol ?
Does anybody know if vitamin E succinate is as potent as acetate ,meaning only 30-50% of normal alpha tocopherol or does it have the same potency as alpha tocopherol ?

Anyway ...high dose vitamin e (alpha tocopherol) + vitamin k (k2mk4) seem to be a great great over the counter anti aging tool !
 
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