I've read some analysis of Pauling's argument re megadosing with Vitamin C. My understanding is that there have been much distortions; the medical-pharmaceutical complex will browbeat anyone (even a two-time Nobel prize winner) claiming good health and longevity can be had from supplementing with "mere" Vitamin C. Sold as a supplement, Vitamin C is a non-proprietary form of medication that can potentially siphon off billions of health care spending from statin medications designed to lower LDL.

The issue here is the connection between Vitamin C and heart disease, which many people are missing. Pauling claimed that Vit C deficiency increases the level of LP(a) in blood. LP(a) gets going when there isn't enough Vit C by stiffening up blood vessels and forming plaques that often break off when inflammation is present. Since Vit C strengthens blood vessels and connective tissues without causing atherosclerosis, this "surrogate" function played by LP(a) is quite lethal.

LP(a) is thought to represent the genetic portion of CVD risk -- this shows up as part of your VAP test and is probably more important than the particle size of your LDL. Genetic because it doesn't seem to respond to treatment with statins and lifestyle changes such as diet and exercise. There are no drugs that will lower Lp(a), though some believe that diet and exercise, and supplements such as Niacin and fish oil, can reduce Lp(a).

If you examine animals that produce Vit C endogenously, they generally do not suffer from heart disease. Take dogs, for example. They may be fed a terrible, Neolithic diet full of refined carbs (Mighty Dog) but they usually do not have heart attacks. Why is that? Perhaps because their Lp(a) is never elevated because of the constant flow of sufficient Vit C in their blood vessels, warding off atherosclerosis?

This is the Pauling argument. He died in 1994. Lp(a) didn't become part of a standard blood test regimen until much later. Well, heck, even now, you can only get this if you order VAP. And most PCPs still don't know how to interpret it or even what to do when it's dangerously elevated. They just scratch their heads when someone who is young, thin, looks healthy with excellent lifestyle and eating habits fall prey to CVD. Chances are, such people also had family members that unexpectedly had heart attacks. Presumably, such people are genetically susceptible to have hyper-sensitive LP(a) triggers that respond quickly to Vit C deficiency.

Pauling may indeed be right if you realize that CVD is a degenerative disease, just like diabetes. If it's Vit C deficiency that causes atherosclerosis, then it's perfectly understandable that we would see plaques more or less in all people regardless of their diet. (Except in those who consistently ate a Vit C rich diet or supplemented with plenty of Vit C.C. Is this perhaps the reason why we didn't see plaques in someone like Pritikin who ate a plant-heavy diet?) Well, we have accounts of atherosclerosis among Inuits who ate nothing but marine mammals. Also, we have confirmed cases of atherosclerosis in Egyptian mummies, 2,000 years ago. These people didn't eat refined carbohydrates like Twinkies or modern versions of wheat. If you see that atherosclerosis is a painfully slow process that takes shape well after sexual maturity, you can see why evolution wasn't too concerned about phasing it out: evolution had a bigger fish to fry in ensuring successful procreation. All the more, if the loss of endogenous Vit C generation was an environmental adaptation, as Pualing points out -- a quid pro quo.

I've read some analysis of Pauling's argument regarding re megadosing with Vitamin C. My understanding is that there have been much distortions; the medical-pharmaceutical complex will browbeat anyone (even a two-time Nobel prize winner) claiming good health and longevity can be had from supplementing with "mere" Vitamin C. Sold as a supplement, Vitamin C is a non-proprietary form of medication that can potentially siphon off billions of health care spending from statin medications designed to lower LDL.

One underlying

The issue here is the connection between Vitamin C and heart disease, which many people here are missing. Pauling claimed that Vit C deficiency increases the level of LP(a) in blood. LP(a) seems to get gets going when there isn't enough Vit C by stiffening up blood vessels and forming plaques that often break off when inflammation is present. Since Vit C serves to strengthen strengthens blood vessels and connective tissues without causing atherosclerosis(nor eventual thrombosis), this surrogate "surrogate" function played by LP(a) is quite lethal.

LP(a) is thought to represent the genetic portion of CVD risk -- this shows up as part of your VAP test and is probably more important than the particle size of your LDL. Genetic because it doesn't seem to respond to treatment with statins and lifestyle changes such as diet and exercise. There are no drugs that will lower Lp(a), though some holistic doctors believe that diet and exercise, and supplements such as Niacin and fish oil, can reduce elevated Lp(a).

If you examine animals that produce Vit C endogenously, they generally do not suffer from heart disease. Take dogs, for example. They may be fed a terrible, Neolithic diet full of refined carbs (Mighty Dog) but they usually do not have heart attacks. Why is that? Perhaps because their Lp(a) is never elevated because of the constant flow of sufficient Vit C in their blood vessels, warding off atherosclerosis?

This is the Pauling argument. He died in 1994. Lp(a) didn't become part of a standard blood test regimen until much later. Well, heck, even now, you can only get this if you order VAP. And most PCPs still don't know how to interpret it or even what to do when it's dangerously elevated. They just scratch their heads when someone who is young, thin, looks healthy with excellent lifestyle and eating habits fall prey to CVD. Chances are, such people also had family members that unexpectedly had heart attacks. Presumably, such people are genetically susceptible to LP(a) triggers that respond quickly to Vit C deficiency.

Pauling may indeed be right if you realize that CVD is a degenerative disease, just like diabetes. If it's Vit C deficiency that causes atherosclerosis, then it's perfectly understandable that we would see plaques more or less in all people regardless of their diet. (Except in those who consistently ate a Vit C rich diet or supplemented with plenty of Vit C.) Well, we have accounts of atherosclerosis among Inuits who ate nothing but marine mammals. Also, we have confirmed cases of atherosclerosis in Egyptian mummies, 2,000 years ago. These people didn't eat refined carbohydrates like Twinkiesnor dine at Carl's Jr. If you see that atherosclerosis is a painfully slow process that usually takes shape well after sexual maturity, you can understand that see why evolution did not actively try to phase wasn't too concerned about phasing it out: evolution had a bigger fish to fry in procreation. Especially All the more, if the loss of endogenous Vit C generation was an environmental adaptation, as Pualing seems to think. A points out -- a quid pro quo.

I've read some analysis of Pauling's argument regarding Vitamin C. My understanding is that there have been much distortions; the medical-pharmaceutical complex will browbeat anyone (even a two-time Nobel prize winner) claiming good health and longevity can be had from supplementing with "mere" Vitamin C. Sold as a supplement, Vitamin C is a non-proprietary form of medication that can potentially siphon off billions of health care spending from statin medications designed to lower LDL.

One underlying issue is the connection between Vitamin C and heart disease, which many people here are missing. Pauling claimed that Vit C deficiency increases the level of LP(a) in blood. LP(a) seems to get going when there isn't enough Vit C by stiffening up blood vessels and forming plaques that often break off when inflammation is present. Since Vit C serves to strengthen blood vessels and connective tissues without causing atherosclerosis (nor eventual thrombosis), this surrogate function played by LP(a) is quite lethal.

LP(a) is thought to represent the genetic portion of CVD risk -- this shows up as part of your VAP test and is probably more important than the particle size of your LDL. Genetic because it doesn't seem to respond to treatment with statins and lifestyle changes such as diet and exercise. There are no drugs that will lower Lp(a), though some holistic doctors believe that diet and exercise, and supplements such as Niacin and fish oil, can reduce elevated Lp(a).

If you examine animals that produce Vit C endogenously, they generally do not suffer from heart disease. Take dogs, for example. They may be fed a terrible, Neolithic diet full of refined carbs (Mighty Dog) but they usually do not have heart attacks. Why is that? Perhaps because their Lp(a) is never elevated because of the constant flow of sufficient Vit C in their blood vessels, warding off atherosclerosis?

This is the Pauling argument. He died in 1994. Lp(a) didn't become part of a standard blood test regimen until much later. Well, heck, even now, you can only get this if you order VAP. And most PCPs still don't know how to interpret it or even what to do when it's dangerously elevated. They just scratch their heads when someone who is young, thin, looks healthy with excellent lifestyle and eating habits fall prey to CVD. Chances are, such people also had family members that unexpectedly had heart attacks. Presumably, such people are genetically susceptible to LP(a) triggers that respond quickly to Vit C deficiency.

Pauling may indeed be right if you realize that CVD is a degenerative disease, just like diabetes. If it's Vit C deficiency that causes atherosclerosis, then it's perfectly understandable that we would see plaques more or less in all people regardless of their diet. (Except in those who consistently ate a Vit C rich diet or supplemented with plenty of Vit C.) Well, we have accounts of atherosclerosis among Inuits who ate nothing but marine mammals. Also, we have confirmed cases of atherosclerosis in Egyptian mummies, 2,000 years ago. These people didn't eat Twinkies nor dine at Carl's Jr. If you see that atherosclerosis is a painfully slow process that usually takes shape well after sexual maturity, you can understand that evolution did not actively try to phase it out. Especially if the loss of endogenous Vit C generation was an environmental adaptation, as Pualing seems to think. A quid pro quo.