Vitamin c and collagen,quick gym workouts,medical weight loss clinic diet - You Shoud Know

admin | Boot Camp Training Routines | 03.08.2015
My cardiologist friend and the rest of the mainstream medical system has no clue about the steamroller (above image) coming to health care aiming right at the huge profits from diagnosis and treatment of heart disease, a multi billion dollar industry in the US. Vitamin C is required to make a protein called collagen which is the major component of connective tissues.  The lack of Vitamin C is a deficiency disease called Scurvy.
Above image courtesy of wikimedia commons  lysyl oxidase.Above image shows three steps in attachment of two fibrils (collagen strands) by combining two lysine molecules with the help of an enzyme lysine hydroxylase which requires vitamin C. In the full blown Vitamin C deficiency disease called Scurvy, the structural elements of the body literally fall apart.  Collagen is broken down and not replaced. Atherosclerotic plaques are not found randomly distributed throughout the arterial tree, rather distribution is restricted to sites of high mechanical stress such as bifurcations, and areas of motion such as the surface of the heart (coronary arteries).
Except for humans and primates, all other animals have the three enzymes in the liver which can synthesize vitamin C from glucose (a simple sugar).
As mentioned above, guinea pigs are especially well suited to study atherosclerosis because guinea pigs are unable to make their own vitamin C, and in addition, they develop atherosclerotic plaques similar to those found in humans. Coronary Calcium Score studies also support the Pauling Theory with favorable results after treatment with Vitamin C and Lysine.
Message boards are a source of anecdotal cases reports supporting the Linus Pauling Protocol.   The Track Your Plaque Message Boards have documented many cases of regression of atherosclerotic disease with protocols which include vitamin C  as well as other nutritional supplements. Using public funds, the NIH (National Institute of Health) funded a large study called The Physicians’ Health Study II which evaluated Vitamins C and E in heart disease and was published Nov. Enstrom showed that increasing vitamin C intake had a dramatic 40% reduction in mortality benefit which exceeds any statin drug study ever conducted. If heart disease is chronic scurvy, caused by chronic vitamin C deficiency, then it makes sense to supplement with vitamin C in the amounts needed to make strong collagen and prevent arterial damage from mechanical stress. In addition to Lysine, some of the collagen crosslinking is done with another amino acid called Proline, so proline was also added to the treatment protocol. A convenient powder containing all the combined ingredients for the Linus Pauling Protocol is called Ascorsine 9 and can be purchased at Tower Laboratories. What would happen if there was a cheap and effective way to reverse and prevent heart disease, (ie. Financial Disclosure:  I have no financial interest in Vitamin C Foundation, Tower Labororatories or LivOn Labs, Track Your Plaque, nor do I receive income from the sale of any books mentioned here.
SOME FACTORS IN THE CAUSATION OF INTIMAL HEMORRHAGES AND IN THE PRECIPITATION OF CORONARY THROMBI, J. Influence of ascorbic acid deficiency on serum and hepatic lipid and on the aorta were studied. Control animals of the experimental groups were fed with the same diet of previous two groups and received 25 mg of ascorbic acid subcutaneously for the same period (group 2 and 4).
Moderate increase of triglyceride and cholesterol ester and beta-lipoprotein in the serum of ascorbic acid deficiency (group 1), and markedly to approximately twice of normal in the ascorbic acid deficiency with coconut oil feeding (group 3). Increase of serum lipids and depression of plasma lipoprotein lipase activity by ascorbic acid deficiency was prevented by ascorbic acid administration as observed in the control groups. Hyperglycemia-induced ascorbic acid deficiency promotes endothelial dysfunction and the development of atherosclerosis.Price KD, Price CS, Reynolds RD.
Dehydroascorbic acid, the oxidized form of vitamin C, is transported into mammalian cells via facilitative glucose transporters and hyperglycemia inhibits this process by competitive inhibition. Basic research and observational studies suggest vitamin E or vitamin C may reduce the risk of cardiovascular disease.
Objective  To evaluate whether long-term vitamin E or vitamin C supplementation decreases the risk of major cardiovascular events among men. Design, Setting, and Participants  The Physicians’ Health Study II was a randomized, double-blind, placebo-controlled factorial trial of vitamin E and vitamin C that began in 1997 and continued until its scheduled completion on August 31, 2007.
Intervention  Individual supplements of 400 IU of vitamin E every other day and 500 mg of vitamin C daily. Main Outcome Measures  A composite end point of major cardiovascular events (nonfatal myocardial infarction, nonfatal stroke, and cardiovascular disease death). Conclusions  In this large, long-term trial of male physicians, neither vitamin E nor vitamin C supplementation reduced the risk of major cardiovascular events.
The formation of mature fibrillar collagen involves many steps beyond gene transcription (Figure). The ascorbate-dependent addition of polar hydroxyl groups to the side chains of proline and lysine may aid the self-assembly and stability of the collagen fibril by forming interchain hydrogen bonds. It is curious indeed that many remain suspicious of pharmacological lipid-lowering, a strategy now proven unequivocally to prevent myocardial infarction and stroke and to prolong life as well. We examined the relation between vitamin C intake and mortality in the First National Health and Nutrition Examination Survey (NHANES I) Epidemiologic Follow-up Study cohort. Epidemiologic studies have suggested a lower risk of coronary heart disease (CHD) at higher intakes of fruit, vegetables, and whole grain.


Design:A cohort study pooling 9 prospective studies that included information on intakes of vitamin E, carotenoids, and vitamin C and that met specific criteria was carried out.
Resultsietary intake of antioxidant vitamins was only weakly related to a reduced CHD risk after adjustment for potential nondietary and dietary confounding factors.
Conclusions:The results suggest a reduced incidence of major CHD events at high supplemental vitamin C intakes. 1) CV Mortality declines after Vitamin C Consumption increases after publication of Linus PAuling Book published 1970.  US is only industrialized country to experience a 40% drop in CV disease. 2) Most high order mammals make their own vitamin C (3-11 g daily) do not have CV (cardiovascular) disease as seen in humans. 3) Animals such as the Guinea pig which cannot make their own vitamin C, also have cardiovascular disease, same as humans if they are fed a Vitamin C deficient diet. 4) The Willis Guinea Pig Experiments in the 1950’s show that depriving the animal of vitamin C causes atherosclerosis which is quite similar to the human lesion. 8) Plaques are often localized to areas of mechanical stress, at bifurcations, and the surface of the heart (coronary arteries or carotid arteries).
9) Vitamin C is required (and used up) making collagen – the most abundant protein in the human body. 10) Scurvy is caused by a deficiency in making collagen which is in turn caused by a lack of vitamin C. 11) The Beisiegel studies in Germany of post-mortem human aortas in 1989 determined that plaque consists of Lp(a) and only Lp(a) – no ordinary LDL. Heart Disease and Vitamin C, Linus Pauling Genius discovered a way to stop and reverse heart disease in humans. The long-term effect of eicosapentaenoic acid on serum levels of lipoprotein (a) and lipids in patients with vascular disease. Vitamin C is required for lysyl hydroxylase, an enzyme responsible for attaching the lysine residues together on adjacent collagen strands. The joints wear out, the small arteries begin to crack and degenerate, the skin shows easy bruising and bleeding as small vessels rupture throughout the body, and the teeth may loosen and fall out. The GLO deficient mice fed a vitamin C deficient diet developed atherosclerotic plaques in the aorta with characteristic deranged collagen crosslinking.
Since there are no patents involved for natural supplements, and no drugs involved, no drug company would ever invest the 250 million dollars to fund such a study with no potential for financial return. Two groups of ascorbic acid deficient guinea pigs were made by feeding with scorbutic diet with or without 5% coconut oil for two weeks (group 3 and 1). Histological examination of the aorta revealed edematous swelling of the ground substance in the intima and media in the scorbutic, and early atheromatous lesions of accumulated foam cells in the intima of the ascorbic acid deficiency with coconut oil feeding. In the guinea pig, marginal AH2 deficiency results in intracellular oxidative damage in the cardiac tissue as evidenced by lipid peroxidation, formation of fluorescent pigment and loss of structural integrity of the microsomal membranes. This inhibited transport may promote oxidative stress and contribute to the increase in atherosclerotic cardiovascular disease observed in patients with diabetes mellitus. However, few long-term trials have evaluated men at initially low risk of cardiovascular disease, and no previous trial in men has examined vitamin C alone in the prevention of cardiovascular disease. These data provide no support for the use of these supplements for the prevention of cardiovascular disease in middle-aged and older men. The absence of sufficient ascorbic acid (vitamin C), a required cofactor for prolylhydroxylase, thus impairs the formation of stable collagen.
Unlike humans, usual experimental animals can synthesize vitamin C and thus cannot be made scorbutic. First, these studies may have employed suboptimal doses of the vitamins used, or interactions among them may have mitigated a beneficial effect of one or the other supplements.
Yet, many individuals readily consume costly vitamin supplements devoid of benefit in clinical trials.
Whether this association is due to antioxidant vitamins or some other factors remains unclear. L-Proline: 3 grams twice per day (acts to release lipoprotein(a) from plaque formation and prevent further deposition of same). L-Lysine: 3 grams twice each day (acts to release lipoprotein(a) from plaque formation and prevent further deposition of same).
Mixing vitamin C into the air conditioner air stream is intended to have a moisturizing effect by being available directly to the skin.To mix vitamin C into the air conditioner's air stream, a ceramic additive in the filter releases vitamin C in the presence of moisture in the air. Willis, a Canadian doctor, conducted research with guinea pigs in the 1950’s showing that guinea pigs deprived of dietary vitamin C developed atherosclerotic plaques, while guinea pigs given plentiful vitamin C were protected. Sesso.  The study found that Vitamin C and E did not prevent mortality from heart disease, results which are completely opposite to massive previously published research and anecdotal case reports. These findings suggest that any factors disturbing ascorbic acid metabolism induce an increase of serum lipids and altered vascular wall metabolism, and consequently follows atherosclerosis.


The oxidative damage does not occur due to lack of enzymatic scavengers of reactive oxygen species such as superoxide dismutase, catalase and glutathione peroxidase. Collagen contains unusual amino acids, hydroxyproline and hydroxylysine, formed by a vitamin C–dependent process that entails enzymatic transfer of hydroxyl groups to selected proline and lysine residues in the nascent procollagen chains. The human phenotype of vitamin C deficiency, scurvy, classically involves fragility of blood vessels. Maeda’s group has recently introduced a targeted mutation that makes mice dependent on dietary vitamin C, allowing manipulation of ascorbate levels. Physiological concentrations of ascorbic acid can inhibit in vitro oxidative modification of LDL, a critical event during atherogenesis.13 For this reason, many individuals take this and other antioxidant vitamins in hope that combating oxidative stress can forestall atherosclerosis and its complications.
In this regard, vitamin E monotherapy showed no benefit on atherosclerotic events in both the Heart Outcomes Prevention Evaluation (HOPE) and GISSI studies.21,22 In these various studies, the degree of preexisting disease or inadequate duration of treatment might have limited the benefit of the antioxidants. This situation may reflect in part a failure of the medical community to communicate effectively with the public regarding evidence-based medicine and the life-saving benefits of preventive strategies. There is no clear relation for individual cancer sites, except possibly an inverse relation for esophagus and stomach cancer among males.
Inositol hexanicotinate is a form of niacin which gives less of a problem with flushing and therefore allows for larger therapeutic doses. Toward a new recommended dietary allowance for vitamin C based on antioxidant and health effects in humans. Serum ascorbic acid and gallbladder disease prevalence among US adults: the Third National Health and Nutrition Examination Survey (NHANES III).
Willis, MD, made these same observations, and they have been confirmed by 60 years of coronary and peripheral arteriography at major medical centers. In this issue of Circulation, Nakata et al8 studied atheroma in hypercholesterolemic and scorbutic mice. Vitamin C has other antiinflammatory effects as well, including decreased leukocyte adhesion to the endothelium and increased bioavailability of atheroprotective nitric oxide (NO).
Yet, the striking beneficial effects observed in the statin treatment arms of both the HPS and HATS20 and of the angiotensin converting enzyme inhibitor in the HOPE study21 establish the mutability of outcomes measured in these patient populations in the same trials.
The present results of Nakata et al8 reinforce the importance of collagen metabolism in determining the structure of atherosclerotic plaques. An index of vitamin C intake has been formed from detailed dietary measurements and use of vitamin supplements. The relation with all causes of death among males remains after adjustment for age, sex, and 10 potentially confounding variables (including cigarette smoking, education, race, and disease history). Lipid peroxidation, fluorescent pigment formation and protein modification disappear after AH2 therapy. The hydroxylated and glycosylated monomers then self-assemble into helical trimers as they traverse several intracellular compartments. Of course, chemical characterization of vitamin C as the antiscorbutic factor did not occur until the 1930s. They find no change in lesion size, but they observe decreased collagen content in the lesions.
Partition of fat-soluble vitamin E into the lipid phase of plaque or lipoproteins might shield it from the cooperative antioxidant effect of water-soluble ascorbate, excluded from these lipid milieux. However, current clinical and experimental evidence suggests that the best way to influence favorably the balance of collagen synthesis and degradation in atheroma at hand today remains lipid-lowering, not vitamin C. The relation of the standardized mortality ratio (SMR) for all causes of death to increasing vitamin C intake is strongly inverse for males and weakly inverse for females. Basic theory is that most of animal species produce own bitamin C in the liver.  Humans cannot make vitamin C, and we suffer cardiovascular disease. Trimming the nonhelical tails (the telopeptides) from both ends of the procollagen molecule by proteinases yields the mature interstitial collagen triple helix secreted by smooth muscle cells in arteries.
Such changes should impair the biomechanical strength of the plaque and make it more prone to rupture.
Thus, more potent or amphipathic antioxidants might interrupt oxidative stress during atherogenesis more effectively than the vitamins. These building blocks then further self-aggregate into multimers and form interstitial collagen fibrils, linear structures as strong as steel wires.
This finding extends the burgeoning evidence that changes in collagen metabolism can influence crucial characteristics of the atherosclerotic plaque. Although vitamin deficiencies lead to disease, consumption of pharmacological amounts of these substances in individuals who maintain vitamin-sufficient diets may not prevent disease.



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