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TLC 3.0 represents a true orthomolecular heart health formulation with testimonials from case reports that indicate amazing results. TLC 3.0 contains an unprecedented combination of nutrients to keep blood vessels strong based on the research of the late Dr. Linus Pauling (along with Dr. Matthias Rath), who made a connection between vitamin C and atherosclerosis.
TLC 3.0 is designed to preserve the health of blood vessels by preventing the build-up of arterial plaques. High-dose vitamin C helps to produce collagen, which in turn heals, strengthens and protects the arteries, particularly against the potential danger posed by a circulating lipoprotein known as Lp(a). Lp(a) binds to injured blood vessels, rapidly delivering the cholesterol needed to regenerate the cell wall. Of course, this is how atherosclerotic plaque is formed. Lysine and proline provide alternate binding sites for Lp(a), reducing its ability to attach to the blood vessels and allowing vitamin C to do its healing work. Taurine, magnesium, potassium and calcium are also essential for maintaining a regular heartbeat, and for good muscle and nerve function in the heart.
TLC 3.0 is ideal for those looking for a high-dose vitamin C formula or electrolyte formula, or for those who are concerned about their cardiovascular health.
TLC 3.0™ is formulated based on the research of Linus Pauling and Matthias Rath into the role of lipoprotein(a) [Lp(a)] in cardiovascular health, and the evolutionary relationship between Lp(a) and vitamin C. The ingredients in TLC 3.0™ are factors in the maintenance of good health.
|AOR04243||80023541||240 G POWDER|
|Serving Size: 1 Level Tablespoon (approx. 11.5 g)||Amount||% Daily|
|Vitamin C (ascorbic acid, calcium and magnesium ascorbates)||3000 mg|
|Magnesium (carbonate, ascorbate)||340 mg|
|Potassium (bicarbonate)||99 mg|
|Calcium (carbonate, ascorbate)||545 mg|
silicon dioxide, natural flavour (lemon), gum Arabic, maltodextrin, dextrose, tricalcium phosphate.
AOR™ guarantees that all ingredients have been declared on the label. Contains no wheat, gluten, dairy, soy, eggs or shellfish.
Stir 1 level tablespoon (approx. 11.5g) into a glass of water or juice without food, or as directed by a qualified health care practitioner.
Consult a health care practitioner prior to use if you are following a low protein diet or if you are pregnant or breastfeeding.
Healthy blood vessels
The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide or replace medical advice to individuals from a qualified health care professional. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes.
Vitamin C with L-Lysine and L-Proline: The Pauling Heart Health Prescription
Many epidemiological studies have linked a higher intake, or blood levels, of vitamin C with lower risk of cardiovascular disease and heart attack. But the reasons remain unclear. Some studies have found that vitamin C supplementation improves many known CVD risk factors, lowering total cholesterol, boosting HDL (“good”) cholesterol, reducing the oxidation of LDL (“bad”) cholesterol, and lowering blood pressure. But other studies have failed to substantiate these findings, leaving the connection between vitamin C and heart health a bit of a mystery.
Lp(a) & Cardiovascular Disease: The Missing Link?
In the last years of his life, the great vitamin C researcher and godfather of orthomolecular medicine Dr. Linus Pauling uncovered a potential explanation for this puzzle – and along with Dr. Matthias Rath, performed a series of key experiments to back it up. But this theory doesn’t just help to explain the protective powers of vitamin C against heart disease. It provides a theoretical basis for a supplement combination to enhance its effects. The missing link: a new cardiovascular risk factor known as lipoprotein (a) [Lp(a)].
High Lp(a) Makes “Bad” Cholesterol Look Good
Lp(a) a lipoprotein, like “high-density lipoprotein” (HDL) and “low-density lipoprotein” (LDL). Lipoproteins are complexes made up of a central core of fats and cholesterol, surrounded by an outer layer of proteins, cholesterol, and phospholipids, which transport fatty substances in your body through the lymph and blood. We know LDL as the “bad” cholesterol, but elevated Lp(a) is an even greater threat to cardiovascular health. There’s a lot less Lp(a) than LDL circulating through your system – but the small numbers on your lab report can belie the size of the threat. Your total cholesterol poses no danger to you if it’s below 180 milligrams per deciliter, and LDL is safe as long as it’s kept under 100 milligrams per deciliter. But Lp(a) cholesterol becomes a threat to your health at levels of just 10 milligrams per deciliter. (Other labs use total Lp(a) instead of Lp(a) cholesterol levels, in which case the danger threshold is pegged at 30 milligrams per deciliter). People with Lp(a) levels greater than 10 milligrams per deciliter are at about twice the risk of coronary heart disease as people with lower levels – and if total cholesterol and LDL are also high, the risk can increase fivefold.
Worse Than LDL
What makes Lp(a) a killer is its structure. At the molecular level, Lp(a) looks a lot like LDL (“bad”) cholesterol. Like LDL, it contains a central protein called apolipoprotein B-100 (apoB-100), some phospholipids, and cholesterol itself. But in Lp(a), the apolipoprotein B-100 is chemically bonded to an additional large protein known as apolipoprotein (a) [apo(a)]. It’s this extra protein that makes Lp(a) behave differently from LDL – and that makes it so deadly.
Prevents Clot Dissolution
The apo(a) component of Lp(a) has a close structural resemblance to plasminogen – a dormant form of the enzyme plasmin, which helps the body to break up blood clots. Because of this structure, Lp(a) interferes with the breakup of blood clots – clots, which can trigger a heart attack by blocking off the delivery of blood to the heart, or contribute to the fibrous, scary mess that makes up a plaque in the blood vessels.
So what is a potential killer doing lurking in your body? It appears that Lp(a) is involved in the body’s response to injury to the blood vessel wall – the kind of injuries that underlie advanced atherosclerotic disease. Lp(a) acts as an acute-phase reactant in the body: a substance released in response to acute injury, infection, or other inflammatory conditions. (Other acute-phase reactants that are linked to higher cardiovascular risk include C-reactive protein (CRP) and fibrinogen).
A Fine Balance
Lp(a) does help injured blood vessels to heal. It binds to the scab material on the wounded blood vessel, preventing the digestion of blood clots on an injured blood vessel, and binds to the cellular matrix of injured vessels, rapidly delivering the cholesterol needed to regenerate the cell wall. This is a great defense to have if you’ve just been pierced by fang or claw – but it’s also a sure way to promote atherosclerosis, as the body’s defenses against short-term, acute trauma are misdirected into a chronic inflammatory process that leads to heart disease.
The Vitamin C Solution
Lp(a)’s role appears to be due to the fact that humans are unable to synthesize vitamin C. Lp(a) is closely linked to vitamin C. When blood vessels are damaged, Lp(a) acts to block blood clots and deposit cholesterol, healing the vessel, but potentially causing long-term damage. Vitamin C, on the other hand, keeps blood vessels strong to prevent blood vessel injuries. When levels of the vitamin are optimal, Lp(a)’s beneficial actions are not required and its harmful effects can be avoided. The amino acids lysine and proline enhance the effects of vitamin C and prevent Lp(a) from binding to blood vessel walls. Proline can block the formation of Lp(a) in the first place.
A Longterm Partnership
Dr. Linus Pauling became interested when it was observed that Lp(a) is found almost exclusively in species which cannot make their own vitamin C: the guinea pig and the primates – including we human primates. The adaptive purpose of Lp(a) is intimately tied into one of the key functions of vitamin C: through its role in collagen synthesis, ascorbate is needed for the maintenance of healthy blood vessels over the long term, while Lp(a) is produced in an effort to repair blood vessels which have suffered short-term damage.
Lp(a) is meant to help heal blood vessels which were more prone to injury because they had been weakened by poor collagen synthesis, owing to their lack of vitamin C – their hypoascorbemia, or genetically-induced “borderline” vitamin C deficiency. In effect, Lp(a) is a “surrogate for ascorbate.”
Guinea Pig Cardiovascular Disease Reversed by Vitamin C
There was already experimental evidence for this. Humans and other primates are nearly the only animals that develop atherosclerosis: rabbits and other rodents can be forced to develop heart disease if they are fed a diet loaded with saturated fat and cholesterol, but the disease process is very different from that seen in humans. The one exception is the guinea pig – the only rodent that does not synthesize its own vitamin C. In the 1950s, the Canadian cardiologist Dr. GC Willis demonstrated that guinea pigs on a diet lacking saturated fat or cholesterol develop lipid deposits in their arteries, which are morphologically identical to human atherosclerosis – if their diet is also low in vitamin C. Even more excitingly, Dr. Willis found that this atherosclerosis could be reversed by high-dose vitamin C supplementation. A small human pilot study confirmed this observation.
3 Grams A Day
Pauling and Rath repeated and expanded Dr. Willis’ work, showing that the amount of vitamin C required to prevent the development of atherosclerosis in the hypoascorbemic guinea pig is 40 milligrams per kilogram of body weight. In a 70 kilogram human, the experimental data thus suggests that a minimum requirement of 2 800 mg of vitamin C per day would be required to prevent heart disease in our own species.
Vitamin C… Plus What?
In a small human trial run by Dr. Rath, people with high Lp(a) levels who supplemented with nine full grams of ascorbate for 14 weeks experienced an average 27% reduction in Lp(a) levels. However, a larger, controlled trial failed to confirm this result. On the one hand, the larger trial used only half of the dose of vitamin C used in Dr. Rath’s trial, so the result could just be due to a failure to use enough ascorbate. But it’s more likely that vitamin C doesn’t lower the level of Lp(a). Lp(a) levels are mostly determined by your genes, and the only conclusively proven ways to lower Lp(a) levels are niacin supplements (which can be taken in the form of inositol hexanicotinate) and estrogen “replacement” therapy in postmenopausal women.
Instead, the relationship between vitamin C and Lp(a) suggest that doses of vitamin C sufficient to correct our genetic lack of vitamin C will neutralize the threat posed by high Lp(a) levels – rather than lowering the simple amount of the lipoprotein. By keeping blood vessel walls strong, vitamin C would prevent the injuries that cause Lp(a) to bind to the cells of the arterial wall. Ultimately, you aren’t at risk from the Lp(a) circulating in your blood, but with the process by which Lp(a) infiltrates your arteries – and it’s this infiltration that ascorbate prevents, as Pauling’s research suggests.
A Misguided Interpretation
Amusingly, some early evidence for this may have come from a trial that reported that vitamin C supplementation led to “thickening” of the blood vessels in elderly subjects, as measured by intima-media thickness (IMT). The media ran screaming headlines about this study, jumping on the findings even though they have never been published in a peer-reviewed scientific journal. “Vitamin C Pills, Artery Clogs Linked” cried one newspaper; “Vitamin C Supplements May Add to Artery Hardening” proclaimed another, as evidence that ascorbate supplementation causes atherosclerosis. But the IMT technique alone cannot actually detect atherosclerotic plaque: to do that, you need more advanced imaging analysis, including the plaque index (a measure of the degree of focal plaque) and the velocity ratio, which assesses any interference with blood flow. What this study may actually have done is to confirm the effectiveness of vitamin C at enhancing collagen synthesis and restoring the normal thickness of blood vessels thinned by the aging process. We know that this thinning happens, just as it does in the skin, because the aging process reduces your body’s ability to synthesize new collagen.
Vitamin C Plus Lysine & Proline
By linking vitamin C’s heart-protective powers to the strengthening of the blood vessels, leading to the prevention of arterial injury and to the reduction of Lp(a) binding to the arterial wall, Pauling’s theory also reveals a way to enhance the effect of ascorbate: by adding the amino acids L-lysine and L-proline to your supplement plan. The elastin and collagen that give strength and flexibility to the arterial wall are rich in both of these amino acids, and apo(a) (the protein sequence which, when tagged on to LDL cholesterol, forms Lp(a) and makes it so deadly) uses its lysine binding site (LBS) as a “grappling hook” to adhere to the blood vessel wall and to bind to fibrin in fibrous caps of atherosclerotic plaques. The importance of the LBS in Lp(a)’s assault on your blood vessels was shown dramatically in a recent study using experimental animals. “Wild-type” mice, which don’t produce apo(a), do not develop atherosclerosis, even if fed a diet high in saturated fat. But when scientists gave one group of mice the gene which encodes the standard human form of apo(a), they rapidly develop fatty deposits in their blood vessels and of apo(a) in their aortas on the same diet. Yet when the same animals are given a version of the apo(a) gene with an altered sequence in the lysine binding site, they remain free of atherosclerosis.
Studies in isolated Lp(a) show that free L-lysine can act as a kind of molecular “chaff,” tying up the LBS and preventing Lp(a) from binding to the kind of lysine residues present in the blood vessels. And L-proline has an even greater binding affinity for Lp(a) than does L-lysine itself, because of a domain outside the LBS which is sensitive to both L-lysine and L-proline.
In fact, L- proline appears to have additional Lp(a)-fighting benefits not shared by vitamin C or L-lysine. In addition to its more potent affinity for Lp(a)’s binding sites, L- proline interferes with the formation of a complex between Lp(a) and triglyceride-rich lipoproteins which is common in people with high triglycerides and which appears to further increase the uptake of Lp(a) by the arteries. As well, recent evidence suggests that L-proline intervenes in the formation of Lp(a) by keeping apo(a) from binding to the apoB in LDL cholesterol molecule to form Lp(a).
Many integrative physicians have reported success with combinations of ascorbate and lysine, often along with proline and/or other nutraceuticals, in treating people suffering with heart disease. Linus Pauling himself reported the first such case: a National Science Medalist who had already undergone several coronary artery bypass grafts (CABG), each of which had successively re-clogged, and who had been prescribed statin drugs for high cholesterol as well as calcium channel blockers and beta-blockers for high blood pressure. After discussing his history with Pauling, this person began an orthomolecular supplement program, including six grams of vitamin C; however, his condition continued to worsen. Pauling then suggested adding L-lysine (peaking at 6g/day) to his cocktail. The result was described as “border[ing] on miraculous” by the patient: his walking distance suddenly recovered, and he was again able to do his own yardwork (including the cutting up of a tree with his chainsaw and the painting of his house).
Other cases have been reported by Dr. Rath, and by a variety of orthomolecular physicians – including the case of Dr. Kathie Dalessandri, MD, who reported her own dramatic improvement after using vitamin C and lysine in the Archives of Internal Medicine.
Based on this groundbreaking research, a new hope for heart health has emerged. The synergistic combination of vitamin C, L-lysine, and L-proline opens up a safe, natural way to defuse the charge before a tragedy strikes.
Most people experience some degree of arterial narrowing by the end of their life. Heart disease is one of the number one killers in developed countries. Modern medical interventions for symptoms of blood vessel disease include blood pressure drugs and cholesterol drugs. However, none of these deal with the root of the problem, and many cause adverse effects.
TLC 3.0 represents a true orthomolecular formulation with testimonials from case reports that indicate amazing results. TLC 3.0 contains an unprecedented combination of nutrients to keep blood vessels strong and healthy and reduce the risk of developing cardiovascular disease. TLC: try for yourself and see!
Boonmark NW, Lou XJ, Yang ZJ, Schwartz K, Zhang JL, Rubin EM, Lawn RM. Modification of apolipoprotein(a) lysine binding site reduces atherosclerosis in transgenic mice. J Clin Invest. 1997 Aug 1;100(3):558-64.
Lippi G, Guidi G. Lipoprotein(a): an emerging cardiovascular risk factor. Crit Rev Clin Lab Sci. 2003 Feb; 40(1): 1-42.
Price KD, Price CS, Reynolds RD. Hyperglycemia-induced latent scurvy and atherosclerosis: the scorbutic-metaplasia hypothesis. Med Hypotheses. 1996 Feb; 46(2): 119-29.
Rath M. and Pauling L. Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig. PNAS. 87(23): 9388-90. Rath M, Pauling L. Hypothesis: lipoprotein(a) is a surrogate for ascorbate. PNAS. 1990 Aug; 87(16): 6204-7.
Rath M. Lipoprotein(a) reduction by ascorbate. J Orthomolec Med. 1992 Aug; 7(1): 81-2.
Rath M. Reducing the risk for cardiovascular disease with nutritional supplements. J Orthomolec Med.1995; 7(3): 153-62.
Trieu VN, Zioncheck TF, Lawn RM, McConathy WJ. Interaction of apolipoprotein(a) with apolipoprotein B-containing lipoproteins. J Biol Chem. 1991 Mar 25; 266(9): 5480-5.
Willis GC. The reversibility of atherosclerosis. CMAJ. 1957 Jul 15; 77(2): 106-9.
Lipoprotein(a): an emerging cardiovascular risk factor.
Crit Rev Clin Lab Sci. 2003 Feb; 40(1): 1-42.
Lippi G, Guidi G.
Lipoprotein(a) is a cholesterol-enriched lipoprotein, consisting of a covalent linkage joining the unique and highly polymorphic apolipoprotein(a) to apolipoprotein B100, the main protein moiety of low-density lipoproteins. Although the concentration of lipoprotein(a) in humans is mostly genetically determined, acquired disorders might influence synthesis and catabolism of the particle. Raised concentration of lipoprotein(a) has been acknowledged as a leading inherited risk factor for both premature and advanced atherosclerosis at different vascular sites. The strong structural homologies with plasminogen and low-density lipoproteins suggest that lipoprotein(a) might represent the ideal bridge between the fields of atherosclerosis and thrombosis in the pathogenesis of vascular occlusive disorders. Unfortunately, the exact mechanisms by which lipoprotein(a) promotes, accelerates, and complicates atherosclerosis are only partially understood. In some clinical settings, such as in patients at exceptionally low risk for cardiovascular disease, the potential regenerative and antineoplastic properties of lipoprotein(a) might paradoxically counterbalance its athero-thrombogenicity, as attested by the compatibility between raised plasma lipoprotein(a) levels and longevity.
Hyperglycemia-induced latent scurvy and atherosclerosis: the scorbutic-metaplasia hypothesis.
Med Hypotheses. 1996 Feb; 46(2): 119-29.
Price KD, Price CS, Reynolds RD.
Latent scurvy is characterized by a reversible atherosclerosis that closely resembles the clinical form of this disease. Acute scurvy is characterized by microvascular complications such as widespread capillary hemorrhaging. Vitamin C (ascorbate) is required for the synthesis of collagen, the protein most critical in the maintenance of vascular integrity. We suggest that in latent scurvy, large blood vessels use modified LDL–in particular lipoprotein(a)–in addition to collagen to maintain macrovascular integrity. By this mechanism, collagen is spared for the maintenance of capillaries, the sites of gas and nutrient exchange. The foam-cell phenotype of atherosclerosis is identified as a mesenchymal genetic program, regulated by the availability of ascorbate. When vitamin C is limited, foam cells develop and induce oxidative modification of LDL, thereby stabilizing large blood vessels via the deposition of LDL. The structural similarity between vitamin C and glucose suggests that hyperglycemia will inhibit cellular uptake of ascorbate, inducing local vitamin C deficiency.
Reducing the risk for cardiovascular disease with nutritional supplements.
J Orthomolec Med.1995; 7(3): 153-62.
Reducing the risk for cardiovascular disease (CVD) is a primary goal of any health care system in the industrialized world. The success of this world-wide effort will largely depend on the proper understanding of the mechanisms responsible for development of this disease. This paper marshals the scientific evidence for the predominant pathomechanisms of CVD and presents new therapeutic approaches. Human atherosclerotic lesions are primarily composed of lipoprotein(a). The extracellular deposition of this lipoprotein directly parallels the extent of the atherosclerotic lesion. The frequency of this pathomechanism today is directly related to its efficacy as a defense mechanism during the evolution of man, particularly in stabilizing the vascular wall during ascorbate deficiency. The deposition of lipoprotein(a) in form of largely intact particles implies the reversibility of this mechanism.On the basis of an improved understanding about the pathogenesis of CVD new therapeutic approaches are defined. Certain vitamins and amino acids are of particular importance for these approaches. Ascorbate is essential for preserving and restoring the integrity and stability of the vascular wall. Niacin and ascorbate were reported to lower lipoprotein(a) plasma levels. It is proposed that this effect is mediated by NADPH. The amino acids L-lysine and L-proline competitively interfere with the binding of lipoprotein(a) to constituents of the vascular wall and atherosclerotic lesions. The therapeutic use of these amino acids could prevent further buildup of lipoprotein(a) accumulation in the vascular wall. More importantly, optimum concentrations of L-lysine and L-proline could release deposited lipoprotein(a) but also other atherogenic lipoproteins form the vascular wall. This paper defines a new therapeutic goal: The pharmaceutical, non-invasive reversal of existing CVD with nutritional supplements.
Lipoprotein(a) reduction by ascorbate.
J Orthomolec Med. 1992 Aug; 7(1): 81-2.
High plasma levels of lipoprotein(a) constitute a strong risk factor for cardiovascular disease. Lipoprotein(a) is primarily found in the plasma of man and other species that are unable to synthesize ascorbate endogenously. Here it is shown that ascorbate, a strong physiologicalreducing agent, lowers elevated lipoprotein(a) plasma levels in man.
Interaction of apolipoprotein(a) with apolipoprotein B-containing lipoproteins.
J Biol Chem. 1991 Mar 25; 266(9): 5480-5.
Trieu VN, Zioncheck TF, Lawn RM, McConathy WJ.
Recombinant DNA-derived apolipoprotein(a) was used to demonstrate that the apo(a) moiety of lipoprotein(a) (Lp(a)) is responsible for the binding of Lp(a) to other apolipoprotein B-containing lipoproteins (apoB-Lp) including LDL2, a subclass of low density lipoproteins (d = 1.030-1.063 g/ml). The r-apo(a).LDL2 complexes exhibited the same binding constant as Lp(a).LDL2 (10(-8) M). Treatment of either recombinant apo(a) or Lp(a) with a reducing agent destroyed binding activity. A synthetic polypeptide corresponding to a portion of apo(a)\’s kringle-4 inhibited the binding (K1 = 1.9 x 10(-4) M) of LDL2 to Lp(a). Therefore, we concluded that binding to apoB-Lp was mediated by the kringle-4-like domains on apo(a). Using ligand chromatography which can detect complexes having a KD as low as 10(-2) M, we demonstrated the binding of plasminogen to apoB-Lp. Like Lp(a), binding of plasminogen to apoB-Lp was mediated by the kringle domain(s). The differences in binding affinity may be due to amino acid substitutions in the kringle-4-like domain. In most of the kringle-4-like domains of apo(a), the aspartic residue critical for binding to lysine was substituted by valine. Consistent with this substitution, we found that L-proline and hydroxyproline, but not L-lysine, inhibited the binding of LDL2 to apo(a). Inhibition by L-proline could be reversed in the binding studies by increasing the amount of apo(a); and L-proline-Sepharose bound plasma Lp(a), suggesting that L-proline acted as a ligand for the kringle-4-like domain(s) of apo(a) involved in the binding of apoB-Lp. The binding of apo(a) to proline and hydroxyproline could be responsible for the binding of apo(a) to the subendothelial extracellular matrix, i.e. domains of proteins rich in proline or hydroxyproline (e.g. collagen and elastin).
Hypothesis: lipoprotein(a) is a surrogate for ascorbate.
Proc Natl Acad Sci U S A 1990 Aug; 87(16): 6204-7.
Rath M, Pauling L.
The concept that lipoprotein(a) [Lp(a)] is a surrogate for ascorbate is suggested by the fact that this lipoprotein is found generally in the blood of primates and the guinea pig, which have lost the ability to synthesize ascorbate, but only rarely in the blood of other animals. Properties of Lp(a) that are shared with ascorbate, in accordance with this hypothesis, are the acceleration of wound healing and other cell-repair mechanisms, the strengthening of the extracellular matrix (e.g., in blood vessels), and the prevention of lipid peroxidation. High plasma Lp(a) is associated with coronary heart disease and other forms of atherosclerosis in humans, and the incidence of cardiovascular disease is decreased by elevated ascorbate. Similar observations have been made in cancer and diabetes. We have formulated the hypothesis that Lp(a) is a surrogate for ascorbate in humans and other species and have marshaled the evidence bearing on this hypothesis.
Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig. P
roc Natl Acad Sci USA 1990 Dec; 87(23): 9388-90.
Rath M, Pauling L.
Lipoprotein(a) [Lp(a)] is an extremely atherogenic lipoprotein. Lp(a) has been found in the plasma of humans and other primates, but until now only in a few other species. The mechanism by which it exerts its atherogenicity is still poorly understood. We observed that Lp(a) has been found in the plasma of several species unable to synthesize ascorbate and not in other species. We have now detected apoprotein(a) in the plasma of the guinea pig. We induced atherosclerosis in this animal by dietary ascorbate depletion and, using SDS/PAGE and subsequent immunoblotting, we identified Lp(a) as accumulating in the atherosclerotic plaque. Most importantly, adequate amounts of ascorbate (40 mg per kg of body weight per day) prevent the development of atherosclerotic lesions in this animal model and the accumulation of Lp(a) in the arterial wall. We suggest an analogous mechanism in humans because of the similarity between guinea pigs and humans with respect to both the lack of endogenous ascorbate production and the role of Lp(a) in human atherosclerosis.
The reversibility of atherosclerosis.
CMAJ. 1957 Jul 15; 77(2): 106-9.
Former studies into the reversibility of experimentally induced atherosclerosis had been seriously hampered by the persistence of the hypercholesterolaemia essential for the production of the lesions. This hypercholesterolaemia actually causes atherogenesis to proceed even when cholesterol feeding is stopped. In the present study this difficulty is avoided by employing scorbutic guinea-pigs in which it had previously been shown that atherosclerosis develops rapidly without cholesterol feeding. When ascorbic acid is given to scorbutic guinea-pigs, the early atherosclerotic lesions resorb quickly. The advanced lesions are considerably more resistant to reversal, apparently because of the islands of lipid whose only contact with resorbing process is at the surface. A correlation is made between the atherosclerosis of the scorbutic guinea-pig and that observed in man, and the results of a previous study of ascorbic acid therapy in human atherosclerosis are quoted.
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