Aor TLC 3 Powder 240 Grams
Aor TLC 3 Powder 240 Grams:
Powerful Heart Health Formula Based on Linus Pauling's Research
- High dose vitamin C, lysine, proline and cofactors
- Promotes healthy blood vessels
- A comprehensive formula to reduce the risk of cardiovascular disease
- Convenient lemon flavoured powder
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.
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. Find Aor Supplements at healthpalace.ca
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.
|Medicinal Ingredients Per 1 Level Tablespoon (approx. 11.5g)|
|Vitamin C (ascorbic acid, calcium and magnesium ascorbates)||3000 mg|
|Magnesium (carbonate, ascorbate)||340 mg|
|Potassium (bicarbonate)||99 mg|
|Calcium (carbonate, ascorbate)||545 mg|
|Non-medicinal ingredients: 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.
(Adult): Stir 1 level tablespoon (approx. 11.5 g) 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.
- Cardiovascular support
- Healthy blood vessels
Relations Between Vitamin C and High Levels of Lipoprotein (a):
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 adaptive purpose of Lp(a) is intimately tied into one of the key functions of vitamin C. Vitamin C plays a role in collagen synthesis, so it 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, due to vitamin C deficiency ( hypoascorbemia), or genetically-induced “borderline” vitamin C deficiency. Therefore, Lp(a) is a “surrogate for ascorbate.”
Cardiovascular Disease could be 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. Find Aor Supplements at healthpalace.ca
Why 3 Grams Vitamin C Per 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
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. Find Aor Supplements at healthpalace.ca
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. Find Aor Supplements at healthpalace.ca
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).Find Aor Supplements at healthpalace.ca
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.
- 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.