TLC 3.0 Buffered Powder

Purchase TLC 3.0 Buffered 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. Lysine and proline beneficially alter the binding properties of Lp(a).

240g Powder (Buffered Vitamin C) AOR01007
Product expiry date: January 2009

100% Vegetarian

SUPPLEMENT FACTS:

Serving Size: 1 Level Tablespoon (11.5g) %DRI
Vitamin C (Ascorbic Acid, Calcium and Magnesium Ascorbates) 3000mg 3333%
L-Lysine 3000mg 113%
L-Proline 2000mg *
L-Taurine 250mg *
Magnesium (Carbonate, Ascorbate) 340mg 81%
Potassium (Bicarbonate) 99mg *
Calcium (Carbonate, Ascorbate) 545mg 55%
*Dietary Reference Intake not established.

Other Ingredients: Silicon dioxide and lemon flavor.

AOR guarantees that no ingredients not listed on the label have been added to the product. Contains no wheat, gluten, nuts, dairy, soy, eggs, fish, or shellfish. Vitamin C is pharmaceutical-grade material derived from commercially-sourced glucose, which may derive from corn, beets, or other sources. No corn allergens are present.

Suggested Use

Stir one level tablespoon (approx. 11.5g) into a glass of water or juice, or as directed by a qualified health consultant.

Main Applications
As reported by literature:
•Antioxidant.
•Oral chelator of lead.
•Cardiovascular Support

Source
Multisource. Hypoallergenic material.

Pregnancy / Nursing
Safe

Cautions
None known.

Key Ingredients: Bromelain, Calcium, L-Lysine, L-Proline, L-Taurine, Magnesium, Potassium, Vitamin C

Related Research of TLC

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.

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)].

Even Badder Cholesterol

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.

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’s 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.

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, scarry mess that makes up an atherosclerotic plaque.

So what is a potential killer doing lurking in your body? For our Paleolithic ancestors, a quick and overwhelming response to an injury was vital to survival. In the short and dangerous life of a hunter-gatherer, getting a lesion in the blood vessel wall patched up ASAP would have been critical for survival. 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).

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.

A Bad Trade in Human Evolution

So what’s the connection with vitamin C? Dr. Pauling became interested when it was observed that Lp(a) is found almost exclusively in species which have lost the ability to make their own vitamin C: the guinea pig and the primates – including we human primates. And intriguingly, these two mutations – the production of Lp(a) and the inability to biosynthesize vitamin C – occurred at almost exactly the same time in the evolution of our primate ancestors, about 40 million years into the past. Thirdly, and most importantly, the adaptive purpose of Lp(a) is intimately tied up with 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.

Pauling’s hypothesis: our primate ancestors evolved Lp(a) to help them heal up blood vessels which were more prone to injury because they had been weakened by poor collagen synthesis, owing their lack of vitamin C – their hypoascorbemia, or genetically-induced “borderline” vitamin C deficiency. In effect, Lp(a) is a “surrogate for ascorbate.”

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.

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.

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 evolutionary 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.

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.

Running Interference

By linking vitamin C’s heart-protective powers to the strengthening of the blood vessels, leading to the prevention arterial injury 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: aNational 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 is 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. Millions of years ago, the fuse on a ticking genetic time bomb was lit by an accident of evolution. 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.

Selected References:
Lippi G, Guidi G. Lipoprotein(a): an emerging cardiovascular risk factor. Crit Rev Clin Lab Sci. 2003 Feb; 40(1): 1-42.
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.
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. 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.
Willis GC. The reversibility of atherosclerosis. CMAJ. 1957 Jul 15; 77(2): 106-9.
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.
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.

This information is copyright the Editor of Advances magazine and may not be reproduced in whole or in part in any medium without the express permission of Advanced Orthomolecular Research. Used with permission

Purchase TLC 3.0 Buffered Powder