By Benjamin V. Treadwell, Ph.D.

Many people, including some medical doctors, advise against supplementing our diets with vitamins, minerals, and other micronutrients. The most common reason given? We can obtain all the nutrients our bodies require from healthy eating.



Is this true? Or is supplementing the key to maintaining sufficient levels of vitamins and nutrients for a balanced metabolism and optimum health? A large group of medical/health professionals has come to this conclusion. Let's take a closer look at one essential nutrient, biotin, as an example of how and why.



Biotin Basics

Our bodies cannot make biotin, the more common name for vitamin B-7. It serves key functions in the production of energy in our cells, including metabolizing glucose, amino acids and fat. (See Juvenon Health Journal Volume 3 Number 10, "B for Biotin.") More recent research supports a role for biotin in regulating gene expression as well.



The micronutrient biotin is present, at varying concentrations, in cow's milk, liver, other meats, fish and many vegetables, fruits and grains. Cooked eggs are also a good source of this nutrient.



The recommended daily allowance (RDA) for biotin is 300 micrograms (mcg). Even though many multivitamins on the market contain less per dose, biotin has actually been shown to be safe at amounts much higher than the RDA. In fact, the upper safe limit remains to be established.



How do you know if your cells aren't getting enough biotin? A rash can be an early warning sign. Almost 10 years ago, it was also part of what led scientists at Juvenon to better understand biotin uptake.



Decade of Discoveries

Pilot studies during the development of the Juvenon Cellular Health Supplement yielded primarily positive feedback (more energy, sharper mind, shinier hair…). But there were a very few people (less than 1 in 1,000) who reported a skin rash, a metallic/salty taste or losing their normal sense of taste.



The Juvenon scientists were somewhat puzzled. The two primary nutrients in the formula -- acetyl-L-carnitine and alpha lipoic acid -- had shown no adverse effects, even at much higher than the supplement's recommended dose.



One of the investigators, however, remembered previous studies that might apply. An expert in the field of biotin research had conducted an experiment that demonstrated lower biotin levels in the tissues of some animals fed large amounts of lipoic acid.



Later work had shown that lipoic acid, biotin and another B-vitamin, pantothenic acid (B5) share structural similarities and the same Multivitamin Transporter (MTV). The MTV moves the nutrients of more than one vitamin from the blood into the cell to perform their functions.



The Juvenon researchers theorized the MTVs of the few individuals reporting side effects might not function efficiently. This small group remained side-effect-free until Juvenon elevated their metabolism. The Cellular Health Supplement provided more lipoic acid, increasing the need for pantothenic acid and biotin.



Pantothenic acid is present at high levels in many foods and most multivitamins (5x RDA). But biotin, from food or multivitamins (low RDA), is not as readily available. If the MTV were not functioning efficiently and the levels of the three nutrients were not balanced, more of one nutrient would be absorbed into the cell at the expense of another.



So, conditions like a rash or loss of taste might actually be a warning of an under-performing MTV that could result in a biotin imbalance.



Biotin Balancing

Based on this research and biotin's safety record, the solution seemed to be adding the vitamin to the Cellular Health formula. The adjustment resulted in a dramatic decrease in reports of side effects: from one in 1,000 users to less than one in 7,000.



The "less than one" led the Juvenon scientists to another important discovery. Suspecting that low biotin might still be producing the symptoms, they recommended that this smaller minority take 5 milligrams (mg) of biotin (17x RDA), along with the Cellular Health Supplement, per day. Over 70% of those following this protocol reported becoming side-effect-free.



The conclusion from these results? Biotin requirements for maximum health vary from person to person, perhaps determined by how well their MTVs function, a genetic predisposition, or both. The case studies that follow seem to support this conclusion.



More Please

In a recent Juvenon Cellular Health clinical trial (designed to evaluate its benefits for human cognition), a female participant experienced loss of taste after a few weeks. A research team documented her condition and were the first to report how this "unexplained loss of taste" was resolved.



Confirming that this development had been previously reported and successfully reversed, the team initially recommended the same protocol, using the 5 mg biotin dose. Surprisingly, this approach produced little change in the subject's symptoms. The investigators suggested increasing the daily dosage to 10 mg (33x RDA). After a few days, the woman regained her normal sense of taste.



Who Needs More and Why?

Did this response to the 10mg dose demonstrate a more individualized (and perhaps pharmacological) need for biotin? The investigators examined another case to find out.



A male patient, unconnected to Juvenon, awoke from abdominal surgery with no sense of taste. Like the first case study subject, he was asked to begin by taking 5 mg of biotin per day and showed no apparent positive response after several days.



Unlike the female patient, however, increasing the daily dosage to 10 mg also had no effect. The researchers continued to give incrementally larger doses to the male participant, eventually reaching 20 mg per day (67 times RDA). It took this mega-dose to fully restore his sense of taste.



Beyond Biotin

The two case studies seem to support the concepts of variable MVT efficiency from one person to another and differences in individual needs for/responses to biotin. Perhaps more importantly, this research suggests that requirements for other nutrients, and the need for supplementing, will vary.



Factors like gene composition, diet, weight, general health, level of stress and age could account for the variations. Speaking of age, studies have also shown a general need for more nutrients as we get older. (The case study subjects were 67 and 60 years old, respectively.) Higher intake compensates for age-associated decreases in absorption from the digestive tract and uptake into the body's cells and tissues (older, inefficient nutrient transporters).



We may require higher concentrations for one more reason. Recent studies are uncovering new tasks performed by other nutrients, similar to biotin's broader function with loss of taste. In view of these findings, a healthy diet alone (fruits, vegetables, whole grains and legumes), although important, may simply not be sufficient, particularly as we age.



In other words, taking supplements (with the guidance of a health professional, of course) seems to be the best option for protecting and promoting optimum health.

Without vitamin E, we essentially turn rancid. Vitamin E is fat-soluble, that is, able to penetrate the fatty areas of our tissues. As it does so, it neutralizes toxic oxidants and protects oxidant-sensitive membranes. Thus vitamin E is justifiably known as an antioxidant, and for helping to prevent age-associated increases in oxidative insults to our bodies.

The Eight Forms of Vitamin E

In reality, vitamin E comes in eight different forms, all of which are derived from plants. The eight E's are divided into two classes:

• The tocopherols consist of 4 types of vitamin E, alpha, beta, gamma, and delta. The features distinguishing each are slight chemical differences (location and number of methyl groups) on its core structure.
• The tocotrienols are virtually identical to the tocopherols in structure, except for the presence of 3 unsaturated bonds (hence trienol). Alpha, beta, gamma and delta tocotrienols are more permeable to cell membranes because of their unsaturated bonds. This chemical difference imparts certain advantages over the less permeable tocopherols.

The most potent antioxidant of the group is alpha tocopherol. For reasons still unknown, this form of E represents the bulk of vitamin E present in our serum. This is puzzling, since the plants we normally consume contain much more gamma tocopherol. Scientists originally speculated that our bodies require high serum levels of alpha tocopherol and have developed mechanisms to retain it. Thus, multi-vitamins almost always contain alpha tocopherol.

It is becoming more evident, however, that all forms of E are important and that they serve very different functions. Laboratory experiments have indicated that gamma and alpha tocopherol may complement one another with respect to antioxidant protection. Alpha tocopherol is most effective at neutralizing oxygen-based free radicals, whereas gamma tocopherol does best with nitrogen-based free radicals. Both types of radicals are destructive to our bodies.

The vitamin E offered on the market is either man-made or isolated from plants. Man-made (or synthetic) vitamin E is designated on the bottle's label as DL alpha tocopherol. The D and L are isomers or mirror images of each other. Only the D form is representative of the natural vitamin E alpha tocopherol. There is considerable controversy as to whether the L form interferes with the natural D form in the body. Some researchers believe it may be toxic.

Natural vitamin E is usually labeled D alpha tocopherol but almost always contains all 4 tocopherols. Typically, the bottle's label mentions only D alpha tocopherol because of the expense the manufacturer would incur to assay for the presence and quantity of the other three. The 4 tocopherols are derived from soybean oil or, less commonly, wheat germ. The 4 tocotrienols are usually prepared from extracts of palm oil or rice bran.

Vitamin E deficiency is not common, but it can occur with poor nutrition and/or a problem with absorption of fats. The RDA for vitamin E is 30 International Units (IU) per day for DL and 22 IU/day for D alpha tocopherol. A diet totally devoid of fats can result in a deficiency of E, since some fat is required for absorption from the intestines.

Fragile red blood cells are a common characteristic of E deficiency. Blood cell membranes, normally protected by E, tend to oxidize and rupture easily. Recent studies indicate vitamin E may help in slowing cognitive decline in Alzheimer's patients, and it may even lower blood pressure and cholesterol levels. Significant evidence also supports the vitamin as important for protecting tissues from the destructive action of oxidants and consequent disease, including heart disease, cataracts, cancer, neurological disorders and disorders of the muscular system. The incidence of these diseases increases with age. Thus it is important to obtain enough E to attenuate the age-associated destructive process.

Vitamin E is more than an antioxidant. Growing evidence supports specific roles for the different forms of vitamin E. For example, recent research demonstrates gamma tocopherol to be capable of blocking the activity of an enzyme involved in producing cellular mediators of inflammation (prostaglandins), which can lead to disease. Other tocopherols, including the more popular alpha, are largely ineffective in this context.

Alpha tocotrienol has now been shown in cell culture experiments to protect cells of the nervous system from the degenerative action created by the overproduction of the neurotransmitter, glutamate. This chemical, better known as monosodium glutamate, is used as a food enhancer and is infamous for its reputation as the agent responsible for the Chinese restaurant syndrome (bad headaches, etc.) in those who consume too much of it. Normally, an excess of this neurotransmitter activates a neurotoxic enzyme (12-LOX). Tocotrienol, in very small amounts, stops this toxic enzyme in its tracks, thus potentially protecting the nervous tissue.

The unique behavior of the different forms of vitamin E helps explain the advice of nutritionists to consume a variety of fruits, vegetables, legumes and grains. All are good sources of the various forms of vitamin E. Grains should preferably be non-refined. The tocotrienols, as well as other micronutrients, are present in the rice bran, which is lost in processing. People on low-fat diets, such as vegans, are often deficient in vitamin E and should consider taking supplements.

How much E should one take, if any? The upper safe limit for D alpha tocopherol is 1,500 IU/day, according to The Institute of Medicine. The major danger in taking high levels of E is its capacity to inhibit the adherence of platelets to the walls of blood vessels. This is positive for cardiovascular health in those with over-active clotting, but too much E can cause bleeding, especially for people taking other anticoagulants, such as aspirin or coumadin. If you are inclined to take vitamin E, 400 IU/day of natural vitamin E is a reasonable target. However, it is advisable to consult with your physician before taking this supplement.

Finally, the E vitamins function as antioxidants only in their reduced, non-oxidized state. In a subsequent newsletter we will describe how the cells of the body maintain these antioxidants in their reduced or active state. We will also describe how the versatile antioxidant, alpha lipoic acid, functions to recycle these and other antioxidants to maintain cellular health as we age.

Substantial progress has been made in understanding the bio- chemistry of the mitochondria - the organelles that power our cells. Similarly, mitochondrial decay is broadly recognized as playing a central role in the aging process. However, much less is known about effective nutritional approaches to maintain and promote mitochondrial health.

A recent literature review in Canada has evaluated the effects of a wide variety of substances that are reported to produce positive effects on the mitochondria. These include coenzyme Q₁₀; other antioxidants, such as ascorbic acid, vitamin E, and lipoic acid; niacin; creatine; carnitine, and some others. For further information, click here.

This Research Update column highlights articles related to recent scientific inquiry into the process of human aging. It is not intended to promote any specific ingredient, regimen, or use and should not be construed as evidence of the safety, effectiveness, or intended uses of the Juvenon product. The Juvenon label should be consulted for intended uses and appropriate directions for use of the product.

Alpha lipoic acid (ALA) is a vitamin-like nutrient that is essential for life. The conversion of food to energy within our cells derives predominantly from a series of reactions within the mitochondria, commonly referred to as the Krebs Cycle. Alpha Lipoic Acid acts like a catalytic converter for the reactions that involve two key enzyme complexes, without which the Cycle would shut down and the cell would die. (For more information visit the following articles Alpha Lipoic Acid: A Marvelous Nutrient, and The Two Faces of Alpha Lipoic Acid.)

Although this conversion of food to energy is its primary function, recent studies have shown that Alpha Lipoic Acid may also be effective in treating many chronic health problems.

Cell culture and animal research, along with human clinical trials and anecdotal evidence, seem to support Alpha Lipoic Acid's therapeutic value for migraine headache, macular degeneration, obesity, inflammation, cataracts, multiple sclerosis, neurodegenerative, cardiovascular and liver disease, and, in particular, type II diabetes.

ALA The Cell Protector

Pain, numbness, tingling, burning sensations.. .the exact mechanism by which Alpha Lipoic Acid lessens these diabetic symptoms is not yet known. However, results from recent cell culture and animal studies appear to provide some exciting clues.

A study examining the effects of Alpha Lipoic Acid on preventing the death of liver cells, after exposure to a death-promoting inflammatory substance produced by the cell (TNF alpha), demonstrated a new function for Alpha Lipoic Acid: the ability to bind to a specific area (tyrosine kinase domain) of the insulin receptor, which results in its activation. Once activated, the receptor initiates a series of reactions forming a biochemical pathway (PI3-K/Akt pathway) in the cell that acts to counter the TNF alpha-induced death pathway.

The investigators also noted that the PI3-K/Akt pathway, although primary, was not the only cell-saving mechanism. Their results indicated that the antioxidant property associated with Alpha Lipoic Acid (ALA) plays some role in preventing cellular death as well. Moreover, only ALA, and not other antioxidants, binds to the insulin receptor and activates the life-saving PI3-K/Akt pathway.

Less Cellular Stress

These results provide valuable insight into how ALA may function to improve the symptoms of diabetic neuropathies and increase insulin receptor sensitivity.

Animal studies of tissue under diabetic conditions have also demonstrated how cellular stress is produced by increased oxidative stress. Similar to what happened in the liver cell study, this stress promotes inflammation and the production of inflammatory substances like TNF alpha. The end-result is damage to nerve tissues and eventual death of some nervous system cells.

Translation: The painful condition of the peripheral nervous system experienced by diabetic patients may be partially caused by this inflammation-induced damage. ALA may neutralize the inflammatory pathway via binding to the insulin receptor which activates the PI3-K/Akt, or pro-survival, pathway.

As to increased insulin sensitivity and its glucose regulating benefits, this, too, seems to be a result of ALA's ability to support insulin in activating the receptor. You might say that ALA converts a rusty non-compliant insulin receptor to a hair-trigger receptor that is more easily set-off, i.e., activated, in response to insulin.

ALA and Us

Recent human clinical trials seem to support cell culture and animal study findings. Patients with certain nervous system pathologies associated with type II diabetes have experienced significant improvement from taking ALA in oral doses (600 mg/day). Clinical trials also indicate that ALA does improve insulin sensitivity.

Whether the actual mechanisms responsible for the positive effects in humans are explained by the results obtained from animal and cell culture studies remains to be determined. However, it is clear from these and other studies on ALA that additional research on this vitamin-like compound is warranted.

By Benjamin V. Treadwell, Ph.D.

Vitamins have taken several significant hits lately for not delivering their purported health benefits. In fact, there are claims that, under specific conditions, some vitamins can actually have a negative effect on health. In contrast, experts have also recently become aware that the current recommended dietary amounts of some vitamins are far below what is needed for maximum health. Who is responsible for those recommendations and how will they change?

Initially, vitamin D was believed to help prevent the inadequate bone mineralization that progressed to the disease known as rickets in children and osteoporosis in adults. Consequently, the RDA for vitamin D was set to prevent bone-mineralization-associated diseases.

Research, however, has identified this vitamin’s contribution to numerous other biological functions, including a potential role in preventing breast and prostate cancer, tuberculosis, autoimmune diseases, and other disorders unrelated to bone mineralization. (For a review of new vitamin D findings, visit the following articles see Vitamin D - Recent Provocative Discoveries, Vitamin D - A Hormone with New Health Benefits, and Vitamin D — A Vitamin In Need of Revision.) Furthermore, there are more vitamin D receptors whose functions have yet to be discovered, in organs such as the brain.

In other words, the current recommended dose of 400 IU appears to be far short of what many require for maximum health, especially the elderly and those with pigmented skin and/or minimal exposure to sunlight. As a result, the government is scrambling to establish a new, significantly higher RDA. The maximum safe dosage may also be increased by a factor of at least 5 to 10 times the current recommended daily intake.

Another Story: Vitamin K

In 1943, Danish biochemist Carl Dam shared a Nobel Prize for his work on discovering a substance required for the clotting of blood: vitamin K. Taking its name from “koagulation,” Danish for coagulation, vitamin K functions as a cofactor for an enzyme (gamma glutamylcarboxylase) involved in modifying specific amino acid residues in several proteins to convert them from inactive to active blood-coagulating proteins.

People who lack sufficient amounts of vitamin K have a prolonged clotting time that can result in severe bleeding problems or hemorrhage. The recommended daily intake of vitamin K was initially estimated to be between 90 and 120 micrograms/day, the amount required for normal clotting time. It turns out that this amount is fairly easy to obtain from a diet rich in green, leafy vegetables (spinach, broccoli, lettuce). Bacteria residing in our intestines produce an even more potent form of vitamin K, vitamin K2, to help supplement what is supplied by diet.

These bone-specific proteins function in a way analogous to the steel reinforcement rods that give concrete its tensile strength. This is especially important in post-menopausal women and the aged, who have an increased rate of bone loss and increased incidence of osteoporosis and fractures.

As an even more effective method of increasing bone formation and strength, new data supports taking vitamin K, vitamin D and calcium in combination. The bottom line, to further our steel and concrete analogy: vitamin D and calcium help to promote the formation of "cement" in bone, while vitamin K may help promote the production of the bone-strengthening "reinforcing rods."

Blood Thinners and Bone Loss

Data from patients taking the blood thinner Coumadin® (aka warfarin) over long periods of time also seems to identify vitamin K as an important factor for bone formation. Coumadin, often used to treat an abnormally high tendency to form blood clots, effectively interferes with the normal process of recycling vitamin K from an inactive oxidized state to an active reduced state. The net result of this interference is that active vitamin K is less available as a cofactor to initiate blood clot formation.

Although Coumadin may help prevent stroke and other clot-related pathologies, it is also associated with a significantly higher incidence of osteoporosis (loss of bone density) than in age-matched people not taking the drug. Even more alarming, however, are recent results from animal studies showing that inhibiting vitamin K with Coumadin can promote the development of calcified plaques in blood vessels.

The implication is that atherosclerosis may, in part, be associated with low levels of vitamin K. In fact, the arterial plaque in the Coumadin-treated animals could be reduced or even eliminated by feeding the animals high doses of vitamin K2. Whether this applies to humans has yet to be determined.

What we do know is that people with atherosclerosis as well as osteoporosis have protein markers in their blood indicative of low levels of vitamin K. Furthermore, as we age, these same markers increase along with the incidence of osteoporosis and atherosclerosis. Consequently, should there be an age-associated increase in daily vitamin K intake?

Enough K Today

Except for Coumadin patients, there is no evidence that taking vitamin K in higher doses – even those far exceeding the RDA -- is dangerous to our health. However, unless a higher dose is recommended by a qualified health professional, the vitamin K from a healthy diet and multi-vitamin supplements should be sufficient for most people. Until more research is completed on higher doses for the prevention of certain diseases as described above, a nutritious diet with lots of green leafy vegetables may be the best method for obtaining a sufficient amount of this vitamin.

American and Japanese physicians, from a number of prestigious institutions specializing in critical care, pediatrics and geriatrics, have summarized recent work that demonstrates the broad range of biological activities associated with vitamin K.

The investigators point out the surprising evidence implicating vitamin K deficiency as potentially associated with a host of diseases including osteoporosis, atherosclerosis, osteoarthritis and liver cancer. They underscore the finding that many individuals who go on to develop these diseases appear to have normal vitamin K status as judged by normal hemostatic or blood-clotting activities.

The accumulated information from studies on vitamin K and its diverse activities suggests that this vitamin should be more intensely investigated. The current studies clearly indicate that some individuals, especially the elderly, may be deficient in this vitamin and could benefit from increased intake of vitamin K.

To read the abstract, click here.

"Pleiotropic actions of vitamin K: protector of bone health and beyond?"

Nutrition, Volume 22, Issue 7-8, Pages 845-852.

This Research Update column highlights articles related to recent scientific inquiry into the process of human aging. It is not intended to promote any specific ingredient, regimen, or use and should not be construed as evidence of the safety, effectiveness, or intended uses of the Juvenon product. The Juvenon label should be consulted for intended uses and appropriate directions for use of the product.

Cholesterol! The word strikes fear into the hearts of many Americans. Popular press and TV have dumbed down the basics of cholesterol:

• High total cholesterol is associated with heart attack and stroke.
• LDL (low density lipoprotein) Cholesterol is bad.
• HDL (high density lipoprotein) Cholesterol is good.

Healthy Cholesterol Levles Aren't Quite That Simple

There is in fact only one kind of cholesterol. Whether obtained from the diet or synthesized by the liver, it is immediately bound to specific carrier substances, lipoproteins, and transported via the blood stream to the 60 trillion cells of the body. LDL is the major lipoprotein responsible for the transport of cholesterol TO the cells of the body. HDL, in contrast, takes cholesterol FROM the cells of the body and transports it back to the liver, where it is sequestered, or metabolized and secreted in the intestine as bile.

Our bodies require a certain amount of cholesterol for numerous cellular functions, including cell membrane integrity, absorption of nutrients such as fat-soluble vitamins, and synthesis of vitamin D and sex hormones. Too much of it can hurt us, however. Research has demonstrated an association between elevated LDL and atherosclerosis, a disease of the arteries causing heart attack and stroke.

How does this work? When the LDL-cholesterol combination (technically, LDLc) is present in the blood at a high level, it diffuses across the endothelial cells that line the interiors of blood vessels and is deposited just underneath these cells. This leaves a pool of LDL within the wall of the blood vessel. LDL is susceptible to attack by common cellular oxidants, which in effect turn it rancid. When LDL is present in the blood at normal healthy amounts, this does not occur, as there are substances, such as HDL and cellular antioxidants, to protect it from oxidation.

When the blood level of LDL Cholesterol is too high, large amounts of LDL transfer across the vessel wall, the antioxidant protection is overwhelmed, and LDL is oxidized (turns rancid). Now it becomes toxic to the cell and surrounding tissue. The process is aggravated by hypertension (high blood pressure), a condition characterized by elevated vascular pressure that can excessively stretch vessels and stimulate the oxidation of LDL.

Since the liver has the capacity to make cholesterol, we really don't need much of it from the foods we eat. In general, western industrialized man has too much LDL, largely as a result of sedentary lifestyles, and a diet high in substances that promote cholesterol synthesis, such as saturated fat, and trans fats. More than 90 million American adults - about 50% - have unhealthy blood-cholesterol levels.

What can you do to avoid being one of them? Recently, new standards have been suggested for the desired level of HDL (>40mg/deciliter), LDL (<100mg/dl) and total cholesterol (<200 mg/dl). As we age, these figures go in the wrong direction. Total cholesterol and LDL go up; HDL goes down. Most people can correct these markers of health to optimal or near optimal levels with minimum effort and cost. This is one area of healthcare that has real solutions. Various approaches are available to either control these precursors of poor health or help maintain levels that are already within the normal range.

Diet and Lifestyle. Diet does have an effect, but the intensity of it varies with age, genetic constitution and physical condition. The diet should include about 25-30% of total calories from fat. Less than 10% of these calories should come from saturated fats (which raise LDL), and none from trans fats (which raise LDL and lower HDL). A diet high in fruits and vegetables (7 servings/day), nuts and fiber has been demonstrated to promote a healthy lipid profile.

Lowering total cholesterol by diet and keeping your total daily intake of cholesterol to less than 300mg/day almost always improves the ratio of HDL/LDL. It stimulates the synthesis of LDL receptors in liver cells, thus decreasing the circulating level of the lousy cholesterol. Avoiding a sedentary lifestyle and maintaining a regular exercise routine can significantly improve the level of HDL.

Drugs. OK, you did all that and your cholesterol level, although improved, remains in the red zone, so now what? Numerous ads on TV and elsewhere promote cholesterol-lowering prescription drugs, but many of us are aware of documented side effects from these drugs. On the other hand these drugs, commonly referred to as statin drugs, do work. They lower cholesterol by as much as 45-50% and raise HDL, while lowering LDL and another circulating neutral fat, triglyceride. The bottom line is they have been shown to work, and they decrease mortality from atherosclerosis.

Supplements. Dietary supplements can help improve and or maintain cholesterol levels. One example is a plant-derived substance commonly known as policosanol. Niacin (vitamin B3), in large doses (>1gm/day), has a significant effect on lowering triglycerides, and raising HDL, especially when used in combination with one of the statin drugs or policosanol. Any decision to try these dietary supplements should be taken under a health professional’s supervision, since these products, like the statin drugs, may have side effects.

Another approach to help maintain cholesterol levels that are already within the normal range is to supplement with antioxidants, since the body's natural inflammation response involves oxidants. The potent antioxidant alpha lipoic acid may help by acting directly to neutralize oxidants and indirectly by increasing levels of two key antioxidants, vitamin C and glutathione, in the cells lining the vessel walls. Lipoic acid also enhances synthesis of the chemical messenger, nitric oxide, which in turn protects the function of these cells and promotes vascular relaxation.

Whichever approach you choose, the important thing for healthy aging is to get your cholesterol under control and keep it there.

This month we highlight once again a study of the powerful antioxidant alpha lipoic acid. Among the general population, double-blind, placebo-controlled clinical trials, with human subjects, are perhaps the most widely known form of healthcare testing. Studies in laboratory animals are even more extensively used by pre-clinical scientists. To understand fundamental biochemistry, however, scientists often use cell cultures.

S cientists at Vanderbilt University School of Medicine examined the antioxidant effects of alpha lipoic acid in cultured human endothelial cells (which line our blood vessels). They found that alpha lipoic acid enhances both the antioxidant defenses and the function of endothelial cells. For details on how alpha lipoic acid protects the cells lining the arteries to prevent inflammation, click here.

This Research Update column highlights articles related to recent scientific inquiry into the process of human aging. It is not intended to promote any specific ingredient, regimen, or use and should not be construed as evidence of the safety, effectiveness, or intended uses of the Juvenon product. The Juvenon label should be consulted for intended uses and appropriate directions for use of the product.