Alpha-Lipoic Acid (ALA) is well documented to be effective in these areas:

According to The Prediabetic Epidemic - Nutrition Science News, 3/01 -  The therapeutic dose for ALA is 600 mg per day (the amt in 2 capsules of this product).

The following was taken from the Youngagain Nutrtients web site and is copyrighted by them.

For those of you who read the Longevity News newsletter on a regular basis, you are aware that alpha lipoic acid is one of our favorite and recommended nutrients. It is considered the "universal" antioxidant, as it has both fat- and water-soluble properties. Physicians world-wide are now routinely recommending it to their patients with peripheral neuropathy, and are seeing patients stabilize and even reverse some of the adverse affects of this potentially disabling disorder.

Alpha lipoic acid (ALA) and acetyl L-carnitine are considered rejuvenating nutrients. Animal studies have shown that these nutrients can actually reverse the effects of aging on the brain. Human studies indicate numerous benefits for the brain, glucose metabolism and nervous system function.

In a recent study published in the Journal of Cerebral Blood Flow Metabolism late last year, researchers from Germany studied advanced glycation end products (AGEs). It is felt that these end products are critically involved in the complications of diabetes, Alzheimer's and other degenerative diseases, not to mention the aging process itself. What happens with these so-called end products is that they cross-link between different proteins in the body, eventually destroying the proteins. The body cannot survive without adequate functioning proteins. The researchers investigated the effects of AGEs regarding glucose metabolism and energy production within a cell line. The AGEs decreased cellular energy production in the form of ATP, while increasing glucose metabolism and consumption. However, the ALA seemed to reverse some of the effects of these end products. Researchers concluded that ALA may be useful against age-related AGE effects in neuro-degeneration by positively affecting cellular energy metabolism.

In a study published in the September 2004 edition of the American Journal of Physiology, Endocrinology and Metabolism, researchers from the University of Arizona indicated that ALA appeared to improve insulin action in insulin-resistant skeletal muscles, thereby improving glucose transport into these tissues. 

We see considerable buzz on the Internet and elsewhere about alpha lipoic acid (ALA). It is represented as an anti-aging agent, as well as a treatment for certain diseases and conditions. Our aim this month is to clarify what it is and how it works.

ALA is a vitamin-like compound, first isolated from potatoes. It was designated lipoic acid over 50 years ago, as it was commonly found associated with lipids, or fatty areas of the cell. ALA was subsequently found to be soluble in water and also able to penetrate lipid environments, a property lending considerable versatility to this nutrient.

ALA is a nutrient that comes close to being a vitamin. Vitamins are nutrients required for health but, for the most part, produced in insufficient amount (or not at all) by the cells of the body. Under certain conditions of cellular stress, ALA may not be synthesized in sufficient quantities. Thus it could be classified a para-vitamin or conditionally essential nutrient.

It is now known that ALA's primary function is to serve as a cofactor during the conversion of food to energy. Energy production in our cells derives predominantly from a series of enzyme-catalyzed reactions, commonly referred to as the Krebs Cycle, and contained within the mitochondria. Reactions involving two key enzyme complexes of the Krebs Cycle require the cofactor ALA. By analogy, it acts as a sort of catalytic converter. Without it, the Cycle would shut down, and the cell would die.

More recent evidence supports another equally important role for ALA, which is to function as a potent antioxidant. The conversion of food to energy in the Krebs Cycle has an inherent inefficiency that results in the creation of toxic oxidants, or free radicals. They are the result of the occasional escape of an electron from the mitochondrial machinery and the incorporation of that electron by molecular oxygen. This aberrant transfer of a single electron to molecular oxygen creates a molecule with an unpaired electron, or free radical, which is highly reactive. If not neutralized, it will react with and damage critical cellular components, including proteins, lipids and DNA.

Approximately 2% of the oxygen delivered to the cell for participation in the production of energy is converted to highly reactive and toxic free radicals. The percentage increases with age. This translates into a whopping one kilogram of oxygen radicals produced per year by each of us, less in youth and lots more as we age. Evidence indicates ALA can help neutralize these free radicals before they can impair cellular molecules.

The ability of ALA to neutralize free radicals derives from its chemical structure. In addition to its role as a catalytic converter, ALA is a potent antioxidant, which simply means it has a higher affinity for unpaired electrons than do other cellular components. It readily combines with the unpaired electron on a free radical, thus neutralizing it and sparing the cell from damage.

Furthermore, because of its aggressive propensity to combine with free radicals, ALA has been shown to have a significant sparing effect on other cellular antioxidants. For example, vitamins C and E, as well as the vital cellular antioxidant, glutathione, are also capable of pairing with free radicals, but if an aggressive ALA molecule gets there first, vitamin C and the others are freed to perform other functions. The net effect is to lower the oxidative stress on our bodies. This stress is the consequence of the tendency of oxidants to attack the body's molecular constituents, analogous to the attack of iron by oxygen to form the degradation product, rust. A high level of free radicals promotes high oxidative stress.

As previously stated, a unique feature of ALA is its ability to enter both lipid and water environments. Unlike other antioxidants that are deficient in this property, ALA can protect the total cell, both the fatty cellular environments such as membranes, as well as the water-soluble cellular components that comprise the bulk of the cell.

The principal dietary source of ALA is plants, such as spinach. However, although ALA is present in our diet and may be synthesized by our cells, recent studies indicate these sources appear to fall below optimum levels, especially in the aged animal. Under certain conditions, such as high oxidative stress, the body's production of ALA may be insufficient for maximum protection. This deficiency can be compensated for through either diet or supplements. Since it is known that the absorption of nutrients declines with age, and oxidative stress increases, supplemental sources of ALA may benefit people as they age, especially those with impaired nutrient absorption.

Animal and cell culture studies support the use of supplemental ALA in the aged. These studies demonstrate the capacity of supplemental ALA to convert old, inefficient mitochondria to ones with more youth-like appearance and activity. Furthermore, additional studies have demonstrated a significant improvement in activity level, as well as learning ability, in aged animals treated with ALA. For these reasons, increasing numbers of healthcare professionals who work with older adults are including ALA in the vitamin and supplement regimens that they recommend to their clients.