Guest guest Posted September 20, 2004 Report Share Posted September 20, 2004 The supplement did nothing for me, but it is very good it may be what you need. Here's some information from my files. Information Alpha Lipolic Acid Studies strongly support supplementation with ALA, A L Carnitine, and Co Enzyme Q10 for increased energy within in the cells. Studies show ALA reduced CATARACT FORMATION by 45% in Rats! Studies show ALA reduces oxidative stress in the heart muscle while raising levels in heart and liver energy (mitochondria). Studies show ALA's special property of chelating free iron from brain cells, and enhancement of vility to regenerate ascorbate. ALPHA LIPOIC ACID PREVENTS BRAIN-AGING. Part of the pathology of brain aging is an increase in the levels of iron with a parallel decrease in vitamin C in the tissue. This leads to increased levels of free radicals in brain cells and subsequent neuronal dysfunction and death. to At The Linus ing Institute, studies demonstrated that a significant reversal of this pattern in rats receiving 4 mg. per day of lipoic acid. Lipoic acid reduced total levels of iron of the forebrain and a substantial increase in the forebrain vitamin C levels. This suggests that the forebrain, a region involved in cognition has a special facility for the uptake and metabolism of lipoic acid. Scientists speculate it has the special property of chelating free iron from brain cells, IMPROVING MITOCHONDRIAL FUNCTION AND PROTECTING AGAINST FREE RADICALS AND ENHANCING BRAIN CELL REGENERATION. Another study reported that lipoic acid reduces oxidative stress in the heart muscle while raising glutathione and ascorbate levels in the heart and liver mitochondria. Researchers recommend lipoic acid as a therapy to prevent cataract formation. Lipoic has the ability to maintain glutathione in the eye lens. Lipoic regulates oxidation of fats and sugars into energy, maintains the critical Kreb's energy production cycle and is able to lower blood glucose levels and prevent the formation of glycation products. GLYCOSYLATION is the abnormal binding of a glucose molecule to a protein molecule to form a non-functioning structure in the body. The inhibition of glycation is critical to diabetics and can slow aging (and wrinkles) in healthy people. * LOWERS GLUCOSE LEVELS BY INCREASING INSULIN METABOLISM AND DECREASES NUMBNESS IN DIABETICS * INCREASES ENERGY LEVELS WITHIN CELLS * CAN DECREASE CHOLESTEROL AND PROTEIN OXIDATION FOR A HEALTHY HEART ALPHA LIPOIC ACID inhibits free radicals more effectively than vitamin E. ALA is an important supplement in the prevention of HEART DISEASE. ALPHA LIPOIC ACID inhibits the oxidation of protein, AIDS MITOCHONDRIAL ENERGY METABOL which he are on ISM, and lowers LDL cholesterol. a-LIPOIC ACID Also known as thioctic acid, a-lipoic acid is a naturally occurring compound that is synthesized by plants and animals, including humans. a-Lipoic acid contains two sulfur molecules that can be _oxidized_ (http://lpi.oregonstate.edu/infocenter/glossary.html#oxidation) or _reduced_ (http://lpi.oregonstate.edu/infocenter/glossary.html#reduction) . This feature allows a-lipoic acid to function as a _cofactor_ (http://lpi.oregonstate.edu/infocenter/glossary.html#cofactor) for several important _enzymes_ (http://lpi.oregonstate.edu/infocenter/glossary.html#enzyme) as well as a potent _antioxidant_ (http://lpi.oregonstate.edu/infocenter/glossary.html#antioxidant) . Only the R-_isomer_ (http://lpi.oregonstate.edu/infocenter/glossary.html#isomers) of a-lipoic acid is synthesized naturally. Conventional chemical synthesis of a-lipoic acid results in a 50/50 (racemic) mixture of the two optical isomers, R-a-lipoic acid and S-a-lipoic acid. _(1)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#reference) . In the text that follows, the term " a-lipoic acid " refers to racemic a-lipoic acid, while " R-a-lipoic acid " or " S-a-lipoic acid " refers to the specific isomer. FUNCTION Enzyme cofactor R-a-Lipoic acid is normally bound to _proteins_ (http://lpi.oregonstate.edu/infocenter/glossary.html#protein) by linkage of its carboxyl (COOH) group to a lysine _residue_ (http://lpi.oregonstate.edu/infocenter/glossary.html#residue) in the protein. In its protein bound form, lipoamide, R-a-lipoic acid is a required _cofactor_ (http://lpi.oregonstate.edu/infocenter/glossary.html#cofactor) for several multi-enzyme complexes that _catalyze_ (http://lpi.oregonstate.edu/infocenter/glossary.html#catalyze) critical energy _metabolism_ (http://lpi.oregonstate.edu/infocenter/glossary.html#metabolism) reactions inside the _mitochondria_ (http://lpi.oregonstate.edu/infocenter/glossary.html#mitochondria) . The pyruvate dehydrogenase complex catalyzes the conversion of pyruvate to acetyl-CoA, an important _substrate_ (http://lpi.oregonstate.edu/infocenter/glossary.html#substrate) for energy production, via the citric acid cycle. The a-ketoglutarate dehydrogenase complex catalyzes another important citric acid cycle reaction. The branched-chain a-keto acid dehyrogenase complex catalyzes the metabolism of three _amino acids_ (http://lpi.oregonstate.edu/infocenter/glossary.html#amino acid) , leucine, isoleucine, and valine, also known as branched-chain amino acids. The glycine cleavage system is a multi-enzyme complex that catalyzes the formation of 5,10 methylene tetrahydrofolate, an important cofactor in _nucleic acid_ (http://lpi.oregonstate.edu/infocenter/glossary.html#nucleic acid) synthesis _(2)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref2) . Antioxidant When large amounts of free a-lipoic acid are available (e.g., with supplementation), a-lipoic acid is also able to function as an antioxidant _(3)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref3) . a-Dihydrolipoic acid (DHLA) is the reduced form of a-lipoic acid, and is the only form that functions directly as an _antioxidant_ (http://lpi.oregonstate.edu/infocenter/glossary.html#antioxidant) (_structure_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/la%20structure.html) ). Free a-lipoic acid is rapidly taken up by cells and reduced to DHLA intracellularly. Because DHLA is also rapidly eliminated from cells, the extent to which its antioxidant effects can be sustained remain unclear. Although only DHLA functions directly as an antioxidant, a-lipoic acid may have indirect antioxidant effects _(4)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref4) . Chelation of metal ions: Certain free metal ions like iron and copper can induce oxidative damage by catalyzing reactions that generate highly reactive _free radicals_ (http://lpi.oregonstate.edu/infocenter/glossary.html#free radical) . Both a-lipoic acid and DHLA may _chelate_ (http://lpi.oregonstate.edu/infocenter/glossary.html#chelate) or bind metal ions in a way that prevents them from generating free radicals _(1)_ (http://lpi ..oregonstate.edu/infocenter/othernuts/la/#reference) . At present, this property has only been demonstrated in the test tube and in _extracellular fluids_ (http://lpi.oregonstate.edu/infocenter/glossary.html#extracellular fluid) . Scavenging free radicals: DHLA may prevent oxidative damage by interacting with potentially damaging _reactive oxygen species_ (http://lpi.oregonstate.edu/infocenter/glossary.html#reactive oxygen species) (ROS) and _reactive nitrogen species_ (http://lpi.oregonstate.edu/infocenter/glossary.html#reactive nitorogen species) (RNS) _(5)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref5) . Regenerating other antioxidants: When an antioxidant like vitamin C neutralizes a free radical, it becomes oxidized itself, and is not able to neutralize other free radicals until it has been reduced or regenerated. DHLA is a potent reducing agent, and has the capacity to regenerate a number of oxidized antioxidants to their active antioxidant forms (_diagram_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/la%20antiox%20network.html) ). Specifically, DHLA is capable of reducing the oxidized forms of vitamin C, _glutathione_ (http://lpi.oregonstate.edu/infocenter/glossary.html#glutathione) , and coenzyme Q10, which are able to regenerate oxidized a-tocopherol (vitamin E), forming an antioxidant network. DHLA can be regenerated from a-lipoic acid through the activity of _enzymes_ (http://lpi.oregonstate.edu/infocenter/glossary.html#enzyme) present in cells _(1)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#reference) . Increasing intracellular glutathione levels: Glutathione is an important water-soluble antioxidant that is synthesized from the sulfur-containing _amino acid_ (http://lpi.oregonstate.edu/infocenter/glossary.html#amino acid) cysteine. The availability of cysteine inside a cell determines its rate of glutathione synthesis. DHLA has been found to increase the uptake of cysteine by cells in culture, leading to increased glutathione synthesis _(1)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#reference) . Although increases in intracellular DHLA are short-lived, DHLA may also improve intracellular antioxidant capacity by inducing glutathione synthesis. Repair of oxidative damage: The protein, a1-antiprotease, is an inhibitor of the enzyme elastase. _Oxidation_ (http://lpi.oregonstate.edu/infocenter/glossary.html#oxidation) inactivates a1-antiprotease, leading to increased activity of elastase and degradation of elastin in the lungs, a process that has been implicated in _chronic obstructive pulmonary disease (COPD)_ (http://lpi.oregonstate.edu/infocenter/glossary.html#chronic obstructive pulmonary disease) .. In the test tube, DHLA can act as a reducing factor for the enzyme, peptide methionine sulfoxide reductase (PMSR), which can reduce and reactivate oxidized a1-antiprotease _(6)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref6) . Whether a-lipoic acid contributes to the repair of oxidized proteins in living organisms remains to be determined. Regulation of gene transcription The protein, NF-kappaB (NF-kB), is known as a _transcription factor_ (http://lpi.oregonstate.edu/infocenter/glossary.html#transcription factor) because it is able to bind to DNA and affect the rate of _transcription_ (http://lpi.oregonstate.edu/infocenter/glossary.html#transcription) of certain _genes_ (http://lpi.oregonstate.edu/infocenter/glossary.html#gene) that have NF-kB binding sites. NF-kB plays an important role in regulating genes related to inflammation and the pathology of a number of diseases, including _atherosclerosis_ (http://lpi.oregonstate.edu/infocenter/glossary.html#atherosclerosis) , cancer, and _diabetes_ (http://lpi.oregonstate.edu/infocenter/glossary.html#diabetes) _(2)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref2) . Physiologically relevant concentrations of a-lipoic acid have been found to inhibit the activation of NF-kB when added to cells in culture _(7)_ (http://lpi.orego nstate.edu/infocenter/othernuts/la/#ref7) . AP-1 is another transcription factor that can be affected by both reactive oxygen species (ROS) and certain antioxidants within cells. Treating cells in culture with DHLA has been found to inhibit the activity of AP-1 by decreasing the expression of c-fos, one of the proteins that makes up the functional AP-1 complex _(8)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref8) . DEFICIENCY a-Lipoic acid deficiency has not been described, suggesting that humans are able to synthesize enough to meet their needs for _enzyme_ (http://lpi.oregonstate.edu/infocenter/glossary.html#enzyme) _cofactors_ (http://lpi.oregonstate.edu/infocenter/glossary.html#cofactors) . Increased destruction of the cofactor form of a-lipoic acid may underlie the pathology of some diseases. In arsenic toxicity, arsenic can form a complex with a-lipoic acid in dehydrogenase enzymes, leaving it inactive _(3)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref3) . Circulating antibodies to lipoamide-containing enzyme subunits have been isolated in patients with an _autoimmune_ (http://lpi.oregonstate.edu/infocenter/glossary.html#autoimmune disease) liver disease known as primary biliary cirrhosis _(9)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref9) . DISEASE PREVENTION Aging _Mitochondria_ (http://lpi.oregonstate.edu/infocenter/glossary.html#mitochondria) are cellular organelles that oxidize dietary fuels (proteins, fats, and carbohydrates) to a usable form of energy, adenosine triphosphate (_ATP_ (http://lpi.oregonstate.edu/infocenter/glossary.html#atp) ). _Free radicals_ (http://lpi.oregonstate.edu/infocenter/glossary.html#free radical) or _reactive oxygen species_ (http://lpi.oregonstate.edu/infocenter/glossary.html#reactive oxygen species) (ROS) are also produced by mitochondria as a byproduct of energy production. If not neutralized by antioxidants, ROS may damage mitochondria over time, causing them function less efficiently and to generate more damaging ROS in a self-perpetuating cycle. Many experts feel that this deterioration in mitochondrial function is directly related to functional declines in aging and age-related diseases _(10)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref10) . In aging rats, short-term dietary supplementation with R-a-lipoic acid has been found to decrease mitochondrial ROS production and improve mitochondrial function _(11, 12)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref11) . A series of studies in aged rats found that combined dietary supplementation of R-a-lipoic acid and acetyl-L-carnitine improved mitochondrial energy metabolism, decreased oxidative stress, increased physical activity, and improved measures of short-term memory _(13, 14)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref13) . Acetyl-L-carnitine is a supplemental form of L-carnitine, an amino acid derivative that plays a crucial role in mitochondrial energy metabolism. (See L-carnitine for more information.) While these findings are very encouraging, the researchers caution that these studies used relatively high doses of the compounds for only for one month. It is not yet known whether taking relatively high doses of R-a-lipoic acid and acetyl-L-carnitine will benefit aging rats in the long-term or will have similar effects in humans. Clinical trials of a combination supplement of a-lipoic acid and acetyl-L-carnitine in humans currently underway, but the results of these trials are not yet available for evaluation. For more information about aging and oxidative stress, see the article, _Aging with Dr. Tory Hagen_ (http://lpi.orst.edu/f-w00/aging.html) , in the Fall/Winter 2000 LPI Newsletter. DISEASE TREATMENT Diabetes Chronically elevated blood glucose levels are the hallmark of _diabetes mellitus_ (http://lpi.oregonstate.edu/infocenter/glossary.html#diabetes) . Type I diabetes is also known as juvenile-onset or insulin-dependent diabetes mellitus (IDDM) because it often develops in childhood or adolescence, and insulin therapy is required to control blood glucose levels. Type II diabetes is also known as adult-onset diabetes or non-insulin-dependent diabetes mellitus (NIDDM) because it is more common in older adults and may not require insulin therapy. However, type II diabetes may also develop in children and adolescents, and its treatment may eventually require insulin therapy. _Pharmacologic doses_ (http://lpi.oregonstate.edu/infocenter/glossary.html#pharmacologic dose) of a-lipoic acid (i.e., many times higher than the amount a person could synthesize or obtain from foods) have been prescribed to treat diabetic patients in Germany since the late 1960's _(4)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref4) . Below is a summary of research on the use of a-lipoic acid supplementation to treat diabetes and its complications. Insulin sensitivity: In type II diabetes, elevated blood glucose levels result from _insulin resistance_ (http://lpi.oregonstate.edu/infocenter/glossary.html#insulin resistance) rather than a lack of insulin, and a number of treatments have been aimed at improving insulin sensitivity. There is limited evidence that high doses of a-lipoic acid can improve insulin sensitivity in individuals with type II diabetes. Intravenous infusions of 600 mg _(15)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref15) and 1,000 mg _(16)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref16) of a-lipoic acid to type II diabetics, improved insulin sensitivity by 27% and 51%, respectively compared to a placebo. An uncontrolled study of 20 type II diabetics found that oral administration of 1,200 mg of a-lipoic acid for 4 weeks significantly improved measures of glucose metabolism _(17)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref17) , and a placebo-controlled study of 72 type II diabetics found that oral a-lipoic acid at doses of 600 mg/day, 1,200 mg/day or 1,800 mg/day for 4 weeks improved insulin sensitivity by 25% _(18)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref18) . However, there were no significant differences between the three doses of a-lipoic acid tested. All of these studies were conducted using racemic a-lipoic acid. Data from animal studies suggests that the R-isomer may be more effective in improving insulin sensitivity than the S-isomer _(19, 20)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref19) , but this possibility has not been tested in any published human trials. Oxidative stress: A number of studies in individuals with diabetes (type I and type II) indicate that they are under increased _oxidative stress_ (http://lpi.oregonstate.edu/infocenter/glossary.html#oxidative stress) , a condition that is believed to contribute to the vascular and neurologic complications of diabetes. Although a-lipoic acid supplementation has been found to reduce measures of oxidative stress in animal models of diabetes, evidence that a-lipoic acid reduces oxidative stress in humans with diabetes is limited. In a non-randomized _cross-sectional study_ (http://lpi.oregonstate.edu/infocenter/glossary.html#cross-sectional study) , 33 patients with type I or type II diabetes who had been taking 600 mg/day of a-lipoic acid orally for at least 3 months had lower levels of _plasma_ (http://lpi.oregonstate.edu/infocenter/glossary.html#plasma) _lipid peroxidation_ (http://lpi.oregonstate.edu/infocenter/glossary.html#lipid peroxidation) than did 74 diabetics who did not take a-lipoic acid _(21)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref21) .. An intervention trial in 10 diabetic patients found that plasma lipid peroxides were significantly lower after taking 600 mg/day of a-lipoic acid orally for 60 days compared to baseline _(22)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref22) . The NF-kB transcription factor is known to increase the transcription of genes related to inflammation in response to increased oxidative stress. Oral a-lipoic acid supplementation (600 mg/day) has been found to decrease NF-kB activation in the white blood cells of type I diabetics _(23) _ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref23) and patients with diabetic nephropathy (kidney damage) _(24)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref24) . The formation of advanced glycation end products (AGEP) also leads to glucose-mediated damage in diabetes. a-Lipoic acid has been found to prevent the formation of AGEP in the test tube _(25)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref25) . Diabetic peripheral neuropathy: Over one third of diabetics develop peripheral _neuropathy_ (http://lpi.oregonstate.edu/infocenter/glossary.html#neuropathy) , a type of nerve damage that may result in decreased sensitivity, numbness, and pain, particularly in the lower extremities. In addition to the pain and disability caused by diabetic neuropathy, it is a leading cause of lower limb amputation in diabetics _(26)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref26) . The results of several large _randomized controlled trials_ (http://lpi.oregonstate.edu/infocenter/glossary.html#randomized controlled trial) indicate that maintaining blood glucose at near normal levels is the most important step in decreasing the risk of diabetic neuropathy _(27, 28)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref27) . However, such intensive blood glucose control may not be achievable in all diabetic patients. Oxidative stress has been implicated in the pathology of diabetic neuropathy, and a-lipoic acid is approved for the treatment of diabetic neuropathy in Germany _(1)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#reference) . At least 15 clinical trials have examined the effect of a-lipoic acid treatment on symptoms of diabetic neuropathy with mixed results, especially in smaller studies _(29)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref29) .. Modest benefits have been observed in several large multi-center trials. More than 300 type II diabetics with symptomatic peripheral neuropathy were randomly assigned to intravenous treatment with 100 mg/day, 600 mg/day, or 1,200 mg/day of a-lipoic acid or _placebo_ (http://lpi.oregonstate.edu/infocenter/glossary.html#placebo) for 3 weeks _(30)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref30) . Symptom scores were significantly improved in those that received intravenous infusions of at least 600 mg/day of a-lipoic acid compared to placebo. A subsequent multi-center trial randomly assigned 509 type II diabetics with symptomatic peripheral neuropathy to one of three treatments: 1) 600 mg/day of intravenous a-lipoic acid for 3 weeks followed by 1,800 mg/day of oral a-lipoic acid (600 mg, 3 times/day) for 6 months, 2) 600 mg/day of intravenous a-lipoic acid for 3 weeks followed by oral placebo for 6 months, or 3) intravenous placebo for 3 weeks followed by oral placebo for 6 months _(31)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref31) . Although symptom scores did not differ significantly from baseline in any of the groups, assessments of sensory and motor deficits by trained physicians were significantly improved after 3 weeks of intravenous a-lipoic acid therapy and non-significantly improved at the end of 6 months of oral a-lipoic acid therapy. A smaller randomized controlled trial examined the effect of long-term oral a-lipoic acid supplementation on the results of electrophysiologic nerve conduction studies in 65 diabetic patients with symptomatic peripheral neuropathy _(32)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref32) . After two years of follow up, those who took either 600 mg/day or 1,200 mg/day of a-lipoic acid orally showed significant improvements in 3 out of 4 nerve conduction assessments compared to those who took placebo. Overall, the available research suggests that oral doses of at least 600 mg/day of a-lipoic acid may offer some benefit in the alleviation of neuropathic symptoms and deficits, especially when used in conjunction with effective treatment aimed at normalizing blood glucose levels. Vascular complications: The inner lining of blood vessels, known as the _endothelium_ (http://lpi.oregonstate.edu/infocenter/glossary.html#endothelium) , plays an important role in preventing vascular disease. Endothelial function in individuals with diabetes (type I and type II) is often impaired, and diabetics are at increased risk for vascular disease. Several small preliminary studies in humans have examined the effect of a-lipoic acid administration on endothelial function. In one study, intra-arterial infusions of a-lipoic acid improved endothelium-dependent _vasodilation_ (http://lpi.oregonstate.edu/infocenter/glossary.html#vasodilation) (blood vessel relaxation) in 39 diabetic patients, but not in 11 healthy controls _(33)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref33) . Oral supplementation of 1,200 mg/day of a-lipoic acid for 6 weeks improved a measure of capillary perfusion in the fingers of 8 diabetic patients with peripheral neuropathy _(34)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref34) . In an uncontrolled, non-randomized study of 84 diabetic patients, plasma thrombomodulin levels, a marker of compromised endothelial function, decreased significantly in the 35 diabetics that took 600 mg/day of a-lipoic acid orally over 18 months, while thrombomodulin levels increased significantly in those that did not take a-lipoic acid over the same period _(35)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref35) . While the results of these small, uncontrolled trials are encouraging, long-term placebo-controlled studies are needed before it can be determined whether a-lipoic acid supplementation can reduce the risk of vascular complications in individuals with diabetes. SOURCES Biosynthesis a-Lipoic acid can be synthesized by plants and animals. The biosynthetic pathway for a-lipoic acid is not known, but it appears to be synthesized in the mitochondria from an 8-carbon _fatty acid_ (http://lpi.oregonstate.edu/infocenter/glossary.html#fatty acid) and elemental sulfur _(5)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref5) . It is currently unclear whether synthesis by normal _gastrointestinal_ (http://lpi.oregonstate.edu/infocenter/glossary.html#gastrointestinal) bacteria is a significant source of a-lipoic acid in humans. Biosynthesis does not appear to result in large amounts of circulating free a-lipoic acid, the form that is likely to function as an antioxidant _(3)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref3) . Food sources Most a-lipoic acid in food is derived from lipoamide-containing _enzymes_ (http://lpi.oregonstate.edu/infocenter/glossary.html#enzyme) and is bound to the _amino acid_ (http://lpi.oregonstate.edu/infocenter/glossary.html#amino acid) , lysine (lipoyllysine). Animal tissues that are rich in lipoyllysine include kidney, heart, and liver, while plant sources that are rich in lipoyllysine include spinach, broccoli, and tomatoes. Somewhat lower amounts of lipoyllysine have been measured in peas, brussel sprouts, and rice bran _(36)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref36) . Digestive enzymes do not break the bond between a-lipoic acid and lysine very effectively. Thus, it has been hypothesized that most dietary a-lipoic acid is absorbed as lipoyllysine, and free a-lipoic acid has not been detected in the circulation of humans who are not taking a-lipoic acid supplements _(3)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref3) . Although a-lipoic acid is found in a wide variety of foods from plant and animal sources, quantitative information on the a-lipoic acid content of food is limited. In the table below, the a-lipoic acid content of some foods was calculated from measurements of lipoyllysine in freeze-dried food samples _(36)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref36) . Food Lipoyllysine (mg/g dry weight) Serving a-lipoic acid*/serving (mg)# Beef kidney 2.6 3 ounces (85 g) 32 Beef heart 1.5 3 ounces (85 g) 19 Beef liver 0.9 3 ounces (85 g) 14 Spinach 3.2 1 cup raw (30 g) 5 Broccoli 0.9 1 cup raw (71 g) 4 Tomato 0.6 1 medium (123 g) 3 Peas 0.4 1 cup raw (145 g) 7 Brussel sprouts 0.4 1 cup raw (88 g) 3 Rice bran 0.2 1 cup (118 g) 11 Egg yolk 0.05 1 large (17 g) 0.3 *Lipoyllysine x 0.62 = a-lipoic acid _(1)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#reference) #1,000 micrograms (mg) = 1 milligram (mg) Supplements Supplemental doses of a-lipoic acid are hundreds of times higher than the amounts that can be obtained from food, and should be considered _pharmacologic_ (http://lpi.oregonstate.edu/infocenter/glossary.html#pharmacologic dose) rather than _physiologic doses_ (http://lpi.oregonstate.edu/infocenter/glossary.html#physiologic dose) . a-Lipoic acid is available by prescription in Germany, where it is approved for the treatment of diabetic and alcoholic _neuropathies_ (http://lpi.oregonstate.edu/infocenter/glossary.html#neuropathy) and alcoholic liver disease. It is available in the U.S. as a dietary supplement _(37)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref37) . Presently, all supplements available in the U.S. contain racemic a-lipoic acid, also called R-, S-a-lipoic acid or D-, L-a-lipoic acid. a-Lipoic acid from supplements is rapidly absorbed, rapidly metabolized, and rapidly cleared from plasma and tissues, suggesting that it should be taken in divided doses throughout the day, rather than in a single daily dose. The bioavailability of an orally administered dose of 200 mg is about 20-30% that of an intravenous dose _(38, 39)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref38) . Recommendations for the use of racemic a-lipoic acid as an _antioxidant_ (http://lpi.oregonstate.edu/infocenter/glossary.html#antioxidant) range from 50 mg/day to 400 mg/day. In the only published study to examine the _in vivo_ (http://lpi.oregonstate.edu/infocenter/glossary.html#in vivo) antioxidant effects of a-lipoic acid in healthy humans, 600 mg/day for 4 months significantly decreased several _biomarkers_ (http://lpi.oregonstate.edu/infocenter/glossary.html#biomarker) of oxidative stress compared to baseline _(40)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref40) . However, the antioxidant effects of lower doses have not been well studied in humans. Racemic vs. R-a-lipoic acid: There is evidence that the two optical _isomers_ (http://lpi.oregonstate.edu/infocenter/glossary.html#isomers) of a-lipoic acid have different biological activities. R-a-lipoic acid occurs naturally in plants and animals and is the only form that functions as a _cofactor_ (http://lpi.oregonstate.edu/infocenter/glossary.html#cofactor) for mitochondrial enzymes (see _Function_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#function) ). Chemical synthesis of a-lipoic acid results in a 50/50 or racemic mixture of S-a-lipoic acid and R-a-lipoic acid. Within the _mitochondria_ (http://lpi.oregonstate.edu/infocenter/glossary.html#mitochondria) , R-a-lipoic acid is reduced to DHLA, the more potent antioxidant, 28 times faster than S-a-lipoic acid. However, in the cytosol S-a-lipoic acid is reduced to DHLA twice as fast as R-a-lipoic acid. One study in humans found R-a-lipoic acid to be more _bioavailable_ (http://lpi.oregonstate.edu/infocenter/glossary.html#bioavailable) than S-a-lipoic acid when taken orally _(38)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref38) . R-lipoic acid was more effective than S-lipoic acid in enhancing insulin-stimulated glucose transport and metabolism in insulin-resistant rat skeletal muscle _(19)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref19) , and R-a-lipoic acid was more effective than racemic a-lipoic acid and S-a-lipoic acid in preventing cataracts in rats _(41)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref41) . Almost all studies of a-lipoic acid supplementation in humans have been performed using racemic a-lipoic acid. At present, it is not known whether R-a-lipoic acid is more effective as an antioxidant than racemic lipoic acid when taken by humans in _pharmacologic doses_ (http://lpi.oregonstate.edu/infocenter/glossary.html#pharmacologic dose) . SAFETY Toxicity In general, a-lipoic acid doses of 600 mg/day have been well tolerated. Doses as high as 1,200 mg/day (600 mg, 2 times/day) for 2 years and 1,800 mg/day (600 mg, 3 times/day) for 3 weeks did not result in adverse effects when given to patients with diabetic neuropathy under medical supervision. There are no reports of toxicity from a-lipoic acid overdose in humans. In individuals with diabetes and/or _impaired glucose tolerance_ (http://lpi.oregonstate.edu/infocenter/glossary.html#impaired glucose tolerance) , a-lipoic acid supplementation may lower blood glucose levels. Individuals on diabetic medications should monitor blood glucose levels. Diabetic medication doses may need to be adjusted to avoid _hypoglycemia_ (http://lpi.oregonstate.edu/infocenter/glossary.html#hypoglycemia) . Because controlled safety studies in pregnant and lactating women are not available, the use of a-lipoic acid supplements by pregnant or breastfeeding women is not recommended _(37)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref37) . Drug Interactions a-Lipoic acid supplements may affect the optimal dose of medications used to control blood glucose in diabetics. Individuals on such hypoglycemic agents should monitor their blood glucose levels and consult their health care provider for dosage adjustments if necessary to prevent _hypoglycemia_ (http://lpi.oregonstate.edu/infocenter/glossary.html#hypoglycemia) _(37)_ (http://lpi.oregonstate.edu/infocenter/othernuts/la/#ref37) . SUMMARY * R-a-lipoic acid functions as a critical _cofactor_ (http://lpi.oregonstate.edu/infocenter/glossary.html#cofactor) in several important _enzymes_ (http://lpi.oregonstate.edu/infocenter/glossary.html#enzyme) related to energy metabolism. * a-Lipoic acid deficiency has not been described, suggesting that humans are able to synthesize enough to meet their needs for enzyme cofactors. * In doses achievable through supplementation, a-lipoic acid can act as an _antioxidant_ (http://lpi.oregonstate.edu/infocenter/glossary.html#antioxidant) . * Controlled clinical trials indicate that 600 mg/day of racemic a-lipoic acid may reduce symptoms and neurological deficits associated with diabetic neuropathy. * Although recent studies in rats suggest that supplementation with the combination of R-a-lipoic acid and acetyl-L-carnitine may be beneficial in preventing age-related declines in energy metabolism and memory, it is not known whether supplementation with these compounds will help prevent such age-related declines in humans. * Although generally well tolerated, a-lipoic acid supplementation may affect the optimal dose of medications used to control blood glucose in diabetics or precipitate _hypoglycemia_ (http://lpi.oregonstate.edu/infocenter/glossary.html#hypoglycemia) . 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Natural sources of lipoic acid: determination of lipoyllysine released from protease-digested tissues by high performance liquid chromatography incorporating electrochemical detection. J Appl Nutr. 1997;49(1 & 2):3-11. 37. Hendler SS, Rorvik DR, eds. PDR for Nutritional Supplements. Montvale: Medical Economics Company, Inc; 2001. 38. Hermann R, Niebch G, Borbe HO, et al. Enantioselective pharmacokinetics and bioavailability of different racemic a-lipoic acid formulations in healthy volunteers. Eur J Pharm Sci. 1996;4:167-174. 39. Teichert J, Kern J, Tritschler HJ, Ulrich H, Preiss R. Investigations on the pharmacokinetics of alpha-lipoic acid in healthy volunteers. Int J Clin Pharmacol Ther. 1998;36(12):625-628. _(PubMed)_ (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=\ 9876998 & dopt=Abstract) 40. Marangon K, Devaraj S, Tirosh O, Packer L, Jialal I. Comparison of the effect of alpha-lipoic acid and alpha-tocopherol supplementation on measures of oxidative stress. Free Radic Biol Med. 1999;27(9-10):1114-1121. _(PubMed)_ (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids =10569644 & dopt=Abstract) 41. Maitra I, Serbinova E, Tritschler HJ, Packer L. Stereospecific effects of R-lipoic acid on buthionine sulfoximine-induced cataract formation in newborn rats. Biochem Biophys Res Commun. 1996;221(2):422-429. _(PubMed)_ (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=\ 8619871 & dopt=Abstract) ____________________________________ Reviewed by: _Tory M. Hagen, Ph.D._ (http://lpi.oregonstate.edu/staff/hagenbio.html) Principal Investigator, Linus ing Institute Assistant Professor, Dept. of Biochemistry and Biophysics Oregon State University Last updated 08/19/2002 Copyright 2002 by The Linus ing Institute ============================================ 3.Alpha Lipolic Acid May naturally in body cells as byproducts of energy release, A. L. A. increases levels of intracellular glutathione, and is a natural antioxidant with free radical scavenging abilities. It has the ability to regenerate oxidize antioxidants like vitamin C and E. and helps to make them more potent ALA is also known for its ability to enhance glucose uptake and may help prevent the cellular damage accompanying the complications of diabetes, it also has protective effect. 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