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R-Lipoic Acid (High Dose)


R-Lipoic Acid (High Dose)

$56.95 CAD

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The Natural, Effective form of Lipoic Acid

  • A powerful antioxidant addition to any supplement regime

  • Supportsblood sugar metabolism, nerve health and youthful cells

  • Enhances weight loss 

  • Promotes longevity by mimicking caloric restriction


Use this product for: Blood Sugar & Weight Management
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Lipoic acid is a versatile antioxidant known for its ability to protect the brain and nerve cells from free radicals and heavy metals that promote cognitive and neurodegenerative diseases. Lipoic acid is known as the “captain of the antioxidants” due to its ability to recycle and recharge other antioxidants such as vitamins C and E. Numerous studies have shown that lipoic acid can balance blood sugar and repair nerves damaged by diabetes. Additionally, this powerful anti-aging nutrient has been shown to mimic some of the effects of caloric restriction, the only proven method of extending health span and lifespan. It does so by protecting the mitochondria against free radical damage. Due to its action on the mitochondria it can revive damaged cells, especially those found in nerves and in the liver. It is a powerful partner for glutathione, the most powerful antioxidant produced in the body. 

In 1999, AOR introduced the world’s first pure R( ) lipoic acid based on the most current research. Unlike most conventional alpha-lipoic acid supplements, AOR’s 95% pure R( ) lipoic acid delivers the most effective form of this valuable antioxidant without the negative actions of S(-) lipoic acid.

R-Lipoic acid is a powerful, natural and well-rounded antioxidant with many actions such as repairing nerves, balancing blood sugar, protecting the brain and increasing energy formation in the mitochondria. Regular doses of lipoic acid are recommended for maintaining overall general health while high doses of R( ) lipoic acid are recommended for the management of high blood sugar, diabetic neuropathy and weight.


Label Info


High Dose R-Lipoic Acid helps to promote healthy glucose metabolism. AOR’s High Dose R-Lipoic Acid provides the natural ‘R’ form of this vital antioxidant produced in the body, unlike most alpha-lipoic acid supplements which also contain equal amounts of the synthetic, inactive ‘S’ form. AOR’s R-Lipoic Acid is in time-release capsules to enhance its stability and effectiveness.

Product Variation

Product Code NPN Size
AOR04289 80032333 60 VEGI-CAPS

Supplements Facts

Serving Size: 1 Capsule Amount % Daily
DL(α) lipoic acid (sodium salt)* 300 mg

*≥95% R(α)-lipoic acid, contains 30 mg sodium per capsule.

 sodium stearyl fumarate. Capsule: hypromellose, gellan gum.


AOR™ guarantees that there is not more than 14 mg of S-lipoic acid per capsule, and that all ingredients have been declared on the label. Contains no wheat, gluten, corn, nuts, peanuts, sesame seeds, sulphites, mustard, soy, dairy, eggs, fish, shellfish or any animal byproduct.

Adult Dosage

Take 1 capsule twice daily with/without food, or as directed by a qualified health care practitioner. 


Consult a health care practitioner prior to use if you are pregnant, breastfeeding or if you have diabetes. If you experience sweating, paleness, chills, headaches, dizziness and/or confusion, discontinue use and consult a health care practitioner as these may be symptoms of serious low blood sugar.


Pharmaceutical synthesis

Main Application

Network antioxidant

Mitochondrial function

Cognitive support

Neurological function



The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide or replace medical advice to individuals from a qualified health care professional. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes.



R-Lipoic Acid for Maintaining Overall Health

The Linus Pauling Institute recommends that 200-400mg of lipoic acid per day is beneficial for people who are in good health. Low doses of lipoic acid taken on a consistent basis help to protect the body from free radical damage and to slow the aging process whereas higher doses may benefit specific concerns such as weight management, insulin resistance or diabetic neuropathy.

Lipoic Acid’s Health Benefits

Lipoic acid is one of the most versatile endogenous antioxidants recently discovered. It has numerous health benefits, such as slowing the cellular aging process, protecting the mitochondria (our energy-producing organelles), contributing to healthy glucose metabolism, chelating iron, protecting against cognitive degenerative disorders, and more! But only the R( ) form of lipoic acid is responsible for these health benefits. Are you taking the right form?

Regular Alpha Lipoic Acid

Unless they say specify otherwise, “lipoic acid” supplements are a 50/50 mixture of the natural R ( ) lipoic acid, and the synthetic S (-) lipoic acid. These mixtures are called “racemates.” In some cases, S (-) lipoic acid – or the racemate – is simply less effective than R ( ) lipoic acid. But in other cases, the S (-) form actually acts in opposition to the activity of R ( ) lipoic acid.

If you’re taking a conventional alpha-lipoic acid pill, then you need to know that the health-promoting, anti-aging benefits associated with this nutrient are only being delivered by half of your supplement. The other half is worse than useless: it actually antagonizes the effects of the good half of the supplement. To put it bluntly: the lipoic acid you’re taking harbors both a hero … and an “evil twin.” Many molecules used by the body have a specific “handedness” (chirality). For example, alpha-tocopherol, or essential fatty acids. In some cases, synthetic versions of these molecules have a different “handedness” than the natural molecule. You’re probably familiar with some examples of this phenomenon, such as natural d- vs. synthetic dl-alpha-tocopherolor natural cis- vs. unnatural trans-fatty acids. Some of these artificial molecules are merely less potent than the natural forms, such as in the case of dl-alpha-tocopherol. But others are actually harmful – for example, trans-fatty acids.

The Bottom Line

Common “lipoic acid” supplements are thus like a house at war with itself. The S (-) form should be removed from supplements in favor of pure R ( ) lipoic acid.

“We’re finding – and others are, too – that the R ( ) form – the natural form – is much more powerful than the racemic mixture … Hopefully … companies are going to be producing on more of a clinical scale the R ( ) form of lipoic acid, because we’re finding very significant effects using this, as opposed to the racemic mixture.” – Dr. Tory Hagen, in Mitochondrial Decay in Aging.

“We have presented in this study new information indicating that this enhancement of glucose metabolism is sterospecific, with the R ( ) enantiomer being much more effective than the S (-) enantiomer.” – Dr. Ryan Streeper and colleagues, in The American Journal of Physiology.

“Lipoic acid sold in a health food store is a synthetic mixture, a racemic mixture. And R( ) is the natural form and S (-) is an unnatural one … And in our hands R( ) works and S (-) doesn’t.” – Dr. Bruce Ames, in Strategies for Engineered Negligible Senescence.

“R ( ) LA [that is, R ( ) lipoic acid], and not a racemic mixture of R ( ) and S (-) LA, should be considered a choice for therapeutic applications.” – Dr. Lester Packer and colleagues, in Free Radical Biology and Medicine.

“The S (-) enantiomer … part of the racemate, which is present as about a 50% impurity, needs to be eliminated.” – Dr. Guido Zimmer and colleagues, in Methods in Enzymology.



Compared with the S(-) Form, R( ) Lipoic Acid is Far Superior

Some studies have compared the effects of the two “lipoic acid” molecules seperately. R ( ) lipoic acid has emerged as the active ingredient in the racemate. R ( ) lipoic acid fights all of the major effects of insulin resistance. The S(-)-form does not help in some of these areas, and even makes things worse in others.

Antioxidant Defenses

Lipoic acid is known as a powerful and versatile antioxidant. R ( ) lipoic acid is more easily absorbed and taken into the cells than S (-) lipoic acid. Peak plasma concentration of R( )-Lipoic Acid has been found to be 40-50% higher than S(-)-lipoic acid. Both forms of lipoic acid can be made more powerful by “charging” them up into their active DHLA form. R ( ) -lipoic acid is “upgraded” much more rapidly than S(-)-lipoic acid. Many studies have found that R ( ) lipoic acid provides much more effective protection than S (-) lipoic acid or the racemate. In some cases, the S (-) lipoic acid actually counteracts the effects of R ( ) lipoic acid.

Glucose Metabolism and Weight Management – Using a Higher Dosage May Be More Effective

Lipoic acid has been used to support healthy blood sugar metabolism. Insulin resistance, in which the cells of the body stop responding properly to the hormone insulin, happens to some degree in almost all of us as we age. Insulin resistance causes higher levels of insulin, blood sugar, and free fatty acids, all of which are threats to your health. Higher bolus dosages of lipoic acid have been proven to benefit those with blood sugar control problems as well as for managing diabetic neuropathy.

A randomized double-blind placebo-controlled clinical trial investigating the effectiveness of oral supplementation of DL-alpha-lipoic acid (ALA) on glycemic and oxidative status in diabetes mellitus (DM) patients was conducted. Thirty eight outpatients with type 2 DM were recruited and randomly assigned to either placebo or treatment in various doses of ALA (300, 600, 900, and 1200 mg/day) for 6 months. Following the treatment, all subjects were evaluated for glucose status and oxidative biomarkers. Results showed that fasting blood glucose trended to decrease in a dose-dependent manner. High dosages such as these have been safely used over extended periods of time in research studies as long as two years. Another study used a dosage of 600mg given two times per day and was shown to significantly improve the symptoms of diabetic polyneuropathy in 73% of the 236 patients enrolled in the study.

A study investigating the effects of ALA supplements on weight loss found that ALA can be used as an adjunctive treatment for obesity. Over a period of 20 weeks, the randomized, double-blind, placebo controlled study enrolled 360 obese individuals whom also had hypertension, diabetes and or high cholesterol levels. Subjects were divided into either treatment groups that received 1200 or 1800 mg/day of ALA or were given a placebo. The group that took the higher level of ALA experienced a 5% decrease in total body weight while the 1200mg/day group also experienced weight loss, although it was less statistically significant.

A new study showed that when combined with a calorie-restricted diet, even 300 mg/day of alpha-lipoic acid over 10 weeks is effective in reducing body weight and supporting fat loss, especially around the belly and hips.

Neurological Health

Lipoic acid is known for its ability to protect brain and nerve cells from free radicals and toxins. Excessive levels of “transition metals” such as iron, copper, and cadmium are believed to play an important role in many neurological disorders. Having too much free iron in a key part of the brain has been implicated as a cause of Parkinson’s disease, for example. In fact, a recent study showed that older people with Alzheimer’s disease had higher accumulation of iron in the hippocampus, while older healthy people did not have this accumulation. The hippocampus is the area of the brain responsible for memory and learning and is highly affected early in Alzheimer’s disease.

R ( ) lipoic acid supplements partially reverse the age-associated loss of spatial and temporal memory seen in old animals. An animal study using R ( ) lipoic acid found that it was able to significantly reduce age-related buildup of iron in the brain. Other studies suggest that S (-) lipoic acid will not work as well.

Protection Against Macular Degeneration

Age related macular degeneration (AMD) is a concern for many people as they advance in age. A study conducted in 62 patients with early and intermediate AMD were assigned to either a treatment or a placebo group. The results of the study showed that there was a statistically significant increase in serum antioxidant Super Oxide Dismutase activity after the lipoic acid intervention. The increase in SOD activity caused by LA supplementation indicates that LA may have a possible preventive effect in the development of AMD through an antioxidant mechanism.

Mitochondrial Function

The biggest source of free radicals in your body are your cellular “power plants,” the mitochondria. They are both the origin, and the target, of most of the free radical damage in the body. As we age, our mitochondria become less and less efficient, generating less and less energy while creating more and more free radicals. R ( ) lipoic acid, in animal experiments and in test-tube studies, makes mitochondria more efficient, so that they produce more energy and create fewer free radicals. Age-associated damage to mitochondrial structure is significantly reduced. S (-) lipoic acid does not have these effects, and may antagonize the action of R ( ) lipoic acid. These benefits have a real impact on the organism. Animals undergoing a simulated heart attack recover heart function more rapidly when infused with R ( ) lipoic acid; S (-) lipoic acid has no such effect. Animals who receive R ( ) lipoic acid supplements look better and are more active.

Fundamental Aging

Nearly all researchers into the biology of aging agree that the decay of mitochondrial function is a major engine of the aging process. Caloric restriction, with adequate nutrition, is the only proven way to slow down the fundamental aging process in mammals. Many of the benefits of R( ) lipoic acid closely mimic those of caloric restriction. R ( ) lipoic acid’s effects on mitochondrial function are the most striking and unique parallel. A study in a short-lived strain of mouse demonstrated that R ( ) lipoic acid can dramatically increase its lifespan. Neither S (-) lipoic acid, nor the racemate, had any significant effect. The National Institutes on Aging are currently funding studies to see if R ( ) lipoic acid can truly slow down the aging process.

With or Without Food?

Higher amounts of lipoic acid are absorbed when the supplement is taken on an empty stomach. When taken with food, the peak plasma lipoic acid concentration was reduced by approximately 20% as compared to fasting plasma levels.


Market Trends

Most consumers purchase alpha-lipoic acid without knowing that there is a disadvantage to using both forms of the supplement. The R( ) form of Lipoic acid is the only form that is of value, while the S (-) form of lipoic acid is of no value and may even negate the effects of the more beneficial form. To obtain maximum beneficial effects, the S (-) form should be removed from supplements in favor of pure R-lipoic acid.

AOR Advantage

In 1999, AOR was the first company in the world to offer pure R( ) Lipoic Acid based on the most current literature. AOR’s pure R-Lipoic acid delivers the most effective form of this valuable antioxidant without the negative actions of lipoic acid’s S (-) form. Regular doses of lipoic acid are recommended for maintaining overall general health while high doses of R( ) Lipoic Acid are recommended for the management of high blood sugar and diabetic neuropathy problems.

High dose R( ) lipoic acid provides a convenient and more economical dosage in a reduced capsule count for those that need to take a higher dosage at one time for that therapeutic treatment and management of high blood sugar levels, and/or for improving neuropathy conditions.



Hagen TM, Ingersoll RT, Lykkesfeldt J, Liu J, Wehr CM, Vinarsky V, Bartholomew JC, Ames AB. “(R)-alpha-lipoic acid-supplemented old rats have improved mitochondrial function, decreased oxidative damage, and increased metabolic rate.” FASEB J. 1999 Feb; 13(2): 411-8.

Hagen TM, Vinarsky V, Wehr CM, Ames BN. “(R)-alpha-lipoic acid reverses the age-associated increase in susceptibility of hepatocytes to tert-butylhydroperoxide both in vitro and in vivo.” Antioxid Redox Signal. 2000 Fall; 2(3): 473-83.

Huerta AE, Navas-Carretero S, Prieto-Hontoria PL, Martínez JA, Moreno-Aliaga MJ. Effects of α-lipoic acid and eicosapentaenoic acid in overweight and obese women during weight loss. Obesity (Silver Spring). 2014 Dec 31. 

Koh EH, Lee WJ, Lee SA, Kim EH, Cho EH, Jeong E, Kim DW, Kim MS, Park JY, Park KG, Lee HJ, Lee IK, Lim S, Jang HC, Lee KH, Lee KU. Effects of alpha-lipoic Acid on body weight in obese subjects. Am J Med. 2011 Jan;124(1):85

Lockhart B, Jones C, Cuisinier C, Villain N, Peyroulan D, Lestage P. “Inhibition of L-homocysteic acid and buthionine sulphoximine-mediated neurotoxicity in rat embryonic neuronal cultures with alpha-lipoic acid enantiomers.” Brain Res. 2000 Feb 14; 855(2): 292-7.

Streeper RS, Henriksen EJ, Jacob S, Hokama JY, Fogt DL, Tritschler HJ. “Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle.” Am J Physiol. 1997 Jul; 273(1 Pt 1): E185-91.

Suh J, Rocha A, Shigeno E, Frei B, Hagen TM. “(R)-alpha-lipoic acid supplementation of old rats decreases age-dependent accumulation of iron and ascorbate depletion in brain.” AGE. 1999 Jul; 22(3): 121(Abs 19).



Effects of α-lipoic acid and eicosapentaenoic acid in overweight and obese women during weight loss.

Obesity (Silver Spring). 2014 Dec 31.

Huerta AE, Navas-Carretero S, Prieto-Hontoria PL, Martínez JA, Moreno-Aliaga MJ.

OBJECTIVE: To evaluate the potential body weight-lowering effects of dietary supplementation with eicosapentaenoic acid (EPA) and α-lipoic acid separately or combined in healthy overweight/obese women following a hypocaloric diet.

METHODS: This is a short-term double-blind placebo-controlled study with parallel design that lasted 10 weeks. Of the randomized participants, 97 women received the allocated treatment [Control, EPA (1.3 g/d), α-lipoic acid (0.3 g/d), and EPA   α-lipoic acid (1.3 g/d   0.3 g/d)], and 77 volunteers completed the study. All groups followed an energy-restricted diet of 30% less than total energy expenditure. Body weight, anthropometric measurements, body composition, resting energy expenditure, blood pressure, serum glucose, and insulin and lipid profile, as well as leptin and ghrelin levels, were assessed at baseline and after nutritional intervention.

RESULTS: Body weight loss was significantly higher (P < 0.05) in those groups supplemented with α-lipoic acid. EPA supplementation significantly attenuated (P < 0.001) the decrease in leptin levels that occurs during weight loss. Body weight loss improved lipid and glucose metabolism parameters but without significant differences between groups.

CONCLUSIONS: The intervention suggests that α-lipoic acid supplementation alone or in combination with EPA may help to promote body weight loss in healthy overweight/obese women following energy-restricted diets.


Increased Iron Levels and Decreased Tissue Integrity in Hippocampus of Alzheimer’s Disease Detected in vivo with Magnetic Resonance Imaging.

J Alzheimers Dis. 2013 Jun 21.

Raven EP, Lu PH, Tishler TA, Heydari P, Bartzokis G.

Background: Iron can catalyze damaging free radical reactions. With age, iron accumulates in brain gray matter regions and may contribute to the risk of developing age-related diseases such as Alzheimer’s disease (AD). Prior MRI studies demonstrated increased iron deposits in basal ganglia regions; however, the hippocampus (Hipp), which is heavily damaged in AD, and comparator regions that are resistant to AD damage, such as thalamus (Th), have rarely been examined.

Objective: To assess iron levels and evidence of tissue damage in Hipp and Th of AD subjects and healthy controls.

Methods: Thirty-one AD and sixty-eight healthy control subjects participated in this study. High- and low-field strength MRI instruments were used in combination to quantify iron content of ferritin molecules (ferritin iron) using the field dependent relaxation rate increase (FDRI) method. Decreased transverse relaxation rate (R2) was used as an index of tissue damage.

Results: Compared with healthy controls, AD subjects had increased ferritin iron in Hipp (p = 0.019) but not Th (p = 0.637), and significantly decreased R2 in Hipp (p < 0.001) but not Th (p = 0.37). In the entire sample, FDRI and R2 were negatively correlated.

Conclusion: The data shows that in AD, Hipp damage occurs in conjunction with ferritin iron accumulation. Prospective studies are needed to evaluate how increasing iron levels may influence the trajectory of tissue damage and cognitive and pathologic manifestations of AD.


Effect of (R)-α-lipoic acid supplementation on serum lipids and antioxidative ability in patients with age-related macular degeneration.

Ann Nutr Metab. 2012;60(4):293-7.

Sun YD, Dong YD, Fan R, Zhai LL, Bai YL, Jia LH.

BACKGROUND/AIMS: Supplementation with antioxidants is of special interest in preventing or delaying the development and progression of age-related macular degeneration (AMD). This investigation aimed to assess the effect of α- lipoic acid (LA) on serum lipids, serum malondialdehyde (MDA) and superoxide dismutase (SOD) in patients with AMD.

METHODS: A total of 62 patients (50-75 years old) with early and intermediate dry form of AMD were randomly assigned to two groups, i.e. LA administration (n = 32) and placebo (n = 30). The levels of serum lipids and MDA and SOD activity were measured before and after LA and placebo intervention.

RESULTS: Compared with the parameters at baseline, serum total cholesterol (CHO), triglyceride and high- and low-density lipoprotein CHO (HDL and LDL) levels were not significantly different after LA and placebo intervention. There was a slight but statistically nonsignificant decrease in serum MDA levels and a statistically significant increase in serum SOD activity after LA intervention. There were no statistically significant differences in serum MDA levels or SOD activity after placebo intervention.

CONCLUSION: The apparent increase in SOD activity caused by LA supplementation indicates that LA may have a possible preventive effect in the development of AMD through an antioxidant mechanism.


Glycemic and oxidative status of patients with type 2 diabetes mellitus following oral administration of alpha-lipoic acid: a randomized double-blinded placebo-controlled study.

Asia Pac J Clin Nutr. 2012;21(1):12-21.

Porasuphatana S, Suddee S, Nartnampong A, Konsil J, Harnwong B, Santaweesuk A.

Despite well-controlled blood glucose levels, diabetic complications still inevitably take place via several mechanisms including excessive generation of free radicals in patients who suffer from diabetes mellitus (DM). A randomized double-blind placebo-controlled clinical trial to investigate the effectiveness of oral supplementation of DL-alpha-lipoic acid (ALA) on glycemic and oxidative status in DM patients was conducted. Thirty eight outpatients with type 2 DM were recruited and randomly assigned to either placebo or treatment in various doses of ALA (300, 600, 900, and 1200 mg/day) for 6 months. Following the treatment, all subjects were evaluated for glucose status and oxidative biomarkers. Results showed that fasting blood glucose, HbA1c trended to decrease in a dose-dependent manner. Increase of urinary PGF2α-Isoprostanes (F2α-IsoP) was noted in placebo but not ALA-treated groups, indicating possible suppressing action of ALA on lipid peroxidation in DM subjects. 8-Hydroxy-2′-deoxyguanosine (8-OHdG) levels, however, were similar in both placebo and ALA groups as well as urinary microalbumin and serum creatinine. Safety evaluation was monitored and treatment was found to be well tolerated despite some minor side effects. Results from this study reflected the benefits of ALA in glucose status with slight efficiency on oxidative stress-related deterioration in DM patients.


Combination of alpha lipoic acid and superoxide dismutase leads to physiological and symptomatic improvements in diabetic neuropathy.

Drugs R D. 2012 Mar 1;12(1):29-34.

Bertolotto F, Massone A.

BACKGROUND AND OBJECTIVE: The management of diabetic neuropathy is still a challenge for physicians. The aim of this study was to assess the efficacy of a new combination of alpha lipoic acid and superoxide dismutase for the treatment of diabetic neuropathy.

METHODS: |The setting of this study was ambulatory (outpatient) care. A prospective, non-randomized, open-label study was conducted in 50 patients with diabetes mellitus and with a deficit in both motor and sensory nerve conduction. Treatment was with a new combination of alpha lipoic acid and superoxide dismutase (ALA600SOD®) for 4 months. Electroneurographic parameters and perceived pain were assessed at baseline and after treatment.

RESULTS: After 4 months of treatment, patients significantly improved their electroneurographic parameters and their perception of pain. Best improvements were observed in sensory nerve conduction.

CONCLUSION: The combination of two powerful antioxidant agents leads to improvement in both subjective and objective parameters in patients with diabetic neuropathy. New profitable directions for investigations are opened for a non-invasive treatment of diabetic neuropathy in the future.


Effect of α-lipoic acid on platelet reactivity in type 1 diabetic patients.

Diabetes Care. 2012 Feb;35(2):196-7.

Mollo R, Zaccardi F, Scalone G, Scavone G, Rizzo P, Navarese EP, Manto A, Pitocco D, Lanza GA, Ghirlanda G, Crea F.

OBJECTIVE: Type 1 diabetes is associated with increased platelet reactivity. We investigated whether α-lipoic acid (ALA) has any effect on platelet reactivity in these patients.

RESEARCH DESIGN AND METHODS: We randomly assigned 51 type 1 diabetic patients to ALA (600 mg once daily) or placebo for 5 weeks. Platelet reactivity was evaluated by the PFA-100 method and by measuring CD41 and CD62 platelet expression. C-reactive protein (CRP) and 8-iso-prostaglandin F2α serum levels also were measured.

RESULTS: Baseline variables were similar in the two groups. After treatment, closure time was longer (P = 0.006) and CD62P platelet expression was lower, both before (P = 0.002) and after (P = 0.009) ADP stimulation in the ALA group compared with the placebo group. CRP and 8-iso-prostaglandin F2α levels showed no differences between the two groups.

CONCLUSIONS: Our data show that ALA reduces measures of platelet reactivity ex vivo in type 1 diabetic patients, independently of antioxidant or anti-inflammatory effects.


Effect of alpha-lipoic acid on blood glucose, insulin resistance and glutathione peroxidase of type 2 diabetic patients. 

Saudi Med J. 2011 Jun;32(6):584-8. A

nsar H, Mazloom Z, Kazemi F, Hejazi N.

OBJECTIVE: To examine the effects of alpha-lipoic acid (ALA) treatment over a period of 2 months on fasting blood glucose (FBG), insulin resistance (IR), and glutathione peroxidase (GH-Px) activity in type 2 diabetes (T2DM) patients.

METHODS:|This study took place in Motahari Clinic, Shiraz, Iran, which is affiliated to Shiraz University of Medical Sciences from May to October 2006. Type 2 DM patients (n=57) were divided into 2 groups to receive either ALA (300 mg daily) or placebo by systematic randomization, and were followed-up for 8 weeks. After an overnight fasting and 2 hours after breakfast, patients’ blood samples were drawn and tested for FBG, 2 hours PPG, serum insulin level, and GH-Px activity.

RESULTS: The result of the study showed a significant decrease in FBG and PPG levels, IR-Homeostasis Model Assessment (IR-HOMA index) and GH-Px level in the ALA group. The comparison of differences between FBG and IR at the beginning and at the end of study in the ALA treated group and the placebo group were also significant.

CONCLUSION: This study supports the use of ALA as an antioxidant in the care of diabetic patients.


[Efficacy and safety of high-dose α-lipoic acid in the treatment of diabetic polyneuropathy]. [Article in Chinese] 

Zhonghua Yi Xue Za Zhi. 2010 Sep 21;90(35):2473-6.

Gu XM, Zhang SS, Wu JC, Tang ZY, Lu ZQ, Li H, Liu C, Chen L, Ning G.

OBJECTIVE: To evaluate the efficacy and safety of high-dose α-lipoic acid in the treatment of diabetic polyneuropathy with regards to sensory symptoms and nerve conduction velocity.

METHODS: A total of 236 diabetics with symptomatic polyneuropathy were enrolled into this 5-center, randomized, double-blind and placebo-controlled study of α-lipoic acid 1800 mg daily (n = 117) or matching placebo (n = 119) for 12 weeks. The primary outcome was total symptom score (TSS). Secondary end points included nerve conduction velocity, individual symptom score, HbA1c and safety parameters. The above parameters were reviewed and recorded at zero point and after treatment for 2, 4, 8, 12 weeks separately.

RESULTS: 73.27% patients with symptomatic polyneuropathy improved after treatment with α-lipoic acid for 12 weeks versus 18.27% with placebo. TSS declined by 2.6 ± 2.3 with α-lipoic acid. And it was more than 0.7 ± 1.4 versus placebo (P < 0.05). TSS decreased quickly after treatment with α-lipoic acid for 2 weeks (P < 0.05). And it was better than placebo. Individual symptom scores of pain, extremity numbness, burning sensation or resting abnormal sensations were significantly diminished as compared to those before treatment and placebo group (all P < 0.05). Nerve conduction velocity had no change. HbA1c further decreased at the end of trial after α-lipoic acid treatment (P < 0.05). The incidence rates of adverse effects were 25.4% vs 11.8% in the treatment and control groups. The major manifestation was burning sensation from throat to stomach (12.7%).

CONCLUSION: Oral treatment with high-dose α-lipoic acid for 12 weeks may improve symptoms in patients with diabetic polyneuropathy. Dose of 600 mg thrice daily for 2 weeks has marked effects with a reasonable safety.


Chronic dietary a-lipoic acid reduces deficits in hippocampal memory of aged Tg2576 mice.

Neurobiology of Aging. 2007;28:213-225.

Joseph F. Quinn, Joseph R. Bussiere, Rebecca S. Hammond, Thomas J. Montine, Edward Henson, Richard E. Jones, Robert W. Stackman Jr.

Oxidative stress may play a key role in Alzheimer’s disease (AD) neuropathology. Here, the effects of the antioxidant, alpha-lipoic acid (ALA) were tested on the Tg2576 mouse, a transgenic model of cerebral amyloidosis associated with AD. Ten-month old Tg2576 and wild type mice were fed an ALA-containing diet (0.1%) or control diet for 6 months and then assessed for the influence of diet on memory and neuropathology. ALA-treated Tg2576 mice exhibited significantly improved learning, and memory retention in the Morris water maze task compared to untreated Tg2576 mice. Twenty-four hours after contextual fear conditioning, untreated Tg2576 mice exhibited significantly impaired context-dependent freezing. ALA-treated Tg2576 mice exhibited significantly more context freezing than the untreated Tg2576 mice. Assessment of brain soluble and insoluble beta-amyloid levels revealed no differences between ALA-treated and untreated Tg2576 mice. Brain levels of nitrotyrosine, a marker of nitrative stress, were elevated in Tg2576 mice, while F2 isoprostanes and neuroprostanes, oxidative stress markers, were not elevated in the Tg2576 mice relative to wild type. These data indicate that chronic dietary ALA can reduce hippocampal-dependent memory deficits of Tg2576 mice without affecting beta-amyloid levels or plaque deposition.


The antioxidants a-lipoic acid and N-acetylcysteine reverse memory impairment and brain oxidative stress in aged SAMP8 mice. J

ournal of Neurochemistry. March 2003;84(5):173-1183.

Susan A. Farr, H. Fai Poon, Dilek Dogrukol, Jeniffer Drake, William A. Banks, Edward Eyerman, D. Allan Butterfield, and John E. Morley.

Oxidative stress may play a crucial role in age-related neurodegenerative disorders. Here, we examined the ability of two antioxidants, a-lipoic acid (LA) and N-acetylcysteine (NAC), to reverse the cognitive deficits found in the SAMP8 mouse. By 12 months of age, this strain develops elevated levels of Aß and severe deficits in learning and memory. We found that 12-month-old SAMP8 mice, in comparison with 4-month-old mice, had increased levels of protein carbonyls (an index of protein oxidation), increased TBARS (an index of lipid peroxidation) and a decrease in the weakly immobilized/strongly immobilized (W/S) ratio of the protein-specific spin label MAL-6 (an index of oxidation-induced conformational changes in synaptosomal membrane proteins). Chronic administration of either LA or NAC improved cognition of 12-month-old SAMP8 mice in both the T-maze footshock avoidance paradigm and the lever press appetitive task without inducing non-specific effects on motor activity, motivation to avoid shock, or body weight. These effects probably occurred directly within the brain, as NAC crossed the blood-brain barrier and accumulated in the brain. Furthermore, treatment of 12-month-old SAMP8 mice with LA reversed all three indexes of oxidative stress. These results support the hypothesis that oxidative stress can lead to cognitive dysfunction and provide evidence for a therapeutic role for antioxidants.


Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: partial reversal by feeding acetyl-L-carnitine and/or R-alpha-lipoic acid.

Proc Natl Acad Sci USA 2002 Feb 19; 99(4): 2356-61.

Liu J, Head E, Gharib AM, Yuan W, Ingersoll RT, Hagen TM, Cotman CW, Ames BN.

Accumulation of oxidative damage to mitochondria, protein, and nucleic acid in the brain may lead to neuronal and cognitive dysfunction. The effects on cognitive function, brain mitochondrial structure, and biomarkers of oxidative damage were studied after feeding old rats two mitochondrial metabolites, acetyl-l-carnitine (ALCAR) [0.5% or 0.2% (wt/vol) in drinking water], and/or R-alpha-lipoic acid (LA) [0.2% or 0.1% (wt/wt) in diet]. Spatial memory was assessed by using the Morris water maze; temporal memory was tested by using the peak procedure (a time-discrimination procedure). Dietary supplementation with ALCAR and/or LA improved memory, the combination being the most effective for two different tests of spatial memory (P < 0.05; P < 0.01) and for temporal memory (P < 0.05). Immunohistochemical analysis showed that oxidative damage to nucleic acids (8-hydroxyguanosine and 8-hydroxy-2′-deoxyguanosine) increased with age in the hippocampus, a region important for memory. Oxidative damage to nucleic acids occurred predominantly in RNA. Dietary administration of ALCAR and/or LA significantly reduced the extent of oxidized RNA, the combination being the most effective. Electron microscopic studies in the hippocampus showed that ALCAR and/or LA reversed age-associated mitochondrial structural decay. These results suggest that feeding ALCAR and LA to old rats improves performance on memory tasks by lowering oxidative damage and improving mitochondrial function.


(R)-alpha-lipoic acid reverses the age-associated increase in susceptibility of hepatocytes to tert-butylhydroperoxide both in vitro and in vivo.

Antioxid Redox Signal 2000 Fall; 2(3): 473-83.

Hagen TM, Vinarsky V, Wehr CM, Ames BN.

Hepatocytes were isolated from young (3-5 months) and old (24-28 months) rats and incubated with various concentrations of tert-butylhydroperoxide (t-BuOOH). The t-BuOOH concentration that killed 50% of cells (LC50) in 2 hr declined nearly two-fold from 721 /- 32 microM in cells from young rats to 391 /- 31 microM in cells from old rats. This increased sensitivity of hepatocytes from old rats may be due, in part, to changes in glutathione (GSH) levels, because total cellular and mitochondrial GSH were 37.7% and 58.3% lower, respectively, compared to cells from young rats. Cells from old animals were incubated with either (R)- or (S)-lipoic acid (100 microM) for 30 min prior to the addition of 300 microM t-BuOOH. The physiologically relevant (R)-form, a coenzyme in mitochondria, as opposed to the (S)-form significantly protected hepatocytes against t-BuOOH toxicity. Dietary supplementation of (R)-lipoic acid [0.5% (wt/wt)] for 2 weeks also completely reversed the age-related decline in hepatocellular GSH levels and the increased vulnerability to t-BuOOH as well. An identical supplemental diet fed to young rats did not enhance the resistance to t-BuOOH, indicating that antioxidant protection was already optimal in young rats. Thus, this study shows that cells from old animals are more susceptible to oxidant insult and (R)-lipoic acid, after reduction to an antioxidant in the mitochondria, effectively reverses this age-related increase in oxidant vulnerability.


Inhibition of L-homocysteic acid and buthionine sulphoximine-mediated neurotoxicity in rat embryonic neuronal cultures with alpha-lipoic acid enantiomers.

Brain Res 2000 Feb 14; 855(2): 292-7.

Lockhart B, Jones C, Cuisinier C, Villain N, Peyroulan D, Lestage P.

In the present report, we have set out to investigate the potential capacity of both the oxidised and reduced forms of RS-alpha-lipoic acid, and its separate R-( ) and S-(-)enantiomers, to prevent cell death induced with L-homocysteic acid (L-HCA) and buthionine sulphoximine (BSO) in rat primary cortical and hippocampal neurons. L-HCA induced a concentration-dependent neurotoxic effect, estimated by cellular 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) reduction, in primary neurons, but was significantly more toxic for hippocampal (EC(50)=197 microM) compared with cortical neurons (EC(50)=1016 microM) whereas D-HCA demonstrated only moderate (


(R)-alpha-lipoic acid-supplemented old rats have improved mitochondrial function, decreased oxidative damage, and increased metabolic rate.

FASEB J 1999 Feb; 13(2): 411-8.

Hagen TM, Ingersoll RT, Lykkesfeldt J, Liu J, Wehr CM, Vinarsky V, Bartholomew JC, Ames AB.

A diet supplemented with (R)-lipoic acid, a mitochondrial coenzyme, was fed to old rats to determine its efficacy in reversing the decline in metabolism seen with age. Young (3 to 5 months) and old (24 to 26 months) rats were fed an AIN-93M diet with or without (R)-lipoic acid (0.5% w/w) for 2 wk, killed, and their liver parenchymal cells were isolated. Hepatocytes from untreated old rats vs. young controls had significantly lower oxygen consumption (P


Influence of selegiline and lipoic acid on the life expectancy of immunosuppressed mice.

Arzneimittelforschung 1997 Jun; 47(6): 776-80.

Freisleben HJ, Neeb A, Lehr F, Ackermann H.

Ten groups of 14 immunosuppressed NMRI-mice (nu/nu) were raised and kept under germ-reduced conditions. The control animals were fed a germ-reduced diet, nine other groups received the same diet with selegiline (CAS 14611-51-9, Deprenyl) or lipoic acid (thioctic acid, CAS 62-46-4) admixed at various amounts. The 50% survival rate, the total life span of each group and the areas under the curves were determined to evaluate life expectancy as compared to the controls. The racemate of lipoic acid at high dosage (350 mg/kg body weight) reduced the life span significantly. The S(-)-enantiomer of lipoic acid (75 mg/kg body weight) increased the 50% survival rate, whereas the physiologic R( )-enantiomer (9 mg/kg body weight) expanded the total life span of its group. Alteration of only one out of three parameters was not considered significant. All other groups except for one did not differ from controls: only animals which obtained 75 micrograms selegiline per kg of body weight and per day exerted increased life expectancies by all three parameters. This group exhibited also in statistical evaluation a significantly (p < 0.05) prolongated survival time up to about 200% as compared to the control animals.


Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle. A

m J Physiol 1997 Jul; 273(1 Pt 1): E185-91.

Streeper RS, Henriksen EJ, Jacob S, Hokama JY, Fogt DL, Tritschler HJ.

The racemic mixture of the antioxidant alpha-lipoic acid (ALA) enhances insulin-stimulated glucose metabolism in insulin-resistant humans and animals. We determined the individual effects of the pure R-( ) and S-(-) enantiomers of ALA on glucose metabolism in skeletal muscle of an animal model of insulin resistance, hyperinsulinemia, and dyslipidemia: the obese Zucker (fa/fa) rat. Obese rats were treated intraperitoneally acutely (100 mg/kg body wt for 1 h) or chronically [10 days with 30 mg/kg of R-( )-ALA or 50 mg/kg of S-(-)-ALA]. Glucose transport [2-deoxyglucose (2-DG) uptake], glycogen synthesis, and glucose oxidation were determined in the epitrochlearis muscles in the absence or presence of insulin (13.3 nM). Acutely, R-( )-ALA increased insulin-mediated2-DG-uptake by 64% (P < 0.05), whereas S-(-)-ALA had no significant effect. Although chronic R-( )-ALA treatment significantly reduced plasma insulin (17%) and free fatty acids (FFA; 35%) relative to vehicle-treated obese animals, S-(-)-ALA treatment further increased insulin (15%) and had no effect on FFA. Insulin-stimulated 2-DG uptake was increased by 65% by chronic R-( )-ALA treatment, whereas S-(-)-ALA administration resulted in only a 29% improvement. Chronic R-( )-ALA treatment elicited a 26% increase in insulin-stimulated glycogen synthesis and a 33% enhancement of insulin-stimulated glucose oxidation. No significant increase in these parameters was observed after S-(-)-ALA treatment. Glucose transporter (GLUT-4) protein was unchanged after chronic R-( )-ALA treatment but was reduced to 81 /- 6% of obese control with S-(-)-ALA treatment. Therefore, chronic parenteral treatment with the antioxidant ALA enhances insulin-stimulated glucose transport and non-oxidative and oxidative glucose metabolism in insulin-resistant rat skeletal muscle, with the R-( ) enantiomer being much more effective than the S-(-) enantiomer.


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