Alpha Lipoic Acid for Fat Loss

Posted: April 15, 2010 in Nutrition

New study on ALA, with a HUGE number of subjects. They were given 800mg/day of ALA, the pre-obese subjects lost 8% of their body weight and the obese subjects lost 9%. Both groups dropped abdominal circumference significantly as well.

Alpha-Lipoic Acid Supplementation: A Tool for Obesity Therapy?

Current pharmaceutical design, 2010

Lipid peroxidation has supposed as the major biochemical alteration underling oxidant-induced cell injury in stress including numerous diseases. One of the natural molecules know to prevent or retard oxidation is alpha-lipoic acid (LA) and, therefore, the lipoic acid/dihydrolipoic acid (LA/DHLA) redox couple has received considerable attention. Recent studies have highlighted the potential of free LA and DHLA as powerful metabolic antioxidants that are able to scavenge the reactive oxygen species, to recycle other antioxidants. Our aim was to investigate the beneficial effects of LA in the treatment of Italian pre-obese and obese subjects. We screened 1612 subjects for enrolment; of these, 1127 subjects (445 men and 682 women, 18-60 age) met enrolment criteria and were enrolled in the study. According to body mass index (BMI) the 53% was obese and the 43% was pre-obese. The subjects were treated for 4 month with 800 mg/day of LA. In pre-obese subject significant reduction (p<0.001) of weight (8%, both gender), BMI (2 points), blood pressure, and abdominal circumference (female 6 cm, male 7 cm) were observed. In obese subjects significant reductions (p<0.001) of weight (9%, both gender), BMI (female 3 point, male 4 point), blood pressure and abdominal circumference (female 9 cm, male 11 cm) were observed. Our study indicated that LA is an ideal antioxidant candidate for the therapy of obesity related diseases. Further clinical studies should be considered to highlight the role and efficacy of LA treatment.


I prefer a stabilized “R” form (pictured above), but the regular old ALA obviously worked very well here. Divide your dose up to 3x/day, about 15 minutes before a meal.

  1. John says:

    Were these subjects on a calorie restricted, macro restricted diet? I’m pretty much a fan of anything that lowers inflammation and increases insulin sensitivity (these two characteristics seem to be pretty tightly interconnected) so it would be beneficial for these subjects to say the least, even if a change in diet wasn’t made. But what I’m not sure about yet is whether or not this yields a noticeable positive effect without a calorie restricted diet.

  2. fitport says:

    John, I haven’t had a chance to track down the full text yet, if anyone has access feel free to send it to your buddy Marc…

    It’s a pretty huge weight loss, so I’m guessing there was some calorie restriction but that should have been mentioned in the abstract if there was. I’ll read the full text and report back as soon as I get it.

    Some other interesting ALA studies I had in the library for anyone interested:

    This last one is in PCOS patients, but it caused a shift from small dense LDLs to larger particle LDLs, which is pretty exciting.

  3. John says:

    That first study is interesting and makes me wonder whether or not Ala is necessary to use with fibrates in order to get the fat loss results we were always hoping to get with fibrates alone. Triglycerides? No problem, Fatty acids? Fibrates eat them up for breakfast (pun absolutely intended) and yet for the average athletic individual, fibrates didn’t lead to a fat loss that was worthwhile for most subjects. I wonder if the AmpK activation is the missing ingredient for body composition purposes?

  4. fitport says:

    The study would certainly seem to suggest that, at least in rats…but it almost seems to simple to be true. Do you have much personal experience with fibrate usage? ALCAR would be another AMPK activator to couple with fibrates, but Spook from Mind and Muscle brought up an interesting point some time ago about the cellular pool of carnitine being prone to acetylation with the excess substrate from the PPAR agonism, so ALA would probably be a good choice here.

    QUOTE(Spook @ May 10 2004, 01:35 PM)
    “The stack is PPAR-alpha agonist (fibrate, fish oil, sesathin) + NAC + pantothenic acid + L-Carnitine base (not ALCAR). I did not base in on that paper from “medical hypotheseis” at all. fibrates are there to increase mitochondrial oxidation enzymes. NAC is there for its ability to act as a mitochondrial anti-oxidant, pantothenic acid is there to provide substrate for CoA formation, and carnitine is added because to much substrate use will acytalate the carnitine pool. So the with carnitine is to provide base not acytal-L-carnitine since we are trying to prevent the entire cellular pool of carnitine from turing in to ALCAR.”

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