- Science-Based
- Dietary Supplement
- Defends against Free Radicals*
Alpha lipoic acid (ALA) is a fatty acid that functions like avitamin, although it is not classified as a vitamin. As a coenzyme, ALAplays an important role in the metabolism of glucose that producesenergy in cells. ALA also has antioxidant properties and this isimportant for controlling free radicals. Because it is soluble in bothwater and fat, ALA is sometimes referred to as the "universalantioxidant."
- Supports the body's defenses against free radicals*
- Recycles antioxidant nutrients such as vitamin C and vitamin E*
- Helps maintain a healthy blood sugar level when used as part of the diet.*
Take one to six capsules daily, with or without food.
| Supplement Facts | ||
| Serving Size 1 Capsule | ||
| Servings per container 90 servings | ||
| Amount Per Serving | %Daily Value | |
| Alpha Lipoic Acid | 150 mg | |
| Daily Value not established. | ||
Cellulose, magnesium stearate, gelatin capsule.
Contains nothing other than listed ingredients.
Alpha Lipoic Acid (ALA) is the only antioxidant that is both fat and water soluble. This is important because Alpha Lipoic Acid can access all parts of the cell, giving it tremendous ability to trap free radicals wherever they may be. One of the leading causes of the symptoms we know as aging is free radical damage,
Alpha Lipoic Acid is one of the very few substances that can actually cross the blood/brain barrier to enter the brain and go directly where it is needed most. Alpha Lipoic Acid supplementation causes increased levels of glutathione, which helps the body dispose of toxins.
This is important as glutathione protects the brain from free radical damage, and low levels of glutathione in the brain are associated with brain disorders such as stroke, dementia, Parkinson's and Alzheimer's disease.
Alpha Lipoic Acid (ALA): The Network Antioxidant
Normally once an antioxidant has eliminated a free radical, it is lost forever. Lipoic acid is the only antioxidant with the unique ability to regenerate/recycle itself, and other antioxidants such as vitamins C & E, so that they can continue destroying free radicals. This is why ALA is known as a network antioxidant.
Stroke and Alpha Lipoic Acid
In one experiment, strokes were induced in laboratory rats by blocking the carotid artery, which delivers blood and oxygen to the brain for 30 minutes. After blood flow was restored, the animals were monitored for 24 hours. Once oxygen was restored, there was a burst in the production of free radicals, overwhelming the brain's antioxidant defenses. This proved deadly as 80% of the rats died within 24 hours. In the follow up experiment, everything was the same except this time lipoic acid was injected into the rats just before blood flow to the brain was restored. After 24 hours, only 25% of the rats had died and the survivors were no worse for wear, recovering completely.
Follow up studies showed that the animals not treated with lipoic acid showed a substantial increase in free radical related damage to the brain but not for the ones who were treated with lipoic acid. Their brains were normal, as if they had not had a stroke at all. Further testing showed that in the non-treated animals, glutathione levels had plummeted after the stroke, causing the antioxidant defenses to be wiped out while the animals treated with lipoic acid had glutathione levels that were quite high, a sign that they were able to successfully fight attack from free radicals.
Alzheimer's Disease and Alpha Lipoic Acid
Excessive free radicals within our bodies cause a condition known as "oxidative stress." Oxidative stress and energy depletion are characteristic biochemical hallmarks of Alzheimer's disease (AD), thus antioxidants with positive effects on glucose metabolism such as thioctic (alpha-lipoic) acid should exert positive effects in Alzheimer's patients. Due to this, a study was conducted in which 600 mg alpha-lipoic acid was given daily to nine Alzheimer's patients with Alzheimer's disease and related dementias in an open study over an observation period of, on average, 337+/-80 days. The treatment led to a stabilization of cognitive functions in the Alzheimer's study group, demonstrated by constant scores in two neuropsychological tests.
Despite the fact that this study was small and not randomized, this is the first indication that treatment with alpha-lipoic acid might be a successful 'neuroprotective' therapy option for Alzheimer's Disease and related dementias.
Benefits for Parkinson's Disease (PD)
Parkinson's Disease (PD) is a disorder of the central nervous system that affects between one and one-and-a-half million Americans. Clinically, the disease is characterized by a decrease in spontaneous movements, gait difficulty, postural instability, rigidity and tremor. PD may appear at any age, but it is uncommon in people younger than 30, and the risk of developing it increases with age.
Oxidative stress appears to play an important role in neuronal degeneration associated with PD (Beal. 1992; Burke, 1998; Adams et al.. 2001; Sayreet al., 2001). The depletion of glutathione (GSH) in the brain is the earliest know indicator of oxidative stress in presymptomatic PD. (Jenner, 1993). Studies using both in vitro and in vivo models have suggested that pretreatment with R-Lipoic acid increases cellular levels of GSH, probably by preventing its depletion thereby protecting mitochondrial integrity (Suzuki et al., 1991; Scott et al., 1994; Hanet al., 1997; Xu and Wells, 1996; Lykkesfeldt et al., 1998; Kagen et al., 1992).
lipoic acid administration has been reported to result in increased ambulatory activity and improved memory in aged animals and to partially restore age-associated mitochondrial decay in both the liver and heart.
Results with previous studies suggest that R-Lipoic acid may be an effective neuroprotective agent in age-associated neurodegeneration. Utilizing the PC 12 cell model system, we propose that Lipoic acid administration could be an effective way of circumventing or delaying mitochondrial dysfunction associated with PD.
Treatment with Lipoic acid alone seems to significantly increase GSH levels only in whole cell preparations but not in mitochondrial extracts. However, pretreatment of cells with R-Lipoic acid appears to prevent BSO-mediated GSH depletion in both whole cells and mitochondria. Decreases in mitochondrial NADH dehydrogenase activity associated with GSH depletion also appear to be preserved via Lipoic acid pretreatment.
