What is ALA?
Alpha-lipoic acid (ALA) is an antioxidant that is found in every cell of our bodies, where it helps turn glucose into energy.
ALA also has a number of important health-promoting and healing actions. These actions are amplified when ALA is administered intravenously.
Like other antioxidants, ALA attacks “free radicals” – the harmful waste products created in the process of turning food into energy.
Free radicals initiate harmful chemical reactions that can damage cells, making it harder for the body to fight infection. Free radicals also damage organs and tissues.
Unlike other antioxidants, which are either water-soluble (e.g., vitamin C) or fat-soluble (e.g., vitamin E), ALA is both fat– and water-soluble. Thus, its positive effects are available throughout the body.
Most antioxidants are depleted as they attack free radicals, but evidence suggests that ALA may help regenerate and reactivate other antioxidants.
Sources of ALA – Food, Oral, and Intravenous
ALA is found in red meat, spinach, broccoli, yam, carrot, beets, potato, and yeast. As a supplement, ALA can be taken orally or administered intravenously in doses up to 600mg.
ALA’s Impressive Benefits
Orally, ALA may be used in the treatment of diabetes, peripheral neuropathy, cardiac autonomic neuropathy, retinopathy, cataracts, and glaucoma.
ALA is also used orally in dementia, chronic fatigue syndrome, HIV/AIDS, cancer, liver disease, Wilson’s Disease, cardiovascular disease, peripheral arterial disease, intermittent claudication, Lyme Disease, and lactic acidosis due to inborn errors of metabolism.
ALA for Cancer and Pre-Cancerous Conditions
Oxidative stress plays an important role in the development of cancer. Although investigation of ALA for the treatment and prevention of cancer is mainly limited to preclinical studies, a handful of randomized and non-randomized trials and case studies support ALA’s use in combination with other cancer therapies.
A small case-control study in 2010 found that ALA in combination with conventional cancer therapy was effective in managing oral submucous fibrosis, a chronic, irreversible condition of the mouth with proven malignant (cancerous) potential. The ALA group exhibited better relief of symptoms such as a burning sensation in the mucosa and mouth opening. ALA also demonstrated greater effectiveness in reversing higher clinical cancer stages to lower ones, compared to the control group.
ALA’s antioxidant activity can help prevent the transformation of healthy cells to cancer cells. ALA was also recently demonstrated to induce cancer cell death in lung cancer.
It’s believed that ALA helps kill cancer cells by activating enzymes that induce cancer cell death. ALA has also been shown to prevent the degradation of a tumor suppressor gene in colon cancer cells.
Furthermore, ALA reduces the amount of lactate produced by cancer cells, slowing their growth. The mechanism is complex: ALA is a cofactor of pyruvate dehydrogenase, an enzyme that converts pyruvate to acetyl-CoA, which reduces the formation of lactate. In cancer cells, lactate is produced from glucose in excessive amounts, as a result of altered cell metabolism (a phenomenon known as the Warburg effect). As mentioned above, ALA slows cancer cell growth by reducing the amount of lactate the cancer cells can produce. In this way, ALA is synergistic with DCA (dichloroacetate) in its ability to alter cancer cell metabolism.
ALA also inhibits a signaling pathway responsible for cancer cell growth and insulin secretion, known as the mTOR pathway. mTOR inhibitors such as Afinitor or everolimus are presently used to reduce cancer growth in certain cancers. Thus, ALA is considered a natural mTOR inhibitor.
Several published case reports have documented improved cancer symptoms and survival time following treatment with ALA, with or without low-dose naltrexone (LDN)
Because it is fat-soluble, ALA can cross the blood-brain barrier to treat neurological conditions such as dementia, Alzheimer’s disease, and multiple sclerosis, as well as possibly aiding in the treatment of cancer in neurological tissue – e.g., gliomas, malignant nerve sheath tumors, and other cancers.
Recent animal studies have yielded promising results from ALA’s ability to promote functional recovery after stroke. ALA (IV and oral) is a frequent component of integrative cancer protocols, as well as treatment protocols for MS, dementia, Alzheimer’s disease, and to aid recovery from traumatic and ischemic brain injury in concussion and stroke.
ALA is required for healthy cell metabolism – specifically in the mitochondria, the “power house” in our cells. Thus ALA plays a critical role in producing energy to fuel other bodily activities.
ALA can lower blood sugar levels. Its ability to kill free radicals may help reduce the pain, burning, itching, tingling, and numbness in patients with diabetes-related nerve damage (peripheral neuropathy).
In Europe, where ALA has been used for years to treat peripheral neuropathy, at least one study found that intravenous (IV) ALA helped reduce the symptoms. In Germany, high doses of ALA have been approved for the treatment of diabetic neuropathy.
ALA has been proposed as a treatment for alcohol-related liver disease, although there is presently no evidence that it works.
ALA has been administered by IV, together with silymarin, to treat people who have ingested the deadly Amanita mushroom, which causes severe liver damage resulting in certain death.
Brain Function and Stroke
Because ALA can easily pass into the brain, its protective antioxidant effects are readily available to brain and nerve tissue.
Scientists are currently investigating ALA’s potential in treating stroke and other brain disorders that involve free radical damage. Animals treated with ALA after stroke suffered less brain damage and had four times higher survival rates than animals not receiving ALA. More research is needed to understand whether ALA can benefit human stroke victims.
Intravenous versus Oral ALA
Many well-designed studies and recent meta-analyses have demonstrated intravenous ALA to be more effective than oral ALA.
Packer L, Tritschler HJ, Wessel K. Neuroprotection by the metabolic antioxidant alpha-lipoic acid. Free Radic Biol Med 1997;22:359-78.
Ziegler D, Hanefeld M, Ruhnau K, et al. Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: A 7-month, multicenter, randomized, controlled trial (ALADIN III Study). Diabetes Care 1999;22:1296-301.
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