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Alpha lipoic acid (ALA) is a naturally occurring fat- and water-soluble antioxidant. ALA is found naturally occurring in certain foods such as 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 at a time.


ALA plays a significant role in several biological processes in the body. It is considered the “universal antioxidant” since it demonstrates such diverse physiological activity.

Free radical scavenger: ALA is a potent anti-oxidant, quenching DNA- and cell-damaging oxidants, such as free radicals (1,2). Free radicals are produced when the body is under significant amounts of physical stress (such as the disease state) and to varying degrees with certain medications (such as chemotherapy and radiation). Free radicals can also cause disease, by damaging healthy cells and genetic material, especially in the face of antioxidant deficiency. Moreover, free radicals can accelerate the aging process.

Enzyme co-factor: ALA is required for healthy cell metabolism – specifically in the mitochondria (aka the “power house”) of our cells – thereby playing a critical role in energy production to fuel other activities in the body (3).

Potentiates other antioxidants: ALA helps regenerate glutathione – another major antioxidant in the body (4). Glutathione is critical to healthy aging and disease prevention, found in highest concentration in the heart, lungs, kidneys and liver. Without sufficient glutathione, these organs are particularly at high risk of disease. Furthermore, ALA augments the function of other key antioxidants such as vitamin E and vitamin C (1,3). Taken together, the synergy of antioxidants reduces the oxidative stress in the body, preventing and reversing tissue damage and initiating cell repair to help reduce tissue inflammation and promote recovery from illness.


Since ALA is required to slow the aging process, any disease of aging (such as cancer, cardiovascular disease, dementia) can be prevented and treated by ALA. Based on the evidence, ALA can be used to treat the following conditions:



Since ALA plays a critical role in energy production, ALA as a supplement has been demonstrated to improve glycemic control, thereby slowing the progression of diabetes and preventing common illnesses that result as a consequence of poorly managed diabetes, including: peripheral neuropathy, retinopathy, cardiovascular disease, kidney disease, erectile dysfunction and cancer (5-9). Overtime, ALA may reverse insulin resistance or borderline diabetes, when combined with appropriate lifestyle and dietary interventions. Interestingly, oxidative-stress related hyperglycemia is now considered to be significant contributor to the development of hyperglycemia (high blood sugar) and its related complications (10).

In terms of treating diabetes-related chronic complications (such as retinopathy), well-designed studies have shown ALA in combination with other anti-oxidants can help reverse many of these complications (11).


ALA has many actions that may result in weight loss and improved cholesterol levels, by improving glucose control, inhibiting formation of fat cells, reducing inflammation associated with fatty tissue, increasing HDL-cholesterol (“good” cholesterol) and reducing LDL-cholesterol (“bad” cholesterol) (12).

For weight loss, studies have used doses of ALA ranging from 1-1.8 grams for up to 20weeks in obese individuals, resulting in a weight loss of 3 kg (13). Based on study findings, it appears weight loss is more pronounced when ALA is combined with other nutritional agents, such as omega-3 fatty acids (14).


Oxidative stress plays an important role in the development of cancer. Although investigation of ALA for role in the treatment and prevention of cancer is mainly limited to preclinical studies, there are a few randomized and non-randomized trials and case studies that support the use of ALA in combination with other therapies for cancer.

A small case-control study in 2010 found ALA in combination with conventional therapy was effective in managing the oral submucous fibrosis (OSF), a chronic irreversible condition of the mouth with proven malignant (cancerous) potential (15). The ALA group exhibited better relief of symptoms such as burning sensation of the mucosa and mouth opening and demonstrated greater reversal of higher clinical stages to lower ones, as compared to the control group.

Besides its antioxidant activity impacting the transformation of healthy cells to cancer cells, ALA was recently demonstrated to induce apoptosis (cancer cell death) in lung cancer cells. It is believed the mechanism of apoptosis induction is via activation of capsases – enzymes that induce cell apoptosis (16,17). ALA has also been shown to prevent degradation of a tumor suppressor gene (p53) in colon cancer cells (18).

Furthermore, ALA is cofactor of pyruvate dehydrogenase, an enzyme that converts pyruvate to acetyl-CoA, which reduces the formation of lactate. Lactate is produced from glucose in excessive amounts by cancer cells, as a result of altered cell metabolism (a phenomenon known as the Warburg effect). ALA reduces the amount of lactate produced by cancer cells, slowing their growth rate (19,20). In this way, ALA is synergistic with DCA (dichloroacetate) in its ability to alter cancer cell metabolism.

Another anti-cancer mechanism of ALA is its ability to inhibit a signaling pathway responsible for cell growth and insulin secretion, known as the mTOR (mammalian target of rapamycin) pathway (21). mTOR inhibitors (such as Afinitor or everolimus) are presently used in the treatment of certain cancers, to reduce cancer growth. Thus, ALA is considered a natural mTOR inhibitor.

There are several published case reports documenting improved symptoms and survival time following treatment with ALA with or without low-dose naltrexone (LDN)(22-24).


For decades, Dr. Berkson, MD, PhD has successfully treated a variety of liver disorders – such as hepatitis – using intravenous ALA (25). Studies have shown that therapeutic doses of IV ALA can remarkably help regenerate the liver, but excessively high doses (greater than 600mg IV ALA) can cause liver necrosis (26).

Non-alcoholic fatty liver disease (NAFLD) is a condition often associated with diabetes or insulin resistance and high cholesterol. Mitochondrial dysfunction, oxidative stress and inflammation play a key role in the development of NAFLD and other fatty liver diseases. Animal studies have demonstrated some promise for the use of ALA in the treatment of fatty liver disease (12).


Due to its lipophilic (fat soluble) nature, ALA can enter cells and cross the blood-brain barrier to treat neurological conditions such as dementia, Alzheimer’s disease or multiple sclerosis and possibly aid in the treatment of malignancies (cancer) in neurological tissue such as gliomas, malignant nerve sheath tumors and other cancers (27,28). Recently, animal studies demonstrate promise in ALA’s ability to promote functional recovery after stroke (29). ALA (IV and oral) is a frequent component of integrative cancer protocols, as well as treatment protocols for diseases such as MS and dementia, Alzheimer’s disease and to aid recovery from traumatic and ischemic brain injury such as concussion and stroke.



A common feature of progressive diabetes and a frequent side effect of certain chemotherapies (also known as “diabetic neuropathy” and “chemo-induced peripheral neuropathy”, respectively), PN can be a debilitating condition with significant impact on quality of life. ALA can help treat PN, especially when used a multi-modal treatment approach, but it is most effective when used prophylactically to prevent PN (30-33). Often IV and oral forms of ALA are used to help prevent neuropathy associated with chemotherapy treatment and to prevent neuropathy that can be associated with DCA treatment.



It is important to know that many well-designed studies and recent meta-analyses have demonstrated greater efficacy with intravenous ALA compared to oral ALA (34). Therefore, outcomes with ALA are dependent on several factors, especially the route of administration.

Furthermore, oral ALA can have adverse effects – predominately in the gastrointestinal tract (nausea, vomiting, acid reflux, indigestion and abdominal pain or discomfort). Hypoglycemia (lowering of blood sugar) is a common effect (often therapeutic) of ALA, but may be amplified in patients taking blood-sugar lowering medications (35). Therefore, caution should be exercised in using ALA for those taking medications that lower blood glucose levels.

Taking oral ALA with food minimizes the tendency for GI-related side effects and hypoglycemia, but compromises absorption of ALA. Since ALA is most beneficial when a bolus dose is administered, it is best to take oral ALA on an empty stomach, in 1-2 doses per day rather than several doses throughout the day. Alternately, an intravenous dose of ALA (not exceeding 600mg or 10mg/kg) is not likely to result in any adverse effects and demonstrates better clinical efficacy than oral ALA.



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13. Koh EH, Lee WJ, Lee SA, Kim EH, Cho EH, Jeong E, Kim DW, Kim MS, Park JY,
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18. Yoo TH, Lee JH, Chun HS, Chi SG. a-Lipoic acid prevents p53 degradation in colon cancer cells by blocking NF-kB induction of RPS6KA4. Anticancer Drugs. 2013; 24(6):555-65.

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35. Ziegler D, Hanefeld M, Ruhnau KJ, Hasche H, Lobisch M, Schütte K, Kerum G, Malessa R: Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: a 7-month multicenter randomized controlled trial (ALADIN III Study). ALADIN III Study Group. Alpha-Lipoic Acid in Diabetic Neuropathy. Diabetes Care. 1999, 22(8):1296–1301.

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