Supplements Reducing Lou Gehrig’s disease Risk: Promising evidence from neurology research
Source: J Biomedicines (2021)
Lifestyle Medicine Update (November 8, 2022)
Lou Gehrig’s disease, also known as ALS (amyotrophic lateral sclerosis) is a progressive and devastating neurodegenerative disease that leads to weakness and paralysis caused by the death of the motor nerves in the brain and spinal cord that enable our muscle function. After Alzheimer’s disease and Parkinson’s disease, it is the third most prevalent neurodegenerative disease, affecting 450,000 people worldwide. It typically strikes after the age of 50, although a minority of cases occur in younger people. A review of the latest breakthroughs in ALS was published in the journal Biomedicines in August of 2021, which provided insights as to how we may be able to prevent many cases of Lou Gehrig’s disease through the use of diet, lifestyle, and especially, supplementation practices.
As a quick summary of how we might achieve this, the authors of the study highlight the critical role of the B vitamin, niacin (B3), which the body converts into NAD (nicotinamide adenine dinucleotide). NAD is required by brain cells for energy production, for protection against toxic substances (excitotoxicity) and states of reduced blood flow, (cerebral ischemia), to preserve the integrity and function of brain cell axons (that relay electrical messages from one nerve cell to the next), to preserve mitochondrial function (where nerve cell energy is generated), support the synthesis of glutathione – an important brain cell antioxidant that prevents damage and death of brain cells from free radicals (oxidative stress – reactive oxygen species), and NAD activates longevity and survival genes in brain cells such as the Sirtuin-6 gene. Research clearly shows that a consistent finding in ALS is a depletion of NAD levels in the brain. In fact, we know that NAD levels tend to decline with age. It appears likely that in persons who are genetically prone to ALS (SOD1 mutation) development, once a critical level of NAD is depleted in the brain, the disease is triggered. In fact, the best documented genetic mutation for ALS risk is the presence of the SOD1 mutation. SOD1 is an antioxidant that normally protects brain cells from free radical damage that otherwise leads to their brain cell and nerve cell death. In individuals who are born with the SOD1 mutation their SOD1 enzyme doesn’t work and thus, free radicals build up more easily, triggering nerve cell death and the onset and progression of Lou Gehrig’s disease. But animal studies and preliminary human studies are showing that supplementation with NAD or its precursors (niacin, vitamin B3) can replenish brain levels of NAD, which in turn, acts to protect nerve cells from dying and increases the synthesis of glutathione – a critically important antioxidant that can, to some degree, compensate for the lack of free radical protection from the faulty SOD1 antioxidant enzyme. Interestingly, like NAD, glutathione is also shown to be lower in the brains of ALS patients than in healthy individuals.
In fact, halting free radical damage to the brain has been a focus of medical intervention in recent years and has led to the approval of an antioxidant drug (edaravone) that is approved for ALS therapy. But the antioxidant drug edaravone is not the only thing that has shown promise and improvement in ALS studies. For example, administration of high-dose melatonin (300 mg/daily via rectal suppository), as well as high-dose oral supplementation of melatonin, combined with a cocktail of other supplements, resulted in the recovery of lost muscle function and/or slowed ALS disease progression, and these patients lived longer compared to those not taking melatonin. Other studies show that the antioxidant supplement NAC (N-acetylcysteine) can replenish brain levels of glutathione and has shown tremendous promise in ALS prevention in animal models of this disease.
So, to summarize what I have outlined in this update and to make it practical, the following considerations that may help reduce the risk of developing Lou Gehrig’s disease during your lifetime include:
1. Consider taking a high-potency multiple vitamin and mineral supplement each day that contains 50 mg of vitamin B3 (niacin). This helps to prevent the age-related depletion in brain NAD levels that is shown to contribute to not only the onset of ALS, but also Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. A high-potency multivitamin and mineral supplement would also have increased amounts of antioxidant vitamins like vitamin C (1,000 mg) vitamin E (400 IU), beta-carotene (15,000 IU), and selenium (200 mcg), as an example, compared to typical drug-store type multiple vitamins.
2. After age 40 (at a time when melatonin synthesis in the brain becomes very low), consider taking 1-3 mg of melatonin an hour before bedtime each day. Melatonin is not only a brain antioxidant (quenching free radicals), but it has also been shown to prevent the death of the motor nerves, which is a critical factor in preventing and treating ALS. Of course, melatonin also helps you reach deeper levels of sleep, which is in itself very renewing, it supports immune function and helps to protect breast and prostate cells from changes linked to cancer.
3. After age 45 -50 consider taking a supplement each day that helps your body synthesize glutathione. Typically, a supplement of this nature includes the following ingredients, NAC (N-acetylcysteine, alpha-lipoic acid, L-glutamine, and Milk thistle, which provides the flavonoid, silymarin).
4. Some evidence suggests that taking 30-100 mg/day of coenzyme Q10 after the age of 45, may also be a prudent step in the prevention of various neurodegenerative diseases. This is especially true for Parkinson’s disease but may have applications for Alzheimer’s disease and ALS.
5. For highly motivated individuals, I might suggest that after age 45- 50 you consider seeing an integrative or anti-aging medical doctor or naturopath, who can administer glutathione (1,000 mg) and/or NAC (500 -1,000 mg) intravenously, once every month or two, to help ensure optimal brain levels of glutathione. The same holds true for NAD, which can also be administered via IV, usually at a dosage of 250, 500 or 750 mg IV dose. There are also NAD sublingual products in the marketplace that can also efficiently deliver NAD to the brain by preventing its degradation via the digestive process.
If this subject is of interest to you, then I would encourage you to read the entire 2019 review article on this subject. I have provided a link to it in the text below.
Obrador E et al. NAD+ precursors and antioxidants for the treatment of amyotrophic lateral sclerosis. Biomedicine. 2021, 9(8): 1000. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8394119/
Eat Smart, Live Well, Look Great,
Dr. James Meschino
ABOUT THE AUTHOR
Dr. James Meschino, DC, MS, ROHP, is an educator, author, and researcher having lectured to thousands of healthcare professionals across North America. He holds a Master’s Degree in Science with specialties in human nutrition and biology and is recognized as an expert in the field of nutrition, anti-aging, fitness, and wellness as well as the author of numerous books.