Niacin may help prevent or treat migraines.

Niacin may help prevent migraines or tension-type headaches when taken daily based on a review of nine articles about niacin use and migraines or tension-type headaches. It may also help end a migraine that is occurring with the cooling effect that follows the skin-reddening niacin flush.

  • The treatment of migraines and tension-type headaches with intravenous and oral niacin (nicotinic acid): systematic review of the literature. (1)

Chronic tension-type headaches are also associated with cerebrospinal pressure or intracranial venous pressure (or both) [26]. In fact, tension-type headaches are more similar to migraine headaches than they are dissimilar, in that they seem to progress into migraine headaches due to an escalating pathophysiological process [27].” (1)

Niacin may also help reduce a migraine that is occurring, with a 500 mg dose taken to cause the niacin flush.

Regarding one of the articles reviewed: “In this [self] report, Hall describes the use of niacin for his migraine headaches remarking that the migraines resolved when intense flushing occurred.” (1)

The vasodilation in the skin that causes the warm feeling and reddening of the skin is followed by a vasoconstriction and cooling effect on the body and brain. Older research confirmed vasoconstriction in the brain occurs as well as in the peripheral blood vessels, however current research is needed. (1)

From the Discussion section (1) : “When taken intravenously or orally, niacin causes cutaneous flushing that might abort the acute symptoms of migraine by vasodilating the intracranial vessels, thus preventing the subsequent vasoconstriction of the extracranial vessels.

There is evidence that niacin is an effective peripheral vasodilator, but its ability to influence central mechanisms (i.e., cerebral blood flow and cranial hemodynamics) involved in migraine headaches have not been well studied. Niacin causes peripheral vasodilation and cutaneous flushing by inducing the production of prostaglandin D2 (PGD2) in the skin, leading to a marked increase of its metabolite, 9α, 11β-PGF2, in the plasma [22].

When niacin is administered orally in amounts of 500 mg or topically via a 6-inch patch of 10-1 M aqueous methylnicotinate on the forearm, PGD2 is markedly released in the skin and its metabolite appears in high amounts in the plasma [2223]. It is not known if PGD2 causes vasodilation of the intracranial arteries, but niacin’s ability to abort acute migraine headaches suggests that this might be what is occurring.

Old reports cited by Bicknell and Prescott [24], demonstrate that niacin does indeed cause vasodilation of the cerebral and spinal vessels, and that intravenous administration increases the rate of intracranial blood flow in human beings for 20–60 minutes without any significant change in blood pressure. Unfortunately, there have not been more recent reports examining the effects that niacin has upon cerebral blood flow in human subjects.” (1)

Niacin (B3) is needed for Mitochondrial function…

…so are riboflavin (B2), other B vitamins; many trace minerals including magnesium; amino acid derived creatine and cysteine; and the internally made antioxidants CoQ10, glutathione and alpha-lipoic acid.

Niacin helps mitochondria function to burn glucose for energy use or to release as heat (such as in brown fat). Riboflavin and coenzyme Q10 and other nutrients are also used by the mitochondria. (1)

A deficit of mitochondrial energy metabolism may play a role in the pathogenesis of migraine. Since niacin improves mitochondrial energy metabolism by increasing substrate availability to complex I, it might also be an effective agent for migraine prevention.” (1)

Citric Acid Cycle – used for aerobic glycolysis of glucose by the many many Mitochondria within all of our cells.

Graphic (via Dmitry Kats, PhD, @NiacinisHealth) shows the many nutrients that are used in the Citric Acid Cycle by mitochondria when they are metabolizing glucose aerobically, with oxygen, as typical of their normal function. Anaerobic glycolysis, fermentation of glucose or glutamate without oxygen, by mitochondria is associated with cancerous cells.
Nutrients include: B1 (thiamin), B2 (riboflavin), B3 (niacin), B5 (pantothenic acid), B6 (pyridoxine), B7 (biotin), B9 (folate), Mg++ (magnesium), Mn++ (manganese), K+ (potassium), zinc, iron, copper, sulfate, CoQ10, carnitine, cysteine, glutathione, Lipoic acid.

B vitamins are very important and we need them in balance because they work as a team. Niacin might not help as much if there is significant lack of the other B vitamins or some of the minerals, amino acids or antioxidants needed for the Citric Acid Cycle to function. The nutrients mentioned as cofactors for the chemical reactions in the above graphic include:

  • B vitamins: B1 (Thiamin) (3) , B2 (Riboflavin) (4), B3 (Niacin) (810), B5 (Pantothenic acid) (5), B6 (Pyridoxine) (67), B7 (Biotin), B9 (Folate) (9),
  • Minerals (17): Mg++ (Magnesium) (111213), Mn++ (Manganese), K+ (Potassium) (13), Zinc (1415), Iron (16), Copper, Sulfate,
  • Amino acids: Carnitine (derived from lysine), Cysteine,
  • Antioxidants: CoQ10, Glutathione, Alpha-Lipoic Acid (ALA).

The cofactors used in the Citric Acid Cycle by mitochondria when they are performing aerobic glycolysis may be a limiting factor in chronic degeneration or cancer. Aerobic glycolysis is the process of metabolizing sugar with the use of oxygen, fermentation is anaerobic glycolysis. Mitochondrial dysfunction and a shift to anaerobic metabolism of sugar or glutamate, fermentation, is associated with cancer cells and other chronic degenerative disease. The cause may be limited nutrients – the list of cofactors needed is long and includes niacin.

Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes.

Reference List

  1. Prousky, J., Seely, D. The treatment of migraines and tension-type headaches with intravenous and oral niacin (nicotinic acid): systematic review of the literature. Nutr J4, 3 (2005).
  2. Dmitry Kats, PhD, @NiacinisHealth Citric Acid Cycle graphic
  3. Thiamin: people with anorexia or alcoholism are more at risk for vitamin B1 deficiency. Aug 21, 2013
  4. Riboflavin – Vitamin B2, May 23, 2018,
  5. Pantothenic Acid – vitamin B5, May 24, 2018
  6. Vitamin B6,
  7. Pyroluria, anxiety and deficiency of B6 and zinc, most recent update, 4/9/2017
  8. Niacin, & early treatment in general for SARS-CoV-2 is sensible, reduces hospitalization and mortality rate.
  9. Folate is essential and Folic Acid is commonly available. Aug 21, 2013,
  10. Niacin, Aug 21, 2013,
  11. To have optimal Magnesium needs Protein and Phospholipids too. July 20, 2018,
  12. Magnesium – essential for eighty percent of our body’s chemistry. July 1, 2019,
  13. Electrolytes are essential, magnesium helps protect brain cells. Feb 10, 2011,
  14. Zinc,
  15. Zinc and the immune system,
  16. Iron and anemia of chronic inflammation.
  17. Trace Minerals – It’s Teamwork.

Demyelination, continued.

The last post got a little long and it included a link to another health writer who was summarizing a large amount of material on the topic of demyelination – it is amazing what you can learn by reading. I only mentioned the article, (22), briefly because it was already a long post and I hadn’t checked the other writer’s references, (it is primarily all medical research from peer reviewed journals (22.1)); and some of his recommendations are not typical, however I had read of them elsewhere so it seemed thorough and well written. The truly intriguing part for me was just how many other conditions there are that may be susceptible to demyelination and increased negative symptoms due to nerve degeneration.

I have a few of the problems that were mentioned and I have had early symptoms of nerve numbness and pain in my extremities – fingertips particularly. Health is easier to maintain then to restore once chronic conditions develop. I have managed to reverse the nerve numbness and occasional pain that I was having in my fingertips but it is with several daily or weekly health habits, not just a simple take-this-medication-once-a-day solution.

The list of psychiatric conditions that may also have demyelination summarized in an article about possible ways to regenerate myelin, (22):

  • Attention deficit hyperactivity disorder
  • Depression 
  • Bipolar disorder 
  • Dyslexia 
  • Language disorders 
  • Stuttering 
  • Autism 
  • Obsessive-compulsive disorder 
  • Cognitive decline 
  • Alzheimer’s disease
  • Tourette’s syndrome 
  • Schizophrenia 
  • Tone deafness
  • Pathological lying
  • (22)

That is quite a list – protect your oligodendrocytes, because they protect your ability to think and communicate, to control your ability to control your movements and to have stable moods, reduce anxiety, and control your ability to be able to read and speak and to be able to control your impulses and ability to prevent yourself from lying or saying things you don’t intend to say, and to be able to understand that your thoughts are your own thoughts, and to be able to hear accurately. The reference given for the information is this article: [45].

Neurology is the study of the nervous system, Psychiatry or Psychology is the study of mental health and neuropsychiatry is the study of mental symptoms caused by neurological conditions.

This topic of psychiatric conditions and other conditions that may also have demyelination is also reviewed in a summary of Neurotoxicology for neurologists: (6.Neurotoxicology). Neurology is the study of the nerves and nervous system. The nervous system includes the brain and spinal cord and all of the nerves throughout the body. It is subdivided into two main categories: the Central Nervous System (CNS) refers to the brain, the spinal cord and nerves of the brain and spinal cord; and the Peripheral Nervous System (PNS) refers to the nerves throughout the rest of the body. Neurologists are medical doctors who specialize in conditions affecting the nervous system. They may focus on a subspeciality within the field of neurology (What is a neurologist?, HealthLine) Interestingly dementia, chronic headaches, and Multiple sclerosis are mentioned as possible conditions they treat but all the other psychiatric conditions mentioned in the list that may involve demyelination are not mentioned.

The overview article on Neurotoxicology does mention that psychiatric symptoms may occur in patients with neurological conditions but that the symptoms tend to be dismissed by neurologists, and are not studied in depth, so more reliable information is needed about psychiatric symptoms presenting with neurological disorders  – see “Psychiatric and behavioural disorders.” (6.Neurotoxicology) An article for neurologists goes into more detail about psychiatric symptoms that might deserve consultation with a neurologist rather than having the patient only see a psychiatrist: Neurological syndromes which can be mistaken for psychiatric conditions. Early symptoms of Multiple sclerosis for example sometimes may be mistaken for a psychiatric condition. (Neurological syndromes) Talk therapy or psychiatric medications are not going to help a patient regenerate their myelin after all. Neuropyschiatrists are neurologists that also have a degree in psychology and specialize in treating patients with mental health and behavioral symptoms related to neurological disorders. (neuropsychiatrists)

PTSD was also mentioned as a psychiatric condition that may have demyelination.[45]

Reading the article that was referenced for the list of psychiatric conditions that may also have demyelination [45] provided an additional condition that was not added to the list in the summary article about potential ways to help regenerate myelin (22) – PTSD also may involve demyelination, and confirmed the rest of the list were mentioned [45] . The article also includes more background information about the function and development of the myelin sheath in learning and behavior.

Nerves with myelin provide a much faster signal and oligodendrocytes myelinate several different nerves so there is additional benefit in signals that work in a coordinated manner to also improve speed of function. The myelination occurs over time so the phrase practice, practice, practice applies. Peak time of life to learn skills is in our youth because that is when the majority of myelination occurs -starting in early childhood and continuing until the early twenties even up to age thirty. Healing after injury or learning a new skill later in life would still require the practice, practice, practice so the speedy pathways between groups of nerve cells develop their myelin sheaths in coordinated connections. [45]

This information may help show the difficulties faced by people with PTSD or other psychiatric conditions – the brain connections are coordinated in patterns learned from traumatic memories or are stuck in Obsessive Compulsive patterns. The problem with impulse control might also make more sense if there is simply “leaky” wiring in the brain. Signals that were intended to do one thing might end up activating other behaviors because the myelin sheath is no longer functioning as expected.

A cognitive therapy technique, involving frequent practice/repetition of new ways to talk to yourself – it might help strengthen more positive neural networks with new myelin sheath connections.

Learning new patterns of thinking, replacing traumatic or anxious thoughts that were learned as a child or during a traumatic phase of life can take time and a lot of repetition but it is possible, just like it can be possible to relearn how to walk or do other basic life skills after a stroke or traumatic physical injury. A book by Shad Helmstetter, PhD discusses how to rephrase your own internal self talk to be more positive and gives examples for a number of different types of concerns. I found the technique helpful for emotional overeating and share phrases that I wrote regarding healthy eating and lifestyle and a link to the book in a previous post: “What to Say When You’re Talking to Yourself.” The recommendation that I followed was to read the statements several times every day – for a while, months even. I don’t remember how long I read them daily but it was for quite a while and I still have the little ring binder of statements that I wrote.

Often changing behavior patterns is easier when the new pattern is created first, rather then trying to stop the old first. Build the new and then the old is no longer needed.  Addition, I found the source of that idea:

“The secret of change is to focus all of your energy not on fighting the old, but on building the new.” – Socrates

A new way to think about demyelination – what is the underlying problem? Possibly excess cell death, at rates above the ability to breakdown and remove nucleotides (ATP, ADP, UTP, UDP).

The article on demyelination and cognitive disorders, [45] , also mentioned that adenosine plays a role in signaling oligodendrocytes to make myelin and an article with more information on the topic mentions that increased amounts of ATP, ADP, UTP, UDP can signal breakdown of myelin. Increased presence of those chemicals was suggested to possibly be due to increased cell death without normal clearing away of the old cellular material. And some types of Multiple sclerosis seems to involve increased levels of the enzyme that breaks down adenosine so there would be less available to signal the production of myelin. (8.adenosine in MS)

Take home point – protect against excessive cell death and/or mitochondria damage by not having excessive glutamate ( or aspartate – excitatory amino acids that may be overly available in the modern processed food diet – and by having adequate magnesium to protect the cells from their interior by providing the needed energy to block ion channels in the cell membrane and prevent excessive amounts of calcium, glutamate or aspartate from being able to cross the cell membrane and enter the cell’s interior.

As usual however, it is not that simple, (not that avoiding glutamate and aspartate in the diet is easy, they are in many processed foods), other things can also cause excessive cell death.

  • Exposure to toxins in the environment or due to drug use, illicit or legal, can cause excessive cell death and lead to demyelination disorders. An overview:(6.Neurotoxicology)
  • Lack of oxygen can also be a cause. Lack of nutrients in general can increase the breakdown of cellular parts to provide enough nutrients however if malnutrition is severe and ongoing the breakdown (autophagy) can become excessive. (7.Metabolic Stress, Autophagy & Cell Death)
  • Traumatic injury and infection can increase the  rate of cell death above the level that the body’s detoxification systems can cope with clearing away the cellular material. Traumatic injury is associated with increased risk for infection for reasons that are not well understood, the immune system is considered functionally suppressed: (10.Immunobiology of Trauma) Also mentioned briefly in the Skeletal Muscle section of this overview: (6.Neurotoxicology).
  • Anything that causes excess oxidative stress may cause increased rates of mitochondria breakdown so protecting against stress is protecting the mitochondria which is protecting the cells. (7.Metabolic Stress, Autophagy & Cell Death) Mitochondria are the main energy producers within cells and make up about thirty percent of the volume of cardiac/heart cells. Other type of mitochondrial problems can also increase risk of their switching from promoting health through energy production into a mode that promotes cell death. One of the roles mitochondria play in normal health is storage of excess intracellular calcium. If the mitochondria become dysfunctional then the extra calcium is released into the cell where it can signal increased activity such as release of cannabinoids from the membranes. (9.mitochondria in CVD)

This is approaching really long again, so I am stopping here for now.

/Disclosure: This information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes./ 

  1. Jordan Fallis, 27 Proven Ways to Promote the Regeneration of Myelin. Feb. 18, 2017, Optimal Living Dynamics, (22)
  2. Reference list: (22.1)
  3. R. Douglas Fields, White Matter in Learning, Cognition, and Psychiatric DisordersTrends Neurosci. 2008 Jul; 31(7): 361–370. [45]
  4. Butler CZeman AZJ, Neurological syndromes which can be mistaken for psychiatric conditions
  5. Anne Masi, Marilena M. DeMayo, Nicholas Glozier, Adam J. Guastella, An Overview of Autism Spectrum Disorder, Heterogeneity and Treatment Options. Neuroscience Bulletin, Vol 33, Iss 2, pp 183–193, (autism link)
  6. Harris JBBlain PG, Neurotoxicology: what the neurologist needs to know.


  7. Brian J. Altman, Jeffrey C. Rathmell, Metabolic Stress in Autophagy and Cell Death Pathways. Cold Spring Harb Perspect Biol. 2012 Sep 1;4(9):a008763 (7.Metabolic Stress & Cell Death)
  8. Marek Cieślak, Filip Kukulski, Michał Komoszyński, Emerging Role of Extracellular Nucleotides and Adenosine in Multiple sclerosisPurinergic Signal. 2011 Dec; 7(4): 393–402. (8.adenosine in MS)
  9. Sang-Bing Ong, Asa B. Gustafsson, New roles for mitochondria in cell death in the reperfused myocardium. Cardiovascular Research, Vol. 94, Issue 2, 1 May 2012, pp 190–196, (9.mitochondria in CVD)
  10. Dr. Daniel Remick, pre-ARC Director, Immunobiology of Trauma, pre-Affinity Research Collaborative (ARC), Boston University Medical Center,  (10.Immunobiology of Trauma)
  11. Howard Prentice, Jigar Pravinchandra Modi, Jang-Yen Wu, Mechanisms of Neuronal Protection against Excitotoxicity, Endoplasmic Reticulum Stress, and Mitochondrial Dysfunction in Stroke and Neurodegenerative Diseases. Oxidative Medicine and Cellular Longevity, Vol. 2015, Article ID 964518, 7 pages, (
  12. Blaylock, R.L. (1996). Excitotoxins: The Taste That Kills. Health Press. ISBN 0-929173-25-2
  13. Blaylock, R.L. (a neurosurgeon) podcast Excitotoxins (Excitotoxins podcast)
  14. Excitotoxicity, Wikipedia, (Excitotoxicity)
  15. Aspartic Acid, Wikipedia, (Aspartic Acid/Aspartate)

Choline and betaine – water soluble nutrients

Choline is a newer discovery in the nutrient world. It is considered to be a member of the water soluble B vitamins group which are nutrients involved in metabolism – the use of energy within the body. We can produce small amounts of choline so it isn’t considered a vitamin but as we can not produce enough for health it is considered an essential nutrient. (1) Betaine is a slightly different form of choline. Choline is found throughout the body but is particularly important within the brain and is needed for the neurotransmitter acetylcholine. Betaine is a metabolite of choline.

Choline, a water soluble nutrient. Foods Sources and symptoms of deficiency.

Choline is most typically found within phospholipids (such as phosphatidylcholine) which are important in membranes and as messenger chemicals within the brain and in the immune system. It may play a role in prenatal brain development but research on supplementation within pregnancy r to protect cognitive skills in the elderly is still in early stages. (1)

Choline is a  methyl donor (1) which means it can share a methyl group – essentially one carbon atom with three hydrogen atoms with an overall neutral charge.

An important role of methyl groups is in the release of energy from sugar within mitochondria. The methyl group is passed back and forth between nutrients and enzymes that are involved in breaking down a molecule of fat or sugar for use of the stored energy that is released when a double bond is broken. The methyl group is combined with an acetyl group when it is removed from the area on the chain of carbon molecules when a double bond is broken. An acetyl group is an atom of carbon combined with one atom of hydrogen and the group has a negative charge. The process for breaking down the glucose sugar molecule is called the Krebs cycle and most beginning level organic chemistry or nutrition students will remember having to memorize all of the steps involved. My summary may be inaccurate – college was a long time ago – the important point is that B vitamins and methyl donors are needed for mitochondria to be able to release energy from glucose/sugar molecules).

  • (The Krebs cycle is also known as the “citric acid cycle or the tricarboxylic acid (TCAcycle.” More info: Krebs cycle.)

Methyl groups are also important in controlling gene activity. They act like an on/off switch for genes. A gene that is fully methylated – all the available double bonds between carbon atoms are broken into single bonds with a methyl group added instead – is in the off position, the protein that the gene would encode is not being made. Genes that are unmethylated have double bonds and are in the on position, the pattern for assembling amino acids into a protein can be read by a matching strand of RNA and the protein can be formed (generally in the endoplasmic reticulum or Golgi apparatus areas of a cell).

Betaine and the more familiar B vitamins folate (B9 if anyone is counting), B6 and B12 are also methyl donors. Folate deficiency has been associated with less gene methylation (a histone is part of a gene). (2) More about methyl donors as a group is available here:  Methyl Donors and BPA.

  • The number system for naming B vitamins was derived at an earlier stage of research and some of the chemicals that were given numbers at the time were discovered to not be essential nutrients – meaning the body was able to form them within the normal health and didn’t essentially need to have them included in the diet (so that is why we don’t hear about a B4, B8, B10 or B11).

Excessive intake of choline above 7500 milligrams may cause a drop in blood pressure, sweating, vomiting and digestive upset, and change in body odor. The recommended Upper Limit is 3,500 mg/day. It would be difficult to reach that amount with food sources. (Safety information,

Food Sources of Choline:

Good sources of choline include meats, fish & shellfish, eggs/egg yolks, cheese, milk, yogurt, broccoli, cauliflower, cabbage, kale, kohlrabi and other cruciferous vegetables, green leafy vegetables, pomegranate seeds, sesame seeds, tahini, peanuts,  soybeans, beans, brown rice, whole grains.

Food Sources of Betaine:

Sweet potatoes, meats, cheese, beets, basil, spinach, green leafy vegetables, brown rice, whole grains.

Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes.


  1. Choline, Linus Pauling Institute, Oregon State University,
  2. Benjamin A. Garcia, Zigmund Luka, Lioudmila V. Loukachevitch, Natarajan V. Bhanu, Conrad Wagner, Folate deficiency affects histone methylation,

    Medical Hypotheses, Volume 88, March 2016, Pages 63-67, ScienceDirect,

  3. Foods used in the 30% Calories from Carbohydrates Menu Plans,

Oxidative stress and aging; trace minerals and antioxidants

For a more detailed review of the current understanding of how oxidative stress and inflammation are involved in the aging process see this chapter from a longer book: Oxidative Stress and the Aging Brain: From Theory to Prevention, [1]

Mitochondria are the main energy producers in cells. They are involved in breaking down each molecule of glucose (one half of the larger molecule that is commonly known as sugar). During the process of breaking the chemical bonds found in the glucose molecule the free radicals that can cause oxidative damage are produced. When adequate antioxidants are available the free radicals are stabilized before they can cause damage. The body’s internally produced antioxidant enzymes also require the trace minerals copper, zinc and manganese. /Separate topic: An imbalance in copper and zinc can cause health problems./

“Free radicals are chemical species with a single unpaired electron. The unpaired electron is highly reactive as it seeks to pair with another free electron; this results in the production of another free radical. The newly produced free radical is unstable in most cases and, as a result, it can also react with another molecule to produce yet another free radical. Thus, a chain reaction of free radicals can occur, leading to more and more damaging reactions.” [1]

“Several antioxidant defense mechanisms have evolved to protect cell components from the attack of oxidative stress and associated oxidative damage. These mechanisms include antioxidant enzymes, such as SOD, superoxide reductases, catalase, glutathione peroxidases (Gpx), and many heat-shock proteins.” “SOD exists in two forms: Cu/ZnSOD is present primarily in the cytoplasm while MnSOD is present primarily in the mitochondria.” [1]

More information about manganese superoxide dismutase (MnSOD) and how mitochondria function is available here: MnSOD in Oxidative Stress Response-Potential Regulation viaMitochondrial Protein Influx [2]

Supplementing the diet with a manganese and other trace minerals may be helpful as manganese and other trace minerals may be chelated by glyphosate, the active ingredient of the herbicide RoundUp. Chelation is a chemical term for the tendency for one chemical to bind with another – take hold and make the other one less freely available in the environment. The process can be helpful in some situations as it can act as a carrier, a taxi cab so to speak, but at other times it is simply removing the other chemical from being available for other uses.

Plant scientists are aware of the problem and there are agricultural suggestions for reducing the negative effects of manganese chelation by glyphosate in the following article: What About Glyphosate-Induced Manganese Deficiency? The effects of glyphosate’s chelation of iron, copper and zinc is also included in addition to the discussion of manganese. [3] The summary of plant yield research found that improved crop yields were produced when manganese, copper and zinc were applied as a supplemental fertilizer a certain amount of time after the glyphosate containing herbicide was applied to the fields:

“The greatest soybean yield response on high organic soils
was with both Mn and Cu applied 8 to 12 days after the glyphosate.
The highest yields for corn were obtained by foliar-applying Zn 15
days after glyphosate was applied in northwestern Indiana,” [3]

So if plant health scientists recommend supplementing with manganese, copper and zinc for best plant health do human health scientists? Some do, but the topic is still considered alternative medicine rather than being a mainstream medical recommendation. [4] Risks of increased toxicity from trace metals that have negative health effects such as aluminum. [4]

Antioxidant rich foods or supplements that were discussed in the chapter on Oxidative Stress and Aging include vitamin E, which had positive results when used as a supplement in animal studies and mixed results in studies with humans, addition of whole foods such as nuts which are a good source of vitamin E and other nutrients had more consistent positive results in human clinical research studies; Green Tea and its active metabolite EGCG; blueberries, spinach and spirulina, a blue-green algae. [1]

  • Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes.
  1. Carmelina Gemma, Jennifer Vila, Adam Bachstetter, and Paula C. Bickford, Chapter 15: Oxidative Stress and the Aging Brain: From Theory to Prevention, from Brain Aging: Models, Methods, and Mechanisms. Riddle DR, editor. Boca Raton (FL): CRC Press/Taylor & Francis; 2007.
  2. Demet Candas and Jian Jian Li, MnSOD in Oxidative Stress Response-Potential Regulation viaMitochondrial Protein Influx, Antioxid Redox Signal. 2014 Apr 1; 20(10): 1599–1617.
  3. Don M. Huber, What About Glyphosate-Induced Manganese Deficiency?, Fluid Journal, Fall 2007,
  4. Anthony Samsel and Stephanie Seneff, Glyphosate, pathways to modern diseases III: Manganese, neurological diseases, and associated pathologies, Surg Neurol Int. 2015; 6: 45.