In Blog, Diet, Exercise, Health, multiple sclerosis, Research

If you have multiple sclerosis or another autoimmune condition with neurological or psychological symptoms, you need to resuscitate your mitochondria. Mitochondria generate adenosine triphosphate (ATP), which are used by cells to drive the chemistry of life.  There is increased recognition that brain cells, including neurons, astrocytes, and microglia, have very high energy needs and need lots of ATP, as do retinal cells and heart cells. If mitochondria are inefficient, cells begin to function inefficiently.

In 2004, I was in my tilt/recline wheelchair and began reviewing the basic science, hoping to learn something that would help slow my decline. I read animal studies of multiple sclerosis, Parkinson’s, Alzheimer’s, Huntington’s, and ALS. In all those conditions there was excessive oxidative stress, meaning the mitochondria were not making enough ATP. I theorized that insufficient ATP was at the heart of neurodegeneration, cognitive decline in Alzheimer’s, Parkinson’s, and multiple sclerosis, and the development of progressive disability in multiple sclerosis.1-3 Mitochondrial dysfunction is a key driver in macular degeneration and retinal aging, which are leading causes of blindness.4

Mitochondria also play a major role in aging. Multiple sclerosis and other neuroimmune and neurodegenerative conditions demonstrate accelerated aging. Diabetes also demonstrates accelerated aging. Mitochondria, in the face of nutritional inadequacy, will triage which functions to perform and which to ignore. This triage process prioritizes immediate survival at the expense of long-term health. The result is accelerated aging, which leads to neurodegenerative damage.5-8 Bruce Ames, a key nutrition scientist, first focused on restoring mitochondrial function to delay aging and slow neurodegeneration. He focused on lipoic acid, creatine, carnitine, magnesium, zinc, and fat-soluble vitamins A, D, and K.7,8 He championed targeted use of those supplements as a strategy to reduce neurodegeneration and prevent accelerated aging.

There is more we can do to improve our mitochondrial efficiency, but first let me review the origin of mitochondria. Mitochondria are ancient bacteria that evolved when oxygen first emerged in the earth’s atmosphere, which occurred when cyanobacteria began photosynthesis with sunlight and carbon dioxide, which created sugar and oxygen as a byproduct. Those events occurred billions of years ago, when all life was limited to single cell organisms. Those ancient bacteria were engulfed by larger bacteria, which eventually evolved into multi-cellular organisms that, a billion years later, evolved into mammals and eventually humans. We rely on our mitochondria to fuel the chemical reactions that are essential to life.

When our mitochondria do not work well, our cells don’t function well. Symptoms accumulate. Chronic diseases accumulate. Brain fog. Fatigue. High blood pressure. Diabetes. Heart disease. Anxiety. Depression. Macular degeneration. Parkinson’s. Rheumatoid arthritis. The longer the mitochondrial nutrition is suboptimal, the more chronic disease states will accumulate.

When patients have brain fog, mental health issues, neurologic symptoms, cardiac problems, or vision problems, I assume the mitochondria are malfunctioning and need to be resuscitated. There are a number of ways to stop poisoning and start feeding the mitochondria. Long term use of antibiotics may impact mitochondria; some individuals are more susceptible to certain classes of antibiotics, particularly the fluoroquinolones class of antibiotics. Another way to support mitochondria is stopping smoking and improving air and water quality in the home, which reduces exposure to cadmium, arsenic, lead, and mercury, all of which damage key proteins in mitochondria. Pesticides and insecticides are also mitochondrial poisons that should be avoided.

As poisons are removed, steps also need to be taken to improve mitochondrial nutrition. Reduce or eliminate added sugars. Replace white flour and processed foods with non-starchy vegetables and berries. Ensure adequate protein and healthy fats. Eat the highest quality of food that your budget will allow. Cooking your meals at home and planning your shopping will reduce food waste and make this dietary approach more affordable. I recommend cooking and meal planning classes to make these changes easier to implement as a family.

To help patients understand why and how to support their mitochondria, I review basic mitochondria biology. The mitochondria (plural) or mitochondrion (singular) have proteins embedded in an inner membrane that facilitate the electron transport chain of reactions that generate ATP much more efficiently than is made outside the mitochondrion. The mitochondrion need healthy cell membranes to hold the proteins in the correct positions, and for that they need a lot of healthy fats, particularly omega-3 fat (which most of us have too little of) and omega-6 fat (which most of us have too much of). In addition, mitochondrial function can be boosted by some of the co-factors that support the reactions in the electron transport chain. These factors include B vitamins, riboflavin, thiamine, niacin, folate, pyridoxine, cobalamin, zinc, and magnesium.9 In addition, ubiquinone (co-enzyme Q), lipoic acid, carnitine, berberine, broccoli sprout extract, and creatine support improved mitochondrial efficiency.9-12 Taking a blend of supplements to provide broad-spectrum support can be very helpful.

I recommend specific supplements based on current symptoms, co-morbid medical diagnoses, and severity of impairment. Most people with mitochondrial issues benefit from a fish oil supplement, activated B vitamins and a mix of carnitine, and lipoic acid. Many are also deficient in zinc and magnesium. Most people in Westernized societies eat less than two servings of vegetables per day and get most of their calories from added sugars and white flour. That means most people have diets that have starved their mitochondria of key nutrition for years.

When I see patients with neurological and psychiatric disorders, I discuss their diet history. I want to know how much sugar and processed foods they consume, how many years they have been vegan or vegetarian, and for how many years they’ve experienced high stress. Ongoing high stress increases loss of magnesium and zinc in the urine. Single nucleotide polymorphisms (SNPs) affect the efficiency of B vitamins, and the presence of SNPs increases risk of mitochondrial strain. Taking activated B vitamins bypasses the SNPs.

People sometimes ask if they can just take supplements and not change their diets. Unfortunately, the answer is no.

Fixing diet to improve nutrition is key. Supplements, while very helpful, are not sufficient. Adding targeted supplements can accelerate the recovery, but continuing the standard Westernized diet with high levels of added sugars and processed foods means mitochondrial strain and accelerated aging will continue.


If you feel overwhelmed by choosing the right combination of targeted supplements, I have put together two bundles from my Wahls Protocol® Supplement Collection that most people with an autoimmune condition may find supportive:

The MS Protect Support Kit

Includes:

  • MonoAbsorb Omega 1300
  • Cytokine Modulator
  • Activated B’s
  • N-Acetyl-Cysteine (NAC)

Click here to SHOP NOW

 

The MS Protect Support Kit COMPLETE

Includes:

  • MonoAbsorb Omega 1300
  • Cytokine Modulator
  • Activated B’s
  • N-Acetyl-Cysteine (NAC)
  • Cytokine Modulator
  • Complete Carnitine

Click here to SHOP NOW


References:

  1. Barcelos IP, Troxell RM, Graves JS. Mitochondrial Dysfunction and Multiple Sclerosis. Biology (Basel). 2019;8(2).
  2. Bueler H. Mitochondrial and Autophagic Regulation of Adult Neurogenesis in the Healthy and Diseased Brain. Int J Mol Sci. 2021;22(7).
  3. Carvalho KS. Mitochondrial dysfunction in demyelinating diseases. Semin Pediatr Neurol. 2013;20(3):194-201.
  4. Eells JT. Mitochondrial Dysfunction in the Aging Retina. Biology (Basel). 2019;8(2).
  5. Ames BN. Delaying the mitochondrial decay of aging-a metabolic tune-up. Alzheimer Dis Assoc Disord. 2003;17 Suppl 2:S54-57.
  6. Ames BN. Delaying the mitochondrial decay of aging. Ann N Y Acad Sci. 2004;1019:406-411.
  7. Ames BN. Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage. Proc Natl Acad Sci U S A. 2006;103(47):17589-17594.
  8. Ames BN, Liu J. Delaying the mitochondrial decay of aging with acetylcarnitine. Ann N Y Acad Sci. 2004;1033:108-116.
  9. Fila M, Chojnacki C, Chojnacki J, Blasiak J. Nutrients to Improve Mitochondrial Function to Reduce Brain Energy Deficit and Oxidative Stress in Migraine. Nutrients. 2021;13(12).
  10. Lewis Lujan LM, McCarty MF, Di Nicolantonio JJ, et al. Nutraceuticals/Drugs Promoting Mitophagy and Mitochondrial Biogenesis May Combat the Mitochondrial Dysfunction Driving Progression of Dry Age-Related Macular Degeneration. Nutrients. 2022;14(9).
  11. Testai L, Martelli A, Flori L, Cicero AFG, Colletti A. Coenzyme Q10: Clinical Applications beyond Cardiovascular Diseases. Nutrients. 2021;13(5).
  12. Naoi M, Maruyama W, Shamoto-Nagai M. Disease-modifying treatment of Parkinson’s disease by phytochemicals: targeting multiple pathogenic factors. J Neural Transm (Vienna). 2022;129(5-6):737-753.
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