2013/01/02 by Keith Abell, RPh cMTM MI
I just completed a continuing education program on Multiple Sclerosis for my Pharmacist License requirements. The interesting thing about MS is the medical system doesn’t really know the causes. There are all kinds of theories about the cause but so far continued research has not proven any of them to be the definitive cause. It seems every time they think they have found something other research finds people with MS that don’t fit into the profile. My personal opinion is that there is not one particular cause. That MS is actually a symptom of multiple mineral and micro-nutrient deficiencies.
We know from research that large populations of MS sufferers come from areas where there are lower levels of sunlight during the winter months. The hypothesis is that Vitamin D – the sunshine vitamin therefore plays some role. This is probably true but since there are people suffering from the disease that do not have low Vitamin D levels we know it is not the only cause.
Many theorize that it is an auto-immune disease, where the immune system itself turns on the body causing damage. I have never been a big proponent of the auto-immune hypothesis. My question is always what started the immune system to turn on in the first place. To me the auto-immune hypothesis of any disease is much like the debate about whether a higher power, ie God, exist and is the cause for creating the universe. For many years the “Big Bang” has been promoted by science as the moment of creation of the Universe. My question is what then caused the Big Bang. Another example, for many years scientist thought the atom was the smallest particle but we now know that there are even smaller particles combined to make the atom and I am sure we will continue as technology allows to find even smaller and smaller particles. I believe the whole thing about auto-immune being the cause of so many diseases is just as flawed as these other theories have been proven to be.
In my opinion so called auto-immune diseases are actually caused by underlying deficiencies in the 90 essential nutrients that the body needs for optimal health. These 90 essential nutrients are involved in an unlimited amount of bio-chemical processes throughout the body and we have only scratched the surface of understanding what role these micro-nutrients play.
Just as an example in MS, we know that something causes the myelin sheaths around the nerve fibers to become inflamed and to become scarred. Science has yet to find one single cause of this probably because there are a multitude of different bio-chemical process that affect the myelin, problems with any one of these processes lead to similar damage. We know that there are a number of micronutrients involved with the overall health of the brain and nervous system yet we do not know every micronutrient and we do not know all the effects of deficiencies and combination of deficiencies have on the overall health. It is my opinion that the cause of this disease is multiple micro-nutrient deficiencies and the best way to prevent this disease and other auto-immune diseases is to supplement with all 90 known essential nutrients at levels according to ones body weight. I have seen other auto-immune diseases go into remission and I believe the same can be accomplished here.
Unfortunately, with the way that research is funded, most research money is spent trying to find medications to treat symptoms. Medications that can be patented and large profits made, whereas micro-nutrients, since they are naturally occurring, can’t be patented so research in these areas are not funded.
Here is a list of just some of the micro-nutrients used by the brain taken from an article from “Mineral Resources International, Inc’s” web site
( http://www.mineralresourcesint.com/basic/micronutrients-and-brain-function ). Remember this is only a partial list, we know that the human body actually needs 90 essential nutrients for optimal health.
Consequences of Select Micronutrient Deficiencies
Phosphorylated forms of thiamin (vitamin B1) are required for reactions involved in the metabolism of carbohydrates, amino acids, and lipids, and one form of the vitamin has been implicated in membrane functions of neurons and in the generation of nerve impulses. Thus, inadequate intake of thiamin can negatively affect cognition. Severe thiamin deficiency causes beriberi; the dry and wet types of beriberi involve peripheral neuropathy, whereas cerebral beriberi can lead to cell death of neurons and the clinical conditions of Wernicke’s encephalopathy and Korsakoff’s psychosis, especially in those who abuse alcohol.
Niacin (vitamin B3) is needed for a number of redox reactions (reduction—”electron gain”, oxidation—”electron loss”) and other reactions in the body. Severe niacin deficiency, known as pellagra, has been historically associated with poverty and consumption of a diet predominantly based on corn, which is low in bioavailable niacin. Today, the condition is uncommon but can occur in cases of chronic alcoholism and in individuals with malabsorption syndromes. Neurologic symptoms of pellagra include headache, fatigue, apathy, depression, ataxia, poor concentration, delusions, and hallucinations, which can lead to confusion, memory loss, psychosis, dementia, and death.
Pantothenic acid (vitamin B5) is needed for the oxidative metabolism of glucose and fats and also for synthesis of fats, cholesterol, steroid hormones, the hormone melatonin, and the neurotransmitter acetylcholine. Pantothenic acid deficiency is very rare and has been observed only in cases of severe malnutrition. However, deficiency of this vitamin has been induced experimentally in humans by co-administering a pantothenic acid antagonist and a pantothenic aciddeficient diet. Participants in this experiment complained of headache, fatigue, insomnia, intestinal disturbances, and numbness and tingling of their hands and feet.
Experimentally induced pantothenic acid deficiency in laboratory animals has been shown to cause loss of the myelin sheath and peripheral nerve damage.
Pyridoxal, pyridoxine, and pyridoxamine are collectively called vitamin B6, which is required for the biosynthesis of several neurotransmitters, including GABA, dopamine, norepinephrine, and serotonin. Severe deficiency of vitamin B6 is uncommon, but alcoholics are thought to be most at risk due to inadequate dietary intakes and impaired metabolism of the vitamin. Neurologic symptoms of severe vitamin B6 deficiency include irritability, depression, confusion, and seizures.
Biotin (vitamin B7) is required for carboxylase enzymes that are important in the metabolism of fatty acids and amino acids. While overt biotin deficiency is quite rare, deficiency of the vitamin has been observed in patients on prolonged intravenous feeding (parenteral nutrition) without biotin supplementation, in individuals consuming high amounts of raw egg white containing a protein that binds biotin and prevents its absorption, and in those with inherited disorders of biotin metabolism. Neurologic symptoms of biotin deficiency include depression, lethargy, hallucinations, and numbness and tingling of the extremities.
Folate (vitamin B9) is required for the metabolism of nucleic acids (DNA and RNA) and amino acids. The vitamin is also needed for the synthesis of several neurotransmitters, including norepinephrine, dopamine, and serotonin, and, along with vitamin B12, folate is required in the breakdown of norepinephrine and dopamine. Dietary folate deficiency in the absence of vitamin B12 deficiency does not cause neurologic symptoms. However, individuals with genetic disorders of folate metabolism have experienced seizures and progressive neurologic deterioration.
In humans, vitamin B12 is a required cofactor for two enzymes: methionine synthase, which is needed for the production of methionine from homocysteine, and L-methylmalonyl-CoA mutase, which is involved in crucial metabolic pathways. Vitamin B12 deficiency affects 10-15% of adults over the age of 60 years. It damages the myelin sheath of nerves and is frequently associated with neurological problems. Neurologic symptoms are the only clinical indicator of vitamin B12 deficiency in about 25% of cases. Such symptoms include numbness and tingling of the extremities, difficulty walking, problems with concentration, memory loss, disorientation, and dementia. Severe B12 deficiency is associated with pernicious anemia and, if untreated, can lead to “megaloblastic madness,” characterized by delusions and hallucinations. Atrophic gastritis, an age-related condition resulting in diminished digestive factors, is often associated with decreased absorption of vitamin B12 from food.
Vitamin C accumulates in the central nervous system, with neurons of the brain having especially high levels. Vitamin C is an important antioxidant that is required for the synthesis of the neurotransmitter norepinephrine, the reduction of metal (e.g., iron, copper) ions in the brain, and for the regeneration of vitamin E. Vitamin C deficiency causes oxidative damage to lipids and proteins in the brain. Severe vitamin C deficiency, called scurvy, is potentially fatal. In scurvy, vitamin C is retained by the brain for neuronal function, and eventual death from the disease is more likely due to lack of vitamin C for the synthesis of collagen—an important structural component of blood vessels, tendons, ligaments, and bone. Vitamin C is also required for the conversion of dietary lysine to carnitine, a compound essential for energy production in the cells’ mitochondria. Hence, scurvy is characterized by fatigue and depression in addition to physical manifestations.
Vitamin D is important for normal brain development and function, and vitamin D deficiency may impair cognitive abilities. Some studies in older adults have either linked lower 25-hydroxyvitamin D levels—the clinical indicator in the blood of vitamin D status&mdwith measures of poor cognitive performance or higher 25-hydroxyvitamin D levels with measures of better cognitive performance. However, the association between 25-hydroxyvitamin D concentrations and cognitive performance is not yet clear.
In the brain and other tissues, the alpha-tocopherol form of vitamin E is a key fat-soluble antioxidant that prevents lipid peroxidation and helps to maintain the integrity of cell membranes. Thus, vitamin E deficiency causes lipid peroxidation in brain tissues. Severe vitamin E deficiency results mainly in neurological symptoms, including impaired balance and coordination (ataxia), injury to the sensory nerves (peripheral neuropathy), muscle weakness (myopathy), and damage to the retina of the eye (pigmented retinopathy).
Calcium ions are important intracellular signals that regulate a number of physiological processes, including neuronal gene expression and neuronal secretion of neurotransmitters. Normal blood levels of calcium are maintained even when dietary intake of calcium is inadequate because the skeleton provides a large reserve of the mineral. Thus, dietary calcium inadequacy primarily affects bone health.
Iodine is required for the synthesis of thyroid hormones, which are important for myelination of the central nervous system. Iodine is critical for normal development of the brain; therefore, deficiency of this mineral during critical periods of fetal development or childhood can have deleterious effects on cognition. The most extreme cognitive effect of developmental iodine deficiency is irreversible mental retardation; milder cognitive effects include various neurodevelopmental deficits, including intellectual impairment.
Iron is an essential component of hundreds of proteins and enzymes involved in various aspects of cellular metabolism. The mineral is needed for proper development of oligodendrocytes (the brain cells that produce myelin) and for several enzymes that synthesize neurotransmitters. Accordingly, iron deficiency during various stages of brain development has negative consequences. Maternal iron deficiency during pregnancy has serious consequences for the woman and the fetus, including permanent learning and memory deficits in the offspring. Iron deficiency during childhood may be associated with impaired cognitive development.
Magnesium is required for more than 300 metabolic reactions, many of which are important for normal brain function. Overt magnesium deficiency has been induced experimentally and results in neurologic and muscular symptoms that include tremor, muscle spasms, and tetany (involuntary muscle contractions). According to recent surveys, many Americans do not have an adequate intake of magnesium.
Selenium is required for glutathione peroxidases (GPx), important antioxidant enzymes in the brain and other tissues. Selenium deficiency has been associated with decreased GPx activity in the brains of laboratory animals and may be linked to a reduced antioxidant capacity in the brain.
Zinc is present at high levels in the brain, where it has catalytic, structural, and regulatory roles in cellular metabolism. In the brain, most of the zinc ion is tightly bound to proteins, but free zinc is present in synaptic vesicles and has a role in neurotransmission mediated by glutamate and GABA. Experimentally induced zinc deficiency in humans has been shown to impair measures of mental and neurologic function. However, deficiency of the mineral during critical periods of cognitive development can be more devastating, causing congenital malformations or deficits in attention, learning, memory, and neuropsychological behavior.
Although not considered a vitamin, choline is an essential nutrient needed for myelination of nerves, synthesis of the neurotransmitter acetylcholine, and synthesis of various structural and cell-signaling molecules, including phospholipids (phosphatidylcholine and sphingomyelin) that are important components of cell membranes. Choline deficiency during the perinatal period in laboratory animals results in persistent memory and other cognitive deficits in offspring.