Vitamin and minerals are better than prescription medications. The targeted use of nutrients can solve simple problems like anemia and complex conditions like autoimmune disease. The sampling below are the leading or the most important nutrients to consider when getting a baseline nutrient status.
Baseline labs we run on new patients and as part of an annual review may include: Iron, Ferritin, Vitamin D, Zinc, Copper, Selenium, Magnesium, Vitamin B12, Folic Acid, and Vitamin B6
Iron is a transport mineral found in red blood that binds oxygen for delivery to all cells and tissues throughout the body. It is vital to good physical and mental health and if it is low, fatigue and lethargy will often be present. Low iron levels are easily observed in standard labs and can be supplemented with chelated forms with good absorption.
Ferritin levels are an indicator often of the long term storage of iron. If ferritin levels are low, fatigue may be present, and patients may also report feeling unable to recover from physical exertion when compared to the recent past. Ferritin levels may also rise in genetic disorders such as Hemochromatosis and are also associated with inflammation generally and from candida overgrowth in the intestines.
Vitamin D is a fat-soluble vitamin with optimal levels in the blood ranging between 50 -70mg/dL. Optimal vitamin D levels offer many health benefits, including promoting bone growth, reducing risks for cardiovascular disease, Multiple Sclerosis, and breast cancer. A small number of patients report improving energy and mood with appropriate dosing of vitamin D. We know that optimal vitamin D levels may be influenced by the amount and time of day of sun exposure. Though even in Arizona, a sunshine state, testing reveals most patients are deficient.
An additional area of intense vitamin D research is its relationship to depression. Seasonal affective disorder, or SAD, is a situational mood disorder brought on by decreasing daylight in the winter months. High doses of vitamin D during these months have proven to be a very effective natural remedy for SAD, leading most practitioners to believe that normal neurotransmitter function depends in part on adequate vitamin D synthesis.
Vitamin D levels are inversely related to those of melatonin, another mood-regulating hormone. Melatonin helps modulate your sleep and wake circadian rhythms, with darkness triggering melatonin secretion by the pineal gland contained within the brain. Melatonin elevations help prepare the mind and the body for a good night of sleep. Insomnia, mood swings, and even food cravings are influenced by melatonin. Sunlight shuts melatonin production off, while triggering release of vitamin D. Most of us can sense the positive influence of sunlight in our own lives by the immediate lift we get from taking a walk outdoors on a beautiful sunny day. Now there may be many factors at work that brighten our mood in such cases, but sun exposure is almost certainly a critical piece. Soaking in the warmth of the sun is one of the most relaxing activities we share with all living creatures.
Oxidation is a chemical reaction necessary to good health. However, many disease conditions result in excessive oxidation with insufficient natural antioxidant protectors. This results in the release of free radicals and undesirable chemical reactions. Free radicals are able to damage proteins, membranes, DNA, and also produce excessive inflammation. As an example, research has shown Autism is linked to oxidative stress as a result of free radicals from toxic metals, smog, pesticides, biotoxins, infections, radiation, and chemical waste products.
We can test for deficiencies of certain nutrients, minerals, and biomarkers that can affect normal free radical control and healthy brain function. Our goal is to support the brain’s already existing mechanisms for oxidative management. Here are a few of the things we test for and why.
Zinc is the most common depleted nutrient found in mental health diseases, including autism. Zinc is a component of more than 200 enzymes functioning as antioxidants, converting B-6 to PLP, supporting synthesis of neurotransmitters, and inhibition of NMDA receptors. In addition Zinc is valuable in building reserves of Metallothionein which blocks and aids in the removal of toxic metals as they try to cross the gastrointestinal and brain barriers. Optimized levels of zinc bring significant improvements to patients and is a powerful generator of superoxide dismutase(SOD), our body’s most important free radical fighter.
Excess copper has been linked to neurological symptoms including schizophrenia, bipolar disorder, postpartum depression, ADHD, and Autism. Copper is used to convert dopamine to norepinephrine and epinephrine. Too much copper leads to an excess of these two chemicals which causes neurological symptoms. Copper also has other functions within the brain that can be affected by having too much, including depression of Zinc levels and oxidative stress.
Copper and Zinc levels are usually inversely related. Where we see high levels of copper, we also see low levels of zinc. Increasing zinc helps the body decrease copper. Normalizing the ratio of copper to zinc is an important area of treatment which is helpful to the various populations.
Selenium is a non-metal chemical element. It can serve many purposes within the brain. It aids in glutathione activity and can affect hormonal and neurotransmitter activity. It is also effective at combating the neurotoxicity of certain metals. A deficiency in selenium can affect any one of these aspects, with the additional activity of helping regenerate our most potent free radical fighter, Super Oxide
Magnesium is another mineral that is vital to healthy brain function. It plays a role in over 300 enzymatic reactions in the body and brain. It aids in muscle contractions, DNA and RNA synthesis, efficient nerve signaling, and protecting neuronal cells from oxidative stress.
Assessment of the methylation pathway is critical in understanding the optimal metabolism of methionine and homocysteine. Methionine is an amino acid critical for cellular methylation of DNA and neurotransmitters, transsulfuration, and folate-dependent transmethylation. The most often recognized concerns with inefficient metabolism of methionine are increased risk of cardiovascular disease, cancer, autoimmunity, mood disorders, neurodegeneration, birth defects, poor detoxification, and autism.
Methylation of Methionine to Homocysteine
Baseline labs we run on new patients and as part of an annual review may include: Homocysteine, Methyl B12, Vitamin B6, Folic acid, and MTHFR. Methionine metabolism is a multi-step process with Homocysteine as an end product of the cycle, that is easily measured in standard labs. Since Homocysteine is used to recycle methionine, elevations in Homocysteine will predict blunting of the methionine and methylation cycle. It is also critical to test for vitamin B12, as a deficiency will also cause a significant increase in Homocysteine levels and blunting of the methylation cycle.
Causes of Elevated Homocysteine
Methionine metabolism defects, often signified by elevated or suboptimal homocysteine levels, are associated with nutritional and vitamin deficiencies, normal aging, environmental toxicants, lead toxicity, and genetics. Evaluating vitamin B12, B6, and Folic acid levels associated with the methylation pathway is easily accomplished through normal lab testing. Environmental testing can be done as a part of a Toxic Metals Chelation challenge to evaluate for lead burden. But for a large percent of individuals, genetics may also be involved.
A large percent of the population carries a polymorphism in an enzyme called 5,10 methyltetrahydrofolate reductase or MTHFR. This polymorphism results in a decline in a number of events that require sufficient folic acid. The effect of this enzyme defect results in a decline of the MTHFR enzyme by approximately 60 percent, leaving the folic acid cycle very sluggish. Folic acid comes in two common forms outside the body known as folate and folic acid. Folic acid status in the US has improved since 1998 when it was added to fortified foods, yet studies show that many people are still deficient in folic acid. Folic acid is essential for the synthesis of purines (the building blocks of DNA), the synthesis of methionine (important in methylation and over 100 reactions requiring SAMe), production of many neurotransmitters, and very importantly, metabolism of homocysteine. Folic acid is absorbed by the gut and is converted to tetrahydrofolate which is converted to methylene tetrahydrofolate and then to methyltetrahydrofolate by the enzyme MTHFR. If the MTHFR polymorphism is present then the pathways reducing homocysteine to methionine, glutathione, phospholipids, and neurotransmitters is reduced by up to 60 percent.
Folic acid deficiency has been linked in numerous studies with depression. It is estimated that 1/3 of all depressed patients have as the sole cause of their depression, a folate deficiency. Studies which have added folic acid to the current antidepressant prescription also showed significant improvement in depression. In addition, studies have also found folic acid deficiency to cause low serotonin(and subsequently low melatonin), which is the brain’s major antidepressant neurotransmitter.
The good news about the folate pathway, it is maintained simply by high doses of folic acid, which will drive the pathway, just like water spilling over a dam, or by taking the form of folic acid that bypasses the need for MTHFR, called 5 Methyltetrahydrofolate (5-MTHF). Other cofactors that also help drive the folate cycle are essential and include vitamins B2 (riboflavin), B6 (pyridoxine), and B12 (methylcobalamin). Patients with depression, without a MTHFR defect, but who are folic acid deficient, will be benefited by taking additional folic acid as contained in a multivitamin mineral complex or methylated B-Complex. Those with the MTHFR are recommended to take a specifically formulated blend of methylated folic acid and co-factors required to maximize folic acid and methionine pathways.
For so many patients who have lived years or decades without knowing they had a MTHFR defect, it is imperative to treat it correctly now. A single blood draw is all that is required to determine the presence of MTHFR. Those who have any symptom of MTHFR polymorphism, or extended family history, should be tested and treated. Click to view DNA Methylation Pathway SNP’s Sample Report. Once the evidence of SNP’s has been determined and supplemental support has been added future evaluation can include specific nutrient levels of the methylation cycle including methionine, homocysteine, S-Adenosyl homocysteine, S-Adenosylmethionine, and cystathionine. Click to view a Methylation Profile Sample Report.