VITAMINS Jul 29, 2019

Vitamin B Deficienes

Request a b12/iron/folate test from your doctor and ask for a copy of the results. If it's anywhere near the bottom-end you may have a metabolic/absoprtion issue and should be supplementing B12 sublingually at the minimum. If you test deficient you require B12 injections as frequently as possible (up to once a day) until symptoms reside. You can then attempt to switch to sublingual for maintence however many need injections for the rest of their lives since they cannot absorb/metabolise b12.

Standard panel result will be elevated if you have inflammation. Request a Full iron panel be done that includes Serum iron, TIBC, and Transferrin saturation % for best measure of iron status. Avoid iron supplementation 5 days prior to test. Keep a check on ferritin levels. Once b12 has transferred to cells the body uses ferritin to produce new blood cells. This process puts a higher demand on folate and ferritin.
Magnesium Aids your body in relaxing, detoxing, and muscle aches and pains, reducing fatigue, heart rate, skin conditions, and aids potassium intake from foods. A 30 minute soak in Epsom salts is also a good source.
Personal genetics play a role here. Some may need a Methyl B-Complex, Keep B6 dosages low (under 10mg/day - 4 months on, 2 off). High dosages can cause neurological damage.
Ideally you should be getting injections - however 1mg sublingual is a close alternative. Recommended dosage if you've tested defecient is injection every 12 weeks until no longer gaining benefit. If Neurological symptoms are present a dose must be administered every other day to attempt to reverse any damage.
Get potassium from whole-foods only. 4700mg - 6000mg daily
When supplementing B12, adequate folate is critical - without it to ensure B12 activation, the B12 will likely worsen your symptoms and cause new ones to manifest - Either Folate, Folic Acid or Methyl-Folate will work best depending on personal reaction/genetics.

B vitamin polymorphisms and behavior: Evidence of associations with neurodevelopment, depression, schizophrenia, bipolar disorder and cognitive decline (2017)

While many epidemiological studies have shown that B vitamin deficiency is associated with various psychiatric and cognitive issues, B vitamin supplementation has had little effect on its own. Since ‘vulnerability’ genotypes such as MTHFR 677TT have low frequencies in many populations and its effects are subtle, the numbers of subjects needed for a B vitamin intervention study, with sufficient groups of homozygotes, is unfeasible. Yet observational studies using cohorts are not appropriate to test whether psychiatric and cognition issues are reversible or even caused by changes in B vitamin intake. Although analyses of variants in several B vitamin metabolic pathways seem promising in genetic association studies, the contribution of a single gene or small subset of genes is not likely to show reproducible effects, due to different genetic populations or different diets. More consistent intervention study outcomes were observed in subjects with baseline homocysteinuria or other markers of imbalanced methyl donor status, where genotype status contributes to an imbalance and thus is amenable to correcting levels of nutrients. However, as stated earlier, selection or stratification of subjects based on self-report questionnaires or even plasma B vitamins may not indicate levels of active forms such as methylcobalamin or methylenetetrahydrofolate. Thus future studies would be well served by selection of subjects with imbalances in active or downstream components of the methyl donor pathways, like SAM/SAH.

In conclusion, diverse clinical studies have revealed weak and in some cases inconsistent associations of cognition, mood and neurodevelopment disorders to genes involved in B vitamin metabolism. Use of new experimental models and designs, more extensive phenotyping, and more detailed understanding of an individual's exposures to stress, diet, and lifestyle will likely improve the consistency and reliability of genotype–nutrient–behavior interaction data.