CoenzymeQ10 is a cofactor produced by the body that aids in energy production in the Krebs cycle and mitrochondrial electron transport chain. It is converted into the antioxidant ubiquinol following ingestion: Dyslipidemia, High Cholesterol, Current statin use. CoQ10 levels decrease with age and have also been observed to be low in patients with certain disorders (e.g. cardiovascular diseases, diabetes). CoQ10 supplementation has been shown to offset some negative side effects of statin medications. Statins + CoQ10 - HMG-CoA reductase inhibitors (lovastatin, pravastatin, rosuvastatin, and simvastatin) decrease the concentration of CoQ10 in the human body.
Ratio of low-density lipoprotein cholesterol to ubiquinone as a coronary risk factor.
A meta-analysis of 12 randomized trials of vitamin supplements to lower homocysteine levels was carried out to determine the optimal dose of folic acid required to lower homocysteine levels and to assess whether vitamin B12 or vitamin B6 had additive effects. This meta-analysis demonstrated that reductions in blood homocysteine levels were greater at higher pretreatment blood homocysteine levels and at lower pretreatment folate concentrations. After standardization for a pretreatment homocysteine concentration of 12 micromol/L and folate concentration of 12 nmol/L (approximate average concentrations for western populations), dietary folic acid reduced homocysteine levels by 25% (95% confidence interval [CI]: 23 to 28%) with similar effects in a daily dosage range of 0.5 to 5 mg… Large-scale randomized trials of such regimens are now required to determine whether lowering homocysteine levels by folic acid and vitamin B12, with or without added vitamin B6, reduces the risk of vascular disease
Folic acid deficiency has been found in people with depression and has been linked to poor response to antidepressant treatment. Homocysteine is considered a significant risk factor for cardiovascular disease and may be modified by B vitamins, including folate or derivatives. Daily doses of > or =0.8 mg folic acid are typically required to achieve the maximal reduction in plasma homocysteine concentrations produced by folic acid supplementation. Doses of 0.2 and 0.4 mg are associated with 60% and 90%, respectively, of this maximal effect. Homocysteine Lowering Trialists’ Collaboration.
Individuals with thermolabile MTHFR may have a higher folate requirement for regulation of plasma homocysteine concentrations; folate supplementation may be necessary to prevent fasting hyperhomocysteinemia in such persons.
Methylenetetrahydrofolate reductase (MTFHR) is an enzyme involved in the processing of amino acids using folic acid, specifically the conversion of homocysteine to methionine. Patients with C677T polymorphism may see increased levels of blood homocysteine when folate levels are low, which may lead to a need for folate supplementation. Various mutations to the MTFHR enzyme may result in altered need and response to folate supplementation.
L-Methylfolate is the centrally active derivative of the vitamin folate and is used for both neurotransmitter synthesis, and vital methylation reactions in all cells. It regulates BH4 (or tetrahydrobiopterin) a critical enzyme cofactor required for serotonin, dopamine and norepinephrine synthesis. Some forms of depression resistant to antidepressant treatment may respond to folate or l-methylfolate. Synthesis of the monoamine neurotransmitters serotonin, dopamine, and norepinephrine is regulated by L-methylfolate, a derivate of the vitamin folate. Copyright 2008 Physicians Postgraduate Press, Inc.
B12 Deficiency: Homocysteine - “Vitamin B12 (mean 0.5 mg) produced an additional reduction in blood homocysteine of 7%, whereas vitamin B6 (mean 16.5 mg) did not have any significant effect. Hence, in typical populations, daily supplementation with both 0.5 to 5 mg folic acid and about 0.5 mg vitamin B12 would be expected to reduce homocysteine levels by one quarter to one third (from about 12 micromol/L to about 8 to 9 micromol/L).”
Pyridoxine (B6) nutritional status has a significant and selective modulatory impact on central production of both serotonin and GABA - neurotransmitters which control depression, pain perception, and anxiety.
Vitamin B6-dependent enzymes play a role in the biosynthesis of five neurotransmitters: serotonin, norepinephrine, epinephrine, dopamine and GABA. Vitamin B-6, comprised of pyridoxal, pyridoxamine, and pyridoxine, is one alternative treatment that may be a mitigating factor in hormone related depression, via its role in the proper metabolism of various neurotransmitters considered relevant in the manifestation of depression.
Several antioxidants, both enzymatic and non-enzymatic, are highly expressed in comparison to other tissues. Ascorbic acid (vitamin C), which recycles a-tocopherol (vitamin A) radicals, is present at the highest levels in the adrenal cortex (Hornig 1975), indeed endogenous ascorbic acid was first isolated from adrenal tissue (Svirbely & Szent-Gyorgyi 1932). Depletion of ascorbic acid secondary to vitamin A deficiency in rats leads to adrenocortical degeneration (Gruber et al. 1976)
Vitamin C enhances absorption of non-heme iron (found in plant-based foods) in the GI tract because an acidic environment favors the ferrous form of iron, which is better absorbed than the ferric form
Some research suggests that vitamin C may reduce cartilage loss and osteoarthritis progression. One randomized, placebo controlled crossover trial and showed that osteoarthritis pain significantly decreased in the vitamin C group in comparison to the placebo.
The objective of this article is to provide a review of the fundamental aspects of body fluid balance and the physiological consequences of water imbalances, as well as discuss considerations for the optimal composition of a fluid replacement beverage across a broad range of applications. Early pioneering research involving fluid replacement in persons suffering from diarrheal disease and in military, occupational, and athlete populations incurring exercise- and/or heat-induced sweat losses has provided much of the insight regarding basic principles on beverage palatability, voluntary fluid intake, fluid absorption, and fluid retention. We review this work and also discuss more recent advances in the understanding of fluid replacement as it applies to various populations (military, athletes, occupational, men, women, children, and older adults) and situations (pathophysiological factors, spaceflight, bed rest, long plane flights, heat stress, altitude/cold exposure, and recreational exercise). We discuss how beverage carbohydrate and electrolytes impact fluid replacement. We also discuss nutrients and compounds that are often included in fluid-replacement beverages to augment physiological functions unrelated to hydration, such as the provision of energy. The optimal composition of a fluid-replacement beverage depends upon the source of the fluid loss, whether from sweat, urine, respiration, or diarrhea/vomiting. It is also apparent that the optimal fluid-replacement beverage is one that is customized according to specific physiological needs, environmental conditions, desired benefits, and individual characteristics and taste preferences.
Alcohol has been known to deplete magnesium, along with other electrolytes including potassium and calcium
Magnesium is especially important in athletes because it is crucial for production of energy and the mineral is lost through sweating (~0.1 mmol/L). Several other electrolytes are lost in sweat including chloride (~30mmol/L), potassium (~5mmol/L), calcium (~0.5 mmol/L).
The effect of ethanol on magnesium excretion was studied in three normal subjects. It was found that the ingestion of 2 ml ethanol/kg body weight produced a marked immediate increase in urinary magnesium excretion, but there was no significant effect on overall magnesium balance when this amount was taken daily for eight days.
Vitamin K has been purported to play an important role in bone health. It is required for the gamma-carboxylation of osteocalcin (the most abundant noncollagenous protein in bone), making osteocalcin functional. There are 2 main forms (vitamin K1 and vitamin K2), and they come from different sources and have different biological activities. Epidemiologic studies suggest a diet high in vitamin K is associated with a lower risk of hip fractures in aging men and women. However, randomized controlled trials of vitamin K1 or K2 supplementation in white populations did not increase bone mineral density at major skeletal sites. Supplementation with vitamin K1 and K2 may reduce the risk of fractures, but the trials that examined fractures as an outcome have methodological limitations. Large well-designed trials are needed to compare the efficacies of vitamin K1 and K2 on fractures. We conclude that currently there is not enough evidence to recommend the routine use of vitamin K supplements for the prevention of osteoporosis and fractures in postmenopausal women.
Interventional studies showed that vitamin K1 provided significant improvement in undercarboxylated osteocalcin (ucOC) levels in postmenopausal women with normal bone mineral density (BMD); however, there are inconsistent results in women with low BMD. There is no study showing any improvement in bone-alkaline-phosphatase (BAP), n-telopeptide of type-1 collagen (NTX), 25-hydroxy-vitamin D, and urinary markers. Improvement in BMD could not be shown in the majority of the studies; there is no interventional study evaluating the fracture risk.
Low intakes of vitamin K may increase the risk of hip fracture in women. The data support the suggestion for a reassessment of the vitamin K requirements that are based on bone health and blood coagulation.
