Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.5.7.1 (methylenetetrahydrofolate reductase)
 2,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Migraine is the most common form of headache disorder globally. The etiology of migraine is multifactorial, with genetic components and environmental interactions considered to be the main causal factors. Some researchers postulate that deficits in mitochondrial energy reserves can cause migraine or an increase in homocysteine levels can lead to migraine attacks; therefore, vitamins could play a vital role in migraine prevention. For instance, riboflavin influences mitochondrial dysfunction and prevents migraine. Genes such as flavoenzyme 5,10-methylenetetrahydrofolate reductase (MTHFR), especially the C677T variant, have been associated with elevated plasma levels of homocysteine and migraine with aura. Homocysteine catalyzation requires the presence of vitamins B6, B12, and folic acid, which can decrease the severity of migraine with aura, making these vitamins potentially useful prophylactic agents for treating migraine with aura. Menstrual migraine, on the other hand, is associated with increased prostaglandin (PG) levels in the endometrium, indicating a role for vitamin E, which is an anti-PG. Vitamin C can also be used as a scavenger of reactive oxygen species for treating neurogenic inflammation in migraine patients. This paper reviews possible therapies based on vitamin supplementation for migraine prophylaxis, focusing on migraine with aura and menstrual migraine.
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PMID:Vitamin supplementation as possible prophylactic treatment against migraine with aura and menstrual migraine. 2581 19

Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases. The con- cept of NAFLD ranges from simple steatosis (NAFL) to non-alcoholic steatohepatitis (NASH) and cirrhosis. The majority of NAFLD has been recognized as a hepatic manifestation of metabolic syndrome with a close association with insulin resistance. Regarding the development of NAFLD/NASH, adiponectin and TNFa are thought to have key roles. Moreover, the gut microbiota may affect energy metabolism in the context of NAFLD. Genetic susceptibility to NAFLD may be determined by polymorphisms of patatin-like phospho- lipase domain-containing 3 (PNPLA3) and methylenetetrahydrofolate reductase (MTHFR). The diagnosis of NAFLD/NASH is made by liver biopsy. The differential diagnosis between NAFL and NASH has been made according to Matteoni's classification, and the progression of liver fibrosis has been determined by Brunt's staging. For the prevention and treatment of NAFLD, the modification of dietary habits and promo- tion of physical activity including aerobic and resistance training are essential. Although vitamin E, pioglita- zone, or liraglutide is used as a first-line treatment for NAFLD, pharmacotherapy for NAFLD has not been established because of the insufficient pharmacological effects of these agents. Among recently developed drugs, farnesoid X nuclear receptor ligand obeticholic acid is the most promising for first-in-class treatment of NASH. In this review, the details of recent advances in knowledge about the epidemiology, etiology, diag- nosis, and treatment of NAFLD/NASH are described. [Review].
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PMID:[Progress in the Management of NAFLD/NASH]. 3069 68

Diabetic retinopathy (DR) is a form of microangiopathy. Reducing oxidative stress in the mitochondria and cell membranes decreases ischemic injury and end-organ damage to the retina. New approaches are needed, which reduce the risk and improve the outcomes of DR while complementing current therapeutic approaches. Homocysteine (Hcy) elevation and oxidative stress are potential therapeutic targets in DR. Common genetic polymorphisms such as those of methylenetetrahydrofolate reductase (MTHFR), increase Hcy and DR risk and severity. Patients with DR have high incidences of deficiencies of crucial vitamins, minerals, and related compounds, which also lead to elevation of Hcy and oxidative stress. Addressing the effects of the MTHFR polymorphism and addressing comorbid deficiencies and insufficiencies reduce the impact and severity of the disease. This approach provides safe and simple strategies that support conventional care and improve outcomes. Suboptimal vitamin co-factor availability also impairs the release of neurotrophic and neuroprotective growth factors. Collectively, this accounts for variability in presentation and response of DR to conventional therapy. Fortunately, there are straightforward recommendations for addressing these issues and supporting traditional treatment plans. We have reviewed the literature for nutritional interventions that support conventional therapies to reduce disease risk and severity. Optimal combinations of vitamins B1, B2, B6, L-methylfolate, methylcobalamin (B12), C, D, natural vitamin E complex, lutein, zeaxanthin, alpha-lipoic acid, and n-acetylcysteine are identified for protecting the retina and choroid. Certain medical foods have been successfully used as therapy for retinopathy. Recommendations based on this review and our clinical experience are developed for clinicians to use to support conventional therapy for DR. DR from both type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) have similar retinal findings and responses to nutritional therapies.
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PMID:Nutritional and medical food therapies for diabetic retinopathy. 3258 7