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A doctor should always include testing for serum folate and vitamin B12 levels during annual checkups and calculate the estimated actual usable folate levels based on the patient’s MTHFR mutations. Pay attention to “normal” laboratory levels vs “Functional” levels.
MTHFR is a very important gene and its mutations may affect your health in many different ways. We gathered a list of 10 important steps to help you learn what to do. Download
Vibrant Health Dr. Fatima Vilich, MD Certified Functional Medicine Practitioner Associate Professor of Anesthesiology Phone: (435) 782-9384 Email: DrFatima@Vibrant-Health.info Wallace Taylor, MD Texas-US
The best time to Burn Fat and Build Muscle. To determine the best time for you to burn fat and build muscle, the saliva test is the best option because it can show an abnormal rhythm of cortisol levels.
Factor V G1691A (FV Leiden), FII GA20210, and methylenetetrahydrofolate reductase (MTHFR) C677T mutations are the most common genetic risk factors for thromboembolism in the Western countries. However, there is rare data in Iran about cerebral venous and sinus thrombosis (CVST) patients.
The MTHFR gene is responsible for the production of an enzyme called methylenetetrahydrofolate reductase, within our bodies. The role of that enzyme is to turn folic acid into folate, which our bodies use in many ways, such as to make new cells (like red blood cells) and neurotransmitters,...
Specifically, elevated homocysteine levels often caused by the MTHFR gene variation have been associated with nutrient deficiencies in Vitamin B9 (folate), B6, and B12. It may seem like common sense to take a supplement to address a deficiency in folate, but not all sources of Vitamin B9 are created equally.
An MTHFR mutation is a problem associated with poor methylation and enzyme production. MTHFR mutations affect every person differently, sometimes contributing to hardly any noticeable symptoms at all, while other times leading to serious, long-term health problems.
Professor Isaac AshkenaziIsaac Ashkenazi (born 1957 in Israel) is an Israeli Professor of Disaster Medicine at Ben-Gurion University of the Negev in Israel and a consultant to Harvard University. He is considered one of the world’s foremost experts in medical preparedness for complex emergencies and disasters.
Vertebral artery dissection (VAD) is a flap-like tear of the inner lining of the vertebral artery, which is located in the neck and supplies blood to the brain. After the tear, blood enters the arterial wall and forms a blood clot, thickening the artery wall and often impeding blood flow. The symptoms of vertebral artery dissection include head and neck pain and intermittent or permanent stroke symptoms such as difficulty speaking, impaired coordination and visual loss. It is usually diagnosed with a contrast-enhanced CT or MRI scan. Vertebral dissection may occur after physical trauma to the neck, such as a blunt injury (e.g. traffic collision) or strangulation but may also happen spontaneously. 1–4% of spontaneous cases have a clear underlying connective tissue disorder affecting the blood vessels. Treatment is usually with either antiplatelet drugs such as aspirin or with anticoagulants such as heparin or warfarin. Vertebral artery dissection is less common than carotid artery dissection (dissection of the large arteries in the front of the neck). The two conditions together account for 10–25% of non-hemorrhagic strokes in young and middle-aged people. Over 75% recover completely or with minimal impact on functioning, with the remainder having more severe disability and a very small proportion (about 2%) dying from complications. It was first described in the 1970s by the Canadian neurologist C. Miller Fisher.
Classical homocystinuria, also known as cystathionine beta synthase deficiency or CBS deficiency, is an inherited disorder of the metabolism of the amino acid methionine due to a deficiency of cystathionine beta synthase. It is an inherited autosomal recessive trait, which means a child needs to inherit a copy of the defective gene from both parents to be affected or can be acquired with a deficiency of B6, B12, or folate.