Stroke
High blood pressure has been identified as the most important risk factor for stroke and elevated homocysteine levels are associated with hypertension(high blood pressure) and play a significant role in the creation. While the most common genetic cause of severe hyperhomocysteinaemia is believed to be the
deficiency of cystathionine-beta-synthase, which has been shown to result in a 40-fold increase in fasting homocysteine. Other causes include the deficiency or impaired activity of methionine synthase due to genetic disorders of vitamin B12 metabolism. Outside of these genetic mutations folate and vitamins B6 and B12 are essential cofactors in the methylation cycle and homocysteine-methionine metabolism, and low bioavailability and function of these nutrients due to the polymorphisms impair the remethylation of homocysteine to methionine, lending to a vicious cycle of compounding Homocysteine levels. Certain nutritional and lifestyle components also play a role in the pathophysiology of hyperhomocysteinaemia. Deficiencies of folate, vitamins B6 and B12 due to poor nutrient intake, malabsorption, leaky gut, medications or the presence of certain diseases may lead to abnormal homocysteine concentrations. Vegetarians may be at a higher risk of hyperhomocysteinaemia due to insufficient vitamin B12 intake. While insufficient physical activity and excessive alcohol consumption have also been shown to contribute to hyperhomocysteinaemia. Other factors can also raise homocysteine levels, including eating a poor diet, leaky gut syndrome/poor absorption, malnutrition, gastrointestinal illness, high amounts of stress, alcohol and drug use, and toxin exposure. Natural treatments include taking specialized forms of B9; B6 and B12; exercising; lowering intake of inflammatory foods, and managing stress.
