Hyperhomocysteinaemia may arise from genetic defects of several enzymes involved in homocysteine metabolism including MTHFR, MTR and CBS.
Low hair magnesium status and high serum homocysteine levels are often seen in children with autism spectrum disorders (ASD). Researchers recently confirmed these findings and hypothesise that magnesium may play a critical role in homocysteine metabolism and methylation.
S-adenosylmethionine (SAMe) is integral to cellular metabolism and as the major methyl donor in the body. SAMe is involved in the methylation of a diverse range of compounds including phospholipids, DNA, RNA, proteins and neurotransmitters. It is also involved in two other important pathways – transsulfuration which produces glutathione, and aminopropylation which synthesises polyamines.
One potential mechanism proposed for the pathogenesis of preeclampsia is elevated homocysteine levels adversely affecting placental functionality, with various data finding a three- to eightfold increase in risk of disease onset associated with hyperhomocysteinaemia.
Homocysteine is an intermediate produced in the metabolism of sulfur-containing amino acids. Elevated levels of homocysteine are associated with heart attack, heart disease, vascular disease as well as dementia and cognitive decline, macular degeneration, migraine, neural tube defects and bone fractures.