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Moderately elevated levels of homocystine are associated with a significantly increased risk of atherosclerosis. High levels in body fluids of this amino acid have been associated with increased risk of cardiovascular disease as well as ocular, neurological, musculoskeletal and joint abnormalities.
A commoncause of this metabolic disorder is impaired function of the enzyme cystathionine β-synthetase for conversion to cystathionine. This enzyme is vitamin B 6-dependent and supplementation of the vitamin has been used to treat elevated homocysteine. A second route in metabolism of homocysteine is remethylation to methionine using vitamin B 12, folic acid and betaine (trimethylglycine).
Supplementation of betaine has proven useful for people with high homocysteine who do not respond to vitamin B 6. Adequate intake of vitamins B 6 and B 12, folic acid and magnesium is necessary for insuring proper methionine metabolism to prevent the accumulation of homocysteine. Homocystine (HCys) Cystathionine.
For lowering of elevated homocysteine, in addition to the supplementation of folate, B 12 and B6, some have advocated the use of betaine to support the betaine-methyl transfer reaction in reformation of methionine. Recent evidence demonstrates that plasma betaine concentration is, indeed, inversely related to homocysteine levels. Because betaine levels are raised by folic acid supplementation, additional betaine supplementation is less likely to be effective when the B vitamins are used at appropriate doses.
Treatment: B6, 100 mg; Folate, 800 µg; B12, 1,000 µg; Betaine, 1,000 mg The supplement from Health Aid that I am taking contains: (up to 4 tablets a day) -Trimetiglicina 500mg - Colina, cloruro 100mg - Inositol 100mg - B6 (Pyridoxine Hydrochloride) 3mg(PN) - B12 1mcg - Folacina 200mcg -Zinc, oxido 8mcg I alternate it with Depyrrol Basis plus B12 & Folic acid that contains- B6 (Pyridoxine Hydrochloride) 10mg(PN) - Mangaangluconaat 41,7mg - Pyridoxal-5-fosfaat 50mg (PLP) - Zincgluconaat 210 mg - B12 10000 mcg - Folic Acid 200 mcg
History of Lab test regarding Homocysteine-Metionine 2007 y 2008
Free Homocysteine 24h. ---------------------------------> (Dec 2008) *5 (0-4) HIGH=> Risk for cardiovascular disease or renal insufficiency=> Current treatment B12+B6+Folic Acid+Zinc
Note: S-adenosylhomocysteine is a more sensitive indicator of renal insufficiency than homocysteine; also appears to be a more sensitive indicator of the risk for cardiovascular disease than is homocysteine.
Metionina------------------------------------------------------> (Dic 2007) * 35,5 19-31 (HIGH) Homocystein was not checked at this time... Cystine (Jun 2008) 30 (21-83)----------------- -------->(Dec 2008) *7
Low cystine levels may impair cellular synthesis of taurine, in which case plasma and urinary taurine will also be low. Low plasma cyst(e)ine may reflect a dietary deficiency of methionine and/or cysteine in which case N-acetylcysteine (NAC) would be an appropriate intervention. High dietary intake of condensed tannins as in heavy users of tea can lower plasma cystine.
Zinc is the cofactor for carnosinase and elevations of carnosine or anserine may be one effect of zinc deficiency. A patient with zinc deficiency who consumes a high-poultry diet would tend to show increased anserine excretion because of low carnosinase activity. Anserine have the capacity to modulate the immune response.
1-Methylhistidine is derived mainly from hydrolysis of the anserine of dietary meat, especially poultry.Carnosinase splits anserine into β-alanine and 1-methylhistidine (Figure 4.27) and since 1-methylhistidine is not normally metabolized in human tissues, most of it rapidly appears in urine. Urinary excretion of 1-methylhistidine has been used as a marker to distinguish meat-eating individuals from vegetarians.Vitamin E deficiency can lead to 1-methylhistidinuria from increased oxidative effects in skeletal muscle509mass (SM) in healthy adults on a meat-free diet. Excessive muscle tissue breakdown can be associated with inadequate antioxidant protection in the muscle.
Supplementation of the natural antioxidants—vitamins A, C, E and B2 and selenium, β-carotene, lipoic acid and coenzyme Q 10 (CoQ10)—may be useful in preventing excessive free radical pathology associated with this problem. BCAAs have also been indicated to lower plasma levels of 3-MHis by preventing muscle proteolysis.
Low levels in plasma are characteristic of one subset of patients with depression.368 The neurodegenerative condition, Huntington’s disease, also manifests as lowered levels of GABA as neuron loss proceeds.Vitamin B6 deficiency impairs GABA formation, offering one option to help assist patients with inadequate GABA production. In animal models of seizure, lysine has dose-dependent anticonvulsant effects that appear to be due to GABA receptor modulation.
Elevated alpha-aminoadipic acid is a clue that a patient is consuming large amounts of lysine. Elevation of a-aminoadipic acid could result from vitamin B 6 deficiency. The high positive correlation between homocysteine and a-amino adipic acid suggests that they share metabolic marker status in the etiology of atherosclerosis and myocardial infarction. Elevated alpha-aminoadipic acid is a risk factor for heart disease. Unlike homocysteine, a-aminoadipic acid is not vitamin B 12 dependent and thus its elevation may indicate a specific need for vitamin B 6
suberic acids are by-products of an alternative fatty acid oxidation pathway that is utilized when mitochondrial oxidation is limited. A secondary cause of elevated adipate and suberate is riboflavin insufficiency.52 Once they are inside the mitochondria, fatty acids cannot undergo oxidative metabolism without riboflavin coenzymes. Functional carnitine deficiency is revealed by elevated urinary excretion of adipic, suberic and ethylmalonic acid. The action of carnitine may be described as a key that opens the gate of energy flow in most cells
Arginine insufficiency quickly leads to hyperammonemia due to failure of ammonia removal. Citric acid, cisaconitic acid, isocitric acid and orotic acid appearance in urine are other biochemical markers of this condition. Elevated Citric acid is also a sign of mitochondrial failure and toxicity or B-Complex deficiencies.