The aim of this work was to investigate the association between homocysteine levels and coffee consumption in a sample of cardiovascular disease-free men and women. From May 2001 to December 2002, we randomly enrolled 1514 men and 1528 women, stratified by age and gender, from the greater area of Athens. Blood samples were collected in the fasting state. Among other investigated factors, dietary habits (including coffee consumption in ml per day, adjusted for 28% caffeine containment) were evaluated using a validated food frequency questionnaire. Men consumed higher quantities of coffee compared with women (250 +/- 55 vs 150 +/- 60 ml/day, P = 0.001), while homocysteine values were also higher in men than in women (14.5 +/- 6 vs 10.8 +/- 3.5 micromol/l, P = 0.001). A dose-response relationship of homocysteine levels with coffee consumption was observed (r = 0.10, P = 0.034). In particular, we found that homocysteine levels were 11.2 +/- 5 micromol/l for no consumption, 11.7 +/- 7 micromol/l for <100 ml/day, 12.5 +/- 7 micromol/l for 200-400 ml/day, and 12.7 +/- 4 micromol/l for >500 ml/day consumption (P = 0.018). The observed trend remained significant even after controlling for the interactions between coffee consumption with gender, smoking habits, physical activity status, and eating habits. However, the sole effect of the consumption of filtered coffee on homocysteine levels was significant only in those who consumed more than 500 ml/day (P = 0.043). Although our findings cannot be evidence for causality, they can be the basis for hypotheses about the relation between homocysteine and coffee that can partially explain the mechanisms by which elevated homocysteine levels may influence coronary risk.
"If tHcy metabolism is impaired, an increase in SAH level and a decrease in the SAM:SAH ratio inhibit transmethylation reactions (Miller et al. 1994; Loehrer et al. 1996; Yi et al. 2000). Studies indicate that actively drinking patients with alcoholism (Bleich et al. 2005), and individuals who consume more coffee than 500 ml/d (Panagiotakos et al. 2004), have increased levels of tHcy. Ethanol has been shown to produce a stimulatory action on PE biosynthesis after chronic ingestion (Carrasco et al. 1996). "
[Show abstract][Hide abstract] ABSTRACT: The effects of high dietary levels of phosphatidylethanolamine (PE) on plasma concentrations of homocysteine (tHcy) have not previously been studied. Eighteen mink (Mustela vison) studied were fed one of three diets during a 25 d period in a parallel-group design. The compared diets had 0, 17 and 67 % extracted lipids from natural gas-utilising bacteria (LNGB), which were rich in PE. The group with 0 % LNGB was fed a diet of 100 % soyabean oil (SB diet). Phospholipids are the main lipid components in LNGB and Methylococcus capsulatus is the main bacteria (90 %). The fasting plasma concentration of tHcy was significantly higher when the mink consumed the diet with 67 % LNGB than when they consumed the SB diet (P=0.039). A significantly lower glutathione peroxidase activity was observed in mink consuming the 17 % LNGB diet or the 67 % LNGB diet than was observed in mink fed the SB diet. The lack of significant differences in the level of plasma PE due to the diets indicates that most of the PE from the 67 % LNGB diet was converted to phosphatidylcholine (PC) in the liver. It has previously been hypothesised that phosphatidylethanolamine N-methyltransferase is an important source of tHcy. The present results indicate that plasma tHcy is at least partly regulated by phospholipid methylation from PE to PC. This methylation reaction is a regulator of physiological importance.
British Journal Of Nutrition 12/2005; 94(5):684-90. DOI:10.1079/BJN20051549 · 3.45 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: This study investigated the role of hyperhomocysteinaemia as a risk factor in Sudanese adults suffering from cardiovascular disease or malaria and children with protein-energy malnutrition. Mean total plasma homocysteine levels (micromol/L) were significantly higher in patients with coronary heart disease (17.64; SD 11.68) recurrent venous thrombosis (5.06; SD 10.55) and recurrent malaria (13.61; SD 4.82) than in healthy adult controls (7.85; SD 3.39). The mean homocysteine level was also significantly higher in children with protein-energy malnutrition (8.41; SD 1.61) than in healthy control children (5.72; SD 1.99).
Eastern Mediterranean health journal = La revue de santé de la Méditerranée orientale = al-Majallah al-ṣiḥḥīyah li-sharq al-mutawassiṭ 01/2009; 15(6):1432-9.
[Show abstract][Hide abstract] ABSTRACT: Elevated plasma levels of the amino acid homocysteine have been associated with schizophrenia, particularly in young male patients. Among other factors, low folate and vitamin B12 levels have been implicated in the increase in homocysteine. In order to investigate this association, we determined plasma homocysteine, folate and B12 levels in 97 (67 males and 30 females) inpatients with chronic schizophrenia and 103 (46 males and 57 females) controls. Patients and controls did not differ in folate or B12 levels, after adjusting for age. Patients with schizophrenia had higher plasma homocysteine than controls (mean=15.42 micromol/l in cases versus 11.54 micromol/l in controls: F(1,195)=17.978; p<0.001). This difference persisted after controlling for folate and B12 concentrations. Both male and female patients had increased plasma homocysteine compared to controls [(males: mean=16.61 micromol/l in cases versus mean=13.72 in controls: F(1,110)=5.54; p=0.020) (females: mean=12.78 micromol/l in cases versus mean=9.79 micromol/l in controls: F(1,84)=13.54; p<0.001)]. When dividing our sample into two age groups (age < and > or =50 years), both young and older females and younger males with schizophrenia had increased plasma homocysteine compared to controls. We therefore suggest that homocysteinemia is a general risk factor for schizophrenia. We further suggest that it is not limited to young male patients and is not necessarily associated with low folate or B12 levels.
Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2007; 31(6):1289-96. DOI:10.1016/j.pnpbp.2007.05.011 · 3.69 Impact Factor
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