Hyperhomocysteinemia
Cystathionine beta-Synthase
Vitamin B 12
Folic Acid
Methylenetetrahydrofolate Reductase (NADPH2)
Betaine-Homocysteine S-Methyltransferase
Folic Acid Deficiency
Vitamin B Deficiency
Vitamin B 12 Deficiency
Pyridoxine
Oxidoreductases Acting on CH-NH Group Donors
Homocystine
Vitamin B 6
Homocystinuria
5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase
S-Adenosylhomocysteine
5,10-Methylenetetrahydrofolate Reductase (FADH2)
Vitamin B 6 Deficiency
Betaine
Methylmalonic Acid
Cystathionine gamma-Lyase
Thrombophilia
S-Adenosylmethionine
Risk Factors
Cystathionine
Amino Acid Metabolism, Inborn Errors
Dietary Supplements
Vascular Diseases
Glycine N-Methyltransferase
Hematinics
Adenosylhomocysteinase
Togo
Choline Deficiency
Lipotropic Agents
Endothelium, Vascular
Dietary Services
Arteriosclerosis
Transcobalamins
Choline
Disease Models, Animal
Cardiovascular Diseases
Genotype
Hydrogen Sulfide
Protein C Deficiency
Oxidative Stress
Factor V
Protein S Deficiency
Diet, Vegetarian
Kidney Failure, Chronic
Rats, Wistar
Heterozygote
Endothelial dysfunction by acute hyperhomocyst(e)inaemia: restoration by folic acid. (1/735)
Recent evidence demonstrates that hyperhomocyst(e)inaemia is a novel risk factor for cardiovascular diseases. In patients with chronic hyperhomocyst(e)inaemia, endothelial function is impaired. However, whether hyperhomocyst(e)inaemia per se is a cause or an epiphenomenon of endothelial dysfunction remains unknown. In this study, we examined the effects of methionine-induced acute hyperhomocyst(e)inaemia on human endothelial function. In healthy volunteers we administered methionine (0.1 g/kg body weight, per os), a substrate of homocyst(e)ine, with or without folic acid (20 mg, per os) and examined flow-mediated vasodilatation of the brachial artery by high-resolution ultrasonography as a non-invasive measure of endothelial function. We also measured plasma levels of homocyst(e)ine before and 3, 8 and 24 h after methionine loading. Methionine administration increased plasma levels of homocyst(e)ine by four times the basal level at 8 h (P<0.0001, ANOVA). The plasma levels returned to baseline at 24 h. Flow-mediated vasodilatation was significantly decreased to half of the baseline value at 8 h and returned to baseline at 24 h (P<0.0001, ANOVA), whereas endothelium-independent vasodilatation by glyceryl trinitrate was not affected by the methionine loading. Co-administration of folic acid did not attenuate methionine-induced hyperhomocyst(e)inaemia but completely prevented endothelial dysfunction. Our results suggest that in humans a methionine-rich diet may acutely impair endothelial function, which can be prevented by folic acid supplementation. (+info)Demonstration of rapid onset vascular endothelial dysfunction after hyperhomocysteinemia: an effect reversible with vitamin C therapy. (2/735)
BACKGROUND: Hyperhomocysteinemia is a major and independent risk factor for vascular disease. The mechanisms by which homocysteine promotes atherosclerosis are not well understood. We hypothesized that elevated homocysteine concentrations are associated with rapid onset endothelial dysfunction, which is mediated through oxidant stress mechanisms and can be inhibited by the antioxidant vitamin C. METHODS AND RESULTS: We studied 17 healthy volunteers (10 male and 7 female) aged 33 (range 21 to 59) years. Brachial artery diameter responses to hyperemic flow (endothelium dependent), and glyceryltrinitrate (GTN, endothelium independent) were measured with high resolution ultrasound at 0 hours (fasting), 2 hours, and 4 hours after (1) oral methionine (L-methionine 100 mg/kg), (2) oral methionine preceded by vitamin C (1g/day, for 1 week), and (3) placebo, on separate days and in random order. Plasma homocysteine increased (0 hours, 12.8+/-1.4; 2 hours, 25.4+/-2.5; and 4 hours, 31. 2+/-3.1 micromol/l, P<0.001), and flow-mediated dilatation fell (0 hours, 4.3+/-0.7; 2 hours, 1.1+/-0.9; and 4 hours, -0.7+/-0.8%) after oral L-methionine. There was an inverse linear relationship between homocysteine concentration and flow-mediated dilatation (P<0. 001). Pretreatment with vitamin C did not affect the rise in homocysteine concentrations after methionine (0 hours, 13.6+/-1.6; 2 hours, 28.3+/-2.9; and 4 hours, 33.8+/-3.7 micromol/l, P=0.27), but did ameliorate the reduction in flow-mediated dilatation (0 hours, 4. 0+/-1.0; 2 hours, 3.5+/-1.2 and 4 hours, 2.8+/-0.7%, P=0.02). GTN-induced endothelium independent brachial artery dilatation was not affected after methionine or methionine preceded by vitamin C. CONCLUSIONS: We conclude that an elevation in homocysteine concentration is associated with an acute impairment of vascular endothelial function that can be prevented by pretreatment with vitamin C in healthy subjects. Our results support the hypothesis that the adverse effects of homocysteine on vascular endothelial cells are mediated through oxidative stress mechanisms. (+info)Prevalence and determinants of hyperhomocysteinemia in hemodialysis and peritoneal dialysis. (3/735)
BACKGROUND: Hyperhomocysteinemia is an independent risk factor for atherosclerotic complications in patients with end-stage renal disease, although the mechanisms remain unclear. The major determinants of plasma homocysteine concentration are usually folate, vitamin B12, pyridoxal 5'-phosphate (vitamin B6), and glomerular filtration rate. METHODS: We measured factors, including plasma folate, vitamin B12, vitamin B6, creatinine, as well as the dose and duration of dialysis, that might affect plasma homocysteine concentrations in 130 patients on hemodialysis (HD) and compared these observations with those in 46 patients on peritoneal dialysis (PD). Independent determinants of total homocysteine were identified using a multiple logistical regression analysis. RESULTS: Total homocysteine values averaged 29.8 mumol/liter in HD patients, significantly higher than the mean value of 19.9 mumol/liter observed in patients on PD (P < 0.001). The prevalence of hyperhomocysteinemia was 90.8% among HD patients, significantly higher than the prevalence of 67.4% among PD patients. Folate values in HD patients averaged 45.5 nmol/liter and were significantly lower than in PD patients (104.2 nmol/liter, P < 0.001). For patients on HD, the only determinant of total homocysteine concentration was plasma folate (r = -0.31, P < 0.001). In contrast, for PD patients, total homocysteine did not correlate with plasma folate, vitamin B12, or vitamin B6. CONCLUSIONS: Hyperhomocysteinemia is more prevalent and intense in HD patients compared with those on PD. The homocysteine response may become refractory to excess folate supplementation in PD patients. (+info)Hyperhomocysteinemia: a risk factor for ischemic stroke in children. (4/735)
BACKGROUND: Moderate hyperhomocysteinemia is a risk factor for arterial vascular disease and venous thrombosis in adults. We performed a case-control study to assess a possible relation between moderate hyperhomocysteinemia and ischemic stroke in Dutch children (age range, 0 to 18 years). METHODS AND RESULTS: We measured plasma total homocysteine levels (tHcy) in 45 patients with ischemic stroke and in 234 controls. Hyperhomocysteinemia was defined as a tHcy above the 95th percentile regression line for the respective age of the controls. Hyperhomocysteinemia was present in 8 (18%) of the 45 patients with ischemic stroke. The odds ratio was 4.4 (95% CI, 1.7 to 11.6). CONCLUSIONS: We conclude that moderate hyperhomocysteinemia is a risk factor for ischemic stroke in children. (+info)Hyperhomocysteinemia and hypofibrinolysis in young adults with ischemic stroke. (5/735)
BACKGROUND AND PURPOSE: Data from epidemiological and case-control studies suggest that increased total homocysteine (tHcy) levels are associated with increased risk for thromboembolic disease. The mechanisms by which hyperhomocysteinemia contributes to thrombogenesis are incompletely understood. The main objectives of this study of young ischemic stroke patients were (1) to examine fasting and post-methionine load levels of tHcy, (2) to ascertain the genotype frequency of the C677CT mutation in the methylenetetrahydrofolate reductase gene (TT genotype), and (3) to study the possible interaction between plasma tHcy levels and fibrinolytic factors. METHODS: This case-control study was based on 80 consecutive patients aged 18 to 44 years admitted between January 1992 and May 1996 as a result of a first-ever ischemic stroke. Forty-one healthy control subjects were recruited. Measurement of fasting tHcy and post-methionine load levels and evaluation of the fibrinolytic system were undertaken at least 3 months (mean, 5.1+/-1. 9 months) after admission. Genotyping of the methylenetetrahydrofolate reductase gene was performed. RESULTS: Although the increase after methionine loading (ie, postload tHcy minus fasting-level tHcy) was significantly higher among patients, there was no difference in fasting and postload tHcy levels. After adjustment for conventional risk factors, elevated postload increase tHcy levels were associated with a 4.8-fold increased risk of ischemic stroke. There was no difference between patients and control subjects in either TT genotype frequency or T allele frequency. Abnormal response to methionine loading was associated with higher tissue plasminogen activator (tPA) mass concentration, higher plasminogen activator inhibitor-1 levels, and lower tPA activity. After adjustment for age, sex, body mass index, serum cholesterol, and triglycerides, an abnormal increase in postload tHcy levels remained significantly associated with tPA mass concentration levels (P=0.03). CONCLUSIONS: A moderately elevated increase in tHcy levels after methionine loading was associated with an increased risk for ischemic stroke in young adults. In contrast, fasting tHcy levels did not differ between patients and controls. A moderately elevated increase in tHcy after methionine loading may provide a additional thrombogenic risk mediated in part by interactions with the fibrinolytic system. In young stroke patients, a methionine loading test to detect hyperhomocysteinemia should always be considered in the convalescent phase of the disease. (+info)Peritoneal elimination of homocysteine moieties in continuous ambulatory peritoneal dialysis patients. (6/735)
BACKGROUND: The amount of total homocysteine eliminated by peritoneal dialysis and its relationship to peritoneal transport characteristics in continuous ambulatory peritoneal dialysis (CAPD) patients are unknown. METHODS: The influence of total homocysteine, folate, and vitamin B12 plasma concentrations, serum albumin levels, age, sex, dialysate to plasma ratio (D/P) creatinine, D/D0 glucose, D/P albumin, dialysate effluent volume, and effluent albumin on the daily peritoneal excretion of total homocysteine was investigated in 39 CAPD patients. The relationship of D/P creatinine to D/P total homocysteine, D/P free homocysteine, and D/P protein-bound homocysteine was analyzed additionally in a subgroup of 25 patients. RESULTS: We observed a significant influence of plasma total homocysteine concentrations (P = 0.0001) of the daily dialysate effluent volume (P = 0.0221) and of the D/P creatinine (P = 0.0132) on peritoneal elimination of total homocysteine. The daily peritoneal excretion of total homocysteine was 38.94 +/- 20.82 mumol (5.27 +/- 2.81 mg). There was a positive linear association of the daily total homocysteine elimination with plasma total homocysteine concentrations (P = 0.0001). A significant linear correlation was observed between D/P creatinine and D/P total homocysteine (P = 0.0001), D/P free homocysteine (P = 0.0001), as well as D/P protein-bound homocysteine (P = 0.0001). CONCLUSIONS: The peritoneal elimination of total homocysteine primarily depends on the plasma total homocysteine concentration. Elevated total homocysteine plasma levels cannot be reduced efficiently by peritoneal dialysis. (+info)Hyperhomocysteinemia but not the C677T mutation of methylenetetrahydrofolate reductase is an independent risk determinant of carotid wall thickening. The Perth Carotid Ultrasound Disease Assessment Study (CUDAS) (7/735)
BACKGROUND: Hyperhomocysteinemia has been identified as a potential risk factor for atherosclerosis. This study examined whether a modest elevation of plasma total homocysteine (tHcy) was an independent risk factor for increased carotid artery intimal-medial wall thickness (IMT) and focal plaque formation in a large, randomly selected community population. We also examined whether vitamin cofactors and the C677T genetic mutation of the methylenetetrahydrofolate reductase (MTHFR) enzyme were major contributors to elevated plasma tHcy and carotid vascular disease. METHODS AND RESULTS: In 1111 subjects (558 men, 553 women) 52+/-13 years old (mean+/-SD; range, 27 to 77 years) recruited from a random electoral roll survey, we measured fasting tHcy and performed bilateral carotid B-mode ultrasound. For the total population, mean tHcy was 12.1+/-4.0 micromol/L. Plasma tHcy levels were correlated with IMT (Spearman rank rs=0.31, P=0.0001). After adjustment for age, sex, and other conventional risk factors, subjects in the highest versus the lowest quartile of tHcy had an odds ratio of 2.60 (95% CI, 1.51 to 4.45) for increased IMT and 1.76 (95% CI, 1.10 to 2.82) for plaque. Serum and dietary folate levels and the C677T mutation in MTHFR were independent determinants of tHcy (all P=0.0001). The mutant homozygotes (10% of the population) had higher mean tHcy than heterozygotes or those without the mutation (14.2 versus 12.3 versus 11.6 micromol/L, respectively, P=0.0001). The inverse association of folate levels with tHcy was steeper in the mutant homozygotes. Despite this, the C677T MTHFR mutation was not independently predictive of increased carotid IMT or plaque formation. CONCLUSIONS: Mild hyperhomocysteinemia is an independent risk factor for increased carotid artery wall thickness and plaque formation in a general population. Lower levels of dietary folate intake and the C677T mutation in MTHFR are important causes of mild hyperhomocysteinemia and may therefore contribute to vascular disease in the community. (+info)Enhanced in vivo lipid peroxidation at elevated plasma total homocysteine levels. (8/735)
An elevated plasma total homocysteine level (tHcy) is considered an independent risk factor for atherosclerosis. The mechanisms by which hyperhomocysteinemia induces atherosclerosis are only partially understood, but promotion of LDL oxidation and endothelial injury have been suggested. The purpose of this study was to test the hypothesis that a high plasma tHcy is associated in men with increased in vivo lipid peroxidation, as measured by plasma F2-isoprostane concentrations. We investigated this association in a subset of the participants in the Antioxidant Supplementation in Atherosclerosis Prevention (ASAP) study. Of 256 male participants, a subsample of 100 consecutive men was selected for F2-isoprostane assays. The mean tHcy was 11.0 micromol/L, and the mean F2-isoprostanes was 29.6 ng/L. The simple correlation coefficient for association between tHcy and F2-isoprostane was 0.40 (P<0.001). In a linear regression model, the variables with the strongest associations with F2-isoprostane were tHcy (standardized coefficient 0.33, P<0.001), serum triglycerides (0.21, P=0.042), carbohydrate-deficient transferrin (0.15, P=0.132), and plasma lipid-standardized alpha-tocopherol (-0.11, P=0.252) (R2=0.24, P<0. 001 for model). Plasma F2-isoprostane levels increased linearly across quintiles of tHcy (P<0.001). The unadjusted mean (95% confidence interval) F2-isoprostanes was 47.5% greater in the highest tHcy quintile (37.4, 31.1 to 43.6 ng/L) than in the lowest quintile (25.3, 21.3 to 29.3 ng/L). Adjustment for the strongest other determinants of F2-isoprostane reduced this difference to 28. 2% (P=0.010). Our present data suggest that elevated fasting plasma tHcy is associated with enhanced in vivo lipid peroxidation in men. (+info)Hyperhomocysteinemia is a medical condition characterized by an excessively high level of homocysteine, an amino acid, in the blood. Generally, a level of 15 micromoles per liter (μmol/L) or higher is considered elevated.
Homocysteine is a byproduct of methionine metabolism, an essential amino acid obtained from dietary proteins. Normally, homocysteine gets converted back to methionine with the help of vitamin B12 and folate (vitamin B9), or it can be converted to another amino acid, cysteine, with the aid of vitamin B6.
Hyperhomocysteinemia can occur due to genetic defects in these enzymes, nutritional deficiencies of vitamins B12, B6, or folate, renal insufficiency, or aging. High homocysteine levels are associated with increased risks of cardiovascular diseases, including atherosclerosis, thrombosis, and stroke. It may also contribute to neurodegenerative disorders like Alzheimer's disease and cognitive decline.
It is essential to diagnose and manage hyperhomocysteinemia early to prevent potential complications. Treatment typically involves dietary modifications, supplementation of the deficient vitamins, and, in some cases, medication.
Homocysteine is an amino acid that is formed in the body during the metabolism of another amino acid called methionine. It's an important intermediate in various biochemical reactions, including the synthesis of proteins, neurotransmitters, and other molecules. However, elevated levels of homocysteine in the blood (a condition known as hyperhomocysteinemia) have been linked to several health issues, such as cardiovascular disease, stroke, and cognitive decline.
Homocysteine can be converted back to methionine with the help of vitamin B12 and a cofactor called betaine, or it can be converted to another amino acid called cystathionine with the help of vitamin B6 and folate (vitamin B9). Imbalances in these vitamins and other factors can lead to an increase in homocysteine levels.
It is crucial to maintain normal homocysteine levels for overall health, as high levels may contribute to the development of various diseases. Regular monitoring and maintaining a balanced diet rich in folate, vitamin B6, and vitamin B12 can help regulate homocysteine levels and reduce the risk of related health issues.
Cystathionine beta-synthase (CBS) is an enzyme that plays a crucial role in the metabolic pathway responsible for the production of the amino acid cysteine from homocysteine. CBS catalyzes the condensation of serine with homocysteine to form cystathionine, which is subsequently hydrolyzed to cysteine and alpha-ketobutyrate by another enzyme called cystathionine gamma-lyase.
CBS requires the cofactor pyridoxal 5'-phosphate (PLP) for its activity and is primarily located in the liver, where it helps regulate homocysteine levels in the body. Elevated levels of homocysteine have been linked to various health issues, including cardiovascular disease and neurological disorders.
In addition to its role in cysteine synthesis, CBS also contributes to the transsulfuration pathway, which is involved in the detoxification of methionine and the production of glutathione, an essential antioxidant in the body. Genetic mutations in the CBS gene can lead to conditions such as homocystinuria, a rare inherited metabolic disorder characterized by elevated levels of homocysteine and methionine in the blood and urine.
Vitamin B12, also known as cobalamin, is a water-soluble vitamin that plays a crucial role in the synthesis of DNA, formation of red blood cells, and maintenance of the nervous system. It is involved in the metabolism of every cell in the body, particularly affecting DNA regulation and neurological function.
Vitamin B12 is unique among vitamins because it contains a metal ion, cobalt, from which its name is derived. This vitamin can be synthesized only by certain types of bacteria and is not produced by plants or animals. The major sources of vitamin B12 in the human diet include animal-derived foods such as meat, fish, poultry, eggs, and dairy products, as well as fortified plant-based milk alternatives and breakfast cereals.
Deficiency in vitamin B12 can lead to various health issues, including megaloblastic anemia, fatigue, neurological symptoms such as numbness and tingling in the extremities, memory loss, and depression. Since vitamin B12 is not readily available from plant-based sources, vegetarians and vegans are at a higher risk of deficiency and may require supplementation or fortified foods to meet their daily requirements.
Folic acid is the synthetic form of folate, a type of B vitamin (B9). It is widely used in dietary supplements and fortified foods because it is more stable and has a longer shelf life than folate. Folate is essential for normal cell growth and metabolism, and it plays a critical role in the formation of DNA and RNA, the body's genetic material. Folic acid is also crucial during early pregnancy to prevent birth defects of the brain and spine called neural tube defects.
Medical Definition: "Folic acid is the synthetic form of folate (vitamin B9), a water-soluble vitamin involved in DNA synthesis, repair, and methylation. It is used in dietary supplementation and food fortification due to its stability and longer shelf life compared to folate. Folic acid is critical for normal cell growth, development, and red blood cell production."
Methionine is an essential amino acid, which means that it cannot be synthesized by the human body and must be obtained through the diet. It plays a crucial role in various biological processes, including:
1. Protein synthesis: Methionine is one of the building blocks of proteins, helping to create new proteins and maintain the structure and function of cells.
2. Methylation: Methionine serves as a methyl group donor in various biochemical reactions, which are essential for DNA synthesis, gene regulation, and neurotransmitter production.
3. Antioxidant defense: Methionine can be converted to cysteine, which is involved in the formation of glutathione, a potent antioxidant that helps protect cells from oxidative damage.
4. Homocysteine metabolism: Methionine is involved in the conversion of homocysteine back to methionine through a process called remethylation, which is essential for maintaining normal homocysteine levels and preventing cardiovascular disease.
5. Fat metabolism: Methionine helps facilitate the breakdown and metabolism of fats in the body.
Foods rich in methionine include meat, fish, dairy products, eggs, and some nuts and seeds.
Betaine-Homocysteine S-Methyltransferase (BHMT) is an enzyme that catalyzes the methylation of homocysteine to methionine using betaine as a methyl donor. This reaction plays a crucial role in maintaining the homeostasis of methionine and homocysteine, which are important for various biological processes such as methylation reactions, protein synthesis, and neurotransmitter production.
The BHMT enzyme is primarily found in the liver and kidneys, where it helps to regulate the levels of homocysteine in the body. Elevated levels of homocysteine have been linked to several health issues, including cardiovascular disease, neurological disorders, and bone diseases. Therefore, BHMT plays an essential role in maintaining overall health by regulating homocysteine metabolism.
Folic Acid Deficiency is a condition characterized by insufficient levels of folic acid (Vitamin B9) in the body. Folic acid plays an essential role in the synthesis of DNA and RNA, the production of red blood cells, and the prevention of neural tube defects during fetal development.
A deficiency in folic acid can lead to a variety of health issues, including:
- Megaloblastic anemia: A type of anemia characterized by large, structurally abnormal, immature red blood cells (megaloblasts) that are unable to function properly. This results in fatigue, weakness, shortness of breath, and a pale appearance.
- Neural tube defects: In pregnant women, folic acid deficiency can increase the risk of neural tube defects, such as spina bifida and anencephaly, in the developing fetus.
- Developmental delays and neurological disorders: In infants and children, folic acid deficiency during pregnancy can lead to developmental delays, learning difficulties, and neurological disorders.
- Increased risk of cardiovascular disease: Folate plays a role in maintaining healthy homocysteine levels. Deficiency can result in elevated homocysteine levels, which is an independent risk factor for cardiovascular disease.
Folic acid deficiency can be caused by various factors, including poor dietary intake, malabsorption syndromes (such as celiac disease or Crohn's disease), pregnancy, alcoholism, certain medications (like methotrexate and phenytoin), and genetic disorders affecting folate metabolism. To prevent or treat folic acid deficiency, dietary supplementation with folic acid is often recommended, especially for pregnant women and individuals at risk of deficiency.
Vitamin B deficiency refers to a condition where an individual's body lacks adequate amounts of one or more essential Vitamin B compounds, including Vitamin B1 (thiamin), Vitamin B2 (riboflavin), Vitamin B3 (niacin), Vitamin B5 (pantothenic acid), Vitamin B6 (pyridoxine), Vitamin B7 (biotin), Vitamin B9 (folate), and Vitamin B12 (cobalamin). These water-soluble vitamins play crucial roles in various bodily functions, such as energy production, nerve function, DNA repair, and the formation of red blood cells.
Deficiency in any of these Vitamin B compounds can lead to specific health issues. For instance:
1. Vitamin B1 (thiamin) deficiency can cause beriberi, a condition characterized by muscle weakness, peripheral neuropathy, and heart failure.
2. Vitamin B2 (riboflavin) deficiency may result in ariboflavinosis, which presents with inflammation of the mouth and tongue, anemia, and skin disorders.
3. Vitamin B3 (niacin) deficiency can lead to pellagra, marked by diarrhea, dermatitis, dementia, and, if left untreated, death.
4. Vitamin B5 (pantothenic acid) deficiency is rare but can cause acne-like skin lesions and neurological symptoms.
5. Vitamin B6 (pyridoxine) deficiency may result in anemia, peripheral neuropathy, seizures, and skin disorders.
6. Vitamin B7 (biotin) deficiency can cause hair loss, skin rashes, and neurological symptoms.
7. Vitamin B9 (folate) deficiency can lead to megaloblastic anemia, neural tube defects in fetuses during pregnancy, and increased homocysteine levels, which may contribute to cardiovascular disease.
8. Vitamin B12 (cobalamin) deficiency can cause pernicious anemia, characterized by fatigue, weakness, neurological symptoms, and, if left untreated, irreversible nerve damage.
Deficiencies in these vitamins can arise from inadequate dietary intake, malabsorption syndromes, or certain medications that interfere with absorption or metabolism. It is essential to maintain a balanced diet and consider supplementation if necessary under the guidance of a healthcare professional.
Vitamin B12 deficiency is a condition characterized by insufficient levels of vitamin B12 in the body, leading to impaired production of red blood cells, nerve function damage, and potential neurological complications. Vitamin B12 is an essential nutrient that plays a crucial role in DNA synthesis, fatty acid metabolism, and maintaining the health of the nervous system.
The medical definition of vitamin B12 deficiency includes:
1. Reduced serum or whole blood vitamin B12 concentrations (typically below 200 pg/mL or 145 pmol/L)
2. Presence of clinical symptoms and signs, such as:
* Fatigue, weakness, and lethargy
* Pale skin, shortness of breath, and heart palpitations due to anemia (megaloblastic or macrocytic anemia)
* Neurological symptoms like numbness, tingling, or burning sensations in the hands and feet (peripheral neuropathy), balance problems, confusion, memory loss, and depression
3. Laboratory findings consistent with deficiency, such as:
* Increased mean corpuscular volume (MCV) of red blood cells
* Reduced numbers of red and white blood cells and platelets in severe cases
* Elevated homocysteine and methylmalonic acid levels in the blood due to impaired metabolism
The most common causes of vitamin B12 deficiency include dietary insufficiency (common in vegetarians and vegans), pernicious anemia (an autoimmune condition affecting intrinsic factor production), gastrointestinal disorders (such as celiac disease, Crohn's disease, or gastric bypass surgery), and certain medications that interfere with vitamin B12 absorption.
Untreated vitamin B12 deficiency can lead to severe complications, including irreversible nerve damage, cognitive impairment, and increased risk of cardiovascular diseases. Therefore, prompt diagnosis and treatment are essential for preventing long-term health consequences.
Pyridoxine is the chemical name for Vitamin B6. According to the medical definition, Pyridoxine is a water-soluble vitamin that is part of the B-vitamin complex and is essential for the metabolism of proteins, carbohydrates, and fats. It plays a vital role in the regulation of homocysteine levels in the body, the formation of neurotransmitters such as serotonin and dopamine, and the synthesis of hemoglobin.
Pyridoxine can be found naturally in various foods, including whole grains, legumes, vegetables, nuts, seeds, meat, poultry, and fish. It is also available as a dietary supplement and may be prescribed by healthcare providers to treat or prevent certain medical conditions, such as vitamin B6 deficiency, anemia, seizures, and carpal tunnel syndrome.
Like other water-soluble vitamins, Pyridoxine cannot be stored in the body and must be replenished regularly through diet or supplementation. Excessive intake of Pyridoxine can lead to toxicity symptoms such as nerve damage, skin lesions, and light sensitivity.
Oxidoreductases acting on CH-NH group donors are a class of enzymes within the larger group of oxidoreductases, which are responsible for catalyzing oxidation-reduction reactions. Specifically, this subclass of enzymes acts on CH-NH group donors, where the CH-NH group is a chemical functional group consisting of a carbon atom (C) bonded to a nitrogen atom (N) via a single covalent bond.
These enzymes play a crucial role in various biological processes by transferring electrons from the CH-NH group donor to an acceptor molecule, which results in the oxidation of the donor and reduction of the acceptor. This process can lead to the formation or breakdown of chemical bonds, and plays a key role in metabolic pathways such as amino acid degradation and nitrogen fixation.
Examples of enzymes that fall within this class include:
* Amino oxidases, which catalyze the oxidative deamination of amino acids to produce alpha-keto acids, ammonia, and hydrogen peroxide.
* Transaminases, which transfer an amino group from one molecule to another, often in the process of amino acid biosynthesis or degradation.
* Amine oxidoreductases, which catalyze the oxidation of primary amines to aldehydes and secondary amines to ketones, with the concomitant reduction of molecular oxygen to hydrogen peroxide.
Homocysteine is an amino acid that is formed from the metabolism of another amino acid called methionine. It is not normally present in significant amounts in the diet, but it can be elevated in some people due to genetic factors or nutritional deficiencies (such as a lack of vitamin B12, folate, or betaine). Elevated levels of homocysteine in the blood have been linked to an increased risk of cardiovascular disease, including heart attack and stroke. Homocysteine can be converted back to methionine through a process that requires the presence of vitamin B12, folate, and betaine. It can also be converted to another amino acid called cystathionine through a reaction that requires the enzyme cystathionine beta-synthase and the cofactor vitamin B6.
Vitamin B Complex refers to a group of water-soluble vitamins that play essential roles in cell metabolism, cellular function, and formation of red blood cells. This complex includes 8 distinct vitamins, all of which were originally thought to be the same vitamin when first discovered. They are now known to have individual structures and specific functions.
1. Vitamin B1 (Thiamin): Necessary for energy production and nerve function.
2. Vitamin B2 (Riboflavin): Involved in energy production and growth.
3. Vitamin B3 (Niacin): Assists in energy production, DNA repair, and acts as a co-factor for various enzymes.
4. Vitamin B5 (Pantothenic Acid): Plays a role in the synthesis of Coenzyme A, which is vital for fatty acid metabolism.
5. Vitamin B6 (Pyridoxine): Needed for protein metabolism, neurotransmitter synthesis, hemoglobin formation, and immune function.
6. Vitamin B7 (Biotin): Involved in fatty acid synthesis, glucose metabolism, and nail and hair health.
7. Vitamin B9 (Folate or Folic Acid): Essential for DNA replication, cell division, and the production of red blood cells.
8. Vitamin B12 (Cobalamin): Necessary for nerve function, DNA synthesis, and the production of red blood cells.
These vitamins are often found together in various foods, and a balanced diet usually provides sufficient amounts of each. Deficiencies can lead to specific health issues related to the functions of each particular vitamin.
Medical Definition of Vitamin B6:
Vitamin B6, also known as pyridoxine, is a water-soluble vitamin that plays a crucial role in various bodily functions. It is involved in the process of making serotonin and norepinephrine, which are chemicals that transmit signals in the brain. Vitamin B6 is also necessary for the formation of myelin, a protein layer that forms around nerve cells. Additionally, it helps the body to metabolize proteins, carbohydrates, and fats, and is involved in the creation of red blood cells.
Vitamin B6 can be found in a wide variety of foods, including poultry, seafood, bananas, potatoes, and fortified cereals. A deficiency in vitamin B6 can lead to anemia, confusion, and a weakened immune system. On the other hand, excessive intake of vitamin B6 can cause nerve damage and skin lesions. It is important to maintain appropriate levels of vitamin B6 through a balanced diet and, if necessary, supplementation under the guidance of a healthcare provider.
Homocystinuria is a genetic disorder characterized by the accumulation of homocysteine and its metabolites in the body due to a deficiency in the enzyme cystathionine beta-synthase (CBS). This enzyme is responsible for converting homocysteine to cystathionine, which is a critical step in the metabolic pathway that breaks down methionine.
As a result of this deficiency, homocysteine levels in the blood increase and can lead to various health problems, including neurological impairment, ocular abnormalities (such as ectopia lentis or dislocation of the lens), skeletal abnormalities (such as Marfan-like features), and vascular complications.
Homocystinuria can be diagnosed through newborn screening or by measuring homocysteine levels in the blood or urine. Treatment typically involves a low-methionine diet, supplementation with vitamin B6 (pyridoxine), betaine, and/or methylcobalamin (a form of vitamin B12) to help reduce homocysteine levels and prevent complications associated with the disorder.
5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase is also known as Methionine Synthase. It is a vital enzyme in the human body that plays a crucial role in methionine metabolism and homocysteine regulation.
The medical definition of 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase is as follows:
A enzyme (EC 2.1.1.13) that catalyzes the methylation of homocysteine to methionine, using 5-methyltetrahydrofolate as a methyl donor. This reaction also requires the cofactor vitamin B12 (cobalamin) as a coenzyme. The enzyme is located in the cytosol of cells and is essential for the synthesis of methionine, which is an important amino acid required for various biological processes such as protein synthesis, methylation reactions, and the formation of neurotransmitters.
Deficiency or dysfunction of this enzyme can lead to several health issues, including homocystinuria, a genetic disorder characterized by elevated levels of homocysteine in the blood, which can cause serious complications such as neurological damage, cardiovascular disease, and skeletal abnormalities.
S-Adenosylhomocysteine (SAH) is a metabolic byproduct formed from the demethylation of various compounds or from the breakdown of S-adenosylmethionine (SAM), which is a major methyl group donor in the body. SAH is rapidly hydrolyzed to homocysteine and adenosine by the enzyme S-adenosylhomocysteine hydrolase. Increased levels of SAH can inhibit many methyltransferases, leading to disturbances in cellular metabolism and potential negative health effects.
Vitamin B6 deficiency refers to the condition in which there is an insufficient amount of vitamin B6 (pyridoxine) in the body. Vitamin B6 is an essential nutrient that plays a crucial role in various bodily functions, including protein metabolism, neurotransmitter synthesis, hemoglobin production, and immune function.
A deficiency in vitamin B6 can lead to several health issues, such as:
1. Anemia: Vitamin B6 is essential for the production of hemoglobin, a protein in red blood cells that carries oxygen throughout the body. A deficiency in this nutrient can lead to anemia, characterized by fatigue, weakness, and shortness of breath.
2. Peripheral neuropathy: Vitamin B6 deficiency can cause nerve damage, leading to symptoms such as numbness, tingling, and pain in the hands and feet.
3. Depression and cognitive impairment: Pyridoxine is necessary for the synthesis of neurotransmitters like serotonin and dopamine, which are involved in mood regulation. A deficiency in vitamin B6 can lead to depression, irritability, and cognitive decline.
4. Seizures: In severe cases, vitamin B6 deficiency can cause seizures due to the impaired synthesis of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter that helps regulate brain activity.
5. Skin changes: A deficiency in this nutrient can also lead to skin changes, such as dryness, scaling, and cracks around the mouth.
Vitamin B6 deficiency is relatively uncommon in developed countries but can occur in individuals with certain medical conditions, such as malabsorption syndromes, alcoholism, kidney disease, or those taking medications that interfere with vitamin B6 metabolism. Additionally, older adults, pregnant women, and breastfeeding mothers may have an increased need for this nutrient, making them more susceptible to deficiency.
Betaine, also known as trimethylglycine, is a naturally occurring compound that can be found in various foods such as beets, spinach, and whole grains. In the body, betaine functions as an osmolyte, helping to regulate water balance in cells, and as a methyl donor, contributing to various metabolic processes including the conversion of homocysteine to methionine.
In medical terms, betaine is also used as a dietary supplement and medication. Betaine hydrochloride is a form of betaine that is sometimes used as a supplement to help with digestion by providing additional stomach acid. Betaine anhydrous, on the other hand, is often used as a supplement for improving athletic performance and promoting liver health.
Betaine has also been studied for its potential role in protecting against various diseases, including cardiovascular disease, diabetes, and neurological disorders. However, more research is needed to fully understand its mechanisms of action and therapeutic potential.
Methylmalonic acid (MMA) is an organic compound that is produced in the human body during the metabolism of certain amino acids, including methionine and threonine. It is a type of fatty acid that is intermediate in the breakdown of these amino acids in the liver and other tissues.
Under normal circumstances, MMA is quickly converted to succinic acid, which is then used in the Krebs cycle to generate energy in the form of ATP. However, when there are deficiencies or mutations in enzymes involved in this metabolic pathway, such as methylmalonyl-CoA mutase, MMA can accumulate in the body and cause methylmalonic acidemia, a rare genetic disorder that affects approximately 1 in every 50,000 to 100,000 individuals worldwide.
Elevated levels of MMA in the blood or urine can be indicative of various metabolic disorders, including methylmalonic acidemia, vitamin B12 deficiency, and renal insufficiency. Therefore, measuring MMA levels is often used as a diagnostic tool to help identify and manage these conditions.
Tetrahydrofolates (THFs) are a type of folate, which is a form of vitamin B9. Folate is essential for the production and maintenance of new cells, especially in DNA synthesis and methylation. THFs are the active forms of folate in the body and are involved in various metabolic processes, including:
1. The conversion of homocysteine to methionine, an amino acid required for protein synthesis and the formation of S-adenosylmethionine (SAM), a major methyl donor in the body.
2. The transfer of one-carbon units in various metabolic reactions, such as the synthesis of purines and pyrimidines, which are essential components of DNA and RNA.
3. The remethylation of homocysteine to methionine, a process that helps maintain normal homocysteine levels in the body. Elevated homocysteine levels have been linked to an increased risk of cardiovascular disease.
THFs can be obtained from dietary sources, such as leafy green vegetables, legumes, and fortified cereals. They can also be synthesized endogenously in the body through the action of the enzyme dihydrofolate reductase (DHFR), which reduces dihydrofolate (DHF) to THF using NADPH as a cofactor.
Deficiencies in folate or impaired THF metabolism can lead to various health issues, including megaloblastic anemia, neural tube defects during fetal development, and an increased risk of cardiovascular disease due to elevated homocysteine levels.
Cystathionine gamma-lyase (CSE or CGL) is an enzyme that plays a role in the metabolism of sulfur-containing amino acids, specifically methionine and cysteine. It catalyzes the conversion of cystathionine to cysteine, releasing α-ketobutyrate and ammonia as byproducts. This reaction also results in the formation of hydrogen sulfide (H2S), a gaseous signaling molecule that has been implicated in various physiological and pathophysiological processes.
Cystathionine gamma-lyase is primarily expressed in the liver, kidney, and brain, and its activity is regulated by several factors, including the availability of its substrates and allosteric modulators like S-adenosylmethionine (SAM) and homocysteine. Dysregulation of CSE has been associated with various diseases, such as cardiovascular disorders, neurodegenerative conditions, and cancer. Therefore, understanding the function and regulation of cystathionine gamma-lyase is crucial for developing novel therapeutic strategies targeting these diseases.
Thrombophilia is a medical condition characterized by an increased tendency to form blood clots (thrombi) due to various genetic or acquired abnormalities in the coagulation system. These abnormalities can lead to a hypercoagulable state, which can cause thrombosis in both veins and arteries. Commonly identified thrombophilias include factor V Leiden mutation, prothrombin G20210A mutation, antithrombin deficiency, protein C deficiency, and protein S deficiency.
Acquired thrombophilias can be caused by various factors such as antiphospholipid antibody syndrome (APS), malignancies, pregnancy, oral contraceptive use, hormone replacement therapy, and certain medical conditions like inflammatory bowel disease or nephrotic syndrome.
It is essential to diagnose thrombophilia accurately, as it may influence the management of venous thromboembolism (VTE) events and guide decisions regarding prophylactic anticoagulation in high-risk situations.
S-Adenosylmethionine (SAMe) is a physiological compound involved in methylation reactions, transulfuration pathways, and aminopropylation processes in the body. It is formed from the coupling of methionine, an essential sulfur-containing amino acid, and adenosine triphosphate (ATP) through the action of methionine adenosyltransferase enzymes.
SAMe serves as a major methyl donor in various biochemical reactions, contributing to the synthesis of numerous compounds such as neurotransmitters, proteins, phospholipids, nucleic acids, and other methylated metabolites. Additionally, SAMe plays a crucial role in the detoxification process within the liver by participating in glutathione production, which is an important antioxidant and detoxifying agent.
In clinical settings, SAMe supplementation has been explored as a potential therapeutic intervention for various conditions, including depression, osteoarthritis, liver diseases, and fibromyalgia, among others. However, its efficacy remains a subject of ongoing research and debate within the medical community.
Medical Definition:
"Risk factors" are any attribute, characteristic or exposure of an individual that increases the likelihood of developing a disease or injury. They can be divided into modifiable and non-modifiable risk factors. Modifiable risk factors are those that can be changed through lifestyle choices or medical treatment, while non-modifiable risk factors are inherent traits such as age, gender, or genetic predisposition. Examples of modifiable risk factors include smoking, alcohol consumption, physical inactivity, and unhealthy diet, while non-modifiable risk factors include age, sex, and family history. It is important to note that having a risk factor does not guarantee that a person will develop the disease, but rather indicates an increased susceptibility.
Cystathionine is a non-proteinogenic amino acid, which means that it is not used in the synthesis of proteins. It is an intermediate in the biosynthetic pathway that converts the amino acid methionine to cysteine in the body. This process involves the removal of a sulfur atom from methionine, resulting in the formation of cystathionine. Further breakdown of cystathionine leads to the production of cysteine and another amino acid called alpha-ketobutyrate.
Cystathionine plays a crucial role in the metabolism of certain sulfur-containing amino acids, and its levels are regulated by an enzyme called cystathionine beta-synthase (CBS). Genetic defects or deficiencies in this enzyme can result in a disorder known as homocystinuria, which is characterized by the accumulation of homocysteine and methionine in the body and an increased risk of various health complications.
In summary, cystathionine is a biologically important amino acid that functions as an intermediate in the conversion of methionine to cysteine, and its levels are tightly regulated by enzymatic processes in the body.
Inborn errors of amino acid metabolism refer to genetic disorders that affect the body's ability to properly break down and process individual amino acids, which are the building blocks of proteins. These disorders can result in an accumulation of toxic levels of certain amino acids or their byproducts in the body, leading to a variety of symptoms and health complications.
There are many different types of inborn errors of amino acid metabolism, each affecting a specific amino acid or group of amino acids. Some examples include:
* Phenylketonuria (PKU): This disorder affects the breakdown of the amino acid phenylalanine, leading to its accumulation in the body and causing brain damage if left untreated.
* Maple syrup urine disease: This disorder affects the breakdown of the branched-chain amino acids leucine, isoleucine, and valine, leading to their accumulation in the body and causing neurological problems.
* Homocystinuria: This disorder affects the breakdown of the amino acid methionine, leading to its accumulation in the body and causing a range of symptoms including developmental delay, intellectual disability, and cardiovascular problems.
Treatment for inborn errors of amino acid metabolism typically involves dietary restrictions or supplementation to manage the levels of affected amino acids in the body. In some cases, medication or other therapies may also be necessary. Early diagnosis and treatment can help prevent or minimize the severity of symptoms and health complications associated with these disorders.
A dietary supplement is a product that contains nutrients, such as vitamins, minerals, amino acids, herbs or other botanicals, and is intended to be taken by mouth, to supplement the diet. Dietary supplements can include a wide range of products, such as vitamin and mineral supplements, herbal supplements, and sports nutrition products.
Dietary supplements are not intended to treat, diagnose, cure, or alleviate the effects of diseases. They are intended to be used as a way to add extra nutrients to the diet or to support specific health functions. It is important to note that dietary supplements are not subject to the same rigorous testing and regulations as drugs, so it is important to choose products carefully and consult with a healthcare provider if you have any questions or concerns about using them.
Vascular diseases are medical conditions that affect the circulatory system, specifically the blood vessels (arteries, veins, and capillaries). These diseases can include conditions such as:
1. Atherosclerosis: The buildup of fats, cholesterol, and other substances in and on the walls of the arteries, which can restrict blood flow.
2. Peripheral Artery Disease (PAD): A condition caused by atherosclerosis where there is narrowing or blockage of the peripheral arteries, most commonly in the legs. This can lead to pain, numbness, and cramping.
3. Coronary Artery Disease (CAD): Atherosclerosis of the coronary arteries that supply blood to the heart muscle. This can lead to chest pain, shortness of breath, or a heart attack.
4. Carotid Artery Disease: Atherosclerosis of the carotid arteries in the neck that supply blood to the brain. This can increase the risk of stroke.
5. Cerebrovascular Disease: Conditions that affect blood flow to the brain, including stroke and transient ischemic attack (TIA or "mini-stroke").
6. Aneurysm: A weakened area in the wall of a blood vessel that causes it to bulge outward and potentially rupture.
7. Deep Vein Thrombosis (DVT): A blood clot that forms in the deep veins, usually in the legs, which can cause pain, swelling, and increased risk of pulmonary embolism if the clot travels to the lungs.
8. Varicose Veins: Swollen, twisted, and often painful veins that have filled with an abnormal collection of blood, usually appearing in the legs.
9. Vasculitis: Inflammation of the blood vessels, which can cause damage and narrowing, leading to reduced blood flow.
10. Raynaud's Phenomenon: A condition where the small arteries that supply blood to the skin become narrowed, causing decreased blood flow, typically in response to cold temperatures or stress.
These are just a few examples of vascular conditions that fall under the umbrella term "cerebrovascular disease." Early diagnosis and treatment can significantly improve outcomes for many of these conditions.
Glycine N-Methyltransferase (GNMT) is an enzyme that plays a crucial role in methionine and homocysteine metabolism. It is primarily found in the liver and to some extent in the kidneys, pancreas, and brain.
GNMT catalyzes the transfer of a methyl group from S-adenosylmethionine (SAM) to glycine, forming S-adenosylhomocysteine (SAH) and sarcosine as products. This reaction helps regulate the levels of SAM, SAH, and homocysteine in the body.
Additionally, GNMT has been shown to have other functions, such as detoxification of xenobiotics and regulation of lipid metabolism. Abnormal GNMT activity or expression has been linked to various diseases, including liver disorders, cardiovascular disease, and cancer.
A diet, in medical terms, refers to the planned and regular consumption of food and drinks. It is a balanced selection of nutrient-rich foods that an individual eats on a daily or periodic basis to meet their energy needs and maintain good health. A well-balanced diet typically includes a variety of fruits, vegetables, whole grains, lean proteins, and low-fat dairy products.
A diet may also be prescribed for therapeutic purposes, such as in the management of certain medical conditions like diabetes, hypertension, or obesity. In these cases, a healthcare professional may recommend specific restrictions or modifications to an individual's regular diet to help manage their condition and improve their overall health.
It is important to note that a healthy and balanced diet should be tailored to an individual's age, gender, body size, activity level, and any underlying medical conditions. Consulting with a healthcare professional, such as a registered dietitian or nutritionist, can help ensure that an individual's dietary needs are being met in a safe and effective way.
Hematinics are a class of medications and dietary supplements that are used to enhance the production of red blood cells or hemoglobin in the body. They typically contain iron, vitamin B12, folic acid, or other nutrients that are essential for the synthesis of hemoglobin and the formation of red blood cells.
Iron is a critical component of hematinics because it plays a central role in the production of hemoglobin, which is the protein in red blood cells that carries oxygen throughout the body. Vitamin B12 and folic acid are also important nutrients for red blood cell production, as they help to regulate the growth and division of red blood cells in the bone marrow.
Hematinics are often prescribed to treat anemia, which is a condition characterized by a low red blood cell count or abnormally low levels of hemoglobin in the blood. Anemia can be caused by a variety of factors, including nutritional deficiencies, chronic diseases, and inherited genetic disorders.
Examples of hematinics include ferrous sulfate (an iron supplement), cyanocobalamin (vitamin B12), and folic acid. These medications are available in various forms, such as tablets, capsules, and liquids, and can be taken orally or by injection. It is important to follow the dosage instructions carefully and to inform your healthcare provider of any other medications you are taking, as hematinics can interact with certain drugs and may cause side effects.
Adenosylhomocysteinase is an enzyme that plays a crucial role in the methionine cycle, which is a biochemical pathway involved in the synthesis and metabolism of various essential molecules in the body. The formal medical definition of adenosylhomocysteinase is:
"An enzyme that catalyzes the reversible conversion of S-adenosylhomocysteine to homocysteine and adenosine. This reaction is the first step in the recycling of methionine, a sulfur-containing amino acid that is essential for various metabolic processes, including the synthesis of proteins, neurotransmitters, and phospholipids."
In simpler terms, adenosylhomocysteinase helps break down S-adenosylhomocysteine, a byproduct of methylation reactions in the body, into its component parts: homocysteine and adenosine. This breakdown is essential for the proper functioning of the methionine cycle and the maintenance of normal levels of homocysteine, which can be toxic at high concentrations.
Deficiencies or mutations in the adenosylhomocysteinase gene can lead to an accumulation of S-adenosylhomocysteine and homocysteine, which can contribute to various health issues, including neurological disorders, cardiovascular disease, and developmental abnormalities.
I'm sorry for any confusion, but "Togo" is not a medical term. It is the name of a country in West Africa, known officially as the Togolese Republic. If you have any questions about medical terminology or health-related topics, please don't hesitate to ask!
Choline deficiency is a condition that occurs when an individual's diet does not provide adequate amounts of choline, which is an essential nutrient required for various bodily functions. Choline plays a crucial role in the synthesis of phospholipids, which are critical components of cell membranes, and it also serves as a precursor to the neurotransmitter acetylcholine, which is involved in memory, muscle control, and other nervous system functions.
Choline deficiency can lead to several health problems, including fatty liver disease, muscle damage, and cognitive impairment. Symptoms of choline deficiency may include fatigue, memory loss, cognitive decline, and peripheral neuropathy. In severe cases, it can also cause liver dysfunction and even liver failure.
It is important to note that choline deficiency is relatively rare in the general population, as many foods contain choline, including eggs, meat, fish, dairy products, and certain vegetables such as broccoli and Brussels sprouts. However, some individuals may be at higher risk of choline deficiency, including pregnant women, postmenopausal women, and those with certain genetic mutations that affect choline metabolism. In these cases, supplementation with choline may be necessary to prevent deficiency.
Lipotropic agents are substances that help to promote the breakdown and removal of fats from the liver. They are often used in weight loss supplements because they can help to speed up the metabolism of fat and prevent the accumulation of excess fat in the liver. Some common lipotropic agents include methionine, choline, inositol, and betaine. These compounds work by increasing the production of lecithin, which helps to emulsify fats in the liver and facilitate their transport out of the body. Additionally, lipotropic agents can also help to protect the liver from damage caused by toxins such as alcohol and drugs.
The endothelium is a thin layer of simple squamous epithelial cells that lines the interior surface of blood vessels, lymphatic vessels, and heart chambers. The vascular endothelium, specifically, refers to the endothelial cells that line the blood vessels. These cells play a crucial role in maintaining vascular homeostasis by regulating vasomotor tone, coagulation, platelet activation, inflammation, and permeability of the vessel wall. They also contribute to the growth and repair of the vascular system and are involved in various pathological processes such as atherosclerosis, hypertension, and diabetes.
Dietary services, also known as food and nutrition services, refer to the provision of medical nutritional therapy and management of food services in healthcare facilities. This includes the assessment, diagnosis, and treatment of nutrition-related problems by a registered dietitian or nutrition professional. Dietary services also involve the planning, preparation, and serving of meals that meet the individualized nutritional needs and preferences of patients, residents, or clients. Additionally, dietary services may include nutrition education and counseling for patients, families, and staff members to promote healthy eating habits and prevent nutrition-related diseases.
Arteriosclerosis is a general term that describes the hardening and stiffening of the artery walls. It's a progressive condition that can occur as a result of aging, or it may be associated with certain risk factors such as high blood pressure, high cholesterol, diabetes, smoking, and a sedentary lifestyle.
The process of arteriosclerosis involves the buildup of plaque, made up of fat, cholesterol, calcium, and other substances, in the inner lining of the artery walls. Over time, this buildup can cause the artery walls to thicken and harden, reducing the flow of oxygen-rich blood to the body's organs and tissues.
Arteriosclerosis can affect any of the body's arteries, but it is most commonly found in the coronary arteries that supply blood to the heart, the cerebral arteries that supply blood to the brain, and the peripheral arteries that supply blood to the limbs. When arteriosclerosis affects the coronary arteries, it can lead to heart disease, angina, or heart attack. When it affects the cerebral arteries, it can lead to stroke or transient ischemic attack (TIA). When it affects the peripheral arteries, it can cause pain, numbness, or weakness in the limbs, and in severe cases, gangrene and amputation.
Transcobalamins are a group of proteins in the human body that are responsible for the transport of vitamin B12, also known as cobalamin. There are three main types of transcobalamins:
1. Transcobalamin I (also known as haptocorrin or R-binders): This is a protein produced in various tissues, including the salivary glands and gastric mucosa. It binds to vitamin B12 in the stomach and protects it from degradation by digestive enzymes. However, this form of vitamin B12 is not available for absorption and must be converted to other forms.
2. Transcobalamin II: This is a protein produced mainly in the kidneys and intestines. It binds to vitamin B12 that has been freed from its binding proteins in the stomach and facilitates its absorption in the intestine. Once absorbed, transcobalamin II transports vitamin B12 to tissues throughout the body.
3. Transcobalamin III (also known as intrinsic factor): This is a protein produced by the parietal cells of the stomach. It binds to vitamin B12 and protects it from degradation in the acidic environment of the stomach. Intrinsic factor is essential for the absorption of vitamin B12 in the intestine, as it facilitates its transport across the intestinal wall.
Deficiencies in transcobalamins can lead to vitamin B12 deficiency, which can result in a range of health problems, including anemia, fatigue, neurological symptoms, and developmental delays in children.
Choline is an essential nutrient that is vital for the normal functioning of all cells, particularly those in the brain and liver. It is a water-soluble compound that is neither a vitamin nor a mineral, but is often grouped with vitamins because it has many similar functions. Choline is a precursor to the neurotransmitter acetylcholine, which plays an important role in memory, mood, and other cognitive processes. It also helps to maintain the structural integrity of cell membranes and is involved in the transport and metabolism of fats.
Choline can be synthesized by the body in small amounts, but it is also found in a variety of foods such as eggs, meat, fish, nuts, and cruciferous vegetables. Some people may require additional choline through supplementation, particularly if they follow a vegetarian or vegan diet, are pregnant or breastfeeding, or have certain medical conditions that affect choline metabolism.
Deficiency in choline can lead to a variety of health problems, including liver disease, muscle damage, and neurological disorders. On the other hand, excessive intake of choline can cause fishy body odor, sweating, and gastrointestinal symptoms such as diarrhea and vomiting. It is important to maintain adequate levels of choline through a balanced diet and, if necessary, supplementation under the guidance of a healthcare professional.
Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.
The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.
Examples of animal disease models include:
1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.
Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.
Cardiovascular diseases (CVDs) are a class of diseases that affect the heart and blood vessels. They are the leading cause of death globally, according to the World Health Organization (WHO). The term "cardiovascular disease" refers to a group of conditions that include:
1. Coronary artery disease (CAD): This is the most common type of heart disease and occurs when the arteries that supply blood to the heart become narrowed or blocked due to the buildup of cholesterol, fat, and other substances in the walls of the arteries. This can lead to chest pain, shortness of breath, or a heart attack.
2. Heart failure: This occurs when the heart is unable to pump blood efficiently to meet the body's needs. It can be caused by various conditions, including coronary artery disease, high blood pressure, and cardiomyopathy.
3. Stroke: A stroke occurs when the blood supply to a part of the brain is interrupted or reduced, often due to a clot or a ruptured blood vessel. This can cause brain damage or death.
4. Peripheral artery disease (PAD): This occurs when the arteries that supply blood to the limbs become narrowed or blocked, leading to pain, numbness, or weakness in the legs or arms.
5. Rheumatic heart disease: This is a complication of untreated strep throat and can cause damage to the heart valves, leading to heart failure or other complications.
6. Congenital heart defects: These are structural problems with the heart that are present at birth. They can range from mild to severe and may require medical intervention.
7. Cardiomyopathy: This is a disease of the heart muscle that makes it harder for the heart to pump blood efficiently. It can be caused by various factors, including genetics, infections, and certain medications.
8. Heart arrhythmias: These are abnormal heart rhythms that can cause the heart to beat too fast, too slow, or irregularly. They can lead to symptoms such as palpitations, dizziness, or fainting.
9. Valvular heart disease: This occurs when one or more of the heart valves become damaged or diseased, leading to problems with blood flow through the heart.
10. Aortic aneurysm and dissection: These are conditions that affect the aorta, the largest artery in the body. An aneurysm is a bulge in the aorta, while a dissection is a tear in the inner layer of the aorta. Both can be life-threatening if not treated promptly.
It's important to note that many of these conditions can be managed or treated with medical interventions such as medications, surgery, or lifestyle changes. If you have any concerns about your heart health, it's important to speak with a healthcare provider.
Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel, obstructing the flow of blood through the circulatory system. When a clot forms in an artery, it can cut off the supply of oxygen and nutrients to the tissues served by that artery, leading to damage or tissue death. If a thrombus forms in the heart, it can cause a heart attack. If a thrombus breaks off and travels through the bloodstream, it can lodge in a smaller vessel, causing blockage and potentially leading to damage in the organ that the vessel supplies. This is known as an embolism.
Thrombosis can occur due to various factors such as injury to the blood vessel wall, abnormalities in blood flow, or changes in the composition of the blood. Certain medical conditions, medications, and lifestyle factors can increase the risk of thrombosis. Treatment typically involves anticoagulant or thrombolytic therapy to dissolve or prevent further growth of the clot, as well as addressing any underlying causes.
Genotype, in genetics, refers to the complete heritable genetic makeup of an individual organism, including all of its genes. It is the set of instructions contained in an organism's DNA for the development and function of that organism. The genotype is the basis for an individual's inherited traits, and it can be contrasted with an individual's phenotype, which refers to the observable physical or biochemical characteristics of an organism that result from the expression of its genes in combination with environmental influences.
It is important to note that an individual's genotype is not necessarily identical to their genetic sequence. Some genes have multiple forms called alleles, and an individual may inherit different alleles for a given gene from each parent. The combination of alleles that an individual inherits for a particular gene is known as their genotype for that gene.
Understanding an individual's genotype can provide important information about their susceptibility to certain diseases, their response to drugs and other treatments, and their risk of passing on inherited genetic disorders to their offspring.
Hydrogen sulfide (H2S) is a colorless, flammable, and extremely toxic gas with a strong odor of rotten eggs. It is a naturally occurring compound that is produced in various industrial processes and is also found in some natural sources like volcanoes, hot springs, and swamps.
In the medical context, hydrogen sulfide is known to have both toxic and therapeutic effects on the human body. At high concentrations, it can cause respiratory failure, unconsciousness, and even death. However, recent studies have shown that at low levels, hydrogen sulfide may act as a signaling molecule in the human body, playing a role in various physiological processes such as regulating blood flow, reducing inflammation, and protecting against oxidative stress.
It's worth noting that exposure to high levels of hydrogen sulfide can be life-threatening, and immediate medical attention is required in case of exposure.
Protein C deficiency is a genetic disorder that affects the body's ability to control blood clotting. Protein C is a protein in the blood that helps regulate the formation of blood clots. When blood clots form too easily or do not dissolve properly, they can block blood vessels and lead to serious medical conditions such as deep vein thrombosis (DVT) or pulmonary embolism (PE).
People with protein C deficiency have lower than normal levels of this protein in their blood, which can increase their risk of developing abnormal blood clots. The condition is usually inherited and present from birth, but it may not cause any symptoms until later in life, such as during pregnancy, after surgery, or due to other factors that increase the risk of blood clots.
Protein C deficiency can be classified into two types: type I and type II. Type I deficiency is characterized by lower than normal levels of both functional and immunoreactive protein C in the blood. Type II deficiency is characterized by normal or near-normal levels of immunoreactive protein C, but reduced functional activity.
Protein C deficiency can be diagnosed through blood tests that measure the level and function of protein C in the blood. Treatment may include anticoagulant medications to prevent blood clots from forming or dissolve existing ones. Regular monitoring of protein C levels and careful management of risk factors for blood clots are also important parts of managing this condition.
Oxidative stress is defined as an imbalance between the production of reactive oxygen species (free radicals) and the body's ability to detoxify them or repair the damage they cause. This imbalance can lead to cellular damage, oxidation of proteins, lipids, and DNA, disruption of cellular functions, and activation of inflammatory responses. Prolonged or excessive oxidative stress has been linked to various health conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and aging-related diseases.
Sarcosine is not a medical condition or disease, but rather it is an organic compound that is classified as a natural amino acid. It is a metabolite that can be found in the human body, and it is involved in various biochemical processes. Specifically, sarcosine is formed from the conversion of the amino acid glycine by the enzyme glycine sarcosine N-methyltransferase (GSMT) and is then converted to glycine betaine (also known as trimethylglycine) by the enzyme betaine-homocysteine S-methyltransferase (BHMT).
Abnormal levels of sarcosine have been found in various disease states, including cancer. Some studies have suggested that high levels of sarcosine in urine or prostate tissue may be associated with an increased risk of developing prostate cancer or a more aggressive form of the disease. However, more research is needed to confirm these findings and establish the clinical significance of sarcosine as a biomarker for cancer or other diseases.
Factor V, also known as proaccelerin or labile factor, is a protein involved in the coagulation cascade, which is a series of chemical reactions that leads to the formation of a blood clot. Factor V acts as a cofactor for the activation of Factor X to Factor Xa, which is a critical step in the coagulation cascade.
When blood vessels are damaged, the coagulation cascade is initiated to prevent excessive bleeding. During this process, Factor V is activated by thrombin, another protein involved in coagulation, and then forms a complex with activated Factor X and calcium ions on the surface of platelets or other cells. This complex converts prothrombin to thrombin, which then converts fibrinogen to fibrin to form a stable clot.
Deficiency or dysfunction of Factor V can lead to bleeding disorders such as hemophilia B or factor V deficiency, while mutations in the gene encoding Factor V can increase the risk of thrombosis, as seen in the Factor V Leiden mutation.
Protein S deficiency is a genetic disorder that affects the body's ability to coagulate blood properly. Protein S is a naturally occurring protein in the blood that helps regulate the clotting process by deactivating clotting factors when they are no longer needed. When Protein S levels are too low, it can lead to an increased risk of abnormal blood clots forming within blood vessels, a condition known as thrombophilia.
There are three types of Protein S deficiency: Type I (quantitative deficiency), Type II (qualitative deficiency), and Type III (dysfunctional protein). These types refer to the amount or function of Protein S in the blood. In Type I, there is a decrease in both free and total Protein S levels. In Type II, there is a decrease in functional Protein S despite normal total Protein S levels. In Type III, there is a decrease in free Protein S with normal total Protein S levels.
Protein S deficiency can be inherited or acquired. Inherited forms of the disorder are caused by genetic mutations and are usually present from birth. Acquired forms of Protein S deficiency can develop later in life due to certain medical conditions, such as liver disease, vitamin K deficiency, or the use of certain medications that affect blood clotting.
Symptoms of Protein S deficiency may include recurrent blood clots, usually in the legs (deep vein thrombosis) or lungs (pulmonary embolism), skin discoloration, pain, and swelling in the affected area. In severe cases, it can lead to complications such as chronic leg ulcers, pulmonary hypertension, or damage to the heart or lungs.
Diagnosis of Protein S deficiency typically involves blood tests to measure Protein S levels and function. Treatment may include anticoagulant medications to prevent blood clots from forming or growing larger. Lifestyle modifications such as regular exercise, maintaining a healthy weight, and avoiding smoking can also help reduce the risk of blood clots in people with Protein S deficiency.
A vegetarian diet is a type of eating pattern that excludes meat, poultry, and fish, and sometimes other animal products like eggs, dairy, or honey, depending on the individual's specific dietary choices. There are several types of vegetarian diets, including:
1. Ovo-vegetarian: This diet includes vegetables, fruits, grains, nuts, seeds, dairy products, and eggs but excludes meat, poultry, and fish.
2. Lacto-vegetarian: This diet includes vegetables, fruits, grains, nuts, seeds, dairy products, and eggs but excludes meat, poultry, fish, and sometimes eggs.
3. Ovo-lacto vegetarian: This is the most common type of vegetarian diet and includes vegetables, fruits, grains, nuts, seeds, dairy products, and eggs but excludes meat, poultry, and fish.
4. Vegan: This diet excludes all animal products, including meat, poultry, fish, dairy, eggs, and sometimes honey or other bee products.
5. Fruitarian: This is a more restrictive form of veganism that includes only fruits, nuts, seeds, and other plant foods that can be harvested without killing the plant.
6. Raw vegan: This diet includes only raw fruits, vegetables, nuts, seeds, and other plant foods that have not been cooked or processed above 115°F (46°C).
Vegetarian diets can provide a range of health benefits, including lower risks of heart disease, high blood pressure, type 2 diabetes, and certain cancers. However, it is important to ensure that vegetarian diets are well-planned and nutritionally adequate to meet individual nutrient needs, particularly for nutrients like vitamin B12, iron, calcium, and omega-3 fatty acids.
Venous thrombosis is a medical condition characterized by the formation of a blood clot (thrombus) in the deep veins, often in the legs (deep vein thrombosis or DVT), but it can also occur in other parts of the body such as the arms, pelvis, or lungs (pulmonary embolism).
The formation of a venous thrombus can be caused by various factors, including injury to the blood vessel wall, changes in blood flow, and alterations in the composition of the blood. These factors can lead to the activation of clotting factors and platelets, which can result in the formation of a clot that blocks the vein.
Symptoms of venous thrombosis may include swelling, pain, warmth, and redness in the affected area. In some cases, the clot can dislodge and travel to other parts of the body, causing potentially life-threatening complications such as pulmonary embolism.
Risk factors for venous thrombosis include advanced age, obesity, smoking, pregnancy, use of hormonal contraceptives or hormone replacement therapy, cancer, recent surgery or trauma, prolonged immobility, and a history of previous venous thromboembolism. Treatment typically involves the use of anticoagulant medications to prevent further clotting and dissolve existing clots.
Chronic kidney failure, also known as chronic kidney disease (CKD) stage 5 or end-stage renal disease (ESRD), is a permanent loss of kidney function that occurs gradually over a period of months to years. It is defined as a glomerular filtration rate (GFR) of less than 15 ml/min, which means the kidneys are filtering waste and excess fluids at less than 15% of their normal capacity.
CKD can be caused by various underlying conditions such as diabetes, hypertension, glomerulonephritis, polycystic kidney disease, and recurrent kidney infections. Over time, the damage to the kidneys can lead to a buildup of waste products and fluids in the body, which can cause a range of symptoms including fatigue, weakness, shortness of breath, nausea, vomiting, and confusion.
Treatment for chronic kidney failure typically involves managing the underlying condition, making lifestyle changes such as following a healthy diet, and receiving supportive care such as dialysis or a kidney transplant to replace lost kidney function.
A homozygote is an individual who has inherited the same allele (version of a gene) from both parents and therefore possesses two identical copies of that allele at a specific genetic locus. This can result in either having two dominant alleles (homozygous dominant) or two recessive alleles (homozygous recessive). In contrast, a heterozygote has inherited different alleles from each parent for a particular gene.
The term "homozygote" is used in genetics to describe the genetic makeup of an individual at a specific locus on their chromosomes. Homozygosity can play a significant role in determining an individual's phenotype (observable traits), as having two identical alleles can strengthen the expression of certain characteristics compared to having just one dominant and one recessive allele.
"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.
Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.
Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.
A heterozygote is an individual who has inherited two different alleles (versions) of a particular gene, one from each parent. This means that the individual's genotype for that gene contains both a dominant and a recessive allele. The dominant allele will be expressed phenotypically (outwardly visible), while the recessive allele may or may not have any effect on the individual's observable traits, depending on the specific gene and its function. Heterozygotes are often represented as 'Aa', where 'A' is the dominant allele and 'a' is the recessive allele.
The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:
1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.
Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.
Hyperhomocysteinemia
Asymmetric dimethylarginine
Homocysteine
Methylenetetrahydrofolate reductase deficiency
Leukoaraiosis
Prevention of dementia
Gluten-sensitive enteropathy-associated conditions
Methionine synthase
Homocystinuria
Pinealon
Kamineni Institute of Medical Sciences
Adenosine kinase
Haptocorrin
Foltx
Jayne Woodside
Cystathionine beta synthase
Methylenetetrahydrofolate reductase
Neurotoxin
Long-term effects of alcohol
Maitree Bhattacharyya
Methylmalonic acid
Complications of diabetes
MTRR (gene)
Lipotropic
Vitamin B12 deficiency
Folate deficiency
Rowena Green Matthews
Osteoporosis
DNA methylation
Histone-modifying enzymes
Hyperhomocysteinemia - Wikipedia
PRIME PubMed | Folic acid and vitamin B6 deficiencies related hyperhomocysteinemia in apparently healthy Pakistani adults; is...
PRIME PubMed | Preventive health care, 2000 update: screening and management of hyperhomocysteinemia for the prevention of...
Hyperhomocysteinemia (HHcy) | The Infographic Guide to Medicine | AccessMedicine | McGraw Hill Medical
KFU. Card publication. Vitamins group B restored the motor deficit of the rats with maternal hyperhomocysteinemia
Hyperhomocysteinaemia is not associated with increased levels of asymmetric dimethylarginine in patients with ischaemic heart...
β-amyloid deposition is shifted to the vasculature and memory impairment is exacerbated when hyperhomocysteinemia is induced in...
ESC 365 - Autophagy insufficiency participates in hyperhomocysteinemia-induced cardiac aging
Hyperhomocysteinemia - Indexed Journals
Hyperhomocysteinemia: an independent risk factor for vascular disease. - Nuffield Department of Population Health
How do you prevent hyperhomocysteinemia? - Moorejustinmusic
Hyperhomocysteinemia - Hematology and Oncology - MSD Manual Professional Edition
Časopis Internal medicine - Článok Hyperhomocysteinemia and vascular disease
Predictive value of folate, vitamin B12 and homocysteine levels in late-life depression | The...
Venous thrombosis and hyperhomocysteinaemia - McMaster Experts
Genetics and Molecular Pathophysiology of Thrombotic States | IntechOpen
Hyperhomocysteinemia and protein S deficiency in complicated pregnancies<...
"Toll-like receptor 4 mutation suppresses hyperhomocysteinemia-mediated" by Anastasia Familtseva
HYPERHOMOCYSTEINEMIA ACCELERATES THROMBOSIS THROUGH ICAM-1 DEPENDENT ENDOTHELIAL ACTIVATION AND DNA HYPOMETHYLATION
Hyperhomocysteinemia in acute hepatic porphyria (AHP) and implications for treatment with givosiran
Mild Hyperhomocysteinemia and Heterozygous Methylenetetrahydrofolate Reductase Mutation Associated with Pulmonary...
First Proposed Evidence-Based Guideline for Alzheimer's Prevention
Should we still look for hyperhomocysteinemia in patients with venous thromboembolism?]. - Université de Bretagne Occidentale
Venous thromboembolism due to hyperhomocysteinaemia and tuberculosis - The National Medical Journal of India
Vitamin B12 | Natural Medicine Journal
Hyperhomocysteinemia potentiates megakaryocyte differentiation and thrombopoiesis via GH-PI3K-Akt axis | Journal of Hematology ...
"Evaluation of hyperhomocysteinemia in the progression of Parkinson's d" by Marisa A. Ducach and Pritpal S. Saggu
HHcy9
- Devitt M.E. Devitt, Michael E. Hyperhomocysteinemia (HHcy). (mhmedical.com)
- We used a dietary model of cerebrovascular disease that relies on the induction of hyperhomocysteinemia (HHcy). (biomedcentral.com)
- Elevated levels of homocysteine, termed hyperhomocysteinemia (HHcy), is considered a risk factor for cardiovascular and cerebrovascular diseases [ 7 ]. (biomedcentral.com)
- Hyperhomocysteinemia (HHcy) has been observed to promote hypertension, but the mechanisms are unclear. (louisville.edu)
- Background: Hyperhomocysteinemia (HHcy) is an established risk factor for thrombotic diseases yet the underlying mechanism remain unclear. (temple.edu)
- Plasma homocysteine elevation, hyperhomocysteinemia (HHcy), has been reported in patients with acute hepatic porphyria (AHP), a family of rare genetic disorders caused by defects in hepatic heme biosynthesis. (unimore.it)
- Hyperhomocysteinemia (HHcy) is closely associated with thrombotic diseases such as myocardial infarction and stroke. (biomedcentral.com)
- Hyperhomocysteinaemia (HHcy) is an established risk factor for cardiovascular, cerebrovascular, peripheral vascular diseases and neurodegenerative disease. (bmrat.org)
- Ly6C high MC is the pro-inflammatory subset and the counterpart of human CD14 ++ CD16 + intermediate MC which contributes to systemic and tissue inflammation in various metabolic disorders, including hyperhomocysteinemia (HHcy). (frontiersin.org)
Folic acid6
- Hyperhomocysteinemia is a medical condition characterized by an abnormally high level of total homocysteine (that is, including homocystine and homocysteine-cysteine disulfide) in the blood, conventionally described as above 15 μmol/L. As a consequence of the biochemical reactions in which homocysteine is involved, deficiencies of vitamin B6, folic acid (vitamin B9), and vitamin B12 can lead to high homocysteine levels. (wikipedia.org)
- Can a folic acid supplement help with hyperhomocysteinemia? (moorejustinmusic.com)
- Intake of Folic acid supplements can be beneficial in lowering homocysteine levels in patients of mild genetic Hyperhomocysteinemia. (moorejustinmusic.com)
- Hyperhomocysteinemia can by lowered simply by adequate taking of folic acid, vitamins B6 and B12. (amedi.sk)
- Folic acid also ameliorates hyperhomocysteinemia, which is a consequence of elevated levels of homocysteine. (elsevierpure.com)
- Therefore, the present study was designed to observe the protective effects of folic acid against hyperhomocysteinemia-induced epigenetic and molecular alterations leading to neurotoxic cascades. (elsevierpure.com)
Homocysteine levels2
- ABSTRACT To investigate the possible relationship between hyperhomocysteinaemia and retinal vascular occlusion, we measured plasma homocysteine levels in 25 patients with a history of retinal vascular occlu- sion in the previous 2 years and in a control group of 24. (who.int)
- However, there is not enough substantial medical proof to show that reducing Homocysteine levels will actually improve health of Hyperhomocysteinemia sufferers. (moorejustinmusic.com)
Causes of hyperhomocysteinemia1
- Other possible causes of hyperhomocysteinemia include genetics, excessive methionine intake, and other diseases. (wikipedia.org)
Abstract1
- 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. (who.int)
Cerebrovascular1
- RESULTS: Hyperhomocysteinemia was detected in 16 of 38 patients with cerebrovascular disease (42 percent), 7 of 25 with peripheral vascular disease (28 percent), and 18 of 60 with coronary vascular disease (30 percent), but in none of the 27 normal subjects. (ox.ac.uk)
Develop hyperhomocysteinemia2
- Experts in the field advocate treatment of elevated tHcy levels in high-risk people, such as those with a personal or family history of premature atherosclerosis or a predisposition to develop hyperhomocysteinemia. (unboundmedicine.com)
- If you have a folate or B vitamin deficiency, you may develop hyperhomocysteinemia. (moorejustinmusic.com)
Coronary artery2
- Preventive health care, 2000 update: screening and management of hyperhomocysteinemia for the prevention of coronary artery disease events. (unboundmedicine.com)
- To establish guidelines for the screening and treatment of hyperhomocysteinemia in the investigation and management of coronary artery disease (CAD). (unboundmedicine.com)
Methylenetetrahydrofolate reductase1
- Hyperhomocysteinemia in CBS +/- + Met mouse brain was accompanied by a decrease in methylenetetrahydrofolate reductase and an increase in S-adenosylhomocysteine hydrolase expression, symptoms of oxidative stress, upregulation of DNA methyltransferases, rise in matrix metalloproteinases, a drop in the tissue inhibitors of metalloproteinases, decreased expression of tight junction proteins, increased permeability of the blood-brain barrier, neurodegeneration, and synaptotoxicity. (elsevierpure.com)
MTHFR1
- Folate and vitamin B 12 deficiency, hyperhomocysteinaemia and the T677 allele of the MTHFR gene, which cause impaired methylation reactions in the central nervous system, have been associated with depressive disorders. (cambridge.org)
Cardiovascular disease2
- In patients who have cardiovascular disease in the absence of more established risk factors, investigation and treatment of hyperhomocysteinemia should be considered. (moorejustinmusic.com)
- Hyperhomocysteinemia has been suggested as a potent new risk factor for premature cardiovascular disease. (ox.ac.uk)
Prevalence3
- The prevalence of hyperhomocysteinemia in the general population is between 5% and 10% and may be as high as 30%-40% in the elderly population. (unboundmedicine.com)
- To assess the prevalence of hyperhomocysteinemia in Parkinson's Disease (PD) and if this elevated serum level can be used as a predictive biomarker in risk assessment for the progression of cognitive decline in PD. (jmu.edu)
- Hyperhomocysteinaemia in stroke: prevalence, cause, and relationships to type of stroke and stroke risk factors. (thieme-connect.de)
Supplementation2
- Hyperhomocysteinemia is typically managed with vitamin B6, vitamin B9 and vitamin B12 supplementation. (wikipedia.org)
- Definitive guidelines for the management of hyperhomocysteinemia await the completion of randomized trials to establish the effect of vitamin supplementation on CAD events. (unboundmedicine.com)
Folate2
- Although there is insufficient evidence to recommend the screening or management of hyperhomocysteinemia at present (grade C recommendation), adherence to recommended daily allowance of dietary sources of folate and vitamins B12 and B6 should be encouraged. (unboundmedicine.com)
- Mild hyperhomocysteinemia was also observed and serum B12, B6 and folate levels were normal. (solunum.org.tr)
Arterial2
- Hyperhomocysteinemia may predispose to arterial and venous thrombosis. (msdmanuals.com)
- Hyperhomocysteinemia is known to be a significant risk factor for arterial occlusive vascular diseases and venous thrombosis. (solunum.org.tr)
Humans1
- Is there a cure for hyperhomocysteinemia in humans? (moorejustinmusic.com)
Vascular disease6
- Hyperhomocysteinemia: an independent risk factor for vascular disease. (ox.ac.uk)
- BACKGROUND: Hyperhomocysteinemia arising from impaired methionine metabolism, probably usually due to a deficiency of cystathionine beta-synthase, is associated with premature cerebral, peripheral, and possibly coronary vascular disease. (ox.ac.uk)
- After adjustment for the effects of conventional risk factors, the lower 95 percent confidence limit for the odds ratio for vascular disease among the patients with hyperhomocysteinemia, as compared with the normal subjects, was 3.2. (ox.ac.uk)
- The presence of cystathionine beta-synthase deficiency was confirmed in 18 of 23 patients with vascular disease who had hyperhomocysteinemia. (ox.ac.uk)
- CONCLUSIONS: Hyperhomocysteinemia is an independent risk factor for vascular disease, including coronary disease, and in most instances is probably due to cystathionine beta-synthase deficiency. (ox.ac.uk)
- Hyperhomocysteinemia is associated with significant risk of stroke, narrowing of the carotid artery due to atherosclerosis and peripheral vascular disease. (amedi.sk)
Vitamin deficiency1
- Hyperhomocysteinemia and B-vitamin deficiency are associated with recurrent abortion. (degruyter.com)
Venous thromboembolism1
- Should we still look for hyperhomocysteinemia in patients with venous thromboembolism? (univ-brest.fr)
Methionine2
- Smoking also causes hyperhomocysteinemia Homocysteine is a non-protein amino acid, synthesized from methionine and either recycled back into methionine or converted into cysteine with the aid of the B-group vitamins. (wikipedia.org)
- METHODS: We first established a diagnostic criterion for hyperhomocysteinemia by comparing peak serum levels of homocysteine after a standard methionine-loading test in 25 obligate heterozygotes with respect to cystathionine beta-synthase deficiency (whose children were known to be homozygous for homocystinuria due to this enzyme defect) with the levels in 27 unrelated age- and sex-matched normal subjects. (ox.ac.uk)
Risk factor1
- Smokeless tobacco is implicated as risk factor for hyperhomocysteinemia. (wikipedia.org)
Rats1
- Gataulina E. Vitamins group B restored the motor deficit of the rats with maternal hyperhomocysteinemia / E. Gataulina, A. Ziganshina, E. Ermakova, N. Khaertdinov, O. Yakovleva, G. Sitdikova // EUROPEAN JOURNAL OF CLINICAL INVESTIGATION. (kpfu.ru)
Systemic1
- Factors such as emotional status and associated systemic disease may play a role in predisposition of retinal vascular occlusion, so more-precise studies are needed to determine the possible risk factors of hyperhomocysteinaemia in retinal vascular occlusion. (who.int)
Peripheral1
- We describe a 38-year-old woman with a mural thrombus in the proximal aorta complicated by peripheral embolisation, due to hyperhomocysteinaemia. (njmonline.nl)
Levels1
- Hyperhomocysteinaemia is not associated with increased levels of asymmetric dimethylarginine in patients with ischaemic heart disease. (lu.se)
Genetic3
- Genetic defects in 5-MTHF reductase can consequently lead to hyperhomocysteinemia. (wikipedia.org)
- Is hyperhomocysteinemia genetic? (moorejustinmusic.com)
- Hyperhomocysteinemia may be either a genetic or an acquired characteristic. (moorejustinmusic.com)
Intake1
- Other than increasing the intake of vitamin B in your diet, there is no proper and prescribed way to treat the high level of homocysteine aka Hyperhomocysteinemia in your body. (moorejustinmusic.com)
Mutation1
- Toll-like receptor 4 mutation suppresses hyperhomocysteinemia-mediated hypertension. (louisville.edu)
Hypertension1
- The mechanism behind this association is unclear but does not appear to involve common risk factors such as hypertension, diabetes or hyperhomocysteinemia. (nih.gov)
Treatment1
- Treatment for Hyperhomocysteinemia. (moorejustinmusic.com)
Role2
- The role of free radicals as mediators of endothelial cell injury in hyperhomocysteinemia. (ox.ac.uk)
- of symptoms of malaria (in addition to The aim of this study was to investigate positive thick-blood film test) after a the role of hyperhomocysteinaemia as a risk previous malarial attack. (who.int)