Talk:Homocysteine

Proposal to move disease related info to Hyperhomocysteinemia

The page Hyperhomocysteinemia already exists and has some overlapping information with this page. It may be more appropriate to move anything related to elevated homocysteine to the Hyperhomocysteinemia page. Manfred Bartz (talk) 12:19, 9 January 2013 (UTC)

Hypothyroid causes high homocysteine levels

Could be most cases are sub-clinical Hypothyroidism? —Preceding unsigned comment added by 63.245.153.165 (talk) 03:19, 29 November 2009 (UTC)

Vitamin B

not helpful

Waster (talk · contribs) inserted the news item that taking B vitamins was not helpful. This has not been published yet - it was an abstract at the European Society of Cardiology, presented on 5/9/2005 by Bonaa KH et al [1] [2]. I think we should scan the literature in a few months to see which large journal will be publishing this finding. JFW | T@lk 16:58, 6 September 2005 (UTC)

absorption and supplementation

This is incomprehensible:

As B12 is inefficiently absorbed from food by elderly persons they could gain a greater benefit from taking vitamin supplements.

Greater than from what? Which of the mentioned vitamins? --Espoo 20:11, 20 June 2006 (UTC)

The above statement is not really a true statement, in addition to being incomprehensible. The decline in absorption of B12 from the stomach is generally believed to be due to lower levels of intrinsic factor being produced by stomach cells. Intrinsic factor, a protein, is essential to absorption of B12 through the stomach lining. So B12 via food and via vitamin supplementation will both be blocked by the lack of intrinsic factor. The traditional way around this is to inject intramuscularly B12. As I recall, Scandanavians have been shown to be low in intrinsic factor especially, as well as older people in general. (Hey, I'm just getting used to this. Haven't figured out the 'Sandbox' yet.)Siam442 (talk) 23:40, 24 February 2009 (UTC)

gluten sensitivity complications

"Prevalence of hyperhomocysteinemia in adult gluten-sensitive enteropathy at diagnosis: role of B12, folate, and genetics." by Saibeni S, Lecchi A, Meucci G, Cattaneo M, Tagliabue L, Rondonotti E, Formenti S, De Franchis R, Vecchi M.; Gastroenterology and Gastrointestinal Endoscopy Service, IRCCS Maggiore Hospital and University of Milan, Milan, Italy.

• BACKGROUND & AIMS: Hyperhomocysteinemia, a risk factor for thrombosis, recurrent miscarriages, and osteoporosis, might derive from acquired folate and vitamin B 12 deficiencies and from a C677T mutation in methylene-tetrahydrofolate reductase (MTHFR) gene. Undiagnosed gluten-sensitive enteropathy (GSE) is associated with vitamin deficiencies, osteoporosis, and recurrent miscarriages. We evaluated the prevalence and the risk factors for hyperhomocysteinemia in patients with newly diagnosed GSE.
• METHODS: In this prospective study performed in a tertiary care setting, 40 consecutive subjects with newly diagnosed GSE were evaluated for homocysteine, folate, and vitamin B 12 levels and for C677T polymorphism. One hundred twenty sex- and age-matched healthy control subjects were studied. Nonparametric tests and multiple regression analysis were used to evaluate the risk factors in inducing hyperhomocysteinemia in the GSE population.
• RESULTS: Hyperhomocysteinemia was more frequent in GSE patients than in control subjects (8/40, 20.0% vs 7/120, 5.8%) (relative risk, 3.4; 95% confidence interval, 1.3-8.9), as well as folate deficiency (17/40, 42.5% vs 10/120, 8.3%) (relative risk, 5.1; 95% confidence interval, 2.5-10.2). Multiple regression analysis showed that folate and B 12 levels were independently and inversely associated with homocysteine levels, whereas homozygosity for the MTHFR thermolabile variant was not. The prevalence of MTHFR variant in GSE population was not different from that reported in racially comparable control groups. Gluten-free diet was able to normalize folate, vitamin B 12 , and homocysteine levels.
• CONCLUSIONS: Hyperhomocysteinemia is frequent in newly diagnosed GSE. Vitamin deficiencies caused by malabsorption are the most important determinants of this condition. Hyperhomocysteinemia might contribute to the occurrence of common complications of undiagnosed GSE.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15952099&dopt=Abstract PMID: 15952099 [PubMed - indexed for MEDLINE]
--Renice 05:11, 24 March 2007 (UTC)

Dementia

I was shocked that there was not a section on the connection between dementia risk and course and homocysteine. It is a fruitful area of research. Also, exercise reduces homosy. in the elderly, and is not mentioned. My vote for adding to this article on these points! —Preceding unsigned comment added by 159.212.71.200 (talk) 17:28, 19 May 2008 (UTC)

I do believe there is a possible link between homocysteine levels and dementia. Does anyone want to verify and add this? Kenkoo1987 01:45, 1 November 2006 (UTC)

I believe that there is definitely link between homocysteine neurotoxicity in neurodegenerative diseases such as Alzeimer's Disease ,Dementia etc.All mechanisms by which it is achieved is explained in article I have referred to.Its interesting to read and understand.

Ref article: FEBS letters 580(2006)2994-3005 [ User: Dipenindia], 22:50,10 November 2006

I agree! I also believe there's a link with an Aspie/systemizer-thinking-style, in addition to a family or personal history of auto-immune disorders, gluten sensitivity, gout (especially in women), menopause, heart attacks, strokes, MS, or Connective Tissue Disorders (e.g., Beal's syndrome and possibly Marfan's syndrome).

Months ago, I figured out that I had a high H-level by comparing symptoms in those disorders (I'm 'true' for at least 8 out of 9) and removing endocannabinoid system symptoms. So I drastically cut animal fat (methionine-rich foods) from my diet then, and started taking B and Folic Acid supplements -- even so, my latest level was 12.7! (Anything over 10.4 is abnormally high (but I suspect the upper limit should be adjusted down for those certain phenotypes).)

If you are one of those phenotypes, get a level taken. You'll have to tell your doctor you want it checked: most of them don't seem to know yet that it may be more important than LDLs and HDLs for certain people.

When you get your H level checked, make sure they also check your iron level. Iron and homocysteine together are especially damaging.

My doctor says "Take folic acid." In light of the Vit B research mentioned above, any other ideas on looking for a remedy? -- Renice 23:49, 23 March 2007 (UTC)

Cystathionine Beta-Synthase Deficiency

Connection with dementia and other neurodegenerative diseases?

"Homocystinuria Caused by Cystathionine Beta-Synthase Deficiency" by Jonathan D Picker, MBChB, PhD; Harvey L Levy, MD

• Characteristics:
  • developmental delay/mental retardation
  • ectopia lentis and/or severe myopia by age 8
  • skeletal abnormalities (excessive height and length of the limbs) [i.e., may look like Marfan's syndrome], prone to osteoporosis
  • thromboembolism (major cause of early death and morbidity)
• Other features that may occur:
  • seizures
  • psychiatric problems
  • extrapyramidal signs such as dystonia
  • hypopigmentation
  • pancreatitis
  • malar flush
  • livedo reticularis
• Two phenotypic variants recognized:

1. B6-non-responsive homocystinuria
2. B6-responsive homocystinuria (typically milder expression)

[just holding this here until someone can incorporate relevant bits]
--Renice 05:58, 24 March 2007 (UTC)

not obtained from diet?

if homocysteine is not obtained from diet as the article claims and homocysteine forms methionine, how can methionine be an essential amino acid? -- Bubbachuck (talk) 09:14, 13 January 2008 (UTC)

homocysteine forms cysteine, not methionine. methionine is what it's formed from. —Preceding unsigned comment added by 79.71.77.24 (talk) 10:27, 23 July 2008 (UTC)

Hi, This article erroneously states; "No study has yet been conducted in a preventive capacity on subjects who are in a relatively good state of health."

       Three such peer reviewed papers reporting on intervention trials are im medline, 

PMID: 15086356 PMID: 10683000 PMID: 19118243 are the ID numbers at pubmed the online portal. As of Jan '09 these may be the only three and all report benefits for hi dose, homocysteine reducing supplementation.

04:54, 10 January 2009 (UTC)Thomas Carter04:54, 10 January 2009 (UTC)67.235.35.232 (talk)

Effect of Homocysteine regarding strokes

I am a 40 year male (Indian - Punjab) and last week experienced a stroke. I felt serious numbness in my right limbs and lost control of the right side of my mouth. I could not talk properly and rushed immediately to the hospital. I was lucky and recovered.

The Docs say there was a very small clot in the brain (the report says - MRI done showed, old infract in the left cerebellar hemisphere with subtle hyper intensity seen inthe left frontal region...).

On testing found everything within limits except for HOmocysteine - which recorder at 74.15 umol / L.

Could this be the reason for the clot in my head?

I work out at the gym 2 hours daily, could heavy exercise give rise to higher levels of homocysteine? I dont want to leave going to the gym.

I would appreciate all who can advice me on further course of action.

Thank you

Parminder.B.Singh parminderbsingh@yahoo.co.in —Preceding unsigned comment added by 121.245.79.251 (talk) 16:55, 9 July 2009 (UTC)

Please do not seek medical advice on Wikipedia. Tony (talk) 12:47, 28 May 2010 (UTC)

Cancer

Try to lower HCy, get cancer risk increase instead http://jama.ama-assn.org/cgi/content/abstract/302/19/2111 JFW | T@lk 22:59, 17 November 2009 (UTC)

Clean up

The list of references needs a good copy-edit. Some refs have inadequate information as well as inconsistent formatting. And the rest of the article could do with updating. Tony (talk) 12:45, 28 May 2010 (UTC)

Non-protein amino acid

The opening sentence declares that homocysteine is a non-protein amino acid. Reading this I'm not sure what it means. Is it that this amino acid (one of "the building blocks of protein") doesn't occur in proteins, doesn't occur in the usual proteins (whatever that set may be) or cannot occur in proteins? Does it mean something else, perhaps that homocysteine has a "non-protein role" in the body? Could someone who knows expand the shorthand "non-protein" to say exactly what is meant? 78.144.77.146 (talk) 11:23, 31 July 2013 (UTC)

intro

"A high level of homocysteine makes a person more prone to endothelial injury, which leads to vascular inflammation, which in turn may lead to atherogenesis... " should that really say atherogenesis, or are we referring to atherosclerosis?24.21.86.182 (talk) 18:44, 1 September 2013 (UTC)