How to Read Homocysteine Levels on Blood Tests

• What Is It?
  • What is the definition of homocysteine? What is it?
• Genetic
  • What are hyperhomycysteinemia and homocystinuria? Are they inherited (genetic)?
• Elevated Levels
  • How many people have elevated homocysteine levels, and who gets the condition?
• Signs/Symptoms
  • What are the signs and symptoms of homocystinuria?
• Causes
  • What are the more than mutual causes of hyperhomocysteinemia?
• Lowering Homocysteine Levels
  • How can homocysteine levels be lowered?
  • Does lowering homocysteine level prevent eye attacks and strokes?
  • Does lowering homocysteine levels prevent middle attacks and strokes?
• Who Needs It?
  • Who should become tested for elevated homocysteine levels? How is it treated?
• Center
  • Homocysteine Blood Test: Normal and Elevated Levels Center
• Comments
  • Patient Comments: Homocysteine - Elevated Levels
  • Patient Comments: Homocysteine - Lowering Levels
  • Patient Comments: Homocysteine - Testing

What is the definition of homocysteine? What is it?

Alcohol can raise homocysteine blood levels.

Homocysteine is an amino acid produced by the body by chemically altering adenosine. Amino acids are naturally fabricated products, which are the edifice blocks of all the proteins in the torso. Most labs report normal ranges of homocysteine every bit nigh 4-15 µml/50.

Can elevated homocysteine levels be genetic? When was homocystinuria discovered?

Homocystinuria was discovered in 1962 past two different groups of researchers. In 1969, Dr. Kilmer Southward. McCully reported that children built-in with a genetic disorder called homocystinuria, which causes the homocysteine levels to be very high, sometimes died at a very young historic period with advanced atherosclerosis in their arteries. Homocysteine levels in the blood may be elevated for many reasons. More specifically, these reasons can be divided into severe genetic causes and other milder causes.

What are hyperhomycysteinemia and homocystinuria? Are they inherited (genetic)?

Homocystinuria was discovered in 1962 past 2 different groups of researchers. In 1969, Dr. Kilmer S. McCully reported that children born with a genetic disorder called homocystinuria, which causes the homocysteine levels to exist very loftier, sometimes died at a very immature historic period with avant-garde atherosclerosis in their arteries. Homocysteine levels in the blood may be elevated for many reasons. More than specifically, these reasons can be divided into astringent genetic causes and other milder causes.

How many people accept elevated homocysteine levels, and who gets the status?

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Mild summit in homocysteine levels (hyperhomocysteinemia) are common, and seen in about 5% to 12% of the general population. In specific populations such as, alcoholics (due to poor vitamin intake) or patients with chronic kidney affliction, this may be more mutual. The severe genetic form, homocystinuria, is rare (0.02%).

What are the signs and symptoms of homocystinuria?

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Homocystinuria has a constellation of signs and symptoms that include:

• Developmental delay
• Osteoporosis (thin bones)
• Visual abnormalities
• Germination of claret clots
• Advanced atherosclerosis or narrowing and hardening of blood vessels, a type of heart disease.

What are the more than common causes of hyperhomocysteinemia?

More mutual causes of elevated homocysteine levels in the blood are milder genetic variations of homocystinuria. In these weather, the mediator molecules malfunction and are less efficient because of a modest aberration in their structure. They also lead to pinnacle of homocysteine levels (to a higher place 15 µmol/L), although much milder than in homocystinuria (to a higher place 100 µmol/L), past slowing down the breakup of homocysteine.

How can homocysteine levels be lowered?

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Eating cereals that are fortified with folic acid, and to a lesser extent vitamins B6 and B12, tin can lower claret homocysteine levels. These supplements may even be beneficial in people with mild genetic hyperhomocysteinemia to lower their homocysteine levels. However, it is noteworthy that so far there is no compelling data to support the treatment of hyperhomocysteinemia for prevention of heart affliction or treatment of known centre affliction or blood clots. Homocysteine levels are non routinely measured in people with heart disease (atherosclerosis) or other diseases.

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Who should become tested for elevated homocysteine levels? How is information technology treated?

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Currently, in that location are no official recommendations as to who should undergo testing for homocysteine claret levels. Before data that are more scientific become available from the currently ongoing studies, many experts do not recommend a screening test for blood homocysteine levels, even in patients with unexplained blood clot formation. In improver, the consensus recommendation is confronting treating elevated homocysteine levels with vitamins to prevent heart disease. Rarely, a few specialists may test for elevated homocysteine levels in patients with early onset of claret clot formation, heart attacks, strokes, or other symptoms related to atherosclerosis, specially if these patients do not have typical adventure factors, such as smoking cigarettes, diabetes, high blood pressure, or high LDL cholesterol levels and they suspect genetic causes

There is likewise no consensus as to the optimal dose of folic acid and other B vitamins for the treatment of elevated blood homocysteine levels. (For example, treatment of patients with high homocysteine levels may require college doses of folic acrid and other B vitamins than the amounts contained in a multivitamin.) Therefore, a decision regarding testing should exist individualized after consulting with your doctor and/or a specialist in genetic diseases. Some researchers recommend treatment guidelines that result in levels of homocysteine below 100 µmol/L but say the recommendation may alter (possibly lowered) with new information.

Does lowering homocysteine level prevent middle attacks and strokes?

Currently, there is no direct proof that taking folic acid and B vitamins to lower homocysteine levels prevents heart attacks and strokes. Notwithstanding, in a big population study involving women, those who had the highest consumption of folic acrid (usually in the grade of multivitamins) had fewer centre attacks than those who consumed the least amount of folic acrid. In this written report, the association betwixt dietary intake of folate and vitamin B6 and gamble of heart illness was more noticeable than between dietary intake of vitamin B12 and heart illness, which was minimal.

Many other observational studies have been performed to appraise the upshot of folate and the other B vitamins on centre disease. Most of these studies take ended that oral intake of folate has been associated to lower gamble of heart affliction, possibly considering due to lowering of homocysteine levels. The relation betwixt oral intake of vitamin B12 and B6 and centre disease was non equally obvious in many of these studies. In one study, it was concluded that even in people with elevated homocysteine levels due to genetic reasons, oral intake of folate and possibly the other B vitamins was related to lower incidence of heart affliction.

Most of these data, however, are obtained from observational studies rather than purely controlled scientific data. Therefore, it is important to mention that despite these studies suggesting an association between the intake of these vitamins and the lower incidence of heart disease, in general, at that place is no compelling clinical evidence to treat hyperhomocysteinemia other than homocystinuria (the severe genetic form) in regards to heart disease, stroke, or claret clots. Homocysteine levels are non routinely measured in people with these problems.

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Does lowering homocysteine levels prevent heart attacks and strokes?

Currently, there is no direct proof that taking folic acid and B vitamins to lower homocysteine levels prevents eye attacks and strokes. Even so, in a large population report involving women, those who had the highest consumption of folic acrid (unremarkably in the course of multivitamins) had fewer middle attacks than those who consumed the to the lowest degree corporeality of folic acid. In this study, the association between dietary intake of folate and vitamin B6 and risk of eye disease was more than noticeable than between dietary intake of vitamin B12 and middle affliction, which was minimal.

Many other observational studies have been performed to assess the effect of folate and the other B vitamins on heart disease. Well-nigh of these studies accept concluded that oral intake of folate has been associated to lower take chances of heart disease, possibly because due to lowering of homocysteine levels. The relation betwixt oral intake of vitamin B12 and B6 and heart disease was not as obvious in many of these studies. In one report, it was concluded that fifty-fifty in people with elevated homocysteine levels due to genetic reasons, oral intake of folate and possibly the other B vitamins was related to lower incidence of heart disease.

Well-nigh of these information, however, are obtained from observational studies rather than purely controlled scientific data. Therefore, information technology is important to mention that despite these studies suggesting an association betwixt the intake of these vitamins and the lower incidence of heart disease, in general, there is no compelling clinical evidence to treat hyperhomocysteinemia other than homocystinuria (the severe genetic form) in regards to middle disease, stroke, or blood clots. Homocysteine levels are not routinely measured in people with these problems.

QUESTION

In the U.S., ane in every 4 deaths is caused by heart disease. See Respond

Medically Reviewed on 9/18/2020

References

REFERENCES:

Abrahaham, MD, J.M. et al. The homocysteine hypothesis: Even so relevant to the prevention and treatment of cardiovascular disease? Cleveland Dispensary Journal of Medicine December 2010 vol. 77 12 911-918.

Homocysteine, Folic Acrid and Cardiovascular Disease.
<http://world wide web.heart.org/HEARTORG/Encyclopedia/Centre-Encyclopedia_UCM_445084_ContentIndex.jsp>

Mandava, P, MD. Homocystinuria/Homocysteinemia. Medscape. Updated: Jun 14, 2017.
<https://emedicine.medscape.com/article/1952251-overview>

Morris, AM, et al, Guidelines for the diagnosis and management of cystathionine beta-synthase deficiency. J. Inherit. Metab. Dis.. 2017; 40(1): 49–74. 40(1), 49-74. 2017 Published online 2016 Oct 24. doi: 10.1007/s10545-016-9979-0
<https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5203861/>

Rosenson, RS, MD, et al. Overview of homocysteine. UpToDate. Updated: May 2018.
<https://www.uptodate.com/contents/overview-of-homocysteine>

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Source: https://www.medicinenet.com/homocysteine/article.htm

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