Hyperhomocysteinemia Treatment


Hyperhomocysteinema Treatment

Scientific work property of Resurgen®.

Date: 17/01/13



High levels of homocysteine in blood can damage the arteries lining. Besides high levels of homocysteine migh cause the blood to clot more easily than it should. This may increase the risk of blockages in the blood vessels.


A clot in a blood vessel is called a thrombus. A thrombus might travel through the blood stream and be trapped in your lungs (known as pulmonary embolism), in your brain (which cause a stroke –embolism-) or in your heart (causing a heart attack).


People with too high levels of homocysteine have a higher risk of developing coronary artery disease.


Also they have a higher risk of having all type of chronic and degenerative diseases given the interconnections of homocysteine with the superoxide ion (oxidative stress) and with the nitric oxide metabolism.


This can produce lipid peroxidation of low density lipoproteins (LDL) and atherosclerosis, besides many other and the most dangerous even increase senescence and diminish the elderly life quality.


What causes a high level of homocysteine?

Usually homocysteine is converted into other amino acids the body uses. If your homocysteine level is too high it is possible you are not getting enough vitamins B to help your body to use the homocysteine.


Majority of people having a high homocysteine level do not get enough folate (also called folic acid), vitamin B6 or vitamin B12 in their diet. Replace these vitamins often helps homocysteine level return down to normal.


It is well known that patients with high homocystein levels (>9 µmol/L) have greater risk to suffer from cardiocirculatory diseases, hence it would be most desirable to obtain lower levels of the same. It has been identified Folic acid. As an efficient tool to lower those levels.


Also have been found high homocysteine blood levels in people suffering from atherosclerosis so much so that recently it is accepted as a predictor of atherosclerosis the homocysteine levels much more than cholesterol o the LDL, even the triglycerides. Although this is a test not routinely performed for blood tests, but since its correction is just to take folic acid and listed vitamins all of those non toxic, it does not matter too much to practice the homocysteine level if we have not that possibility.


For all that I advocate to take phytoestrogens since endogen estrogens physiologically accelerate the homocysteine catabolism and contributes to its fall in blood and since phytoestrogens in the body acts similarly to estrogens, we get the desired. (RESURGEN has in its composition all that is needed to lower the homocysteine) .


How can I reduce a high homocysteine level?

Eating more fruits and vegetables – mainly those with green leaves- that might help to lower your homocysteine level by increasing the amount of folate obtained in your diet.


Many cereals for breakfast, fortified grain products, lentil’s, asparagus, spinachs and majority of grains are good folate sources.


If adjusting your diet is not enough to lower your homocysteine level, your physician might suggest you to take a folic acid supplement. It might be possible as well for you to take supplements of vitamins B6 and B12 according with my own phytoestrogens studies.


Newly risk factors in cardiovascular diseases.

In the last years new risk factors have been discovered related with a higher incidence of cardiovascular diseases. Among them we can quote the homocysteine, the fibrinogen, increased platelets reactivity, the lipoprotein (a), hypercoagulability, etc. it is believed all these factors, although in different proportions, could contribute to the atherosclerosis development. Conventional risk factors predict less than half of cardiac events, hence these new risk factors could be related to a great extent with cardiac diseases where none of conventional factors is present. Homocysteine is one of the most outstanding factors. Recent studies confirm that its increased in plasma concentration is related in linear way with a higher risk of cardiac disease.


A 10% increase homocysteine blood level, just about in the same way it is increased the risk to suffer a severe cardiovascular disease.


These vitamins participate as coenzymes or substrate in the methionine and homocysteine metabolism because of what there is strong relationship in between these vitamins plasmatic levels and homocysteine level. Folic acid regulates the metabolic pathway catalyzed by Metilen-TetrahydroFolate reductase (MTHFR), the Cyanocobalamine (B12) in turn regulates the catalyzed way by the sintetase methionine . Vitamin B6 acts as cofactor for the sintetase cystationine .


In people who had a marked deficiency of vitamin B12 with intermediate or severe hyperhomocysteinemia the administration of this vitamin normalized the concentrations in 70% of cases. Numerous studies establish that moderately high circulating homocysteine levels are important independent risk factor for the development and progress of occlusive vascular diseases.


There are several factors causing increased plasmatic homocysteine; among those are hereditary metabolic disorders, nutritional status and treatment with certain drugs. Possible mechanisms whereby high homocysteine levels might caused vascular diseases include effects on the endothelium, platelets and coagulation factors.


Clinical Essay

Objective: A clinical essay was conducted aiming to evaluate the use of folic acid to reduce high homocysteine in patients having some other associated cardiovascular risk factors such as cholesterol LDL, etc.


Method: were added consecutively 33 patients both sexes (20 women and 13 men) running hyperhomocysteinemia carriers of two or more atherosclerotic risk factors, participants on a preventive cardiovascular programme (age 62,15+10,18 years). While fasting were dosed the level of plasmatic homocysteine on the first day and were administered with folic acid 2,5 mg/day. After 60 days again was dosed the homocysteine level which was compared with the initial one.


Results: initial average homocysteinemia value was 17,20+6,63µmol/L and after those 60 days of treatment with folic acid decreased down to 12,36+4,49µmol/L. Achieving a meaningful reduction of 28,14% with p<0,0001.


Conclusion: In this group of patients running high levels of plasmatic homocysteinemia and risk factors for atherosclerosis, treatment with folic acid reduced significatively their homocysteinemia.


Many years back it has been observed among those patients who develop morbid cardio circulatory episodes the striking frequency with which it did appear the association of predisposing factors for those conditions.. It has been detailed the effect produced by arterial hypertension, hypercholesterolemia and smoking amongst some other important factors.


Similarly has been documented the association found in between homocysteine high levels and coronary disease.


Numerous investigators suggest even moderately high homocysteine levels cause as well atherogenesis (1-5). Being as it is homocysteine an amino cid product of the methionine cycle, it is believed that its growth is an independent risk factor, frequent for atherosclerosis, particularly for aorto-iliac vascular disease, coronary, brain vascular and venous and arterial thromboses.


The pathophysiological mechanism proposed for this risk becomes out of the vascular modifications induced by homocysteine. (cells proliferation of the smooth vascular muscle, endothelial dysfunction), in addition to other effects produced over the platelets and a procoagulant state. So much so when we consider coronary artery disease, hyperhomocysteinemia bears with a risk similar to smoking one or hyperlipidemia. Those patients running a certain coronary disease, plasmatic homocysteine level appoints as a strong death predictor.


Hence evidence concludes being associated factors with coronary disease, if they were modified could decrease its incidence. Amongst those can cause homocysteine increase we can mention Piridoxin deficit (vitamin B6) and vitamin B12, important cofactors for methionine metabolism , but, no question about, the most principal known factor is folate deficit. Hence it has been proposed supplementary treatment with folic acid as well as with vitaminB as therapeutic alternatives to lessen plasmatic homocysteine values.


It is thought over than two thirds of hyperhomocysteinemia cases happen to be associated to low folate concentrations or of vitamin B12.


Those studies establishing hyperhomocysteinemia as an independent risk factor for the development of atherosclerotic artery disease are settled on a basis of the tested association existing in between this particular vascular disease and the presence of increased homocysteinemia levels, capable of producing endothelial injury as well as induce platelet activation.


Folic acid is involved in modulating the Homocysteine levels through its participation of methionine metabolism adjusting the catalyzed metabolic route by the Metilen-TetraHydroFolate reductase (MTHFR). Treatment with folic acid has been informed in different publications as accountable of plasmatic homocysteine levels diminution, in about 25% (if combined with vitamin B 12 those level will be reduced plus 7% additional).


With this group of patients having risk factors for atherosclerosis and hyperhomocysteinemia, treatment with folic acid brought forth meaningful reduction of plasmatic homocysteine value.


Recommended folic acid daily doses is 400 micrograms, although in some specific conditions used treatment might become up to 1000 micrograms. In United States the Drugs and Foods Federal Agency does not allow supplements containing over 800 micrograms, due to the fact that, high amounts of folic acid can make it difficult to detect anaemia’s because of vitamin B12 deficiency.


By mouth non toxic effects are known.


After small doses administration, most part of folic acid is reduced and methylated into Methyltetrahydrofolate. Nevertheless after large doses. the drug appears into the plasma not altered. Active forms of folic acid are recovered by enterohepatic reabsorption. Folic acid is eliminated under the form of metabolites through the urine. After quite large doses it might appear unmetabolized in the urine.


Secondary Effects

Practically folic acid is free from secondary effects.


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