Homocysteine as a marker of cardiovascular risk

Cardiovascular disease (CVD) remains one of the leading causes of morbidity and mortality worldwide.
Identifying reliable markers for cardiovascular risk assessment is crucial for the early detection, prevention, and effective management of this complex condition.
In recent years, homocysteine has gained attention as a potential biomarker for cardiovascular risk.
This article explores the role of homocysteine as a marker of such risk, focusing on its biological importance and summarizing the important relevant research existing to date.
In addition, we will make a contribution about one of our products, which could provide important help.

Understanding Homocysteine

Homocysteine is an amino acid derived from the metabolism of methionine, which is an essential amino acid obtained from dietary sources.
Depending on the metabolic pathway that comes into play, homocysteine is converted to cysteine through the transsulfuration pathway or resynthesized into methionine through the remethylation pathway.
Defective metabolism of methionine can increase homocysteine levels, and elevated serum or plasma concentrations of this sulfur-containing amino acid increase cardiovascular risk.

Hyperhomocysteinemia has been strongly associated with increased cardiovascular risk by causing endothelial dysfunction through the induction of inflammation and oxidative stress.
Homocysteine concentrations can increase primarily as a result of specific genetic defects of the enzymes responsible for its metabolism, as well as deficiencies of cofactors involved in this pathway, such as vitamins B6, B12, and folic acid.
Such deficiencies are secondary to reduced intake or absorption and the use of specific medications. https://doi.org/10.1177/1179573520962230

Homocysteine and cardiovascular risk

Numerous epidemiological studies have established a close link between elevated homocysteine levels and cardiovascular disease.
However, the underlying mechanisms and causal relationship between homocysteine and CVD are still being studied.
The research has explored the association between homocysteine and various aspects of cardiovascular risk, shedding light on its potential as a predictive marker.
Current predictive parameters of specific cardiovascular risk indicate that a high plasma level of homocysteine significantly increases the incidence of vascular damage in both small and large vessels.

In 1997, a very important study was carried out in Europe to establish the magnitude of the risk of CVD associated with an elevated level of plasma homocysteine and to examine the effects of interaction between these and conventional risk factors.
The result was that an elevated plasma level of total homocysteine confers an independent risk of vascular disease similar to that of smoking or hyperlipidemia, and this risk is powerfully increased when associated with hypertension.
DOI: 10.1001/jama.1997.03540460039030

Homocysteine can promote endothelial dysfunction, oxidative stress, inflammation, and thrombosis, all of which contribute to the development and progression of atherosclerosis.
In addition, elevated homocysteine levels can affect vascular endothelial cell function, disrupt nitric oxide production, and lead to arterial stiffness and hypertension.

Another study conducted in 2020 attempted to determine the relationship between elevated homocysteine levels and peripheral artery disease. The result obtained ratified the previously existing studies and highlighted the joint effect of high homocysteine concentration and traditional cardiovascular risk factors such as smoking, diabetes and aging on the incidence of peripheral arterial disease.
DOI: 10.2147/DMSO. S267122

Perspectives

While clinical trials have provided valuable insights into the relationship between homocysteine and cardiovascular risk, it is important to note that they primarily serve as examples in our research during the preparation of this article.
However, these important findings contribute to a better understanding of the role of homocysteine in CVD.

However, the impact of homocysteine-lowering therapy on cardiovascular outcomes has been inconsistent, so it is important to consider the potential benefits of managing homocysteine levels.
Lifestyle modifications, including a healthy diet rich in B vitamins (folate, vitamin B6, and vitamin B12), can help maintain optimal homocysteine levels.
In addition, individuals with certain genetic variations may have a greater predisposition to hyperhomocysteinemia and may benefit from personalized interventions.
DOI: 10.1055/s-2000-8101

Although homocysteine is not currently recommended as a stand-alone marker for cardiovascular risk assessment, it may be useful in combination with other established risk factors.
Assessing homocysteine levels along with traditional risk factors such as age, smoking, blood pressure, lipid profile, and family history can provide a more comprehensive assessment of an individual’s cardiovascular risk.

Possible interventions

Homocysteine-lowering supplements often contain nutrients such as folic acid, vitamin B6, and vitamin B12, which are involved in your metabolism.
These supplements are commonly recommended for people with elevated homocysteine levels or those at increased risk of cardiovascular disease.
While the specific benefits of taking two capsules of Active Homocystrol+TMG daily cannot be disputed, it is good to inquire a little more about the benefits.

One of them is the maintenance of the proper functioning of their metabolism and metabolic processes that require methyl group donation.
Remethylation of homocysteine to methionine requires folic acid in its active form 5-methyl TFH.
To obtain 5-methyl TFH, the MTHFR gene is needed as a catalyst and riboflavin as a cofactor.
Once in their active form, folate can cede its methyl group to homocysteine, allowing the remethylation process.
This process is catalyzed by the MS gene and requires methylcobalamin as a cofactor.
An alternative route for methionine remethylation to occur is from betaine degradation by the BHTM gene.
Betaine can be obtained from the diet or from choline oxidation.

It has been strongly hypothesized that lowering homocysteine levels has cardiovascular benefits.
While the direct impact on cardiovascular outcomes continues to be studied, it is suggested that lowering homocysteine levels may help improve endothelial function, reduce inflammation, and improve vascular health.
These effects could potentially contribute to a decreased risk of developing cardiovascular disease, such as coronary artery disease and stroke.

Homocysteine-lowering supplements can synergistically complement other interventional strategies for reducing cardiovascular risk.
They can be used in conjunction with lifestyle modifications, including a healthy diet, regular exercise, and smoking cessation for good. The combination of these interventions may provide a more comprehensive approach to managing cardiovascular risk factors.

In some individuals, genetic variations can be observed that predispose them to higher levels of homocysteine.
In such cases, reducing supplements may be particularly beneficial.
These supplements can help compensate for impaired enzyme activity and help maintain optimal homocysteine levels, thereby reducing the associated cardiovascular risk.

It is important to note that before starting any new supplement regimen, it is recommended to consult with a healthcare professional so that they can assess your individual health status, the suitability of the supplements, and provide personalized recommendations based on your specific needs.

Conclusion

Homocysteine has emerged with greater emphasis lately as a potential marker of cardiovascular risk, with elevated levels associated with increased susceptibility to CVD.
Although clinical trials have provided mixed results regarding the impact of homocysteine-lowering therapy on cardiovascular outcomes, the biological importance of homocysteine in the development and progression of atherosclerosis warrants further investigation and possible interventions.

Active Homocystrol+TMG helps by providing specific nutrients that are widely demonstrated to be useful in the metabolic pathways of homocysteinemia descent.