Coronary Artery Disease (CAD) is a disease claiming the lives of over 370,000 people each year in the United States (US). Making CAD the most common type of heart disease for men and women living in the US. (1)
There are typical risk factors in the development of CAD such as: diabetes, hypertension, hyperlipidaemia, family history, smoking, and diet. But, are there genetic components involved in the development of CAD? And what might they be?
Lately, there is a growing interest in the scientific community to study the role of MTHFR in the development of heart disease and CAD. This is because scientists suspect, and have some evidence, that: (2,3)
Impaired MTHFR activity may lead to homocysteine accumulation in plasma, and this condition may contribute towards progressive atherosclerosis through several mechanisms, including arterial endothelial function impairment, oxidative stress induction and promotion of inflammation and thrombosis
What genetic polymorphisms result in impaired MTHFR activity? If you don’t know, read are post “What is MTHFR?” for a quick refresher. To keep it simple, the MTHFR C667T polymorphism has the greatest potential to reduce the activity of the MTHFR enzyme.
In a new study, researchers looked at how the MTHFR C667T polymorphisms influences the development of heart disease and CAD. (4) They compared the genetic status of 100 people with cardiovascular disease and 110 healthy controls. They found a significant correlation between the MTHFR C667T polymorphisms and higher levels of CAD, total cholesterol, and LDL-cholesterol compared to healthy controls. The researchers also compared risk factors for heart disease and CAD between the two groups and found individuals within both groups often had one or more risk factors for heart disease and CAD.
The researchers concluded that having a MTHFR C667T polymorphism is a major contributor to the development of heart disease and CAD when combined with other associated risk factors.
What you can do to minimize heart disease and CAD risk if you have MTHFR C667T?
We know the biochemical and physiological consequences associated with the MTHFR C667T polymorphism, so if we work towards correcting and/or preventing these consequences, we can minimize the risk of MTHFR C667T contributing to the development of heart disease and CAD. Risk can potentially be minimized by ensuring folate levels are stable and sufficient. This can be done through diet (See: What to eat if you are low in folate) and through supplementation (See: Folate Supplementation Guide). If you do not know your MTHFR status (See: How to find out if you have the MTHFR gene mutation).
- Castro, R., Rivera, I., Blom, H. J., Jakobs, C., & de Almeida, I. T. (2006). Homocysteine metabolism, hyperhomocysteinaemia and vascular disease: an overview. Journal of inherited metabolic disease, 29(1), 3-20.
- Wald, D. S., Law, M., & Morris, J. K. (2004). The dose-response relation between serum homocysteine and cardiovascular disease: implications for treatment and screening. European Journal of Cardiovascular Prevention & Rehabilitation, 11(3), 250-253.
- Tantray, J. A., Reddy, K. P., Yerra, S. K., & Jamil, K. A Study of C677T Polymorphism of Methylenetetrahydrofolate Reductase (MTHFR) Gene and It’s Susceptibility in Coronary Artery Disease.