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Betaine supplementation: a double-edged sword for CVD markers

This meta-analysis suggested that betaine doses under 4 grams daily can lower homocysteine without necessarily raising LDL-C, but there's still a lot of uncertainty.

Study under review: Effects of betaine supplementation on cardiovascular markers: A systematic review and Meta-analysis

Introduction

Complex systems tend to have weak points by nature of being made up of many interwoven parts. Identifying a weak point is a great way to approach what may seem like an insurmountable problem. Many diseases are both complex and can appear overwhelming when it comes to curing them or treating the associated symptoms. But if a disease state has a weak point, those weaknesses can be targeted.

One possible weakness when it comes to targeting cardiovascular disease (CVD) is high homocysteine levels. Homocysteine might be considered the weak point of the complex, metabolic sensing [1]homocysteine-methionine cycle (see sidebar). Elevated homocysteine is a disease biomarker[2] that is generally recognized as an independent risk factor for CVD, suggesting that interventions that lower homocysteine can also lower the risk of CVD. However, this idea is quite controversial because it’s not clear[3] whether high homocysteine is a consequence or a cause of CVD. This uncertainty hasn’t stopped research looking at interventions that reduce homocysteine levels, which is understandable given that CVD is the leading cause[4] of global mortality, and homocysteine levels could be a modifiable risk factor[5]. Beyond ensuring adequate status of vitamins B6[6], B9[6] (folate), and B12[6], which can support the homocysteine-methionine cycle, supplementation of betaine has emerged as a potential homocysteine-lowering intervention, as it is involved in another transmethylation pathway independent of[7] B vitamin intake.

What was studied?

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What were the findings?

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The bigger picture

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Frequently asked questions

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