A key underlying factor in cardiovascular conditions such as heart disease and stroke is a process known as atherosclerosis (also known as arteriosclerosis), which is essentially a furring up of arteries with a fatty ‘plaque’. For decades now, we’ve had it instilled in us that the chief dietary factor influencing atherosclerosis is fat, which saturated fat being painted as the main villain of the piece. This is despite the fact that the notion that saturated fat causes cardiovascular diseases like heart disease is not supported by the science [1]. See here for more about this.
The focus on fat the primary problem in cardiovascular disease has, to a degree, diverted our attention away from other ‘macronutrients’ that may play a role here, notably carbohydrates. Because carbohydrate rich foods, such as starchy breakfast cereals, are low in fat, there is sometimes an implicit assumption that these foods are healthy regarding arterial health. This, of course may not stand up to scrutiny.
In recent years there has been growing recognition that disruption in blood sugar levels might contribute to an enhanced risk of cardiovascular disease. It might be that one of the reasons diabetics are generally at increased risk of cardiovascular disease is because they tend to run elevated levels of blood sugar. If that’s the case, then maybe even transient rises in blood sugar might be a risk factor for cardiovascular disease.
The speed and extent to which foods release sugar into the bloodstream can be measured and expressed as something known as the glycaemic index of GI. High GI foods can cause spikes in blood sugar which can predispose to cardiovascular and other diseases through a number of mechanisms including increased ‘oxidative stress’ (free radical damage), increased inflammation, protein glycation (glucose ‘bonding’ to proteins in the body and damaging them) and increased coagulation (essentially, making the blood ‘stickier’ and more likely to clot). On top of this we have evidence linking high GI foods with an increased risk of cardiovascular disease [2]. You can read more about this here.
Partly as a result of this background, my eye was caught recently by a study which assessed the relationship between the eating of different sources of carbohydrate on something known as ‘flow mediated dilatation’ (FMD) in the brachial artery (a major artery in the arm). This measurement essentially tests the ability of arteries to relax, which is something that is good for blood flow in the artery, and is associated with a reduced risk of cardiovascular disease risk. Reduced FMD is a sign of reduced health in the artery, and is a potential risk factor for heart attacks and stroke.
The subjects in this study were overweight and obese, non-diabetic men with an average age of 48. On separate occasions, each of these men were fed with one of four test ‘meals’, after which FMD was assessed 2 hours later. The four text meals were water (placebo), glucose (high GI), cornflakes (high GI) and bran flakes (low GI). Compared to the placebo, FMD was reduced after all of these meals, but only to a statistically significant degree after the two high GI meals [3]. The authors of this study concluded that, High- compared with low-glycemic carbohydrate consumption significantly suppresses FMD in nondiabetic overweight and obese volunteers, suggesting a mechanism whereby high-glycemic meals may enhance cardiovascular risk.
This study provides more evidence that carbohydrates, specifically those that are disruptive to blood sugar, pose serious risks for our health, including our heart and circulation.
References:
1. Mente A, et al. A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Arch Intern Med. 2009;169(7):659-669
2. Brand-Miller, et al. The Glycemic Index and Cardiovascular Disease Risk. Current Atherosclerosis Reports 2007;9:479-485
3. Lavi T, et al. The Acute Effect of Various Glycemic Index Dietary Carbohydrates on Endothelial Function in Nondiabetic Overweight and Obese Subjects J Am Coll Cardiol 2009;53:2283 – 2287
