The pendulum swings in nutrition are extreme. In Part 1 we critiqued the meta-analyses which generated momentum for the “saturated fats are fine” movement, but there was another suggested conclusion from certain of these meta-analyses: that carbohydrates are to blame, not saturated fats [1][2].

These conclusions were timely in the nutrition sphere, coming as they were at a time when a confused nutrition public was being exposed to the cult of “clean eating”, powered by the unprecedented access of totally unqualified “wellness gurus” to reach the masses via social media. And sugar was, and remains, Public Enemy No.1 for the “clean eating” paradigm.

So, what is the role of sugar in cardiometabolic disease? Why did these meta-analyses find “no association” between saturated fat and cardiovascular disease [CVD] when replaced by carbohydrates in the diet?

 

Comparing Saturated Fat to Carbohydrate in Meta-Analyses

Certain meta-analyses have suggested that replacing saturated fat with carbohydrates does not reduce risk of CVD [1][2]. Reiterating the point made in the previous article, the quality of the primary included studies will define the results of any meta-analysis. In these meta-analyses, the primary studies included substitution trials which failed to specify the type of carbohydrate replacing saturated fat [1][2]. This is a significant error. In population studies differentiating between unrefined, wholegrain carbohydrates and refined, simple sugar carbohydrates, substitution of saturated fat for unrefined carbohydrates decreases CVD risk, while substitution with refined carbohydrate either increases risk or at isocaloric levels risk remains unchanged [3][4].

Therefore, any pooled analysis that suggests a neutral effect of overall carbohydrate replacement of saturated fat arrives at a null association due to the fact that the studies showing increased risk and decreased risk cancel each other out [3]. In addition, the de Souza et al. (2015) meta-analysis concluded that there was no association between saturated fat, CVD or type-2 diabetes [T2DM] when saturated fat replaces refined carbohydrates. That would be expected given that risk remains relatively similar at isocaloric replacement [4]. Consequently, cohort studies that fail to address the quality of carbohydrate will generally result in a neutral effect of carbohydrate on CVD risk in replacing saturated fats.

These studies add to the confusion, because while they suggest carbohydrate to be a greater issue than saturated fat, they also obscure the true role of sugar in the development of CVD.

 

Lipoprotein Metabolism and Cardiometabolic Risk Factors

You’ll note I used the term “cardiometabolic” in relation to sugars. This term reflects the fact that CVD is a complex multifactorial disease, for which the influence of saturated fat on blood cholesterol levels is only one aspect. Other metabolic factors increase CVD risk by influencing the “atherogenic lipoprotein phenotype” defined by high blood LDL-cholesterol, low HDL-cholesterol levels, high circulating triglycerides [TGs], and a remodelling of LDL into small, dense lipoprotein subparticles [5]. “Cardiometabolic” refers to these risk factors: central adiposity, insulin resistance, fatty liver, and the influence of these factors on other markers of CVD disease like triglycerides [TGs], HDL and lipoprotein subtypes [6][7][5].

Let’s go a bit deeper into the mechanisms by which CVD risk is increased through adverse effects on these biomarkers. Other than LDL, high blood TGs are an independent risk factor for heart disease even in otherwise healthy weight, normal individuals [8]. LDL cholesterol has two patterns: A-type patterns are defined by large, less dense particles while B-type patterns are defined by remodelling of LDL into small, dense, atherogenic particles [9]. LDL remodels into the B-type pattern when circulating TGs exceed a threshold around 1.5-1.6nM [8].

This is where we need to grasp some lipid metabolism. The density of a lipoprotein refers to its ratio of proteins to lipids: increasing density means less lipid storage. Chylomicrons [CMs] – which transport TGs absorbed from dietary intake – are 99% lipid, 85-90% TGs and 1-3% cholesterol, while very low-density lipoprotein [VLDL] is 90% lipid, 55% TGs and 25% cholesterol. CMs and VLDL are thus designed primarily for transporting TGs and other lipids. Conversely, HDL only consists of 44% lipids and 6% TGs, as its primary function is the transport of cholesterol for recycling. Neither LDL, and more specifically HDL, are designed to carry much TGs.

When circulating TGs reach that threshold of 1.5-1.6nM, the usual equimolar exchange – where HDL offloads its cholesterol to VLDL in return for equal parts TGs, so VLDL can remove cholesterol to the liver – is impaired, and VLDL offloads too much TGs onto HDL and LDL [8]. HDL is then burdened with TGs, and remodels into small dense subparticles, which are rapidly catabolized in the liver: thus, the low HDL aspect of the phenotype [9]. With impaired TG clearance, LDL also remodels into smaller, denser subparticles, which remain in circulation for prolonged periods and are capable of penetrating the arterial endothelium [9].

The key point here is that there are two ways in which we end up with elevated circulating TGs: by impaired clearance – i.e. breakdown – of TGs from CMs and VLDL, and/or from increased TG synthesis in the liver. Both of these factors are strongly influenced by free sugars.

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