Is there a link between carbohydrate consumption and heart disease?
At this point blood glucose will be elevated, as will insulin levels, and peripheral tissues will be preferentially burning glucose and therefore have a significantly reduced uptake of fats from the lipoproteins. This is a recipe for a true lipoprotein log-jam. Increased apoB100 particle numbers due to ramped up VLDL production, and competition at the LPL receptor due to the common saturable removal mechanism, will increase all smaller particles’ time in circulation.
The high number of VLDL particles in circulation causes the triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, over enriching them with triglycerides (via the action of cholesteryl-ester transfer protein, or CETP), which in turn reduces HDL functional capacity.
The triglyceride-rich LDL is "remodelled" during its excessive circulation by enzymes like hepatic lipase, becoming delipidated and smaller and denser, thus creating small-dense LDL. Once these particles get smaller it would appear that their clearance from circulation becomes hindered by their degenerated affinity for the LDL receptor, leading to an excessive time in circulation (Ref,Ref), which in turn further increases their susceptibility to oxidation (Ref).
As an aside, to demonstrate that the link between high carbohydrate intakes and heart disease is not a direct one, it is worth identifying the example of the Kitavans. This South Polynesian island population, eat generous quantities of carbohydrates. On average, they get 69% of their 2200 calories per day from high-glycemic starchy tubers and fruit (380 g carbohydrate), with not much fat to slow down digestion. Yet they have low fasting insulin, very little body fat and an undetectable incidence of diabetes, heart attack and stroke. That's despite a significant elderly population on the island and the tendency of many Kitavans to smoke like chimneys .
For more information of the above process see "Lipoprotein Metabolism & Heart Disease"
The short answer to that question is "No, not directly!" However, in the typical modern diet, carbohydrates may be contributing to a metabolic state which is intimately involved in the development of heart disease. This is especially relevant when eating a diet which is unnaturally high in polyunsaturated fats, and when the carbohydrates being consistently consumed are in excess of the body's capacity to use or store them, in rate or volume.
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In an attempt to improve health and reduce the risk of heart disease the common mainstream nutritional advice from the health authorities is to "Reduce your animal fat and cholesterol intake and replace them with complex carbohydrates and polyunsaturated oils." I believe that this is the worst advice a person could be given. For a start, it makes much more sense for a person to minimize omega-6 polyunsaturated fat intake, consume lower carbohydrate levels, create a calorie deficit if ‘over-fat’, get the majority of your fat-calories from the stable saturated fats, and whatever amount of carbohydrate calories you choose to consume from fruits and vegetables rich in anti-oxidants and other phytonutrients.
When addressing heart disease risk and assessing the effects of interventions, such as diet, certain blood-borne bio-markers are used. When reading about these, it is important to always be aware that these are just bio-markers which tend to associate with the condition.
When using nutritional changes to address the risk of heart disease, low-carb diets do appear to have repeatedly proved successful in reducing certain blood lipid bio-markers of heart disease risk (Ref), whilst increased carbohydrate levels and reduced animal fat has been found to have the opposite effect.
For example, it has been demonstrated that reducing animal fat in the diet, and replacing it with proportionate calories from carbohydrates, will in particular increase levels of the undesirable small-dense LDL [Ref 1 & 2 ]. This is said to be due to the increase in carbohydrates rather than the decrease in fats (Ref). This study found that an increase in dietary saturated fat increases numbers of another desirable type of lipoprotein - large buoyant cholesterol-enriched LDL, which are found to negatively correlate with heart disease; whilst reducing small-dense sdLDL. But as I said earlier these are just bio-markers which can divert attention away from the real background causes.
The most popular theory of the cause behind the correlation between these sdLDL and atherosclerosis appears to be a little too mechanistic. It proposes that these pattern-B small dense LDL particles are so small that they slip through cellular gaps in the endothelial lining of the coronary arteries and cause vascular damage.
An alternative and more credible theory is that their existence is a consequence of slow and dysfunctional lipoprotein metabolism, which in turn is contributing to the cause of the atherosclerosis.
Relatively speaking, we are only able to store a limited amount of carbohydrate in our body; with individual variations affected by habitual diet, muscle mass, and physical activity levels. This is stored mainly as glycogen in the muscles, the liver, and also in the brain in very small amounts. When these stores of glycogen become saturated and the body is faced with a continued carbohydrate intake, its first response in order to deal with the excess is to increase the use of glucose as its primary fuel in all tissues. But these tissue will only burn what they need to meet their metabolic needs. The remainder is either returned to the liver, or converted into fats by adipose tissue.
In the face of high carbohydrate delivery above and beyond its own capacity to store it, the liver will increase its output of glucose into the blood, even when insulin levels have increased above a point which would normally cause the liver to reduce its glucose output and start converting it into glycogen. (Incidentally, the fructose and galactose sugar molecules preferentially stock liver glycogen and are therefore more likely to contribute to liver saturation if/when they are the dominant carbohydrate sources)
An alternative and more credible theory is that their existence is a consequence of slow and dysfunctional lipoprotein metabolism, which in turn is contributing to the cause of the atherosclerosis.
Relatively speaking, we are only able to store a limited amount of carbohydrate in our body; with individual variations affected by habitual diet, muscle mass, and physical activity levels. This is stored mainly as glycogen in the muscles, the liver, and also in the brain in very small amounts. When these stores of glycogen become saturated and the body is faced with a continued carbohydrate intake, its first response in order to deal with the excess is to increase the use of glucose as its primary fuel in all tissues. But these tissue will only burn what they need to meet their metabolic needs. The remainder is either returned to the liver, or converted into fats by adipose tissue.
In the face of high carbohydrate delivery above and beyond its own capacity to store it, the liver will increase its output of glucose into the blood, even when insulin levels have increased above a point which would normally cause the liver to reduce its glucose output and start converting it into glycogen. (Incidentally, the fructose and galactose sugar molecules preferentially stock liver glycogen and are therefore more likely to contribute to liver saturation if/when they are the dominant carbohydrate sources)
When saturated, the liver initiates de novo lipogenesis – the creation of new fat – using the excess carbohydrates to do so. These fats are packaged into high numbers of apoB100 particles called very low density lipoproteins (VLDL) and shipped out into the bloodstream in a rush, most likely with a poor anti-oxidant capacity.
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| A metaphorical lipoprotein log-jam |
The high number of VLDL particles in circulation causes the triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, over enriching them with triglycerides (via the action of cholesteryl-ester transfer protein, or CETP), which in turn reduces HDL functional capacity.
The triglyceride-rich LDL is "remodelled" during its excessive circulation by enzymes like hepatic lipase, becoming delipidated and smaller and denser, thus creating small-dense LDL. Once these particles get smaller it would appear that their clearance from circulation becomes hindered by their degenerated affinity for the LDL receptor, leading to an excessive time in circulation (Ref,Ref), which in turn further increases their susceptibility to oxidation (Ref).
If we then combine this abundance of lipoprotein molecules caused by excessive carbohydrates, and add easily oxidised polyunsaturated fats to the recipe, the outcome is obvious. Peroxidation of the vulnerable polyunsaturated fats leads to degenerated lipoprotein particles being taken up by the endothelium as an immune response. This then leads to an inflammatory reaction, the production of foam cells, and eventually the formation of arterial plaque.
As an aside, to demonstrate that the link between high carbohydrate intakes and heart disease is not a direct one, it is worth identifying the example of the Kitavans. This South Polynesian island population, eat generous quantities of carbohydrates. On average, they get 69% of their 2200 calories per day from high-glycemic starchy tubers and fruit (380 g carbohydrate), with not much fat to slow down digestion. Yet they have low fasting insulin, very little body fat and an undetectable incidence of diabetes, heart attack and stroke. That's despite a significant elderly population on the island and the tendency of many Kitavans to smoke like chimneys .
However, it should be noted that they are not eating excessive calories, their diet is extremely low in omega-6 polyunsaturated fats, with only some omega-3 polyunsaturated fats from occasional fish, and their main fat source is from highly-saturated and oxidation-resistant coconut fats.
For more information of the above process see "Lipoprotein Metabolism & Heart Disease"
