When people think of cholesterol the two most common things you will hear is HDL being your “good cholesterol” and LDL being your bad “cholesterol”. These are not actually your cholesterol, these are lipoproteins, which are protein and fat, and their job is to package cholesterol into these transporters and send them where they need to go. While high LDL is a major risk factor for heart disease, looking at HDL and LDL as good and bad can be a little hasty and miss other markers of risk for cardiovascular disease.
Cholesterol is a major constituent of all our cell membranes, it is needed for steroid hormone synthesis like testosterone and oestrogen and aids in the synthesis of vitamin D and bile. The need for dietary cholesterol is actually zero, as cholesterol synthesis happens in the liver, and the liver can endogenously produce all of the cholesterol it needs. This begs the question, is dietary cholesterol even needed?
There are many different types of cholesterol, but we will be looking at HDL & LDL subfractions and triglycerides, which is not cholesterol but a type of fat that is highly correlated with heart disease if levels are high.
- High-Density Lipoproteins (HDL) Also known as your “good cholesterol”, the main constituent is APOA (the protein bit of lipoprotein). The main role of HDL is to bring cholesterol back to the liver for recycling. High levels in comparison to LDL are associated with reduced mortality from cardiovascular disease (CVD). HDL also picks up cholesterol in blood vessels to make sure it does not stay there.Optimal levels:- >60 mg/dl or >1 (males) >1.2 (females)mmol/L
- Low-Density Lipoproteins (LDL) Also known as your “bad cholesterol” the main constituent of LDL is APOB. The main role of LDL is to bring cholesterol to cells and peripheral tissue. So you can see that without LDL you would actually die! You need some LDL, the body has the transporters for a reason. This is often overlooked in the medical world when talking about cholesterol. You need LDL. A more accurate predictor of CVD risk is to look at the APOA/APOB ratio, as this is one of the scientific gold standards to measure CVD risk. This shows the level of HDL in comparison to LDL transporters in the body. If the ratio is skewed towards more APOB this implies LDL cholesterol will be too high. [1] Optimal levels :- <100 mg/dl or <3 mmol/l
Small Dense LDL (sdLDL) These are a specific subfraction of LDL that can penetrate blood vessel walls easily because of their size. They are also very reactive and can be easily oxidised or glycated (removal of electrons by sugar). This triggers an atherosclerotic response and increased levels of cholesterol in the endothelium (interior layer of blood vessels).
Higher levels of sdLDL are correlated with increased triglycerides, less HDLF and increased risk of CVD than LDL alone. Oxidised LDL is also another more recent exploration of the cholesterol research. As PUFA have more than one carbon double bond they are more vulnerable to lipid peroxidation (free radicals stealing electrons) This makes them very unstable
If the LDL particle has been modified in any way the immune system is more likely to take it up and form a plaque in a ditch effort to protect the body from this modified foreign particle. Macrophages (immune cells) see these modified sdLDL, and are more likely to form a plaque to protect the sensitive endothelium from these oxidised particles. Oxidised PUFA= more likely sdLDL uptake into the endothelium [12].
Why do i need to know this?
Most fried foods will heat sunflower, soybean and other PUFA at very high temperatures multiple times which leads to the fatty acid composition becoming very unstable. Ingestion of fried foods on a regular basis will increase consumption of oxidised PUFA, and increasing the risk of oxidised LDL deposition in the endothelium.
Triglycerides. Triglycerides are a type of fat that are elevated after you eat a meal and are stored in fat tissue to be used as energy later on. They are transported by carriers called chylomicrons. They make up the majority of human body fat stores. Triglycerides are raised with diets high in sugar and fat, specifically sugar, this is know as hypertriglyceridemia . [2] High triglycerides are a major risk factor for CVD. Triglycerides are also mainly transported by VLDL (very low-density lipoproteins) VLDL remnants(left and not used) are elevated and remain circulating when you eat due to their triglyceride carrying effects, and much of the CVD literature finds a strong correlation between remnant lipoproteins and atherosclerotic cardiovascular disease [5] Optimal levels:- <150 mg/dl or <3 mmol/L
Early studies looked at feeding rabbits high amount of dietary cholesterol and seeing whether this had a detriment to serum cholesterol. The rabbits were fed purified cholesterol and there was a dose-dependent correlation between cholesterol in the diet and atherosclerotic plaque build up in the arteries [3]. There are two main issues with these kinds of study:
- Rabbits are not humans and have different fatty acid metabolism, and are particularly sensitive to dietary cholesterol.
- No human eats purified cholesterol on its own.
So if we turn to more relevant literature in humans and look if dietary cholesterol does, in fact, raise serum cholesterol. There are 3 things we need to look at within the research:
- The relationship between saturated fat and dietary cholesterol levels in the food we are eating.
- The relationship between saturated fat intake compared to poly and monounsaturated on serum cholesterol.
- High saturated fat intake and high dietary cholesterol effect on blood cholesterol.
- Foods high in cholesterol are often high in saturated fat, think beef, pork, lamb, bacon and other processed red meats. Eggs being an exception as they are very high in cholesterol but lower in saturated fat. The most significant reduction in cholesterol often comes from replacing saturated fats with either poly or monounsaturated fats. Reducing dietary cholesterol is not as pronounced [4]. Clearly, if you reduce a lot of foods high in saturated fat you are in turn probably removing a lot of cholesterol, but the hypercholesterolemic effects are mainly from the saturated fat.
- High intakes of saturated fat suppress the LDL receptor, whereas PUFA upregulates the removal of cholesterol from the bloodstream. Saturated fat also remains in your blood longer after a meal than both PUFA and MUFA, which can cause endothelial damage. Saturated fats do not need to be consumed as the body can produce all of the saturated fatty acids it needs, it may be prudent in people who struggle to control their blood lipids or have existing CVD to replace saturated fats with fats that have a lowering effect on blood cholesterol. This is a very important thing to consider as with pretty much all things in nutrition it is the skewing of ratios that lead to adverse outcomes, rarely is one compound inherently unhealthy.
- Meta-analysis on saturated fat intake and heart disease often pool different results, some conclude “no association” and some conclude “strong association”. This is where the hierarchy of research can be called into question. A meta-analysis looks at a number of different studies with specific exclusion criteria and looks at trends, results and possible conclusions. The issue with some meta-analysis’ is the quality of the studies that they are looking at in the first place. Bad data= bad conclusion. LDL is a risk factor and not an endpoint (dying from CVD). [6] is one of the most cited studies in the “SFA does not cause CVD argument” this study found an 18% (borderline significant) increased mortality with high SF intakes and CVD instances (total and fatalities) This meta-analysis included 40% studies that controlled for LDL levels. This means that almost half of the studies made sure LDL levels were under a certain level to be included. As we know from earlie,r LDL is a major risk factor for CVD and with almost half of the studies having this variable controlled calls into question this meta analysis’ validity. When not controlled for LDL the study shows a 32% increase in risk with SFA content, this is very statistically significant. Meta-analysis are supposedly the “gold standard” but it is so important to look at the studies included in the analysis to test its validity. High saturated fat intake will raise blood cholesterol in more people than not, there will outliers in which it does not.
[7] Finland CVD trend study. SFA intake fell from 22% to 13% with the majority of this coming from reduced butter consumption from 40lbs to 7lbs average per year. A 70% reduction in CVD mortality mainly attributed to decreases in LDL.
Considering PUFA and MUFA both reduce cholesterol it is a prudent recommendation to reduce saturated fat intake in relation to these other types of fatty acid.
A note on Sodium and blood pressure
Cholesterol and blood lipids are not the only factor affecting CVD risk, blood pressure can be affected by cholesterol levels, and is an independent risk factor.
Blood pressure is made up of systolic (when the heard beats) and diastolic (when the blood vessels relax) optimal levels are 120/80 but 115/83 would still be considered healthy. 140/90 is considered hypertensive, and can often require prescription medication.
Sodium is an essential electrolyte mineral which is essential for muscle contractions, blood pressure, and blood volume. As it is an electrolyte is has charged ions so is also essential in normal nerve transmission. Sodium is very important, and it is recommend to consume between 3-8g of salt every day which at the upper end is around 3,400mg of sodium. Very low salt intakes are correlated with an increased risk of insulin resistance, increased blood glucose and an increased risk of mortality, which is your risk of death [8] [9]. The Renin angiotensin system is responsible for maintenance of blood volume and pressure, and chronically low sodium intakes negatively affects this system, as sodium is essential.
The biggest issue is that processed foods and “unhealthy” foods are often very high in sodium and very low in potassium. Potassium is another essential mineral which has the opposite effect to sodium. Potassium lowers blood pressure and volume whereas sodium raises it. The real issue is when peoples diets are very high in salt and lacking in potassium. The NRV (nutrient reference value) is 4,600mg which is much higher than the average consumption.
What foods are high in potassium?
Fruits & Vegetables.
The consensus among a large body of literature is that the sodium-to-potassium ratio appears to be more strongly associated with blood pressure outcomes than either sodium or potassium alone in hypertensive adult population [10].
Public health messages to reduce salt are pointless in the fight against CVD, and only very modest transient reductions in blood pressure are observed with salt restriction. Focus should be on other factors, such as maintaining a healthy body weight, consuming the right kind of fats (PUFA & MUFAs), not smoking and doing a mix of aerobic and anaerobic activity. [11]
Comments
Post a Comment