Hypercholesterolaemia is a general term that is used to describe dyslipidaemia, a suboptimal blood lipid profile, and a key marker for increased cardiovascular disease risk and development of cardiometabolic disease.
Cholesterol is an essential fat that humans produced in the liver and some other tissues. Cholesterol is important for the production of steroids, sex hormones, bile acids, and as a component of all cell membrane structures. Our bodies only require a small amount of cholesterol to perform these important functions, and when dietary cholesterol and saturated fat intake is high the blood lipid profile becomes altered. Cholesterol is transported in the blood attached to lipoproteins, which is why a lipid profile will usually include:
High Density Lipoprotein (HDL-c) 1.0-2.0mmol/L
Low Density Lipoprotein (LDL-c) 2.0-3.5mmol/L
Total Cholesterol (TC) 3.0-5.5mmol/L
Non-HDL Cholesterol <3.37mmol/L
In addition to the standard lipid profile it is advisable to also measure:
Apolipoprotein B (APO-B) <130mg/dL
Very Low Density Lipoprotein (VLDL) <30mg/dL
HDL-c is often referred to as “good” cholesterol as it is responsible for transporting cholesterol out of the cells and back to the liver where it is synthesised into bile acids and excreted.
LDL-c is often referred to as “bad” cholesterol as it transports cholesterol from the liver to the cells where it is used in cell structures or to make various hormones. For this reason LDL-c should not be considered “bad” but recognised as being in excess.
VLDL is responsible for transporting triglycerides to the cells of the body to make energy. If triglycerides are high VLDL will transport them to adipose tissue where they are stored as body fat.
APO-B is another type of protein that is associated with cardiovascular disease. APO-B attaches to other atherogenic lipoproteins such as LDL-c and VLDL to provide structural support to the macromolecular structure. Having a high level of APO-B correlates to a high level of atherosclerotic plaque forming lipoprotein structures in the blood. Current evidence suggests that APO-B is a better marker than cholesterol, HDL, and LDL to determine cardiovascular disease risk.
The main problem with hypercholesterolaemia then is less about the cholesterol and more about the lipoproteins that are responsible for the transport of cholesterol and triglycerides around the body. It is these lipoprotein structures (LDL, VLDL, APO-B) that correlate to cardiovascular disease development.
Less commonly some people may have a hereditary predisposition to hypercholesterolaemia and there are certain populations of people, such as indigenous persons or those with an African heritage, who have a hereditary predisposition to developing dyslipidaemia and cardiovascular or cardiometabolic disease.
Shapiro, M. & Fazio, S. (2017) Apolipoprotein B-containing lipoproteins and athersclerotic cardiovascular disease, F1000Research, 6(F1000 Faculty Rev.), doi:10.12688/f1000research.9845.1
Wengrofsky, JL. & Makaryus, AN. (2019) Dyslipidemia and its role in the pathogenesis of atherosclerotic cardiovascular disease: Implications for evaluation and targets for treatment of dyslipidemia based on recent guidelines, Dyslipidemia, IntechOpen, USA, doi:10.5772/intechopen.05772
Hypercholesterolaemia refers to an elevated level of total cholesterol in the blood. Australian guidelines currently recommend a total cholesterol level of less than 4.0mmol/L for people at high risk for the development of cardiovascular disease, or less than 5.5mmol/L for the general healthy population.
Elevated total cholesterol however, is not a reliable indicator for cardiovascular disease risk, and the standard medical approach is to test for High Density Lipoprotein (HDL) often referred to as good cholesterol, Low Density Lipoprotein (LDL), HDL:LDL ratio and triglycerides. If these markers are outside the normal ranges then dyslipidaemia is diagnosed.
Dietary modification and lifestyle factors such as exercise and smoking cessation are the first line strategies in convention medical care for dyslipidaemia. If these strategies are not successful in correcting the lipid profile within 3 months, then pharmaceutical medications may be prescribed.
The most common class of medications used to treat dyslipidaemia are statins which inhibit a metabolic pathway (HMG-CoA reductase) for endogenous production of cholesterol. One of the most common side effects of statins is persistent muscle aches and pains.
If the use of statins alone are not effective in lowering cholesterol and correcting the lipid profile, or if a patient is unable to tolerate statin medications, other medications such as fibrates, nicotinic acid, or Ezetamibe may be prescribed.
Treating elevated cholesterol and dyslipidaemia in isolation of a total cardiovascular risk profile can be problematic as it may not necessarily reduce cardiovascular disease risk.
Unfortunately most people who develop hypercholesterolaemia will have no overt signs and symptoms, and the dyslipidaemia is only discovered by chance when the blood is tested during a routine health check. This is why it is vitally important to have your lipid profile checked regularly especially if you are 40+ years of age, overweight or obese, smoke, have excessive alcohol intake, consume a diet high in saturated fats and low in fibre, lead a sedentary lifestyle or have a family history of hypertension or cardiovascular disease.
There isn’t one single cause of eczema but a range of potential contributing factors that are unique to each person. These include:
Research has found people with the ‘atopic triad’ have a defective barrier of the skin and upper and lower respiratory tracts.
These genetic alterations cause a loss of function of filaggrin (filament aggregating protein), which is a protein in the skin that normally breaks down to create natural moisturisation and protect the skin from penetration by pathogens and allergens.
Filaggrin mutations are found in approximately 30 percent of people with atopic dermatitis, and also predispose people to asthma, allergic rhinitis (hayfever), keratosis pilaris (dry rough patches and bumps on the skin), and ichthyosis vulgaris (a chronic condition which causes thick, dry, scaly skin.)If one parent carries this genetic alteration, there is a 50 percent chance their child will develop atopic symptoms. And that risk increases to 80 percent if both parents are affected.
The connection between the gut microbiome and skin health is complex, however, research has found the microbiota contributes to the development, persistence, and severity of atopic dermatitis through immunologic, metabolic and neuroendocrine pathways.
Deficiency of Omega-6 essential fatty acids (EFA) has been linked with the increased incidence of atopic dermatitis, along with the inability for the body to efficiently metabolise EFA’s to gamma linoleic acids (GLA) and arachidonic acids (AA).
Changing weather conditions can certainly aggravate eczema symptoms, but the triggers are subject to change among individuals.
Mould exposure and susceptibility to mould can cause Chronic Inflammatory Response Syndrome (CIRS), of which dermatitis is a manifestation.
In most people the root cause for elevated cholesterol levels and dyslipidemia will be dietary. A diet high in saturated and trans- fats, low unsaturated plant based fats, or omega 3 fatty acids (fish oils), and low in fruits, vegetables and fibre will contribute to elevated cholesterol and an altered lipid profile.
However dyslipidaemia should not be considered in isolation, but should be considered as one part of a complete cardiovascular or cardiometabolic risk assessment. As with all cardiometabolic disease the principle underlying problems are dysregulation of the neuro-endocrine and immuno-inflammatory pathways which is impacting on the cardiovascular system in some way. The systemic vascular inflammation that is present, makes the vessel tissue fragile and prone to injury. When this occurs atherosclerotic plaque forms, and immune cells migrate to the site progressively impeding blood flow, and potentially fragmenting the plaque leading to emboli and the potential for heart attack and stroke. The risk of this occurring is higher in people with dyslipidemia.
The primary contributing factors for development of dyslipidaemia are a diet that is high in saturated and trans fats, low in unsaturated fats, low in fruits, vegetables and fibres.
Exercise has also been shown to be favourable for improving the lipid profile, so a sedentary or low physical activity lifestyle may increase the risk for dyslipidaemia.
Other contributing factors are those common to all cardiovascular and cardiometabolic diseases:
Family history of cardiovascular/cardiometabolic disease
Development of insulin resistance
Chatterjee, A., Harrid, S., Leiter, L., Fitchett, D., Teoh, H. & Bhattacharyya, O. (2012) Managing cardiometabolic risk in primary care; summary of the 2011 consensus statement. Canadian Family Physician, 58(4), 389-393.
A comprehensive cardiovascular profile screens for the most important markers for cardiovascular disease and cardiometabolic disease, including mulitple sub-fractions of LDL-c, blood clotting factors, and inflammatory markers.
In some cases it can be helpful to have certain general pathology tests done for things like vitamin B12, folate, vitamin D and iron studies, kidney function and liver function.
The most common misconception about cholesterol is that it is “bad” and therefore if you lower cholesterol you lower your risk for developing cardiovascular disease. Cholesterol and more broadly dyslipidemia should not be considered in isolation, but instead, as one component of a comprehensive cardiovascular and cardiometabolic disease risk assessment.
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