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Lowering cholesterol in primary care settings

Key learning points:

 - Gain awareness of the causes of dyslipidaemia and the importance of being able to recognise conditions including inherited high cholesterol 

 - Be aware of the many secondary conditions that may have an influence on thelipid profile

 - Diet and lifestyle should be a key focus for cholesterol lowering, regardless of whether a statin is prescribed or not

The link between cholesterol and coronary heart disease (CHD) is well established. In 2002, the World Health Organisation (WHO) estimated that 56% of people with CHD have cholesterol concentrations greater than 3.8mmol/l.  INTERHEART, a case controlled study, ably demonstrated that the risk of heart attack is over three times higher in people with an abnormal lipid profile. They established the rule of thumb that every 1mmol/l reduction in low-density lipoprotein cholesterol (LDL-C) produced a 10% reduction in all causes of mortality. The term dyslipidaemia refers to a pattern of abnormal lipids (cholesterol and triglycerides) and the lipoproteins that carry them in the blood. It includes elevated total cholesterol (TC) and LDL-C, elevated triglycerides, small dense low-density lipoproteins (LDL) and reduced high-density lipoprotein (HDL). 

Primary causes of dyslipidaemia

Polygenic hypercholesterolaemia is the most common cause of high cholesterol and is associated with an increased risk of developing CHD. Although the condition is still not fully understood, it is thought to occur due to the small effects of a number of genes which influence lipid levels. These effects may be compounded by other risk factors such as poor diet, smoking and inactivity. Familial hypercholesterolemia (FH) and familial combined hyperlipidaemia (FCH) also have a genetic origin, but are slightly less common. Around one in 500 people have FH which is characterised by very high levels of plasma TC and LDL-C from birth (TC 7.5-12mmol/l, LDL-C >4.9). The most common form of FH is where one faulty LDL receptor gene is inherited from one parent resulting in only half the normal number of working LDL receptors on the surface of their cells. This means they struggle to remove LDL-C from the blood. Because LDL-C levels are usually two to three times higher than normal, FH is associated with an increased risk of premature cardiovascular disease, morbidity and mortality. If left untreated, approximately 50% of men will develop CHD by the age of 50 and 30% of women by the age of 60. Worryingly only 15% of the 120,000 people estimated to have FH have been formally diagnosed. It is therefore imperative that nurses are vigilant when screening for high cholesterol as most practices will have undiagnosed cases. Typically, these are patients with a history of high cholesterol (see levels above) and who have a history of premature heart disease in close family members. The Simon Broome diagnostic criteria are set out in NICE FH Guidelines. 

FCH affects one in 100 people and is relatively common. It is normally associated with insulin resistance and diabetes but may not be triggered until people are in their 20s or 30s, or even older. It is thought to be caused by several genes that act upon critical metabolic processes, and is associated with premature CVD. There can be considerable variability in presenting lipid levels (TC levels between 6-10mmol/l, triglycerides 2-3mmol/l or above). 

Secondary causes of dyslipidaemia

Before diagnosis it is important to exclude any possible secondary causes of dyslipidaemia, for example medications and conditions which can influence lipid levels, such as type two diabetes and untreated hypothyroidism.

People with type two diabetes frequently show a characteristic lipid pattern, referred to as diabetic dyslipidaemia, which increases the risk of developing CHD. This consists of elevated triglyceride, low levels of HDL-C and smaller sized LDL-C particles, which are more atherogenic. An underactive thyroid can cause severe hyperlipidaemia which is thought to be caused by the down regulation of LDL receptors due to the lack of thyroxine. Once properly treated, the lipid profile will usually normalise within three months. Hypothyroidism appears to increase the risk of developing side effects from medications such as statins so it is important that patients are not unnecessarily medicated.3

Other causes which should be considered include renal disease, liver diseases (cholestasis, alcoholic liver disease), obesity, diet, immune disorders, menopause, and certain medications including beta blockers, thiazides and anabolic steroids.

How nurses can help patients

Statin therapy has proven to be lifesaving, primarily as a result of their 25-55% LDL-cholesterol reducing effect and their plaque stabilising ability. However dietary and lifestyle interventions should always be first line therapy whether or not a patient has been prescribed a statin. The two should be complimentary. 

The ultimate cholesterol-lowering plan

Cholesterol charity Heart UK has developed an evidence-based dietary strategy called the 'the ultimate cholesterol-lowering plan' (UCLP) which focuses on key dietary changes that bring about significant cholesterol lowering. With a stepped approach and visual resources, the UCLP helps to make dietary interventions more deliverable. The diet is realistic and can be tailored to the patient's needs.

Step one involves motivational interviewing. This focuses on what motivates the patient, helping to get them started and enabling them to make and sustain dietary change.

Step two is about building strong foundations by encouraging the patient to adopt a heart healthy diet. This is achieved by reducing saturated fat and replacing it with healthier unsaturated fats and ensuring the five-a-day and oil rich fish once-a-week targets are met.

Step three is a pick-and-mix of four key foods (soy foods, nuts, soluble fibre and plant sterols and stanols). The patient can choose one or more over time. Each one of these foods can help reduce cholesterol further, and together they have an additive effect.

A change in diet can have a dramatic effect on the lipid profile. If fully adopted, the UCLP could lead to reductions in cholesterol of up to 24%. To enable nurses to access the UCLP, Heart UK has developed a toolkit of resources and an online teaching tool (see Resources). Even modest alcohol intake can cause weight gain due to its high calorie content. Excessive alcohol can affect the liver and lead to an increased triglyceride level. While drinking in moderation is thought to offer some protection against heart disease, the effect is small. The emphasis should be on not exceeding recommended levels and having at least two alcohol free days per week. Smoking is a well-known modifiable risk factor for CHD. Smoking affects the lipid profile by lowering HDL-C levels and raising LDL-C. Acrolein, a chemical found in cigarettes, stops HDL-C from transporting LDL-C to the liver, leading to unhealthy lipid profile levels and increased risk of CHD. Regular aerobic activity (for example, walking, jogging, swimming and cycling) which raises the heart rate for at least 20-30 minutes at a time, most days of the week, can improve lipid profiles. During exercise people should be slightly out of breath but still able to hold a conversation. Physical activity has an effect on the whole lipid profile, improving LDL-C, lowering triglyceride levels and increasing HDL-C. Mechanisms are unclear but it is thought to be due to the action of several enzymes and factors which interact to alter the rates of synthesis, transport and clearance of cholesterol from the blood. The benefits of being active are numerous and include being a healthier size and shape, reduced stress, better overall health and improved self esteem. 


Heart UK factsheets

Drink Aware



1. Dr. Mackay, J and Mensah, A. World Health Organisation. The Atlas of Heart Disease and Stroke. Part two Risk factors. 

2. Yusuf S, Hawken S, Ounpuu S et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case control study. Lancet 2004;364:93752.

3. Reckless J, Morrell J. Lipid Disorders: Your Questions Answered. London: Churchill Livingstone; 2005.

4. National Institute for Heath and Clinical Excellence (NICE). Identification and Management of Familial Hypercholesterolaemia. NICE Clinical Guidance 71; 2008.

5. What is FH? FH facts and figures; HEART UK. 

6. Neely, D. How can we improve clinical diagnosis of dyslipidaemia? In The British Journal of Cardiology 2012;(19):Supplement 1.

7. Joint ESC Guidelines: European Heart Journal: doi 10.1093/eurheartj/ehs092

8. The UCLP; 2011; HEART UK; Eating to our heart's content, saving lives and money.

9. Viljoen A. Improving dyslipidaemia management: focus on lifestyle intervention and adherence. Br J of Cardiology; 2012;(19):Supplement 1.