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Managing risk factors associated with cardiovascular disease

Despite advances in the diagnosis and treatment of cardiovascular disease (CVD), this condition remains a concerning public health issue in Australia, accounting for more than one in four deaths annually.

Patient improvement in modifiable risk factors has the potential to significantly decrease the incidence of CVD and its associated morbidity, mortality and economic burden. Yet, risk factors and management protocols associated with CVD remain widely misunderstood by the general public. With unique accessibility to patients, pharmacists are in the position to provide education and eliminate misconceptions offering advice on both effective lifestyle and pharmacological treatment options.

Risk factors for CVD: Cholesterol & Lipoproteins

Cholesterol is an important structural component of cell membranes, an essential precursor for steroid hormones in the body and a key molecule in digestion processes. Yet, abnormally elevated levels of serum cholesterol remain the most important indicator of CVD risk.

The cholesterol present in the body is derived from two sources: endogenously synthesised by the body and exogenously consumed through the diet. In the diet, cholesterol is a steroid exclusively found in animal tissues predominantly in egg yolk, beef, pork, poultry, dairy fat and crustaceans, such as shrimp, lobster and crab. In early days it was acceptable to assume that dietary cholesterol would increase serum cholesterol. However, modern-day research has demonstrated that the impact of dietary cholesterol is relatively insubstantial. The balance between endogenous and exogenous cholesterol is regulated very efficiently through a negative feedback loop. The efficiency of this loop has been demonstrated in animal studies, notably in guinea pigs who synthesised lower amounts of endogenous cholesterol when dietary intake was increased.

More recent studies have investigated the amounts of cholesterol transport proteins and their impact on CVD risk. The two major blood cholesterol carriers are low-density lipoprotein (LDL) and high-density lipoprotein (HDL). The normal function of LDL is to transport cholesterol from the liver to peripheral cells. LDL is taken up by the cells through specific receptor-mediated endocytosis. When LDL is unable to bind to receptors, serum concentrations can increase and particles can form deposits and become trapped in the artery walls. This can lead to plaque formation and narrowing blood vessels, a hallmark trait of atherosclerosis. And while LDL levels correlate with CVD risk, HDL has an inverse ratio of risk because HDL particles scavenge cholesterol from peripheral cells and artery walls to transport them back to the liver to be synthesised into bile salts or excreted as bile.

While lowering serum cholesterol remains the treatment goal for lowering CVD risk, the best means to achieve this is through lowering LDL and increasing HDL levels. From a dietary perspective, recommendations should include modifying the fatty acid composition of the diet through replacing saturated and trans fats with unsaturated fats and increasing the intake of whole grains and soluble dietary fibre.


A lot of misconceptions were generated from initial dietary recommendations which focused solely on reducing fat intake as a means to lowering risk factors associated with CVD.2 However, a solid backbone of evidence has now indicated that the composition of fats in the diet plays a more significant role than total fat. Thus, managing the types of fats consumed is now widely accepted as a more effective means for lowering risk factors associated with CVD.

Dietary saturated fats and trans fats have been recognised as having the most detrimental effect on CVD risk. While the excessive intake of saturated fat has been shown to raise LDL cholesterol levels in the bloodstream, trans fats have been shown to not only raise LDL cholesterol but also lower HDL cholesterol levels. It is hypothesised that these types of fatty acids may modify membrane fluidity which significantly alters LDL ability to bind to receptors and ultimately results in high levels of LDL cholesterol circulating in the bloodstream.

Contrary to this, unsaturated fats appear to reduce LDL cholesterol concentrations through upregulating LDL receptors. In addition, unsaturated fats provide a protective effect against CVD through increasing HDL cholesterol concentrations.

Recommendations should encourage patients to replace saturated and trans fats in their diet with unsaturated fats. This means limiting fatty meat, poultry skin, processed animal products and full-fat dairy, as well as fried foods and processed baked goods such as cookies, cakes and biscuits while increasing consumption of fatty fish, such as tuna, salmon, mackerel and sardines, as well as walnuts, flaxseeds and olive oil.

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Increasing consumption of dietary fibre, particularly soluble fibre, may also reduce LDL cholesterol levels. Soluble fibre found in oats, barley, rice bran, nuts, seeds, fruit and vegetables is the type of fibre that is fermentable by intestinal bacteria. The cholesterol-lowering abilities of soluble fibre have been attributed to its ability to bind to bile acids, inhibiting reabsorption and increasing the rate of its disposal. These beneficial effects of soluble fibre have been documented in both observational and RCT studies. On the other hand, insoluble fibre, found mostly in wheat, passes through the digestive tract intact and is generally understood to be beneficial for intestinal motility, yet has no effect on normalising cholesterol levels.

It is currently recommended that Australians consume at least 30 g of dietary fibre daily and, as previously mentioned, patients with elevated cholesterol should be encouraged to focus on insoluble sources of fibre. Patients introducing fibre into a traditionally low-fibre diet should be recommended to do so gradually, with an additional increase in water consumption in order to tolerate and ameliorate problems with gas and bloating.


Eggs are a major source of dietary cholesterol yet are the only dietary source of cholesterol that is low in saturated fat, which has made them a topic of intense debate for the past decade. Over the years, various studies have produced inconsistent results in regards to whether there is a dose-response association between egg consumption and risk of cardiovascular disease.11 Recently, researchers have tried to explain the lack of consistency and have mostly agreed that it comes down to different population groups exhibiting varying levels of sensitivity.

For healthy populations, egg consumption has quite consistently shown to not increase levels of fasting cholesterol nor increase risk of CVD. In-vitro studies have even shown that egg consumption might perhaps be beneficial for this population group.

However, the effect of egg consumption on serum cholesterol can be significant for populations with type 2 diabetes and individuals with hyperlipidaemia. In addition, it has been estimated that 15–25% of the population are hyper-responders to dietary cholesterol, which is poorly understood but possibly due to nutrient–gene interactions.

Therefore, in healthy populations, there is insufficient evidence supporting the restriction of egg intake as part of a healthy diet. For potential hyper-responders and high-risk populations, excessive egg consumption should not be encouraged and in some cases restriction should be considered.


Dietary intervention has emerged as a powerful tool in the management of CVD risk factors. A diet that replaces saturated and trans fats with unsaturated fats while increasing the intake of dietary soluble fiber can produce reductions in both LDL and serum concentrations of cholesterol.2 Pharmacists should feel empowered to offer education regarding dietary interventions which may enhance the efficacy of traditional pharmacological therapies.

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