Cholesterol and statins

3. Foods with good evidence for lowering cholesterol, and supplements. Plant sterols/stanols, sometimes added to margarine, yoghurt or other fortified foods, reduce LDL-C by blocking cholesterol absorption in the intestine; typically doses of 2 to 3 g/day are needed to reduce LDL-C by ~0.3 to 0.4 mmol/L. Soluble fibre, when combined with liquid, helps remove bile acids so that the liver uses more LDL-C to make new bile acids: oats and barley (3 daily servings of oats lowers LDL-C <0.13 mmol/L), psyllium husk (the most evidence behind it; at least 10 g per day to reduce LDL-C), legumes (soluble fibre and plant protein). Nuts: one serving per day reduces LDL-C by 0.12 mmol/L. Polyunsaturated fats (fish, nuts, flax, chia seeds) and monounsaturated fats (olive oil, avocados, canola oil), the "good" fats. Soy protein, especially in place of animal protein. Vegan diets. Foods to avoid: saturated fats such as red meat, butter, high-fat dairy and coconut oil, which raise LDL-C. Supplements: red yeast rice extract contains naturally occurring statins (monacolins), particularly monacolin K, which is chemically the same as lovastatin, and there is evidence it can reduce LDL-C. The 2024 SPORT trial challenged this when it compared supplements like red yeast rice extract to low-dose rosuvastatin: rosuvastatin reduced LDL-C by 37.9% and the supplements showed no reduction in LDL-C compared to placebo. There are safety concerns as it is unregulated, and a contamination risk: some products have been found contaminated with citrinin (a nephrotoxic mycotoxin). Berberine shows modest LDL-C reduction in combination with other compounds. Fish oil (over the counter): no benefit for LDL-C or any outcomes. Plant sterols as a supplement: no benefit, though food-fortified sources have better evidence.

4. Lipoprotein(a) and familial hypercholesterolaemia. Lipoprotein(a) [Lp(a)] is a blood test which is not currently covered by Medicare and generally costs around $50 to $90 in Australia. Typically we only need to test it once in a person’s life; however, as treatments targeting Lp(a) emerge, we may start testing it more frequently. It may also be useful to test again after a woman has completed menopause. Lp(a) is like LDL cholesterol with an additional protein attached. Levels are mostly genetically determined (diet and exercise have little influence). People with elevated Lp(a) are 2 to 4 times more likely to develop coronary artery disease, calcific aortic stenosis (a type of valve disease), and cerebral (strokes) and vascular disease. It causes inflammation, increased risk of clots and coronary artery disease. International guidelines recommend measuring Lp(a) at least once in a lifetime for adults, especially for those with a family history of premature ASCVD; familial hypercholesterolaemia; onset of coronary artery disease without typical risk factors; family members with high Lp(a); calcific aortic valve stenosis; or persistently high LDL despite good medical treatment. Treatment targeting Lp(a) is still being investigated in large-scale trials. PCSK9 inhibitors have been found to reduce levels of Lp(a); however, this has not been studied independently and is not approved in Australia for the treatment of Lp(a) alone. People with elevated Lp(a) should be treated as high risk for heart disease, receive intensive management of other risk factors and be monitored closely. Familial hypercholesterolaemia (FH) is a genetic condition which results in a mutation in the LDL receptor, meaning LDL cannot enter the cells and builds up in the bloodstream, eventually depositing in the artery walls. It causes early-onset heart disease. It is one of the most common inherited conditions and 1 in 300 people in Australia have it. It is more common in some ethnic groups, such as Afrikaner, Christian Lebanese, Ashkenazi and French-Canadians. Dr Isobelle Smith (FRACP) manages complex and inherited lipid disorders in the same clinic.