LDL, HDL cholesterol and triglycerides: understanding your lipid panel

01Understanding the different cholesterol fractions#

Cholesterol is a lipid molecule essential to body function. Often demonised in everyday language, it actually plays several essential roles: it participates in the structure of cell membranes, serves as a precursor for the synthesis of steroid hormones (cortisol, aldosterone, oestrogens, progesterone, testosterone), enters the composition of vitamin D, and constitutes the skeleton of bile acids necessary for fat digestion. The major part of circulating cholesterol is actually produced by the liver (about 80%), only about 20% comes from food. The problem therefore does not come from cholesterol itself, but from an excess in certain fractions, which becomes a major cardiovascular risk factor.

As cholesterol is insoluble in water, it circulates in the blood associated with transport proteins, forming lipoproteins with different characteristics and functions. This distinction is fundamental to understanding your lipid panel.

LDL is called "bad cholesterol" because its excess oxidises and deposits in artery walls as atheroma plaques. These plaques progressively narrow arteries (stenosis) and can rupture, triggering the formation of a clot that suddenly obstructs circulation: this is the mechanism of myocardial infarction when it affects the coronary arteries, or stroke when it affects the cerebral arteries. The higher LDL is over the long term, the more cardiovascular risk increases — each 1 mmol/L (0.4 g/L) reduction in LDL decreases cardiovascular risk by 22% according to international meta-analyses.

HDL, conversely, exerts a protective effect by capturing excess cholesterol from tissues (including incipient atheroma plaques) to bring it back to the liver where it will be eliminated. High HDL is associated with decreased cardiovascular risk. However, artificially raising HDL with medications has not demonstrated cardiovascular benefit in recent trials — what counts is "functional" HDL resulting from good lifestyle.

Triglycerides are the main form of fat storage in the body. Their moderate elevation is associated with metabolic syndrome (abdominal obesity, diabetes, hypertension), while severe elevations (above 5 g/L) expose to acute pancreatitis risk through hyperchylomicronaemia.

02Figures in Morocco and the public health issue#

According to data from the Moroccan Society of Cardiology (SMC) 2020 and the Epidemiology Directorate of the Ministry of Health, dyslipidaemias (blood lipid abnormalities) represent a real public health problem in Morocco.

Approximately 30% of Moroccan adults have an LDL above 1.60 g/L, i.e. nearly 8 million people with hypercholesterolaemia. This prevalence increases with age and reaches more than 50% after age 60. Approximately 22% of adults have hypertriglyceridaemia (triglycerides above 1.50 g/L), often associated with overweight, diabetes and excessive consumption of rapid sugars and alcohol. Low HDL is present in approximately 25% of men and 15% of women, more frequent in smokers, sedentary individuals and diabetics.

The worrying observation is that the majority of these patients are unaware of their situation: less than 50% of hypercholesterolaemic patients are diagnosed in Morocco, and among diagnosed high-risk patients, less than 30% achieve their therapeutic targets. Yet the consequences are considerable: cardiovascular diseases are the leading cause of death in Morocco, with approximately 17,000 annual deaths from myocardial infarction and as many from stroke, a significant part of which is directly attributable to untreated high cholesterol. Improving the screening and management of dyslipidaemias is therefore one of the major challenges of Moroccan cardiovascular medicine.

03How to read your lipid panel#

The lipid panel is a simple, inexpensive biological examination (60 to 150 MAD in Morocco, reimbursed at 70-80% by AMO) and widely available in all laboratories. It should be prescribed in any adult every 5 years after 40 (35 years in case of family history or risk factors), and more frequently in patients already on treatment.

Sampling is classically done fasting for at least 12 hours, which is necessary to correctly interpret triglycerides (which transiently rise after meals). Recent recommendations (ESC 2019) however accept non-fasting dosing for total cholesterol, LDL and HDL if triglycerides are normal. For the first determination or in case of abnormality, fasting dosing remains preferable.

The reference values for the general population, regardless of individual cardiovascular risk, are as follows.

But these general reference values are not enough — the LDL target must be adapted to individual cardiovascular risk of the patient, as we will see. An LDL at 1.40 g/L may be entirely acceptable in a young adult without risk factors, but largely insufficient in a patient who has already had an infarction.

04Targets according to your cardiovascular risk#

The recommendations of French HAS and the European Society of Cardiology (ESC) 2021, taken up in Morocco by SMC, classify global cardiovascular risk into four levels and define LDL targets differentiated according to this risk level.

Low risk concerns adults under 40 without particular risk factors (non-smokers, normotensive, non-diabetic, no early family history, normal BMI). For these patients, the LDL target is below 1.90 g/L.

Moderate risk concerns adults with one or two moderate risk factors. The LDL target is below 1.30 g/L.

High risk concerns type 2 diabetic patients without complications, patients with severe hypertension, those with moderate chronic kidney disease, patients with high calculated risk according to SCORE2 or Framingham scores. The LDL target is below 1.00 g/L.

Very high risk concerns patients who have already had a cardiovascular event (infarction, stroke, coronary syndrome, peripheral artery disease), diabetics with complications or several risk factors, patients with severe chronic kidney disease, patients with homozygous familial hypercholesterolaemia. The LDL target is below 0.70 g/L, and even below 0.55 g/L for patients having had a recent event (updated ESC 2019 recommendations).

This individual stratification is crucial. A patient who has had an infarction with "reassuring" LDL at 1.10 g/L in absolute value is in reality largely above his target and requires therapeutic reinforcement. Conversely, a patient without risk factors with LDL at 1.55 g/L can be monitored without medication. Calculation of global cardiovascular risk must therefore systematically precede any therapeutic decision.

05Causes of dyslipidaemia#

Several factors contribute to the elevation of cholesterol and triglycerides. Identifying them allows both proposing adapted management and motivating lifestyle changes.

Modifiable causes are the most frequent and represent the majority of dyslipidaemias in the general population. Diet rich in saturated fats of animal origin (butter, cream, fatty cheeses, fatty red meats, processed meats) is the leading cause of LDL elevation — these fats increase hepatic cholesterol synthesis and reduce LDL receptor expression. Trans fats present in some industrial pastries, biscuits, commercial fried dishes, are even more deleterious. Sedentary lifestyle reduces HDL and increases triglycerides. Overweight and obesity, particularly abdominal, are strongly associated with the entire unfavourable lipid triad. Smoking lowers HDL and favours LDL oxidation (which becomes more atherogenic). Excessive alcohol consumption significantly increases triglycerides and can cause major hypertriglyceridaemia. Excess rapid sugars (sodas, juices, pastries, sweets) increase triglycerides through hepatic lipogenesis.

Non-modifiable causes are important to recognise. Genetics plays a major role: familial hypercholesterolaemia, transmitted in an autosomal dominant mode, affects about 1 person in 200 in the general population (heterozygous form). It is characterised by very high LDL from childhood (generally above 1.90 g/L), cardiovascular risk multiplied by 20 without treatment, and the possibility of coronary events from the thirties. Cascade screening (screening of first-degree relatives as soon as a case is identified) is crucial. The homozygous form (1/250,000), much rarer and serious, gives LDL above 5 g/L and infarctions from childhood. Age (over 40 in men and 50 in women), male sex before menopause, and post-menopause in women (loss of oestrogenic protection) are non-modifiable factors. Several pathologies can cause secondary dyslipidaemias: hypothyroidism (always dose TSH in front of hypercholesterolaemia), type 2 diabetes, nephrotic syndrome, chronic cholestasis, certain treatments (corticosteroids, oestrogenic contraceptives, antiretrovirals, some antipsychotics).

06Treatment: lifestyle first, medications if necessary#

Management of dyslipidaemias is based on two complementary pillars. The first step is systematically constituted by lifestyle measures, which must be applied for at least 3 to 6 months before considering medication in moderate forms. These measures remain essential even when medication is initiated.

Weight loss in overweight or obese patients can decrease LDL by 5 to 15% and triglycerides by 20 to 50%. Regular practice of physical activity (at least 150 minutes per week of moderate intensity) increases HDL by 5 to 10% and reduces triglycerides. Smoking cessation progressively restores HDL and decreases global cardiovascular risk. Alcohol moderation (less than 2 glasses per day) lowers triglycerides in regular consumers. Diet, detailed below, is central.

When lifestyle measures are not enough after 3 to 6 months, or when cardiovascular risk is very high from the outset (justifying immediate treatment), medication is initiated. Several therapeutic classes are available.

Statins are the cornerstone of treatment, with cardiovascular benefit largely demonstrated by dozens of controlled studies on hundreds of thousands of patients. They inhibit the HMG-CoA reductase enzyme which synthesises cholesterol at hepatic level, which increases LDL receptor expression and favours its capture. The molecules available in Morocco are numerous: atorvastatin (Tahor, Lipitor generics), rosuvastatin (Crestor, generics), simvastatin, pravastatin, fluvastatin. Statins allow an LDL reduction of 30 to 55% depending on molecules and doses, with demonstrated reduction in cardiovascular mortality and total mortality. Monthly cost in Morocco is between 50 and 250 MAD depending on molecules, with a wide choice of very affordable generics. AMO reimbursement is 70-80% on prescription.

Ezetimibe (Ezetrol) inhibits intestinal cholesterol absorption and provides additional 15-20% LDL reduction in addition to a statin. Indicated when the target is not reached with the statin alone, or in case of statin intolerance. Monthly cost: 200 to 400 MAD.

Fibrates (fenofibrate, gemfibrozil) are mainly indicated in severe hypertriglyceridaemias or mixed dyslipidaemias. They decrease triglycerides by 30-50% and modestly increase HDL. Limited effect on LDL.

PCSK9 inhibitors (evolocumab/Repatha, alirocumab/Praluent) represent the most recent and most powerful therapeutic class. Administered by bi-monthly subcutaneous injection, they allow an additional 50-60% LDL reduction in addition to statins. Their high cost (about 6,000 MAD per month) still limits their access, and they are reserved for severe familial hypercholesterolaemia or very high-risk patients unable to reach their targets with other treatments.

ATP-citrate lyase inhibitors (bempedoic acid) and PCSK9 RNAi inhibitors (inclisiran) are novelties currently arriving on the market.

Statin side effects are at the heart of many concerns often disproportionate to scientific reality. Muscle pain is reported by 5 to 10% of patients, generally moderate and tolerable; in case of disabling pain, never stop without medical advice but discuss with your doctor a molecule change, dose reduction, or vitamin D and coenzyme Q10 dosing. The rare rhabdomyolysis (severe muscle destruction) occurs in less than 0.1% of cases, generally with drug interactions. Liver transaminase elevation is observed in 1-3% of patients, generally benign and reversible, justifying dosing at 3 months then annually. A slight increased risk of type 2 diabetes (+10-15% relative risk) has been demonstrated in at-risk patients, but this risk is largely compensated by the cardiovascular benefit of statins. Several myths circulating on the internet (statins responsible for cancer, cognitive disorders, ALS) have been refuted by Cochrane meta-analyses on hundreds of thousands of patients — these are false information that must be recognised so as not to refuse a potentially life-saving treatment.

07The anti-cholesterol diet#

Diet is probably the most powerful action lever in the majority of patients. The Mediterranean diet, validated by countless studies (PREDIMED in particular), is now considered the reference in cardiovascular prevention and is particularly suited to Moroccan culinary culture.

To favour in your daily diet. Extra virgin olive oil, main source of fat, at the rate of 2 to 4 tablespoons per day for cooking and seasoning — its monounsaturated fatty acids and polyphenols are protective. Fatty fish (sardines, mackerel, anchovies, salmon, tuna) at least 2 times a week — rich in anti-inflammatory and triglyceride-lowering omega-3. Dried fruits and oilseeds (almonds, walnuts, hazelnuts, unsalted pistachios) at the rate of a small handful (30 g) per day — rich in good fats, fibres, magnesium. Legumes (lentils, chickpeas, beans) at least 2-3 times a week — excellent source of vegetable proteins and soluble fibres that reduce intestinal cholesterol absorption. Coloured fruits and vegetables at the rate of 5 portions per day. Oats (flakes, oat bran) at breakfast — rich in beta-glucans which reduce LDL. Whole grains (whole bread, brown rice, whole semolina) rather than refined.

To limit or avoid. Red meats (beef, lamb, mutton) less than 500 grams per week according to WHO, favouring lean cuts. Cured and processed meats to a minimum (occasional consumption only). Industrial pastries rich in trans fats and added sugars. Fatty cheeses in large daily quantities — prefer fresh cheeses, plain yoghurts. Butter, fresh cream, lard in cooking — prefer olive oil or liquid vegetable oils. Fried foods and commercial fried dishes. Sugary drinks (sodas, industrial juices, syrups) which increase triglycerides. Alcohol in excess, to be limited to less than 2 glasses per day with alcohol-free days.

The DASH diet (Dietary Approaches to Stop Hypertension) and the Mediterranean diet share many common principles and can be combined. Consultation with a qualified nutritionist to personalise this approach according to your tastes and your Moroccan culinary culture brings considerable benefit. In Morocco, several nutritionists now offer these approaches adapted to traditional cuisine, which makes the advice more applicable on a daily basis.