Lipid Profile: Understanding Your Blood Test Series

1. Overview: What this panel reveals and why it is important

The lipid profile is not merely a set of cholesterol numbers; it is a surrogate marker of lipoprotein metabolism and a cornerstone of global cardiovascular risk assessment. Unlike an enzyme panel that localises organ injury, the lipid panel quantifies the concentration and distribution of lipid‑carrying particles that, when perturbed, promote atherogenesis, inflammation, and end‑organ vascular damage.

The panel measures four core analytes—total cholesterol, LDL‑cholesterol, HDL‑cholesterol, and triglycerides—from which additional derived values (non‑HDL cholesterol, VLDL cholesterol, atherogenic ratios) are calculated. No single lipid value is diagnostic in isolation. The clinical power lies in the integrated pattern: the balance between pro‑atherogenic (LDL, non‑HDL, remnant particles) and anti‑atherogenic (HDL) lipoproteins, the degree of triglyceride elevation, and the presence of secondary or genetic drivers.

Critically, the decision to intervene—whether lifestyle or pharmacologic—is never based on lipid values alone. It is anchored in the patient’s absolute cardiovascular risk (age, sex, blood pressure, diabetes, smoking, family history, target organ damage). A “high” LDL in a young, low‑risk individual has a different implication than the same value in a diabetic with established coronary disease. Thus, the lipid profile is a conversation between the laboratory and the global risk algorithm, not a standalone diagnostic verdict.

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2. What does it measure

A standard lipid profile includes the following components. Reference ranges are laboratory‑specific; values below are approximate adult ranges and do not define treatment targets, which are risk‑stratified.

Core lipid fractions:

· Total cholesterol (TC): <200 mg/dL (<5.2 mmol/L). Represents cholesterol content of all lipoproteins (LDL, HDL, VLDL, remnants). Non‑specific; requires fractionation.

· Triglycerides (TG): <150 mg/dL (<1.7 mmol/L). Energy‑rich particles (VLDL, chylomicrons). Elevated levels reflect excess caloric intake, insulin resistance, or genetic disorders.

· HDL‑cholesterol (HDL‑C): >40 mg/dL (male), >50 mg/dL (female) (>1.0/1.3 mmol/L). Anti‑atherogenic; facilitates reverse cholesterol transport. Very high levels (>80 mg/dL) may not confer additional benefit.

· LDL‑cholesterol (LDL‑C): Optimal <100 mg/dL (<2.6 mmol/L); near‑optimal <130 mg/dL. Primary atherogenic lipoprotein. Calculated via Friedewald formula (valid when TG <400 mg/dL) or measured directly.

Derived / calculated parameters:

· Non‑HDL cholesterol: TC – HDL‑C. Captures cholesterol content of all atherogenic lipoproteins (LDL, VLDL, IDL, Lp(a)). Superior to LDL‑C alone, especially when triglycerides elevated.

· VLDL cholesterol: TG ÷ 5 (if mg/dL). Represents triglyceride‑rich lipoproteins.

· Atherogenic ratios:

· TC/HDL‑C ratio: <3.5 ideal; higher values predict risk.

· LDL‑C/HDL‑C ratio.

· TG/HDL‑C ratio: Surrogate for insulin resistance.

Advanced lipoprotein markers (not in standard panel, but sometimes added):

· Apolipoprotein B (ApoB): Number of atherogenic particles; stronger predictor than LDL‑C.

· Lipoprotein(a) [Lp(a)]: Genetic, pro‑thrombotic, pro‑atherogenic; measured once in lifetime.

· Apolipoprotein A‑I (ApoA‑I): HDL content.

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3. Other factors connected to this panel

Preanalytical variables:

· Fasting status: Traditional fasting (9–12 hours) minimises postprandial triglyceride variation. Non‑fasting samples yield slightly lower glucose, similar LDL‑C, and higher triglycerides (by ~20–30 mg/dL). Non‑fasting is acceptable for initial screening if TG <400 mg/dL.

· Posture: Prolonged recumbency (hospitalised) lowers cholesterol by ~10% (plasma shift).

· Tourniquet use: Prolonged application causes haemoconcentration, falsely elevating all lipid fractions.

· Sample handling: Lipids stable 7 days at 4°C; haemolysis falsely lowers some assays.

· Acute illness / surgery / MI: Lipid levels fall transiently (acute phase response). Do not measure lipids during or immediately after acute coronary syndrome – wait 4–8 weeks for steady state.

· Pregnancy: TC and TG rise progressively (peaks 30–35% above baseline at term). Return to pre‑pregnancy levels by 6–12 weeks postpartum.

Medications affecting lipid components:

· Increase LDL‑C: Thiazide diuretics, cyclosporine, amiodarone, progestins, some antiretrovirals (protease inhibitors).

· Increase triglycerides: Oral oestrogens, tamoxifen, beta‑blockers (non‑cardioselective), thiazides, glucocorticoids, isotretinoin, bile acid sequestrants, second‑generation antipsychotics (clozapine, olanzapine).

· Decrease LDL‑C: Statins, ezetimibe, PCSK9 inhibitors, fibrates (modest), plant sterols, red yeast rice (contains monacolin K).

· Decrease triglycerides: Fibrates, high‑dose omega‑3 fatty acids (≥2 g/day), niacin, statins (modest).

· Increase HDL‑C: Moderate alcohol, oestrogens, niacin, fibrates (modest); Note on alcohol: not recommended due to addiction potential.

· Decrease HDL‑C: Androgens, progestins, anabolic steroids, beta‑blockers, thiazides, smoking.

Physiological and demographic factors:

· Age: TC and LDL‑C rise until ~60 years (men) and ~70 years (women), then plateau or decline.

· Sex: Premenopausal women have lower LDL‑C and higher HDL‑C than men; postmenopausal LDL‑C rises, HDL‑C falls.

· Race/ethnicity: South Asians have higher triglycerides, lower HDL‑C, and increased Lp(a); African ancestry populations often have higher HDL‑C and lower triglycerides.

· Genetics: Familial hypercholesterolaemia (LDL receptor defects), familial combined hyperlipidaemia, familial hypertriglyceridaemia, Lp(a) excess.

· Body mass index: Positive correlation with TG, negative with HDL‑C; weight gain increases LDL‑C.

· Physical activity: Regular aerobic exercise raises HDL‑C, lowers TG; acute exercise transiently lowers lipids.

· Diet: Saturated and trans fats raise LDL‑C; dietary cholesterol has modest effect; excess simple carbohydrates raise TG.

· Seasonal variation: TC and LDL‑C slightly higher in winter (2–5 mg/dL).

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4. Disorders related to abnormal values: Pattern recognition

The lipid profile is best interpreted by dominant lipoprotein phenotype. Five patterns account for the vast majority of dyslipidaemias.

a. Isolated hypercholesterolaemia (elevated LDL‑C, normal TG)

Laboratory profile:

· LDL‑C ↑ (often >160–190 mg/dL)

· TC ↑ (proportional to LDL‑C)

· TG normal (<150 mg/dL)

· HDL‑C normal or slightly ↓

Differential diagnosis:

· Polygenic hypercholesterolaemia: Most common; multiple gene variants + diet/lifestyle; LDL‑C usually 130–190 mg/dL.

· Familial hypercholesterolaemia (HeFH, HoFH): Autosomal dominant (LDLR, ApoB, PCSK9). HeFH: LDL‑C >190 mg/dL in adults, tendon xanthomata, premature CAD family history. HoFH: LDL‑C >400 mg/dL, cutaneous xanthomata in childhood.

· Secondary causes: Hypothyroidism (low T4 increases LDL receptors), nephrotic syndrome (increased hepatic synthesis), cholestatic liver disease (lipoprotein X), anorexia nervosa.

· Dietary: High saturated fat, trans fat intake.

Outlier scenarios:

· LDL‑C >190 mg/dL in adult without secondary cause: Suspect HeFH until proven otherwise. Requires cascade screening, genetic counselling, and high‑intensity statin regardless of risk score.

· LDL‑C >400 mg/dL: Homozygous FH or severe HeFH; refer to lipid specialist.

· Isolated hypercholesterolaemia with normal LDL‑C but elevated non‑HDL: Occurs when TG borderline and VLDL contributes; check ApoB.

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b. Isolated hypertriglyceridaemia (elevated TG, normal LDL‑C)

Laboratory profile:

· TG ↑ (150–499 mg/dL mild; 500–880 moderate; ≥880 severe)

· LDL‑C normal or low (may be falsely low by Friedewald if TG >400)

· Non‑HDL cholesterol ↑ (due to VLDL)

· HDL‑C often low

Differential diagnosis:

· Primary: Familial hypertriglyceridaemia (autosomal dominant, elevated VLDL), familial combined hyperlipidaemia (may have mixed pattern), lipoprotein lipase deficiency (severe, chylomicronaemia syndrome).

· Secondary: Insulin resistance / type 2 diabetes, obesity, excess alcohol, oestrogen therapy, hypothyroidism, chronic kidney disease, pregnancy, glucocorticoids, antipsychotics.

· Dietary: High refined carbohydrate, excess caloric intake.

Outlier scenarios:

· TG ≥500 mg/dL: Risk of acute pancreatitis rises exponentially. Immediate lifestyle intervention and pharmacotherapy (fibrate, high‑dose omega‑3) indicated.

· TG >1000 mg/dL: Severe chylomicronaemia; may present with eruptive xanthomata, lipaemia retinalis, abdominal pain. Requires very low‑fat diet (<20 g/day) and fibrate.

· Mild TG elevation (150–200) with low HDL‑C: Highly characteristic of metabolic syndrome; treat underlying insulin resistance.

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c. Mixed hyperlipidaemia (elevated LDL‑C + elevated TG)

Laboratory profile:

· LDL‑C ↑

· TG ↑ (usually 200–500 mg/dL)

· Non‑HDL cholesterol ↑↑

· HDL‑C often low

Differential diagnosis:

· Familial combined hyperlipidaemia (FCHL): Common (1–2% of population); autosomal dominant with variable expression; elevated ApoB, small dense LDL, premature CAD.

· Diabetic dyslipidaemia: Elevated TG, low HDL‑C, normal or mildly elevated LDL‑C (often small dense LDL – pattern B).

· Secondary: Nephrotic syndrome, hypothyroidism, chronic kidney disease.

· Lifestyle: High caloric intake, high saturated fat, high refined carbohydrate.

Outlier scenarios:

· Mixed pattern with TG >500 and LDL‑C >160: Severe combined hyperlipidaemia; high risk of both atherosclerosis and pancreatitis.

· Mixed pattern in young adult with strong family history of premature CAD: Suspect FCHL or familial defective ApoB.

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d. Isolated low HDL‑C

Laboratory profile:

· HDL‑C <40 mg/dL (male), <50 mg/dL (female)

· LDL‑C normal, TG normal or mildly elevated

· TC may be low or normal

Differential diagnosis:

· Primary: Familial hypoalphalipoproteinaemia (mutations in ApoA‑I, ABCA1, LCAT – rare), Tangier disease (very low HDL, cholesterol esters in tissues).

· Secondary: Metabolic syndrome, insulin resistance, type 2 diabetes, smoking, sedentary lifestyle, very high carbohydrate intake, anabolic steroids, progestins.

· Physiological: Some individuals have genetically low HDL‑C without increased risk if other lipids and ApoB are normal.

Outlier scenarios:

· HDL‑C <20 mg/dL: Rare; suspect genetic causes (ApoA‑I deficiency, LCAT deficiency, Tangier). May be associated with corneal opacification, neuropathy, tonsillar discolouration.

· Isolated low HDL‑C with normal TG and LDL‑C: Controversial risk factor; current guidelines do not mandate pharmacotherapy specifically to raise HDL‑C. Focus on lifestyle and non‑HDL target.

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e. Secondary hyperlipidaemia: always consider underlying conditions

Any lipid abnormality—especially when recent onset, severe, or accompanied by systemic symptoms—should prompt evaluation for secondary causes:

· Hypothyroidism: ↑ LDL‑C, ↑ TG; check TSH.

· Diabetes / metabolic syndrome: ↑ TG, ↓ HDL‑C, ↑ small dense LDL.

· Nephrotic syndrome: ↑ LDL‑C, ↑ TG; hypoalbuminaemia.

· Chronic kidney disease: ↑ TG, ↓ HDL‑C.

· Obstructive liver disease: ↑ TC (lipoprotein X), normal TG.

· Pregnancy: Physiological rise; resolves postpartum.

· Drugs: As listed in Section 3.

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5. Best way to address aberrant levels: A holistic approach

Critical principle: The lipid profile is a modifiable risk marker, not a disease. Do not treat the number; treat the patient’s global cardiovascular risk. Empiric lipid‑lowering therapy without risk stratification is inappropriate and may delay investigation of reversible secondary causes.

a. Diagnostic algorithm, not therapeutic trial

Step 1: Confirm the abnormality

· Repeat lipid profile if initial value is borderline, severe, or suspected to be non‑fasting/acute illness‑related.

· Exclude secondary causes: TSH, creatinine, glucose/HbA1c, LFT, urine dipstick (protein).

· For severe hypercholesterolaemia, consider FH clinical criteria (Dutch Lipid Clinic, Simon Broome).

Step 2: Quantify absolute cardiovascular risk

· Use validated risk calculators (ASCVD risk estimator, SCORE2, QRISK3) incorporating age, sex, race, BP, diabetes, smoking, lipid values.

· High‑risk conditions (diabetes, CKD, established ASCVD, familial hypercholesterolaemia) automatically qualify for pharmacotherapy.

Step 3: Identify the dominant lipid phenotype

· Isolated high LDL‑C

· Isolated high TG

· Mixed

· Isolated low HDL‑C

· Secondary cause

Step 4: Treat the underlying cause and target the dominant abnormality

· LDL‑C dominant: Statin first‑line (moderate or high intensity based on risk). Ezetimibe, PCSK9 inhibitors for persistent elevation or statin intolerance.

· TG dominant: Lifestyle (diet, exercise, weight loss, alcohol cessation). If TG >500 or >200 with high risk: add fibrate, high‑dose omega‑3, or icosapent ethyl (pure EPA).

· Mixed: Statin first; if TG remain >500 or non‑HDL not at target, add fibrate or omega‑3.

· Isolated low HDL‑C: No pharmacotherapy specifically for HDL‑C. Lifestyle optimisation; non‑HDL or ApoB target.

Step 5: Treat genetic and severe disorders

· HeFH: High‑intensity statin + ezetimibe; consider PCSK9 inhibitor if not at goal. Cascade screen relatives.

· HoFH: Refer to specialist; statins, ezetimibe, PCSK9 inhibitors, lomitapide, evinacumab, LDL apheresis.

· Severe hypertriglyceridaemia: Fibrate + very low‑fat diet; avoid alcohol, oestrogens.

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b. Role of supplements and holistic medicine – supportive only

LDL‑C lowering (adjunctive):

· Plant sterols/stanols: 2 g/day reduces LDL‑C by 5–10%. Found in fortified spreads, supplements. Mechanism: inhibit intestinal cholesterol absorption.

· Soluble fibre: Psyllium husk, oats, barley, legumes, flaxseed. 5–10 g/day reduces LDL‑C by 5–8%.

· Red yeast rice: Contains monacolin K (lovastatin). Not regulated; variable potency, potential for contamination (citrinin). May cause same myopathy and drug interactions as statins. Not recommended as unregulated supplement.

· Berberine: Modest LDL‑C and TG reduction; gastrointestinal side effects; drug interactions. Limited evidence.

· Garlic, green tea extract: Minimal effect; not recommended for primary therapy.

Triglyceride lowering (adjunctive):

· Omega‑3 fatty acids (EPA/DHA): 2–4 g/day reduces TG by 20–50%. Prefer algae‑derived EPA/DHA (ecologically sustainable, no fish bioaccumulation). Icosapent ethyl (prescription pure EPA) reduces cardiovascular events in high‑risk patients with TG 150–499.

· Flaxseed oil (alpha‑linolenic acid): Weak TG lowering; inferior to EPA/DHA.

· Fenugreek, cinnamon: Very modest effect; insufficient evidence.

HDL‑C raising (adjunctive):

· No supplement reliably raises HDL‑C in a clinically meaningful or event‑reducing manner. Exercise and smoking cessation are most effective.

· Niacin: Raises HDL‑C but does not reduce cardiovascular events when added to statin; causes flushing, hepatotoxicity, hyperglycaemia. Not recommended.

Herbs and Phytochemicals from Indian subcontinent (adjunctive, not primary):

· Guggul (Commiphora mukul): Traditional use; modern trials show minimal or no LDL‑C reduction, potential rash. Not recommended.

· Arjuna (Terminalia arjuna): Bark extract; small studies suggest modest lipid lowering; insufficient for recommendation.

· Curcumin: Anti‑inflammatory; minimal direct lipid effect.

· Amla (Emblica officinalis): High vitamin C, antioxidant; some small trials show modest LDL‑C reduction. Adjunctive only.

· Never use as substitute for evidence‑based therapy in high‑risk patients.

Critical warning:

· Do not use red yeast rice with statins – risk of cumulative toxicity.

· Avoid all products containing undisclosed statins (common in adulterated “herbal” cholesterol supplements).

· Omega‑3 supplements should be from algal sources; fish‑derived contribute to marine ecosystem depletion and bioaccumulation of heavy metals.

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c. Dietary and lifestyle approach (plant‑forward, ecologically sustainable)

Core principles for all dyslipidaemias:

· Mediterranean dietary pattern – highest evidence level: Emphasises vegetables, fruits, legumes, whole grains, nuts, seeds, extra‑virgin olive oil. Reduces LDL‑C, TG, inflammation, and cardiovascular events.

· Replace saturated fat with unsaturated fat: Saturated fat <7% total calories. Use olive, avocado, nut, seed oils. Avoid coconut and palm oil (high saturated fat, ecological concerns).

· Eliminate industrial trans fats: Fully hydrogenated oils, partially hydrogenated oils (banned in many countries, still present in some ultra‑processed foods).

· Reduce refined carbohydrates and added sugars: Fructose drives hepatic de novo lipogenesis → hypertriglyceridaemia.

· Dietary cholesterol: No longer a primary target; eggs and shellfish do not significantly affect plasma LDL‑C in most individuals.

· Achieve and maintain healthy weight: 5–10% weight loss reduces LDL‑C by 5–10%, TG by 20–30%.

· Regular physical activity: ≥150 minutes/week moderate aerobic; raises HDL‑C, lowers TG.

· Complete cessation of alcohol and tobacco: Alcohol raises TG, contributes to hypertension, and has addiction potential. No cardioprotective benefit is worth the harm. Tobacco lowers HDL‑C and is pro‑atherogenic.

Plant‑based protein sources (ecologically responsible):

· Legumes, tofu, tempeh, edamame, mycoprotein, quinoa, hemp seeds, spirulina, chlorella.

· No requirement for animal protein for optimal lipid management.

· Saturated fat and dietary cholesterol are minimal in plant‑based diets; such diets consistently lower LDL‑C by 10–20%.

Specific considerations:

· Familial hypercholesterolaemia: Diet alone insufficient; requires pharmacotherapy. Adjunctive plant sterols and fibre may modestly enhance LDL‑C reduction.

· Hypertriglyceridaemia: Very low‑fat diet (<20% calories) if TG >500; restrict fructose, sucrose, alcohol.

· Metabolic syndrome: Insulin resistance drives lipid abnormalities; dietary carbohydrate restriction (not necessarily ketogenic) and weight loss are paramount.

Note on substances with addiction potential:

This guide does not recommend tea, coffee, alcohol, or tobacco in any form. While some observational studies have associated coffee with reduced cardiovascular mortality or moderate alcohol with higher HDL‑C, such substances carry addiction potential, contribute to hypertension, and (in the case of alcohol) directly raise triglycerides and cause hepatic steatosis. Non‑addictive lifestyle measures – particularly a whole‑food, plant‑based diet, regular exercise, and maintenance of healthy body weight – are both safer and more foundational for long‑term cardiometabolic health. No addictive substance is necessary for the management of dyslipidaemia.

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6. How soon can one expect improvement and the ideal time frame to retest

Improvement timelines are intervention‑ and phenotype‑dependent.

Dietary and lifestyle changes:

· LDL‑C reduction: 5–15% within 4–8 weeks of sustained diet modification.

· TG reduction: 20–50% within 2–4 weeks of carbohydrate restriction, weight loss, alcohol cessation.

· HDL‑C increase: Slow (1–3 mg/dL over months) with regular aerobic exercise.

Pharmacotherapy:

· Statins:

· LDL‑C reduction maximal at 4–6 weeks.

· Retest lipids at 6–12 weeks after initiation or dose change.

· Once stable, retest annually or more frequently if non‑adherence suspected.

· Fibrates:

· TG reduction evident within 2–4 weeks.

· Retest at 6–8 weeks.

· Omega‑3 fatty acids (≥2 g/day):

· TG reduction at 4–8 weeks.

· Ezetimibe:

· LDL‑C reduction at 4–6 weeks.

· PCSK9 inhibitors:

· LDL‑C reduction at 4–8 weeks; maximal effect 12 weeks.

Retesting intervals in stable disease:

· Primary prevention, low risk, on lifestyle only: Every 3–5 years if values near goal.

· Primary prevention, moderate/high risk, on pharmacotherapy: Every 6–12 months.

· Secondary prevention (ASCVD, diabetes with target organ damage): Every 6–12 months.

· Familial hypercholesterolaemia (on treatment): Every 6–12 months; more frequently if adjusting therapy.

· Severe hypertriglyceridaemia (TG >500): Every 4–8 weeks until TG <500, then every 6–12 months.

Special situations:

· After acute coronary syndrome: Do not measure lipids during hospitalisation; wait 4–8 weeks for steady state.

· Pregnancy: Lipid levels physiologically elevated; do not initiate statins; retest 6–12 weeks postpartum.

· Medication change: Retest 6–12 weeks after any change in dose or agent.

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Conclusion

The lipid profile is a window into the efficiency of hepatic lipoprotein synthesis, intestinal absorption, and peripheral catabolism. Yet its greatest clinical utility lies not in the isolated numbers, but in their integration with global cardiovascular risk. A mildly elevated LDL‑C in a low‑risk young adult is a prompt for dietary education; the same value in a diabetic with microalbuminuria mandates high‑intensity statin therapy.

Dyslipidaemia is not a unitary diagnosis. The pattern—isolated LDL‑C, isolated triglycerides, mixed, or secondary—dictates the diagnostic workup and therapeutic strategy. And while lifestyle is foundational, genetic hyperlipidaemias and high‑risk conditions require pharmacotherapy. Supplements and nutraceuticals are adjunctive, never substitutive.

The holistic management of an abnormal lipid profile is therefore diagnostic rigour first, absolute risk stratification second, cause‑specific therapy third, and supportive, ecologically sustainable lifestyle interventions always. The plant‑forward Mediterranean diet, regular physical activity, weight optimisation, and complete abstinence from alcohol and tobacco provide the substrate for durable cardiometabolic health.

No addictive substance—whether caffeine, alcohol, or nicotine—is required to achieve or maintain optimal lipid levels. Safe, non‑addictive, ecologically responsible dietary and lifestyle interventions are always preferred.

As with all blood tests, the lipid profile is a conversation between the laboratory, the clinician, and the patient. Interpret the pattern. Stratify the risk. Treat the patient—not the number.

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Note on dietary recommendations on this site:

For the sake of our environment we adhere to the following dietary preference hierarchy:

1. Plant‑based

2. Fungi / algae / fermented

3. Biotechnology / lab‑grown / cultures

4. Dairy / eggs

5. Meat / fish / poultry (only if no effective alternative exists)

This approach reflects ecological responsibility, antibiotic stewardship, and the urgent need to reduce the environmental footprint of dietary recommendations.

Special note on protein in dyslipidaemia:

Plant‑based protein sources are nutritionally adequate for all individuals requiring lipid management, including those with familial hypercholesterolaemia, diabetes, and established cardiovascular disease. Soy, legumes, mycoprotein, and algae provide complete or complementary amino acid profiles and are free from dietary cholesterol and low in saturated fat. Meat and fish are neither necessary nor preferred.

Special note on addictive substances:

This guide does not recommend tea, coffee, alcohol, or tobacco in any form. While some observational studies have associated coffee with reduced cardiovascular mortality or moderate alcohol with higher HDL‑C, the addiction potential, contribution to hypertension, and (for alcohol) direct triglyceride‑raising and hepatotoxic effects outweigh any putative benefit. Safe, non‑addictive lifestyle interventions are always preferred.

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