A Deadly Combination of Durian with Alcohol Consumption

My mother in the 1940’s used to tell me when I was only  a small child, never eat durians and drink alcohol at the same time or soon after that. She told me it will result in death.  I was then very small when she told me this.

Today, I am a clinician, a nutritionist, a retired senior medical researcher, but above all  - a medical and food toxicologist - formerly with the Massachusetts Institute of Technology working in collaboration with the Institute for Medical Research. I believe today I am in a much better position to speak on the scientific truth behind this traditional, social and cultural belief.

 

This deadly traditional belief has struck on for generations among most Malaysians. There were several reports I read in the newspaper and have also heard unconfirmed stories telling the same -  of deaths resulting from the consumption of durian together with alcohol. Especially currently in the peak durian season we need to be careful with what we eat.

 

This paper is meant for all healthcare professionals, including medical doctors who have no clue on this traditional belief.  Some doctors has even  dismissed it as an  “unscientific superstition”  

 

Title: Durian and Alcohol  -  Biochemical Evidence Supporting a Traditional Malaysian Dietary Prohibition

 

Abstract

 

For generations, Malaysians have been cautioned against consuming durian together with alcohol, with traditional warnings ranging from severe illness to sudden death. Often dismissed as folklore, this belief has persisted across cultures and decades. This paper examines the biochemical basis of this traditional prohibition by analyzing the metabolism of ethanol in the human body and the inhibitory effects of sulphur-containing compounds found in durian on key hepatic enzymes. Evidence suggests that durian can significantly impair aldehyde dehydrogenase activity, leading to toxic acetaldehyde accumulation. While the claim of inevitable fatality is exaggerated, the combination poses genuine physiological risks, particularly in individuals with underlying metabolic or cardiovascular disease. This work demonstrates how traditional dietary wisdom may align closely with modern biochemical understanding.

Introduction

Durian (Durio zibethinus), revered as the “King of Fruits” in Southeast Asia, is cherished for its distinctive aroma, rich taste, and high nutritional value. Alongside its popularity, however, exists a long-standing traditional warning: durian should never be consumed together with alcohol. This belief was widely known in Malaysia as early as the first half of the twentieth century and was often conveyed with grave seriousness, sometimes invoking the possibility of death.

With advances in biochemistry, toxicology, and nutritional science, it is now possible to examine whether this traditional belief has a physiological basis. To do so, one must first understand the normal metabolic fate of ethanol in the human body.

Ethanol Metabolism: A Biochemical Overview

Absorption and Hepatic Processing

Ethanol is rapidly absorbed from the gastrointestinal tract into the bloodstream and transported to the liver, which serves as the primary organ for its metabolism. The detoxification of ethanol occurs via a tightly regulated two-step enzymatic pathway involving:

Alcohol dehydrogenase (ADH)  and  Aldehyde dehydrogenase (ALDH)

This system normally prevents the accumulation of toxic intermediates.

Step 1: Ethanol to Acetaldehyde (Alcohol Dehydrogenase)

The first step occurs in the cytoplasm of hepatocytes, where alcohol dehydrogenase (ADH) catalyzes the oxidation of ethanol into acetaldehyde:

Ethanol + NAD⁺ → Acetaldehyde + NADH + H⁺

Acetaldehyde is a highly toxic and carcinogenic compound, far more harmful than ethanol itself. It is responsible for many acute alcohol-related symptoms, including facial flushing, nausea, headache, tachycardia, and tissue injury. Therefore, rapid removal of acetaldehyde is essential for physiological safety.

Step 2: Acetaldehyde to Acetate (Aldehyde Dehydrogenase)

Acetaldehyde is promptly transported into the mitochondria, where aldehyde dehydrogenase (ALDH), particularly the mitochondrial isoenzyme ALDH2, oxidizes it into acetate:

Acetaldehyde + NAD⁺ + H₂O → Acetate + NADH + H⁺

This step is normally highly efficient, ensuring that circulating acetaldehyde levels remain extremely low.

Final Metabolic Fate

Acetate is relatively non-toxic and exits the liver to circulate to peripheral tissues such as muscle and brain. There, it is converted into acetyl-CoA, enters the citric acid (Krebs) cycle, and is fully oxidized to carbon dioxide and water, generating metabolic energy in the form of ATP.

In summary, under normal conditions: ADH initiates ethanol metabolism. ALDH completes detoxification. Toxic intermediates do not accumulate.

ADH and ALDH: Distinct but Complementary Roles

Although ADH and ALDH function sequentially, their physiological roles differ profoundly. Alcohol dehydrogenase (ADH) converts ethanol into acetaldehyde
Cytoplasmic localization produces a highly toxic intermediate . Aldehyde dehydrogenase (ALDH) converts acetaldehyde into acetate
ALDH2 is predominantly mitochondrial. Detoxifies aldehydes and protects tissues

ALDH enzymes form a family of NAD(P)+-dependent enzymes responsible for oxidising a wide range of toxic endogenous and exogenous aldehydes. ALDH2 deficiency or inhibition leads to acetaldehyde accumulation, manifesting clinically as the alcohol flush reaction.

Crucially, ADH activity often exceeds that of ALDH. Therefore, any impairment of ALDH function rapidly results in acetaldehyde buildup and systemic toxicity.

Durian and Enzyme Inhibition

Sulphur Compounds in Durian

Durian contains several volatile sulfur-containing compounds responsible for its characteristic aroma. Among these, diethyl disulfide has been shown to significantly inhibit aldehyde dehydrogenase activity.

Experimental studies, including those from the University of Tsukuba (Japan), demonstrate that diethyl disulfide can reduce ALDH (particularly ALDH2) activity by up to 60–70%.

Biochemical Consequences of Co-Consumption

When alcohol is consumed together with durian. ADH continues to convert ethanol into acetaldehyde. ALDH activity is inhibited by durian sulfur compounds. Acetaldehyde like formaldehyde  accumulates rapidly in the bloodstream and may even cause blindness. Other results in symptoms resembling severe alcohol intolerance like,  intense facial flushing, severe nausea and vomiting, dizziness and headache, palpitations and chest discomfort and profound malaise and distress

Additional Metabolic and Cardiovascular Stress

Durian is also high in natural sugars, calorically dense, and capable of transiently increasing blood pressure and heart rate

Alcohol contributes further physiological strain through vasodilation, dehydration, and sympathetic activation. In individuals with diabetes mellitus, hypertension, coronary artery disease, or cardiac arrhythmias, this combined metabolic burden may precipitate serious adverse events, including hypertensive crises, arrhythmias, or myocardial ischemia.

This provides a plausible explanation for rare but credible reports of collapse or death following durian–alcohol co-consumption.

Discussion: Tradition Anticipating Science

The traditional Malaysian warning against consuming durian with alcohol is not merely cultural superstition. While claims of inevitable or immediate death are exaggerated, modern biochemistry clearly demonstrates that the combination is physiologically hazardous, particularly in vulnerable individuals.

This case exemplifies how empirical cultural wisdom, transmitted across generations, can precede and is in line in the same frequency with scientific discovery.

The consumption of durian together with alcohol disrupts normal ethanol metabolism by inhibiting aldehyde dehydrogenase, leading to toxic acetaldehyde accumulation. While not universally fatal, the combination can cause severe adverse reactions and may be dangerous in individuals with underlying medical conditions.

Accordingly, avoidance of alcohol for several hours before or after durian consumption is strongly advisable. In this instance, traditional dietary guidance stands validated by modern biochemical science.

Selected References

1. Zakhari, S. (2006). Overview: How is alcohol metabolized by the body? Alcohol Research & Health, 29(4), 245–254.

2. Edenberg, H. J. (2007). The genetics of alcohol metabolism. Alcohol Research & Health, 30(1), 5–13.

3. Yokoyama, A., et al. (2010). Alcohol flushing, alcohol and aldehyde dehydrogenase genotypes, and risk for esophageal cancer. Alcohol, 44(2), 123–130.

4. Maninang, J. S., et al. (2009). Inhibition of aldehyde dehydrogenase by sulfur compounds in durian. Journal of Agricultural and Food Chemistry, 57(21), 10342–10347.

5. Lieber, C. S. (1997). Ethanol metabolism, cirrhosis and alcoholism. Clinical Chimica Acta, 257(1), 59–84.

 

1. thanol + NAD

 

The Progression of Atherosclerosis and Coronary Heart Disease with Age

 

From Linear Wear to Exponential Risk: The Age-Dependent Kinetics of Atherosclerosis

-  by Blogger Lim ju boo

Abstract

Atherosclerosis is often simplistically portrayed as a steadily progressive, linear consequence of aging. In reality, its biological behavior is far more complex. Accumulating evidence indicates that atherosclerosis follows an approximately linear trajectory during early life and mid-adulthood, but frequently transitions into an accelerated, near-exponential pattern in later decades. This shift reflects the convergence of biological aging, cumulative risk exposure, declining vascular defense mechanisms, and changes in plaque composition. Understanding this non-linear progression is essential for accurate risk prediction, timely prevention, and rational interpretation of vascular biomarkers.

1. Introduction: Beyond the Linear Model

A theoretical linear model of atherosclerosis, where plaque burden increases by a fixed amount each year, offers conceptual simplicity but fails to reflect biological reality. Human arteries are living, adaptive structures whose responses to injury, metabolic stress, and aging evolve over time. While early arterial changes may progress slowly and predictably, later stages are characterized by amplification phenomena in which small additional insults produce disproportionately large clinical consequences.

2. Early Life and Mid-Adulthood: Predominantly Linear Progression

In childhood, adolescence, and early adulthood, atherosclerosis typically begins as fatty streaks and minimal intimal thickening. During these phases, progression is generally slow and approximately linear. Longitudinal and cross-sectional studies of extra-cranial arteries, particularly the carotid arteries and abdominal aorta have shown that lesion size and intima-media thickness (IMT) increase in a near-linear fashion through early and middle adulthood.

This apparent linearity reflects several protective factors, namely:

 

(a) . Preserved endothelial function.

(b)  Robust antioxidant and repair mechanism.

(c) Lower cumulative exposure to metabolic and hemodynamic stressors

At plaque-free arterial sites, IMT often continues to increase linearly across much of the lifespan, serving as a marker of vascular aging rather than advanced atherosclerotic disease.

3. Transition in Later Life: From Linear Accumulation to Accelerated Growth

As individuals enter their sixth decade and beyond, the kinetics of atherosclerosis frequently change. Both structural arterial changes (such as stiffness) and clinically relevant plaque burden begin to accelerate. This transition marks a shift from simple accumulation to biological amplification.

Several age-related mechanisms drive this acceleration. These are cellular senescence that reduces the capacity for endothelial repair. Chronic low-grade inflammation (“inflammaging”) promotes plaque expansion and instability, oxidative stress increases as endogenous antioxidant defenses decline. Plaque vulnerability rises, with lipid-rich cores, thinning fibrous caps, and increased propensity for rupture.

The result is not merely larger plaques, but more dangerous ones.

4. Metric-Specific Patterns of Progression

4.1 Intima-Media Thickness (IMT)

At plaque-free sites, IMT generally increases linearly with age, reflecting diffuse arterial remodeling. However, when plaque-containing segments are included, several studies demonstrate an accelerated—often exponential, rise in IMT up to the seventh or eighth decade of life.

4.2 Coronary Artery Calcium (CAC)

Once calcification begins, coronary artery calcium tends to accumulate in a distinctly non-linear manner. CAC scores frequently demonstrate exponential growth, with doubling over defined time intervals. This reflects the transition from early, potentially reversible lesions to advanced, mineralized plaque.

5. Clinical Events and Mortality: Exponential Risk with Age

While anatomical measures may show gradual acceleration, clinical outcomes exhibit an even more dramatic pattern. The incidence of first cardiovascular events, including myocardial infarction and stroke, increases exponentially with age. In men, for example, first cardiovascular event rates may rise more than 20-fold between ages 40 and 90.

This divergence underscores a critical point: modest increases in plaque burden can translate into disproportionately large increases in clinical risk once biological reserves are exhausted.

6. Cumulative and Regional Influences

The shift from linear to accelerated progression is strongly influenced by cumulative exposure to traditional risk factors:

(a) Long-standing hypertension (b) Chronic hyperlipidemia (c) Diabetes and insulin resistance

These factors exert compounding effects over decades, leading to rapid progression later in life even if risk levels appear stable.

Regional differences further illustrate this principle. Intracranial arteries, for example, are relatively protected in early and mid-life by superior antioxidant and structural defenses compared with extra-cranial arteries. However, once these protections wane in advanced age, intracranial atherosclerosis may accelerate abruptly, contributing to late-life cerebrovascular events.

Atherosclerosis I should explain,  is not governed by a simple linear clock. Rather, it represents a biologically dynamic process in which early, slow accumulation gives way to accelerated progression as aging, cumulative risk exposure, and declining vascular resilience converge. Appreciating this non-linear trajectory helps explain why cardiovascular disease often appears suddenly in later life and emphasizes the importance of early, sustained prevention long before exponential risk emerges.

 

References & Further Reading:  

1. Libby P, Ridker PM, Hansson GK. Progress and challenges in translating the biology of atherosclerosis. Nature. 2011.

2.Lakatta EG, Levy D. Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises. Circulation. 2003.

3. Bots ML, et al. Common carotid intima-media thickness and risk of stroke and myocardial infarction. Circulation. 1997.

4. Budoff MJ, et al. Coronary artery calcium scoring: past, present, and future. JACC. 2018.

5. North BJ, Sinclair DA. The intersection between aging and cardiovascular disease. Circ Res. 2012.

6. Benjamin EJ, et al. Heart disease and stroke statistics—update. Circulation. Annual reports.

Letters of Reflection from Ms Sofea - A Physiotherapy in Kuala Lumpur Hospital

Sofea is a registered physiotherapist working  in Kuala Lumpur Hospital. 

 

She wrote this letter to share with me in my WhatsApp chat group many weeks ago. 

 

Thank you very much Sofea for sharing your thoughts and letters in my WhatsApp chat group. I value this very much, something most people lack - "yet it is more blessed to give than to receive".   

Let me reproduce what you wrote in blue below with your earlier permission

 

"Found this so beautiful 

 

Letting Go: The Grace in Accepting Change

 

There was a time when we believed we had control over everything—our days, our children, our careers, even the direction of life itself. We planned carefully, held tight to dreams, routines, people. And perhaps that was needed then. Life asked us to build, to care, to lead, to protect.

 

But slowly, life shifts.

 

One by one, the things we held so tightly start slipping away—not always with pain, but sometimes with quiet dignity.

 

The children grow up and move away—not out of disregard, but because they must build their own lives.

Beloved homes are sold, not because they weren't cherished, but because climbing those stairs became harder.

Our roles—as manager, mother, engineer, teacher—fade into the background, like names written in soft sand.

 

And then, there is a moment—a quiet afternoon, perhaps—when we look around and realise: life has changed.

The people we used to call every day now send messages. The faces around us are new. Even our own reflection carries gentle lines we never noticed forming.

 

But instead of grief, something else begins to settle in.

A kind of peace.

 

We understand, slowly, that letting go is not about losing. It’s about making room—for stillness, for peace, for reflection.

Letting go means allowing our hearts to carry memories without chains.

It means accepting that we are no longer the centre of the world—but we are still part of it, deeply and beautifully.

 

Letting go is not a weakness. It is grace—the grace of the river that flows forward, not resisting the rocks, but dancing around them.

 

It is in these years—when the world becomes quieter—that we learn the true strength of acceptance.

We hold less, but we feel more.

We chase less, but we appreciate more.

We speak less, but what we say carries depth" 

 

And so we sit by the window, sip our tea, and smile—not because life was perfect, but because we lived, we loved, and we let go… with grace.

 

- Sofea 

 

Yesterday, after reading my blog article on 

 

"Beyond Blockages: Can Atherosclerosis and Stable Angina Be Stabilized, or Even Reversed—Without Stents or Bypass Surgery? here: 

https://scientificlogic.blogspot.com/2026/01/can-atherosclerosis-and-stable-angina.html

 

Ms Sofea again wrote three letters  to me here: 

 

1. " [10/01, 6:50 am] Sofea Physio HKL: 

Thank you, Dr Lim, for the reminder. Life has been very busy and demanding lately. I am truly grateful.

2. [10/01, 7:06 am] Sofea Physio HKL: 

Thank you again, Dr Lim, for writing such a holistic approach to managing atherosclerosis. Disease is like a large puzzle that needs to be solved, with every piece fitting together nicely. I feel as though I could extend my life by 20 years after reading this.

3. [10/01, 10:40 pm] Sofea Physio HKL: 

Dear Dr Lim, Thank you so much for being so generous with your time and for always making yourself available to me despite your busy schedule. I truly appreciate your kindness and dedication.

I have always wanted to write a proper message that is worth your time to read. Unfortunately, I often put it off as my days are quite hectic juggling work and caring for my four children at home.

Thank you once again for your patience, understanding, and support. It truly means a lot to me. On the days when you feel slightly better, try to move your ankle and toes to help maintain the available range of motion. Even if strengthening is limited at this stage, preserving mobility is important. I’m concerned that reduced movement may affect ankle stability. Please also remember to stretch your calf muscles, as they are equally important for ankle function. 

- Sofea 

 

Can Atherosclerosis and Stable Angina Be Stabilized, or Even Reversed—Without Stents or Bypass Surgery?

Beyond Blockages: Can Atherosclerosis and Stable Angina Be Stabilized, or Even Reversed—Without Stents or Bypass Surgery?

 

Here are my answers and discussions for those who suffers from coronary heart disease and who cares and values what I write

 

by  lim ju boo, alias lin ru wu (林 如 武)

 

Atherosclerosis, the progressive buildup of lipid-rich plaques within the walls of arteries, lies at the heart of coronary artery disease (CAD), stroke, and peripheral vascular disease. For decades, it was regarded as an inexorably progressive condition, one that could be bypassed or mechanically opened but never truly altered. This view has changed substantially. Modern cardiovascular science now recognizes atherosclerosis as a dynamic biological process, one that can be slowed, stabilized, and in selected circumstances partially reversed, provided intervention is sufficiently early, sustained, and comprehensive.

The Biology of Atherosclerosis: Can Plaques Really Regress?

Atherosclerosis is fundamentally an inflammatory disease driven by the accumulation of low-density lipoprotein (LDL) cholesterol within the arterial wall. LDL particles penetrate a damaged endothelium, become oxidized, and trigger an inflammatory cascade involving macrophages, foam cells, smooth muscle proliferation, and extracellular lipid deposition. Over time, this process forms plaques that narrow arteries and compromise blood flow.

Although atherosclerosis remains a chronic condition, it is no longer correct to say it is entirely irreversible. Imaging studies using intravascular ultrasound (IVUS) and coronary CT angiography have demonstrated that intensive lipid-lowering therapy, particularly with high-dose statins and newer agents, can produce modest but measurable reductions in plaque volume, typically in the range of 1–5% over one to two years. While this degree of shrinkage may appear small, its clinical impact can be significant.

More important than plaque size reduction is plaque stabilization. Intensive therapy transforms plaques from soft, lipid-rich, rupture-prone structures into more fibrotic, stable lesions with thicker caps. Since most heart attacks result not from gradual narrowing but from sudden plaque rupture followed by thrombosis, stabilization dramatically reduces the risk of catastrophic events even when angiographic stenosis remains unchanged.

The stage of disease is crucial. Early, lipid-rich plaques respond far better to intervention than advanced, heavily calcified lesions. Once calcification dominates, true regression becomes difficult, though stabilization remains achievable.

Lowering Risk Aggressively: Medical and Lifestyle Foundations

To achieve plaque stabilization or regression, cardiovascular risk factors must be managed aggressively, often aiming for LDL cholesterol levels below 70 mg/dL, and in very high-risk patients, below 50 mg/dL.

Statins remain the cornerstone of therapy. High-intensity statins such as atorvastatin and rosuvastatin lower LDL cholesterol, reduce vascular inflammation, and stabilise plaques. When statins alone are insufficient or poorly tolerated, ezetimibe can further reduce intestinal cholesterol absorption, and PCSK9 inhibitors, powerful injectable agents, can lower LDL dramatically, with studies showing plaque regression in a substantial proportion of patients.

Lifestyle modification is not an adjunct but a biological intervention. Very low-fat, whole-food, plant-based diets, such as those studied by Ornish and others, have demonstrated regression of coronary disease in selected patients.

Besides nutrition and dietary changes other lifestyle modifications need to be addressed.

If you smoke, stop at once or at least gradually.  Quitting smoking is considered the most powerful and cost-effective step for protecting the heart. Tobacco toxins cause direct endothelial damage, promote plaque buildup, and increase the risk of blood clots. This includes avoiding vaping and secondhand smoke, both of which trigger arterial inflammation.

 

Smoking cessation is immediate and critical; it halts ongoing endothelial injury and reduces thrombogenicity within weeks.

 

Regular physical activity comes next.  Aim for at least 150–300 minutes of moderate-intensity aerobic exercise (e.g., brisk walking, cycling, swimming) or 75–150 minutes of vigorous activity per week. Exercise helps stabilize plaques by reducing the lipid core and thickening the fibrous cap, making them less prone to rupture.

 

High volumes of aerobic exercise improve endothelial function, insulin sensitivity, and lipid metabolism. However, do NOT engage in excessive, prolonged, and strenuous exercises if you know you already already suffering from coronary heart disease and angina pectoris (chest pains). You may suddenly collapse from an AMI (acute myocardial infraction or heart attack), or even a total cardiac arrest from cardiac electrical transmission failure. See my explanation here: 

Do You Think Exercise and Jogging are All Health Beneficial? Think Again and Read On

 

https://scientificlogic.blogspot.com/search?q=jogging+and+exercise

   

If you are obese or overweight weight management is crucial.  Losing even 5–10% of body weight can significantly improve cholesterol and blood pressure levels. Reducing central obesity (waist circumference) is particularly important as visceral fat has a direct link to plaque formation.

 

Consider stress management.  Chronic mental stress can double the risk of heart attacks by increasing blood pressure and triggering inflammatory responses. Effective techniques include mindfulness, meditation, deep breathing (e.g., the 4-7-8 method), and cognitive behavioral therapy. 

 

Optimal sleep hygiene is another helpful factor.  Aim for 7–9 hours of quality sleep per night. Inadequate sleep (≤4 hours) or excessive sleep (≥10 hours) is associated with an increased risk of coronary artery disease.

 

If you drink, limit alcohol intake. While some studies previously suggested benefits for red wine, 2026 health guidelines increasingly emphasize that any amount of alcohol may increase atherosclerotic risk. If consumed, limit to no more than one drink daily for women and two for men.

 

Regular health checkups is useful. Schedule annual physicals to monitor "silent" risk factors like blood pressure, cholesterol, blood sugar (A1c). Early detection allows for intervention before plagues become unstable.

Ensure  strict control of underlying conditions. 

Actively managing diabetes and hypertension is essential, as these conditions significantly accelerates plague hardening and progression 

Stable Angina: A Symptom, Not a Sentence

Stable angina represents the most common clinical manifestation of CAD. It is characterized by predictable chest discomfort arising when myocardial oxygen demand exceeds supply, typically during exertion, emotional stress, heavy meals, or exposure to cold. The pain is usually brief, lasting less than five minutes, and resolves with rest or nitroglycerin. It is often described as pressure, tightness, or heaviness rather than sharp pain, and may radiate to the arms, neck, jaw, or back. Importantly, certain groups, particularly women, older adults, and individuals with diabetes, may present with atypical symptoms such as breathlessness, nausea, or profound fatigue. Stable angina is usually caused by fixed, stable plaques that limit coronary flow during increased demand rather than by acute plaque rupture. Its predictability distinguishes it from unstable angina, which signals imminent risk of myocardial infarction and requires urgent evaluation. While stable angina is manageable, it is not benign. Any change in pattern such as pain at rest, prolonged discomfort, lack of response to nitrates, or increased severity, should prompt immediate medical attention.

Whether stable angina can be managed without angioplasty or coronary artery bypass grafting (CABG) depends largely on the extent, location, and physiological impact of coronary stenosis, a discussion that must be individualized.

Blood Thinners: Protection Without Plaque Removal

The term “blood thinners” is commonly misunderstood. It refers broadly to two distinct classes of medication: anticoagulants and antiplatelets.

Anticoagulants, including direct oral anticoagulants such as apixaban, rivaroxaban, dabigatran, and edoxaban, as well as warfarin and injectable heparins, interfere with the clotting cascade. Antiplatelet agents such as aspirin, clopidogrel, ticagrelor, and prasugrel prevent platelets from aggregating at sites of vascular injury.

These drugs do not thin the blood, nor do they prevent or reverse atherosclerosis. Their role is to prevent clot formation on top of existing plaques, especially when plaques rupture or endothelial surfaces become thrombogenic. This is why they reduce the risk of heart attacks and strokes without altering plaque burden.

Medications that truly modify plaque biology are lipid-lowering and anti-inflammatory agents, most notably statins and their adjuncts. Blood thinners are protective but not curative, and they cannot substitute for revascularisation when severe flow-limiting disease is present.

Nutrition and Diet is Exceedingly Important in Preventive and Curative Medicine: Can Food Stabilize or Reverse Disease?

By 2026, clinical consensus increasingly supports a “portfolio approach” to lipid management, combining multiple foods and nutrients that act through different mechanisms to improve cholesterol profiles and vascular health.

In tropical countries like Malaysia, nature offers a rich array of fruits and vegetables high in soluble fibre, antioxidants, and phytochemicals. These compounds reduce cholesterol absorption, improve bile excretion, dampen inflammation, and enhance endothelial function.

Avocados, rich in monounsaturated fats and fibre, have demonstrated the ability to lower LDL cholesterol while modestly raising HDL cholesterol in controlled studies. Guava provides abundant pectin and vitamin C, supporting cholesterol excretion and antioxidant defence. Mangoes contribute fibre and polyphenols that reduce dietary cholesterol absorption. Vegetables like lady's fingers and brinjals bind bile acids in the gut, while water spinach (kangkong) supplies antioxidants and potassium that support blood pressure regulation. Emerging research suggests that the leaves of the miracle fruit may possess lipid-lowering properties, though further study is needed.

 What about drinking green and oolong teas?  While both teas come from the Camellia sinensis plant, they undergo different processing that affects their specific bioactive compounds. Green tea is highly effective at reducing total and LDL ("bad") cholesterol due to its high concentration of catechins, specifically epigallocatechin gallate (EGCG).  Catechins inhibit the absorption of dietary cholesterol in the intestines and promote its excretion. Studies show green tea can reduce total cholesterol by 5–10%. although  most research indicates green tea has little to no significant effect on HDL ("good") cholesterol or triglycerides  Consuming 2–4 cups daily or supplements with at least 150 mg of catechins is often recommended for optimization. 

Oolong tea is partially fermented, giving it a unique profile of both green tea catechins and black tea's polymerized polyphenols.  It contains oolong tea polymerized polyphenols (OTPP), which are thought to inhibit pancreatic lipase, the enzyme that digests fats, thereby preventing fat absorption. Regular long-term consumption has been associated with significant reductions in total cholesterol, LDL, and notably, triglycerides (up to nearly 12% in some long-term studies). 

Drinking at least 10 ounces (roughly 1.5 cups) per week or 1 cup daily has been linked to lower risks of high cholesterol. Best for LDL: Green tea typically shows a stronger direct effect on lowering LDL cholesterol compared to oolong.

Oolong tea may be more effective than green tea at managing triglyceride levels.

For maximum benefit, brew tea at high temperatures (over 80°C / 176°F) for at least 3–5 minutes to ensure full extraction of polyphenols.

However,  tea contains caffeine, which may slightly raise blood pressure in sensitive individuals. It can also interfere with certain medications, such as statins or beta-blockers. 

Beyond whole foods, certain supplements provide concentrated doses of bio-active compounds. Niacin (vitamin B3) remains one of the most effective agents for raising HDL cholesterol while lowering LDL and triglycerides, though high doses require caution. Omega-3 fatty acids from fish oil or its supplements primarily reduce triglycerides and exert anti-inflammatory effects. I recommend frequent consumption of salmon, mackerel. herring and trout that are very rich in heart-protective EPA and DHA.  

Plant sterols and stanols block intestinal cholesterol absorption and can lower LDL by approximately 10% when taken at adequate doses. Plant sterols and stanols are naturally found in vegetable oils, nuts, seeds, whole grains, fruits and vegetables, but in small amounts; for therapeutic cholesterol lowering. Look for foods fortified with them, like some yogurts, spreads, orange juice, and cereal bars, which have significantly higher effective doses.   

Red yeast rice contains monacolin K, chemically identical to statins, and can significantly lower LDL cholesterol. Psyllium husk provides potent soluble fibre, while berberine may reduce both LDL cholesterol and triglycerides.

Other core heart-healthy foods besides oily fish, are extra virgin olive oil rich in polyphenols, nuts containing healthy fats and phytosterols, whole grains rich in beta-glucan, and deeply pigmented purple fruits and vegetables high in anthocyanins.

Dietary and nutritional strategies do not mechanically remove plaques. Their benefit lies in lowering LDL cholesterol, reducing inflammation, improving endothelial function, and stabilizing existing plaques. In carefully selected patients, such approaches, when combined with medication, may delay invasive procedures such as angioplasty or even open-heart by-pass surgery (CABG) . However, dietary approaches alone cannot universally replace angioplasty or bypass surgery, particularly in advanced multi-vessel disease with critical stenosis.

It is essential to note that some supplements, including red yeast rice and high-dose niacin, can cause adverse effects or interact with prescribed medications. Medical supervision is always advised.

Revascularisation: Treating Flow, Not Disease

Angioplasty with stenting and coronary artery bypass surgery remain powerful tools for restoring blood flow in critically narrowed vessels. However, they do not cure atherosclerosis. They treat focal obstructions while leaving the underlying systemic disease intact. Long-term outcomes, therefore, still depend on aggressive risk factor modification, medical therapy, and lifestyle change.

Let me summarize what I have explained and written: 

Atherosclerosis is no longer a hopelessly progressive disease. It is a modifiable biological process. Stable angina is not an automatic sentence to the catheterization lab or operating theater. Through intensive lipid lowering, appropriate medications, disciplined lifestyle change, and evidence-based nutrition, many patients can stabilize their disease and significantly reduce their risk of heart attack and death. 

But it also is exceedingly important to note that it does not mean after angioplasty or a coronary bypass surgery all the problems is solved permanently without any need to change our dietary lifestyles and other lifestyles such as continue to eat what we like, continue to be obese and overweight, continue to consume a lot of sugar, or continue to smoke or live aggressively with unnecessary anger and unnecessary stress, in which case the same heart problem will return, and nothing else, whether medical or surgical  can be done after that. Note this well written in red. .      

Nevertheless, medicine must remain honest. Not all plaques regress. Not all patients can avoid procedures. The art of cardiovascular care lies in matching the right patient to the right intervention at the right time, guided by science, compassion, and humility.

 

Selected References for Further Reading

 

1. Nissen SE et al. Statin therapy, LDL cholesterol, C-reactive protein, and coronary artery disease. N Engl J Med.

2. Nicholls SJ et al. Effect of intensive lipid lowering on coronary atherosclerosis. JAMA.

3. Sabatine MS et al. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med.

4. Ornish D et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA.

5. Stone NJ et al. 2018 AHA/ACC Guideline on the Management of Blood Cholesterol. Circulation.

6. Libby P. Inflammation in atherosclerosis. Nature.

7. Yusuf S et al. Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med.