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A useful way to spread a health myth is not to invent something entirely false.
Start with something true.
Then remove the denominator, the competing mechanisms, the boundary conditions, and the uncertainty.
What remains is much easier to remember.
That pattern appears repeatedly in public statements by the Portuguese physician Manuel Pinto Coelho. He has argued that cholesterol has been turned into a distraction, described statins in highly negative terms, attributed inflammation largely to sugar, claimed that sunlight protects more against cancer than it causes, and described fasting as a kind of surgery without a scalpel.
These are not random internet rumours. They are publicly documented statements made in interviews and media appearances.
The interesting question is therefore not whether every sentence is "true" or "false".
The interesting question is:
Which part of the statement is supported, and at what point does the claim become stronger than the evidence?
That is a much more useful exercise.
The anatomy of a persuasive health myth
Before looking at the individual claims, it helps to define the structure.
A common pattern is
The first arrow may be justified.
The second may be plausible.
The third often needs much stronger evidence.
The fourth may be completely unsupported.
For example:
- LDL particles participate in atherosclerosis.
- Inflammation also participates in atherosclerosis.
- Therefore inflammation matters.
- Therefore cholesterol is merely a distraction.
The first three statements can coexist.
The fourth does not follow.
That logical failure is the recurring theme of this article.
Claim 1: cholesterol is a distraction and inflammation is the real problem
In a March 2026 interview, Pinto Coelho described cholesterol as an "arma de distração massiva" and argued that the real problem is inflammation, much of it originating in sugar.
There is a small piece of truth inside this argument.
Atherosclerosis is an inflammatory disease. Inflammatory signalling participates in plaque formation, progression, and rupture. Modern cardiovascular medicine does not deny this. Anti-inflammatory mechanisms are actively studied, and some anti-inflammatory interventions have reduced cardiovascular events in selected populations.
But that does not make LDL irrelevant.
The causal evidence for LDL in atherosclerotic cardiovascular disease is unusually strong because several independent lines of evidence converge.
Genetic variants that raise lifelong LDL exposure increase cardiovascular risk. Variants that reduce LDL exposure lower risk. Prospective cohort studies show dose-dependent associations. Most importantly, randomized trials of LDL-lowering therapies reduce cardiovascular events in proportion to the absolute reduction in LDL burden.
The European Atherosclerosis Society reviewed evidence from genetic studies, epidemiology, Mendelian randomization, and randomized trials involving millions of participants and concluded that LDL is causally involved in atherosclerotic cardiovascular disease.
The World Health Organization currently describes elevated LDL cholesterol as one of the principal modifiable cardiovascular risk factors and notes that lipid-lowering medicines, including statins when indicated, reduce the risk of myocardial infarction and stroke.
Inflammation and LDL are therefore not competing explanations in the sense implied by the claim.
A simplified causal graph is closer to:
with inflammation acting throughout the process.
Calling LDL a distraction because inflammation also matters is like calling smoking a distraction because carcinogenesis involves DNA damage and inflammation.
Multiple causal layers can be true at the same time.
Verdict: inflammation matters, but the claim that cholesterol is essentially a distraction is incompatible with a large body of genetic, mechanistic, epidemiological, and randomized evidence.
Sources:
- Manuel Pinto Coelho interview, NiT, 5 March 2026: https://www.nit.pt/fit/saude/manuel-pinto-coelho-o-jejum-e-uma-cirurgia-sem-bisturi
- European Atherosclerosis Society consensus on LDL causality: https://academic.oup.com/eurheartj/article/38/32/2459/3745109
- WHO, Dyslipidaemia, 15 September 2026: https://www.who.int/news-room/fact-sheets/detail/dyslipidaemia
Claim 2: statins are a medical mistake
In an earlier interview, Pinto Coelho described the widespread use of statins in strongly negative terms and connected their use to what he considers a mistaken focus on cholesterol.
Again, there is a legitimate issue hidden inside the rhetoric.
Not everyone with an elevated cholesterol value should automatically receive a statin.
Treatment depends on absolute cardiovascular risk, age, comorbidities, prior cardiovascular disease, LDL concentration, diabetes, familial hypercholesterolaemia, potential adverse effects, competing risks, and patient preferences.
Over-treatment is a valid concern.
So is under-treatment.
But those questions are fundamentally different from claiming that statins as a class are based on a false premise.
Statins inhibit HMG-CoA reductase and lower circulating LDL cholesterol. Large randomized trials and meta-analyses have repeatedly shown reductions in major vascular events. Their benefit is particularly clear in secondary prevention and in higher-risk primary-prevention populations.
The 2025 focused update of the European Society of Cardiology and European Atherosclerosis Society dyslipidaemia guidelines continues to recommend statins as first-line lipid-lowering therapy when pharmacological treatment is indicated.
This does not mean statins are harmless.
They can produce adverse effects, including muscle symptoms in some patients, a small increase in diabetes risk in susceptible individuals, drug interactions, and rare serious complications.
Evidence-based medicine is not the claim that a treatment has no harms.
It is the comparison
for a particular patient or risk group.
The internet version often replaces that calculation with one of two slogans:
- statins save everyone;
- statins are poison.
Neither is medicine.
Verdict: criticism of indiscriminate prescribing is reasonable. Treating statins themselves as a failed or shameful medical idea is not consistent with randomized evidence or current cardiovascular guidelines.
Sources:
- Manuel Pinto Coelho interview, Expresso: https://leitor.expresso.pt/semanario/semanario2324/html/revista-e/-e/manuel-pinto-coelho-o-sol-protege-mais-contra-o-cancro-do-que-o-provoca
- ESC/EAS 2025 focused guideline update: https://www.escardio.org/communities/councils/cardiology-practice/education/cardiopractice/what-is-new-in-the-2025-focused-update-of-the-2019-esc-eas-guidelines-for-the-m/
- WHO, Dyslipidaemia: https://www.who.int/news-room/fact-sheets/detail/dyslipidaemia
Claim 3: sugar is the principal cause of inflammation behind most diseases
The podcast Sem Remédio has presented Pinto Coelho's position that sugar is the principal driver of inflammation and that this inflammation sits behind a very large proportion of disease.
This is rhetorically effective because all three components sound plausible:
- excessive sugar intake can be unhealthy;
- chronic inflammation contributes to many diseases;
- diet influences inflammation.
The difficulty is the causal compression between them.
"Inflammation" is not one disease and not one pathway.
It is a broad set of immune and tissue responses involving many mediators, tissues, triggers, and timescales.
Inflammation can result from infection, autoimmunity, adipose dysfunction, smoking, tissue injury, environmental exposures, sleep disturbance, chronic disease, ageing, periodontal disease, and numerous other processes.
Diet is one contributor.
Sugar intake can also contribute indirectly through excess energy intake, weight gain, insulin resistance, hepatic fat accumulation, and adverse dietary substitution.
But the proposition
is not an adequate causal model.
Controlled feeding studies are particularly revealing here. A systematic review and meta-analysis of intervention studies found no consistent evidence that fructose produced more systemic inflammation than glucose or sucrose, although the evidence base had limitations.
A later meta-analysis of controlled trials found that the inflammatory effect depended strongly on the food source and energy context. Sugar-sweetened beverages behaved differently from fruit or other foods containing fructose.
That distinction matters.
The molecule, food matrix, dose, total energy intake, replacement food, baseline metabolic health, and duration of exposure all affect interpretation.
A can of sugar-sweetened soda and a whole orange both contain sugars.
They are not metabolically identical exposures.
None of this is an argument for high added-sugar intake. Excess intake of sugar-sweetened beverages is associated with obesity, type 2 diabetes, dental disease, cardiovascular risk, and other adverse outcomes.
The point is narrower:
"Too much added sugar is unhealthy" is well supported. "Sugar is the principal inflammatory cause of most disease" is not.
Sources:
- Sem Remédio, NiTfm: https://www.nitfm.pt/programas/sem-remedio/
- Systematic review and meta-analysis of dietary sugars and inflammatory biomarkers: https://pubmed.ncbi.nlm.nih.gov/29757229/
- Controlled feeding meta-analysis of fructose-containing food sources and inflammation: https://pubmed.ncbi.nlm.nih.gov/36235639/
Claim 4: the sun protects more against cancer than it causes
This is one of the claims where imprecise communication can become particularly consequential.
Pinto Coelho has argued publicly that the sun protects against cancer more than it causes, linking the argument largely to vitamin D.
There is a correct starting point.
Ultraviolet B radiation stimulates cutaneous vitamin D synthesis.
Vitamin D is physiologically important.
Very low vitamin D status can be clinically relevant.
Outdoor activity also has health benefits that have nothing to do with ultraviolet exposure itself.
But solar ultraviolet radiation is also a known carcinogenic exposure.
The International Agency for Research on Cancer concluded that solar radiation is carcinogenic to humans and causes cutaneous malignant melanoma and non-melanoma skin cancer.
The World Health Organization states that skin cancers are caused primarily by ultraviolet radiation from the sun or artificial sources and recommends sun protection when the UV index is sufficiently high.
This does not mean that every photon of sunlight is harmful or that humans should avoid going outdoors.
The correct relationship is dose dependent.
We can represent the problem abstractly as
where $x$ is exposure, $B(x)$ represents benefits, and $H(x)$ represents harms.
There is no reason for either function to be linear.
A small or moderate exposure may provide benefits while excessive exposure sharply increases harm.
That is fundamentally different from the statement that sunlight protects more against cancer than it causes.
The latter requires a population-level causal comparison across multiple cancers, exposure patterns, skin types, latitudes, behaviours, confounders, and competing mechanisms. That is a much stronger proposition.
Vitamin D also does not require uncontrolled UV exposure. Dietary sources and supplementation can address deficiency in appropriate circumstances without introducing the same UV dose.
Verdict: sunlight contributes to vitamin D synthesis and outdoor activity has health benefits. Solar UV is nevertheless an established human carcinogen. The broad claim that the sun protects more against cancer than it causes is not supported as a general medical rule.
Sources:
- Manuel Pinto Coelho interview, Expresso: https://leitor.expresso.pt/semanario/semanario2324/html/revista-e/-e/manuel-pinto-coelho-o-sol-protege-mais-contra-o-cancro-do-que-o-provoca
- IARC Monograph on solar and ultraviolet radiation: https://publications.iarc.who.int/73
- WHO ultraviolet radiation fact sheet: https://www.who.int/news-room/fact-sheets/detail/ultraviolet-radiation
- WHO guidance on known health effects of UV: https://www.who.int/news-room/questions-and-answers/item/radiation-the-known-health-effects-of-ultraviolet-radiation
Claim 5: intermittent fasting is "surgery without a scalpel"
This phrase is memorable.
It is also a good example of how metaphor can smuggle in a biological claim.
Intermittent fasting can be a useful eating pattern for some people. Randomized trials and meta-analyses show that several forms of intermittent energy restriction can reduce body weight and improve some metabolic markers.
But fasting does not literally perform surgery.
The metaphor appears to imply something more specific: that fasting selectively removes harmful biological material while preserving what is beneficial.
Human metabolism is not that tidy.
During fasting, insulin falls, glycogen use changes, lipolysis increases, fatty-acid oxidation changes, and longer fasting periods can increase ketone production. Cellular nutrient-sensing pathways also respond.
Autophagy is frequently invoked in popular explanations.
Autophagy is a real cellular process.
But the leap from
fasting influences pathways associated with autophagy
to
fasting cleans the body and removes what is bad
is not a clinically validated equivalence.
Even the magnitude and timing of fasting-induced autophagy in specific human tissues are difficult to quantify directly.
For weight loss, much of the practical effect of intermittent fasting can often be explained by reduced energy intake and adherence to a restricted eating window. When intermittent fasting is compared with continuous calorie restriction under controlled conditions, differences are usually much smaller than popular descriptions suggest.
Intermittent fasting can therefore be useful without needing a detoxification narrative.
That distinction is important because metaphors such as "cleaning", "detox", and "surgery without a scalpel" encourage people to infer selectivity that has not been demonstrated.
Verdict: intermittent fasting can alter metabolism and can help some people reduce energy intake and body weight. Describing it as a process that selectively removes harmful material is a metaphor, not an established physiological result.
Source documenting the claim:
- Manuel Pinto Coelho interview, NiT, 5 March 2026: https://www.nit.pt/fit/saude/manuel-pinto-coelho-o-jejum-e-uma-cirurgia-sem-bisturi
- Sem Remédio, NiTfm: https://www.nitfm.pt/programas/sem-remedio/
The recurring method: replace a multivariable system with one villain
There is a common structure behind these claims.
Cardiovascular disease becomes inflammation.
Inflammation becomes sugar.
Obesity becomes insulin.
Cancer prevention becomes vitamin D.
Ageing becomes autophagy.
Once a complex system has one dominant variable, a corresponding solution becomes obvious.
Remove sugar.
Ignore cholesterol.
Avoid statins.
Fast.
Seek more sun.
The problem is not that these variables are irrelevant.
The problem is that biological systems rarely have the form
They look more like
where genetics, environment, behaviour, medication, age, time, interactions, baseline risk, and unobserved variables all contribute.
Medicine is difficult precisely because the function $f$ is complicated.
A persuasive health communicator can make the world feel simpler by deleting most of the variables.
The resulting model becomes easier to explain.
It also becomes less true.
Partial truth is more persuasive than nonsense
This is why these claims deserve more careful analysis than obviously absurd medical misinformation.
Consider the following statements:
- chronic inflammation matters;
- excess added sugar can be harmful;
- sunlight contributes to vitamin D synthesis;
- fasting changes metabolism;
- prevention is important;
- lifestyle matters enormously for long-term health.
All are defensible.
If every public claim were obviously false, misinformation would be easy to recognize.
The persuasive move is to place an unsupported conclusion immediately after a supported premise.
For example:
Inflammation causes disease. Sugar can promote adverse metabolic states. Therefore sugar is the cause of most inflammation.
Or:
Vitamin D is important. Sunlight produces vitamin D. Therefore sunlight prevents more cancer than it causes.
Or:
LDL is not the only cardiovascular risk factor. Therefore LDL is a distraction.
The word therefore is doing almost all the work.
How to test a strong health claim
A useful checklist is to ask five questions.
1. What exactly is the exposure?
"Cholesterol", "sugar", "sun", "fasting", and "inflammation" are broad categories.
A claim becomes testable only after defining dose, duration, biological compartment, and population.
2. What is the outcome?
A biomarker is not automatically a clinical outcome.
Lower insulin is not the same as lower mortality.
Higher vitamin D is not the same as fewer cancers.
Lower CRP is not automatically fewer myocardial infarctions.
3. Is the evidence observational or interventional?
Associations can suggest hypotheses.
Randomized interventions are often needed to establish whether modifying the exposure changes the outcome.
4. What is the comparator?
"Fasting works" is incomplete.
Compared with what?
Usual diet?
Continuous energy restriction?
Another eating pattern with the same calories?
No intervention?
The comparator determines the question being answered.
5. What population was studied?
A treatment that helps someone with established cardiovascular disease cannot automatically be generalized to a healthy 25-year-old.
A vitamin D trial in deficient adults cannot automatically be generalized to people with adequate status.
Transportability is part of the evidence.
Prevention does not require mythology
One theme in Pinto Coelho's public communication deserves to be retained: prevention matters.
Modern medicine does not dispute that.
Smoking cessation, vaccination, blood-pressure control, physical activity, healthy dietary patterns, sleep, appropriate cancer screening, lipid management, and diabetes prevention are all forms of preventive medicine.
The disagreement is not between prevention and conventional medicine.
It is between prevention grounded in evidence and prevention grounded in oversimplified causal stories.
There is no need to claim that cholesterol is a distraction to encourage exercise.
There is no need to call statins a disgrace to promote better nutrition.
There is no need to deny the carcinogenicity of ultraviolet radiation to recognize the importance of vitamin D.
There is no need to describe fasting as surgery to study whether it is a useful dietary strategy.
Good preventive medicine becomes stronger, not weaker, when the dramatic claims are removed.
Conclusion
The most interesting public-health myths are rarely pure inventions.
They are often built from accurate fragments.
Manuel Pinto Coelho's statements provide several clear examples.
Inflammation is important, but LDL is not a distraction.
Excess sugar can be harmful, but it is not a universal explanation for inflammation and disease.
Sunlight contributes to vitamin D synthesis, but solar UV is an established carcinogen.
Intermittent fasting can be useful, but "surgery without a scalpel" is metaphor rather than demonstrated physiology.
Statins can be overprescribed in poorly selected patients, but their cardiovascular benefit in appropriate risk groups is supported by randomized evidence.
The scientific problem is therefore not simply that these claims are wrong.
It is that they repeatedly make the same inferential move:
That equation is worth remembering.
It appears everywhere.
References
-
NiT. Manuel Pinto Coelho: “O jejum é uma cirurgia sem bisturi”. 5 March 2026. https://www.nit.pt/fit/saude/manuel-pinto-coelho-o-jejum-e-uma-cirurgia-sem-bisturi
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NiTfm. Sem Remédio. 2026. https://www.nitfm.pt/programas/sem-remedio/
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Expresso. Manuel Pinto Coelho: “O sol protege mais contra o cancro do que o provoca”. https://leitor.expresso.pt/semanario/semanario2324/html/revista-e/-e/manuel-pinto-coelho-o-sol-protege-mais-contra-o-cancro-do-que-o-provoca
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Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. European Heart Journal. 2017;38:2459–2472. https://academic.oup.com/eurheartj/article/38/32/2459/3745109
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Borén J, Chapman MJ, Krauss RM, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights. European Heart Journal. 2020;41:2313–2330.
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World Health Organization. Dyslipidaemia. 15 September 2026. https://www.who.int/news-room/fact-sheets/detail/dyslipidaemia
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European Society of Cardiology. 2025 Focused Update of the 2019 ESC/EAS Guidelines for the management of dyslipidaemias. 2025. https://www.escardio.org/communities/councils/cardiology-practice/education/cardiopractice/what-is-new-in-the-2025-focused-update-of-the-2019-esc-eas-guidelines-for-the-m/
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Della Corte K, Perrar I, Penczynski KJ, et al. Effect of Dietary Sugar Intake on Biomarkers of Subclinical Inflammation: A Systematic Review and Meta-Analysis of Intervention Studies. Nutrients. 2018;10:606. https://pubmed.ncbi.nlm.nih.gov/29757229/
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Qi X, et al. Effect of Important Food Sources of Fructose-Containing Sugars on Inflammatory Biomarkers: A Systematic Review and Meta-Analysis of Controlled Feeding Trials. American Journal of Clinical Nutrition. 2022. https://pubmed.ncbi.nlm.nih.gov/36235639/
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International Agency for Research on Cancer. Solar and Ultraviolet Radiation. IARC Monographs, Volume 55. https://publications.iarc.who.int/73
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World Health Organization. Ultraviolet radiation. 21 June 2022. https://www.who.int/news-room/fact-sheets/detail/ultraviolet-radiation
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World Health Organization. The known health effects of ultraviolet radiation. https://www.who.int/news-room/questions-and-answers/item/radiation-the-known-health-effects-of-ultraviolet-radiation
This article evaluates publicly documented health claims and the evidence supporting or contradicting them. It does not assess Manuel Pinto Coelho's motives, character, or private clinical practice, and it is not individual medical advice.
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Diogo Ribeiro (2026). Manuel Pinto Coelho, Health Myths, and What the Evidence Actually Says. Faculty of Media Arts and Design, Technical University of Porto. https://diogoribeiro7.github.io/healthcare/manuel_pinto_coelho_health_claims_evidence/.
