What Low-Carbohydrate Conferences Get Right—and Where the Evidence Still Demands Caution
For decades, the public conversation about heart disease has often been reduced to one command: lower cholesterol.
Low-carbohydrate conferences challenged this approach by asking an important question: What if metabolic health, blood pressure, glucose control, triglycerides, inflammation, smoking, genetics and overall lipoprotein burden matter more than one total-cholesterol result?
That challenge was necessary.
However, the scientifically responsible conclusion is not that cholesterol is irrelevant, all statins are harmful or a ketogenic diet automatically makes high LDL safe.
The better conclusion is more demanding: assess the whole person, distinguish relative benefit from absolute benefit, and make treatment decisions through informed consent.
Cardiovascular disease cannot be understood through one cholesterol number. Metabolic dysfunction may damage the arterial “road,” while ApoB-containing particles provide material that can become trapped within the artery wall. Both sides of that biology deserve attention.
A CONFERENCE MOVEMENT WITH SEVERAL DIFFERENT VIEWPOINTS
The speakers discussed here do not belong to one medical society, and they do not agree on everything.
Their presentations form part of a broader low-carbohydrate and metabolic-health movement. The fairest way to examine their work is to understand each person’s area of expertise and then compare their claims with the wider scientific evidence.
Dr Philip Ovadia
Dr Philip Ovadia is a cardiothoracic surgeon whose central message is prevention: improve metabolic health before a patient reaches the operating table.
His surgical experience and personal health transformation are compelling. However, statements such as “meat is medicine” or population trends proving that red meat is harmless go beyond what those observations can establish.
Dr Aseem Malhotra
Dr Aseem Malhotra is a British consultant cardiologist and public-health campaigner.
He emphasises sugar, lifestyle, commercial influence, absolute cardiovascular risk and informed consent when statins are discussed.
He addressed a European Parliament event about low-carbohydrate treatment and vested interests. I could not verify the frequently repeated claim that this was a formal address to the British Parliament specifically about statins.
Some of his conclusions remain controversial. His valuable questions about commercial influence and informed consent should therefore be separated from claims that may extend beyond the available evidence.
Dr Nadir Ali
Dr Nadir Ali is an interventional cardiologist who presents the low-carbohydrate case for interpreting LDL within the broader context of insulin resistance, triglycerides and HDL.
That context is useful. However, low triglycerides do not automatically cancel the potential risk associated with a high number of ApoB-containing particles.
Dr Bret Scher
Dr Bret Scher is a cardiologist and lipidologist.
He provides a valuable bridge between metabolic therapy and conventional cardiovascular risk assessment, particularly when LDL rises significantly on a low-carbohydrate or ketogenic diet.
His approach supports careful investigation rather than automatic reassurance or automatic medication.
Associate Professor Ken Sikaris
Associate Professor Ken Sikaris is a chemical pathologist.
He explains what routine blood tests can—and cannot—tell us about insulin resistance, triglycerides, HDL and different LDL patterns.
His work provides valuable laboratory interpretation, but LDL particle size should not be used to ignore LDL particle number.
Ivor Cummins
Ivor Cummins is a chemical engineer rather than a physician.
He applies systems thinking to insulin resistance, cardiovascular risk factors and coronary artery calcium scoring.
His models can generate valuable questions, but clinical claims must still be tested through appropriate clinical research.
Dave Feldman
Dave Feldman is a software engineer and citizen scientist.
By repeatedly changing his diet and measuring his blood lipids, he demonstrated how rapidly cholesterol results can change in some people. He later helped develop the Lipid Energy Model.
His experiments are scientifically interesting and useful for developing hypotheses. However, a short-term protocol that changes a cholesterol test is not evidence that long-term cardiovascular risk has been reduced.
Dr Paul Mason
Dr Paul Mason is a sports and exercise medicine physician.
His presentations connect low-carbohydrate nutrition with metabolic health, inflammation and musculoskeletal health.
His talks provide an educational perspective, but individual treatment still requires a clinician who understands the person’s full medical history and medications.
Dr Doron Sher
Dr Doron Sher is an orthopaedic surgeon.
His work connects body weight, metabolic health and arthritis with preparation for orthopaedic treatment.
His contribution is most relevant to metabolic and musculoskeletal health rather than specialist lipidology.
WHAT THE LOW-CARBOHYDRATE MOVEMENT GETS RIGHT
- METABOLIC HEALTH IS NOT A SIDE ISSUE
Insulin resistance, type 2 diabetes, high blood pressure, abdominal obesity, smoking and physical inactivity are major cardiovascular risks.
Diabetes approximately doubles the risk of coronary heart disease. High added-sugar consumption is also associated with increased cardiovascular mortality.
It is therefore poor medicine to celebrate a lower LDL result while ignoring worsening glucose, blood pressure, waist circumference, sleep or physical fitness.
Low-carbohydrate diets can be a legitimate therapeutic option.
A major 2021 systematic review found that low-carbohydrate diets improved diabetes remission and several metabolic markers after six months. However, the certainty of the evidence was limited, and much of the advantage had diminished after 12 months.
The American Diabetes Association also recognises carbohydrate reduction as one evidence-based dietary option—but not the only option.
The practical conclusion is not that everyone must follow a ketogenic diet.
It is that the quantity and quality of dietary carbohydrates can matter greatly, particularly for people with insulin resistance. Long-term adherence, food quality, nutritional adequacy and medication safety matter as much as the name given to the diet.
- TOTAL CHOLESTEROL IS A CRUDE STARTING POINT
Total cholesterol combines several different types of cholesterol and particles. It does not reveal the full metabolic or cardiovascular picture.
A more complete assessment may include:
• LDL cholesterol
• HDL cholesterol
• Triglycerides
• Non-HDL cholesterol
• ApoB
• Lipoprotein(a), also called Lp(a)
• Blood pressure
• Glucose and HbA1c
• Smoking history
• Family history
• Kidney and thyroid function
• Existing cardiovascular disease
The latest cardiovascular guidelines recognise that ApoB, Lp(a) and coronary artery calcium scoring can sometimes provide additional information when the treatment decision remains uncertain.
- ABSOLUTE BENEFIT MATTERS MORE THAN A DRAMATIC RELATIVE NUMBER
A treatment may produce an impressive relative-risk reduction while providing only a small absolute benefit to a person whose original risk is low.
For example, reducing a risk from 2% to 1% represents a 50% relative-risk reduction. However, the absolute reduction is only one percentage point.
That difference is central to informed consent.
People who have already experienced a heart attack, stroke or documented atherosclerotic disease generally have more to gain from LDL-lowering treatment than young, low-risk people without cardiovascular disease.
This is where Dr Malhotra’s emphasis on transparent communication is most valuable.
Patients should be told the expected absolute benefit, the relevant timeframe, the uncertainties, possible side effects, the monitoring plan and available alternatives—not simply that one laboratory number is “high.”
LDL: TRANSPORT PARTICLE, RISK PARTICLE—OR BOTH?
LDL is not a toxin. It is a normal lipoprotein that transports mainly cholesterol and other fat-soluble material through the bloodstream.
Triglycerides are carried predominantly in chylomicrons and VLDL particles, while free fatty acids travel mainly attached to albumin.
Therefore, the popular statement that LDL simply “carries fat to the cells” is directionally understandable but biologically incomplete.
At the same time, decades of genetic, mechanical, epidemiological and randomised-treatment evidence support ApoB-containing lipoproteins—including LDL—as a cause of atherosclerotic cardiovascular disease.
The problem is not that LDL exists.
The problem is cumulative exposure to particles capable of entering and becoming retained within the artery wall.
PATTERN A, PATTERN B AND THE PARTICLE-NUMBER TRAP
Pattern A describes predominantly larger, more buoyant LDL particles.
Pattern B describes smaller, denser LDL particles and is commonly associated with high triglycerides, low HDL and insulin resistance.
Pattern B is an important metabolic warning sign. Improving insulin sensitivity frequently moves this pattern in a healthier direction.
However, there is a crucial correction.
Large LDL particles are not automatically harmless, and small LDL particles do not remain in the bloodstream simply because the liver fails to recognise them.
Both large and small LDL particles contain ApoB, and every ApoB-containing particle has the potential to contribute to atherosclerosis.
When LDL cholesterol and ApoB provide different impressions of risk, ApoB may be more informative because it estimates the number of atherogenic particles rather than the amount of cholesterol being carried inside them.
THE TRIGLYCERIDE-TO-HDL RATIO
A low triglyceride-to-HDL ratio commonly accompanies better insulin sensitivity and a lower probability of small, dense LDL particles.
It is a valuable metabolic clue that can be followed over time.
However, its interpretation varies according to measurement units, sex and ethnicity.
The triglyceride-to-HDL ratio does not replace ApoB, blood pressure, smoking status, diabetes status, family history or appropriate cardiovascular imaging.
Low triglycerides and high HDL may indicate improved metabolic health.
A high LDL cholesterol level can sometimes reflect cholesterol-rich particles without an equally large increase in particle number—but sometimes ApoB also rises substantially.
The next step should be measurement and proper risk assessment, not assumption.
WHAT HAPPENS TO LIPIDS ON A KETOGENIC DIET?
Nutritional ketosis shifts the body towards greater fat oxidation and ketone production.
Ketones are a normal alternative fuel that can be used by the brain and other tissues. However, describing ketones as universally “cleaner” or as “jet fuel” is a useful metaphor—not a demonstrated cardiovascular outcome.
What matters is whether the person’s complete health profile improves and whether any new risks appear.
On average, ketogenic diets tend to lower triglycerides and increase HDL.
The LDL response varies considerably. LDL changes very little in some people, decreases in others and rises dramatically in a subgroup—often leaner, insulin-sensitive people sometimes described as “lean-mass hyper-responders.”
A 2026 meta-analysis of 53 randomised trials found that ketogenic diets generally lowered triglycerides and raised HDL. However, LDL cholesterol and total cholesterol also increased overall.
Dave Feldman’s experiments helped demonstrate that recent energy intake can alter measured cholesterol in some people following low-carbohydrate diets.
This is scientifically interesting and supports testing under consistent conditions.
However, it does not prove that diet-induced high LDL is safe, and it does not prove that manipulating food intake for several days lowers long-term atherosclerotic risk.
Long-term cardiovascular outcome evidence for this specific group remains incomplete.
STRESS, THE NERVOUS SYSTEM AND DAY-TO-DAY VARIATION
The nervous system can change our physiology very quickly.
Acute stress activates sympathetic and hormonal responses that may raise blood pressure and blood glucose.
Cholesterol and triglycerides also display normal biological and laboratory variation. Some short-term changes during acute stress may partly result from changes in plasma volume.
This supports repeating surprising blood results under comparable conditions and examining long-term trends.
It does not mean that chronic high blood pressure, diabetes or high ApoB can be dismissed as temporary feelings of danger.
A useful personal record may include:
• Home blood-pressure readings
• Sleep quality
• Recent illness
• Fasting conditions
• Alcohol consumption
• Recent exercise
• Emotional stress
• Medication or supplement changes
STATINS: NEITHER MIRACLE NOR MENACE
Statins lower LDL cholesterol and reduce cardiovascular events.
Their absolute value depends heavily upon the person’s original cardiovascular risk.
The argument for statin treatment is strongest after a heart attack, stroke or documented atherosclerotic disease. The decision becomes more dependent on individual preferences in lower-risk primary prevention.
Contemporary guidelines therefore use overall cardiovascular risk, risk-enhancing factors and shared decision-making rather than total cholesterol alone.
WHAT THE BENEFIT NUMBERS MEAN
A 2022 review prepared for the United States Preventive Services Task Force examined statin treatment for primary prevention.
Across the studies, statins were associated with approximate absolute reductions of:
• 0.35 percentage points in all-cause mortality
• 0.39 percentage points in stroke
• 0.85 percentage points in heart attack
• 1.28 percentage points in combined cardiovascular outcomes
These figures represent averages across different people and trial durations.
People with higher starting risk generally receive a greater absolute benefit.
A frequently quoted analysis translated statin benefits into a median postponement of death measured in days during the limited duration of certain clinical trials.
That is an unusual statistical way of presenting the results.
It does not mean that a person can gain only a few days across an entire lifetime. It also does not include the possible prevention of non-fatal heart attacks and strokes.
It is reasonable to discuss this research, but it should not be presented as the complete answer.
STATIN SIDE EFFECTS ALSO REQUIRE ACCURACY
Symptoms reported by patients should never be mocked or ignored.
However, blinded clinical trials show that most muscle symptoms reported during statin treatment are not actually caused by the statin.
A 2022 individual-participant meta-analysis found a small increase in mostly mild muscle pain or weakness, concentrated primarily during the first year of treatment.
A major 2026 analysis examined 23 double-blind trials involving more than 150,000 participants.
It found no convincing increase in most of the adverse effects currently listed on statin product labels. It did confirm small risks including liver-test abnormalities and rare muscle injury. Statins may also produce a modest increase in diabetes risk among susceptible individuals.
When someone experiences possible statin intolerance, the correct response is proper evaluation.
That may include checking the timing of symptoms, medication interactions and reversible causes. A clinician may consider changing the dose, trying another statin or discussing appropriate non-statin treatments.
The answer should not be, “Keep taking it regardless.”
It should also not be, “All statins are dangerous.”
WHAT ABOUT PEOPLE OVER 70?
Observational studies have produced apparently conflicting headlines.
Some studies found that lower LDL among older populations was associated with higher all-cause mortality. Other studies found that higher LDL continued to predict more heart attacks and cardiovascular disease.
Illness, frailty, weight loss and chronic inflammation can lower cholesterol before death. This creates the possibility of reverse causation: the illness may be lowering the cholesterol rather than low cholesterol causing the illness.
All-cause mortality also answers a different question from cardiovascular events.
The 2026 STAREE randomised trial provides important new evidence.
The trial involved almost 10,000 adults aged 70 or older without known cardiovascular disease, diabetes or dementia.
Over a median period of 5.9 years, atorvastatin reduced major cardiovascular events. However, it did not significantly improve disability-free survival.
Serious adverse events were similar overall, although certain muscle-related, liver-related and diabetes-related events occurred more frequently.
These findings support neither automatic statin treatment for every older person nor automatic rejection of statins.
Personal goals, life expectancy, existing illness, medication burden and individual preferences must still be considered.
MARKETING, MOVING TARGETS AND JUSTIFIED SCEPTICISM
Statins have been marketed very aggressively.
Pfizer’s Lipitor campaign became a famous example of pharmaceutical advertising. Atorvastatin and rosuvastatin remain among Australia’s most frequently prescribed medications.
Commercial success is a valid reason to examine the evidence, conflicts of interest and marketing messages carefully.
However, aggressive marketing is not proof that a medication does not work.
Cholesterol recommendations have also changed across different decades and countries.
Human biology did not suddenly change. What changed were the available clinical trials, risk calculators, treatment thresholds and recommended targets.
European guidance establishes very low LDL targets for people at extremely high cardiovascular risk. Australian primary-prevention guidance places greater emphasis on absolute cardiovascular risk.
A laboratory reference range is not the same thing as an individual treatment target.
CAN CHOLESTEROL BE LOWERED WITHOUT MEDICATION?
In many cases, cholesterol and other cardiovascular risk factors can improve without medication, although the size of the response varies considerably.
Helpful strategies may include:
• Weight reduction when appropriate
• Stopping smoking
• Regular physical activity
• Improving sleep
• Reducing refined carbohydrates and added sugars
• Increasing soluble fibre
• Replacing some saturated fat with unsaturated fat
• Managing blood pressure
• Improving glucose and insulin sensitivity
The Portfolio dietary pattern—which combines viscous fibre, nuts, plant sterols and plant protein—has reduced LDL cholesterol, non-HDL cholesterol and ApoB in controlled studies.
A low-carbohydrate approach may also improve triglycerides and blood glucose, particularly in people with insulin resistance.
Low carbohydrate does not have to mean extremely high saturated fat.
A well-designed low-carbohydrate diet can include fish, extra-virgin olive oil, avocado, nuts, seeds, eggs, unsweetened dairy products, adequate protein and non-starchy vegetables.
Anyone taking insulin, sulfonylureas, SGLT2 inhibitors or blood-pressure medication requires clinical supervision when making major dietary changes because medication requirements may change quickly.
A BETTER CLINICAL CONVERSATION THAN “YOUR CHOLESTEROL IS HIGH”
The strongest practical lesson from these conferences is that we must ask better questions.
A responsible clinician-patient conversation may include:
• Is this primary prevention or secondary prevention following known cardiovascular disease?
• What is the estimated absolute cardiovascular risk over an appropriate timeframe?
• Were the lipid tests repeated under comparable conditions?
• What is the long-term trend?
• What do blood pressure, smoking history, waist measurement, physical activity, sleep, HbA1c and fasting glucose show?
• What are the triglycerides, HDL cholesterol, LDL cholesterol and non-HDL cholesterol?
• Would ApoB help clarify the number of potentially atherogenic particles?
• Has Lp(a) been measured at least once, particularly when there is premature cardiovascular disease or a strong family history?
• Could familial hypercholesterolaemia, kidney disease, thyroid disease or medication effects be present?
• Would coronary artery calcium imaging genuinely change the decision?
• What absolute benefit could reasonably be expected from a statin?
• What harms are plausible, and what monitoring or alternative treatments are available?
• What lifestyle program would be safe, measurable and long enough to evaluate properly?
• What result would cause the treatment decision to be reconsidered?
Coronary artery calcium scoring is not an appropriate screening test for everyone.
However, in selected people with borderline or intermediate risk, it may help clarify the decision.
A zero calcium score can sometimes support delaying medication, while substantial coronary calcium strengthens the case for intensive prevention.
Important exceptions exist, including diabetes, smoking, a strong family history and extremely high LDL cholesterol.
THE CONCLUSION: PERSONALISED PREVENTION WITHOUT DENYING SCIENCE
The low-carbohydrate conference movement has made an important contribution by encouraging cardiology to look beyond total cholesterol.
It has restored attention to insulin resistance, food quality, lifestyle, absolute risk and patient choice.
Its strongest message is not that every mainstream medical recommendation is wrong.
Its strongest message is that medicine becomes safer and more honest when risk is explained rather than imposed.
The responsible conclusion is neither:
“Everyone with total cholesterol between 5 and 7 mmol/L needs a statin.”
Nor is it:
“Healthy-looking Pattern A LDL cannot cause harm.”
The stronger conclusion is this:
Metabolic health and ApoB exposure provide complementary information.
Sugar and insulin resistance are major cardiovascular drivers, but they are not the only drivers.
Statins may offer a substantial absolute benefit to some people and a very small benefit to others.
Treatment decisions should be based on a complete cardiovascular risk profile, reliable measurements and the informed priorities of the person sitting in front of the clinician.
Do not prescribe from one number.
Do not dismiss one number either.
Measure the whole risk—and make the decision together.
MEDICAL NOTE
This article is provided for educational purposes. It does not diagnose, prescribe or replace individual medical care.
Do not start, stop or alter statins, diabetes medication, blood-pressure medication or a ketogenic diet without discussing your health, medications and personal cardiovascular risk with an appropriately qualified healthcare professional.
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