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Modern Life Pulled Humans Away From The Very Things That Keep Them Healthy.
Links and info to real updated research. ✔️🇨🇦 Movement.
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Dr. Alo, saying LDL particle size “does not matter, not one bit” is not what the evidence says. Stop lying. 🤥
You are correct that ApoB particle number is generally more useful clinically than simply classifying LDL as small or large. But the European Atherosclerosis Society specifically describes small dense LDL as biologically different from larger LDL. Small dense LDL has longer circulation time, greater susceptibility to oxidation and glycation, greater arterial-wall proteoglycan binding, and appears to enter the arterial intima faster.
The problem is that small dense LDL commonly occurs alongside high triglycerides, insulin resistance, remnant particles and elevated ApoB, so separating the independent effect of particle size is difficult. That is why ApoB is usually the better clinical marker.
But “particle size is not the primary treatment target” is not the same statement as “size does not matter at all.” And saying every LDL particle that enters the artery wall “will destroy your arteries” is also inaccurate. ApoB-containing particles can cross into the intima, but atherosclerosis depends on their retention and accumulation within susceptible areas of the arterial wall.
So the accurate message is: particle number matters greatly, particle size has biological relevance, and neither should be reduced to a social-media slogan.
European Atherosclerosis Society consensus on LDL particle heterogeneity:
https://academic.oup.com/eurheartj/article/41/24/2313/5735221
EAS consensus on LDL and atherosclerosis:
https://academic.oup.com/eurheartj/article/38/32/2459/3745109
National Lipid Association consensus on ApoB:
https://pubmed.ncbi.nlm.nih.gov/39256087/
08/18/2026
Dr. Alo, this post mixes some correct trial results with an incorrect conclusion.
PROMINENT is actually a good example of why triglycerides cannot be interpreted by themselves. Pemafibrate lowered triglycerides 26%, but ApoB increased 4.8% and cardiovascular events did not fall. That does not prove triglycerides are “clinically meaningless.” It suggests that lowering triglycerides without adequately reducing the number of atherogenic particles may not reduce ASCVD risk. (New England Journal of Medicine)
Then you say “fish oil will not save you,” while acknowledging REDUCE-IT produced a 25% relative reduction in cardiovascular events with prescription icosapent ethyl. The mineral-oil placebo issue is a legitimate scientific debate, but it does not allow you to simply discard a randomized outcome trial because you dislike the comparator. STRENGTH tested a different EPA plus DHA formulation and was neutral. Those two trials do not prove that all omega-3 therapies are equivalent or useless. (JAMA Network)
The new olezarsen imaging study is also being overstated. It lowered triglycerides about 64% and remnant cholesterol about 72%, but did not significantly change noncalcified coronary plaque over only 12 months. The investigators concluded that plaque volume did not change over that period. They did not conclude that triglyceride-rich lipoproteins are irrelevant to cardiovascular disease. (PubMed)
And there is an important distinction you leave out. Very high triglycerides are treated for another reason entirely, pancreatitis risk. Cardiovascular prevention and severe hypertriglyceridemia are not the same clinical question.
The more accurate conclusion is that triglycerides are a risk marker and triglyceride-rich ApoB-containing particles can be atherogenic. Simply lowering the triglyceride concentration does not guarantee fewer cardiovascular events. ApoB particle burden, metabolic health and the specific treatment matter.
That is very different from saying “triglyceride lowering is clinically meaningless,” “fibrates will not save you,” or “fish oil will not save you.”
PROMINENT, New England Journal of Medicine:
https://www.nejm.org/doi/abs/10.1056/NEJMoa2210645
STRENGTH, JAMA:
https://jamanetwork.com/journals/jama/fullarticle/2773120
ESSENCE-TIMI 73b coronary imaging study:
https://pubmed.ncbi.nlm.nih.gov/41910513/
ESSENCE-TIMI 73b main trial, New England Journal of Medicine:
https://www.nejm.org/doi/full/10.1056/NEJMoa2507227
🚨 You can drop your triglycerides 50% with a pill and still walk away with the same heart attack risk you started with.
Multiple large trials prove it.
But the data says otherwise on what actually works, and no, it is not fish oil.
I am a cardiologist. I have hundreds of patients with elevated triglycerides. I have watched the industry sell triglyceride lowering as a goal in itself for two decades. The trials say otherwise.
🩺 Here is what the science actually says.
Triglycerides are a marker. They are not a lever you pull to save a life. When you lower them with the wrong tool, nothing happens to your risk of heart attack or stroke. When you lower them with the right tool, your triglycerides fall as a side effect of fixing the actual problem.
💓 The fibrate failures.
✅ ACCORD-Lipid (fenofibrate): triglycerides reduced 25.6%, cardiovascular events unchanged, HR 0.92.
✅ FIELD (fenofibrate): triglycerides reduced 29%, no significant benefit for coronary events.
✅ PROMINENT (pemafibrate): triglycerides reduced 26.2%, remnant cholesterol reduced 25.6%, zero cardiovascular benefit, HR 1.03. LDL-C actually rose 12.3%.
That matters because you can hand a patient impressive numbers on a lab report and send them home with the same clogged arteries.
🔬 Omega-3 fatty acids tell a similar story.
STRENGTH tested EPA plus DHA against corn oil in 13,078 high-risk patients. The trial was terminated early for futility. Event rates were 12.0% versus 12.2%. HR 0.99. That is not a rounding error. That is no effect.
REDUCE-IT showed a 25% reduction in cardiovascular events with icosapent ethyl. I know this is the trial everyone quotes. But the placebo used was mineral oil, and mineral oil raised LDL-C by 10.2% and pushed hs-CRP from 2.1 to 2.8 mg/L. That means the comparison group looked artificially worse, which inflates how good the drug looks. The ACC Expert Consensus says this is unlikely to explain the full 25% reduction, but I call it unresolved. I use icosapent ethyl as a last resort, not a first move.
ESSENCE-TIMI 73B tested olezarsen. Triglycerides fell 64%. Remnant cholesterol fell 70%. Plaque volume on the actual coronary artery did not improve over 12 months. Read that twice.
❌ Fibrates will not save you.
❌ Fish oil will not save you.
❌ Niacin should never be used. Full stop.
🫀 So what actually works.
Weight loss is the most powerful triglyceride-lowering intervention that exists, and it works because it fixes the underlying metabolic disease, not because triglycerides move on a lab slip.
✅ Losing 5% to 10% of body weight drops triglycerides approximately 20%.
✅ Every 1 kg lost reduces triglycerides approximately 4 mg/dL through lifestyle change alone.
✅ Highly responsive patients on GLP-1/GIP therapy can see triglyceride reductions of 50% to 70%.
✅ Look AHEAD showed the more weight patients lost, the more their triglycerides fell, with the biggest losers dropping more than 60 mg/dL.
✅ Semaglutide reduced cardiovascular events 20% to 26% regardless of starting BMI in the Wegovy trials.
✅ Moderate aerobic exercise, 150 minutes per week, cuts triglycerides approximately 18.6 mg/dL, up to 30%.
🩺 A patient scenario.
A patient who loses 15% of body weight through GLP-1 therapy and 150 minutes of weekly exercise can see triglycerides fall by half and cardiovascular risk fall alongside it, in the same 6 to 12 month window where a fibrate would have moved the lab number and done nothing else.
That is the difference between a good-looking chart and a good-looking outcome.
❤️ Bottom line:
Triglyceride lowering in isolation is clinically meaningless. It is not the goal. The number on your lab report is not the target. The metabolic disease driving that number is the target.
This conclusion is built on trials covering more than 38,000 patients across ACCORD-Lipid, FIELD, PROMINENT, and STRENGTH, all showing the same pattern.
My framework: statins first. Metformin and diabetes optimization second. Anti-obesity medication when indicated. Alcohol cessation. Exercise. Fibrates and fish oil sit at the bottom of the list, if they belong there at all.
A patient who addresses weight and insulin resistance can lower cardiovascular risk in months, not years, while a patient chasing a triglyceride number with a pill gets a better lab report and the same arteries.
The question is no longer how do I lower my triglycerides. The question is what is causing them to be high in the first place.
What is your triglyceride number, and has anyone ever explained to you why it is elevated?
Comment "blog" and I will send you the link.
“Grass-finished beef has nearly a 4X better omega-6 to omega-3 ratio than grain-finished beef.”✔️🇨🇦❤️
Sounds like a huge nutritional difference.
But look at the actual amounts.
A recent North American study comparing 337 ribeye samples found an average omega-6 to omega-3 ratio of 2.14:1 in grass-finished beef and 8.28:1 in grain-finished beef.
That difference is real. Grass-finished beef has the more favorable omega-6 to omega-3 profile.✔️🇨🇦❤️
But ratios can make small absolute differences look enormous.
A review of the research estimated that 100 grams of grass-finished beef contained about 175 mg of omega-6 and 68 mg of omega-3, compared with about 330 mg of omega-6 and 45 mg of omega-3 in grain-finished beef.✔️✔️❤️❤️
For perspective, one tablespoon of olive oil contains roughly 1.3 grams, or 1,300 mg, of omega-6.
That does not make olive oil unhealthy. It shows why looking at a fatty-acid ratio without looking at the actual amounts can be misleading.
There is another misconception worth clearing up.✔️🇨🇦❤️
Grain-finished does not mean an animal ate grain its entire life. Conventionally raised grain-finished cattle generally spend much of their lives consuming their mother’s milk, grass and other forage. The grain-heavier finishing ration typically comes during the final months.
Grass-finished beef has the better omega-6 to omega-3 ratio. That is a legitimate nutritional advantage.
But an 8.28:1 versus 2.14:1 ratio sounds much larger than the absolute quantities involved.
When somebody gives you a nutritional ratio, ask one more question.
How much is actually there?✔️🇨🇦🇨🇦❤️
Dale Reynolds
Dr. Alo, the main SELECT result you quoted is correct, but you are stretching what the trial actually established.
SELECT randomized 17,604 adults without diabetes, but these were not generally healthy overweight people. Every participant was at least 45, had a BMI of 27 or higher, and already had established cardiovascular disease. Semaglutide reduced the primary endpoint from 8.0% to 6.5%. That is a 20% relative reduction, but about a 1.5 percentage point absolute reduction over roughly 40 months. The bigger problem is calling that a 20% reduction in “heart attacks, strokes, peripheral artery disease, stents, cardiovascular death.” The primary SELECT endpoint was specifically cardiovascular death, nonfatal heart attack, or nonfatal stroke. Individual outcomes were not all reduced by 20%. Nonfatal stroke, for example, was 1.7% versus 1.9%, HR 0.93, with a confidence interval crossing 1.
And the saturated-fat explanation is speculation. SELECT did not establish that semaglutide worked because people ate less saturated fat. The investigators themselves discuss several possible mechanisms, including weight loss, blood pressure, glucose regulation, inflammation, lipids and potentially direct drug effects. They explicitly say the mechanism remains uncertain. So there is a legitimate and important cardiovascular benefit here. But the accurate message is narrower. Semaglutide reduced major cardiovascular events in overweight or obese people without diabetes who already had cardiovascular disease. SELECT did not prove that GLP-1 drugs prevent atherosclerosis generally, nor did it prove that eating less saturated fat explains the benefit.
Here is the full study to see for yourself, I did.
https://www.nejm.org/doi/full/10.1056/NEJMoa2307563
You’re overstating what the National Academies actually concluded.
Their 2024 review did find that moderate alcohol consumption was associated with lower all-cause mortality compared with never drinking, with moderate certainty. But it did not conclude that red wine itself lowers mortality by 10%, and it specifically did not compare health outcomes among wine, beer and spirits. Association is not proof that alcohol caused the lower mortality. (National Academies)
The same evidence base does not make alcohol a health food. Alcohol is a known human carcinogen. Even relatively low consumption increases the risk of some cancers, and the National Academies review itself found an increased breast cancer risk with moderate drinking. (National Academies)
Saying Mediterranean populations have consumed wine for thousands of years tells us nothing about whether wine extends life. And saying that many older people in a Blue Zone drink wine is classic survivor and observational evidence. It does not establish that the wine helped them reach 90.
So the accurate statement is this. Some observational studies associate moderate alcohol consumption with lower overall mortality and cardiovascular risk, while alcohol simultaneously increases certain cancer risks. That is very different from claiming that the National Academies says red wine lowers mortality by 10%.
And “science tends to refute itself” is the wrong lesson. Better studies refine weaker evidence. That is exactly what science is supposed to do.
08/16/2026
“A 400 ppm pesticide limit on livestock feed does NOT mean there is 400 ppm in your steak.” ✔️🇨🇦❤️
That is the trick behind this argument.
The number being quoted is a regulatory tolerance for certain feed commodities. It is not a measurement of glyphosate in beef. You cannot take the legal residue limit for something an animal eats and present that number as the contamination level of the animal itself.
The argument gets even weaker when glyphosate is mixed together with dioxins, PCBs and other persistent pollutants.
These chemicals do not behave the same way.✔️🇨🇦❤️
Dioxins and certain persistent pollutants can bioaccumulate in animal fat. That does not establish that glyphosate does the same thing. Evidence about one class of chemicals cannot simply be transferred to another because both are called “chemicals” or “pesticides.”
This is why measured residues matter.
FDA testing of 879 samples of corn, soybeans, milk and eggs found no glyphosate tolerance violations. Glyphosate was not detected in the milk or egg samples.
There are legitimate discussions to have about pesticide use, environmental contamination and persistent pollutants.
But comparing a regulatory limit on animal feed with a completely different limit on human food, then implying that the difference represents what ends up in meat, is not a valid comparison.
Compare measured residues.
Not unrelated regulatory limits.✔️🇨🇦❤️
~ Dale Reynolds
EPA:
https://www.epa.gov/ingredients-used-pesticide-products/glyphosate
FDA:
https://www.fda.gov/food/pesticides/questions-and-answers-glyphosate
WHO:
https://www.who.int/news-room/fact-sheets/detail/dioxins-and-their-effects-on-human-health
Dr. Alo, I looked up the Ference paper. It does not support the claim that “only LDL causes heart disease.”
It supports something much more specific. LDL is causal in atherosclerosis.
In fact, the authors themselves explicitly stated that LDL particles are “not the only cause” of ASCVD.
The paper also discusses other atherogenic ApoB containing particles, including VLDL remnants, IDL and Lp(a). It even explains that LDL C can become discordant with LDL particle number, and in those situations ApoB or particle number can better represent the atherogenic burden.
The newer 2026 ACC/AHA guideline makes this distinction even clearer. LDL C measures the cholesterol mass carried inside LDL particles. ApoB measures the number of atherogenic particles and can predict risk better when the two disagree.
So yes, LDL is causal.
No, that does not mean LDL C is the only cause of heart disease, the only cardiovascular risk factor, or even always the best measurement of atherogenic particle burden.
Your own Ference reference does not say that.
https://academic.oup.com/eurheartj/article/38/32/2459/3745109
https://academic.oup.com/eurheartj/article/41/24/2313/5735221
https://www.ahajournals.org/doi/10.1161/CIR.0000000000001423
THE BIGGEST FAT MYTH WASN’T THAT FAT MATTERS.
IT WAS THAT EATING LESS FAT AUTOMATICALLY MEANT BETTER HEALTH.
For decades, dietary fat was treated as something we should simply reduce.
Then large randomized trials actually tested the idea.
The Women’s Health Initiative followed nearly 49,000 women for more than eight years.
Reducing total dietary fat did not significantly reduce coronary heart disease, stroke, or cardiovascular disease.
That does not mean every fat is equal.
Industrial trans fats are harmful.
Extra virgin olive oil, nuts and fish have strong evidence behind them.
Saturated fat can raise LDL and ApoB containing particles, so context and what replaces it still matter.
And despite what is commonly claimed online, ordinary seed oils have not been proven to be toxic inflammatory poisons in humans.
The lesson from the last 50 years is much simpler.
Stop judging food by one nutrient.
Ask what food it comes from, what replaces it, how processed it is, and what it does to the overall metabolic picture.
FAT WAS NEVER THE WHOLE PROBLEM.
THE OVERSIMPLIFIED NUTRITION STORY WAS.
Dale Reynolds
08/15/2026
“THE BIGGEST FAT MYTH WASN’T THAT FAT MATTERS.
IT WAS THAT EATING LESS FAT AUTOMATICALLY MEANT BETTER HEALTH.”❤️✔️🇨🇦
For decades, dietary fat was treated as something we should simply reduce.
Then large randomized trials actually tested the idea.
The Women’s Health Initiative followed nearly 49,000 women for more than eight years.
Reducing total dietary fat did not significantly reduce coronary heart disease, stroke, or cardiovascular disease.
That does not mean every fat is equal.
Industrial trans fats are harmful.
Extra virgin olive oil, nuts and fish have strong evidence behind them.❤️✔️🇨🇦
Saturated fat can raise LDL and ApoB containing particles, so context and what replaces it still matter.
And despite what is commonly claimed online, ordinary seed oils have not been proven to be toxic inflammatory poisons in humans.❤️✔️🇨🇦
The lesson from the last 50 years is much simpler.
Stop judging food by one nutrient.
Ask what food it comes from, what replaces it, how processed it is, and what it does to the overall metabolic picture.
FAT WAS NEVER THE WHOLE PROBLEM.
THE OVERSIMPLIFIED NUTRITION STORY WAS.❤️✔️🇨🇦
Dale Reynolds
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