Is high LDL cholesterol (or apoB) harmful ONLY with poor metabolic health, characterized by low HDLc? New study from preeminent lipidologist Sniderman: "when HDL-C is high ... effect of changing apoB vanishes" PS: A low-carb diet potently increases HDLc academic.oup.com/eurjpc/adva…

US obesity has dropped from 39.9% in 2022 to 36.4% this year, while the share of adults on a GLP-1 for weight loss went from 3% to 11%. That's real progress, and the drugs deserve credit. But the weight usually comes back when the drug stops. The progress only lasts if a person uses that time to build protein-centered meals and a lifting habit.

The push to put everyone on statins over the age of 40 is not about health but about making money. There is no such thing as “bad” cholesterol. LDL isn’t the villain they told you it was. LDL is a delivery truck. It carries nutrients, vitamins, antioxidants, and hormones to your cells. Your brain is about 25% cholesterol, and LDL helps keep you sharp. It repairs damaged blood vessels and helps you fight infections. When LDL drops too low, testosterone, estrogen, and cortisol can crash with it. LDL often rises when your body is healing. That’s protective, not dangerous. Humans ate cholesterol-rich food for millions of years without the heart-disease epidemic we see now. The “LDL equals death” story really took off in the 1970s. LDL is a repair crew and a transporter. Blaming it is like blaming the firefighters for the fire. There isn’t bad cholesterol. There’s a bad environment—inflammation in your arteries.

A new study looking at overall cardiovascular risk after going low carb So many improvements!! Cardiovascular risk has many components we should not simply obsess about LDL cholesterol but look at the wider picture BP, weight, triglycerides, HbA1c .., LOOK ! sciencedirect.com/science/ar…

New YouTube video - Why Calorie Counting always Fails - Check it out - youtu.be/JLvLyCaiI4g

@garytaubes with another great substack on how even discussing controversy is medicine has become taboo Very applicable to heart disease. The mainstream views it as a solved problem while heart disease remains the #1 killer and continues to get worse. Anyone questioning that the accepted solution may be wrong is seen as the problem, not that the solution keeps failing. Discussing Controversy in Medical Science: Air It Out or Sweep It Under the Rug? uncertaintyprinciples.substa…

🚨New TFP_ Newsletter 🥳 🤔Not an LMHR at Hour 10… but One at Hour 12? We gave our ✌🏻cents on the new "atypical" LMHR case report. We dive into an old throwback Cholesterol Code article — Dave’s “triglyceride carryover” experiment + controlled data and had some fun doing some (highly caveated) modeling🤓 Enjoy! feldmanprotocol.substack.com…

First they told us LDL caused heart disease, then is was the oxidized LDL or small dense particles, now it's the ApoB and Lp(a). We can't keep reducing a whole disease process down to individual molecules in the blood and expext to prevent heart disease. The underlying causes of heart disease are insulin resistance and pathologic clotting. So the most effective way to prevent heart disease is not tracking numbers or making your blood test look a certain way, it's to learn about what aspects of our modern day environment are creating insulin resitance and pathologic clotting and learning how to change your environment to prevent them. This is what I teach people in my heart health mentorship program. Click the link below to learn more about it. Https://stephenbhussey.com/r…

Therapeutic carbohydrate reduction (TCR) now has a peer-reviewed implementation guideline. Published today in the Journal of Metabolic Health (JMH)! buff.ly/w0Fe0Yn Developed to help address the growing epidemic of metabolic dysfunction.

I don't sell private supplements dummy.

My questioning of lipids began in PA school in 2016, when a physician gave our class a lecture on evidence-based medicine. He showed us mortality data on statins. When you look at mortality alone, the number needed to treat can look underwhelming. He also explained relative risk reduction in a way that made it feel, to me at the time, like a Big Pharma manipulation of data. That lecture planted a seed. I adopted the paradigm that LDL elevation was overblown. More importantly, I convinced myself that I was the exception: lean, fit, insulin-sensitive, weight training, eating “clean,” and therefore somehow protected from the overwhelming evidence linking ApoB-containing particles to cardiovascular disease. After graduation, I kept studying lipids. In 2019, I became fascinated with arguments built around Eskimo, ancestral, and prehistoric populations. Looking back, I can see how selectively I interpreted that material. I focused on evolutionary narratives and ignored the obvious limitation: many of those populations died young, before modern atherosclerotic disease had decades to develop. Around the same time, I discovered the Quest Diagnostics Cardio IQ panel. It was still early in its life cycle, and I was excited by advanced lipid testing. I became the primary of a patient who found me at the mom and pop urgent care and somehow knew that I was open to alternative thinking and who wanted to use the same test because, like me, he was lean, fit, and a weightlifter. Neither of us wanted to believe that someone who looked metabolically healthy could still be at risk for myocardial infarction, stroke, or vascular disease. Then came 2020. During the pandemic, my questioning of medical authority intensified. I studied the disease as it moved through Asia, then Europe, and by the time it reached the United States, I felt prepared. I worked in urgent care and treated thousands of patients. I wrote to local mayors and sheriffs, pleading with them not to lock us down. I became part of the anti-lockdown resistance, protesting on the streets and am proud of that. That period changed how many of us viewed institutions, public health messaging, and medical authority. But that skepticism came with a cost. In 2021, I published a YouTube lecture on the Quest Cardio IQ test. At the time, very few clinicians were talking publicly about these advanced lipid panels. The lecture received thousands of views. In 2022, I found the Labcorp NMR panel and made another lecture. That one also reached thousands of people. I was not just studying this material anymore. I was teaching it. From 2021 through 2024, I listened to nearly every countercultural medical authority I could find. It started with keto physicians like Gary Fettke and low-carb advocates on social media. Then came the carnivore movement, organ-meat influencers, alternative medicine conferences, and the online war between lipid denialists and lipid-lowering advocates. I even met Shawn Baker at an alternative medicine conference in 2023. The movement reached peak absurdity, in my mind, with the rise and fall of Paul Saladino and Liver King. I learned that they both sourced their supplement line from a manufacturer from a businessman in the supplement industry. I had a decision to make. Do I go full in on this and make millions selling supplements and become such an absurd online personality. I recognized for the first time the meaning of grift. The carnivore influencers had capitalized on a growing health conscious and skeptical market with a “natural” supplement. It was fancied as science perhaps with loose inspiration derived from the anthropological studies of a dentist Weston A Price who found less tooth decay in ancestral populations that at a traditional meat based diet. I started Iron Direct Primary Care in 2021 as an alternative healthcare home for patients who wanted something outside the conventional system. For years, I cared for many patients who did not believe elevated lipids mattered. We ordered everything: MPO, homocysteine, hs-CRP, omega-3 testing, IL-6, Lp-PLA2, and thousands of NMR panels. Desperately searching for an answer to cardiovascular disease other than LDL and APO B burden. The pattern was always the same. Patients had elevated LDL particle number and elevated ApoB, and we often kicked the can down the road. We focused instead on insulin sensitivity, clean diet, seed-oil avoidance, exercise, nitric oxide supplements, methylated vitamins, inflammation markers, and metabolic optimization. On Instagram, X and podcasts, the lipid battle raged. I listened to lipid skeptics like MD Tro and ex-carnivore MD Paul Saladino, some were compelling. Some were charismatic. Some wore white coats and spoke with absolute confidence. I thought some of them were brilliant. I even referred patients into that ecosystem. Then reality started to break through. In 2024 and 2025, I began seeing heart attacks and strokes in my own patient population. That floored me. These were not the stereotypical patients people imagine when they think of cardiovascular risk. These were patients who avoided seed oils, lifted weights, ate clean, took nitric oxide boosters, optimized methylation, and followed the advice of wellness influencers. Yet they still had events. There are carnivore FB groups that Carnivorecringe on instagram screenshots and posts revealing a toxic subculture. These self-help groups will gaslight patients who suffer from keto and carnivore with absurd claims like “they weren’t eating enough fats” or “they didn’t give carnivore long enough.” One patient had a stroke and left my practice to pursue high-priced “natural cardiology” advice form Wolfson for $7,000. Another patient pursued an alternative cardiology path by surgeon Philip Ovadia for also $7,000 and later required triple bypass surgery. These cases forced me to confront something uncomfortable: if I continued to minimize ApoB and LDL particle burden, I might be helping patients feel reassured while their arteries continued accumulating risk. So I re-read the data. This time, I looked at the totality of evidence instead of the cherry-picked fragments that confirmed what I wanted to believe. I looked at Mendelian randomization, familial hypercholesterolemia, randomized trials, plaque regression imaging, PCSK9 biology, ezetimibe, statins, and the simple fact that lifetime exposure to ApoB-containing particles is causal in atherosclerosis. That does not mean inflammation, insulin resistance, blood pressure, smoking, sleep, strength, or diet are irrelevant. They matter. But they do not make ApoB disappear. They do not make LDL particles magically harmless. A lean body and a good fasting insulin do not give the artery immunity from particle exposure. I have now delisted my older YouTube lectures that were influenced by this lipid-denial ecosystem. I no longer want to contribute to the confusion. One of the most common patterns I now see online is a medical influencer who has moved away from ordinary patient care, sells supplements, lives in another country (likely to avoid legal consequence) sells expensive diet consults, or gives generalized advice under the protection of “no doctor-patient relationship.” Many of these figures profit from the fear and distrust that exploded during the COVID era. That distrust is real. Some of it was earned. But bad institutional behavior does not make bad science true. The people most affected by this misinformation are often conservatives. These are my people. They are skeptical of the system, suspicious of pharmaceutical companies, and deeply motivated to take responsibility for their health. I respect that. But skepticism without correction becomes a trap. A recent literature on the political polarization of health outcomes suggests that health and mortality are increasingly diverging along political and ideological lines, favoring better health in liberals. My mission now is to stop the preventable damage. I went from lipid denialist to lipid-lowering advocate because my patients, my data, and the broader evidence forced me to change. I still believe in strength training. I still believe in metabolic health. I still believe in nutrition, sleep, sunlight, and personal responsibility. But I no longer believe those things cancel out ApoB. The new message is simple: ApoB matters. LDL particle exposure matters. Prevention matters. And changing your mind when the evidence demands it is not weakness. It is clinical maturity. I was wrong before. Now I am trying to make it right. Further readings: Ference et al., 2017 — “Low-density lipoproteins cause atherosclerotic cardiovascular disease” This is probably the single best paper for the intellectual foundation of my reversal. It integrates epidemiology, Mendelian randomization, genetic disorders, and randomized trials. The authors conclude that the totality of evidence establishes LDL/ApoB-containing particles as causal in ASCVD, with risk depending heavily on magnitude × duration of exposure. Read the full open-access paper Borén et al., 2020 — the mechanistic follow-up EAS consensusThis is the one to read for how atherosclerosis happens: entry, retention, and accumulation of ApoB-containing lipoproteins in the arterial intima and the subsequent inflammatory response. It helps resolve the false choice of “cholesterol versus inflammation” both matter, but ApoB particle retention is upstream in the atherosclerotic process.Read the full open-access paper Cohen et al., NEJM 2006 — PCSK9 loss-of-function mutationsThis is one of the most persuasive natural experiments. Genetically lower LDL from PCSK9 variants produced dramatically lower coronary disease risk. In one population, roughly a 28% lifelong LDL reduction was associated with an 88% reduction in CHD; in another, a ~15% LDL reduction was associated with ~47% lower risk.Read the NEJM paper Ference et al., JACC 2012 — lifelong genetically lower LDLExtremely important because it explains why short drug trials can make LDL lowering look unimpressive compared with lifelong exposure. Genetic randomization allows us to ask what happens when LDL is lower beginning early in life.Read the PubMed article and access the full text CTT Collaboration, Lancet 2010 — 170,000 participants / 26 randomized trialsThis is an excellent paper to revisit for objection about statin statistics. Rather than focusing on one mortality NNT, it looks at outcomes per absolute LDL reduction across a huge randomized dataset.Read the complete paper free on PMC CTT Collaboration, Lancet 2012 — statins even in lower-risk populationsThis one is particularly relevant to “NNT ≈100” arguments. One important distinction: an NNT around that range can describe major vascular events in relatively low-risk people over a limited follow-up period, but it is not a universal “statin mortality NNT.” Absolute benefit necessarily looks smaller when baseline short-term risk is low.Read the paper / abstract My original skepticism was not irrational—the mistake was extrapolating a modest short-term absolute benefit in low-risk people into the conclusion that lifetime ApoB exposure was unimportant. FOURIER — Evolocumab cardiovascular outcomes, NEJM 201727,564 patients with ASCVD. PCSK9 inhibition lowered LDL dramatically and reduced cardiovascular events on top of statin therapy. This is important because it dismantles the argument that the benefit is some peculiar “pleiotropic statin effect.” Different mechanism, same direction: reduce ApoB/LDL exposure → fewer events.Read FOURIER in NEJM ODYSSEY OUTCOMES — Alirocumab, NEJM 2018Another PCSK9 inhibitor, another randomized trial, another reduction in ischemic events. Primary endpoint: 9.5% versus 11.1% after ACS.And yes. Events were lower in the alirocumab arm. Lipid denialists will say mortality wasn’t reduced enough. But these were patients already managed and in the system able to get emergency care to save from death. Primary composite (CHD death, nonfatal MI, ischemic stroke, or unstable angina hospitalization):903 patients (9.5%) vs 1,052 patients (11.1%).All-cause death:334 patients (3.5%) vs 392 patients (4.1%). That is 149 fewer first primary events and 58 fewer deaths over a median 2.8 years. The relative reduction on the primary endpoint was 15% and met the pre-specified significance threshold.Read ODYSSEY OUTCOMES IMPROVE-IT — Ezetimibe + statin, NEJM 2015Also philosophically important: lower LDL using a nonstatin mechanism, and cardiovascular outcomes improve further. Again, it is difficult to sustain a hypothesis that the benefit is merely a special property of statins.Read IMPROVE-IT GLAGOV — Evolocumab and actual coronary plaque regressionThis was one is Anti Aging Medicine. We can reverse plaque? That is regenerative medicine!. LDL reached about 36.6 mg/dL; percent atheroma volume fell, and 64.3% of evolocumab patients demonstrated regression versus 47.3% with placebo.Read GLAGOV in JAMA PACMAN-AMI — Alirocumab, JAMA 2022This is even more visually compelling because multimodality intracoronary imaging showed not only greater plaque regression but changes consistent with plaque stabilization: reduced lipid burden and thicker fibrous caps. Again, this is Anti Aging and Regenerative Medicine.Read PACMAN-AMI in JAMA ApoB vs LDL-C discordance — JAMA Cardiology 2024It demonstrates how widely ApoB can vary among people with the same LDL-C or non-HDL-C and quantifies clinically important discordance.Read the JAMA Cardiology paper There is also a 2025 systematic review of 15 discordance studies involving 593,354 people. ApoB outperformed LDL-C in all 9 studies directly comparing the two in the review. That one is particularly relevant to explaining why I moved away from obsessing over LDL subfractions/NMR toward ApoB. Read the ApoB systematic review on PubMed And REACT is especially important The REACT study was just published in NEJM on August 29, 2026. It examined almost 17,000 ostensibly healthy adults aged 18–70 in Denmark and Spain. Atherosclerosis was already detectable in the 18–29-year-old group—8.7% of men and 6.7% of women—and plaque prevalence and volume climbed dramatically with age. Read the new REACT paper in NEJM “I am young, lean and fit, therefore these lipid numbers probably do not apply to me.” REACT shows why that reasoning is dangerous: subclinical disease can already exist decades before the person looks or feels like a cardiovascular patient. The conservative-vs-liberal mortality paper Elder & O’Brian, Nature Human Behaviour, May 14, 2026 — “The political polarization of health outcomes in the USA.” They found that conservatives in their cohort experienced worsening health during the 2010s and higher mortality in the early 2020s, particularly from internal causes such as heart disease, cancer, and stroke. Read the full Nature Human Behaviour article The authors found a mortality divergence associated with political identity; they also found that changing socioeconomic composition of the coalitions, including education, income, and insurance, explained part of the difference

🥳 So proud of my friend, @realDaveFeldman 🥳 🤗 my humble synopsis of #TheCholesterolCode: 👉🏻stories of pure turmoil turned hopeful 👉🏻spreading awareness of a therapeutic strategy that may be helpful for some 👉🏻attempting to provide more clinical information to a number of people concerned about these LDLc levels 👉🏻inspirational grassroots, crowdfunded effort through nonprofit to provide these data 👉🏻encourage metabolic health to gain more focus for longevity and vitality 👉🏻encourage better risk stratification through imaging 👉🏻encouraging provider-patient relationships and the use of medications if needed based on shared-decision At the end of the day, it never ceases to move me seeing the relief from profound human suffering 🙏

Tro - I appreciate the cordial response, but this isn't like political opinions where differing views can be justified. This is about empirical science. The demonization of LDL has been perpetuated by the food and drug industries. I don't doubt your sincerity, but the actual benefits of LDL reduction by any means are minuscule, at best, even for secondary prevention. To advocate LDL reduction in #LMHRs is unsupported by any research, and is in fact, opposed to published research that indicates higher LDL in these people would be associated with better health and greater longevity. @markkaplan20