So in our last episode, we laid out the case for traditional limpidology. We traced 150 years of science from rabid autopsies in St. Petersburg to Mendelian randomization and massive satin trials showing why mainstream cardiology views ApoB containing particles as an independent causal driver of heart disease. If you watch that, the conclusion might have seemed pretty or tight. So that brings us to the natural question: why is there an entire counterculture of physicians, researchers, and citizen scientists who aren't buying it? Are they just contrarian influencers selling beef tallow and conspiracy theories? Or is there a genuine evidence-based critique buried beneath the Internet noise?
Today we're going to look at the other side of the ledger. We're going to walk through this countercultural case, not to pick an ideologic term or team, but to look at the data and alternate models, and most importantly, what the evidence actually shows. To understand the cholesterol counterculture, you have to understand where it all began, right? So it didn't begin on TikTok. It began with the collapse of trust in 20th century nutritional guidelines. In 1977, the U. S. Dietary Goals was the first time the government ever really gave suggestions on how its citizens should eat, and it told the entire population that dietary fat and cholesterol were enemy number one, steering millions of people towards refined carbohydrates. grains and margarine. Fast forward fifty years and people are sicker than ever.
People are starting to wonder was the government wrong? On top of that, people were trying fringe diets where they're eating no carbs and eating lots of animal protein and were having Big successes. They were losing weight, reversing prediabetes, and it opened a massive psychological door. If the guidelines are wrong about what to eat, what else might they be wrong about? And that skepticism wasn't purely anecdotal. It gained serious academic traction when researchers dug up raw historical data from the original gold standard diet heart trials. Between 2013 and 2016, an NIH team led by Dr. Christopher Ramsden recovered previously unredacted raw data from two landmark randomized controlled trials: the Sydney Diet Heart Study in Australia.
And the Minnesota Coroner Experiment, co-led by Ansell Keys. These were strict institutional feeding trials conducted in the 60s and 70s, where saturated fats were replaced with vegetable oils rich in limoly acid. In both trials, the interventions worked biochemically. Switching to vegetable oils and margarines significantly drove down total blood cholesterol. Except the clinical outcomes completely inverted the hypothesis. In the Sydney trial, the group eating vegetable oils had higher cardiovascular mortality. And higher all-cause mortality.
In the Minnesota trial, for every 30 milligram per deciliter drop in serum cholesterol, the risk of death rose by 22% among participants over the age of 65. And the question skeptics asked was obvious. If driving down cholesterol by replacing dietary fat is universally life-saving, why did the rigorous, randomized feeding trials fail to show a survival benefit? While historians still debate confounding factors like trans fat and early margins, the fact that these critical findings set unpublished for decades fueled lasting skepticism towards consensus nutrition. The next major crack in the narrative comes from looking at aging populations. If L-DL cholesterol is a universal linear toxin, you would expect its relationship with cardiovascular events and mortality to be even more pronounced as people age and cumulative vascular exposure increases over time. In 2016, Dr. Uffay Ravenskoff, an international group of researchers, published a systematic review in BMJ Open, examining 19 prospective cohort studies covering over 68,000 adults aged 60 and older.
And what they found defied conventional wisdom. In roughly 80% of cohorts, higher LDL was either inversely associated with all-cause mortality or showed no assaying at all. People with the highest LDL levels frequently live just as long or longer than those with the lowest. So mainstream lipidologists explain this via reverse causation, that frail, dying individuals suffer from chronic wasting and end stage illness, which artificially suppresses their cholesterol before death. But skeptics counter that LDL particles also play a crucial physiologic role in immune defense and neutralizing bacterial endotoxins like LPS. If LDL is purely a metabolic byproduct that destroys arteries, why does having more of it appear to have neutral or protective effects in our most vulnerable demographic? This discrepancy pushed contrarian thinkers to start to wonder: why might this be the case?
What is the physiology that would explain this? Physician Dr. Malcolm Kendrick modernized an old theory called the encrustation theory, where atherosclerosis starts with microscopic blood clots. And form into the thrombogenic model of heart disease. So Kendrick argues that the primary initiating event of atherosclerosis is not the concentration of ABOB floating in the lumen, but repeated injury to the subendothelioglycocalyx caused by smoking. high blood pressure, glycation from chronic hyperglycemia, emotional stress, or chronic systemic inflammation. When an injury occurs, platelets and fibrin form a microclot to patch the hole. Normally, the endothelium heals over it, but if repair mechanisms are overwhelmed, that clot gets incorporated into the arteriole wall where red blood cells, membranes, and traph lipoproteins break down, leaving behind cholesterol-rich plaques and secondary calcification.
Under this framework, LDL is not the arsonist setting fire, it is part of the repair squad and structural debris caught in the collateral damage. Now, let's turn to the central argument of the modern lipid skeptics: the power of metabolic context. In conventional cardiology, APOB is treated as an independent risk factor, meaning high numbers carry risk regardless of whether or not your other markers are pristine or broken. Contrarians push back here. They argue that cardiologists spent decades studying a sick population. In the general Western population, people with high LDL almost universally have metabolic syndrome, elevated blood pressure, insulin resistance, evisceral obesity, and chronic systemic inflammation. Skeptics ask, does high LDL carry the same vascular consequence in a body that is completely incident-sensitive and metabolically healthy? Consider this landmark Danish study led by Dr. Martin Mortensen in 2022, published in Jack.
Researchers tracked over 23,000 asymptomatic individuals without known heart disease and evaluated their coronary artery calcium or CAC scores alongside their LDL levels. What they found was striking. In individuals with a CAC score of zero, meaning no detectable calid plaque in their coronary arteries, having high LDL did not translate into an elevated risk of heart attack or stroke over the medium-term follow-up. Risk only scaled significantly with LDL and those who already had established subclinical atherosclerosis. To skeptics, this was evidence that an intact, healthy artery with zero underlying disease behaves very differently from an artery that has already begun to degrade. That brings us to the modern battleground today, the explosion of carbohydrate-restricted and ketogenic diets. Over the past few decades, hundreds of thousands of people have adopted low-carb, high-fat lifestyles to manage type 2 diabetes, metabolic syndrome, or various other medical conditions. For many, the results on paper looked miraculous. HVA1C plummeted, blood pressure normalized, visceral fat melted away, triglycerides plummeted into the double digits, and HGL skyrocketed Everything was great except for one glaring problem that sent their primary care doctors in a panic.
In a distinct subset of these individuals, their LDL, cholesterol, and APOB didn't just tick up, they went into the stratosphere. We're talking LDLC jumps from an average of 130 to 300, 400, or even 600 milligrams per deciliter. In standard clinical guidelines, an LDLC of over 190 is an automatic red alert and recommendation for a statin. If an otherwise healthy 32-year-old walks into a clinic with an LDL of 450, they're immediately treated as an emergency and told they have familial hypocholesterolemia. But these individuals didn't have high cholesterol their whole lives. They cut out carbs, ate much more saturated fat, and their lipid panel exploded. Why was that? The medical establishment originally dismissed this as an outlier anomaly or dangerous dietary recklessness. Enter Dave Feldman, a software engineer with a background in systems analysis.
When Feldman went keto, his own LDL skyrocketed. Instead of immediately taking a statin, he did what an engineer does. He began to test his blood every few days, running detailed N of one experiments, mapping changes against macronutrient shifts. And crowdsourcing data from thousands of other low-carb dieters. He identified a consistent recurring phenotype that he named as a lean mass hyperresponder, or LMHR. The LMHR phenotype is strictly defined by a specific lipid triad. First, markedly elevated LDL cholesterol, typically 200 mg per deciliter higher, often exceeding even 400.
Second, exceptionally high HDL cholesterol, which is 80 milligrams per deciliter higher. And third, rock bottom fasting triglycerides, which is 70 milligrams per deciliter or lower. Now, notice what this triad looks like. In classic insulin resistance, triglycerides are high, HDL is low, and LDL particles are small and dense. In the lean mass hyperresponder profile, Triglycerides are typically low, HDL is high, and the LDL profile shifts towards pattern A, which are large, buoyant particles. And proponents argue that these large particles are far less susceptible to oxidative modification. And sub endothelial entrapment in an artery that is completely free of inflammation.
But Feldman and later academic researchers noticed something even stranger. The cholesterol spike was inversely correlated with body mass index. If you were carrying 80 pounds of excess fat, And went on a keep-junk diet, your LDL barely moved and often actually went down. But if you were lean, athletic, and had low body fat, your LDL spiked the hardest. So think about how counterintuitive this is under conventional thinking. We're told that dietary saturated fat simply clogs the clearance receptors in the body. But why would the leanest, fittest marathon runners have three times the cholesterol response of someone with obesity who's just eating the exact same steak? It didn't make sense. So, to explain this biological phenomenon, Feldman teamed up with other researchers, including Dr. Nick Norowitz and Dr. Ajan Sotomoda, publishing a mechanistic framework called the lipid energy model in the journal metabolites.
The model treats the liver not as a damage filter, but as a dynamic logistic center managing energy delivery across the body. Now, here are the high-level mechanics, but we'll touch more about this in a future video. But here's what happens in simple terms. When you eat carbs, your liver stores glycogen and your body runs on sugar. When you stop eating carbs, your liver runs out of glycogen. Your body has to switch entirely to burning fat. Your fat cells release fatty acids. The liver grabs them, packages them into triglycerides, and puts them aboard a delivery ship called the VLDL and sends it to your body for energy. Under the lipid energy model, the explosion of LDL and HDL in the collapsed tetraglycerides isn't pathology.
It's a natural downstream byproduct of an ultra-efficient fat-fuel energy delivery system running at full throttle in a lean person with limited storage. Then, as those VLDL cruise ships move throughout the body, your muscles suck the triglycerides into the muscles for fuel to burn the energy. What happens when you suck the fuel out of a VLDL ship? Well, it shrinks. And when it shrinks down, that leftover particle becomes LDL. Because this turnover is happening at lightning speed, you get a buildup of empty LDL boats in the blood while surface fats get transferred over to HDL. The result? High LDL, high HDL, and rock bottom triglycerides.
It's not a broken liver, it's a bustling fuel delivery system. And to prove this was about fuel and glycogen, not a problem with the liver, Dr. Nick Norwitz ran an experiment on himself. Norwitz was a lean mass hyperspawner on a keto diet with an LDL nearly 400 mg per esliter, but he ran a test. In one trial, he took 20 milligrams of resuvastatin, a powerful prescription statin, for six weeks. And the other trial, while off the statin, he simply added 100 grams of carbs back on his diet for 16 days, using 12 Oreo cookies each day. The high-dose statin dropped his LDL by about 32%, which is standard and expected for that medication. However, the Orioles dropped his LDL by 71% in just two weeks, from 384 down to 111 milligrams per deciliter.
Now, Norwitz wasn't telling anyone to eat cookies. He proved the same thing by eating bananas and sweet potatoes. His point was scientific, though, and he's arguing for the lipid energy model. To him, it showed that replenishing the liver's glycogen turned off the need to ship fat fuel, and his massive LDL spike vanished almost overnight. But here's where we have to be completely honest. Explaining why LDL rises does not prove that having sky-high LDL for years is safe. Mainstream cardiologists looked at the ellipit energy model and said, okay, this is a neat little theory, but you still have hundreds of API B particles banging against the arterial wall. Does this healthy metabolic state actually protect you from the plaque?
There's only one way to find out: to look directly into people's hearts. So, Norwitz and others, including Dr. Matthew Budoff at UCLA. An expert in CT cardiac imaging, led the landmark keto CTA trial. They took 80 keto participants who fit the LMHR profile, and they'd have been on keto for the average of five years with an average LDL of 272 milligrams per deciliter. They matched them one to one against people of the exact same age, sex, and health status who ate a standard diet and an average LDL of about 123. They then performed advanced CT scans. Scans that detect both calcivide and soft early plaque.
And the baseline result, after roughly five years of an average LDL nearly 150 points higher than the controls , The keto group had no statistically significant difference in coronary plaque burden compared to the match cohorts. Now, what happened over time? Well, the team followed 100 participants for another full year to track progression. An initial 2025 paper suggested that baseline plaque rather than LDL or APOB drove progression. However, in 2026, that specific one-year follow-up paper was formally retracted.
Now there's Lots of controversy over this retraction and what it means for the study, and we'll unpack that in a future video, but I wanted to mention it. Then in 2026, a case report co-authored by Dr. Norwitz again was published detailing a lean young man who'd maintained an LDL nearly 700 milligrams per deciliter for almost seven years. on a ketogenic diet. According to traditional textbooks, maintaining an LDL of 700 milligrams per deciliter over seven years should produce rapid, aggressive atherosclerosis. Yet, when they performed advanced AI-analyzed coronary CT angiography, his calcium score was zero, and his total plaque volume across all his coronators was zero. To skeptics, this was living proof of concept.
LVID LDL alone does not instantly or uniformly guarantee arterial disease in every human being. So, does this mean that ApoB doesn't matter? In fact, no, that's not the case. In their published responses, the authors of the Keto-CTA study explicitly stated that their findings remain, quote, compatible with the causal role of ApoB in atherosclerosis. And so, let's let that sink in. The researchers aren't arguing that AFOB is harmless. They are arguing for effect modification: that metabolic health, low inflammation, and proceeding insulin sensitivity might change the rate or threshold of disease. But athosclerosis is a multi-decade process, the biological equivalent of compounding interest over 30 or 40 years.
Five or seven years of clean scans cannot guarantee clean arteries at year 25. So, now one of the most common things you'll see in this community is the term n equals 1. In scientific papers, n stands for the number of participants. So, this is saying that n equals 1. Means you are the only person in this study. And what they mean by that is that everybody is different and you need to treat yourself based on your own specific needs. So the argument is that if your cholesterol spikes after adopting a low-carb diet, you don't need to panic, but you also shouldn't put your head in the sand. You should take your own health in your own hands.
Instead of arguing over internet theories, measure your actual biology. Get a coronary artery calcium scan, or maybe get a CCTA to evaluate the non-calcified plaque. Check your APO B, your blood pressure, your fasting insulin, your inflammation via high-sensitive ECRP. Have an adult, individualized conversation with your doctor based on your vascular scans rather than relying solely On a generic population risk calculator. And so, this is just the start. I wanted to introduce this, but we are going to talk more about these topics a lot more in my future videos. So, I really hope you found this helpful and have a better understanding of the current landscape of conventional non-traditional lipidology.
Join me for my next video as we discuss more cholesterol controversies. We'll see you next time.
Disclaimer, this podcast is for entertainment, education, and informational purposes only. The topics discussed should not solely be used to diagnose, treat, or prevent any condition. The information presented here was created with an evidence-based approach, but please keep in mind that science is always changing, and at the time of listening to this, there may be some new data that makes this information incomplete or inaccurate. Always seek the advice of your personal physician or qualified healthcare provider for questions regarding any medical condition.
