The Great Overcorrection: Statins, Seed oils, and Saturated fats

The Ember⁸ | #8002

What we’re exploring this week…

🕳️🐇 The Rabbit Hole

I listened to two podcasts this week that got me thinking about the same underlying question, even though they were on seemingly different topics:

What happens when we make generalized interventions based on incomplete understanding?

Both statins and seed oils exist because we decided saturated fat causes heart disease. So we created drugs to lower cholesterol. We swapped butter for vegetable oil. We changed the American diet and put half the adult population on medication.

Eighty years later, we’re still figuring it out. Did we just trade in one problem, for a list of new problems?

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I.

Lipitor and Heart Disease: Drug Story Podcast

👉 The origin story we forget:

It was only 80 years ago that we weren’t treating any of this. High blood pressure? Normal aging. High cholesterol? Not even on the radar.

President Franklin Roosevelt died in office in 1945 with a blood pressure of 300/190.¹ His personal physician — an ear, nose, and throat specialist — had assured him for years that his rising blood pressure was “no more than normal for a man of his age.” The standard belief at the time: acceptable systolic pressure equals 100 plus your age.

Three years after FDR’s death, President Truman signed the National Heart Act, funding the Framingham Heart Study. That study, still running today, gave us the concept of “risk factors.” It changed everything.

We quickly went from treating nothing to treating everyone. I’m not sure we found the balance in between yet, but instead, may have overcorrected.

👉 The threshold creep:

When guidelines first emerged from Framingham-era research, doctors started treating total cholesterol above 260.

By 1986, the threshold dropped to 240. By 1990, it was 200. When Lipitor launched in 1997, the target had fallen to 160.

Each drop expanded the market, putting more people on medication.
📊 Get this…one in two Americans over 40 is now taking a statin!

👉 The 1997 moment:

Speaking of 1997 — that’s the year the FDA changed the rules allowing TV drug advertising for the first time.³ Before then, ads had to include the full list of side effects (if you’ve ever read a prescription insert you know that won’t fit in a 60-second commercial). The new rules let companies just mention “major risks” and refer viewers to a website or phone number.

The timing is interesting. David Kessler, who had been FDA Commissioner since 1990, left in February 1997. The broadcast advertising guidance came out in August. Lipitor launched that same year with a massive TV campaign.

So who was the new head of the FDA as of March ‘97? He later went to work for Monsanto’s pharmaceutical division, then Pharmacia (which merged with Pfizer), then became Chief Medical Officer at PhRMA — the pharmaceutical industry’s lobbying group. 🤔

I’m not saying there’s a conspiracy. But I am saying the revolving door is real, and the timing is worth noticing.

The number needed to treat (NNT):

Here’s where it gets interesting. In primary prevention — meaning healthy people taking statins to prevent a first heart attack — the numbers needed to treat (NNT) are interesting:²

• To prevent one death over 5 years: 167-250 people need to take statins

• To prevent one heart attack: 60-77 people

• To prevent one stroke: 250-313 people

For people at very high risk (familial hypercholesterolemia, previous cardiac events), the math looks different. NNT drops to 20-30. That’s a meaningful benefit.

But for low-risk people with mildly elevated cholesterol? The NNT can exceed 400.

🎯 Does 50% of our adult population over 40 need to be on this medication to function as human beings? I don’t think so.

👉 The Nuance:

Statins clearly help some people. If your LDL is over 250-300, that’s often a genetic issue (familial hypercholesterolemia) that genuinely needs treatment. If you’ve already had a heart attack, secondary prevention makes sense.

But I think we overcorrected. We found one target and focused on it, which led to “if my cholesterol is controlled, I can eat whatever I want” thinking.

🧬 What I expect to happen as we learn more: statin decisions will be based on a combination of data points, not a single number. We’ll look at inflammation markers. Coronary artery calcium scores. Genomics — because some people process cholesterol differently than others. Some people may actually be harmed by aggressively lowering a molecule their body needs.

Guidelines will change. That’s not a failure or one side winning over the other — that’s science working, which is a win for everyone! The question is whether changes are driven by new evidence or new revenue opportunities.

🎧

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II.

The Seed Oil Debate: The Drive by Peter Attia Podcast

The other podcast debated seed oils — canola, soybean, corn, sunflower — which have become the latest wellness villain.

Here are a couple of thoughts (among many) that came up for me while listening.

I’ll be honest: I think that we overuse poor-quality oils and that they can be inflammatory. When I eat at restaurants, I can feel it — phlegm in my throat, gut discomfort. My body sends clear signs that I’m eating something it doesn’t agree with. So this isn’t just a philosophical, political, or virtue-based opinion.

But the podcast pushed back on some of the more extreme claims, and I appreciated that. I always like to hear both sides of any argument so that I can have an informed opinion. So let me share where I agree and where I don’t.

👉 It’s not the seeds. It’s the process.

Seeds aren’t inherently toxic. The problem is what we do to them.

You don’t just squeeze corn and get corn oil. Industrial seed oil extraction looks like this:

1. Preparation: Seeds are cleaned, cracked, dehulled, flaked, and cooked at 180-220°F to rupture cell walls

2. Mechanical pressing: Extracts 60-75% of the oil (cold-pressed oils stop here)

3. Solvent extraction: The remaining press cake is saturated with hexane — a petroleum-derived solvent — which dissolves the remaining oil. This gets yield up to 95%+⁴

4. Solvent recovery: The oil-hexane mixture is heated to evaporate the hexane. About 95% is recaptured and recycled. Trace amounts remain.⁵

5. Refining:

   • Degumming — removes phospholipids

   • Alkali refining — caustic soda removes free fatty acids

   • Bleaching — activated clay removes pigments

   • Deodorization — high-heat steam distillation (400-500°F) removes odors

What comes out the other end is technically “food” — but it’s been through a chemical transormation that leaves no nutrients behind and potentially creates oxidation products and toxic aldehydes that weren’t in the original seed.

👉 The hexane argument I didn’t buy:

The podcast mentioned that to have toxic effects from hexane, you’d need to consume an absurd amount — like 11,000+ kilograms of oil at once. They pointed out that someone once drank straight hexane and just got an upset stomach.

Okay, but... if “you can drink it and not immediately die” is the safety standard, then what’s wrong with saturated fat? You can eat a stick of butter and you won’t drop dead.

That’s not how chronic disease works. Heart disease doesn’t happen because you ate one cheeseburger. Diabetes doesn’t appear overnight. These are cumulative effects over decades.

The same logic should apply to industrial chemicals in our food supply. We don’t know the long-term effects of daily low-dose hexane exposure, oxidized oils, and toxic aldehydes — because we’ve only been eating this way for a few generations.

👉 The fertility question nobody’s asking:

Here’s something that deserves more attention: hexane has been classified as “toxic to human reproduction” by the Nordic criteria (Group 1B).⁶ It’s been known for more than 50 years for its neurotoxicity and reproductive toxicity — and recent evidence suggests it’s also a potential endocrine disruptor.⁷

A 2020 study of women working in a Mexican leather shoe factory — who were occupationally exposed to hexane — found they had longer time to pregnancy and higher rates of menstrual irregularities compared to unexposed controls. The researchers concluded that hexane’s metabolite (2,5-hexanedione) was associated with decreased gonadotropin levels (FSH and LH), and that n-hexane should be considered an endocrine disruptor in reproductive-age women.⁸

🎯 Yes I understand that this was occupational exposure, inhalation, higher levels, etc., but… we’re in the middle of a fertility crisis according to the people who study this stuff. Sperm counts have dropped 50%+ over the past 50 years. Endocrine disruption is everywhere. And we’re bathing our food supply in a petroleum-derived solvent with known reproductive toxicity? 🤨

I’m not saying seed oils are the cause of declining fertility. I’m saying we don’t know what the cumulative, lifelong effects of low-dose hexane exposure are — because we’ve never studied it in that context.
🔥 The absence of evidence isn’t evidence of absence.

Meanwhile, studies have found that infertile men have more than double the omega-6 to omega-3 ratio in their blood and sperm compared to fertile men.⁹ And 4-hydroxynonenal — a toxic aldehyde that forms when omega-6 fatty acids oxidize — has been shown to damage human sperm.¹⁰

Is it the seed oils? The processing chemicals? The imbalanced omega ratios? Some combination? We don’t know. But “nobody’s died from drinking hexane” isn’t a satisfying answer when we’re talking about reproductive health and endocrine function.

👉 Where I land:

I’m not going to pretend I can avoid all seed oils. They’re in everything. If I eat at a restaurant or buy anything packaged, I’m consuming them.

But I choose my battles. At home, I use olive oil, butter, avocado oil, coconut oil — things that don’t require an industrial chemistry lab to produce. When I have the option to eat somewhere that doesn’t use industrial oils, I take it.

The podcast hosts seemed annoyed by restaurants advertising “no seed oils” — like it’s just a trendy gimmick. I disagree. There are plenty of us who would love more options to eat food that isn’t processed with petroleum solvents. Please leave it on the menu.

My philosophy on most things: we’re biological creatures and should, as much as possible, eat real food in its natural state. I’m not looking for excuses to consume highly processed chemical oils when unprocessed alternatives exist.

🎧

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III.

🌀 The Spiral: What If Cholesterol Isn’t the Enemy?

Here’s something I’ve been thinking about while researching cholesterol treatment recommendations (mainly because I have what is typically considered “high” cholesterol):

💡 What if aggressively lowering cholesterol has unintended consequences?

We talk about cholesterol like it’s a toxin — something to be minimized. But cholesterol isn’t arterial sludge waiting to kill you. as it’s often portrayed. Poor cholesterol, it’s one of the most essential molecules in your body and everyone is always hating on it. Here’s what it actually does:

👉 Your Brain Runs on It

Twenty-five percent of your body’s cholesterol is in your brain — more than any other organ.¹¹ Cholesterol is essential for forming the myelin sheath that insulates your neurons and allows them to conduct signals efficiently. It’s critical for synapse formation and neurotransmitter function — including serotonin.¹²

Very low cholesterol levels have been associated with depression, anxiety, and cognitive impairment.¹³ When cholesterol in neuronal membranes drops too low, it affects membrane fluidity and can impair neurotransmitter synthesis.

👉 Every Steroid Hormone Starts Here

Cholesterol is the precursor molecule for all steroid hormones:¹⁴

• Sex hormones: Testosterone, estrogen, progesterone

• Stress hormones: Cortisol, corticosterone

• Mineral regulation: Aldosterone

• Plus: Vitamin D synthesis and bile acid production

Without adequate cholesterol, your body can’t make the hormones it needs for reproduction (back to fertility again), stress response, metabolism, and mineral balance.

👉 Your Immune System Needs It

This one surprised me. Multiple studies show a U-shaped relationship between cholesterol and infectious disease — meaning both very low AND very high levels increase your risk.¹⁵

One study found that men with total cholesterol averaging 150 mg/dL had significantly weaker immune systems than those at 260 mg/dL.¹⁶ Low cholesterol levels are predictive of mortality in patients with severe sepsis.¹⁷ TB patients with low cholesterol have higher death rates — high-cholesterol diets are now part of tuberculosis treatment.¹⁸

Why? LDL and VLDL appear to help sequester pathogens like bacteria and viruses. They’re part of your body’s defense system.¹⁹

👉 The U-Shaped Mortality Curve

Multiple large studies show a similar pattern for all-cause mortality
LDL Level Mortality Risk:
Very low LDL (<100 mg/dL)» Increased risk;
Moderate LDL (100-160 mg/dL)» Lowest risk;
High LDL (>190 mg/dL)» Increased risk

👉 So What Are We Optimizing For?

• CVD risk alone → lower is better

• All-cause mortality → moderate may be optimal

• Hormone synthesis → requires adequate cholesterol

• Immune function → very low may be harmful

• Brain function → essential for cognition

🎯 The blanket application of “lower is always better” may be overly simplistic — especially for older adults whose bodies may have reasons for maintaining higher cholesterol that we don’t fully understand.

None of this means high cholesterol is good. It means we might be treating the wrong target in the wrong people.

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IV.

🔬 The Marker: hs-CRP (High-Sensitivity C-Reactive Protein)

If we’re moving toward multi-factor cardiovascular risk assessment, this is one marker worth knowing.

What it measures: Systemic inflammation — specifically, a protein produced by the liver in response to inflammation

Why it matters for heart disease: Inflammation drives atherosclerosis. You can have “normal” cholesterol and still have inflamed, unstable arterial plaques. Conversely, you can have elevated cholesterol with minimal inflammation and lower risk.

Reference ranges:

• 👉 < 1.0 mg/L: Low cardiovascular risk

• 👉 1.0 - 3.0 mg/L: Moderate risk

• 👉 > 3.0 mg/L: Higher risk

• 👉 > 10 mg/L: Likely acute inflammation (infection, injury) — retest later

The nuance: hs-CRP can be elevated by many things — infections, autoimmune conditions, obesity, poor sleep, stress. A single high reading doesn’t mean much. Patterns over time tell the story.

How to get it: Standard lab test, often included in comprehensive metabolic panels. Inexpensive. Ask your doctor to add it to your next bloodwork, or order through direct-to-consumer labs.
🔥 Automatically included in our Comprehensive Foundational Lab Panel

This marker, combined with lipid panels, coronary artery calcium scoring, and eventually genomics, points toward a future where we make individualized decisions rather than applying population-level blanket treatments to everyone.

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V.

🔥 The Ember

We spent 80 years building a medical framework around one molecule — cholesterol — and one hypothesis — that saturated fat causes heart disease.

We created drugs to lower the molecule. We engineered oils to replace the fat. We put half the country on statins and seed oils.

Now we’re asking: did we get it right? Did we overcorrect? What did we miss?

🌀 The answer isn’t that statins are bad or seed oils are poison. The answer is that biology is complex, and single-target interventions always have unintended consequences. Half of adults over 40 are on a statin and their LDL is under 100, but that tunnel vision has now given us obesity, diabetes, fatty liver disease, and reduced fertility.

The next era of medicine will be about understanding individuals, not populations. Measuring multiple factors, not single numbers. And having the humility to update our guidelines when the evidence demands it — regardless of whose revenue it affects.

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💡 On My Radar

This issue ran a little longer that I intended so I’ll save my latest radar recommendations for next week. Until then…!

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Would love to hear your thoughts in the comments. Keep the conversation going!
Exploring and being open-minded is how we learn…not to mention it’s fun.

Until next week….

Stay curious!

Heather | Ember 8

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📖 References

1. Bruenn HG. “Clinical notes on the illness and death of President Franklin D. Roosevelt.” Annals of Internal Medicine. 1970;72(4):579-591.

2. Byrne P, et al. “Statins for primary prevention of cardiovascular disease.” BMJ. 2019;364:l4541.

3. FDA Guidance for Industry: Consumer-Directed Broadcast Advertisements. August 1997. Ventola CL. “Direct-to-Consumer Pharmaceutical Advertising.” P&T. 2011;36(10):669-684.

4. AOCS (American Oil Chemists’ Society). “Solvent Extraction.” Technical Resources.

5. Durand E, et al. “Towards Substitution of Hexane as Extraction Solvent of Food Products and Ingredients with No Regrets.” Molecules. 2022;27(21):7432.

6. Hansen OC. “Evaluation of health hazards by exposure to n-hexane and proposal of health-based quality criteria.” Nordic Council of Ministers. 1992.

7. ATSDR (Agency for Toxic Substances and Disease Registry). “Toxicological Profile for n-Hexane.” April 2025.

8. Ruiz-García L, et al. “Possible role of n-hexane as an endocrine disruptor in occupationally exposed women at reproductive age.” Toxicology Letters. 2020;330:73-79.

9. Safarinejad MR. “Effect of omega-3 polyunsaturated fatty acid supplementation on semen profile and enzymatic anti-oxidant capacity of seminal plasma in infertile men.” Clinical Nutrition. 2011;30(6):819-825.

10. Aitken RJ, et al. “Cis-unsaturated fatty acids stimulate reactive oxygen species generation and lipid peroxidation in human spermatozoa.” J Clin Endocrinol Metab. 2006;91(10):4154-4163.

11. Dietschy JM, Turley SD. “Cholesterol metabolism in the brain.” Current Opinion in Lipidology. 2001;12(2):105-112.

12. Schultz BG, et al. “The role of statins in both cognitive impairment and protection against dementia: a tale of two mechanisms.” Translational Neurodegeneration. 2018;7:5.

13. Beasley CL, et al. “Reductions in cholesterol and synaptic markers in association cortex in mood disorders.” Bipolar Disorders. 2005;7(5):449-455.

14. StatPearls. “Biochemistry, Cholesterol.” NCBI Bookshelf. 2023. Miller WL, Bhagwat AS. “Cellular cholesterol delivery, intracellular processing and utilization for biosynthesis of steroid hormones.” Nutrition & Metabolism. 2010;7:47.

15. Madsen CM, et al. “U-shaped relationship of HDL and risk of infectious disease: two prospective population-based cohort studies.” European Heart Journal. 2018;39(14):1181-1188.

16. Muldoon MF, et al. “Immune system differences in men with hypo- or hypercholesterolemia.” Clinical Immunology and Immunopathology. 1997;84(2):145-149.

17. Endotext (NIH). “Effect of Inflammation and Infection on Lipids and Lipoproteins.” NCBI Bookshelf. 2025.

18. Pérez-Guzmán C, et al. “A cholesterol-rich diet accelerates bacteriologic sterilization in pulmonary tuberculosis.” Chest. 2005;127(2):643-651.

19. Tall AR, Yvan-Charvet L. “Cholesterol, inflammation and innate immunity.” Nature Reviews Immunology. 2015;15(2):104-116.

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The Ember⁸ Newsletter January 2026