Source: Gasiorowski et al, JAMA Network Open 2022. Article with the numbers: https://t.co/TCnj7DgeNg Telehealth second opinions: https://t.co/PJvLJQm0YE
Giving blood is the only proven way to lower forever chemicals in your body. A cardiologist explains.
PFAS, the chemicals in nonstick pans, waterproof gear and fast food wrappers, bind to albumin in your blood and stay there for years. Your kidneys cannot remove them. They track with higher cholesterol and higher blood pressure in big population studies.
In 2022 an Australian group randomized 285 firefighters with high PFOS levels. Plasma donation every 6 weeks for a year cut PFOS by about 30 percent. Whole blood every 12 weeks cut it about 10 percent. Controls did not change.
Bonus: it lowers ferritin also. Iron is a strong oxidant.
maybe LDL is the wrong target. Look at the curve from the FOURIER trial, we reduced LDL from 92 to 30. If LDL were the villain everyone thought then why are the results so....weak? 11.3 percent had a heart attack, stroke, stent or cardiac death on placebo, 9.8 percent on the drug. Death from any cause 3.1 vs 3.2. Nobody lived longer. Similar results in the SPARCL trial with high dose atorvastatin. Strokes down 2 in 100 after 5 years, an increase in hemorrhagic strokes which are usually much worse, no change in mortality. Maybe we should target things that help patients in all aspects of life. Nutrient rich diet, HIIT, fewer glucose and insulin spikes, better sleep, more time in the sun, avoid chemicals mold and heavy metals. You aren't living in your grandmother's world, over 80,000 chemicals are registered for use in the US. If your cardiologist quotes you 15 percent ask for the absolute number.
The most useful number on your cholesterol panel isn't printed on it.
Triglycerides ÷ HDL. Labs don't report it. I check it before I look at LDL.
Why: "LDL" isn't one thing. High triglycerides + low HDL = small, dense LDL particles — the kind that slip under the arterial lining and oxidize. Oxidized LDL is what the immune system attacks; that's plaque. Low triglycerides + high HDL = large, buoyant LDL, which resists oxidation and mostly does no harm. Two people with an identical LDL of 150 can be carrying completely different cargo. The ratio tells you which.
It's also the cheapest insulin-resistance test in medicine — a ratio over 3 flags it years before glucose or A1c move.
The hard number: in a Boston case-control study of first heart attacks (Gaziano, Circulation 1997), the highest quartile of TG/HDL had ~16x the risk of the lowest. Neither number alone came close.
How I read it: under 1.8 to 1, optimal (normal is not optimal — no lab will flag a 3). Over 3, insulin resistance until proven otherwise. Over 4, high risk whatever the LDL says.
Best part: it moves fast. Statins barely touch it. Cutting refined carbs, protein and fiber first, a walk after meals, resistance training, and real sleep can halve it in months.
The 82-year-old in persistent AFib I wrote about last week: his ratio had drifted from 1.6 to 2.6 over two years. At our first visit: triglycerides 93, HDL 36, not one flag on the report — that lab calculated his cholesterol/HDL ratio for him but never this one. A particle test along the way showed the small dense LDL the ratio predicts. Normal. Not optimal.
LDL is the number we're taught to treat. The ratio is the number that tells you why it's there.
Full piece + source: https://t.co/VCKiRM6blR
The niacin/NAD post this follows: https://t.co/Kr60wlm1V2
Second-opinion consults: https://t.co/PJvLJQm0YE
In 1951 a researcher gave rats every known vitamin, then put them in 20°C water. They quit in 13 minutes.
Ershoff's three groups, fed from weaning:
- purified diet + all 11 known vitamins: 13.3 min
- same + the full B-complex: 13.4 min
- same + 10% dried liver: 63, 83, 87 min, and 9 of 12 still swimming at the 2-hour cutoff
He called it the anti-fatigue factor. It has never been isolated.
Skeptics say the diet was low in iron. Maybe that's part of it. But nobody reproduced the result by adding iron, and the factor was never found, because it isn't a factor. It's synergy: iron with copper, B12 and folate in their natural forms, CoQ10, cofactors nobody has named, in ratios nature worked out before we started counting.
Isolated vitamins are a guess about which nutrient you need and how much. Megadose the guess and you get the excess too (see: niacin, 4PY, inflamed arteries). Whole organs, fish roe, shilajit: the body sorts the ratios.
We know copper to zinc. We don't know copper to boron. We're still copying nature.
The list, or the liver?
An 82-year-old with 2 years of persistent AFib came to me asking about ablation.
10 weeks later, the smartwatch that had documented his AFib around the clock for 2 years flipped to sinus rhythm. No ablation. No antiarrhythmic. No cardioversion. And it's held — every recording since shows sinus, confirmed by a hospital 12-lead during an unrelated procedure in July. His only remaining pharmaceutical: the anticoagulant.
His AFib was documented half a dozen ways — office EKGs, echo, nuclear stress test, a continuous monitor reading AFib 100% of the time (its sinus column: "NONE") — yet naturally rate-controlled, no rate-slowing drugs at all, which is rare in itself. I wrote in his consult letter that natural methods were "unlikely" to convert him — every electrophysiologist is trained on the same one-way street: AFib begets AFib.
What he did instead: ate like his ancestors (organs, sardines, salmon roe, fermented foods). Flattened his glucose spikes — vegetables first, savory breakfast. Rebuilt his sleep: cold dark room, elevated head of bed, magnesium. Did postural training up to 10x a day — body-weight squats, soleus pushups, calf raises — which improved his insulin resistance and cleared his leg swelling; breathwork and humming in the hours between for vagal tone. Fixed his gut (high TMAO), repleted his minerals down to the trace minerals, lowered his homocysteine. Took FEWER pills — traded a cabinet of synthetic supplements for a few whole-food ones.
None of those converts persistent AFib. That's the point — none of them had to. Small inputs compound until the atrium isn't a place fibrillation can live.
One patient is one patient. Keep your anticoagulant, keep your EP appointment. But I put "unlikely" in writing, and he proved me wrong — I've stopped saying it so quickly.
The riskiest part of a heart scan isn't the radiation. It's what happens next.
The screening cascade: a calcium scan "just to know" → high score → stress test → abnormal → cath → elective stent. Every step feels logical. The ending is wrong.
The scan sees old, stable, calcified plaque — not the soft, inflamed plaque that actually ruptures and causes heart attacks.
The stent doesn't change your odds. ISCHEMIA (NEJM 2020) randomized 5,179 stable patients with abnormal stress tests — exactly who the cascade funnels to the cath lab — to invasive vs. medical therapy. Death at 3.2 years: 5.6% vs. 5.6%. Identical.
And the patient leaves with a false story: most elective-stent patients believe it saved their life. Only ~1 in 5 of their own cardiologists agree (Rothberg, Annals of IM 2010). The real drivers of the disease go untreated because the problem feels solved.
A stent DURING a heart attack is lifesaving. That's different.
Assume the disease is there — it almost always is — and treat root causes for everyone. And if you're mid-cascade with a cath on the calendar and no emergency: get a second opinion first. It costs you a week.
One of the most popular “longevity” supplements may be quietly inflaming your arteries.
Niacin was cardiology’s darling for decades — it raises HDL and lowers LDL, so we assumed it saved lives. Then the trials came back negative. Now the wellness world is megadosing its cousins, NR and NMN, to “boost NAD.”
What the newest science shows:
1. Your body can only use so much niacin. The excess is broken down into terminal metabolites — 2PY and 4PY — and they don’t leave quietly.
2. 4PY switches on vascular inflammation. In the Cleveland Clinic study it activated VCAM-1 — the molecule that makes artery walls sticky for inflammatory cells. That may help explain why the big niacin trials (AIM-HIGH, HPS2-THRIVE) improved cholesterol numbers but didn’t prevent events.
3. NAD boosters feed the same pathway. NR and NMN are catabolized into the same 2PY and 4PY. Megadosing a precursor is megadosing niacin’s leftovers.
The hard stat: in Nature Medicine (2024), the top quartile of blood 4PY carried roughly double the risk of heart attack, stroke, or death over 3 years — HR 1.89 in the US cohort, 1.99 in the European validation cohort.
This is what happens with isolated, megadosed nutrients. We know the copper-to-zinc ratio — but what about copper to boron? In whole-food form — freeze-dried organs, shilajit resin, freeze-dried wild salmon roe — your body decides what to absorb, and in what ratios. We are always studying and copying Mother Nature, and we will never fully learn all of her secrets.
Are you taking an NAD booster — and did anyone mention this study when you started?
Full write-up, including the one honest caveat (coffee days cost people ~36 minutes of sleep, and short sleep IS an AFib trigger): https://t.co/hEFae3fbcN
The first question almost every AFib patient asks me: "Do I have to give up my coffee?"
For 30 years cardiologists said yes. The evidence now says the opposite.
That advice was never built on a trial. Caffeine is a stimulant, patients blame their morning cup, and we repeated it back to them.
Tested at scale — 386,258 people in the UK Biobank — each additional daily cup tracked with about 3% LOWER arrhythmia risk (JAMA Internal Medicine, 2021).
Tested with continuous monitors, coffee days produced no more premature atrial beats than caffeine-free days (NEJM, 2023).
And then tested in AFib patients themselves. DECAF (JAMA, 2025): 200 patients randomized after cardioversion to a daily coffee or total abstinence. Coffee group: 39% lower probability of recurrence at six months. The ones told to quit did worse.
I stopped telling AFib patients to give up coffee. I tell them to go after what actually drives it: sleep apnea, alcohol, insulin resistance, weight, poor sleep, stress.
Coffee was never the villain. It was the easiest thing to blame.
An unpopular opinion from a cardiologist: statins are the most oversold drug in medicine.
Not useless. Oversold.
Ask a patient on a statin what it's doing for them. Most will tell you it's keeping them alive. Here's what the randomized trials actually show:
1. The number patients hear is the relative risk reduction — "statins cut death by 9%." Relative numbers always sound bigger than they are.
2. The absolute numbers: across 21 randomized trials, statins reduced all-cause mortality by 0.8% over roughly four and a half years. Heart attack: 1.3%. Stroke: 0.4%. (JAMA Internal Medicine, 2022)
3. That works out to less than two-tenths of a percent per year. Not nothing — but not the life-or-death drug patients believe they're taking.
If you've had a heart attack or you're at genuinely high risk, a statin has a real place. My issue isn't the drug. It's the salesmanship.
I'd rather see every patient attack the root causes — insulin resistance, inflammation, poor sleep, chronic stress — where the payoff is likely larger, and comes with side effects you actually want.
When your statin was prescribed, were you shown the absolute numbers — or just "9%"?
Most patients who get an elective stent believe it saved their life. Most of their own cardiologists know it didn't.
This was actually measured: over 80% of elective-stent patients believed the stent would prevent a heart attack. Only about 1 in 5 of their own cardiologists agreed (Rothberg, Annals of Internal Medicine).
The doctors were right. In stable coronary disease — including stable angina — elective stents don't prevent heart attacks or extend life (COURAGE, ORBITA, ISCHEMIA). Their real job is symptom relief. And in ORBITA, even that barely beat a sham procedure.
Stents during an actual heart attack are lifesaving. That distinction is everything.
The odds change upstream: insulin resistance, blood pressure, sleep, inflammation. If patients knew what their cardiologists know, how many elective stents would still get placed?