Preventing Silent Heart Attacks: The Tests & Tools Your Doctor Isn’t Using | Dr. Michael Twyman

Dr. Twyman uses these strips as a first‑pass evaluation of the exogenous NO pathway. He explains that chewing nitrate‑rich vegetables like spinach, kale, arugula, and beets introduces nitrates that oral bacteria reduce to nitrites; when swallowed, stomach acid converts nitrites to nitric oxide. The strip measures salivary nitrite as a proxy for this process. A pale strip suggests the person isn’t getting enough nitrates or has disrupted oral flora. He notes that mouthwash and fluoride‑containing products wipe out the necessary bacteria. He keeps them in his travel kit and often sees people with low readings who are carnivore or vampire‑like (no sun, no greens).

Dr. Twyman describes the arginine paradox: most people are not arginine‑deficient, but the eNOS enzyme that converts arginine to NO declines with age and oxidative stress. Taking oral arginine is often ineffective because the enzyme is ‘uncoupled.’ Lozenges developed by Dr. Nathan Bryan contain compounds that generate NO gas upon dissolving, delivering it directly to the oral and systemic circulation. He draws an analogy with PDE5 inhibitors (Viagra, Cialis): those drugs keep NO around longer but don’t create it; the lozenges actually produce the NO. In his practice, he combines lifestyle (greens, sun, exercise), lozenges, and sometimes PDE5 inhibitors for a synergistic effect. He also cautions that oral strips and NO supplements alone are not a panacea; the root cause of NO deficiency (e.g., high uric acid from fructose, high homocysteine, chronic stress) must also be addressed.

Dr. Twyman emphasizes that CoQ10 is a vital component of the electron transport chain in mitochondria. Since statins and beta‑blockers can reduce endogenous synthesis, he routinely recommends testing and replacing. He doesn’t prescribe a blanket dose because absorption varies; instead, he targets a blood level above 3 (presumably µg/mL) and adjusts the dose accordingly. He shares that many of his patients on statins notice fewer muscle complaints after optimizing CoQ10. He also clarifies that the form—ubiquinone vs ubiquinol—matters less than achieving the target blood level; ubiquinol absorbs a bit better but costs more.

Dr. Twyman explains that the endothelium is a one‑cell‑thick layer protected by a carbohydrate gel coat, the glycocalyx. Injury to this gel coat allows LDL particles and white blood cells to penetrate the artery wall, initiating atherosclerosis. He now structures his workup around three buckets: nitric oxide bioavailability (blood pressure, salivary strips, EndoPAT, uric acid, homocysteine), oxidative stress/inflammation (hsCRP, Lp‑PLA2, myeloperoxidase, GGT), and only then the lipid profile. This sequence means patients are assessed for the integrity of their arterial lining before lipid numbers dictate treatment. He argues that cardiology does a great job treating end‑stage disease but is too lipid‑focused, and that maintaining the glycocalyx makes downstream plaque less likely.

Dr. Twyman describes his own clinical experience with patients whose LDL reached 500 mg/dL on keto. He applauds the trial for using CT angiography and Cleerly AI to quantify plaque types, not just calcium. The primary outcome was change in non‑calcified plaque, but the published paper glossed over it. When he examined the graphs, he saw that soft plaque increased in nearly every participant, at a rate that would be considered elevated compared to a healthy population. He cautions that the trial does not prove the diet is dangerous in the short term, but it does mean that a ‘calcium score of zero’ is not reassuring if soft plaque is still accumulating. He ties the risk back to glycocalyx health: if the glycocalyx is undamaged, maybe one can tolerate high LDL for years; but if nitric oxide is low and arteries are stiff, the same LDL becomes a ‘time bomb.’ He advises people with this phenotype to measure central blood pressure, pulse wave velocity, or ideally endothelial function to decide how aggressive to be.

He notes that I’ve seen some calcium scores go down on statins, but more often they go up because the soft, vulnerable plaque is being converted to stable, calcified plaque—essentially forming a ‘bone’ over the lesion to prevent rupture. Untreated, calcium scores typically escalate about 20% per year; if a patient’s score rises less than 5% after intervention, they’ve likely halted the disease. True plaque regression (shrinking the lipid core) is visible only on CT angiography, not on a calcium scan. He advises patients not to panic if their score increases modestly while on optimal therapy.