I don’t find this all that surprising. IL-6 was never a great target IMO. It’s pretty clear that it’s a biomarker, but not really an active player. And IL-6 is so central to many things (not all bad), inhibiting it systemically will have consequences. I’m still glad somebody tried to investigate this, at least.
hsCRP seems to be a better marker for the inflammation in HFpEF, from what I’ve read.
Can’t ask for better than this IMO. This is what we all want - freedom from death and the causes of death! And of course, even a non-fatal MI is still a very strong negative health effect that you never fully recover from.
Health effects (healthspan) is underrated, some claim to have no problem with skin cancer if it’s not melanoma if it doesn’t affect ACM. So don’t use sunscreen according to them.
Yet there are skin cancers that require such invasive skin and tissue removal that it significantly affect appearance, especially if people wait for long.
Well, one thing to consider is the “field effect”, where once somebody has had cancer, they are more likely to get it again. In fact, one of the largest risk factors for getting cancer is… previously having had cancer. Plus, recurrences are almost always more aggressive and less treatable than the primary. So IMO, never getting cancer is the best situation by far.
Jason Fung explaining why cholesterol has no effect on heart disease. Lol. I know we’ve seen these things before but I really enjoy watching Dr. Fung go over it. It’s even more fun watching at 1.25 x the normal speed.
Also wanted to add that I agree with all the people that have written in saying Leqvio did nothing for them. It did nothing for me either. I tested LDL of 130 with treatment and it varies between 130 and 160 without. This helped me enjoy the video even more.
The video presents a sharp critique of the American Heart Association’s (AHA) lipid guidelines, arguing that clinical medicine’s fixation on lowering LDL and total cholesterol is drastically exaggerated compared to major metabolic drivers like diabetes, smoking, and hypertension.
1. Critique of the AHA Lipid Guidelines
Aggressive Screening and Stricter Targets: The guidelines recommend screening children as young as 9–11, testing every 5 years starting at age 20, and forcing LDL down to 55–70 mg/dL with immediate drug therapy.
Universal Medicalization: Following these criteria, 56.5% of adults aged 30–79—rising to 85% of people aged 60–69 and 93% of those over 70—would be prescribed lipid-lowering drugs (adding over 21 million Americans to medication rolls). The speaker compares this to “putting statins directly into the public water supply”.
2. Relative Risk Data: LDL vs. Primary Metabolic Drivers
Contrasting hazard ratios (HR) drawn from risk calculators and clinical cohorts highlights the disparity between risk factors:
High-Impact Risk Factors:
Diabetes: In the Women’s Health Study (Dugani et al., JAMA Cardiology, 2021), diabetes increased coronary heart disease risk in younger women by over 10-fold (HR ~10.71), while universally raising risk by 60%–65% in population equations.
Smoking and Hypertension: Elevate cardiovascular risk by roughly 60% and 36%, respectively.
Insignificance of LDL / Non-HDL: In the AHA PREVENT risk equations (Khan et al., Circulation, 2024), elevated non-HDL yielded a hazard ratio of 1.0 (0% added risk) in women and only a 5% increase in men.
Misdirection via “Non-HDL”: The guidelines rely on non-HDL to bundle in triglycerides—which are driven by refined carbohydrate consumption—even though statins target LDL without correcting underlying diet-driven dyslipidemia.
Lifespan Reductions: Two large multinational studies from the Global Cardiovascular Risk Consortium (NEJM, 2023; NEJM, 2025) show that modifying smoking or diabetes adds 4–6 years of life, whereas treating cholesterol yields virtually no reduction in all-cause mortality. In cohort models, aggressively driving down cholesterol was associated with a loss of 0.4 to 1.3 healthy life-years.
The U-Shaped All-Cause Mortality Curve: A large Copenhagen cohort study (Johannesen et al., BMJ, 2020) demonstrated that all-cause mortality was lowest at an LDL of ~140 mg/dL (the 60th–95th percentile). Forcing LDL below 55 mg/dL was associated with a ~50% higher risk of all-cause death.
The Dialysis Paradox: Dialysis patients typically exhibit very low LDL (68–81 mg/dL) yet experience 10- to 20-fold higher cardiovascular mortality, disproving the claim that low cholesterol guarantees vascular protection.
Statin Deprescribing in Older Adults: A randomized trial in adults aged 75 and older (Bonnet et al., The Lancet Healthy Longevity, 2026) found that discontinuing statins caused no increase in cardiovascular events or overall mortality.
4. Clinical Incentives and Priorities
Systemic Misalignment: Writing a statin prescription takes seconds, while coaching patients through dietary lifestyle changes to reverse insulin resistance and metabolic dysfunction requires time the healthcare system fails to incentivize.
Focusing on What Matters: While not advising every patient to discontinue needed drugs, the speaker calls for weighing side effects and reorienting clinical focus: stop fixating on cholesterol numbers, and prioritize smoking cessation, blood pressure management, and dietary carbohydrate restriction to reverse diabetes and metabolic disease.
Interestingly, in the MR study, genetically mediated statin targets were also associated with a 0.31–0.39 year reduction in lifespan per 1SD reduction in LDL/TG. It didn’t reach statistical significance, but it lines up surprisingly well with the cohort study mentioned in the video
Peter Attia has an interesting new interview with the CEO of NewAmsterdam Pharma, the makers of obicetrapib.
The drug lowers LDL-C by approx 40% but ApoB by only 15%, so it’ll be interesting to see if any reduction in CVD events tracks mainly with the ApoB or with the LDL. Results should be out within the next 3 months.
AI (Gemini Flash) Summary (posted by RapAdmin):
I. Executive Summary
This clinical discussion between Peter Attia, MD, and lipidologist/biotech executive Michael Davidson, MD (CEO of NewAmsterdam Pharma), addresses the convergence of lifelong atherogenic particle exposure and neurodegenerative risk, specifically targeting low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (apoB), and apolipoprotein E epsilon 4 (APOE4) biology.
The primary thesis is that current cardiovascular risk paradigms fail because they intervene too late in the disease process. The dialogue advocates for aggressive primordial and primary prevention: initiating lipid-lowering therapies decades before clinical thresholds are breached to minimize cumulative lifetime exposure (the “area under the curve” of apoB-bearing particles). The discussion reviews the historical failure of the “HDL-raising hypothesis,” detailing how early cholesteryl ester transfer protein (CETP) inhibitors (e.g., torcetrapib) failed due to off-target aldosterone induction and hypertension, while clinical trials evaluating niacin on top of statins (AIM-HIGH, HPS2-THRIVE) failed to produce clinical benefit.
The conversation pivots to next-generation therapeutic strategies, specifically selective CETP inhibition via obicetrapib and recombinant klotho development. Unlike ancestral compounds, obicetrapib demonstrates potent LDL-C reduction (up to 40–50% on top of maximally tolerated statins) alongside apoB and lipoprotein(a) lowering without off-target pressor toxicity. Furthermore, the dialogue examines CETP inhibition in the context of Alzheimer’s disease (AD) pathobiology: CETP activity influences brain lipid transport, and pharmacologic inhibition or genetic loss of function appears to attenuate blood-brain barrier dysfunction and amyloid deposition, disproportionately benefiting high-risk APOE4 carriers.
Finally, the participants caution against reliance on unvalidated surrogate longevity biomarkers that induce clinical anxiety without therapeutic actionable value, emphasizing lifestyle optimization (resistance/aerobic exercise, blood pressure control, metabolic homeostasis) alongside targeted pharmacology for APOE4 management.
II. Insight Bullets
Atherosclerosis requires both cumulative exposure to apoB-containing lipoproteins and endothelial transcytosis; preventing initiation is clinically superior to attempting plaque regression.
Primordial prevention aims to stop early vascular lipid deposition entirely rather than managing advanced subclinical disease in older adults.
Lifelong cumulative exposure to apoB-containing particles determines total lifetime atherosclerotic cardiovascular disease (ASCVD) risk.
Intervening early in young adults (in their 20s and 30s) alters long-term cardiovascular trajectory far more effectively than intensifying therapy after calcification occurs.
The historical focus on raising HDL-C was an epidemiological correlation that failed to demonstrate a causal protective mechanism in prospective intervention trials.
Niacin raised HDL-C significantly by 20% to 30%, but landmark clinical trials failed to translate this biochemical shift into major adverse cardiovascular event (MACE) reductions on modern statin backgrounds.
The AIM-HIGH Trial showed that adding extended-release niacin to intensive statin therapy provided no clinical outcome benefit despite substantial HDL-C increases.
The HPS2-THRIVE Trial confirmed the absence of clinical efficacy for niacin while documenting increased risks of bleeding, myopathy, infections, and new-onset diabetes.
Species lacking endogenous CETP activity, such as canines, demonstrate marked resistance to diet-induced atherosclerosis relative to humans and primates.
Transgenic expression of human CETP in murine models induces marked susceptibility to vascular lipid lesion development.
Early-generation CETP inhibitors failed because of off-target toxicities rather than the biological mechanism of CETP inhibition itself.
Torcetrapib failed clinically because of off-target activation of the renin-angiotensin-aldosterone system, which caused severe hypertension, electrolyte abnormalities, and excess mortality.
Pfizer halted development of torcetrapib following fatal cardiovascular outcomes observed in the ILLUMINATE trial.
Obicetrapib is an orally administered, highly potent, next-generation selective CETP inhibitor designed without off-target pressor effects.
NewAmsterdam Pharma is advancing obicetrapib as an adjunct oral therapy to maximally tolerated statin regimens for high-risk ASCVD and heterozygous familial hypercholesterolemia.
Phase 3 clinical evaluation of obicetrapib demonstrated marked LDL-C reductions in the BROOKLYN Trial for familial hypercholesterolemia.
The pivotal BROADWAY Trial evaluated obicetrapib 10 mg daily in patients with established ASCVD needing additional apoB lowering.
The definitive cardiovascular outcomes validation for obicetrapib is underway in the large-scale PREVAIL CVOT Trial.
CETP inhibition redistributes cholesteryl esters to HDL particles while upregulating hepatic LDL receptors, facilitating systemic LDL clearing.
Obicetrapib achieves concurrent decreases in circulating lipoprotein(a) [Lp(a)], a genetically determined, independent causal risk factor for ASCVD.
APOE4 status markedly increases lifetime vulnerability to both coronary artery disease and late-onset Alzheimer’s disease pathology.
APOE4 impairs astrocytic and microglial lipid trafficking within the central nervous system, driving neuroinflammation and impaired amyloid clearance.
Genetic loss-of-function variants in the CETP gene correlate epidemiologically with reduced incidence of cognitive decline and preserved hippocampal volume.
Obicetrapib exhibits central nervous system penetrance and modulation of lipid-protein interactions that could potentially protect APOE4 carriers from neurodegenerative cascade acceleration.
Human cohort analyses of CETP inhibition show favorable downstream trends on circulating and cerebrospinal fluid AD biomarkers, including phosphorylated tau and amyloid ratios.
Recombinant klotho therapy is being evaluated as an exogenous endocrine agent targeting longevity pathways, cognitive enhancement, and synaptic plasticity.
Klotho deficiency accelerates systemic endothelial stiffness, cognitive degradation, and multiorgan senescence phenotypes in preclinical models.
Klotho administration enhances NMDA receptor-mediated synaptic transmission and long-term potentiation in aging brain regions.
Managing vascular risk factors such as blood pressure and glycemic stability remains one of the few validated strategies to decelerate dementia progression in APOE4 carriers.
Untreated hypertension accelerates microvascular rarefaction, white matter hyperintensities, and neurovascular unit breakdown in high-risk genotypes.
High-dose docosahexaenoic acid (DHA) supplementation may support brain lipid balance, though transport across the blood-brain barrier is often impaired once mature APOE4-associated pathology is established.
Over-testing unvalidated surrogate biomarkers generates clinical anxiety and overtreatment without providing reliable clinical utility.
Lifestyle optimization—encompassing zone 2 aerobic conditioning, heavy resistance training, and nutritional management—is necessary but insufficient to overcome high monogenic or polygenic lipid loads.
III. Adversarial Claims & Evidence Table
Claim from Video
Speaker’s Evidence
Scientific Reality (Current Data)
Evidence Grade
Verdict
Primordial LDL-C reduction prevents CAD far more effectively than late-life intervention
Epidemiological modeling and lifetime cumulative exposure curves (“area under the curve”).
Mendelian randomization confirms that a 1 mmol/L lifelong reduction in LDL-C yields an ~50% drop in CAD risk, compared to ~22% from late-life statin therapy (Ference et al., 2012).
Level A
Strong Support
Niacin’s failure was due to biology on top of statins, not lack of HDL raising
AIM-HIGH and HPS2-THRIVE clinical trials.
Meta-analyses verify that pharmacologically elevating HDL-C via niacin or fibrates yields no incremental MACE reduction on statin backgrounds (Briel et al., 2009; HPS2-THRIVE, 2014).
Level A
Strong Support
Obicetrapib reduces LDL-C by >40% safely as an adjunct to maximally tolerated statins
BROADWAY and BROOKLYN Phase 3 trial readouts.
Phase 3 randomized trials confirm that 10 mg obicetrapib added to maximally tolerated statins lowers LDL-C by 40–50% and apoB by ~25–30% without elevating blood pressure (Ray et al., 2024).
Level B
Strong Support
CETP inhibition directly prevents or delays Alzheimer’s disease progression in humans
Preclinical brain lipid data and exploratory biomarker signals in APOE4 carriers.
Human outcomes trials are ongoing. Observational/genetic data link CETP loss-of-function to reduced dementia risk, but prospective phase 3 clinical disease-slowing data remain unproven (Circulation Research, 2026).
Level C
Plausible
Recombinant klotho enhances human cognition and slows neurodegeneration
Non-human primate cognitive testing and preclinical longevity models.
Recombinant klotho improves memory and synaptic plasticity in aging rhesus macaques (Castner et al., 2023), but human clinical efficacy and systemic safety profiles are unverified in phase 2/3 trials.
Level D
Speculative(Translational Gap)
Supplemental DHA significantly improves brain lipid architecture and prevents AD in APOE4 carriers
Neurometabolic hypotheses and clinical lipid clinic anecdotes.
Meta-analyses show high-dose DHA does not arrest cognitive decline once pathology is established in symptomatic APOE4 carriers; early primary prevention benefits remain equivocal (Yassine et al., 2017).
Level B
Speculative
IV. Actionable Protocol (Prioritized)
1. High-Confidence Tier (Level A/B Evidence)
Lifelong ApoB & LDL-C Optimization: Measure apoB directly to quantify circulating atherogenic particle count. For primary prevention in moderate-to-high risk individuals, maintain apoB <65–80 mg/dL (or <55 mg/dL in secondary prevention or very high genetic risk) using low-dose, high-potency statins (e.g., rosuvastatin, atorvastatin) and ezetimibe as first-line combination therapy.
Strict Blood Pressure Regulation: Maintain systolic blood pressure <120 mmHg and diastolic <80 mmHg. Managing hypertension protects microvascular endothelial junctions and preserves neurovascular autoregulation against vascular dementia and secondary amyloid acceleration.
Intense Metabolic Control: Prevent insulin resistance and maintain HbA1c <5.5% via diet, resistance training, and aerobic conditioning to limit chronic endothelial inflammation and vascular basement membrane thickening.
2. Experimental Tier (Level C/D Evidence, High Safety Margin)
High-Dose Triglyceride-Form DHA in Pre-Symptomatic APOE4: If identified as an APOE4 carrier prior to symptom onset, consider 2 g/day of purified EPA/DHA (specifically phospholipid- or triglyceride-bound formulations) to support central nervous system membrane liquidity. Discontinue if AFib signals emerge or bleeding parameters are compromised.
Targeting CETP via Clinical Trials: Patients with refractory dyslipidemia or elevated Lp(a) on maximum statin/ezetimibe combinations should consider enrollment in ongoing CETP inhibitor trials (e.g., the PREVAIL CVOT Trial).
Sad to see the downfall of this guy. Unfortunately he’s another that realised he can make more money and become more famous and powerful by being a contrarian.
Absolutely nobody is saying that smoking, blood pressure and diabetes aren’t important. This is a straw man argument to say LDL-C isn’t important.
Hell, the AHA and ESC have both released papers in the last 12 months talking about the need to control inflammation as part and parcel of reducing CVD. So nobody is saying that you should only think about cholesterols and nothing else. To say we should prioritise smoking cessation, hypertension and diet… yeah, no shit, we’ve only been trying to do that for decades.
The rest is a bunch of straw man arguments too. The U-shape curve is well known, and explained because extremely sick people have lower lipoproteins. Dialysis patients too. They may have low lipoproteins while actually ON dialysis, but it’s lifetime cumulative exposure which matters the most.
To critique the AHA guidelines for aggressive screening and stricter targets is… well, retarded. Sorry I don’t have a better word for it. You know what happens to those children age 9-11 who have high cholesterol? They’re the ones having heart attacks and suddenly dying in their 40s.
In the above landmark Dutch trial, among 156 affected parents with familial hypercholesterolemia (high LDL-C) , 27 (17%) had already suffered an MI before age 40. 11 had died of MI before 40. The youngest cardiovascular death was a 23 year old .
On the other hand, none of their children who had begun statins in childhood died from cardiovascular disease during 20 years follow-up and only 1% had an MI. To be crystal clear, that’s 1% versus 17% for MIs, and 0% versus 7% for death.
And people say LDL-C doesn’t matter and that statins don’t work.
Non-HDL/LDL cholesterol is an insignificant risk factor compared to diabetes and smoking.
Multivariable HRs in AHA PREVENT tool (non-HDL HR 1.00 in women, 1.05 in men vs HR 1.65 for diabetes).
PREVENT models short-term 10-year risk where acute metabolic and thrombotic insults (smoking, diabetes) manifest earlier. In contrast, lifelong Mendelian randomization proves cumulative apoB particle exposure is the causal agent for atherogenesis (Ference et al., 2017).
Level A
Unsupported(misinterprets collinear 10-year risk model as lack of biological causality)
Lowering LDL cholesterol does not reduce all-cause mortality.
Large-scale meta-analyses by the Cholesterol Treatment Trialists’ (CTT) Collaboration confirm a 9% to 12% all-cause mortality reduction per 1 mmol/L (38.7 mg/dL) LDL-C reduction, with maximal effects in secondary prevention (Cholesterol Treatment Trialists’ Collaboration, 2012). In low-risk primary cohorts, all-cause mortality signals attenuate due to low baseline absolute event rates.
Copenhagen General Population Study prospective cohort showing a U-shaped mortality curve nadir at 140 mg/dL.
The U-shaped curve in observational epidemiology is driven by reverse causation (frailty, undiagnosed occult malignancies, end-stage organ failure lowering cholesterol). High-intensity PCSK9 inhibitor trials (FOURIER, ODYSSEY OUTCOMES) titrating LDL below 30 mg/dL demonstrated linear reductions in MACE with zero neurocognitive or non-cardiovascular mortality signals.
Level A
Unsupported(reverse causation artifact)
Statins provide no clinical survival benefit in patients 75 and older for primary prevention.
Deprescribing trials (SAGA/SITE) in non-frail elders without prior ASCVD showed non-inferiority over 3 years. However, meta-analyses (Giral et al., 2019) confirm continuation benefits in patients with high vascular calcification or established microvascular disease. Discontinuation is safe in select primary-prevention elders with low 5-year horizons, but not universal.
Level B
Plausible(strictly limited to non-frail primary prevention)
End-stage renal disease (dialysis) patients prove LDL is irrelevant to heart disease.
Dialysis-associated cardiovascular death is overwhelmingly driven by medial arterial calcification (Mönckeberg sclerosis), uremic cardiomyopathy, hyperkalemia, and sudden cardiac death—not classic intimal atheromatous plaque rupture (4D Trial; AURORA Trial). Extrapolating uremic vascular calcification to general atherogenesis represents an egregious pathophysiologic category error.
Level B
Unsupported(false equivalence of disease mechanisms)
Aggressive targets in guidelines exist primarily to enrich pharmaceutical pipelines.
Rhetorical assertions; reference to 56.5% adult eligibility under new thresholds.
Guideline thresholds (such as 2018 AHA/ACC and 2019 ESC/EAS) are driven by systematic meta-analyses of clinical trial endpoints demonstrating that proportional reductions in major vascular events scale directly with absolute LDL reduction (Mach et al., 2020). Generic statin pricing ($4–$10/month) invalidates simple profit-driven expansion models.
Level A
Unsupported
IV. Actionable Protocol (Prioritized)
High Confidence Tier (Level A/B Evidence)
Comprehensive Atherogenic Particle Quantification: Assess true particle burden using Apolipoprotein B (apoB) or LDL-P rather than relying solely on Friedewald-calculated LDL-C, particularly in patients with hypertriglyceridemia, metabolic syndrome, or low HDL. Target apoB under 65 mg/dL for high-risk and under 80 mg/dL for moderate-risk individuals (Grundy et al., 2019).
Metabolic Syndrome & Glycemic Eradication: Treat insulin resistance via lifestyle and pharmacotherapy to target HbA1c under 5.7% (or under 6.5% in established diabetes). The hazard ratios of diabetes for vascular endothelium damage are indisputable. Implement carbohydrate quality control, caloric restriction, and exercise to attenuate visceral adiposity.
Aggressive Secondary Prevention: In documented coronary artery disease, previous myocardial infarction, or ischemic stroke, titrate high-potency statins plus ezetimibe (and PCSK9 inhibitors if required) to reach an LDL-C target under 55 mg/dL (or under 40 mg/dL for recurrent events) (Mach et al., 2020).
Rigorous Blood Pressure Management: Target systolic blood pressure under 120–130 mmHg per the SPRINT Trial, eliminating the primary physical shear stress driver of intimal mechanical injury.
Experimental Tier (Level C/D Evidence, High Safety Margins)
Coronary Artery Calcium (CAC) Stratification for Borderline Primary Prevention: In asymptomatic patients aged 40 to 75 with intermediate 10-year risk (5% to 7.5%) and elevated LDL (100–189 mg/dL), obtain a non-contrast cardiac CT scan. A CAC score of zero supports withholding or delaying statin therapy, while a CAC score greater than 100 or above the 75th percentile warrants immediate lipid-lowering therapy (Nasir et al., 2015).
Deprescribing Trial in Frail Geriatric Primary Prevention: In individuals aged 75 and older with no clinical history of ASCVD, life expectancy under 3 to 5 years, or significant polypharmacy, a structured deprescribing of statins is clinically reasonable with close monitoring of vascular markers (AAFP Guidance).
Red Flag Zone (Debunked or Dangerous Claims)
Halting Statin Therapy in Documented ASCVD Patients: Ceasing lipid-lowering pharmacotherapy in individuals with established plaques, stents, or bypasses based on “cholesterol is irrelevant” rhetoric dramatically escalates plaque instability, coronary syndrome recurrence, and cardiovascular mortality within 12 months.
Ignoring Extreme Hypercholesterolemia (LDL ≥190 mg/dL): Attributing extreme familial or dietary hypercholesterolemia to harmless normal variation risks rapid atheroma accumulation, even in young adults with optimal glycemic metrics.
My doctor no longer tests CRP whereas 10-20 years ago it was always included in my bloodwork. Something changed and I’m a heart patient. So probably not as important as was once thought.
Looking at my two main labs high sensitivity CRP is called hsCRP on one (which has a minimum test level of 0.3) and CRP HS on the other (which has a minimum test level of 0.15). The original CRP test used for producing Morgan Levine’s algorithm had a minimum test level of 0.6 and high sensitivity implied going below that. She made the point on this that this causes results with values under 0.6 to be less reliable as it was not calculated for that and uses a logarithm which means a small movement in CRP gives a larger change in the delta on the mortality.
Personally I am inclined to call both CRP and worry moreso about how sensitive the test is as this varies quite a lot. (even for the high sensitivity tests).
I did watch this whole thing. He is an expert, no doubt and if they ever get obicetrapib here I will give it a try. Nir says the CETPi will make us live longer. I don’t know if this is the one, but it’s worth a try.
Having said that, he is the CEO of a company that is trying to sell a drug. Not only is he really biased (as we all are), but his job is to spend all day and night figuring out how to move this drug. He says we need lower LDL. Also raising HDL will do amazing things. Also alzheimers is a huge problem. Coincidentally his drug will solve all three of these problems. I’m not saying it won’t, but don’t bet money you might need on it.
Leqvio cost novartis 9.7 billion dollars and it could have been saline for all I got out of it.
I thought he came across as educational and hopeful rather than promotional. The evidence from the trials will tell us whether or not it lowers risk of CVD events. If it doesn’t, it won’t get approved. After the recent failures of other meds, I’m trying not to get my hopes up too much.
What exactly were you expecting Leqvio to do for you (other than lower your LDL-C)?
That’s pretty much it, lower LDL. I had slight hope that it would prefer the small LDL like he says the CETP does. Anyway it has done almost nothing, I think the Ezetimbe did more. And we have heard from a couple other people here with actual experience that was the same as mine.
So we reward the predictions and hype by buying the drugs for a while and it helps them pay back some of their expenses I guess.
Good thing LDL is unimportant right? LOL joking. Trolling actually.
Lowering LDL reduces your risk of future CVD events. You’re not supposed to feel anything, and it’s not supposed to “do” anything else. Unfortunately, preventative treatments never get the praise they deserve because you never know about the heart attack you might have otherwise had. Waiting for a disease to happen and then curing it is much easier to process cognitively.
Right, but in the USA we have to wait for the outcome study, which kinda makes more sense now in light of the recent outcome failures with the IL-6 and Lp(a) blockers.
