7 Needs context
CT coronary angiography causes blooming artifact around preexisting coronary stents, preventing clear visualization inside the stent.
"And if you've had a stent already, you get what we call a blooming around that stent. So you can't read inside that." (said at 0:06:35)
Coronary CT angiography (CCTA) does indeed produce blooming artifacts around metallic stent struts due to beam hardening and partial volume effects. This artifact causes the metallic struts to appear thicker and artificially narrows the visible internal lumen (reducing visualized lumen diameter by approximately 30% compared to invasive angiography), creating substantial diagnostic challenges for detecting in-stent restenosis. However, stating that clinicians 'can't read inside' a stented vessel is an overstatement: while smaller stents (<3.0 mm) and certain alloys are frequently non-evaluable or obscured, larger stents (≥3.0 mm) and scans performed with newer technologies (such as high-definition CT, dual-source CT, and photon-counting detector CT) often permit diagnostic assessment of in-stent patency, exhibiting high negative predictive values.
Research indicates that approximately three-quarters of physicians cannot adequately assess prediabetes or metabolic disease.
"I mean, the research has shown that unfortunately three-quarters of docs can't really assess pre-diabetes, metabolic disease that well, but it's not because they can't. It's because they're too busy." (said at 0:10:12)
The statement reflects published survey findings evaluating primary care physicians' knowledge of prediabetes screening and diagnostic criteria, though framing it as 'three-quarters cannot adequately assess' requires context. In a cross-sectional survey of primary care providers by Tseng et al. (2017), only 17% correctly identified the complete laboratory diagnostic criteria (both fasting plasma glucose and HbA1c thresholds) for prediabetes, and only 6% identified all screening risk factors. A subsequent national survey (Tseng et al., 2019) similarly documented substantial knowledge deficits regarding diagnostic criteria and preventive management guidelines, while noting system-level barriers and time constraints. Because these findings stem from cross-sectional surveys testing guideline recall rather than direct audits of clinical competence, the evidence is rated low certainty.
Clinical guideline committees state that if a patient has a coronary artery calcium score of zero, they do not need a statin.
"And the standards committees, to their credit, have said, look, if you have a zero calcium score, in other words, if you have plaque imaging and it shows no plaque, you don't need a statin." (said at 0:41:30)
The claim is partially accurate but requires qualification. The 2018 ACC/AHA Multi-Society Cholesterol Management Guideline endorses coronary artery calcium (CAC) testing in primary prevention for adults at borderline or intermediate risk to inform shared decision-making, and notes that if CAC is zero, statin therapy may be withheld or delayed (re-evaluating in 5 to 10 years). However, this recommendation applies specifically to primary prevention in intermediate/borderline-risk individuals, and the guidelines explicitly outline important exceptions where statins are still recommended despite CAC = 0 (e.g., severe hypercholesterolemia with LDL-C ≥ 190 mg/dL, diabetes mellitus, active cigarette smoking, or family history of premature ASCVD). Therefore, CAC = 0 does not unconditionally mean a patient does not need a statin.
The American Association of Clinical Endocrinologists advises against relying solely on HbA1c for the diagnosis of diabetes because hemoglobin variants, liver disease, kidney disease, and pregnancy can alter HbA1c levels.
"I'm going to tell you the American Association of Clinical Endocrinologists has said in their own standards, don't rely on A1C for diagnosis of diabetes. There are things like hemoglobin differences like Jesus has that can really impact this test. At the end of the day, it's a hemoglobin test. Liver disease, kidney disease, pregnancy, genetics from where you're from in the world, all these things can change A1C." (said at 0:52:03)
The claim provides helpful clinical context regarding the limitations of HbA1c, but overstates the American Association of Clinical Endocrinologists (AACE) stance as a blanket rejection of HbA1c for diabetes diagnosis. Published AACE guidelines explicitly include and recommend HbA1c ≥6.5% as an established diagnostic criterion alongside fasting plasma glucose and oral glucose tolerance testing. However, AACE consensus statements and guidelines advise caution and recommend relying on glucose-based testing rather than HbA1c when confounding conditions that alter erythrocyte turnover or hemoglobin glycation are present—such as hemoglobinopathies, pregnancy, hemolytic anemia, and advanced renal or liver disease.
- context: Utilizing current diagnostic criteria and treatment algorithms for managing type 2 diabete… (Postgraduate medicine 2011) · cited 14x in the literature
"Within the past 2 years, the American Diabetes Association (ADA)/European Association for the Study of Diabetes (EASD) and the American Association of Clinical Endocrinologists (AACE)/American College of Endocrinology (ACE) have revised their guidelines for the diagnosis and treatment of type 2 diabetes mellitus (T2DM). Both organizations recommend a diagnostic glycated hemoglobin (HbA1c) of >6.5% (based on a new appreciation of the relationship between glycemia and complications) and fasting plasma glucose levels or an oral glucose tolerance test." (abstract, results, passage verified)
pubmedfull study (doi)
Studies by Paul Ridker and others have shown that low doses of statins taken intermittently (such as 5 mg every other day or twice a week) significantly reduce vascular inflammation.
"I know a lot of people and have discussed with people using even 5 every other day, even twice a week. And again, Paul Ridker, Gavin Blake, some other folks have demonstrated that you get an impact on vascular inflammation with these lower doses and taking them less often." (said at 0:53:50)
Randomized trials demonstrate that intermittent or alternate-day statin administration (such as rosuvastatin or atorvastatin administered every other day) significantly reduces high-sensitivity C-reactive protein (hs-CRP), a recognized biomarker of vascular and systemic inflammation. However, attributing intermittent dosing protocols specifically to Paul Ridker and Gavin Blake is slightly conflated: Ridker and Blake conducted foundational landmark research demonstrating that statin therapy directly reduces vascular inflammation and hs-CRP independently of LDL lowering, but their major clinical trials evaluated daily dosing regimens.
A high coronary calcium score reflects stable calcified plaque but does not indicate whether soft plaque is present.
"You understand what a high calcium means. You know, for example, as we've discussed already today, a high calcium score doesn't mean that you've got a ton of soft plaque. One of the things that I would advise my patients to do, one of the things I would do if I had a high calcium score, the next thing is we look and say, "Well, okay, that means we've got plaque, but it means we've got stable plaque. It does not mean that we've got soft plaque."" (said at 1:17:13)
The host's claim requires important context. Non-contrast coronary artery calcium (CAC) scoring specifically measures calcified atherosclerotic plaque, which represents dense, calcified regions. CAC imaging cannot directly visualize or quantify non-calcified ("soft") plaque; detailed characterization of soft plaque requires contrast-enhanced coronary computed tomography angiography (CCTA). However, while CAC scoring does not directly measure non-calcified plaque, higher CAC scores generally correlate with an increased overall burden of non-calcified plaque across patient strata. For example, median non-calcified plaque volume increases progressively from ~18 mm³ in patients with CAC of 0 to over 100–150 mm³ in those with CAC of 100–299. Therefore, while a high CAC score specifically quantifies calcified plaque, it does not mean soft plaque is absent, as calcified and non-calcified plaque burdens frequently coexist.
- context: CCTA-Derived coronary plaque burden offers enhanced prognostic value over CAC scoring in s… (European heart journal. Cardiovascular Imaging 2025) · cited 21x in the literature
"AI-driven assessment of coronary plaque burden enhances prognostic accuracy for future adverse cardiovascular events, highlighting the critical role of comprehensive plaque characterization in refining risk stratification strategies." (abstract, conclusions, passage verified)
pubmedfull study (doi) - context: Using AI-Quantitative CT to evaluate the relationship between coronary artery calcium and … (The international journal of cardiovascular imaging 2026)
"Reliance on either CAC or SIS alone may result in risk misclassification, especially for patients with CAC = 0, the majority of whom had non-calcified plaque by AI-QCT." (abstract, conclusion)
pubmedfull study (doi) - context: Symptom status and non-calcified plaque burden across CAC strata: insights from AI-based C… (The international journal of cardiovascular imaging 2026)
"Median NCP volumes were similar in both groups for CAC 0 (17.7 vs. 18.6 mm³, p = 0.96) and CAC 1-99 (50.8 vs. 56.3 mm³, p = 0.37). A significant difference emerged in the CAC 100-299 category: symptomatic patients had higher NCP (152.3 vs. 112.3 mm³, p = 0.035)." (abstract, results)
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Coronary stents do not prevent heart attacks.
"You mentioned, I think you mentioned stents or bypass or something, and yeah, a stent, as we've seen in multiple places, stents don't really prevent heart attacks. What does prevent it is lifestyle, appropriate use of lifestyle." (said at 1:17:50)
In patients with stable coronary artery disease, large randomized controlled trials (including the COURAGE and ISCHEMIA trials) have demonstrated that coronary stenting (percutaneous coronary intervention, or PCI) combined with optimal medical therapy does not reduce the rate of myocardial infarction or all-cause mortality compared with medical therapy alone. However, the blanket claim requires context: in the setting of acute coronary syndromes (such as ST-elevation myocardial infarction, or STEMI), emergent stenting is an established, life-saving standard of care that limits infarct size and prevents recurrent ischemic events.
- supports: Optimal medical therapy with or without PCI for stable coronary disease. (The New England journal of medicine 2007) · cited 4721x in the literature
"There were no significant differences between the PCI group and the medical-therapy group in the composite of death, myocardial infarction, and stroke (20.0% vs. 19.5%; hazard ratio, 1.05; 95% CI, 0.87 to 1.27; P=0.62)... or myocardial infarction (13.2% vs. 12.3%; hazard ratio, 1.13; 95% CI, 0.89 to 1.43; P=0.33). As an initial management strategy in patients with stable coronary artery disease, PCI did not reduce the risk of death, myocardial infarction, or other major cardiovascular events when added to optimal medical therapy." (abstract, results and conclusions, passage verified)
pubmedfull study (doi) - supports: Initial Invasive or Conservative Strategy for Stable Coronary Disease. (The New England journal of medicine 2020) · cited 2439x in the literature
"Among patients with stable coronary disease and moderate or severe ischemia, we did not find evidence that an initial invasive strategy, as compared with an initial conservative strategy, reduced the risk of ischemic cardiovascular events or death from any cause over a median of 3.2 years." (abstract, conclusions, passage verified)
pubmedfull study (doi) - context: COURAGE, ORBITA, and ISCHEMIA: Percutaneous Coronary Intervention for Stable Coronary Arte… (Interventional cardiology clinics 2020) · cited 8x in the literature
"Anginal relief remains the primary indication for PCI in stable CAD... PCI in stable CAD has not been shown to improve mortality or overall myocardial infarction rates, even in the presence of significant ischemia. Rather, risk reduction medical therapy remains the main intervention for improving outcomes." (abstract, conclusions)
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8 Supported by research
An individual can have a coronary artery calcium score of zero and still experience a heart attack due to non-calcified soft plaque.
"A man can have a calcium score of zero and still have soft plaque building in there, the young kind, the kind that ruptures and causes heart attacks. And guess what? Yes, they've already looked at that. The the research, the science has been done. And there are people that have had heart attacks with a zero calcium score because their plaque was entirely soft." (said at 0:05:07)
Clinical trial data and prospective cohort studies confirm that individuals with a coronary artery calcium (CAC) score of zero can still harbor non-calcified (soft) plaque and experience myocardial infarction. In a post-hoc analysis of the SCOT-HEART trial, 10% of patients who suffered a myocardial infarction had a baseline CAC score of zero, and CAC scoring could not rule out adverse low-attenuation (soft) plaque phenotypes.
- supports: A zero coronary artery calcium score in patients with stable chest pain is associated with… (Open heart 2019) · cited 47x in the literature
"Of the 751 (82.1%) patients with a zero CAC in whom CTCA was performed, 674 (89.7%) had normal coronary arteries, 63 (8.4%) had non-calcified CAD with < 50% stenosis and 14 (1.9%) had ≥ 50% stenosis in at least one coronary artery." (abstract, results)
pubmedfull study (doi) - supports: Association of coronary artery calcium score with qualitatively and quantitatively assesse… (European heart journal. Cardiovascular Imaging 2022) · cited 63x in the literature
"In patients with stable chest pain, zero CACS is associated with a good but not perfect prognosis, and CACS cannot rule out obstructive coronary artery disease, non-obstructive plaque, or adverse plaque phenotypes, including low-attenuation plaque." (abstract, conclusions, passage verified)
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Medical literature has recognized cardiovascular-kidney-metabolic syndrome, acknowledging that cardiovascular disease, heart attacks, and strokes are driven by metabolic disease.
"there's a new paper that came out about cardiometabolic syndrome, which is kidney cardiometabolic syndrome, which is acknowledging that cardiovascular disease, heart attacks, and strokes are a metabolic problem" (said at 0:13:33)
In 2023, the American Heart Association (AHA) published a Presidential Advisory formally defining cardiovascular-kidney-metabolic (CKM) syndrome. The advisory establishes a clinical and pathophysiological framework recognizing the strong interplay between metabolic risk factors (such as obesity and type 2 diabetes), chronic kidney disease, and cardiovascular disease (including heart failure, coronary heart disease, and stroke), highlighting that metabolic dysfunction directly drives cardiovascular morbidity and mortality.
Stress tests do not predict heart attacks.
"Stress tests don't predict heart attacks. So when you get a recommendation, "Let's do a stress test," ask what the purpose is. If the purpose is "We want to see your risk for a heart attack," that's not a good test for that." (said at 0:39:40)
Cardiac stress testing (such as exercise electrocardiography, stress echocardiography, or nuclear perfusion imaging) is designed to detect inducible myocardial ischemia caused by hemodynamically significant, flow-limiting coronary artery stenoses. It is not an effective screening tool to predict future acute myocardial infarction (heart attack), because most myocardial infarctions result from the sudden rupture of non-flow-limiting, non-calcified atherosclerotic plaques that do not produce ischemia during stress testing. Consequently, major guideline bodies, including the U.S. Preventive Services Task Force (USPSTF), recommend against screening asymptomatic adults with exercise or resting ECG to predict coronary heart disease events or assess cardiovascular risk, noting that stress testing does not improve clinical outcomes beyond standard cardiovascular risk assessment tools.
High fasting insulin levels inhibit the body from burning fat.
"The reality is an optimum level of basal insulin is more like less than five. So when I see somebody whose basal insulin levels or fasting insulin levels are 10 or more, they will typically start telling me, "Doc, I promise I'm doing everything I can. I still cannot lose weight." And one of the things that people forget about, many of them never knew, is that high insulin levels keep you from burning your fat." (said at 0:46:58)
A fundamental principle of human lipid metabolism is that insulin exerts a potent antilipolytic effect. Elevated circulating insulin concentrations inhibit lipolysis (the breakdown of stored triglycerides in adipose tissue into free fatty acids) and decrease whole-body lipid oxidation, while shifting substrate utilization toward carbohydrate oxidation and promoting fat storage. Conversely, lower basal insulin levels permit adipose tissue lipolysis and downstream fatty acid oxidation.
- supports: Shift to Fatty Substrate Utilization in Response to Sodium-Glucose Cotransporter 2 Inhibit… (Diabetes 2016) · cited 728x in the literature
"Along with decrements in plasma glucose and insulin levels and increments in glucagon release... empagliflozin administration raised EGP, lowered TGD, and stimulated lipolysis, LOx, and ketogenesis." (abstract, results)
pubmedfull study (doi) - supports: Why hyperinsulinemia is detrimental to weight loss: insights from type 1 diabetes. (BMC medicine 2026)
"Insulin is a major regulator of body weight. It not only mediates glucose uptake but also inhibits hepatic glucose production, lipolysis, and enhances lipogenesis... During fasting or adherence to low-carbohydrate diets, circulating insulin concentrations remain low, permitting unrestrained adipose tissue lipolysis and promoting fatty acid oxidation for energy production." (abstract, results)
pubmedfull study (doi)
Berberine improves arterial health, blood glucose control, and metabolism.
"But even if you don't know yet, if there is one supplement that has proven time and time again to have an impact on arterial health and metabolism, that's going to be berberine." (said at 0:56:40)
Multiple systematic reviews and meta-analyses of randomized controlled trials demonstrate that berberine supplementation significantly improves glycemic control (fasting plasma glucose, HbA1c, insulin, and HOMA-IR), metabolic profiles (triglycerides, total cholesterol, LDL cholesterol, waist circumference, and BMI), and cardiovascular risk markers including systolic blood pressure and circulating inflammatory markers (CRP, TNF-alpha, IL-6).
- supports: The effects of berberine supplementation on cardiovascular risk factors in adults: A syste… (Frontiers in nutrition 2022) · cited 27x in the literature
"The pooled results showed BBR significantly reduced triglyceride (WMD = -23.70 mg/dl; 95%CI -30.16, -17.25; P < 0.001), total cholesterol (WMD = -20.64 mg/dl; 95%CI -23.65, -17.63; P < 0.001), low-density lipoprotein WMD = -9.63 mg/dl; 95%CI, -13.87, -5.39; P < 0.001), fasting blood glucose (FBG) (WMD = -7.74 mg/dl; 95%CI -10.79, -4.70; P < 0.001), insulin (WMD = -3.27 mg/dl; 95%CI -4.46,-2.07; P < 0.001), HbA1c (WMD = -0.45%; 95%CI -0.68, -0.23; P < 0.001), HOMA-IR (WMD = -1.04; 95%CI -1.55, -0.52; P < 0.001), systolic blood pressure (WMD = -5.46 mmHg; 95%CI -8.17, -2.76; P < 0.001), weight (WMD = -0.84; 95%CI -1.34,-0.34; P < 0.001), body mass index (WMD = -0.25 kg/m 2 ; 95%CI -0.46, -0.04; P = 0.020), while increased high-density lipoprotein (HDL) (WMD = 1.37 mg/dl; 95%CI 0.41,2.23; P = 0.005)." (abstract, results)
pubmedfull study (doi) - supports: The Effect of Berberine Supplementation on Glycemic Control and Inflammatory Biomarkers in… (Clinical therapeutics 2024) · cited 20x in the literature
"BBR supplementation was effective in reducing fasting blood glucose (FBG) (ES WMD : -0.77; 95% CI: -0.90 to -0.63, and ES SMD : -0.65; 95% CI: -0.83 to -0.47), hemoglobin A1C (HbA1C) (ES WMD : -0.57; 95% CI: -0.68 to -0.46), homeostasis model assessment for insulin resistance (HOMA-IR) (ES WMD : -1.04; 95% CI: -1.66 to -0.42, and ES SMD : -0.71; 95% CI: -0.97 to -0.46), insulin (ES WMD : -1.00; 95% CI: -1.70 to -0.30, and ES SMD : -0.63; 95% CI: -0.94 to -0.32), interleukin (IL)-6 (ES SMD : -1.23; 95% CI: -1.61 to -0.85), tumor necrosis factor-α (TNF-α) (ES SMD : -1.04; 95% CI: -1.28 to -0.79), and C-reactive protein (CRP) (ES WMD : -0.62; 95% CI: -0.74 to -0.50, and ES SMD : -1.70; 95% CI: -2.21 to -1.19)." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Efficacy and safety of berberine on the components of metabolic syndrome: a systematic rev… (Frontiers in pharmacology 2025) · cited 17x in the literature
"The results indicate that berberine significantly reduces triglycerides (TG) (WMD: -0.367 mmol/L; 95% CI: -0.560 to -0.175; p < 0.001), fasting plasma glucose (FPG) (WMD: -0.515 mmol/L; 95% CI: -0.847 to -0.183; p = 0.002), and waist circumference (WC) (WMD: -3.270 cm; 95% CI: -4.818 to -1.722; p < 0.001) among the components of MetS" (abstract, results)
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A 20 mg dose of atorvastatin is roughly equivalent in potency to a 10 mg dose of rosuvastatin.
"Atorvastatin 20 is more equivalent to rosuvastatin 10, as I've shared before." (said at 0:53:43)
Clinical trial evidence and major cholesterol guidelines show that rosuvastatin is approximately twice as potent as atorvastatin on a milligram-for-milligram basis. In randomized head-to-head dose-comparison studies such as the STELLAR trial, a 10 mg dose of rosuvastatin produces lipid-lowering efficacy (LDL-C reduction of roughly 45–46%) closely matching that of a 20 mg dose of atorvastatin (roughly 43%). Both fall into the moderate-intensity statin dosing regimen.
HDL cholesterol levels exceeding 100 mg/dL are frequently dysfunctional or ineffective as cardiovascular bioindicators.
"Having an HDL over 100 starts to get into a place where doctors question and say, "Is that HDL actually being effective? Is it actually being an appropriate bioindicator or is there something else going on?" ... The people that have ineffective HDL are folks that tend to hang around 105, 110, 115" (said at 0:30:45)
Epidemiological data and meta-analyses support the observation that HDL cholesterol (HDL-C) levels exceeding approximately 90–100 mg/dL lose their conventional protective cardiovascular association and exhibit a paradoxical U-shaped curve, where extremely high levels are associated with increased all-cause and cardiovascular mortality rather than additional protection. A meta-analysis of over 1 million individuals without baseline coronary disease found that very high HDL-C levels significantly increased cardiovascular death at thresholds above 94 mg/dL in men and 116 mg/dL in women. Large prospective cohorts, including a study of 3.3 million individuals, also demonstrated a U-shaped relationship, confirming elevated cardiovascular and all-cause mortality when HDL-C exceeds 90 mg/dL.
- supports: Association of high-density lipoprotein cholesterol with all-cause and cause-specific mort… (The Lancet regional health. Western Pacific 2024) · cited 40x in the literature
"This study found U-shaped associations of HDL-C with all-cause, cardiovascular and cancer mortality. When compared with the groups with the lowest risk, the adjusted hazard ratios (95% CIs) for HDL-C <30 mg/dL was 1.23 (1.17-1.29), 1.33 (1.23-1.45) and 1.18 (1.09-1.28) for all-cause, CVD and cancer mortality, respectively. For HDL-C >90 mg/dL, the corresponding HR (95% CIs) was 1.10 (1.05-1.15), 1.09 (1.01-1.18) and 1.11 (1.03-1.19)." (abstract, results)
pubmedfull study (doi) - supports: Association between very high HDL-C levels and mortality: A systematic review and meta-ana… (Journal of clinical lipidology 2024) · cited 20x in the literature
"Subgroup dose-response analysis revealed that very high HDL-C levels increased cardiovascular death in women above 116 mg/dL (HR 1.47; 95% CI 1.01-2.15) and in men above 94 mg/dL (HR 1.29; 95% CI 1.01-1.65) (p_nonlinearity <0.01). These findings suggest that very high HDL-C levels are not protective against CV mortality and may, in fact, increase CV mortality risk especially in men." (abstract, results and conclusions, passage verified)
pubmedfull study (doi)
The FOURIER clinical trial demonstrated that reducing LDL cholesterol down into the 20s mg/dL appeared to be safe.
"Now, one of the big studies that came up a few years ago was called the FOURIER trials, F-O-U-R-I-E-R. And those trials said, look, we got people down into the 20s. And to me, that was a flashing red light because I said that's an area where I clearly would at that time thought it would have been very dangerous, especially, you know, for things like brain fog, long-term cognition. And I looked at them with the assumption that they really couldn't have had enough people in those low 20s for long enough to be able to make the statement that that was safe. Actually, when I went deeper into the studies, reviewed them, I thought they did have some good numbers and they did make a good case that, you know what, even into the 20s did appear to be safer than a lot of people fear." (said at 1:04:03)
The host's statement accurately summarizes published prespecified secondary and follow-up analyses of the FOURIER randomized clinical trial. In these analyses, thousands of patients achieved low-density lipoprotein cholesterol (LDL-C) levels below 20 mg/dL (0.5 mmol/L) or in the 20s mg/dL range using evolocumab. Over follow-up periods ranging from 2.2 years in the main trial to up to 8.6 years in its open-label extension, achieving these very low LDL-C levels showed no significant increase in serious adverse events or neurocognitive decline compared to higher LDL-C levels.
- supports: Clinical efficacy and safety of achieving very low LDL-cholesterol concentrations with the… (Lancet (London, England) 2017) · cited 685x in the literature
"Conversely, no significant association was observed between achieved LDL cholesterol and safety outcomes, either for all serious adverse events or any of the other nine prespecified safety events... There were no safety concerns with very low LDL-cholesterol concentrations over a median of 2.2 years." (abstract, results and conclusions)
pubmedfull study (doi) - supports: Cognition After Lowering LDL-Cholesterol With Evolocumab. (Journal of the American College of Cardiology 2020) · cited 92x in the literature
"The proportion of patients reporting a decline in total cognitive score was similar among the 2,338 patients who achieved very low LDL-C levels (<20 mg/dl) compared to the 3,613 patients with LDL-C ≥100 mg/dl (3.8% vs. 4.5%, p = 0.57). The addition of evolocumab to maximally tolerated statin therapy had no impact on patient-reported cognition after an average of 2.2 years of treatment, even among patients who achieved LDL-C <20 mg/dl." (abstract, results and conclusions)
pubmedfull study (doi) - supports: Association Between Achieved Low-Density Lipoprotein Cholesterol Levels and Long-Term Card… (Circulation 2023) · cited 185x in the literature
"In patients with atherosclerotic cardiovascular disease, long-term achievement of lower LDL-C levels, down to <20 mg/dL (<0.5 mmol/L), was associated with a lower risk of cardiovascular outcomes with no significant safety concerns." (abstract, conclusions)
pubmedfull study (doi)
Unverified means no publication matching the claim was located; it does not prove the claim false. Spotted an error? See the corrections policy - disputes from the people quoted are prioritized.