http://www.daniellebelardomd.com/

Dr. Danielle Belardo, MD, Los Angeles, CA (2025)

10/08/2025

Many thanks to the New York Times and brilliant journalist Ashwin Rodrigues for featuring me in this important piece on the risks of supplement overuse and the culture that fuels it, alongside my brilliant colleague

https://www.nytimes.com/2025/10/07/well/doctors-supplements.html

When the New York Times reached out, I was thrilled that Ashwin wanted to include real patient stories (privacy protected, of course). So often, our discussions about evidence-based medicine on social media focus on data, research, statistics and confidence intervals, and of course guidelines, all essential… but through Ashwin’s dynamic storytelling, this piece brings the human side of science to life.

I’m grateful to contribute to a conversation that helps people navigate health misinformation with clarity, empathy, and evidence.

We know that supplements when used outside of deficiency or guideline indication (ie folic acid in women of childbearing age, B12 for those who are plant based, vitamin D for individuals in certain regions, to name a few) do not lead to any benefit, and can have significant harm. If a supplement truly delivered the benefits its promoters claim, it wouldn’t be sitting in an influencer’s link in bio - it would be in the clinical guidelines. And that’s the point. The wellness economy thrives not on rigorous evidence, but on aspiration and fear, turning unproven hope into a business model far more profitable than proof ever could be.

10/03/2025

Sharing this again as a reminder that every single day, I receive emails from supplement companies offering me an insane amount of money to market their supplements and herbals—and I will never accept. These companies are part of a multi-billion dollar industry that thrives not on evidence, but on exploiting fear and pseudoscience. The reality is clear: outside of treating a true deficiency or a guideline-directed medical indication, there is no credible scientific evidence that supplements improve cardiovascular outcomes, prevent chronic disease, or extend life. When a physician or influencer pushes you to buy supplements under the guise of “optimization” or “detox,” they are not practicing medicine—they are participating in a scam designed to siphon money from consumers while providing no proven health benefit. Supplement companies spend hundreds of millions of dollars annually on aggressive marketing because they know that advertising sells, not science. Patients deserve real evidence-based care, not snake oil rebranded in glossy bottles.

I recommend for anyone who is confused about how we determine guideline recommendations, and why things like over the counter fish oil and supplements like turmeric are not recommended by any major medical organization guidelines, check out my highlight called “EBM” (evidence based medicine) where I provide resources for how you can start to learn critical scientific appraisal, statistics, the grading of scientific evidence, and understand how we rigorously evaluate science to formulate our medical guidelines. It’s a good start, and once you have a foundational understanding of EBM, the rest makes a ton of sense and is easy.

10/01/2025

Hot off the press! 🗞️🔥 It was such an honor to be a part of this landmark global obesity guideline paper. This guideline reflects truly global collaboration, with representation from experts across the USA, Germany, China, Australia, Nigeria, Mexico, Denmark, Canada, Malaysia, Morocco, Brazil, UK, Slovakia, Japan, India, Portugal, UAE, Singapore, Guatemala, Italy, Spain, Cameroon, Russia, Honduras, Egypt. Many congratulations to the brilliant colleagues I had the privilege to work with!! Especially the amazing

This guideline is open access and free for everyone to read! I will link it in my stories/highlights🩷
Link: https://www.globalcardiology.info/site/article/view/86

The iCARDIO Alliance Global Implementation Guidelines for the Management of Obesity 2025 represent the first international, implementation-focused framework for obesity care. Recognizing obesity as a critical driver of cardiometabolic disease, the guideline integrates lifestyle, pharmacologic, and procedural interventions for both prevention and treatment. A major innovation is the introduction of “economic adjustment” pathways, offering practical, graded options that can be adapted across high-, middle-, and low-resource health systems.

Key principles include:
• Equity and access: ensuring patients worldwide can benefit from proven therapies regardless of setting.
• Patient-centered, multidisciplinary care: emphasizing shared decision-making and integration of medical, surgical, and lifestyle strategies.
• Cutting-edge evidence: including GLP-1/GIP receptor agonists, bariatric surgery, and other effective interventions.

This guideline brings together experts across continents to unify obesity management, and provide clinicians with a pragmatic roadmap to translate science into practice worldwide.

09/27/2025

LDL, HDL, Triglycerides, oh my. Have you heard the myth from influencers or pseudoscience doctors that you should be trying to “raise your HDL cholesterol?”, especially those who tell you to take a supplement to raise it? (I’m looking at you niacin - straight to the dumpster 🚮🗑️) Often these individuals make false claims about how your LDL cholesterol doesn’t matter, and it’s all about triglycerides and HDL. Well then, what actually causes cholesterol to build up in your arteries? What is LDL? What is a triglyceride? What do we even know about HDL? Which lipid markers are most relevant when looking at your cardiovascular disease risk?

Everything and anything you may have ever wanted to know about a standard lipid panel.

And… maybe more than you actually want to know 🤠

Scroll through to learn the difference between LDL-C and LDL-P.

Learn about triglycerides.

Learn about how you have probably been misled about HDL being “good cholesterol” (it is much more nuanced than that), the myth that HDL/TG ratios are useful, and, any lipid ratios that use the enigma which is HDL (they are not useful🥲)

But before you start: if you haven’t read my post on apo B or LDL-C, scroll down ⬇️ to read that first.

Happy lipidology learning!

And remember, prevention is the best intervention! Know your numbers! Knowledge is power in reducing your risk for heart disease.

09/27/2025

What is Lipoprotein(a)? *Swipe through the slides for the latest updates on Lp(a)*

Lp(a) is a complex lipoprotein containing LDL-like particles and apolipoprotein(a), which shares homology with plasminogen but lacks fibrinolytic activity.

High Lp(a) levels contribute to atherosclerosis and inhibit clot dissolution, making elevated Lp(a) an independent risk factor for cardiovascular disease (CVD) in 20% of the population. Current management focuses on controlling other CVD risk factors until Lp(a)-lowering therapies become available.

Lp(a) concentrations are over 90% genetically determined and largely unaffected by lifestyle. High levels lead to plaque buildup, thrombus formation, and an increased risk of events like myocardial infarction, heart failure, and aortic stenosis.

Measurement and Screening:

It is estimated that elevated levels of Lp(a) are found in approximately 20% of the population.
Despite its importance, research shows that Lp(a) is rarely screened for.
Fewer than 1% of Americans have ever had their Lp(a) levels tested!

Lp(a) as a Cardiovascular Risk Factor:

High Lp(a) increases the risk of various CVD outcomes, including myocardial infarction, aortic valve stenosis, stroke, and peripheral artery disease. Genetic studies confirm that elevated Lp(a) is a significant risk factor for CVD.

Current Management:

With no approved Lp(a)-lowering drugs, management focuses on reducing other CVD risk factors, particularly LDL cholesterol/apoB.
To reduce LDL/apoB we recommend diet/lifestyle & if lipid lowering therapy is needed we have many options, including statins, ezetimibe, PCSK9i, bempedoic acid, inclisiran.
We also want to aggressively modify all other CV risk factors (HTN, diabetes, etc)

Future Therapies: Several Lp(a)-lowering drugs are in development. Scroll through the slides to see where we stand in the future of Lp(a) target therapeutics.

Swipe through the slides to find the answers to some of your most common questions about Lp(a), including why we don’t use niacin, questions about PCSK9i, and more.

Have you had your Lp(a) checked?

09/27/2025

Part 1: 2025 AHA/ACC/Multisociety Hypertension Guideline Takeaways

High blood pressure is the most prevalent and modifiable risk factor for cardiovascular disease, including coronary artery disease, heart failure, atrial fibrillation, stroke, dementia, chronic kidney disease, and all-cause mortality.

Guidelines matter because they represent expert consensus grounded in the best available evidence. They provide a standardized framework to ensure patient care is driven by science rather than opinion.

This is the first in our top 10 series on the top takeaways from the 2025 Hypertension Guideline, with Dr. Michael Gibson and Dr. Danielle Belardo of the Baim Institute.

06/11/2025

Tonight! Presenting on my favorite topic (nutrition and cardiovascular disease prevention) for our California chapter of American College of Cardiology. Will be discussing all of the greatest hits: myths surrounding high carb vs low carb diets, dietary interventions for hyperlipidemia, hypertension, diabetes, why so many supplements on the market are harmful, and dietary patterns for cardiovascular disease risk reduction.

Head to CAacc.org for more info ❤️

05/07/2025

Apo B vs LDL-C: Part 2! How do we compare them and evaluate for concordance or discordance?

Let’s start off with: if you haven’t read my post on apoB directly before this one, read that one first!

If you don’t fully understand the concept of discordance between lipid metrics (like LDL-C and non–HDL-C) and lipoprotein metrics (like apoB and LDL particle number)… I am happy to clarify here!

You can’t compare their absolute values (mg/dL or nmol/L) directly, but you can compare their positions across population percentiles.

If your LDL-C and apoB fall at similar percentiles (e.g., both at the 50th), they’re concordant. In that case, either metric reasonably reflects atherogenic burden and ASCVD risk.

But if their percentiles differ by more than 10 percentile points, they’re discordant, and when lipid and lipoprotein metrics disagree, apoB provides the more accurate assessment of cardiovascular risk.

This is common in individuals with insulin resistance, metabolic syndrome, type 2 diabetes, or elevated triglycerides, where LDL-C may appear “normal,” but apoB reveals high particle burden.

The table here, from the NLA apoB Consensus Statement, shows how various LDL-C and apoB values correspond to percentile cut points in the general population.

Example: Your patients lab shows:
• LDL-C = 112 mg/dL → 50th percentile
• apoB = 113 mg/dL → 80th percentile
This mismatch reveals a patient with many more atherogenic particles than LDL-C alone suggests.

So how low should LDL-C or apoB be?
Being at a lower percentile for apoB/LDL-C reduces long-term cardiovascular risk. Since ASCVD eventually affects over half the population, it makes sense to aim toward the lower end of the curve. But how low to go & whether medical treatment is needed depends on individual risk factors, and should always be guided by a cardiologist.

05/06/2025

What is apoB—and do you need to know yours?

You’ve probably heard apoB mentioned in discussions about cholesterol, but is it important? The answer is: yes! But whether or not you need to have it tested depends.

Apolipoprotein B (apoB) is the structural protein found on all atherogenic lipoprotein particles—this includes LDL, VLDL, IDL, and lipoprotein(a). Each atherogenic particle carries one apoB100 molecule, so measuring apoB gives a direct count of the total number of particles that can enter the artery wall and initiate plaque formation.

So how is this different from LDL cholesterol (LDL-C)?

LDL-C is the total mass of cholesterol carried within LDL particles. ApoB, on the other hand, reflects the number of atherogenic particles in circulation. In approximately 85–90% of individuals, LDL-C and apoB are concordant—meaning LDL-C reasonably estimates atherogenic particle burden and cardiovascular risk.

But in some people—especially those with metabolic syndrome, diabetes, obesity, elevated triglycerides, or high Lp(a)—these measures can become discordant. A patient may have a “normal” LDL-C but still harbor a high number of small, cholesterol-depleted particles (i.e., elevated apoB). In such cases, risk always tracks with particle number, not cholesterol content.

Should everyone measure apoB?

Not necessarily—at least not yet. While apoB is a more precise indicator of atherogenic burden, U.S. guidelines (2018 ACC/AHA Cholesterol and 2023 ACC/AHA Chronic Coronary Disease) recommend its use selectively—particularly in patients with insulin resistance, hypertriglyceridemia, or residual ASCVD risk. The 2023 AHA Scientific Statement confirms that apoB outperforms LDL-C in risk prediction, though broader adoption is limited by cost, clinician familiarity, and healthcare system barriers.

ESC/EAS guidelines already reflect this shift, recommending apoB more strongly in high-risk groups.

Bottom line: If you have insulin resistance, high triglycerides, or unexplained cardiovascular risk, checking apoB may uncover hidden risk that LDL-C alone can miss—and help guide more personalized prevention.

04/23/2025

Despite recurrent attempts in popular media and niche scientific circles to undermine the role of LDL-C in atherosclerosis, the totality of rigorous scientific evidence remains unequivocal: elevated LDL cholesterol is causative, not merely associated, with atherosclerotic cardiovascular disease (ASCVD).

This conclusion is not derived from a single study, nor is it contingent on isolated data. It is the result of a vast and consistent body of evidence, including:

✔️Mendelian randomization studies, which leverage genetic variants as natural experiments, demonstrate that lifelong exposure to lower LDL-C results in proportionally lower rates of ASCVD—confirming a dose-dependent, causal relationship.

✔️Randomized controlled trials of LDL-lowering therapies (statins, ezetimibe, PCSK9 inhibitors) show that reducing LDL-C levels consistently reduces the incidence of major cardiovascular events, regardless of mechanism, baseline LDL-C, or patient subgroup.

✔️Prospective epidemiological cohort studies, encompassing over 2 million individuals and 20 million person-years of follow-up, reveal a log-linear, dose-dependent relationship between LDL-C burden and ASCVD risk.

✔️Genetic evidence from familial hypercholesterolemia and rare variants affecting LDL receptor function shows a direct correlation between cumulative LDL-C exposure and early-onset ASCVD.

Causality frameworks such as Bradford Hill’s criteria have been robustly fulfilled, as detailed in the European Atherosclerosis Society consensus statement. Biological plausibility, strength and consistency of association, experimental evidence, and temporal sequence all align.

No recent data—not even when selectively framed or misrepresented—undermines this vast, integrated body of evidence. In fact, when critically appraised, the very study being used to cast doubt on LDL’s role in atherosclerosis actually reinforces the causal model by demonstrating plaque progression in the setting of markedly elevated LDL-C, even among individuals considered otherwise metabolically healthy. To misconstrue such findings as exculpatory for LDL is a profound misreading of the data—and a disservice to evidence-based medicine.

03/24/2025

Have you seen the news headlines? Published in JACC, a multicenter retrospective study evaluated long-term cardiovascular risk associated with cannabis use. This study serves as a fantastic teaching tool about strengths & limitations of different levels of evidence.

First, it’s essential to recognize inherent limitations of retrospective studies. These include confounding (measured & unmeasured), selection bias, information bias & reverse causation. While such studies are useful for hypothesis generation & exploring associations in real-world settings, alone they are often limited in their ability to establish causality.

Study Highlights:
• Data Source: TriNetX (53 healthcare orgs)
• Population: Adults 4.6 million; ~93,000 cannabis users (2%) vs ~4.5M non-users
• Method: Propensity score matching
• MI Risk:
Relative risk ↑ 6x (0.55% vs 0.09%)
Absolute risk: 0.45%
NNH: ~220
• Ischemic Stroke:
Relative risk ↑ 5x
Absolute risk: 0.3%
• MACE:
Relative risk ↑; modest absolute risk
• AF:
Relative risk ↑ 2x
Absolute risk: 0.43%
• All-Cause Mortality:
Relative risk ↑ 1.5x
Absolute risk: 0.45%

Retrospective studies like this contribute a single dimension to causal inference. Without RCTs or complementary inferential pillars—ie consistent replication, dose-response gradients, biological plausibility, demonstration of temporality—causality cannot be inferred. The absence of data on quantity, frequency, formulation & route of cannabis use further weakens the exposure assessment. Additionally, reliance on ICD coding introduces misclassification bias, & even with propensity score matching, residual confounding remains a major threat to internal validity.

Cannabis research has been limited by regulatory barriers, limiting RCTs. Given consistent associations w/ ⬆️ CV risk even in the absence of definitive causality—the precautionary principle warrants exercising caution with cannabis use until higher-quality evidence can clarify long-term safety. Yet: rigorous, prospective research is still needed to draw definitive conclusions.

Dr. Danielle Belardo, MD

10/08/2025

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