Dr. Danielle Belardo, MD

Dr. Danielle Belardo, MD Preventive Cardiologist focusing on preventing heart disease, cardiometabolic health, & weight loss

Tonight! Presenting on my favorite topic (nutrition and cardiovascular disease prevention) for our California chapter of...
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 ❤️

Apo B vs LDL-C: Part 2! How do we compare them and evaluate for concordance or discordance? Let’s start off with: if y...
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.

What is apoB—and do you need to know yours?You’ve probably heard apoB mentioned in discussions about cholesterol, but is...
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.

Despite recurrent attempts in popular media and niche scientific circles to undermine the role of LDL-C in atheroscleros...
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.

Have you seen the news headlines? Published in JACC, a multicenter retrospective study evaluated long-term cardiovascula...
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.

Hi all! It has been brought to my attention that this fake facebook account is pretending to be me - using my photos, ...
03/17/2025

Hi all! It has been brought to my attention that this fake facebook account is pretending to be me - using my photos, and messaging people directly. Please report this user: https://www.facebook.com/share/1JSi8nc3R3/?mibextid=wwXIfr

Please keep in mind that I have only one facebook account (this one), and only one instagram account. Both are verified with a blue check.

Thank you!

Familial hypercholesterolemia (FH) leads to lifelong high LDL cholesterol, increasing the risk of coronary heart disease...
01/20/2025

Familial hypercholesterolemia (FH) leads to lifelong high LDL cholesterol, increasing the risk of coronary heart disease and premature death. Global FH registration has been limited, but Denmark has tracked cases since 1978 using modified ICD codes. This study examined whether prognosis for individuals with FH improved from 1978 to 2021, focusing on age at death and CHD onset.

Methods:
-Nationwide cohort study (1978–2021) including all Danish residents.
-FH (n = 10,199) vs. non-FH (n = 9,174,926) analyzed for trends in mortality and CHD onset.

Results:
Mortality Trends
-1978: FH patients died 22 years earlier than non-FH (P < .001).
-2021: Age at death equalized between FH and non-FH (P = .16).

CHD Trends
-1978: CHD occurred 20 years earlier in FH vs. non-FH (P < .001).
-2021: CHD still occurred 7 years earlier in FH (P < .001).

Findings were consistent across men, women, and a 1:100 matched analysis (s*x, ethnicity, birth year).

Over four decades, life expectancy normalized for FH patients, reflecting major progress in management. CHD onset remains earlier, despite treatment advancements. Denmark is the only country with FH registry data since 1978, making this study uniquely valuable.

So what does this mean?

-Early Screening & Detection Are Critical: Genetic screening & lipid testing drive earlier diagnosis and intervention.
-Denmark’s systematic FH registration improved awareness and management.
-Lipid-Lowering Therapies Changed FH’s Trajectory: Statins, ezetimibe, and PCSK9 inhibitors have been game changers in reducing LDL and cardiovascular risk. Early initiation of therapy is key to optimizing outcomes.

Future challenges and questions
-CHD still occurs earlier in FH, highlighting the need for aggressive LDL-lowering strategies starting younger in those with FH.
-Further research is needed on:
The negative impact of lifetime LDL exposure on risk.
Optimal timing for lipid-lowering therapy.
The potential role of gene therapies and novel lipid-lowering agents.

This study demonstrates how early screening, detection, and aggressive treatment can transform FH prognosis- prevention is the best intervention!

If you follow me on social media —- you know that I make a BIG deal about nutrition and lifestyle change for cardiovascu...
01/20/2025

If you follow me on social media —- you know that I make a BIG deal about nutrition and lifestyle change for cardiovascular disease prevention. Nutrition and lifestyle change are the cornerstone of preventing cardiovascular disease. But for some individuals, medical lipid lowering therapy will also be needed. The great news is that in cardiology, we have a TON of safe and effective medications in our arsenal for heart disease prevention.

Why is LDL cholesterol so important?

LDL Cholesterol & ASCVD: A robust body of evidence, including over 200 cohort studies, Mendelian randomization studies, randomized trials, involving more than 2 million participants & over 150,000 cardiovascular events, demonstrates a clear, dose-dependent, log-linear association between LDL-C levels and the risk of atherosclerotic cardiovascular disease. The risk increases with prolonged exposure to high LDL-C.

So how do we lower LDL-C/ApoB with medical therapy?

-Statins: Reduce LDL-C by 20-65%, showing improvements in mortality in both primary and secondary prevention.
-Ezetimibe: Blocks intestinal sterol absorption, used as an adjunctive therapy.
-Bempedoic Acid: Inhibits ATP citrate lyase, leading to ⬇️ cholesterol synthesis in the liver.
-PCSK9 Inhibitors: Block PCSK9 protein, increasing the number of LDL receptors & reducing LDL-C by about 50%.

And the latest kid on the block **Inclisiran**
A first-in-class small interfering RNA (siRNA) therapy, uniquely targets and silences the PCSK9 gene in the liver. It degrades the messenger RNA for PCSK9, preventing its synthesis, increasing LDL receptors and enhancing LDL-C clearance from the bloodstream.
And…Bi-annual dosing! This means patients can have their inclisiran dosed just TWICE A YEAR, offering a promising option for patients not achieving LDL-C goals with current therapies or those with statin intolerance.

Stay tuned: CV outcomes trials for Inclisiran: ORION-4 and VICTORION-2P, are in progress, with estimated completions in 2026 & 2027!

Before the wildfires devastated LA County, the shelter system was already overwhelmed and in crisis. Now, with the fires...
01/15/2025

Before the wildfires devastated LA County, the shelter system was already overwhelmed and in crisis. Now, with the fires’ aftermath, hundreds of dogs and cats have been deeply affected. Some are burned or injured, while others have been surrendered—temporarily or permanently—by families who lost their homes and are struggling to find pet-friendly housing.

If you’re in Southern California and able to help, consider fostering for one of the shelters or rescues listed here.

As a foster for and , I’ve seen just how much these organizations do to save the countless lives of so many beautiful, sweet, innocent animals. Their work is truly life-changing.

If you’re thinking about adding a pet to your family this year, adopting from one of these organizations can make a world of difference.

For those outside the area, you can still help. If you are able, consider donating to any of these incredible organizations - any donation goes a long way in supporting animals impacted by the wildfires. Every bit makes a difference.










Also - follow Ashley who is a volunteer who shares dogs looking for adoption and foster throughout the LA Shelter System ❤️

Fostering saves lives.

▪️Foster homes reduce the risk of euthanasia by providing temporary care, giving dogs a better chance of being adopted.
▪️80% of fostered dogs are adopted within the first three months of being in a foster home.
▪️Fostering helps reduce shelter overcrowding, making room for more dogs in need.
▪️Foster dogs often show significant improvement in behavior and health, making them more adoptable.
▪️Fostering is flexible: Even short-term fostering can make a big difference!

Fostering saves lives: Every dog that is fostered opens up space for another dog in a shelter, effectively doubling the impact.

If you made it to the end of this caption, thank you for reading❤️🥹

The devastation caused by the LA wildfires is beyond measure. While we remain evacuated, we are incredibly grateful to b...
01/12/2025

The devastation caused by the LA wildfires is beyond measure. While we remain evacuated, we are incredibly grateful to be safe and healthy. My heart goes out to everyone facing the immense hardship of displacement, destruction, and loss.

Tragically, sixteen lives have been lost.
Approximately 153,000 people are still under evacuation orders, though this number has decreased from 180,000.
First responders continue their heroic efforts to contain the flames, while authorities investigate the causes of these devastating wildfires.

Wildfire smoke poses a serious health risk, especially to vulnerable populations, including those with lung conditions such as asthma, COPD, and pulmonary fibrosis, as well as individuals with heart disease, pregnant women, older adults, and children. These groups should take extra precautions and consider consulting their healthcare providers for personalized guidance.

However, inhaling wildfire smoke is harmful to everyone. It can cause inflammation of the airways and lungs, exacerbating respiratory conditions and increasing susceptibility to lung infections. Taking steps to minimize exposure is essential for protecting your health.

Scroll through for the top 10 tips from the American Thoracic Society for protecting your lungs from wildfire smoke.

Sending unending love and support to everyone in LA County, the beautiful community that I call home ❤️

Our neighborhood, our town, our community continues to be ravaged by the LA fires 💔😢 We are evacuated and safe, but is ...
01/09/2025

Our neighborhood, our town, our community continues to be ravaged by the LA fires 💔😢 We are evacuated and safe, but is on the front lines saving hundreds of dogs and cats and animals who are now being rescued with burns all over their bodies 😭

For everyone and anyone who has been asking me how you can help, if you are able, please donate to for their animal fire rescue 🙏

Pasadena Humane rescued my Kaya when I adopted her 8 months ago. Today they are rescuing hundreds of dogs in our community who are burned and in need. Our community is suffering. The humans and the animals 😢🙏

Praying for all of the humans and animals of LA County as we deal with the utmost devastation to our communities.

Thank you to anyone who is able to donate to to help save these animals from the fire. Every penny counts and no donation is too small 🙏 Please share the page as well ❤️

Thank you for supporting our community in this tragic time.

Huge news: FDA has approved Zepbound (tirzepatide- GLP-1/GIP receptor agonist) for the treatment of moderate to severe o...
12/28/2024

Huge news: FDA has approved Zepbound (tirzepatide- GLP-1/GIP receptor agonist) for the treatment of moderate to severe obstructive sleep apnea in adults with obesity.

As a cardiologist, this is a huge deal for my patients, and cardiovascular disease prevention overall.

Untreated sleep apnea significantly raises the risk cardiovascular disease, including:

Hypertension: Hypoxia & sympathetic activation ⬆️ nocturnal & daytime blood pressure.

Arrhythmias: Sleep apnea is strongly linked to atrial fibrillation, bradyarrhythmias, & ventricular ectopy due to intermittent hypoxemia & autonomic instability.

Heart Failure: OSA can accelerate & worsen both heart failure with reduced and preserved ejection fraction.

Coronary Artery Disease: Promotes endothelial dysfunction & accelerates atherosclerosis.

Stroke Risk: ⬆️ risk of ischemic stroke due to systemic inflammation & hypercoagulability.

Zepbound’s approval for moderate to severe OSA in adults with obesity is based on two randomized, double-blind, placebo-controlled studies of 469 adults without type 2 diabetes. One study enrolled participants using positive airway pressure (PAP), the standard of care for moderate to severe OSA, and one study enrolled participants unable or unwilling to use PAP. In both studies, participants received either 10 or 15 mg of Zepbound or placebo once weekly for 52 weeks. The primary measure of efficacy was the change from baseline in the apnea hypopnea index (AHI), a measurement of how many times a person stops breathing (apnea) or breathes shallowly (hypopnea) per hour during sleep, at week 52. After 52 weeks of treatment in both studies, participants who received Zepbound experienced a statistically significant & clinically meaningful reduction in events of apnea or hypopnea as measured by AHI compared with placebo, & greater proportions of participants treated with Zepbound achieved remission or mild OSA with resolution of symptoms compared to placebo. Participants treated with Zepbound had a significant ⬇️ in body weight & improvement in AHI.

Hopefully this approval helps to expand insurance coverage for this life changing medication.

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