Dr. Danielle Belardo, MD

Anti-science “toxin free” fear mongering on social media is nothing new, as toxin free pseudoscience is one of the largest money making scams in wellness.

The global wellness industry is valued at over $4.5 trillion, capitalizing on consumer fears about health and wellness.

The rise of influencers and social media platforms has amplified fear-mongering, leading to increased sales and profits for “all-natural” and “toxin-free” products.

I love this great project created by James Kennedy, a chemistry teacher, who wanted to demonstrate that everything is made up of “chemicals”, by listing the chemical composition of various fruits.

It’s mind blowing how many people on social media list things that are “toxins” and they ignore (or don’t even realize) that we even have formaldehyde normally circulating in our own blood. (Formaldehyde is essential in human metabolism and is required for the synthesis of DNA and amino acids - the building blocks of protein. Therefore, all humans have detectable quantities of natural formaldehyde in their circulation (about 2.5 ug of formaldehyde per ml of blood).

The more I’m involved in scientific communication with the public, the more I am realizing that people are being taken advantage of by the wellness industry. It’s actually really sad. I can only imagine how confusing it must be for consumers of social media - to determine “who is telling you the truth” when there are of course people telling you that “big pharma” is out to get you.

Remember that scientific guidelines and large public health recommendations aren’t based on one study or one individual. They are based on the rigorous and thorough evaluation of the totality of many levels of scientific evidence. 🙏

PS... if someone tells you fruit is bad for you, hit that unfollow button fast😂

What is peripheral artery disease (PAD)? A circulatory problem where narrowed arteries reduce blood flow to your limbs.

The majority of PAD is atherosclerotic (from plaque formation) categorized as claudication, chronic limb ischemia, or acute limb ischemia.

Or it can be non-atherosclerotic (less common)

How prevalent is PAD?
-In the US: over 8.5 million people, but it is very underdiagnosed!
-prevalence ⬆️ w/ age
-patients w/ PAD are more likely to die of cardiovascular disease:
*stable claudication 5 yr mortality = 15-30%
*critical limb ischemia 1 yr mortality = 25%
⁣
Risk factors:
Smoking, Diabetes – highest risk
hypertension, hyperlipidemia

How do we diagnose it?
Most common: Ankle Brachial Index (Swipe through to learn about it!)

Who do we screen w/ ABI?
Exertional leg symptoms & non-healing wounds. Currently: insufficient evidence for asymptomatic screening

Symptoms:
Only 10% of people w/ symptomatic PAD have typical symptoms of classical claudication! (cramping pain in legs induced by exercise)
50% have atypical leg pain, often confused w/ arthritis, spinal stenosis, or fatigue
40% will actually not have well described symptoms at all – asymptomatic PAD!

Asymptomatic PAD is common in women
In a study of 933 women > 65 yr old, 35% had ABI

Increase your dietary fiber intake to improve blood pressure control!

According to several international, regional, and national guidelines on hypertension, lifestyle interventions are the first-line treatment to lower blood pressure (BP). Although diet is one of the major lifestyle modifications described in hypertension guidelines, dietary fiber is not specified. Suboptimal intake of foods high in fiber, such as in Westernized diets, is a major contributing factor to mortality and morbidity of noncommunicable diseases due to higher BP and cardiovascular disease. In this recently published review, the authors address this deficiency by examining and advocating for the incorporation of dietary fiber as a key lifestyle modification to manage elevated BP.

According to the evidence reviewed, the minimum daily dietary fiber for adults with hypertension should be >28 g/day for women and >38 g/day for men, with each extra 5 g/day estimated to reduce systolic BP by 2.8 mm Hg and diastolic BP by 2.1 mm Hg. The authors propose this would support healthy gut microbiota and the production of gut microbiota-derived metabolites called short-chain fatty acids that may lower BP.

We already know from an enormous amount of evidence derived from well designed randomized controlled trials, that eating a diet rich in fruits and vegetables, legumes, whole grains, and low in sodium and eliminating/greatly reducing alcohol intake, can help to reduce blood pressure and overall cardiovascular risk.

Focus on increasing fiber through eating whole plant foods, and skip the fiber supplements, as data has demonstrated that the benefits of fiber come from the whole food, not the fiber in pill form.

Prevention is the best intervention!

What causes high blood pressure, and why does finding out the underlying cause matter?

It’s shocking to me as a cardiologist how many patients I see with hypertension who have been treated with meds for *years*, without having an appropriate work up for HTN. Yes, it’s important for high BP to be treated, but it’s ALSO important to evaluate for the root cause of HTN. In many cases, if the root cause is addressed, patients can eventually either ⬇️ BP meds dramatically, or put their HTN into remission & go off of BP meds safely!

When diagnosing high BP, we want to figure out whether it’s “primary” hypertension, or if there is an underlying cause of “secondary” hypertension.

1️⃣The pathogenesis of primary hypertension is most likely the result of numerous genetic & environmental factors that have multiple compounding effects on cardiovascular & kidney structure & function.

Primary hypertension does not have a single known cause, but certain risk factors ⬆️ risk, including:

Genetics/Family History
Overweight & Obesity
High Sodium Diet
Potassium intake (low)
Physical Inactivity
High Alcohol Consumption

Vs:

2️⃣Secondary Hypertension:
A number of common & uncommon medical conditions may increase BP & lead to HTN. In many cases, these causes may coexist with risk factors for primary HTN and can be significant barriers to achieving adequate BP control. A specific, remediable cause of hypertension can be identified in approximately 10% of adult patients with HTN. If a cause can be correctly diagnosed & treated, patients with secondary hypertension can achieve a cure or experience a marked improvement in BP control, with a reduction in CVD risk.

Some common causes of secondary hypertension:
Renal parenchymal disease
Renovascular disease
Primary aldosteronism
Obstructive Sleep Apnea
Medications
Alcohol Induced

Some uncommon causes of secondary hypertension:
Pheochromocytoma
Cushing’s Syndrome
Hypothyroidism
Hyperthyroidism
Aortic Coarctation
Primary Hyperparathyroidism
Congenital Adrenal Hyperplasia
Mineralocorticoid excess syndromes other than primary aldosteronism
Acromegaly

Know your numbers. Get screened. Prevention is the best intervention.

An important reminder for everyone this holiday weekend!

Across all of my social media platforms, I have always received countless messages from individuals who feel stress & anxiety about eating on holidays 💔

Many of you message me that holidays bring up a lot of anxiety & feelings about food: candy, bbqs, big meals w/ family & the stress of what you can/can’t eat just ruins your entire day. For some of you, the anticipation of seeing desserts & feeling uncomfortable/worried about “unhealthy” food has even ruined your whole weekend💔

In a world where online “diet wars” have depicted some diets to be perfect, some foods to be evil & perfect abs to be the ultimate goal, it’s no wonder why so many feel this way, especially on holidays🥺

But no one’s diet is “perfect”

No one food, in one dose, will cause disease

Just know that you are doing amazing. Give yourself some grace and enjoy time with people you love ❤️

Food is an important part of your overall physical health, yes.

Food is also an important part of your overall mental health, spiritual health, your interpersonal relationships, community & culture!

I have messages from all across the spectrum. Some of you said that you’re so happy now following your healthier diet, whether you started a GLP-1, a new exercise program, you feel amazing & you worry your family members will shame you for your new preferred dietary choices and even shame you for your new found weight loss.💔

And on the other end, some of you have messaged me that you are feeling stressed to even look at an Oreo, because you’re worried you’ll gain weight, suddenly develop chronic disease, or harm your health.

So whether you are worried your family will give you a hard time for “eating healthy”, or bc you want to eat the chocolate chip cookies but it’s stressing you out:

Eat the kale if that makes you happy❤️

Eat the chocolate chip cookies if that makes you happy❤️

Put yourself 1st. Enjoy this weekend with loved ones ❤️ and ignore the noise on social media.

Your body, and your dietary choices, are no one’s business but your own 🙂

Happy 4th!

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 newest 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!

Heart Disease is the #1 killer of women and men, causing 1 in 3 deaths each year, claiming more lives yearly than all forms of cancer combined. As a cardiologist, it’s my goal and life dream to make a difference and change those statistics for good.

✔️Risk Factors: Several risk factors heighten the risk - high blood pressure, elevated cholesterol, smoking, diabetes, obesity, and physical inactivity. Know your family history. Know your pregnancy history & tell your doctor if you have a history of pre-eclampsia or gestational diabetes.

‼️64% of women who die suddenly of coronary heart disease had no previous symptoms.

✔️Early Detection: Regular health screenings for blood pressure, cholesterol levels, and diabetes are crucial. Know your numbers. A normal blood pressure is

Happy MDW from my new foster pup Kaya the Jindo ☀️❤️

Kaya is a gorgeous and sweet 2 year old girl who was found as a stray and brought into . She was just spayed last week, and it seems this pup was used for breeding in her past life 🥺

She’s incredibly kind, sweet, loving, and a major cuddle bug! She’s a little scared and timid at first, but she warmed up so quickly and gives me kisses non stop! If you read and learn about the jindo, they are an incredible breed. They are brilliant, thoughtful, loyal, athletic, calm, and very easy to house-train (they are obsessed with being clean, but do apparently dislike baths lol)

Kaya’s likes:
Peanut butter
Walks
Cuddling
Kisses

Kaya’s dislikes:
Vegan cheese (I tried 🤷🏼‍♀️)
Baths (she refused lol)
The crate 😅 (working on this! lol)

If you or anyone you know is interesting in giving this incredibly sweet, loving, and gorgeous 2 year old girl her forever home, please email [email protected] ❤️

Contrary to popular belief: GLP-1 weight loss medications are NOT all about aesthetic weight loss, they REDUCE risk of cardiovascular death, all cause mortality, and now, progression of kidney disease!

Just published today in NEJM 🚨
Semaglutide’s Impact in the FLOW Trial: A Game-Changer for Type 2 Diabetes and Chronic Kidney Disease

Semaglutide 1.0mg weekly shows disease-modifying benefits for kidney, cardiovascular health, and mortality in T2D+CKD patients, becoming a cornerstone in treatment.

Background:
* T2D and CKD patients face high risks of kidney failure, cardiovascular events, and death.
* The trial explored if semaglutide could reduce these risks.
Methods:
* 3533 participants with T2D and CKD were randomly assigned to receive semaglutide or placebo and followed for 3.4 years.
* Vital status known in 98.6%
* High treatment adherence (89%)

Results:
* Semaglutide group saw a 24% lower risk of major kidney events compared to placebo.
* Slower decline in kidney function in the semaglutide group, with improved eGFR slope by 1.16 ml/min/1.73 m² per year
* 20% reduction in mortality (mainly CV death) with an NNT of just 39 to prevent one death over 3 years.  This means for every 39 people treated with semaglutide, one death is prevented over three years. This shows the effectiveness of the drug in improving survival rates among individuals with CKD and T2DM
* 18% lower risk of major cardiovascular events
* Survival curves start to separate at 12 months

Safety and Tolerability:
* No unexpected safety issues
* Consistent safety profile with previous GLP1RA trials
* Fewer serious adverse events (mainly fewer infections and CV events)

Clinical Benefits Beyond Weight Loss:
* This trial highlights the weight-independent benefits of GLP-1 RA therapy in individuals with CKD and T2DM.

The multitude of benefits this class of medications continues to demonstrate in trial after trial are truly a clinical game changer.

A beautiful night with my favorite women in cardiology celebrating my amazing friend !❤️ Happy Birthday Martha!

In a specialty that is 90% male, I am so lucky to have so many incredible inspiring women as colleagues and friends ❤️ So proud to know and love every single one of you!

Sending out so much love and gratitude to every nurse on the planet for National Nurses Day.

As a cardiologist, throughout my career, from medical school through residency and fellowship training, nurses were my lifeline more times than I can count. From the ICU as an intern to a brand new cardiology fellow in the cath lab, they have showed up, stepped up, and lifted me up.

When I was a baby doctor and new intern, I will never forget starting night float, covering a heart transplant/mechanical support service & caring for a patient with a total artificial heart overnight. I had never even heard of Syncardia as a medical student. And here I was, suddenly called to evaluate a patient with a low blood pressure, who literally had their heart explanted, with a 100% artificial mechanical heart keeping them alive. I ran to the patients room, called my senior resident, but she was busy with a different patient who was decompensating. But I was NOT alone. I’ll never forget Patrick, a brilliant heart failure nurse, sprung into action. He knew EXACTLY what to do, he had been working with advanced heart failure & mechanical support patients for years. He knew exactly which attending to call (nope it wasn’t the attending on call, it can be more nuanced than you think!) and he was able to help me stabilize the patient, STAT.
⠀⠀
I’ll never forget intern year being in the cardiac ICU, and my patient who just landed from the cath lab after a massive STEMI, stent & pericardial effusion, went into SVT. Their heart rate was 180. My senior resident was putting in a line in another patient. I had only been a doctor for a month & although I knew ACLS protocol, I was overwhelmed. Two incredible nurses named Briana & Asia , came over immediately, with the crash cart. The two of them calmly said “you got this” and helped me push adenosine, and we broke the patient out of SVT. His oxygen returned back to normal and he stabilized.

Nurses have been such an integral part of my medical career. Nurses save lives. Nurses save our patients. Nurses help us become better doctors

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 gaslit about HDL being “good cholesterol”, HDL/TG ratios being useful, and, any lipid ratios that use the enigma which is HDL.🥲

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

Happy lipidology learning!

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

Clinical atherosclerosis is the end result of a disease that develops slowly over many decades.

Atherosclerosis is often a silent asymptomatic disease until it suddenly presents as a myocardial infarction (heart attack), or as chronic ischemia, angina or claudication.

Sudden plaque rupture can be fatal 1/3 of the time.

So you might wonder - well how early does heart disease begin if it stays silent for so long?

The PDAY Study on the Natural History and Risk Factors of Atherosclerosis in Children and Youth studied 3,000 subjects who died between ages 15 and 34 due non cardiac reasons.

The study found
1. Atherosclerosis begins in *childhood*
2. Young adults often have “significant” lesions
3. Even at young ages, the risk of atherosclerosis is associated with risk factors such as hyperlipidemia, to***co, obesity, abdominal circumference, diabetes, and hypertension

Recent PDAY studies have shown that a significant number of advanced coronary artery lesions have microscopic qualities associated with susceptibility to rupture and that coronary artery disease risk factors are associated with the development of these characteristic microscopic qualities.

The PDAY archive continues to provide an important resource for new investigators throughout the world that contribute to the understanding of atherosclerosis, the underlying cause of most cardiovascular disease and the leading cause of debilitating illness and death in this country. The PDAY findings emphasize the need to modify risk factors in young people to re**rd the development of atherosclerotic lesions, particularly clinically significant lesions. Thus, true primary prevention of atherosclerosis must being in childhood or early adolescence.

It’s never too early to focus on prevention!

Evidence Based Medicine: what does this mean?

Well - it’s a topic meant for more than one post – but let’s start with… how do we evaluate levels of evidence?

First: whether you are looking at medical or nutrition research, no evidence ranking system or decision tool can be used without a healthy dose of judgment & thought.

It is important to realize that any hierarchy of evidence is a general guideline, not an absolute rule. There certainly are cases where a study that used a relatively weak design can trump a study that used a more robust design, & there is no one universally agreed upon hierarchy, but it is widely agreed that the order presented here does rank the study designs in order of robustness.

This is the reason why I appreciate guidelines at the very top. For example, in Cardiology, our ACC/AHA guidelines translate scientific evidence into clinical practice guidelines. Based on systematic methods to evaluate & classify evidence, they provide a foundation for the delivery of quality cardiovascular care.

Swipe through to learn about the various levels of evidence.

But note: as important as it is to understand various levels of evidence when making recommendations, it is meaningless if you aren’t considering your patient directly in front of you.
Even if a treatment’s effects are supported by best evidence, you must consider several variables:
Is your patient sufficiently similar to the patients in the studies you have examined?
Does the treatment have a clinically relevant benefit that outweighs the harms?
Which outcomes are improved?
Are the patient’s values and circumstances compatible with the treatment?
Shared decision making is literally *the* most evidence based way to practice: having a thorough discussion with your patient about their views and circumstances is vital to clinical decision making.

So the next time you hear a headline like “superfood x,y,z can prevent a scary disease” stop & think:
What level of evidence was the study? What about outcomes? And is this even generalizable or clinically meaningful for me or my patients?

Honored to be elected to the board of the American Society of Preventive Cardiology ❤️ at our 2024 strategic planning session in Dallas with some of the most brilliant cardiologists on earth! Prevention is the best intervention ❤️

What is Lp(a)?

Lipoprotein(a) aka Lp(a) is an atherogenic lipoprotein and is unique because it is genetically inherited. 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!

Elevated Lp(a) is associated with several cardiovascular disease outcomes such as increased risk of aortic valve stenosis, myocardial infarction (heart attack), heart failure, ischemic stroke, as well cardiovascular and all-cause mortality.

Q: So what is the current treatment for high Lp(a)?
A: Until we have targeted therapeutics for Lp(a), the rec is still to lower apoB/LDL as much as possible.But why? Bc 95% of apoB particles are LDLs, thus anything that lowers apoB, reduces LDL/apoB (LDL-P) and LDL-C/non HDL-C.

Q: What about Niacin for Lp(a)?
A: Despite the fact that Niacin may lower the lab value for Lp(a), Niacin has shown to have no benefit in reducing CV risk in 3 large RCT outcome trials (CDP, HATS, HPS-THRIVE). Niacin doesn’t work for heart disease prevention. Period.

Q: What about PCSK9i for Lp(a)?
A: PSCK9i reduces the synthesis of apo(a), and thereby reduces Lp(a) by approximately 25%. But at this time we do not know FOR SURE if reducing Lp(a) reduces MACE, and if it does, how much Lp(a) lowering is needed. Trials are underway to answer these questions.

Q: So then what treatment do we use?
A: Currently we do not have targeted Lp(a) therapy, so to reduce CVD risk in individuals with elevated Lp(a) our rec is to reduce LDL/apoB, with diet/lifestyle, and for those who also need lipid lowering therapy, we use statins +/- ezetimibe as first line, and other agents if necessary (PCSK9i, bempedoic acid, inclisiran). In addition to controlling all other ASCVD risk factors (HTN, diabetes, etc)

Q: So what trials are pending for Lp(a)?
Lots of promising research trials on the horizon for targeted Lp(a) therapy:
1- Lp(a) HORIZON will read out early 2025
2- OCEAN(a) will read out late 2026
3- At least 2 other therapeutics are poised for phase 3, readouts will be closer to 2029-2031

Stay tuned!

What is apoB? You have probably heard this mentioned when people discuss cholesterol - but is it important? Do you need to know your apoB? The answer is… well, it depends.

Apolipoprotein B (apoB) is an “atherogenic lipoprotein” – meaning, it causes plaque build up and atherosclerosis.

ApoB lipoproteins move through the blood, and over a certain threshold, enter the artery wall, leading to plaque buildup and heart disease. For each LDL particle (LDL-P), there is one apo B lipoprotein. So when you’re measuring apoB, you’re measuring your LDL-P concentration.

How is this different from your LDL cholesterol (LDL-C) measurement?
LDL-P is an LDL particle, and LDL-C is the cholesterol CARRIED within your LDL particle.
If you took all LDL particles and weighed the cholesterol in those particles, that would give you your LDL-C. LDL-C is a lipid profile metric, used to estimate apoB.

So who can depend on their LDL-C as a measurement for CVD risk, and who should instead check their apo B? It depends whether you have concordance between your LDL-C and apo B:

Concordance: Typically 90-95% of your atherogenic apoB particles are LDL-Particles. Which means, for the majority of people, their LDL-C will be concordant with their apoB. So this is why it is not necessary to check apoB in everyone.
But…
Discordance: For individuals with metabolic dyslipidemia, diabetes, and high triglycerides (TG) – it can be valuable to check an apoB, as there could be discordance between their apoB and LDL-C. When particle numbers (apoB, LDL-p) are discordant from cholesterol metrics (LDL-C, non HDL-c) risk always traffics with the particle number.

What drives LDL cholesterol into the artery wall is LDL particle number & apoB. Once you exceed a certain threshold in the plasma, the liver can’t clear them – so they go into the arteries and deposit cholesterol in the artery wall, and causing plaque build up in the arteries, which is atherosclerosis.

The vast majority of cardiovascular disease is preventable! But action needs to be taken early, instead of waiting for someone to *develop* heart disease to initiate treatment!

Phenomenal paper just published in AHA:
Eradicating Atherosclerotic Events by Targeting Early Subclinical Disease: It Is Time to Retire the Therapeutic Paradigm of Too Much, Too Late

🔹Atherosclerosis begins early in life, yet often aggressive treatments are delayed until patients already have advanced arterial disease. The paradigm is too much, too late.

🔹 A heart attack is a medical failure. It is a manifestation of longstanding arterial disease that we had allowed to progress to its end-stage, despite knowing that atherosclerosis begins early in life and despite the availability of remarkably safe and highly effective therapies.

🔹 Once we know the root cause of a disease—and have powerful, convenient tools to target the known causative agent in a timely fashion—we can seriously discuss eradicating its clinical burden. These conditions have been met for atherosclerosis. It is a common-source pandemic caused by the retention of LDL (low-density lipoprotein) and other apoB-containing lipoproteins within the arterial wall, modification by other processes, and maladaptive responses to the modified material.

🔹 In the most successful medical fields, the focus is early prevention or early intervention. Included in this review are specific proposals for screening programs and then treatments for subclinical plaques that are still early enough perhaps to heal with the proper interventions. A vivid image of the patient’s plaque has proven to be a powerful motivation for clinicians and for the patient: you have a lump in your coronaries!

🔹 We need to shift the paradigm out of end-stage management and into early interventions that hold the possibility of eradicating the clinical burden of atherosclerotic cardiovascular disease, the #1 cause of death worldwide.

Prevention is the best intervention. Know your numbers: know your blood pressure, lipids, Lp(a), diabetes risk (HgbA1c), family history, pregnancy history, and remember, it’s never too early to see a preventive cardiologist.