Season 1 Episode 10: Inflammation + Season 1 Wrap-Up

Inflammation! 

We use the word all day in the clinic. We blame it for half the problems in medicine. Yet when you strip it down to its core, inflammation is one of the most misunderstood forces in cardiometabolic medicine. 

In this episode of LipidCurious, we discuss

1.    What is inflammation?

2.    How do we measure it?

3.    How do we treat it?

By the end, you’ll walk away with a sharper, cleaner understanding of inflammation’s role in cardiometabolic disease — and how to act on it in everyday practice. 

And finally, a heartfelt wrap-up of Season 1, the journey behind building LipidCurious, and where this platform may go next. 

Bonus: For the full collection of visuals across Season 1, visit the Podcast page.

Download the Free LipidCurious Starter Kit here

Questions or feedback? Reach out at hello@lipidcurious.com 

Disclaimer: This podcast is for educational purposes only. It is NOT medical advice.

Transcript

SEASON 1 EPISODE 10: Inflammation + Season 1 Wrap-Up 

Hi everyone,

I thought we wrapped up LipidCurious Season 1 pretty neatly we spoke about lipids, triglycerides, fatty acids, cholesterol, lipoproteins, lipid pathways, ApoB, Lp(a), and even the birth of an atherosclerotic plaque. 

It felt like one big lipid family reunion, and everyone showed up. 

And then I remembered we’d barely touched one of the most overused and under-explained concepts in medicine: Inflammation.

Inflammation is one of those ideas I thought I understood in med school… assumed I still remembered. We use the word all day in the clinic. We blame it for half the problems in medicine.

But the moment I asked myself, “If someone forced me to explain inflammation in one sentence, could I actually do it?” I had to pause.

So today, we’re fixing that with a clear, short note on inflammation.

Welcome to LipidCurious, the podcast dedicated to simplifying lipids for clinicians.
I’m your host, Dr. Vishnu Priya Pulipati, a board-certified Endocrinologist and Lipidologist.

This is Season 1, Episode 10: Inflammation.

Here’s what we’ll cover today:

1.    What is inflammation?

2.    How do we measure it?

3.    How do we treat it?

And finally, a heartfelt wrap-up of Season 1  

If you’re new here, welcome. This season builds step by step, so you might want to start with Episode 1 to get the full picture. 

You’ll find the bonus visual handouts for every episode plus the free Starter Kit at www.lipidcurious.com.

And as always, this podcast is for educational purposes only, not medical advice.

Alright, let’s dive in.

What is inflammation?

Inflammation is the body’s built-in emergency response to an injury, infection, or irritation.

The five classic signs of inflammation are: redness, warmth, swelling, pain, and loss of function.

Here’s the play-by-play:

• After an insult such as injury, cells release chemical messengers like histamine and prostaglandins.
• Blood vessels widen → more blood flow → redness and warmth.
• Vessels get leaky → immune cells rush in → swelling and pain.
• That pain is partly mechanical and partly a protective signal, your body’s way of saying, “Hey, don’t mess with this while we fix it.”
• Immune cells clean up debris, fight pathogens, and start repairs.

This entire process is normal, essential, and adaptive.

Without inflammation, wounds wouldn’t heal. Even a paper cut would be life-threatening.

But, and here’s the catch, inflammation is helpful only when it’s short-lived and targeted.

Now, there is no perfect cut-off for what's considered acute vs. chronic. But, in general, acute inflammation is sharp and focused, resolving within 1 month.

Chronic inflammation is slow, quiet, and persistent lasts more than 3 months to years. Chronic inflammation shows up with metabolic dysfunction, autoimmune conditions, poor sleep, smoking, obesity, stress, chronic infections and sometimes we don’t even feel it.

This chronic, low-grade background inflammation is the kind that directly ties to cardiovascular disease. 

And here’s the key connection:

If ApoB-containing particles are the “spark,”
Inflammation is the fuel that keeps the fire burning.
You need both for atherosclerosis to grow, progress, and rupture.

Inflammation worsens endothelial dysfunction, pulls immune cells into the arterial wall, promotes foam cell formation, drives oxidative stress, and expands the necrotic core.
 It’s not a side character, it’s in every scene of plaque development.

How do we measure inflammation?

In real-world practice, one biomarker stands far above the rest: hsCRP or high sensitivity C-reactive protein

It’s quick. It’s cheap. It’s widely available.
 And it predicts cardiovascular risk as strongly as blood pressure or cholesterol.

Here’s how we interpret it:

• <1 mg/L → lower risk
• 1–3 mg/L → average risk
• >3 mg/L → higher relative risk
• >10 mg/L → think infection; repeat in 2–3 weeks

Other biomarkers exist such as serum amyloid A, interleukin-6, fibrinogen, white blood cell count, neutrophil-to-lymphocyte ratio, lipoprotein-associated phospholipase-A2, myeloperoxidase, eicosapentaenoic acid/arachidonic acid ratio; but none of them beat hsCRP in terms of practicality or regulatory recognition.

And clinicians don’t act on numbers they never check
 Which is why universal hsCRP screening is recommended in both primary and secondary prevention (as long as the patient isn’t acutely ill).

Imaging?

Yes, CT, MRI, ultrasound, and PET with FDG can visualize vascular inflammation in research, but they are not routinely used in clinical practice.

How do we treat inflammation?

There are three main treatments for inflammation: Lifestyle, lifestyle, and lifestyle! And it works.

• Mediterranean or DASH diet. 
• Plenty of fruits, vegetables, whole grains, legumes, nuts, and olive oil
• Omega-3s: aim for 2–3 servings of fatty fish per week
• Minimize red/processed meat, sugary drinks, refined carbs
• Regular exercise: 150 min moderate / 75 min vigorous per week
• Quit smoking
• Maintain a healthy weight

Medications: We currently have two options available.

1.    Statins lower LDL and inflammation. In primary prevention, a persistently elevated hsCRP, especially >3 mg/L, is a reason to initiate or intensify statin therapy, regardless of LDL. On statins, but hsCRP still >2 mg/L? Consider higher intensity.

2.    Low-dose colchicine is now FDA-approved for reducing CV events in stable ASCVD. It’s an adjunct to lipid-lowering, not a replacement.  It does not help if started during acute ischemia. Avoid in significant renal or liver disease.

Inflammation is no longer just a background character. It’s a modifiable risk factor.

These are the 3 take-home points

1.    Chronic, low-grade inflammation is directly tied to cardiovascular disease. You need both ApoB particles and inflammation for atherosclerotic plaque to grow, progress, and rupture.

2.    hsCRP is the most practical inflammatory marker we have. Use it.

3.    Lifestyle is your strongest anti-inflammatory prescription, other options include statins and low dose colchicine

Alright folks,

If you’ve been here since Episode 1, thank you.
Your curiosity is what made this season come alive. 

You showed up for ten episodes of pathways, particles, metabolism, and biology. And you stayed engaged through all of it.

When I started LipidCurious, I didn’t have a grand plan, a strategy, or a budget. We already have incredible resources that break down trials, guidelines, and therapies. I just felt something was missing in our usual lipid conversations: a bridge back to the foundations. It started from a space of inspiration.

You showed that clinicians want clarity, that foundations matter, and that lipid science can actually feel exciting when it’s understood in a way that makes sense.

Along the way, many of you reached out with questions, insights, and encouragement. That feedback shaped this season more than you know.Your messages reminded me that this effort mattered, that there was a need for this kind of conversation.

Of course, I had moments where I wondered, “Why am I doing this? And for whom?”
 But LipidCurious gave me confidence, a creative outlet, and a deeper connection to a field I love. I learned and unlearned so much along the way. And every time I reached out to a mentor with a question, they responded with contagious enthusiasm. That energy reminded me why curiosity matters.

And somewhere between Episode 1 and Episode 10, it became clear that LipidCurious isn’t just about lipids. It’s about prevention, lifespan, and the quiet power of small changes.

So, what’s next?

Season 1 will remain available until May 2026 while we take a thoughtful pause. The future depends on time, resources, and where this community wants to go. And your input matters here — more than ever.

If this platform has supported your learning, and you’d like to see it grow — whether through collaboration, sharing it with colleagues, or small contributions — you’re always welcome to reach out. If you have ideas for episodes, partnerships with societies, or creative ways to expand this mission, I’m listening.

You can always reach me at hello@lipidcurious.com.
 And don’t forget to grab the free Starter Kit and the Season 1 Visual Guide at www.lipidcurious.com.

To the mentors, colleagues, and every listener who believed that curiosity deserves space — thank you. This has been one of the most meaningful projects of my career, and it’s because of you.

Whether this is a pause or a beginning of something new — thank you for being part of the LipidCurious community.

Until next time — stay curious, and stay confident.

Signing off, Dr. Pulipati.

Bonus: For the full collection of visuals across Season 1 episodes, visit the Podcast page.

Download the Free LipidCurious Starter Kit here

Questions or feedback? Reach out at hello@lipidcurious.com