Dr. Kara Fitzgerald

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Sandy Hook, CT
Dr. Kara Fitzgerald

Actively engaged in award-winning clinical research on epigenetics & longevity. IFM Faculty & renowned international speaker.

Director of New Frontiers Functional Medicine & Nutrition Clinic. Subscribe to get latest content at www.drkarafitzgerald.com

05/17/2026

It’s not just sugar. It’s what your gut does with it.

New research is shedding light on a critical (and overlooked) driver of liver disease progression, from MASLD to MASH.

Here’s what’s happening: Excess dietary sugar (especially fructose) doesn’t just stress the liver directly.

It alters the gut microbiome→ shifting it toward microbes that produce acetaldehyde (a toxic compound also linked to alcohol metabolism)

That acetaldehyde then travels to the liver, where it can:
• Activate hepatic stellate cells
• Increase MMP-7 expression
• Drive fibrosis progression

In a dataset of 210,000+ individuals, higher sugar intake was associated with increased liver-related mortality, in a clear dose-dependent pattern.

But here’s where it gets interesting:

Researchers were able to interrupt this pathway using a targeted probiotic strain designed to break down acetaldehyde, effectively halting fibrosis progression in preclinical models.

This is a big shift.

We’re not just looking at what we eat, we’re looking at how the microbiome metabolizes it.

And that opens the door to entirely new therapeutic strategies.

If you want to better understand the metabolic impact of fructose (and why it matters so much here),

🎧 Don’t miss my conversation with Robert Lustig. Comment FOOD PYRAMID and we’ll DM you the link.

It will change how you think about sugar.

05/16/2026

What if we could nudge cells toward a more youthful, repair-ready state, without full reprogramming?

A new study on cardiomyocytes (heart cells) explores just that.

Researchers looked at a subset of the Yamanaka factors, specifically OSK (OCT4, SOX2, KLF4), without c-Myc, and found something interesting:

Instead of forcing cells to divide, OSK appears to prime them.
→ Cardiomyocytes entered a more flexible, dedifferentiated state
→ Structural components (sarcomeres) temporarily disassembled
→ This “priming” helped cells overcome key barriers to regeneration
→ Result: improved cardiac repair after myocardial infarction

Not full cellular reprogramming, but a shift in readiness.

This is where things get especially interesting for us.

We’re actively exploring whether key nutrients may support similar biological terrain—not turning back the clock, but helping cells express some of the same regenerative characteristics.

Early days. But an exciting direction.

Because the future of longevity may not be about rewriting cells entirely…
…but helping them remember how to repair.

Source: Yan Y, Huang Y, Cao C ...
OSK-mediated partial reprogramming induces cardiomyocyte dedifferentiation, overcomes cytokinesis barriers, and promotes post-MI endogenous cardiac regeneration
Journal of Molecular and Cellular Cardiology, 2026; 215, 36-50

05/15/2026

In this conversation, Montel Williams shares the moment he realized something was actually shifting in his energy levels after starting mitochondrial support with MitoQ.

We also discuss the connection between inflammation, mitochondrial function, and neurodegenerative conditions like MS and why supporting cellular energy may matter more than we once realized.

This is a powerful conversation about resilience, healing, and the evolving science of mitochondrial medicine.

Comment MONTEL and we’ll DM you the link to the episode, or visit https://www.drkarafitzgerald.com/2026/05/15/montel-williams-mitoq-ms-resilience/.

05/14/2026

Most people think there is one “best” diet for longevity. But the science shows something very different. Following generic trends or influencer driven protocols can actually move you further away from optimal health if they are not aligned with your biology.

In this episode of Extend, I sit down with Darshan Shah to explore why personalized nutrition matters more than any trending diet. I explain how fasting protocols, restrictive diets, and one size fits all approaches can backfire, and why longevity nutrition must be tailored to the individual.

We also cover:
➡️ Why influencer driven diets often fail
➡️ The risks of stacking restrictive protocols like fasting and carnivore
➡️ Why bio-individuality is key in longevity nutrition
➡️ How nutrient diversity supports epigenetic health
➡️ Why the right diet depends on your biology, not trends

🎧 Listen to Episode 160: Dr. Kara Fitzgerald on Biological Age, Epigenetic Clocks, and the Future of Aging Reversal on Apple Podcasts or Spotify.

05/13/2026

When we’re young, our bodies are incredibly efficient at building muscle.

We can take in almost any amino acids (yes, even from less-than-ideal sources) and put them to work.

Muscle growth is responsive. Forgiving. Easy.

But over time, that changes.

We develop what’s called muscle anabolic resistance, a reduced sensitivity to the muscle-building effects of protein.

Same protein intake. Different response.

Which means:
→ We need more intentional protein intake
→ We need the right nutrients to support muscle synthesis
→ And we need to prioritize muscle as a key part of healthy aging

This is one of the most overlooked shifts in midlife physiology.

Also, a small exhale for the parents out there: kids are naturally in a highly anabolic state.
They don’t need perfection. They’re doing more with less.

We, on the other hand?

We need to be a little more strategic.

COMMENT ANABOLIC or head to https://www.drkarafitzgerald.com/2026/04/21/overcome-muscle-anabolic-resistance-nutrients-aging/ for the full blog.

05/12/2026

We’re very good at naming diseases. Less good at asking what’s driving them.

There’s a mechanism showing up across the literature, linking iron dysregulation, lipid damage, and chronic disease progression.

And most clinicians still aren’t looking for it.

It’s called ferroptosis.

And it may be sitting underneath what we diagnose as:
• metabolic dysfunction
• fatty liver disease
• cardiovascular decline
• cognitive aging

This isn’t just another pathway.

It’s a pattern, one that may help explain why some patients don’t fully respond…and where we may be missing intervention opportunities.

Join Dr. Stephanie Venn-Watson and me from fatty15 as we break it down:
✔ How ferroptosis shows up clinically
✔ What to look for (including key biomarkers)
✔ Where it fits into chronic disease progression
✔ Why this may represent a correctable deficiency state
✔ What emerging strategies could look like in practice

If you’re thinking, “this might explain a few of my patients…” you’re probably right.

👉 Save your spot. Comment ferroptosis and we’ll DM you the link or head to https://www.drkarafitzgerald.com/2026/05/04/ferroptosis-aging-biomarkers-treatment/ to register

05/11/2026

It’s not A1C.
Not LDL.
It’s Lipopolysaccharide (LPS).

An endotoxin that enters circulation when gut barrier function is compromised, quietly driving systemic inflammation.

And the data are hard to ignore:
→ In a 9-year cohort, LPS was the only biomarker that predicted both the presence and severity of anxiety and depression
→ Tracks with progression from prediabetes to diabetes
→ Drives hypothalamic inflammation → central insulin resistance
→ Associated with chronic low-grade inflammation and even skin conditions like acne

In women, this becomes especially relevant.
As estrogen declines in peri- and menopause:
↓ microbiome diversity
↑ intestinal permeability
↑ LPS translocation
Shifting the body toward a more inflammatory, catabolic state.

LPS isn’t just a marker. It’s a signal.

And if you’re not addressing it, you may be missing a root driver of metabolic and neurological decline.

COMMENT NITRIC or head to https://www.drkarafitzgerald.com/2026/05/05/perimenopause-gut-cardiovascular/) for my full conversation with Kiran Krishnan from Calroy Health Sciences .

05/10/2026

It all starts with mom, even your cells. 🧬💛

Today I’m thinking about something pretty amazing: all of our mitochondria, the little engines that power every cell in our body, come directly from our mothers.

It’s a reminder that the energy we use to move through the world, to heal, to thrive; it all begins with them.

So here’s to the moms, grandmothers, and mother figures who gave us more than we can ever fully appreciate, starting with the very first spark.

Happy Mother’s Day. 🌸

05/09/2026

How you brew your coffee matters more than you think.

Unfiltered methods (French press, espresso) let a compound called cafestol through, which has been shown to raise LDL by ~5–10 mg/dL in clinical trials.

Paper filters? They trap most of it.

In a 20-year study of 500,000+ people, filter coffee was linked to lower mortality, while unfiltered showed a signal toward higher cardiovascular risk in older men.

This isn’t about cutting coffee; it’s about how you make it.

If you’re watching lipids or cardiovascular risk, a simple switch to paper-filtered coffee may be worth considering.

Sources: Tverdal, Eur J Prev Cardiol, 2020, Cai, Eur J Clin Nutr, 2012, Cornelis & van Dam, J Nutr, 2020, Urgert, BMJ, 1996, Ludwig, Food & Function, 2014, Orrje, Nutr Metab Cardiovasc Dis, 2025, Rendón, Food Res Int, 2017

05/08/2026

Alcohol consumption is shifting, and quickly.

Recent data suggests fewer Americans are drinking, and younger generations are leading the change. But the conversation deserves nuance.

Yes, alcohol is a known carcinogen.
Yes, even moderate intake carries measurable risk.
And yes, our understanding of alcohol and health has evolved significantly over the last decade.

But behavior change isn’t just about fear or headlines. It’s about informed, sustainable choices.

In clinical practice, I see a growing number of patients asking better questions:
How does alcohol affect my hormones?
My sleep?
My long-term disease risk?

This is where the real opportunity lies, not in absolutism, but in awareness.

If you choose to drink, do so intentionally.

If you’re reconsidering your relationship with alcohol, you’re not alone.

This is what a more informed, prevention-focused culture looks like.

Source: Source: Gallup Poll, 2026 (U.S. adults) https://news.gallup.com/poll/693362/drinking-rate-new-low-alcohol-concerns-surge.aspx

05/07/2026

Colon cancer at 35. A legacy herbicide. And the epigenome holds clues. 🧬 Read to the end.

⬇️⬇️⬇️

A recent paper in Nature Medicine adds an important layer to how we think about environmental exposures and early-onset cancer.

Researchers used epigenetic profiling to compare tumor tissue from individuals under 50 with those over 70 and identified distinct exposure-linked signatures.

One signal that emerged in the analysis: Picloram, a herbicide first introduced in 1963 and still in use today.

📊 Context from the data
• Rising rates of colorectal cancer in younger populations
• Geographic variation in incidence alongside agricultural use patterns
• Associations that persisted after adjusting for multiple confounders

🧠 Why this matters clinically
For years, I’ve emphasized that environmental inputs can influence gene expression not only through direct toxicity, but through epigenetic signaling: subtle, cumulative shifts in how genes are regulated over time.

This study doesn’t establish causation. But it does highlight something I believe is critical: 👉 Our exposures may leave biological “imprints” that are measurable in human tissue.

💡 The bigger picture
What’s most compelling here is the approach: using epigenetic patterns within tumors to better understand long-term environmental influences.

If validated and refined, this could expand how we evaluate chemical safety, moving beyond short-term toxicity toward long-term biological impact.

💬 I’m curious. Does this shift how you think about environmental exposures and risk?

♻️ Share with a colleague who’s thinking about early-onset disease.

Source: https://doi.org/10.1038/s41591-026-04342-5

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http://www.drkarafitzgerald.com/

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