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Andreea Nitescu RD MSc, 128 City Road, London (2026)

03/06/2026

We talk a lot about the gut microbiome in longevity — but what about the skin microbiome?

A new 2026 study published today in the journal Microbiome used multi-omics analysis to explore how skin microbes may relate to visible skin aging.
doi: 10.1186/s40168-026-02433-6

One of the most interesting findings was that Stenotrophomonas maltophilia was enriched in individuals with a “younger” skin phenotype, defined using AI-predicted skin age and skin elasticity.

Why is this interesting?

Because this microbe appeared to interact with pathways involved in redox balance — especially the glutathione cycle.

Glutathione is one of the body’s key antioxidant systems, and oxidative stress is a major biological driver of skin aging.

In cell experiments, metabolites from S. maltophilia increased glutathione synthesis and upregulated genes involved in antioxidant defense and stress resilience, including GCLM, PGD, SOD2, and NQO1.

This does NOT mean we should all be putting random bacteria on our skin.

But it does suggest something important:

Your skin is not just a surface.
It is an ecosystem.

And the microbes living there may influence skin biology through metabolites, antioxidant pathways, pigmentation pathways, and host-microbiome signaling.

As a dietitian and molecular biologist, this is exactly why I find microbiome research so exciting. Longevity is not just about calories, collagen, or creams — it is about the biological systems that regulate resilience, inflammation, oxidative stress, and repair.

The gut microbiome gets most of the attention, but the skin microbiome deserves a seat at the longevity table too.

31/05/2026

Summer is one day away – but it's been feeling like summer for quite a few days already: hot, bright and cheerful.

On warm days I often don't feel like eating hot food, so I often gravitate to diverse salads or platters.

Today, I had this colorful mix of:
• potato salad with green beans and peas
• roasted chicken
• boiled egg
• beetroot
• bell peppers
• cucumber
• black olives
• pickled gherkins

It was delicious, refreshing and quick to whip up from leftovers.

Yumm!

31/05/2026

🔹 Your colon cells need fuel.
And under normal conditions, mature colonocytes get an estimated 70–80% of their energy from 𝗯𝘂𝘁𝘆𝗿𝗮𝘁𝗲 oxidation.

But here’s the important part:
you don’t make much butyrate yourself.

Your gut microbes do — but not always in one step.

Dietary fibres and resistant starches feed a microbial food web: some bacteria break them down into smaller sugars and fermentation products, while others convert those into butyrate.

Butyrate is a short-chain fatty acid produced by gut microbes as part of a microbial food web.

Complex carbohydrates are broken down into smaller compounds, and certain bacteria convert these into butyrate.

Your colon cells can then oxidize butyrate for energy — making it part of the basic energy economy of the colon, not just another “gut health” buzzword.

🔹 Meet butyrate.
Butyrate production depends on your microbial ecosystem.

Key butyrate-producing groups include bacteria within genera such as Faecalibacterium, Roseburia, Eubacterium, Anaerobutyricum and related taxa.

If you don't have the right microbes, your gut is not producing enough butyrate to fuel the day-to-day activities of your colon cells.

🔹 Not all gut microbes make butyrate.
But these microbes can't survive if you're not feeding them. If your diet is low in dietary fiber and resistant starch, you may be starving your butyrate-producing bacteria.

🔹 Can I take a probiotic to add these bacteria?
Not quite — at least, not in the way people often imagine.

Most standard probiotics do not contain the major butyrate-producing bacteria we typically look for, such as Faecalibacterium prausnitzii, Agathobacter rectalis, or Roseburia intestinalis.

These organisms are often highly oxygen-sensitive and difficult to formulate as conventional probiotics.

But some probiotics may still support butyrate production indirectly.

Certain strains of Bifidobacterium, Lactobacillus, and newer candidates such as Akkermansia muciniphila may help produce substrates, alter pH, support barrier function, or shape the gut environment in ways that favor butyrate-producing microbes.

So the goal is not always to “add butyrate bacteria.”

Usually, it is to support the ecosystem that allows them to thrive.

🔹 Can I take a butyrate supplement?
Yes — but formulation matters.

Butyrate exists in supplement form, usually as salts such as sodium butyrate, calcium/magnesium butyrate, or as tributyrin.

Some people may benefit from supplemental butyrate, but a key question is whether the formulation actually delivers meaningful butyrate to the lower gut.

Free butyrate and some simple butyrate salts may be absorbed earlier in the digestive tract, which can limit how much reaches the colon.

𝗧𝗿𝗶𝗯𝘂𝘁𝘆𝗿𝗶𝗻 is different: it is a triglyceride made of three butyrate molecules attached to glycerol. It is generally considered a more efficient delivery form because it can act as a prodrug, releasing butyrate during digestion rather than simply providing free butyrate upfront.

That said, supplements are not a replacement for feeding the microbial ecosystem.

Long-term butyrate production still depends on having the right microbes, the right substrates, and the right gut environment.

✨ Feeling lost with persistent gut symptoms?
I use evidence-based, microbiome-informed strategies to support gut health.

Consultations available via the link in the comment section.

29/05/2026

Removing the polyp may be necessary — but it may not be enough.

New research in Cell Host & Microbe suggests that long after adenoma removal, the gut microbiome can still resemble a higher-risk colorectal cancer terrain — and lifestyle may matter even more in that post-polyp window.

The takeaway: colonoscopy matters, but so does what happens after.

Here's the study:
PMID: 42202778

20/05/2026

Oat Groats vs Processed Oats: Not the Same

Oats can be a great breakfast option — but not all oats behave the same metabolically.

Even when an oat product is technically whole grain, processing can change its structure, particle size, starch availability, and digestion speed.

That matters because your body does not only respond to “carbs.”
It responds to food architecture.

Oat groats, steel-cut oats, rolled oats, quick oats, instant oats, and oat flour can produce different glucose curves — especially depending on portion size, cooking method, toppings, and what you eat them with.

The goal is not to fear oats.
The goal is to understand that:
whole grain ≠ always slow glucose response

For better glucose stability, I usually prefer oats closer to their original structure — like oat groats, steel-cut oats, or large-flake rolled oats — and I recommend building the bowl with protein, fat, and fiber.

Think Greek yogurt, chia, flax, nuts, berries, protein powder, or eggs and meat on the side.

Same whole grain.
Different processing.
Different structure.
Potentially different glucose curve.

Swipe to read more →

20/05/2026

My little rosemary + sage bushes are doing important work 🌿

I use them constantly in cooking and teas because culinary herbs are such an easy way to add more polyphenols, aromatic compounds, and diversity to your diet.

Rosemary and sage have been studied for their anti-inflammatory, antimicrobial, and gut-supportive properties, and they also make food taste better — which is very underrated when we talk about healthy eating.

Sometimes I also simmer a few sprigs on the stove to naturally freshen the kitchen.

Tiny garden.
Big flavor.
Longevity habits don’t always have to be complicated.

19/05/2026

⏳ Do glucose spikes matter for longevity?
In my view: absolutely — but with nuance.

This is not about fearing carbohydrates or trying to keep glucose perfectly flat. Glucose rises after eating are normal.

The question is whether your glucose is going too high, too often, and staying elevated for too long.

In longevity research, glucose and insulin signalling are deeply connected to nutrient sensing, metabolic health, inflammation, oxidative stress, cardiovascular risk, and ageing biology. Animal data from the ITP (NIA Intervention Testing Program) also show that glucose-lowering therapeutics like acarbose and canagliflozin can extend late-life survival.

In humans, observational studies suggest that post-meal glucose responses, glucose AUC, and 1-hour or 2-hour glucose after an OGTT may predict long-term risk — sometimes even when fasting glucose or HbA1c look less concerning.

This is where CGMs can be useful.
→ Not because everyone needs to track glucose forever.
→ Not because one spike is harmful.
→ But because understanding your personal glucose response to foods, meal timing, stress, sleep, exercise, and food processing can be incredibly informative.

For longevity-focused nutrition, I care less about “is this food good or bad?” and more about:
How does your body respond to it?

Because one glucose spike won’t age you overnight — but thousands of high glucose excursions over years might matter.

Swipe to read more →

19/05/2026

Yesterday's dinner was one of those simple meals that felt extra special because of the little details: pork cooked in EVOO with freshly picked rosemary from the garden, onions, and all those savory pan juices doing their thing. 🌿

Rosemary is one of my favorite herbs to cook with because it brings so much flavor, along with some interesting gut-supportive compounds.

Its polyphenols, like rosmarinic acid, carnosic acid, and carnosol, may act in a prebiotic-like way by helping support a more favorable gut microbiome environment. Its aromatic oils, including 1,8-cineole, camphor, and α-pinene, also have mild antimicrobial properties, which is one reason rosemary has traditionally been used in food preservation and digestion-supportive cooking.

I served it with steamed carrots and green beans, potato & cauliflower mash, and a delicious gravy made from the pork juices, thickened with arrowroot.

Simple, herby, comforting, and exactly the kind of meal I love making at home. 🥩

15/05/2026

May is Hypermobility/EDS/HSD Awareness Month 🦓

When most people hear “hypermobility,” they picture someone who is very flexible.

But for a lot of people, it is not just about joints that move beyond the usual range.

Connective tissue is found throughout the body — in blood vessels, the gut, skin, fascia, pelvic floor, airway, and around the structures that support nerves and organs.

So when connective tissue behaves differently, the symptoms do not always stay neatly in one place.

This is one of the reasons hypermobility can come with such a confusing mix of symptoms: dizziness, reflux, constipation, IBS-type symptoms, fatigue, brain fog, food reactions, adrenaline surges that feel like anxiety, pelvic pain, TMJ issues, easy bruising, poor exercise tolerance, and pain that seems to move around.

That does not mean every symptom is automatically caused by hypermobility.

But it does mean the pattern is worth looking at properly.

The joints are often the most visible part, but behind the scenes there may also be changes in blood-flow regulation, nervous system compensation, gut motility, histamine or mast cell reactivity, pain signalling, and immune sensitivity.

This is why so many people talk about the overlap between hypermobility, POTS/dysautonomia, and MCAS.

And this is also why “it’s just anxiety” is such an unhelpful answer.

A racing heart, nausea, dizziness, shaking, flushing, breathlessness, or a sudden adrenaline surge can absolutely feel like panic. But in someone with hypermobility, the body may also be responding to changes in blood flow, autonomic signalling, histamine, pain, or gut-brain communication.

The symptoms are real, and they make much more sense when they are seen in context.

Nutrition can matter here too, but not in a generic “eat healthier” way.

From a nutrition and systems-biology perspective, I’m often thinking about the terrain: iron, B12, vitamin D, protein intake, gut motility, constipation, reflux, histamine load, microbiome patterns, blood sugar stability, inflammation, mast cell activation, and how much stress the nervous system is already carrying.

The goal is not to restrict everything or make people afraid of their bodies.

The goal is to understand why the body might be working so hard, and where we can support it so things feel a little more stable.

Hypermobility is not just being bendy.

For many people, it is a whole-body pattern that finally helps explain symptoms they were told were random, unrelated, or “all in their head.”

12/05/2026

📢 PCOS has a new name: PMOS.

Today, 12 May 2026, PCOS was announced as being renamed PMOS: polyendocrine metabolic ovarian syndrome. This was published in The Lancet and announced at the European Congress of Endocrinology 2026 in Prague. The transition is expected to be supported over three years, with full implementation in the 2028 International Guideline update.

Honestly, it’s about time. Especially because PCOS was never “just about cysts”.

As a dietitian, I sometimes meet patients who have 2 out of the 3 Rotterdam criteria — for example, irregular cycles and signs of androgen excess — but because their ultrasound doesn’t show polycystic ovaries, they’ve been told: “You don’t have PCOS.”

At that point, I usually refer them to another doctor.

Because we’ve known for a long time that this condition is not defined by ovarian “cysts”. In fact, many people with PCOS — now PMOS — do not have cysts at all.

PMOS is a much more accurate name because it reflects what this condition actually is: a complex hormonal syndrome, often with metabolic implications, which may affect insulin regulation, weight, skin, cycles, fertility, mood and long-term cardiometabolic health.

It is also a syndrome (meaning an umbrella constellation of signs and symptoms), not one single disease process that looks the same in every person.

My hope is that this name change helps patients be taken more seriously, diagnosed earlier, and treated more holistically.

PCOS was never just an o***y problem.
PMOS makes that clearer.

Andreea Nitescu RD MSc

03/06/2026

31/05/2026

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