I was recently asked by The Times to comment on a fascinating story. A journalist in their 30s found that after switching to a vegetarian diet, their chronic hay fever—which had plagued them for years—suddenly and dramatically improved.

Was this just a happy coincidence, or is there a biological link between what we put on our plates and how our noses react to pollen?

The Gut: Your Immune System’s Training Ground

To understand hay fever, you have to look past the nose and down into the gut. It might surprise you to learn that 70% of your immune system lives in your gut.

Our immune system doesn’t operate in a vacuum; it is constantly being “trained” by the trillions of microbes in our microbiome. From early life, these microbes teach our immune cells what is a genuine threat (like a pathogen) and what is harmless (like pollen).

When your microbiome is diverse and well-balanced, your immune system is “tolerant.” But when that balance is thrown off, the system becomes hyper-reactive. It starts launching full-scale attacks on harmless pollen, leading to the inflammation we know as hay fever.

What the Research Tells Us

We are seeing increasingly strong evidence that dietary patterns dictate our allergy risk:

• The Plant Powerhouse: Large epidemiological studies show that people who follow plant-rich, high-fiber diets (like the classic Mediterranean diet) suffer from significantly fewer allergies. These fibers feed beneficial microbes that produce anti-inflammatory compounds.

• The UPF Penalty: On the flip side, diets high in ultra-processed foods (UPFs) and low in fiber are linked to a doubling of the risk for allergic conditions. UPFs drive the very inflammation that makes an allergic response worse.

• The Probiotic Signal: A meta-analysis of over 30 randomized controlled trials found a small but consistent signal: probiotics can reduce allergy scores. They appear to shift the immune balance (technically known as the Th1 to Th2 ratio), resulting in significant improvements in nasal symptoms.

Is There a “Silver Bullet”?

While the data on probiotics is encouraging, it isn’t a “cure-all.” Because everyone has a unique gut microbiome, a probiotic that works for one person might do nothing for another.

This is why I believe the bigger picture—the overall health of your “microbial garden”—is far more important than any single supplement. By building up your internal resilience and tolerance through food, you are giving your immune system the best chance to stay calm when the pollen count rises.

My Takeaway

There isn’t a definitive clinical trial yet that proves a diet change will “cure” your hay fever. However, the anecdotal evidence is mounting, and the biological reasoning is sound.

If you suffer from seasonal allergies, spring is the perfect time to experiment. Unlike antihistamines, which can leave you feeling drowsy or “flat,” the “side effects” of improving your gut health are entirely positive—ranging from better energy to improved mental clarity.

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🌿 Tim’s Hay Fever Protocol:

1. The Rule of 30: Aim for 30 different plants a week. Diversity in plants leads to diversity in the microbes that calm your immune system.

2. Eat the Rainbow: Focus on high-color vegetables. These are packed with polyphenols, which act as fuel for your “good” bacteria and have natural anti-inflammatory properties.

3. The “Three-a-Day” Ferment Rule: Include three small portions of fermented foods (kefir, kombucha, sauerkraut, or kimchi) every day to support your gut lining.

4. Cut the UPFs: Reduce ultra-processed snacks and meals, which act as “pro-inflammatory” triggers for your immune system.

5. Stop Late-Night Snacking: Give your gut microbes a rest. A longer overnight fast (at least 12–14 hours) allows the “cleaner” microbes to repair the gut lining.

6. Trial a Prebiotic: If you want to go a step further, consider a high-quality prebiotic like the ZOE Daily 30. Our trials show it significantly increases the number of healthy microbes in the gut, which may help bolster that all-important immune tolerance.

The Bottom Line: Your diet might not just change your health—it might just help you breathe a little easier this summer.

I recently returned from a microbiome conference in Serbia where the atmosphere was electric. My colleagues and I were discussing a wave of new research that is turning our traditional view of the “mind-body connection” completely on its head.

For decades, we viewed the brain as the master commander and the gut as a mere subordinate—receiving orders to speed up or slow down digestion. We now know that the reality is far more “bottom-up” than we ever dared to imagine.

The Longest Highway in the Body

The Vagus nerve is the longest cranial nerve we have. It is the only one that travels outside of the head, stretching roughly 50 centimeters down through the neck, past the heart and lungs, and weaving itself into every corner of the gut.

The real bombshell? 80% of the traffic on this highway is one-way, from the gut back to the brain.

Rather than the brain telling the gut how to feel, the gut is constantly “reporting” to the brain on the state of our internal world. It is the primary way the brain keeps up with our physiology, and the “reporters” filing those reports are your gut microbes.

Microbial Messengers

Recent studies published in journals like Nature have mapped out exactly how our microbes “talk” to the endpoints of the Vagus nerve. They do this through a variety of chemical signals called metabolites:

• The Good Guys (SCFAs): Microbes ferment fiber to produce Short-Chain Fatty Acids. These send beneficial, anti-inflammatory signals up to the brain.

• The Disruptors (MCFAs): We’re now learning about Medium-Chain Fatty Acids produced by certain bacteria. Unlike their short-chain cousins, these can actually inhibit Vagal signals and trigger general inflammation.

• Direct Stimulation: Microbes can even trigger immune cells to release signals or use their own cell wall components (like lipopolysaccharides) to “poke” the nerve directly.

Rewriting the Rules of Reward and Addiction

Perhaps the most ground-breaking research, including a study in Science Advances by Onimus et al., shows that this gut-brain axis actually governs the reward mechanisms in our brainstem and hypothalamus.

This explains a phenomenon we are seeing globally with GLP-1 drugs like Ozempic. These drugs mimic gut hormones to signal the brain, but patients often find that their addictions—to alcohol, smoking, or shopping—simply vanish. This isn’t a coincidence. By modulating the signals traveling up the Vagus nerve, we are directly tapping into the brain’s “addiction centers.”

It turns out that your “willpower” might actually be a reflection of the chemical signals being sent by your microbiome. My colleague Dr Federica Amati’s new book ‘The Appetite Reset’ covers this in fascinating detail.

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My Takeaway

Every year, the science moves further away from the idea that we are “thinking” beings who happen to have a digestive system. Instead, we are starting to see that our gut microbiomes are really the ones in charge.

If we want to fix our mental health, our cravings, and our moods, we have to stop looking only at the “top floor.” We have to look at the “engine room”—the trillions of microbes that are currently dictating what your brain should do next.

🧠 Tim’s Tips for a Healthy Gut-Brain Axis:

• Feed the “Good” Signals: To increase those beneficial Short-Chain Fatty Acids, you must eat a diverse range of fiber. Aim for 30 plants a week to ensure your microbes have the fuel they need to send “happy” signals to your brain.

• The Fermentation Effect: Traditional fermented foods (like kefir, kimchi, and kombucha) provide the “live” signals that help prime the Vagus nerve and support immune regulation.

• Listen to Your “Gut Feeling”: That phrase exists for a reason. Often, feelings of anxiety or “butterflies” are literal signals from your Vagus nerve. Before reaching for a pill, consider if you’ve been reaching for too much ultra-processed food.

The Bottom Line: You are not just what you eat; you are what your microbes tell your brain you are. Look after them, and they will look after your mind.

Recent statistics show that Ebbw Vale is now one of the most overweight places in the UK. The numbers are truly stark: nearly 40% of residents are obese, and more than 70% are overweight. Even more concerningly, the wider county records the highest female mortality rates in the country.

These aren’t just statistics on a spreadsheet; they are a clear signal of a community in a downward spiral, facing deep-rooted health and economic challenges. But Ebbw Vale isn’t an outlier—it’s a magnifying glass for a problem playing out across the entire country.

A Masterclass in a “Broken Food Environment”

When you walk through the town center, the problem becomes visible. The landscape is dominated by a “food swamp” of fast-food outlets: burgers, fried chicken, kebabs, and pizza.

Where is the real food?

• The thriving local market has all but disappeared.

• There is now just one butcher serving the entire town.

• “Eating in the street” has become the norm, while cooking at home has become the exception.

This is what a broken food environment looks like. It is a world where the easiest, cheapest, and most visible options are also the most damaging to our health. When ultra-processed foods are the only accessible fuel, we cannot blame the individual for the outcome.

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What Can a Local Council Actually Do?

The local council is now asking the right questions, but the answers require more than just a few posters. While their first instinct—restricting the advertising of ultra-processed foods—is a reasonable start, it won’t be enough on its own.

To truly turn the tide, we need a structural “reset” of what normal eating looks like:

1. Lead by Example: Every school, hospital, and council-run building must serve real, minimally processed food. We need to stop feeding our most vulnerable citizens the very UPFs that drive disease.

2. Change the Retail Landscape: Local authorities have the power to limit new fast-food licenses. They can use business rates and rent incentives to support the “good guys”—greengrocers, markets, and whole-food retailers.

3. Rebuild Food Culture: We need to make cooking a normal, accessible skill again through subsidized community kitchens and food education in schools.

4. Make Healthy the Easy Choice: Lowering rents for fruit and veg shops and supporting local supply chains ensures that fresh food isn’t just available—it’s affordable.

The Elephant in the Room: National Policy

As much as I admire the proactive stance of Ebbw Vale’s local authority, no town is an island. A council cannot compete with the multi-billion-pound advertising budgets of global UPF corporations that reach our children through social media and streaming services.

If we are serious about prevention, local action must be matched by national will. We need:

• Stronger regulation of junk food marketing.

• Fiscal measures, including meaningful taxes on UPFs.

• A shift in NHS spending toward public health infrastructure and prevention.

The costs of inaction are staggering—not just in NHS spending, but in lost productivity and rising welfare dependency.

My Final Word

Ebbw Vale has recognised it has a problem, and that is the first step toward a cure. It will not be a quick fix, but it is possible.

If this town can successfully push back against the tide of ultra-processed foods and rebuild its food culture, it could become a blueprint for the rest of the UK. I say good luck to them; we should all be watching closely.

🍎 How to Fight the “Food Swamp” in Your Own Life:

• The 80% Rule: Aim for at least 80% of your diet to be whole foods. If it comes in a packet with more than five ingredients (especially ones you don’t recognize), it’s likely a UPF.

• Diversify Your Basket: Try to find your local butcher or greengrocer. Supporting these independent shops isn’t just good for your health; it’s vital for the survival of your community’s food culture.

• Advocate Locally: Ask your local school or workplace what they are doing to reduce ultra-processed options on their menus. Change often starts with a single question.

Mushrooms are often lumped into the vegetable category, but they are genetically closer to humans than they are to plants. Because they belong to a distinct kingdom, they offer a nutritional profile that is entirely unique.

If you aren’t already making mushrooms a staple of your weekly shop, here is why you should start.

Beyond the Plant Kingdom

Unlike plants, which have cell walls made of cellulose, mushrooms have cell walls made of chitin. This provides a unique type of fiber that our gut microbes love.

When you cook or dry a mushroom, you remove the water and are left with a powerhouse of nutrition: a full range of B vitamins, a surprising amount of protein, and essential minerals like selenium. They are also one of the few non-animal sources of Vitamin D; in fact, a single serving can provide about a quarter of your daily requirement.

The Secret Weapon: Ergothioneine (ET)

The most exciting part of mushroom science right now is a specific amino acid called ergothioneine (ET).

ET is a powerful antioxidant that humans cannot produce ourselves; we have to get it from our food. What makes it fascinating is that humans have actually evolved a highly specific transporter protein just to move ET around our bodies. This suggests it plays a critical role in our biology.

Some scientists have dubbed ET the “longevity vitamin.” It helps reduce oxidative stress and aids our gut microbes in fighting inflammation. While all mushrooms contain some ET, the levels vary wildly:

• The King: The Boletus variety (known as Porcini in Italy or Seps in France) has the highest levels.

• The Runners Up: Oyster and Shiitake mushrooms are also excellent sources.

• A Note on Cooking: Be careful not to overboil your mushrooms, as you can leach out that “magical” ET into the water. Sautéing or roasting is much better for preserving these benefits.

What Does the Science Actually Say?

As always, we have to look at the data. In Asia, mushrooms have been used as remedies for thousands of years, but Western clinical trials are still catching up.

We have some very compelling “association” studies. For instance, a study of 36,000 Japanese men showed a clear inverse relationship between mushroom consumption and the development of prostate cancer. Similar trends have been seen in meta-analyses regarding women and breast cancer.

The most striking evidence comes from a Cochrane review of five randomized trials looking at Reishi mushrooms in cancer patients. While the study quality was described as “patchy,” the researchers found a 50% improvement in clinical response in patients who took Reishi supplements alongside their chemotherapy. It appears to act as an immune-system primer, helping the body fight back more effectively.

My Takeaway

We are currently seeing a huge surge in “functional” or “adaptogenic” mushrooms. While many of the marketing claims remain unproven, the underlying science is solid: mushrooms are a potent tool for our immune systems.

The evidence for mushrooms as a “superfood” might not be 100% “proven” in long-term human trials yet, but the theoretical benefits and the lack of downside make them a no-brainer.

The Bottom Line: Eat more mushrooms. I certainly do. In fact, if I were undergoing treatment for an immune problem or chemotherapy, I would be making sure to eat them every single day.

Daily30 contains mushrooms

🍄 Tim’s Tips for Maximum Benefit:

1. Diversify your fungi: Don’t just stick to white button mushrooms. Try oyster, shiitake, and porcini to get a broader range of polyphenols.

2. Sun-dry your mushrooms: If you leave shop-bought mushrooms on a sunny windowsill for a few hours, their Vitamin D content can skyrocket.

3. Think Umami: Mushrooms are a “cheaty” way to add deep, savory flavor to meals without excess salt or ultra-processed seasonings.

The study, from Sapien Labs, shows a dramatic decline in mental health among younger generations, particularly those aged 18–34. What’s striking is how different this looks compared to older adults.

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In the early 2000s, younger people actually reported better mental wellbeing than older generations. That pattern has now flipped. Today, young adults are around four times more likely to report mental health problems than people over 60.

This isn’t a small or local effect. It shows up across most of the world.

What’s driving the decline?

The researchers point to four main factors that consistently track with poorer mental health in younger people:

1. Growing up with smartphones from early childhood

2. High consumption of ultra-processed foods (UPFs)

3. Weaker family and social bonds

4. Lower levels of spirituality or sense of meaning (not necessarily religion, but social cohesion and purpose)

When the data are broken down by country, the patterns become even clearer.

Find out more about UPFs here

The UK and US stand out — and not in a good way

In the UK, average mental health scores were:

• 78 out of 100 for people aged 55+

• Just 20 for those under 35

That puts the UK among the worst-performing countries in the study.

The US shows a similar pattern. Mental health scores for over-55s were strong, but far lower for younger adults. Notably, the US also leads the world in ultra-processed food consumption.

One region bucked the trend: sub-Saharan Africa, where younger people did not show the same steep decline. That alone should make us stop and think about what aspects of modern lifestyles are driving this elsewhere.

Is this just COVID?

The timing matters. Mental health in older adults has remained relatively stable since 2019. The sharp decline is concentrated almost entirely in younger groups — and it starts around the same time.

COVID may have played a role, but this pattern also appears in countries that were less affected by lockdowns. That suggests something broader and more structural is going on.

More on mental health here

So what can we actually change?

Some of these factors are hard to tackle quickly. Family structures and social cohesion don’t change overnight. Regulating smartphones for children is starting to happen in some countries, but progress is slow and fiercely resisted by tech companies.

One factor is immediately modifiable: diet.

Ultra-processed foods are strongly linked with poorer mental health in this dataset, just as they are with metabolic disease. This fits with what we’ve seen repeatedly in ZOE research.

The good news? You don’t need perfection.

If we focus on cutting out the worst 25% of ultra-processed foods — the high-risk products full of refined starches, sugars, additives, and industrial fats — we could see meaningful improvements in mental as well as physical health.

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The bottom line

This report should be a wake-up call. We’re asking younger generations to live in environments that are biologically and psychologically hostile and then acting surprised when mental health collapses.

The crisis isn’t inevitable. Much of it is preventable.

And if governments are serious about mental health, they’ll need to look well beyond therapy apps and start with the food system.

In good health,

Tim

Recently, I was offered a new blood test that can detect one of the earliest biological signals of Alzheimer’s disease, the most common cause of dementia. I paused. Not because the science isn’t extraordinary—it is—but because the personal implications are profound.

The test measures a protein in the blood called plasma P-tau-217. In simple terms, it looks at a specific chemical change in a tau protein that we know is central to Alzheimer’s disease. Tau proteins, when they misbehave, form tangles inside brain cells. These tangles are one of the hallmarks of Alzheimer’s, alongside amyloid plaques.

What makes this test revolutionary is not just that it can identify people at very high risk of developing Alzheimer’s, but that new research suggests it may also tell us how long it might be until symptoms begin.

A paper published this week in Nature Medicine suggests this blood marker acts a bit like a biological clock. Once it becomes abnormal, it tracks a slow, predictable journey: from invisible molecular changes, to subtle brain damage, to mild cognitive impairment, and eventually to dementia. This process can take a decade or more.

That long gap is crucial.

Until now, diagnosing Alzheimer’s early has been incredibly difficult. Brain scans often pick up changes late. Lumbar punctures to test spinal fluid are invasive and unpleasant. Brain biopsies—thankfully—are not an option. For over 20 years, researchers have been trying to develop reliable blood tests, and only recently has the technology become accurate enough for clinical use.

Better Brain Health Guide

In the US, the FDA has now approved several of these blood tests. They are impressively predictive. If P-tau-217 is significantly raised, there’s around a 90% chance that Alzheimer’s pathology is present.

So when I was offered the test, I took it.

Mine was negative, and I felt an immediate sense of relief. That reaction surprised me. I hadn’t realised how heavy the knowledge might feel until the possibility of a positive result became real.

Imagine being told: you’re very likely to develop dementia, but probably not for another 10 years. What would you do with that information? Change your lifestyle? Try experimental drugs? Worry quietly? Or live differently?

At the moment, this is where things get uncomfortable. While we’re making huge strides in detection, we still have relatively few proven ways to delay or prevent Alzheimer’s once these biological changes have started. That imbalance—early diagnosis without effective early treatment—raises ethical and psychological questions we’re only beginning to grapple with.

For now, I think the most immediate value of this test lies in research. It could transform drug trials. Instead of waiting years to see whether a treatment works, researchers could use this “P-tau clock” to see whether a drug slows, stops, or even reverses disease progression at a very early stage.

That would be a genuine breakthrough.

All the evidence we have suggests that if we’re going to prevent or meaningfully treat Alzheimer’s, we need to intervene before symptoms appear—just as we’re learning with other neurodegenerative diseases like Parkinson’s, which may begin many years earlier in the gut rather than the brain.

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So this test represents both hope and a challenge. Hope, because we can finally see the disease process unfolding in real time. Challenge, because knowing earlier forces us to ask difficult questions about what we do with that knowledge.

We’re entering an era where dementia may no longer arrive unannounced. The science is moving fast. Now we need to catch up—clinically, ethically, and socially—to make sure that early detection leads not just to early fear, but to early action.

Best,

Tim

The short answer is no. But I understand why so many people think they do — because until recently, I was one of them.

Like many people in my age group, I’ve had a long-running interest in statins. The epidemiological evidence is actually overwhelming: for most people with even a moderate risk of heart disease, the benefits of taking statins far outweigh the downsides. We now have over 20 years of high-quality research showing that these drugs are effective. They don’t just reduce LDL cholesterol; they also lower inflammation, which is why their benefits extend beyond heart disease to a range of conditions associated with inflammation and ageing.

Despite knowing this, I avoided taking statins for nearly a decade. I’d been flagged as “high risk” since my early 60s — mildly raised blood pressure, a strong family history, and a father who died of a heart attack at 57. I ticked all the boxes. But like many people, I wasn’t fully convinced, and I was particularly concerned about side effects. Muscle pain, cramps, weakness — these stories are everywhere.

So when I was advised about a year ago that I should really start statins, I did so with some trepidation. And, interestingly, about two weeks in, I started experiencing quite severe night cramps. I’d had cramps before, but these felt worse. Naturally, I assumed the statins were to blame. Muscle cramps are, after all, clearly listed on the patient information leaflet.

Read more about cholesterol here

I stopped taking the statin, and the cramps continued. I restarted it, and the cramps were still there. At that point, I was genuinely confused. Was this a side effect, or was I simply noticing something I’d already been experiencing?

This question became particularly relevant when I read a major new meta-analysis published in The Lancet. The researchers examined randomised controlled trials of statins — crucially including studies with proper placebo groups, where participants didn’t know whether they were taking the statin or a dummy pill. Across these trials, statin labels list 66 possible side effects, ranging from muscle symptoms and liver changes to mood disturbances, sleep problems, tingling sensations, memory loss, and depression. It’s hardly surprising that many people stop taking them.

But when the data were analysed properly, something remarkable emerged. Of those 66 reported side effects, 62 disappeared. In other words, they occurred just as often in people taking the placebo as in those taking the statin. Only four side effects showed consistent evidence of being genuinely caused by the drug.

This tells us something important — and uncomfortable — about how powerful expectations can be. Reading long lists of adverse effects doesn’t just inform us; it can actively shape what we feel. This isn’t people “imagining” symptoms in a dismissive sense. The symptoms are real. But the cause isn’t the drug — it’s the expectation.

There are genuine side effects to be aware of. Rare liver enzyme changes, very uncommon muscle injury, or specific tissue reactions are real and should always be monitored. But the vast majority of commonly feared symptoms don’t stand up when tested rigorously.

The takeaway isn’t that we should ignore medical information or dismiss people’s experiences. It’s that we need to be far more careful about how we communicate risk. When we overwhelm people with poorly contextualised lists of potential harms, we may actually be doing more damage than good — particularly when the benefits of a treatment are so substantial.

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Statins save lives. For people at increased cardiovascular risk, avoiding them because of misunderstood side effects may be one of the biggest missed opportunities in modern medicine. And sometimes, paradoxically, reading less and understanding more is the healthier choice.

There’s a term for this phenomenon. When an expectation leads to a negative effect, it’s called the nocebo. When it leads to a positive one, it’s the placebo. Both are extremely common, well-documented, and very real. They’re not about pretending or exaggerating symptoms — they’re about how powerfully the brain and body interact.

So my practical advice is this. Before you start a new medication, especially one with strong evidence behind it, I wouldn’t rush to read the patient information leaflet in detail. Much of it is outdated, poorly contextualised, and more likely to alarm than inform — particularly if you know you’re sensitive to these things. Instead, try the medication with an open mind, pay attention to how you actually feel, and stay in dialogue with your clinician. You may well find yourself in a better place for having done so.

Good luck.

Tim

During a recent trip to Japan, I kept coming back to the same question:

Why are obesity rates roughly five times lower than in the United Kingdom?

Rates are creeping up slowly among Japanese adults. But unlike the UK, they’re not rising in children. And Japan is starting from a far lower baseline.

At first glance, it doesn’t make sense.

Both are island nations. Both love snacks. Both have busy lives, convenience foods, sweet treats and fast food. I found matcha Kit Kats, chocolate galore, and mochi balls stuffed with sweet bean paste on almost every corner.

So why the dramatic difference?

As usual in nutrition, the answer isn’t a single “superfood” or magic ingredient.

It’s the system.

The convenience store paradox

One of the biggest surprises was the sheer density of convenience stores.

Chains like Lawson, FamilyMart and 7‑Eleven are everywhere — around 50,000 stores nationally. Roughly one for every 2,000 people.

In Japan, about a quarter of all food purchases happen in these shops.

If you’re British, that sounds like a public-health disaster waiting to happen. Our corner shops tend to be temples of ultra-processed snacks, fizzy drinks and very little fresh food.

But step inside a Japanese one and it’s a different world.

Yes, there are sweets. But you also see:

• Freshly made onigiri (rice balls with salmon, seaweed, vegetables)

• Bento boxes with fish, tofu, pickles and greens

• Soups and salads made daily

• Hard-boiled eggs, beans, fermented foods

• Unsweetened teas and black coffee

I watched a woman quietly making onigiri behind the counter — real food, assembled that morning.

It’s not just convenience.

It’s convenient whole food.

Imagine if your local petrol station sold lentil salads and grilled fish instead of meal deals and energy drinks.

Snacking — but differently

We often blame “snacking” for rising obesity in the UK.

But it’s not snacking per se — it’s what and how we snack.

In Japan, portions are small. Truly small. Bite-sized. Individually wrapped. There’s very little of the “family-size bag for one person” phenomenon.

There’s also a cultural principle called hara hachi bu — eat until you’re about 80% full.

I tried it.

With Japanese meals, it’s surprisingly easy. Meals are naturally lighter, more varied, and less hyper-palatable than Western ultra-processed food designed to override satiety signals.

You simply stop earlier.

Contrast that with eating crisps or pizza on the sofa. The “stop” signal never arrives.

Children: where the real difference starts

This, to me, is the most striking contrast.

In Japanese schools:

• Meals are cooked fresh on site

• Nutrition standards are strict

• Snacks are not allowed

• Children sit down together and eat slowly

• They help serve and clear up

It’s communal and deliberate.

Food isn’t a rushed, lonely refuelling exercise between screens.

It’s part of education.

Parents pay the equivalent of a few pounds a week. In some areas it’s free.

Compare that to the UK, where packed lunches often mean ultra-processed snacks, and we worry that weighing children might “cause stress”.

We’re protecting feelings while ignoring physiology.

Timing and context matter

There are subtle behavioural differences too:

• Eating while walking? Frowned upon

• Eating on commuter trains? Rare

• Late-night sofa snacking? Uncommon

From our ZOE research, we know late-night eating disrupts metabolic health and glucose control. Yet it’s normalised in the West.

Japan quietly discourages it without needing calorie counting or diet culture.

Even the vending machines are different

Japanese vending machines are everywhere — but look closely.

Instead of mostly sugary drinks, you’ll find:

• Green tea

• Black tea

• Coffee (hot and cold)

• Zero-calorie options

Water isn’t the only healthy choice. It’s one of many.

Again, the environment nudges better decisions.

No lectures required.

What happened to my own body?

I logged everything with the ZOE app while I was there.

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At home in the UK, I average about 30 different plants per week.

In Japan?
47 plants per week.

Almost accidentally.

Tiny portions of seaweed, mushrooms, pickles, tofu, beans, greens, miso, herbs — diversity sneaks in everywhere.

More plant diversity means a healthier gut microbiome. And a healthier microbiome helps buffer the occasional indulgence. Interestingly, my healthy protein intake nearly doubled too — lots of fish, tofu and legumes — without me trying.

No protein shakes. No tracking macros. Just food culture.

So what’s the “secret”?

Not willpower. Not genetics. Not some mystical superfood.

It’s:

• Smaller portions

• More plants and fibre

• Fermented foods

• Less ultra-processing

• Slower, communal eating

• Fewer late-night calories

• Healthier default options everywhere

In other words:

A food environment that makes the healthy choice the easy choice. That’s the lesson we keep missing in the UK. We focus on telling individuals to “try harder”. Japan quietly redesigns the system. And the results speak for themselves. We don’t need to become Japanese or give up the occasional treat. But we could absolutely learn from their defaults.

Because obesity isn’t just about personal responsibility. It’s about the world we build around food.

Read more in my interview here

Tim

It appeared in JAMA, the Journal of the American Medical Association, which usually sets a fairly high bar. The study involved around 340 participants and looked at vitamin K2, in this case in a Chinese population. Participants were given what seemed like a sensible dose, and over the course of about a month, those taking vitamin K2 reported roughly a 50% reduction in leg cramps compared with the control group.

That was enough to pique my interest. I managed to get hold of some vitamin K2 myself and decided—very much unscientifically—to try it. Interestingly, after about ten days, I did notice a difference. I was no longer being woken up at night by leg cramps, and my sleep improved as a result. So I’ve continued taking it, sourced from the internet, and for now at least, the effect seems real to me.

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Now, an important caveat. That original study was later retracted due to problems with the randomisation. That clearly weakens the evidence, and it means we shouldn’t draw firm conclusions from it. Still, the signal itself was intriguing, and I wouldn’t be surprised if vitamin K2 attracts more research interest going forward.

Vitamin K2 is a lesser-known variant of vitamin K and is thought to play roles in bone and muscle health, blood coagulation, and possibly other metabolic pathways we don’t yet fully understand. As with many nutrients, its effects may be subtle, context-dependent, and hard to capture cleanly in trials.

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Leg cramps remain a common and frustrating problem, particularly as we get older. While we don’t yet have robust answers, studies like this—despite their flaws—help point researchers in new directions. With better-designed trials, we may eventually find clearer, more reliable ways to help people struggling with these issues.

As always, curiosity is useful—but so is caution.

Vitamin D is a particularly interesting topic for me. I spent close to 20 years studying it, published a couple of dozen papers on the subject, and for a long time I was a firm believer in its benefits. Like many others, I was convinced it played a major role not just in bone health, but in preventing fractures and a wide range of chronic diseases.

Over time, however, the evidence forced a rethink. As better-quality clinical trials emerged—properly randomised studies with placebo controls—the story began to unravel. The world’s favourite “vitamin” (which, strictly speaking, isn’t really a vitamin at all) slowly started to lose its clothes.

Across the board, vitamin D supplements failed to deliver on many of their promises. They do not meaningfully prevent fractures for most people, except in a very small minority with severe deficiency—levels approaching conditions like rickets or osteomalacia. Outside of that group, the benefits are far more modest than once claimed.

This pattern has repeated itself in study after study: strong observational associations, followed by disappointing results when tested in rigorous trials. It’s a useful reminder of how easily correlation can be mistaken for causation, particularly in nutrition science.

So where does that leave vitamin D and type 2 diabetes? The data suggest there may be a small benefit in people who are genuinely deficient, but for the majority, supplementation is unlikely to be a metabolic silver bullet. As with so much in nutrition, context matters far more than headlines—and good evidence should always be allowed to change our minds.

The reason liver fat matters is simple. When fat builds up in the liver, it interferes with how the liver does its job. Glucose isn’t stored as efficiently, fats aren’t processed properly, and a cascade of metabolic problems can start to develop. Even moderate levels of fatty liver are associated with around a 50% higher risk of heart attacks, type 2 diabetes, and several cancers.

What makes this especially important is that fatty liver is usually silent. Many people have no symptoms at all, and you don’t need to be visibly obese for it to be a problem. That’s why I think it’s a useful thing to know about—it flags risk that might otherwise go completely unnoticed.

I was particularly curious about my own results when they came back. I have a strong family history of type 2 diabetes, and my blood sugar has always hovered uncomfortably close to the pre-diabetic range. So I was genuinely relieved to see that my liver fat levels were very low, and that the tissue itself was healthy, elastic and functioning well. For once, a test came back reassuring.

That’s not something to take for granted, and it reinforced for me how valuable this kind of information can be. If you ever get the opportunity to have a liver fat assessment, it’s probably worth considering—especially if you have risk factors that don’t show up on the bathroom scales.

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At the moment, this sort of testing isn’t routinely available through the NHS, and we’re some way off that becoming standard practice. But it’s an area I expect we’ll hear a lot more about, because understanding internal fat tells us far more about metabolic health than weight alone ever could.

The documents don’t go into much detail on how to do this well, and that’s an important caveat. But even so, this represents a genuinely welcome shift away from nutritional advice that has dominated for the last two decades and has proven remarkably resistant to change, despite mounting evidence that it hasn’t delivered better health outcomes.

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What’s encouraging is that this isn’t just about cutting carbs. The guidance continues to emphasise fruit and vegetables, which is sensible, but it also makes several meaningful departures from the old playbook. There’s a clear move towards prioritising protein, a stronger stance against ultra-processed foods, and a long-overdue recognition that many fats are not only harmless but beneficial, and shouldn’t be routinely demonised.

Perhaps most importantly, there’s explicit advice aimed at schools and parents: reducing sugar intake in young children and avoiding artificial sweeteners. That alone would mark a significant public health win if taken seriously.

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Taken together, this feels less like a tweak and more like a course correction. It aligns far better with what we now understand about metabolic health, gut biology, and long-term disease risk. There are issues with conflicts of interest and involvement of the beef and dairy industry, but that’s nothing new in the US.

The question, as ever, is whether other countries are paying attention. One can only hope that the UK and others finally wake up and follow suit, rather than clinging to outdated models that have served neither children nor adults particularly well.

Thank you for reading,

Tim

The overall data are reassuring. Yes, side effects exist, and some can be unpleasant—but serious adverse effects are rare, occurring in roughly one in a thousand people. When you weigh that against the reductions we see in heart disease, diabetic complications, strokes and certain cancers, the balance is clear. From a public-health perspective, these medications are cost-effective.

In real-world use, most people experience around a 10–15% reduction in body weight. That’s significant. But I think the most important message as we move into the next year is this: these drugs should never be seen as the end point.

What they really do is switch down appetite signals in the brain. That creates a unique window of opportunity—a golden moment, in fact. For perhaps the first time, people are freed from constant hunger and cravings. And that is exactly when we should be helping them transition to a healthier food pattern.

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This is the moment to break the grip of ultra-processed junk foods—by which I mean the highly engineered combinations of sugar, fat, salt and additives that are designed to be addictive. With appetite quietened, people can relearn what normal portions look like, rediscover whole foods, and build meals around plants, fibre and diversity rather than constant snacking.

If the taxpayer is funding these drugs, I think it’s entirely reasonable that they’re offered alongside meaningful dietary change. Not as punishment, but as partnership. Medication can help in the short term, but habit change is what delivers benefits over decades.

Used this way, these drugs aren’t just about weight loss. They’re a catalyst for changing behaviour for good—and that’s where the real return on investment lies.

When it comes to the perfect dinner party, I don’t think food is the most important factor at all. A relaxed atmosphere matters far more, as does having the right mix of people—those who are happy to chat, laugh, and not overthink things. If you’re worrying that your food isn’t perfect, you’re missing the point. With good friends, it really doesn’t matter. No one remembers whether the sauce split; they remember how they felt.

That said, I’ve noticed an unintended consequence of writing about food for a living. I hardly ever get invited to dinner parties anymore. I suspect people are nervous about cooking for me, which is ironic given how little I care about culinary perfection. If anything, I’m far more interested in what’s on the table around the food.

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If you want surprisingly good party food that also happens to be good for your gut, it’s the nibbles that do the heavy lifting. Mixed nuts, cashews, stuffed olives, hummus, and other bean-based dips all deliver fibre and plant diversity. Even something as simple as good olive oil with rye bread ticks several gut-friendly boxes.

One recent discovery I didn’t expect to enjoy quite so much is kefir ice cream. It’s not something you’ll have every day, but as treats go, it’s an interesting way to bring fermented foods into places you wouldn’t normally expect them.

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And yes, I’ll say it again: a glass or two of red wine can be part of a healthy gut pattern. Not because alcohol is magical, but because red wine is rich in polyphenols—the compounds your gut microbes love. As always, moderation matters more than mythology.

So don’t stress about hosting. Focus on people, conversation, and a table that encourages sharing. The gut, it turns out, thrives on exactly the same things we do.

Bon appétit.

What do I think about drinking? Do I drink myself? And why haven’t I joined the growing chorus of health experts calling for total abstinence?

Part of the reason this question keeps coming up is that I’ve been unusually open. I’ve said publicly that I do drink alcohol, and that I particularly enjoy a glass of red wine. Ten years ago, that barely raised an eyebrow. Today, it attracts criticism.

So let’s be clear about the science.

If you look at the totality of epidemiological evidence, alcohol is bad for health. It is associated with increased risks of cancer, heart disease, liver disease, addiction, violence, and major social harm. There is no credible argument that alcohol is “good for you” in any simple or general sense. And for a significant minority of people, alcohol causes devastating damage.

Those facts are not in dispute.

The question I’m usually asked, however, is not whether alcohol is harmful, but how harmful, and whether all alcohol is equal. That’s where nuance disappears in most public discussions.

When you dig into the data, a consistent and intriguing anomaly appears. Across multiple large population studies, red wine drinkers tend to have better gut health than people who drink other forms of alcohol. Importantly, this effect is not seen with white wine, beer, or spirits. That tells us it isn’t just an epidemiological quirk or a marker of lifestyle.

The most plausible explanation is polyphenols.

Red wine contains high levels of plant polyphenols, which act as fuel for beneficial gut microbes. In this specific context, the positive effects of polyphenols on the gut appear to partially offset the negative biological effects of alcohol itself—something we do not see with spirits or more highly processed alcoholic drinks.

This does not mean red wine is a health food. It means that not all alcoholic drinks behave the same way in the body.

What’s also missing from most discussions is proportional risk.

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Recent headlines declaring that “there is no safe level of alcohol” are technically correct. Any amount of alcohol slightly increases overall risk of death, even if certain disease risks (such as heart disease) go down. But risk is not binary; it exists on a spectrum.

For most people, drinking a single glass of wine a day over a lifetime increases absolute risk by a very small amount. You would need to drink thousands of bottles before that incremental risk is likely to translate into a measurable adverse event. To put it into context, statisticians have estimated that driving a couple of hours a week on a motorway carries a similar level of risk.

We accept that risk without much thought.

Health is not about eliminating every possible hazard. It’s about balancing risk, benefit, enjoyment, and sustainability. Social connection, relaxation, and pleasure matter too—and they have measurable effects on wellbeing.

So my position hasn’t changed.

If you don’t drink, there is no health reason to start.
If alcohol causes you harm, you should avoid it completely.
But if you enjoy an occasional drink, particularly red wine, and it enhances your social life and quality of life, then for most people, that small risk is a reasonable one to take.

Public health messaging needs honesty, not absolutism.

And biology, as ever, is more complicated than the headlines allow.

For years, gut microbiome testing has had a credibility problem.

Critics have argued that results fluctuate too much, that the science is immature, and that the tests tell you little more than you already know. Some of that criticism was fair; at least historically. Early metrics were blunt tools. Interesting, but not sensitive enough to track meaningful change.

That is exactly what we set out to address.

In our latest study, published in Nature, we developed a new gut health ranking score and tested it rigorously. When we compared people following targeted dietary changes with those taking probiotics, the difference was striking. In the diet group, we saw substantial shifts in gut health. In the probiotic arm, only around 5% showed meaningful change.

That contrast matters. It tells us the signal is real. More importantly, it tells us the test is sensitive enough to detect genuine biological improvement—not noise.

We then stress-tested this new score against published microbiome and obesity data from around the world. Obesity, as we know, is one of the most reliable population-level markers of poor metabolic health. Across countries, ethnicities, and datasets, our new score consistently outperformed the older diversity-based measures that have dominated the field for the past decade.

This is why we’ve introduced this new metric into the ZOE gut microbiome test.

It doesn’t just tell you where you stand at a single point in time. It allows you to track direction. Are the changes you’re making—dietary, lifestyle, behavioural—actually improving your gut health, or quietly making it worse? That longitudinal insight is what’s been missing.

And it’s why I believe gut microbiome testing has reached a turning point.

For the first time, we have a measure that is reproducible, biologically meaningful, and responsive to change. That directly addresses the long-standing criticism that microbiome testing is unreliable or little more than curiosity science.

Looking ahead, I expect this field to become mainstream.

As costs continue to fall and evidence continues to accumulate, I believe that within ten years we’ll see gut microbiome testing embedded in routine healthcare systems—not as a novelty, but as a standard tool. The advantages are hard to ignore: it’s non-invasive, information-dense, and uniquely capable of capturing how diet, lifestyle, and environment interact inside the body.

For me, this represents something bigger than a new test.

The gut microbiome integrates signals from nearly every aspect of modern life—food quality, sleep, stress, exercise, medication. When measured properly, it offers perhaps the single best overall snapshot of long-term health that we currently have.

We’re finally moving beyond vague diversity scores and into something actionable.

And that’s why I think gut microbiome testing isn’t just here to stay—it’s about to come of age.

This week it was portion sizes.

Professor Naveed Sattar and his co-authors wrote a short letter to The Lancet Diabetes & Endocrinology, later picked up by the Daily Mail, suggesting that food retailers should be required to offer different portion sizes for men and women. The logic is intuitive: on average, women and children need fewer calories than men; smaller people need less energy than larger people. Give people appropriately sized portions, and they’ll naturally eat the right amount.

It sounds reasonable. It’s also wrong.

This argument belongs to an older way of thinking about obesity—one where calories are king, arithmetic rules the body, and small daily deficits neatly add up to long-term weight loss. We’ve been here before. Remember the idea that cutting half a banana’s worth of calories a day would lead to a kilo of weight loss per year? Ten years later, ten kilos gone. Neat. Mathematical. And completely disconnected from biology.

The human body does not behave like a bank account.

When you reduce calorie intake, the body adapts. Hunger signals increase. Metabolism shifts. Hormones push back. This is precisely why calorie-controlled diets fail so reliably and why the majority of people regain weight—often with interest.

Portion size matters, but not in the way this proposal suggests.

The much bigger problem is what we are eating, not how much appears on the plate at any one moment. A small portion of ultra-processed food—engineered to be rapidly eaten, intensely rewarding, and biologically confusing—does not lead to restraint. It does the opposite. These foods reliably increase hunger after consumption, driving people to eat an extra 25–30% more calories across the rest of the day.

This is not a failure of willpower. It’s design.

Ultra-processed foods act on the brain and gut in ways that override normal appetite regulation. They alter satiety signals, disrupt glucose responses, and keep us reaching for more. You can shrink the portion, colour-code it, or label it “for women”—the downstream biology doesn’t change.

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The strongest evidence we have for this comes from an unexpected place: weight-loss drugs. The new GLP-1 agonists don’t work by shrinking portion sizes. They work by altering hunger and fullness signals. Slight changes in appetite regulation produce dramatic effects on weight—far more than any mandated portion ever could. Biology, not arithmetic, is doing the heavy lifting.

That doesn’t mean portion size is irrelevant.

At home, simple changes can help. Smaller plates and bowls consistently reduce intake. Eating at a table, without screens, leads to lower consumption than eating distracted on the sofa. These effects are modest but real. Context matters.

But legislating gender-specific portion sizes in shops risks distracting us from the central issue: an appalling food system that prioritises profit over health. A system where flavourings, sweeteners, emulsifiers, and food structure are carefully engineered to make us eat faster, eat more, and feel less full—sometimes consuming several hundred calories in seconds, something that is virtually impossible with real food cooked from scratch.

If we focus narrowly on portions, we let the system off the hook.

Obesity is not caused by people choosing the “wrong” size. It is driven by foods that hijack appetite regulation and environments that make overeating the default. Until we address food quality—how food is made, not just how much is served—we will continue to chase simple fixes that fail.

So yes, let’s talk about portion sizes. But only in the right context.

The real solution is not smaller portions of the same broken food.
It’s better food.

And it’s long past time we stopped pretending otherwise.

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So, today, I’d like to share with you why I’m so excited about the world-leading technology that I’m using in my research and at ZOE, and how gut microbiome testing works.

Before I get too technical, let’s consider why we should all care about our gut microbiomes at all, and so about the ever evolving field of gut microbiome testing. 

The science of the gut microbiome is still relatively young. Most scientists and doctors – including myself – didn’t pay much attention to the microbes in our gut until advances in DNA sequencing technology revealed their amazing capabilities. Around twenty years ago, less than 1 percent of bugs were able to be reviewed by painstakingly growing them in a petri dish.

Photo by CDC

Since then, we’ve learned a huge amount about the importance of our microbial passengers. They play a central role in our health, from our immune system to our metabolism, fighting cancer and even our mental health. 

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A particularly stubborn and common myth about protein is that plants are somehow incomplete or inferior when it comes to protein so you desperately need supplements,  combine them with other foods or better yet, eat animal protein. 

Another myth, used to market vegan products, is that animal free protein foods are actually healthier than their non-vegan counterparts. 

Both take a reductionist view and neither is going to serve you well if you’re worrying about your protein intake. 

Photo by Anna Hecker

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