Over the last few years, my diet has shifted. I used to eat meals that included vegetables. Now I eat meals built around them. I have oily fish two or three times a week, dairy most days, the odd egg, and red meat only rarely - mostly when I’m eating at someone else’s house.

Since we love putting each other into labelled boxes, I tried to work out which one I belong in.

Am I a pescatarian: someone who eats fish and seafood, perhaps dairy and eggs, but no meat? A flexitarian: predominantly plant-based but with animal foods, including meat, occasionally? Or simply an omnivore who eats a lot of vegetables?

As I looked at the research for this issue, it turns out I could be any of these, depending on which study’s classification you apply. On the one hand, that’s a little unsatisfying. On the other, I’ve never been one for putting people in boxes, so perhaps it doesn’t matter.

We know eating more plants is associated with better health and a longer life. But how far do we need to go? Is eating mostly plants enough, or would eliminating fish, eggs and dairy and committing to veganism help us live even longer?

I wasn’t sure of the answer, so that’s what I’ve been trawling through this week.

Does giving up more animal foods mean living longer?

It’s tempting to imagine dietary patterns forming a neat health ladder: omnivore at the bottom, vegetarian in the middle, vegan at the top. Each rung you climb, the longer you live. It’s a tidy idea, but it doesn’t match the data.

American researchers followed more than 30,000 Seventh-day Adventists for almost six years and compared rates of death from any cause across dietary groups. Compared with regular meat-eaters, mortality was:

• 19% lower among pescatarians, who ate fish but not meat.

• 15% lower among vegans, who excluded all animal foods.

• 9% lower among lacto-ovo vegetarians, who ate eggs and dairy but no meat or fish.

• 8% lower among occasional meat-eaters, who ate meat or fish less than once a week.

The associations were stronger in men than in women.

Notice the order. Pescatarians, not vegans, came out on top.

Seventh-day Adventists tend to have healthier lifestyles overall: they smoke and drink less and have lower rates of obesity. So does this pattern hold in broader populations?

A meta-analysis of 12 prospective studies involving more than half a million participants found that those with the highest adherence to plant-based diets were 10% less likely to die from any cause.

When the researchers broke this down by dietary pattern, those following a healthful plant-based diet were 8% less likely to die prematurely, while pescatarians were 19% less likely. The same pattern again.

So, diets emphasising plants are associated with better survival, and regular fish consumption appears to be linked to particularly favourable outcomes. There’s little evidence that going fully vegan offers an additional longevity advantage over an otherwise healthy, predominantly plant-based diet that includes some animal foods.

Of course, these studies are observational, so they can’t establish causation, and definitions of dietary groups vary between studies. But the case for fish doesn’t rest solely on pescatarians doing well. A meta-analysis of 39 prospective studies found that those eating the most fish had a 5% lower risk of dying during follow-up than those eating the least.

Do we see the same pattern in other populations?

A recent analysis of almost 155,000 UK Biobank participants living with obesity provides another useful comparison.

During follow-up, 12.8% of regular meat-eaters died, compared with 13.0% of occasional meat-eaters, 8.2% of vegetarians and vegans, and 7.6% of pescatarians.

That’s approximately 128 deaths per 1,000 regular meat-eaters versus 76 per 1,000 pescatarians. But these are crude, unadjusted rates. Differences in age, health or lifestyle might help explain the contrast. Still, the consistency of this pattern across studies is notable.

In a separate US study, researchers followed almost 118,000 participants of a cancer-screening trial for an average of 18 years. After adjusting for measured differences between participants, the estimated mortality risks relative to omnivores were:

• Pescatarians: 19% lower (hazard ratio 0.81; 95% confidence interval 0.64–1.03)

• Lacto-ovo vegetarians: effectively unchanged (0.99; 0.81–1.22)

• Vegans: 27% higher (1.27; 0.99–1.63)

This study has a problem that makes it unwise to draw firm conclusions: 99.3% of participants were omnivores, so only 0.7% followed other dietary patterns. With so few participants in the pescatarian and vegetarian/vegan groups, the estimates are imprecise, reflected in their wide confidence intervals. Both narrowly missed conventional statistical significance, although the point estimates were quite different. Larger groups might have given us a clearer answer.

My reading of this study is that it’s aligned with other studies finding the greatest benefits from a pescatarian diet. The higher risk associated with veganism is an outlier and may be linked to the fact that vegan participants also had more pre-existing illness. Some might have adopted their diet because they were unwell, an example of reverse causation.

Not all plant-based diets are created equal

Consider someone living on fish and chips and cans of Coke. Technically, that meets the definition of a pescatarian, but so does someone eating grilled salmon with lentils and roasted vegetables. I think we’d all agree that those two meals aren’t nutritionally equivalent.

What matters is which plant-based foods you’re eating.

A meta-analysis of 11 studies involving almost a million participants examined this difference. Using a plant-based dietary index, the researchers found that participants in the highest fifth for overall plant-based eating had 15% lower mortality than those with the lowest adherence.

But when the researchers separated healthy and unhealthy plant foods, they found diverging associations. Those in the highest fifth for eating unhealthy plant foods had approximately 20% higher mortality, as the graph below illustrates.

Labelling someone’s diet as omnivorous, vegan or vegetarian tells you very little about nutritional quality. A thoughtfully constructed omnivorous diet can be nutritionally superior to a poorly constructed vegan one.

Could the best diet at 75 be different from the best diet at 45?

In a later study of Seventh-day Adventists, researchers followed more than 88,000 participants for around 11 years and examined how the associations between dietary patterns and mortality changed with age.

At age 65, lacto-ovo vegetarians had a 12% lower modelled mortality risk than omnivores, and pescatarians a 15% lower risk.

By age 85, those advantages had substantially weakened: to just 3% for lacto-ovo vegetarians and 10% for pescatarians. Vegans showed essentially no mortality difference from omnivores at any age.

This isn’t a one-off finding. Researchers looking at almost 13,000 adults aged 65 and over in China and the US found that vegetarians had a 19% higher risk of dying from any cause in China and a 52% higher risk in the US, compared with meat-eaters.

Why might this happen? I suspect it’s because the balance of health risks shifts as we age.

In younger adulthood, preventing cardiovascular disease, diabetes, and cancer contributes substantially to longevity, and plant-rich diets are associated with lower rates of all three. But in our seventies and beyond, sarcopenia, frailty, falls and impaired recovery from illness become increasingly important threats to survival. Meeting these challenges requires adequate protein and energy.

Think of the same person at two points in life. At 45: a generous appetite, plenty of food intake, and long-term cardiometabolic risk as the primary concern. At 75: a smaller appetite, perhaps unintentional weight loss, and preserving muscle and resilience now competing with chronic disease prevention as priorities. At this point, the diet may need greater protein and nutrient density.

That’s where a predominantly plant-based diet can become more challenging. Many plant foods contain less protein per unit weight than concentrated animal sources. And the fibre that brings so many health benefits can also fill you up before you’ve eaten enough protein, at the exact point in life when appetites are declining and protein needs are rising. Fish, eggs, dairy and meat make meeting these needs easier, although well-planned vegetarian and vegan diets can achieve it too.

There are some important caveats here. The Adventist age-specific estimates are modelled from population data, not a direct measurement of what happens when an individual ages from 65 to 85. Survivor selection may contribute - the more vulnerable omnivores may have died earlier, leaving a comparatively resilient older group. And the Chinese and US findings may also reflect differences in baseline health and confounding, even though the researchers tried to account for these.

Protein or energy inadequacy wasn’t established as the cause of the mortality findings in these studies, but the nutritional challenge is real, including for omnivores. A diet that meets your needs at 45 may need adjusting at 75.

What this means for your health

I think three priorities emerge from the evidence.

First, choose nutritious foods before worrying about dietary labels. The most useful distinction isn’t vegan versus vegetarian versus pescatarian; it’s the quality of the foods dominating your diet. Make whole or minimally processed plant foods the foundation, rather than making avoidance of meat the sole objective.

Second, don’t eliminate all animal foods simply because you think it must be healthier. Pescatarian diets repeatedly show some of the most favourable longevity outcomes, making a good case for eating fish regularly, particularly oily fish. Dairy, the occasional egg (I’d suggest no more than two a week) and modest amounts of lean meat can also be part of a healthy, predominantly plant-based diet.

Third, give increasing attention to protein and nutritional adequacy as you get older. From your sixties onwards, nutrient density becomes increasingly important as appetite and food intake decline. Vegetarians and vegans can meet these needs, but doing so requires more deliberate planning.

As always, your responses are anonymous, but they really help me tailor future content to what’s most helpful to you. Please take a moment to click a button.

HEALTH TWEAK OF THE WEEK

The evidence consistently links predominantly plant-based diets with better longevity, with pescatarian patterns frequently performing particularly well. Fish consumption itself is also associated with better cardiovascular outcomes and lower mortality.

But the quality of those plant foods matters enormously: unhealthy plant-based diets are associated with worse, not better, outcomes. And as we get older, maintaining sufficient protein and energy becomes increasingly important.

1. Make nutritious plants the foundation of your diet. Build meals around vegetables, beans, lentils, whole grains, fruit, nuts and seeds. Replace some refined carbohydrates and less nutritious processed foods with more nutrient-rich alternatives.

2. Include fish regularly, especially oily fish, if you eat animal foods. Aim for at least two portions a week, including one of oily fish such as salmon, sardines, mackerel or trout. Fish provides high-quality protein, while oily fish is particularly rich in EPA and DHA, omega-3 fats that most of us don’t get enough of. Consider replacing some red meat meals with fish. Dairy and occasional eggs and lean meat can also contribute valuable nutrients.

If you’re vegetarian or vegan, you can still meet your nutritional needs through carefully chosen protein-rich foods, particularly soya products and pulses, with algal sources of EPA and DHA worth considering.

3. Reassess your nutritional needs as you get older. From your sixties onwards, include a substantial protein source at each meal, rather than leaving nearly all of it until supper. For many older adults, around 30–40g per main meal is a useful target, adjusted to individual needs. If you’re unintentionally losing weight, eating less or losing strength, reassess whether you’re getting enough food, not just whether it’s ‘healthy’.

By the time I’d finished reviewing these papers, I found myself feeling content with the diet I’ve grown into: definitely plant-based, but including dairy, fish and the odd egg, with red meat occasionally on high days and holidays.

I still can’t decide whether that makes me a pescatarian, a flexitarian or an omnivore. Given that the researchers can’t agree on the definitions either, I don’t think I’ll lose much sleep over it.

What does this mean for your own kitchen?

You don’t necessarily need a different diet. You might just need a clearer picture of what’s already working and what’s missing.

That’s what my Kitchen Snapshot Audit offers. Send me photographs of your fridge, freezer and cupboards, along with a few answers about how you eat, and I’ll give you a personalised, evidence-based second opinion: the strengths to build on, the gaps worth addressing and the changes I’d prioritise.

Find out more about the Kitchen Snapshot Audit

🎧 Prefer to listen while wondering whether you really need to give up cheese to live longer?

🎙️ This week’s One Health Tweak a Week podcast explores a surprisingly complicated question: how far towards plant-based eating do we need to go to maximise our chances of living a longer, healthier life?

We look at the evidence comparing omnivores, vegetarians, pescatarians and vegans, including some findings that challenge conventional wisdom.

You’ll hear:

• Why pescatarians repeatedly show some of the lowest mortality rates, sometimes outperforming vegetarians and vegans

• Whether going fully vegan offers any additional longevity benefits, and what the research actually tells us

• Why not all plant-based diets are healthy, with some associated with a substantially higher risk of premature death

• The unexpected finding that some vegetarian longevity advantages diminish as we get older, and why our nutritional priorities may need to change

• How to build a predominantly plant-based diet that supports long-term health, including the role of fish, other animal foods and adequate protein

👉 Good company for your next walk, commute, or while contemplating whether your dinner makes you a pescatarian, flexitarian or just an omnivore who likes vegetables.

👉 Listen now!

🧭 Before you go

💬 Has the way you eat changed as you’ve got older? Perhaps you’ve shifted towards a more plant-based diet, started eating more fish, or become more conscious of getting enough protein. What prompted those changes? Have you noticed any difference in how you feel?

Leave a comment

📤 Know someone who’s wondering whether they should become vegetarian or vegan to live longer? Or someone who’s been eating mostly plants for years? Share this week’s article with them. The findings might challenge a few assumptions and help them make more informed choices about what goes on their plate.

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👥 Paid corner – If you’re trying to improve your diet but aren’t sure how far to go, join us in the private chat. We can discuss ways to eat more nutritious plants, include fish if you wish, and make sure you’re getting enough protein as you get older, without turning every meal into a nutritional calculation.

Until next Saturday – eat well, keep an eye on your protein, and leave the dietary labels to the researchers.

– Ben

If you’d like to know more about getting sufficient protein on a plant-based diet, you might find this recent issue helpful:

In this episode of One Health Tweak a Week, we examine the evidence from large studies comparing the longevity of omnivores, vegetarians, pescatarians and vegans. And some of the findings might surprise you.

Pescatarians repeatedly show some of the lowest mortality rates, while going fully vegan doesn’t appear to offer additional longevity benefits.

But there’s more to a healthy diet than avoiding animal products. Research involving nearly a million participants reveals a striking difference between healthy and unhealthy plant-based diets, with the latter associated with a higher risk of premature death.

We also explore an unexpected twist: the longevity advantages of vegetarian diets appear to diminish as we get older. Could declining appetites, increasing protein needs and the growing risk of frailty explain why the best diet at 75 might differ from the best diet at 45?

Finally, we’ll share three practical ways to optimise your diet for a longer, healthier life, without unnecessary restrictions or sacrificing the foods you enjoy.

I’m lucky. My joints don’t ache, and I can take the stairs without thinking about it. But I have family members for whom that’s not the case, and watching someone wince as they stand up from a chair changes how you think about supplements you’d normally dismiss.

I’ll admit, I’ve tended to roll my eyes at collagen. It’s marketed as some kind of wonder supplement for joints, muscles, hair, skin, nails... the list never ends. But if it can genuinely help people with painful or stiff joints, it deserves a proper hearing, even from a sceptic like me. So this week, I’ve been rummaging through the research.

Osteoarthritis is estimated to affect 300–500 million people worldwide, and those numbers are expected to climb sharply as populations age. For many of you, that’s not a statistic - it’s the aching knee on the stairs, the stiff fingers first thing in the morning, the hip that stops you going out for a walk.

And our treatment options are frustratingly limited. We don’t have anything that reverses the underlying joint damage. That leaves us managing symptoms, mostly with painkillers and anti-inflammatory drugs, which often work well but can carry real costs, like damage to the gastrointestinal tract and kidneys, and an increased risk of cardiovascular disease.

So, does collagen actually help symptoms? Does it protect cartilage? And is it worth the money?

Why might swallowing collagen help your joints?

The logic sounds appealing. Cartilage contains collagen. Osteoarthritis involves cartilage breaking down. So taking extra collagen should help repair it, right?

Not quite. Your digestive system breaks collagen down into its component parts before anything reaches the bloodstream. Whether those fragments then find their way to damaged cartilage and stimulate repair is a different question entirely. Providing raw materials isn’t the same as persuading a damaged joint to rebuild.

That said, there is some biological plausibility. In the lab, certain collagen peptides do encourage cartilage cells to produce more of the proteins that maintain cartilage, while reducing some processes that break it down. Similar effects have been seen in animals. But findings are inconsistent, particularly with human cartilage, and we don’t have convincing evidence that swallowing collagen rebuilds cartilage in people.

Two main formulations are used, with different proposed mechanisms:

• Hydrolysed collagen peptides: pre-digested collagen containing amino acids and peptides. Some animal studies suggest these accumulate in cartilage tissue and may influence cartilage-cell metabolism. Typical doses are 5-20 g per day.

• Undenatured type II collagen (UC-II): thought to work through the immune system. It’s taken up by immune-cell clusters in the gut called Peyer’s patches, where it may activate T cells that suppress inflammation in joint cartilage. UC-II doses are measured in milligrams.

Both mechanisms remain proposed, not proven. But there’s enough biological plausibility to make the clinical trials worth looking at.

So what happens when researchers give collagen to people?

The pooled evidence initially looks encouraging.

A meta-analysis of 35 studies involving 3,165 participants with joint symptoms found that collagen derivatives had a small-to-moderate effect on pain, equivalent to an 8.5-point decrease on a visual pain scale that went from 0 to 100.

They also found significant improvements in joint function, no clear differences between collagen formulations, and no concerning safety signals. Most studies lasted less than six months, so we can’t say much about longer-term effects.

That 8.5-point drop is a modest improvement on a scale of 0 to 100, but potentially worthwhile if you’re struggling with painful joints. And it’s an average; some people will experience greater relief, others little or none.

A systematic review of 14 randomised controlled trials told a similar story. Most studies found some positive results, typically less pain and better joint function. But doses ranged from 1.2 to 20g per day across studies lasting 12 to 48 weeks, and the researchers felt this wide variation made it hard to generalise results. They were also concerned that about 20% of participants dropped out of some studies, possibly because they weren’t experiencing benefit.

At this point, you might reasonably conclude collagen works. The meta-analyses suggest a modest benefit, and the safety picture looks clean. But when I looked more closely at individual trials, I started getting swatted around the ears by red flags.

How much of that improvement is actually due to collagen?

In a six-month trial, 107 adults with knee osteoarthritis took either undenatured type II collagen or a placebo. Those taking collagen had less pain, less stiffness and better function.

But look at the graph.

The solid lines show clear overall improvements in knee pain (red) and joint function (green).

But see the dotted lines? Those participants were taking a placebo, yet their pain and function also improved substantially. For the first month, improvements were essentially the same for those taking collagen and those taking a dummy supplement.

We see this regularly in clinical trials, especially when patients are reporting their own symptoms. These participants were seen in clinic monthly, far more attention than most arthritis patients typically receive. They wanted the treatment to work. They may have wanted to please the researchers, even subconsciously. The result was that even those taking nothing found their symptoms improving significantly.

So yes, people taking collagen felt better, but the relevant question is “How much better did they feel than those taking placebo?” The answer is a little, but not nearly as much as the headline numbers suggest.

And whose assessment of pain should count most? In a separate trial, 182 adults with hip or knee pain (but without established osteoarthritis) took collagen peptides or a placebo for 12 weeks. Physician assessments favoured collagen. But when the patients themselves rated their pain, there was mostly no significant difference, apart from some specific activities like climbing stairs, squatting and kneeling.

For a treatment intended to relieve pain, the patient’s experience should carry more weight than the doctor’s assessment. It’s their pain. Yet it was the doctor’s assessment that made the headline results.

How much confidence should we place in the positive trials?

Beyond the placebo challenge, there are broader concerns.

The methodological issues are widespread: small samples, subjective endpoints, considerable protocol variation, and high dropout rates in some studies. A meta-analysis can only be as good as the trials it pulls together.

Then there’s the question of who’s funding the research. Many collagen trials have been financed by companies that manufacture or sell the supplements, and some investigators have commercial relationships with those companies. That doesn’t automatically make findings unreliable; industry-funded research can be excellent. But it means we should examine the evidence carefully rather than accepting the researchers’ conclusions at face value.

In the UC-II trial I described above, two investigators worked for the supplement company and a third was an adviser. They disclosed these relationships, so we can interpret the findings with that in mind.

But when I dug deeper into another trial, the picture was more troubling.

The lead researcher owned the company conducting the study and held collagen-related patents assigned to the manufacturer supplying the supplement being tested. The publication acknowledged that the manufacturer supplied the supplement but didn’t explain who paid for the much greater cost of running the trial.

Public records listed the researcher’s company as both responsible for the trial and a source of funding. Yet the paper claimed that funders had no involvement in designing the study or analysing the results, even though researchers from that company did both.

The study also wasn’t registered publicly until more than three years after it began. Trials are supposed to be registered before they start, partly to create a public record of what was planned, and partly to prevent researchers from publishing only positive results and quietly shelving failures. Registering years later defeats both safeguards.

Despite all these connections, the authors declared no conflicts of interest.

To be clear, the available evidence doesn’t establish that these interests influenced the results. But the incomplete disclosures make it harder to evaluate the findings with confidence. And they underscore why independent confirmation matters.

The two most recent independently funded trials aren’t encouraging:

• 108 patients with knee osteoarthritis received UC-II or placebo for 24 weeks. No significant differences in pain, stiffness, function, or X-ray appearance.

• 68 patients took hydrolysed collagen plus UC-II or placebo. Both groups improved, but with no significant difference between them.

Neither trial is large enough to prove collagen is ineffective. But together with the methodological and transparency concerns, they strengthen the case for caution.

Could collagen still protect your joints?

This is one of the most persuasive bits of collagen marketing - not just pain relief, but cartilage protection or repair.

The evidence doesn’t support it. There’s no convincing human evidence that collagen supplementation prevents osteoarthritis, rebuilds cartilage, or slows disease progression. The 2026 trial found no difference in X-ray appearance between collagen and placebo after 24 weeks, though that’s a short window for detecting structural change.

It helps to distinguish two separate questions: “Does my knee feel better?” and “Is the disease progressing more slowly?” A supplement could affect the first without touching the second.

If we rank the claims by the strength of the evidence, there’s uncertain support for modest relief of existing knee symptoms, much less for other joints, and essentially none for preventing arthritis or repairing damaged cartilage.

On a practical note, collagen has an incomplete essential amino acid profile, making it a poor substitute for a quality protein supplement like whey. Don’t assume it’s doing double duty for your muscles while addressing your joints.

So where does this leave us?

Collagen may relieve knee pain and stiffness modestly, but the evidence is more uncertain than the positive headlines suggest. The average additional benefit over placebo appears small, and there’s no convincing case that collagen protects cartilage, prevents arthritis, or helps joints other than the knee.

That said, conventional painkillers and anti-inflammatory drugs carry their own costs with long-term use: gastrointestinal, renal and cardiovascular risks that accumulate over time. Collagen’s short-term safety profile looks reassuring, and the main practical downside is cost.

Speaking of which, a quick scout on Amazon.com shows collagen hydrolysate/peptides powder coming in at around $0.50 to $1 per day for a 10g dose.

For someone with troublesome joint symptoms, a short trial is reasonable. If you feel meaningfully better, that improvement matters to you, even if you can’t know how much is attributable to collagen versus expectation or natural symptom fluctuation.

But continuing indefinitely without noticeable relief, in the hope that collagen is quietly protecting your cartilage, isn’t supported by the evidence.

If I developed troublesome knee pain, I’d be inclined to try collagen for a couple of months. And if it relieved my symptoms as well as my usual painkillers or anti-inflammatories, I’d have little hesitation in making the switch. Collagen appears to have a much better safety profile, and neither treatment has been shown to reverse the underlying joint damage.

As always, your responses are anonymous, but they really help me tailor future content to what’s most helpful to you. Please take a moment to click a button.

HEALTH TWEAK OF THE WEEK

Collagen supplements may offer modest relief from joint pain and stiffness, particularly in knee osteoarthritis, though the evidence is less convincing than the positive headlines suggest. There’s no good evidence that collagen prevents arthritis or repairs cartilage, but a time-limited personal trial is reasonable if your joints are giving you trouble.

1. Don’t take collagen solely to prevent arthritis. No study has shown that collagen supplementation prevents osteoarthritis or protects healthy cartilage. If your joints are comfortable, the evidence doesn’t justify the expense.

2. Consider trying a straightforward hydrolysed collagen supplement if your joints are troublesome. Take around 10g of hydrolysed collagen peptides daily for eight weeks, particularly for knee osteoarthritis. This is a commonly studied dose, not a proven optimum. There’s no convincing evidence that higher doses work better. Eight weeks ought to be enough to determine if it’s helping you. Choose an ordinary product rather than an expensive formulation promising cartilage regeneration.

Before you start, identify the symptoms you most want to improve: walking pain, morning stiffness, difficulty on stairs, whatever matters most to your daily life. Keep other treatments and activities as consistent as reasonably possible, so you can judge the collagen fairly. And don’t count collagen towards your protein needs; its amino acid profile is incomplete compared with whey or other quality protein sources.

3. Decide whether it’s earning its place after eight weeks. If you feel no meaningful improvement, stop. There’s no good reason to continue in the hope of cartilage protection. If you feel substantially better, continuing is reasonable, provided the cost is acceptable and the supplement is well tolerated. You won’t be able to separate collagen’s effect from expectation or natural symptom fluctuation, but relief is still relief. Keep expectations modest for joints other than the knee, where the evidence is thinner.

Hopefully, this has helped you make a bit more sense of the collagen claims. There’s probably something worthwhile here for painful joints, but a lot of the marketing goes well beyond what the evidence supports. At least now you can decide whether it’s worth giving it a go, without being taken in by promises of rebuilding your cartilage.

And we haven’t finished with collagen yet. Apparently, it’s also supposed to give us younger-looking skin, thicker hair and stronger nails. Quite a lot of work for one supplement! We’ll have a closer look at those claims in a future issue.

🎧 Prefer to listen while wondering when standing up from a chair became quite such an undertaking?

🎙️ This week’s One Health Tweak a Week podcast takes a closer look at collagen for joint health. There’s some encouraging evidence that it can relieve pain and stiffness, but the story gets rather more complicated when we examine the trials behind the headlines.

You’ll hear:

• Why collagen sounds like a sensible way to repair damaged cartilage, but the biology doesn’t necessarily work that way

• What the clinical trials tell us about pain relief and joint function, and why improvements in people taking a placebo are so revealing

• Why I became increasingly sceptical as I investigated commercial interests, research funding and some rather questionable disclosures

• Why collagen might help painful knees, but there’s little convincing evidence that it prevents arthritis or rebuilds damaged cartilage

• How to decide whether collagen is worth trying for eight weeks, which formulation and dose I’d choose, and what it might cost

👉 Good company for your next walk, commute, or while wondering whether the collagen powder in your cupboard has been earning its keep.

👉 Listen now!

(Episodes are free for now. Paid subscribers support the deeper research - and unlock practical tools to help you improve your health without turning it into a second job.)

🧭 Before you go

💬 Have you tried collagen supplements for your joints? Did you notice any improvement in pain or stiffness, or was it money down the drain?

Leave a comment

📤 Know someone who’s taking collagen for their joints, or considering giving it a try? Share this week’s article with them. It might help them decide what’s worth paying for and which promises to take with a pinch of salt.

Share

👥 Paid corner – If you’re already taking collagen, or wondering whether to start, drop me a message in our private chat. We can look at the formulation and dose you’re considering, whether you’re paying over the odds, and how to judge whether it’s actually helping.

Until next Saturday – keep those joints moving, and don’t expect a scoop of collagen to perform miracles.

– Ben

In this episode of One Health Tweak a Week, we take a closer look at the research behind collagen supplements for joint health, including some findings that aren’t quite as encouraging as the headlines suggest.

We explore:

• What clinical trials actually show about collagen’s effects on joint pain, stiffness and mobility, particularly in people with knee osteoarthritis.

• Why people taking placebo supplements often improve substantially, and what that tells us about collagen’s true benefits.

• The commercial interests and questionable research practices we uncovered when examining some of the more positive studies.

• Whether collagen can rebuild damaged cartilage or prevent arthritis, or whether those promises go beyond the evidence.

• Which type of collagen to consider, how much to take and how long to try it, before deciding whether it’s worth continuing.

We also consider whether collagen might offer a safer alternative to regular painkillers or anti-inflammatories for some people.

If painful joints are becoming a nuisance, or you’re wondering whether collagen supplements deserve a place in your routine, this episode will help you separate the promising evidence from the hype and make an informed decision.

Lena’s friends call her the Green Goddess. Most of her spare time is spent digging, hauling, planting and generally transforming her garden into something spectacular. She’s been vegan for decades, eats well, and gets plenty of strength work without stepping inside a gym.

But she’s beginning to worry about her muscles.

Her mum became frail in her seventies: struggling with stairs, unsteady on her feet, eventually needing help with things she’d done effortlessly for decades. Lena is determined not to follow the same path. At 52, she’s still fit and strong. Yet she’s never had a big appetite, and hitting her daily protein target has always been a stretch.

The question she keeps asking herself is whether a plant-based diet gives her the strength she needs to age well.

It’s an interesting dilemma. We have substantial evidence supporting the long-term health benefits of plant-forward diets. But the foods that are so good for our cardiovascular and metabolic health aren’t necessarily the easiest way to obtain enough protein for our muscles.

And as we get older, those muscles become increasingly demanding.

So, should Lena be eating more protein? Does it matter whether it comes from plants or animals? And could a protein supplement help her preserve her strength without abandoning the diet she values and enjoys?

Why worry about muscle loss when you’re still fit and active?

Sarcopenia, the progressive loss of muscle mass and strength, affects up to a third of community-living older adults. It’s associated with frailty, falls, depression, hospitalisation, loss of independence and premature death. And studies consistently link lower protein consumption with lower muscle mass and strength.

That might sound like a problem for people in their seventies and eighties, not a fit 52-year-old with soil under her fingernails. But muscle loss accumulates slowly over decades, and the reserves you build and maintain in your forties and fifties determine the starting point when age, illness or a spell of immobility begin to erode what’s there. Think of it as a savings account: the more you’ve accumulated by middle age, the more you can afford to draw down later without running into trouble.

That’s why Lena’s thinking about this now, rather than waiting another twenty years.

Importantly, the goal isn’t to replace healthy plant foods with animal protein. Plant-forward diets bring genuine nutritional advantages: fibre, polyphenols, unsaturated fats. Many animal foods provide fewer of these while contributing more saturated fat. The objective is to make sure that an otherwise excellent diet is also meeting your muscles’ requirements.

Can plant protein fully maintain muscle?

There’s a widespread belief that animal proteins are inherently better for building and maintaining muscle.

Animal proteins do have some advantages, but the longer-term studies tell a rather different story.

In 2025, researchers published a meta-analysis of 30 randomised controlled trials comparing plant and animal protein supplements. They found that soy protein was just as effective as dairy protein, predominantly whey, at maintaining or increasing muscle mass.

Other plant proteins performed slightly less well, although the differences were generally small.

Animal protein did show a modest advantage for leg strength, particularly in some younger adults and resistance-training studies. But there was no clear advantage for upper-body strength or overall physical performance.

Another useful piece of evidence comes from a study of more than 3,200 adults aged 40–80. Researchers examined their protein intake, skeletal muscle mass and the proportion of protein coming from animal versus plant foods.

Higher total protein consumption was associated with greater relative muscle mass. You can see this in the blue line of the graph below.

However, the proportion coming from animal versus plant sources wasn’t linked to differences in muscle mass. (That’s the green to orange line).

Average protein consumption was approximately 1.3g/kg body weight daily, with the lowest-intake group consuming no more than 0.96g/kg and the highest consuming at least 1.7g/kg.

Animal protein does have some advantages. Gram for gram, it tends to stimulate muscle protein synthesis more strongly, and some studies find a small advantage for leg strength. But the longer-term evidence suggests that plant protein can maintain muscle effectively when you consume enough of it.

For Lena, the more important question is whether she can comfortably eat that much.

If plant protein works, why can getting enough be difficult?

Simply eating more tofu, beans or lentils might seem the obvious answer. But several things make that harder than it sounds.

Protein density. Most whole plant foods contain less protein per serving than meat, eggs or dairy. Their fibre content also makes you feel full, which is normally a good thing, except that you may feel full long before you’ve consumed enough protein.

Digestibility. We don’t absorb all the protein listed on the label. Studies suggest we digest and absorb roughly 85–95% of protein from lean meat, eggs and dairy, compared with 50–75% from legumes, although these values vary considerably with the specific food and how it’s prepared.

Amino acid profile. Your muscles require nine essential amino acids that you can’t manufacture yourself. Most animal proteins provide all nine in favourable proportions. Individual plant proteins often contain relatively little of one or more. For example, cereals are often relatively low in lysine, while legumes help supply it.

That’s why combining different plant foods makes sense: beans and rice, bread and hummus, or pasta and beans. You don’t need to construct a perfectly balanced amino acid profile at every meal, but variety becomes increasingly important when you’re relying entirely on plants.

Then there’s leucine. This essential amino acid plays a particularly important role in stimulating muscle protein synthesis, the process through which our muscles build and replace their proteins. Many plant proteins contain less leucine per gram than animal proteins.

As we age, our muscles also become less responsive to a given protein dose, a phenomenon called anabolic resistance. Consequently, an older adult may need more protein, including more leucine, to stimulate muscle protein synthesis effectively.

That’s why animal proteins often produce a stronger immediate muscle-building response gram for gram, even though longer-term studies suggest that adequate plant protein can produce comparable muscle outcomes.

That’s not to say you need to eat more animal food, but it does mean you need to be sure your plant-based diet supplies enough total protein and essential amino acids.

What “enough protein” looks like on a plate

For younger and middle-aged adults, the usual minimum recommendation is approximately 0.8g of protein per kg body weight daily.

If you eat a predominantly plant-based diet, I’d suggest aiming a little higher, around 0.9g/kg, as a practical allowance for differences in protein availability.

Try to obtain roughly 20–25g protein and 2–2.5g leucine per meal. If you’re doing demanding resistance training, your requirements may be higher.

From around 60–65 onwards, I’d increase the daily target to approximately 1.2g/kg, or around 1.3g/kg for predominantly plant-based eaters.

During illness, recovery or particularly demanding training, requirements may rise towards 1.5g/kg.

I’d also aim for approximately 30–35g protein and 3–3.5g leucine per meal.

These are practical targets. Protein needs increase progressively with age, rather than suddenly changing on your 65th birthday, but there’s a surprising lack of data as to how and when those changes occur. The additional 10% for plant-based diets is also a reasonable allowance, not an established requirement for everyone.

But let’s translate those numbers.

For someone weighing 70kg:

• Younger or middle-aged, plant-based: approximately 63g protein daily.

• Older, plant-based: approximately 91g daily.

That’s nearly 30g more protein every day.

And the higher per-meal targets can be particularly challenging. The table below shows clearly the difference in volume between plant-based and animal-derived food to hit these targets.

No disrespect to tofu or chickpeas, but half a kilo is a fairly ambitious lunch.

In a major review, almost half of older adults consumed less than 1g of protein per kilogram of body weight daily, with around 60% of their protein coming from animal foods. Given that many plant foods contain less protein per serving, those relying mostly or entirely on plants find it even harder to meet their needs.

I see this in my own diet. My breakfast of muesli, milk and fruit has plenty going for it, but protein isn’t one of its great talents. It provides only about 16g of protein: far short of the 20–25g I need now and well below the 30–35g I’ll be aiming for in my sixties. My other meals meet current targets, but I already top up breakfast with a protein shake - a 50:50 mix of whey concentrate and pea protein powder. I can see myself using the same tactic for other meals when my requirements increase.

For Lena, and for anyone relying mainly on plant foods, this presents a genuine dilemma. We know plant protein can maintain strong muscles, but we still have to eat enough of it. And as our requirements increase with age, that becomes harder.

Consistently falling short isn’t just a matter of missing a nutritional target. Over time, inadequate protein intake can contribute to the loss of muscle and strength that leaves us increasingly vulnerable to frailty, falls and loss of independence.

The obvious solution is to eat more protein-rich plant foods. And if you can comfortably manage that, excellent.

But as we’ve seen, getting enough protein from plants alone can require rather more food than some of us want to eat.

Fortunately, there’s another option: using a protein supplement to close the gap without turning every meal into an endurance sport.

Supplements, leucine and the exercise question

The advantage of protein powder is that you can add protein to an existing meal without substantially increasing its size. You still get the fibre, polyphenols, unsaturated fats and other nutrients from your whole plant foods, but you can bring the protein content up to where it needs to be.

For example, if your breakfast provides 16g of protein and you’re aiming for 25g, you need another 9g, not a 25g protein shake. Or, for an older adult, if lunch provides 20g, adding 10–15g of protein from a supplement brings it into the target range without requiring another plateful of food.

For these modest top-ups, the type of protein powder probably isn’t terribly important. But if you’re regularly relying on larger amounts, protein quality and amino acid composition deserve more attention:

• Soy has the strongest comparative evidence against dairy protein: a sensible first choice for vegans.

• Pea–rice blends offer complementary amino acid profiles and are another good plant-based option.

• Whey is highly effective and digestible for anyone not avoiding dairy, and may offer a modest edge if you’re already losing muscle.

• Sodium: check the label, particularly with soy-based powders, where content can vary considerably between brands.

Since leucine helps trigger muscle protein synthesis, and plant proteins tend to be less leucine-rich, you might wonder whether adding a little extra would solve the problem. The evidence says no.

Dutch researchers found that adding 2g of leucine to a 20g dose of either plant or whey protein didn’t improve the muscle protein synthesis response when the protein dose itself was insufficient. In a separate trial, giving 30 older men (average age 71) 2.5g of leucine with their meals three times daily for three months produced no measurable improvement in muscle mass or strength.

Leucine helps trigger muscle building, but construction still requires the full set of essential amino acids. Extra leucine can’t rescue insufficient protein.

I’d prioritise adequate, good-quality protein over buying separate leucine or branched-chain amino acid supplements.

There’s something even more important than your protein powder

Muscle is metabolically expensive tissue. Without sufficient demand, our bodies have little reason to maintain more of it than they need.

Resistance exercise provides that demand.

In the meta-analysis comparing plant and animal proteins, every trial combining protein interventions with resistance exercise reported improvements in muscle mass and/or strength.

Among trials without resistance exercise, only 21% reported improvements.

You don’t need to join a gym or start lifting heavy weights. Resistance exercise simply means making your muscles work against a load, whether that’s weights, resistance bands or your own body weight.

The important thing is to keep challenging them. As an exercise becomes easier, gradually increase the weight, resistance or number of repetitions. That gives your muscles a reason to maintain their strength and, ideally, become stronger.

Lena’s gardening certainly provides useful muscular work, particularly all that digging and hauling. But adding some regular exercises that challenge all her major muscle groups would help ensure she’s doing enough to preserve her strength as she gets older.

Getting enough protein is important, but there’s little point agonising over whether soy or whey is the better supplement if you’re not regularly giving your muscles a reason to use it.

What this means for your health

I wouldn’t encourage anyone to abandon a healthy plant-forward diet simply because animal proteins can be more efficient at stimulating muscle protein synthesis.

Plant foods bring fibre, polyphenols and unsaturated fats, alongside their broader nutritional benefits. Many animal foods supply much less of these and may also contribute substantial saturated fat.

One research group has suggested that an ideal dietary pattern might emphasise plant proteins earlier in adulthood, introducing more animal protein in later life as muscle requirements increase.

That’s a reasonable option for people happy to eat both. But it’s not essential.

With sufficient protein and regular strength exercise, Lena can carry on cultivating her garden and enjoying the foods she loves. There’s no need for her to abandon the vegan diet that’s served her so well.

For some people, ordinary food will be sufficient. For others, especially those with smaller appetites or higher requirements, concentrated protein supplements can make life considerably easier.

You don’t need animal protein to maintain strong muscles. But you do need enough protein, and a reason for your muscles to use it.

As always, your responses are anonymous, but they really help me tailor future content to what’s most helpful to you. Please take a moment to click a button.

HEALTH TWEAK OF THE WEEK

A plant-forward diet can support long-term muscle health, but whole plant foods sometimes make adequate protein intake difficult, particularly as requirements increase with age.

Supplements are useful when they close a consistent gap between what your meals provide and what your muscles need. That dietary strategy works best when paired with regular resistance exercise.

Here’s how I’d approach it.

1. Find out how much protein you’re actually eating

Use a free app such as Cronometer or MyFitnessPal to record your normal diet for 3–4 days. It’s very hard to guess just by eyeballing your plate.

Calculate your average daily protein intake relative to body weight.

As practical targets for predominantly plant-based eating:

• Younger and middle-aged adults: Around 0.9g/kg daily, with 20–25g per meal.

• Adults approximately 60–65+: Around 1.3g/kg daily, with 30–35g per meal.

Higher intakes may be appropriate during illness, recovery or demanding training.

Look at individual meals, particularly breakfast. You may discover that your overall diet is adequate, but one meal consistently provides little protein.

If you’re already meeting your requirements, you probably don’t need a supplement.

2. Close the gap, not the manufacturer’s suggested serving size

For small shortfalls, try adding ordinary protein-rich foods: tofu, soy yogurt, beans, lentils, nuts or seeds.

If you’re substantially short, a protein supplement may be more practical.

I’d favour soy or a balanced plant blend, such as pea and rice, for vegans. Whey is another effective option if you consume dairy.

Calculate the actual protein you need, rather than automatically taking a full scoop. A 15g protein shortfall doesn’t require 30g of powder.

Check the protein and sodium content on the label. Don’t rely on separate leucine or BCAA supplements to compensate for inadequate protein.

3. Keep challenging your muscles

Maintain regular, progressively demanding resistance exercise, ideally 2–3 times weekly, involving the major muscle groups.

Weights, resistance bands and bodyweight exercises can all help.

As the exercises become easier, gradually increase the weight, resistance or number of repetitions.

A little attention to your protein intake, alongside regular exercise, can help you enjoy the benefits of a plant-forward diet while keeping your muscles strong. And the stronger you remain as you get older, the better your chances of staying active, independent and able to enjoy the life you’ve worked hard to build.

🎧 Prefer to listen while wondering whether your healthy plant-based diet is giving your muscles everything they need?

🎙️ This week’s One Health Tweak a Week podcast explores a dilemma for anyone eating mostly plants: how to enjoy the long-term health benefits of a plant-forward diet while ensuring you’re getting enough protein to keep your muscles strong as you age.

You’ll hear:

• Why plant protein can be just as effective as animal protein for maintaining muscle, and what the research actually shows

• Why getting enough protein from plants becomes increasingly challenging as we get older, even when we’re eating a healthy diet

• How much protein to aim for each day and at individual meals, and why the amount of food required might surprise you

• When soy, pea–rice or whey supplements can help, and why topping up your existing meals makes more sense than replacing nutritious whole foods

• Why resistance exercise is at least as important as protein intake for keeping your muscles strong

👉 Good company for your next walk, commute, or while contemplating whether half a kilogram of tofu really is a reasonable lunch.

👉 Listen now!

(Episodes are free for now. Paid subscribers support the deeper research - and unlock practical tools to help you improve your health without turning it into a second job.)

🧭 Before you go

💬 Do you eat a predominantly plant-based diet? Have you ever checked whether you’re getting enough protein, particularly at breakfast or lunch? I’d be interested to hear how you manage it, and whether you use protein supplements.

Leave a comment

📤 Know someone who’s embraced plant-based eating but might be overlooking their protein needs? This could help them protect their muscles without giving up the foods they enjoy.

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👥 Paid corner - If you’re eating mostly plants and struggling to meet your protein targets, drop me a message in our private chat. We can look at your usual meals, identify where you might be falling short, and work out whether a little extra food or a carefully chosen supplement would help.

Until next Saturday - keep enjoying your plants, give your muscles something to work on, and remember that protein powder belongs alongside your healthy food, not in place of it.

– Ben

In this episode, we explore a dilemma facing vegans, vegetarians and anyone who eats mostly plant-based foods: how to preserve the benefits of a healthy diet while protecting against age-related muscle loss, frailty and declining strength.

The research offers some reassuring answers. Plant protein can be just as effective as animal protein for maintaining muscle, provided you’re getting enough. But that’s where things become complicated.

We’ll explore:

• Why plant protein can be harder to obtain and use, particularly as our protein requirements increase with age.

• How much protein you actually need, with practical daily and per-meal targets.

• When protein supplements make sense, and how to use them to top up healthy meals rather than replace nutritious whole foods.

• Which protein powders to consider, including soy, pea–rice blends and whey, and whether extra leucine offers any benefit.

• Why resistance exercise is essential, regardless of where your protein comes from.

Our goal is simple: to help you enjoy the benefits of plant-forward eating while keeping your muscles strong and preserving your independence for years to come.

For a few years, I worked at a hospital in Central London. Popping out at lunchtime to run a few errands meant sharing the pavement with a multitude of tourists from all around the world, leisurely taking in the sights and changing direction unpredictably.

The short time I had available and my Type A personality combined to make this a genuinely stressful experience. I’d take lengthy detours just to have a free path ahead of me and be able to walk at a brisk pace. One thing I’m not is a dawdler.

My London days are behind me now, and I live in the countryside. I still walk every day, but field edges, mud, gates and an endless supply of things worth looking at have slowed me down considerably.

The walks are lovely, I’m still getting my steps in, and I’m not weaving around selfie sticks any more. But it got me wondering: am I actually getting the same health benefit at this gentler pace?

Most of us who track our walking think of step count as the number that matters. But 6,000 slow steps and 6,000 brisk ones are very different cardiovascular workouts. The evidence suggests that how fast you walk may matter at least as much as how many steps you accumulate.

Steps are the starting point, not the whole story

Long-time readers may remember an earlier article where we looked at the relationship between daily step count and long-term health. The 10,000-step target is still everywhere, but a meta-analysis of 88 studies tells a more useful story - most of the reduction in all-cause and cardiovascular mortality accumulates within roughly the first 6,000 daily steps.

That makes 6,000 a sensible minimum target, but not the finish line. Additional steps are associated with further reductions in cardiovascular disease, cancer, diabetes, falls and depression. But the steepest part of the curve is behind you once you’re regularly hitting that range.

Step count captures volume: how much walking you accumulate over the course of a day. But it says nothing about how demanding that walking is. A thousand steps at a gentle amble and a thousand steps at a brisk, purposeful pace ask very different things of your heart and lungs.

So once you’re already getting a reasonable daily step count, is there something to gain from walking some of those steps faster?

Faster walkers, lower risk

Researchers followed more than 50,000 British walkers for an average of 9 years. Compared with slow walkers, those walking at a normal pace had a 20% lower risk of dying from any cause and a 24% lower risk of dying from cardiovascular disease.

The association appeared even stronger for those aged 50 and over: 24% less likely to die from any cause and 23% less likely to die from cardiovascular disease.

Increasing the pace further was associated with additional risk reductions. At a fast pace, those aged thirty and above were 24% less likely to die from any cause, and those aged fifty and above were 32% less likely to die prematurely.

Encouragingly, walking faster was associated with lower mortality even among people not meeting recommended physical activity guidelines, though the gains were greater in those who did.

Another study of almost 22,000 male American physicians, average age 68, followed for nearly 10 years, found a strikingly similar pattern.

Compared with those who didn’t walk regularly, those walking at 2–2.9mph were 28% less likely to die from any cause and 12% less likely to develop cardiovascular disease. At 3–3.9mph, those figures were 37% and 25%. At 4mph or above, 37% and 30%.

Two large studies, in different populations on different continents, land on essentially the same dose-response pattern - those two graphs look very similar. The biggest practical gain is between slow and purposeful walking. The further gains from brisk to fast are smaller. You don’t need to start overtaking joggers.

How much faster?

A meta-analysis of 48 studies involving almost 102,000 older adults (average age 72), followed for about five and a half years, helps put some scale on this. Each 0.1m/s slowing in walking speed was associated with 12% higher all-cause mortality and an 8% increased risk of cardiovascular disease.

This doesn’t prove that simply walking 0.1m/s faster will produce those same reductions in risk. Some of the difference will reflect the fact that slower walkers are often less fit or less healthy to begin with. But it does tell us that fairly modest differences in walking speed are associated with meaningful differences in outcome. In everyday terms, 0.1m/s is roughly equivalent to covering a familiar route about 10% faster.

If your usual loop takes 30 minutes, aim for around 27. That gives us a useful sense of what “pick up the pace” actually means - not speed-walking, just moving with noticeably more purpose.

Are healthier people just faster walkers?

There’s an obvious problem with all this.

Walking speed is unusual because it’s both a behaviour and a health marker. To walk quickly, your heart, lungs, muscles, joints, balance and nervous system all have to work well together. Frailty, arthritis, neurological disease, heart or lung disease and simple loss of fitness can all slow you down.

So part of the association almost certainly runs in the opposite direction: people aren’t healthier simply because they walk faster; they may walk faster because they’re healthier.

So is there evidence that intentionally walking faster actually does something useful? A large British commuting study offers a clue.

Researchers followed more than 263,000 mostly midlife adults for an average of 5 years, comparing health outcomes by how they got to work.

Those who walked to work were 27% less likely to develop cardiovascular disease and 36% less likely to die from it. But despite being more physically active than drivers and public-transport users, walking commuters didn’t have greater cardiorespiratory fitness. And they didn’t see reductions in all-cause mortality or cancer risk. The cardiovascular benefits in walkers only appeared in those walking more than about six miles a week - equivalent to roughly two hours at a typical pace.

Cyclists told a different story. They were 46% less likely to develop cardiovascular disease, 52% less likely to die from it, 41% less likely to die from any cause, and 45% less likely to develop cancer. Ninety per cent of cycling commuters met recommended weekly physical activity levels; only 54% of walking commuters did.

This isn’t proof that intensity is the key factor, but it’s a suggestive clue. Cycling generally demands more from the cardiovascular system than a typical walking commute, and the walkers and cyclists also differed in total activity amount, so the study can’t isolate intensity on its own.

But the pattern is consistent with a broader idea. You can accumulate quite a lot of movement without necessarily giving your cardiovascular system much of a training stimulus.

A gentle walk is still movement, but with a brisk walk, your heart and lungs have to work harder, and over time that provides a stimulus to adapt and build reserve.

What happens when you deliberately speed up?

The observational studies leave us with a strong association, but the intervention studies get closer to answering whether deliberately increasing pace actually changes anything.

Researchers randomly assigned 246 people, average age 63, to one of three groups for five months: no added walking programme, regular moderate walking of at least 8,000 steps a day on four or more days a week, or a programme alternating three minutes of easier walking with three minutes at a much brisker pace.

Aerobic fitness barely changed in the first two groups. That’s notable because the steady walkers were doing 8,000 steps a day on four or more days each week: a substantial amount of walking. By contrast, the group adding repeated three-minute brisk intervals increased walking aerobic capacity by about 9%, improved leg strength by 13–17%, and lowered blood pressure further.

A Japanese study strengthened that finding and gave us a useful dosing target. Among 679 participants doing different proportions of fast and slow interval walking over five months, peak aerobic capacity improved progressively with the amount of fast walking, up to about 50 minutes a week, after which it tended to plateau. Neither slow-walking time nor total walking time was associated with the improvement.

So, simply accumulating more walking wasn’t what predicted better aerobic fitness; it was the time spent walking fast enough to challenge the cardiovascular system. Put together with the previous trial, the implication is that easy walking can give you plenty of movement, but improving cardiorespiratory fitness requires enough intensity to give your heart and lungs a reason to adapt.

Now, these trials measured intermediate outcomes: aerobic fitness, leg strength and blood pressure, not mortality or cardiovascular events. But they address the central weakness of the observational studies by showing that when intensity is deliberately increased, real physiological change follows.

What this means for your health

Ordinary walking remains valuable, and nobody should come away from this thinking their daily stroll has been a waste of time. A slow walk still gets you moving, outdoors and, if you’re lucky, somewhere pleasant. Walking of any kind is associated with many benefits.

But if you’re already walking regularly and want to maintain or improve cardiovascular fitness as you get older, the next useful lever is probably pace rather than simply adding more easy steps.

That doesn’t mean every walk needs to feel like exercise. A slow countryside meander or a long conversation with a friend serves purposes that a brisk session doesn’t: enjoyment, connection, time in nature. But those purposes aren’t interchangeable with cardiovascular training.

A reasonable target from the intervention evidence is about 50 minutes of brisk walking accumulated over the week: enough to make your heart and lungs notice.

As always, your responses are anonymous, but they really help me tailor future content to what’s most helpful to you. Please take a moment to click a button.

HEALTH TWEAK OF THE WEEK

Walking regularly is a strong foundation. But the evidence suggests that pace matters alongside step count.

Large observational studies link faster walking with lower cardiovascular and all-cause mortality, while intervention trials show that brisk walking can improve aerobic fitness, leg strength and blood pressure in ways that steady, easy-paced walking may not.

1. Make some of your usual walking brisk. Aim to accumulate about 50 minutes of brisker walking over the course of the week: enough to make your heart and lungs noticeably work harder, but not so much that you can’t hold a (slightly breathless) conversation. You don’t need to do it all at once. Short bursts of three to five minutes scattered through your regular walks add up. Shift from “I’m out for a stroll” to “I’m going to miss the bus.”

2. Prefer something measurable? Pick a familiar route and try to cover it in roughly 10% less time. If your usual loop takes 30 minutes, aim for around 27. That gives you a concrete benchmark to gauge whether you’re pushing the pace enough.

3. Keep your leisurely walks too. This isn’t about turning every walk into a training session. Countryside rambles, conversation walks and time in nature all have their own value. The point is to make sure that some of your weekly walking is vigorous enough to challenge your heart and lungs.

If walking is already part of your routine, you’ve done the hard part. Now make some of those walks brisk enough to give your cardiovascular system something to adapt to

Enjoyed this? There’s more to explore.

If today’s article has made you rethink your daily walk, you might enjoy some of my earlier newsletters exploring how much movement we really need, whether exercise can offset a day of sitting, and why strength training is so important for healthy ageing.

Paid subscribers can explore these and the entire One Health Tweak a Week archive, covering everything from nutrition and exercise to sleep, metabolic health and longevity, with newsletters and podcast episodes to read or listen to whenever you like.

Unlock the full archive →

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🎧 Prefer to listen while deciding whether your next walk needs a little more urgency?

🎙️ This week’s One Health Tweak a Week podcast takes a closer look at walking pace: why step count is only part of the story, what changes when you start walking briskly, and how much faster you may need to go to improve your cardiovascular fitness.

You’ll hear:

• Why 6,000 slow steps and 6,000 brisk ones aren’t the same cardiovascular workout

• Why faster walkers have lower risks of premature death and cardiovascular disease

• Why some of that association reflects the fact that healthier people can simply walk faster

• What happens when researchers ask people to speed up their walking

• Why 8,000 steady steps may do surprisingly little for aerobic fitness

• How about 50 minutes of brisk walking a week could be enough to make a meaningful difference

👉 Good company for your next walk, commute, or while testing whether “I’m going to miss the bus” is a more useful pace than “I’ve got nowhere particular to be”.

👉 Listen now!

(Episodes are free for now. Paid subscribers support the deeper research - and unlock practical tools to help you improve your health without turning it into a second job.)

🧭 Before you go

💬 When you go for a walk, what usually determines your pace: fitness, habit, company, terrain, the dog, or simply whether you’re in a hurry?

Leave a comment

📤 Know someone who proudly hits their step target but rarely gets out of strolling mode? Forward this to them.

Share

👥 Paid corner - If you try adding some brisk walking this week, drop me a message in our private chat. I’d be interested to hear whether the “miss the bus” cue or the 10%-faster route works better for you.

Until next Saturday - keep the leisurely walks, but give your heart and lungs something to do as well.

– Ben

But 6,000 slow steps and 6,000 brisk ones are very different cardiovascular workouts.

In this episode of One Health Tweak a Week, we look at what walking pace adds beyond step count. We’ll explore studies showing that faster walkers have lower risks of cardiovascular disease and premature death, while also asking the obvious question: are they healthier because they walk faster, or do they walk faster because they’re healthier?

Then we move to the evidence that helps untangle that problem. In intervention studies, people doing plenty of steady walking saw little improvement in aerobic fitness, while those adding brisk intervals became fitter, stronger and lowered their blood pressure.

We’ll also look at how much brisk walking may be enough to make a difference, why around 50 minutes a week is a useful target, and how a simple 10%-faster familiar-route test can help you judge your pace.

The takeaway is that if you already walk regularly, making some of those steps brisk may do more for your cardiovascular fitness than simply adding more easy ones.

I’ve been meaning to look into this for years.

Every time another “forever chemicals” headline landed, I’d glance at my non-stick frying pan, notice the scratches across the bottom, and feel a small twinge of unease. Not enough to sit down and research the evidence. Just enough to worry me a little before I carried on making dinner. Maybe you’ve felt that, too.

Eventually I bought a new pan with a ceramic non-stick coating instead of the usual Teflon. Problem solved.

Then I noticed the non-stick basket in my air fryer. And the baking tins. And then I started wondering about the lining of the oven. Non-stick had colonised my kitchen while I was busy worrying about one pan.

I hadn’t removed non-stick coatings from my kitchen. I’d replaced one pan.

So had I reduced a meaningful health risk, or simply responded to a very effective scare story? I honestly didn’t know.

So I’ve finally sat down with the research to answer the question properly. Much of the evidence is reassuring, but there are a few findings that are worth knowing.

PFAS are a real problem. That doesn’t tell us much about your pan.

PFAS, or per- and polyfluorinated alkyl substances, are a huge family of man-made chemicals valued because they resist water, grease, stains and heat.

They’re found in food packaging, waterproof clothing, carpets, personal care products and, of course, non-stick cookware. One member of the family is polytetrafluoroethylene, or PTFE, better known by the brand name Teflon.

They’re called “forever chemicals” for good reason. We produce around a million tonnes of PFAS every year, and many persist in the environment for thousands, possibly tens of thousands, of years. Virtually all of us have detectable PFAS in our blood.

There are at least 8,000 different PFAS, with more than 600 in commercial use, yet only a small proportion have been studied well enough to understand their health effects. The ones that have been studied give genuine cause for concern.

They’re associated with a lowered response to childhood vaccines, higher rates of childhood infections, increased risk of thyroid disorders, disruption to liver function, higher LDL cholesterol, increased risk of chronic kidney disease and kidney cancer, reduced fertility in both men and women, and higher rates of pregnancy-related hypertension and pre-eclampsia.

That’s a serious list. But before we blame the frying pan, we need to know how much exposure actually comes from cookware.

We’re exposed to PFAS from many overlapping sources: food, drinking water, house dust, indoor air and consumer products. Diet may account for at least 40% of exposure in some settings; house dust perhaps 3-25%; indoor air less than 4%.

The mix varies enormously depending on where you live, local industrial history and drinking-water contamination. And some of the best exposure data we have is now over 20 years old, predating regulations that restricted several PFAS, so the picture has likely shifted since then.

Nobody has reliably calculated what proportion of our total PFAS exposure comes from cookware. But the available evidence suggests it is a small contributor compared with food, drinking water and other environmental sources.

What happens when you heat a non-stick pan?

To understand the cookware question, it helps to think about two types of PFAS.

The first is the very large PTFE polymer molecules that form the non-stick coating: too big to be absorbed into the bloodstream. The second is much smaller PFAS molecules, either left over from manufacturing or released when the coating breaks down under extreme heat. It’s these smaller molecules that can be absorbed, circulate in the blood, and accumulate in our tissues over years. They’re the ones worth worrying about.

German researchers heated 5 commercial non-stick frying pans, 9 baking trays and 4 baking mats to 250°C/480°F for 30 minutes. None of the frying pans released any of the small PFAS they were testing for. One baking tray and one baking mat did, but only on the first heating, pointing towards manufacturing residues rather than a breakdown of the coating.

The same experiment detected many volatile organic chemicals from new cookware on the first heating, but not subsequently. That’s a good reason to wash new coated cookware thoroughly, follow the manufacturer’s first-use instructions and ventilate well for the first few uses.

Temperature, however, changes things dramatically.

In another study of 13 pans, emissions of small PFAS molecules were about 4.75ng/hour under normal-use conditions. At 370°C / 700F, they climbed to 12,190ng/hour: more than 2,500 times higher.

A pan containing food is very unlikely to reach 370°C. An empty pan forgotten over a fierce burner can.

The German Federal Institute for Risk Assessment reaches much the same conclusion: properly used PTFE cookware isn’t expected to cause adverse health effects; the meaningful hazard arises when empty cookware is strongly heated to around 360°C or above.

At those temperatures, the fumes can cause polymer fume fever: fever, chills, headache, muscle and joint pains and general malaise beginning several hours after exposure. Overheated non-stick cookware is one recognised cause.

You can preheat a non-stick pan moderately, but don’t leave it empty on high heat long enough to get screaming hot.

The “millions of particles” story

You may remember headlines in 2022 claiming that damaged Teflon pans could release thousands or even millions of micro- and nanoparticles.

The study didn’t actually show that millions of particles were ending up in anyone’s food.

That study was designed to develop a method for detecting coating abrasion. The researchers removed non-stick surfaces from their pans, then deliberately attacked them with steel wool and barbecue clamps before examining the results under a scanning electron microscope.

They didn’t actually cook any meals, and most of the particles they identified were still attached to the coating or to a utensil. That’s a long way from showing what happens when you sauté potatoes for dinner.

A 2024 study using more realistic food-preparation activities did find particles coming from plastic utensils, containers and non-stick coatings. But the researchers estimated that all the plastic/non-stick cookware studied, including chopping boards, might contribute around 2,400-5,000 particles a year to home-cooked food. It still represents some exposure, but on a very different scale from the headlines suggesting millions of particles in every meal.

You might reasonably argue that any non-stick particles we swallow are irrelevant anyway, since the material is famously inert: it shouldn’t react with anything on its way through the system. But recent cell-culture work complicates that assumption.

Spanish researchers found that PTFE nanoparticles could get inside cells, where they disturbed cellular structure, damaged mitochondria, triggered inflammation, caused oxidative stress and damaged DNA. The particles didn’t kill the cells, but that’s still a concerning set of effects.

This is laboratory cell-culture evidence, not clinical evidence. It can’t tell us the dose that reaches human tissues during ordinary cooking, and it doesn’t demonstrate that using an intact pan causes harm. But it does weaken the blanket assumption of biological inertness, and it strengthens the case for replacing pans whose coatings are substantially scratched, blistering, flaking or peeling, rather than continuing to cook on them.

There’s no perfectly inert pan

Media coverage leaves the impression that non-stick is uniquely suspect and everything else is clean.

But, of course, nothing is ever that simple.

US researchers found small amounts of titanium, silicon and aluminium migrating from ceramic coatings, with more released after aggressive scouring.

Korean researchers tested 88 kitchen items made from stainless steel, aluminium alloys, copper alloys and cast iron and found small amounts of metals migrating into food, particularly under acidic conditions or with abrasive scrubbing.

In most studies, the amounts released under ordinary use are too small to be expected to cause harm. Stainless steel, ceramic, cast iron, aluminium and copper all interact with food to some degree. Every material comes with its own small set of trade-offs.

Each material brings a different compromise:

• PTFE non-stick: Effortless food release; coating eventually wears; risk from overheating or damaged coatings.

• Ceramic non-stick: PFAS-free; may lose non-stick properties sooner; coating constituents can migrate under abrasion.

• Stainless steel: Very durable, dishwasher-safe; food sticks more easily; small nickel and chromium release, especially with acidic foods.

• Cast iron and carbon steel: Extremely durable; heavy, requires seasoning; transfers iron to food (generally harmless unless you have an iron overload disease like haemochromatosis).

• Enamelled cast iron: Durable glass-like enamel surface; heavy, not truly non-stick; very little concern with quality enamel.

• Aluminium: Lightweight, responsive to heat; bare metal reacts with acids; aluminium leaching possible from uncoated pans.

• Lined copper: Excellent heat control; expensive; minimal concern while the stainless lining is intact. Unlined pans can leach harmful amounts of copper.

For most of us, the nuisance factor matters too. I don’t think maintaining a frying pan should become a hobby unless you want it to. Some people genuinely enjoy seasoning cast iron. I’m happy for them, but that’s not me.

Product quality matters too.

Aggressive testing of 35 cookware samples in Turkey detected PFAS in six and aniline-related chemicals, which are presumed carcinogens, in all of them. They also found small amounts of arsenic, cadmium, chromium and nickel migrating from stainless-steel cookware into food, particularly under acidic conditions and after scrubbing with abrasives like steel wool.

That testing was harsher than normal household use, but it’s a reason to buy from reputable suppliers rather than simply going for the cheapest pan available, which might be made from non-food-safe recycled metal.

I should stress that this isn’t intended as a definitive guide to buying frying pans. I’m looking at them primarily through the lens of health risk and everyday practicality.

I know a number of professional chefs read the newsletter, and I’d love to hear your perspective: what do you actually use in your own kitchen, and what would you recommend to someone who wants a durable, practical pan without turning its care and maintenance into a hobby?

The same principles apply to kitchen appliances with non-stick coatings: air fryers, rice cookers, waffle irons, sandwich makers and electric grills. None of them come close to the 360°C / 700°F temperatures at which coatings start to break down during normal use, and the same care rules apply.

And, just so you know, oven linings are usually ceramic, so no PTFE coatings to worry about there, so at least the oven can come off the suspect list. Though new ovens do give off chemical residues from the manufacturing process, as you’ll know from that ‘new oven’ smell.

What about non-stick baking trays?

There’s one finding I want to circle back to. In the German study, the frying pans performed well, but some of the non-stick-coated baking trays and mats released small PFAS when heated to 250°C (480°F). None were detected when the same samples were heated a second and third time, suggesting these were residues left over from manufacture rather than the coating steadily breaking down.

For ordinary baking, that’s fairly reassuring. Most of us cook well below 250°C, and PTFE doesn’t begin to seriously break down until considerably higher temperatures.

I’d be more cautious if you use a non-stick baking sheet for very high-temperature cooking, such as pizza with the oven turned up as far as it will go. Check the manufacturer’s maximum temperature, and personally I’d use an uncoated metal tray, pizza stone or steel for that job. As with a frying pan, replace coated bakeware once the surface is badly scratched, peeling or flaking.

For now, I wouldn’t rush off to buy silicone baking sheets or cake tins. These come with their own worrying findings, and deserve an article of their own.

The bigger picture

There’s a risk here of focusing so closely on the pan that we overlook what frying itself puts into the kitchen air.

British researchers measured the volatile organic compounds released while shallow-frying flatbread, frying spices and making a chicken curry. Concentrations of acetaldehyde and acrolein, both linked to lung irritation and cancer, ran two to ten times higher than recommended limits for safe indoor air.

We’ve spent a lot of time worrying about nanograms of chemicals coming off the pan. Meanwhile, frying itself fills the kitchen air with a much larger mixture of irritant, pro-inflammatory and cancer-causing chemicals, such as acetaldehyde and acrolein. In experimental kitchens, some of these have reached several times recommended indoor-air limits.

In a factory or professional kitchen, you’d be expected to control fumes at those levels to protect workers. At home, many of us fry dinner blissfully unaware, while the extractor fan sits unused.

What this means for your health

So what does this add up to for you?

PFAS really are harmful, but the evidence doesn’t support the idea that routine cooking in PTFE-coated non-stick pans is a significant source of harmful PFAS exposure.

The risk picture changes in a few specific, avoidable situations: severely overheating an empty pan, continuing to cook with a pan whose coating is substantially damaged, or buying poor-quality cookware of uncertain provenance. Those are definitely worth avoiding.

Every material we looked at comes with its own small exposure issues, alongside practical strengths and weaknesses. Changing pans means choosing a different set of trade-offs.

And perhaps more importantly, frying itself carries real risks. Heating food and oil to high temperatures produces harmful chemicals, whatever pan you use. If you’re concerned about your long-term health, fry infrequently, and always have the extractor on when you do.

As always, your responses are anonymous, but they really help me tailor future content to what’s most helpful to you. Please take a moment to click a button.

HEALTH TWEAK OF THE WEEK

PFAS - the so-called “forever chemicals” - are a genuine health concern, and reducing unnecessary exposure makes sense. But for most of us, a sound non-stick frying pan used properly is unlikely to be an important source. The bigger cookware risks are much more specific: badly damaged coatings, severe overheating, and poor-quality products.

Take one minute today to check the coated cookware you actually use.

Start with your frying pan, then look at your air-fryer basket, baking trays, and any other regularly used non-stick surfaces.

Keep using them if the coating is intact or only lightly marked.

Replace them if they’re heavily scratched, blistering, peeling or flaking, or if the non-stick surface has clearly started to fail.

Then make three small habits automatic:

• Don’t leave an empty non-stick pan sitting over high heat.

• Use wooden or other non-abrasive utensils and avoid steel wool or harsh scourers.

• Turn on an externally vented extractor whenever you fry, and keep frying as an occasional cooking method rather than an everyday one.

If you buy new coated cookware, choose a reputable manufacturer, wash it before first use, follow its care instructions and ventilate well during the first few uses.

Once you’ve done that, I’d give your cookware rather less mental bandwidth. The evidence doesn’t support treating a sound non-stick pan as a hidden health threat. A quick check, a few sensible habits and replacing coatings when they genuinely deteriorate will take you most of the way.

🎧 Prefer to listen while wondering whether your frying pan is secretly poisoning you?

🎙️ This week’s One Health Tweak a Week podcast takes a close look at non-stick cookware, PFAS and the question most of us actually want answered: is the pan we cook with every day something we need to worry about?

You’ll hear:

• Why PFAS really are a health concern, but your frying pan is probably a very small part of the problem

• What researchers actually find when they heat modern PTFE non-stick cookware

• Why overheating an empty pan changes the picture dramatically

• What scratches, peeling and flaking really mean, and when I’d replace a pan

• What we know about air fryers, baking trays, rice cookers and other coated appliances

• Why switching to ceramic, stainless steel, or cast iron doesn’t make every potential exposure disappear

• The simple cookware check and cooking habits that can reduce the risks that are worth worrying about

👉 Good company for your next walk, commute, or while standing in front of the pan cupboard wondering whether that scratch really means it’s time for a new one.

👉 Listen now!

(Episodes are free for now. Paid subscribers support the deeper research - and unlock practical tools to help you improve your health without turning it into a second job.)

🧭 Before you go

💬 Have a look at the cookware you actually use. Are you keeping your non-stick pan, replacing a badly worn one, changing how you heat it, or finally remembering to turn on the extractor?

And if you’ve already moved away from conventional non-stick, I’d be interested to hear what you chose instead and how you’ve found it in everyday use.

Leave a comment

📤 Know someone who has been eyeing their frying pan suspiciously after another headline about “forever chemicals”? Forward this to them.

Share

👥 Paid corner - Do the one-minute cookware check from this week’s Health Tweak and tell us what you found. I’m particularly interested in the pans and appliances that turned out to be in much better shape than you feared - and the ones that clearly deserved retirement.

Until next Saturday - check the coating, avoid heating an empty non-stick pan hard, and then give your cookware a little less mental bandwidth.

– Ben

In this episode, we look past the “forever chemicals” headlines to ask a much narrower and more useful question: how much health risk actually comes from everyday cooking with PTFE-coated cookware?

We examine what intact non-stick pans release during normal use, what changes when they’re severely overheated, and whether scratched or damaged coatings really shed meaningful amounts of particles into food. We also look at the evidence behind some of the more alarming microparticle claims, and where those studies do, and don’t, reflect real-world cooking.

Then we widen the lens. Would switching to ceramic, stainless steel, cast iron, aluminium or copper actually make your kitchen safer? And what about air fryers, electric grills, sandwich makers and ovens?

The answer is more reassuring, and more nuanced, than most cookware scare stories suggest.

By the end, you’ll have a simple framework for deciding what to keep, what to replace, which habits genuinely matter, and why the fumes produced by frying itself may deserve more attention than the material your pan is made from.

Last week, we looked at why fibre deserves your attention. The headline numbers were hard to ignore: people who eat the most fibre have a 15% lower risk of premature death from any cause and a 24% lower risk of coronary heart disease. And the benefits don’t seem to plateau at 30g a day - studies suggest they keep accruing beyond that.

The obvious response is to eat more of the stuff. And most of us badly need to. In the US, fewer than 10% of women and just 3% of men reach the recommended 25–30g a day. Among UK adults over 65, fewer than 6% manage 30g.

So, we’re agreed. More fibre would be a good idea.

But what does that actually mean when you’re standing in the kitchen tomorrow morning? You could eat a bowl of All-Bran and congratulate yourself, but those extra grams of fibre could just as easily come from oats, beans, nuts, fruit, vegetables or a spoonful of psyllium. And, as it turns out, they’re not all doing quite the same thing.

Fibre is rather more complicated than the number on the nutrition label.

Most fibre-rich foods contain a mixture of types, but not in the same proportions. That affects what they do in the gut, and some foods also make it much easier to reach 30g in the first place.

So this week, I want to tackle the practical question we left hanging last time. If you’re going to eat more fibre, how should you get it?

Much of our fibre comes in the wrong package

A UK national dietary survey examined fibre sources for adults over 65. The average intake was just 18.3g/day, and the breakdown of where that fibre came from was just as revealing as the number itself.

It’s not a picture that fills you with confidence.

There are some whole grains, some peas and a few legumes. But major contributors otherwise include baked beans (okay in principle; in practice, often full of sugar and paired with processed meat), French fries and other fried potatoes, breakfast cereal (mostly ultra-processed, frequently sugar-laden), pizza, white bread and non-fried potatoes.

I can’t help but feel we could do better.

If we’re going to eat more fibre, I’d rather those extra grams came from foods that bring plenty of other useful things with them, rather than arriving incidentally in pizza, fries and sugary breakfast cereal.

And there’s another reason to care where our fibre comes from: different foods don’t give us the same mix of fibres.

Different fibres do different things

Most of us picture fibre as rough stuff: plant material that passes through largely undigested. That’s insoluble fibre, and it’s genuinely useful. It absorbs water, adds bulk, and speeds transit through the gut. This is partly why higher fibre intake is linked to lower rates of colon cancer. Waste material spends less time sitting against the gut wall, and increased bulk dilutes potential carcinogens.

But insoluble fibre is no one-trick pony.

In a study of more than 86,000 US adults, those consuming the most fibre had a 29% lower risk of premature death from any cause, a 27% lower risk of dying from cardiovascular disease, and a 23% lower risk of dying from cancer. Both soluble and insoluble fibre showed broadly similar associations.

Soluble fibre behaves rather differently. Some types form gels in the gut that are particularly effective at binding bile acids.

Bile acids are made from cholesterol in the liver and used to help absorb fats. Normally they’re recycled, but those bound by fibre are carried out of the body. The liver has to make replacements, and to do that it pulls additional cholesterol from the bloodstream. Do that every day, and your blood LDL cholesterol levels can fall meaningfully.

A third important property is fermentability. Some fibres, whether soluble or insoluble, are broken down by gut bacteria. This produces short-chain fatty acids, which may help explain some of fibre’s broader health effects. As we discussed last week, though, that evidence remains plausible rather than conclusive.

Most whole foods contain more than one type of fibre, but not in the same proportions. Oats contain both soluble and insoluble fibre; legumes provide both fermentable and bulking fibres, but their overall fibre profiles are different. No single food gives you the same mix in the same amounts, which is why variety still makes sense.

And, of course, we’re not just eating for fibre. Different foods also bring along different combinations of proteins, resistant carbohydrates, vitamins, minerals and polyphenols.

Getting to 30g: what makes it easier

So, how do you actually reach 30g a day? Some foods are more fibre-dense than others, but you might be surprised at how much they vary.

Before you look at the graph below, try putting these five foods in order from most to least fibre-dense: broccoli, brown rice, prunes, wholewheat bread and an apple.

How did you do? Any surprises? Broccoli perhaps gets a little more credit than it’s properly earned.

(I realise you’ll need to zoom in to see the detail here, but that felt more useful than just giving you a handful of foods).

A common piece of advice for getting more fibre is to eat more fruit and vegetables. That’s a great strategy for long-term health, but as you can see, fruits (yellow) and vegetables (green) sit mostly to the right of the graph - you need to eat considerably more of them to get 10g of fibre. The left side, the most fibre-dense foods, is dominated by grains, seeds and nuts, with legumes holding the middle ground.

Fruit and vegetables remain valuable for many reasons beyond fibre. But if you’re trying to increase your fibre intake efficiently, grains, nuts, seeds and legumes generally provide fibre more efficiently.

Why whole grains deserve a place on your plate

Not all fibre sources appear to be equally associated with long-term health outcomes. Cereal fibre, in particular, has shown unusually consistent links with lower disease risk.

In a study of more than 39,000 mid-life Australian adults followed for almost 14 years, those eating the most cereal fibre were 25% less likely to develop type 2 diabetes. Fruit and vegetable fibre did not show the same protective association. Cereal fibre has also been consistently linked to lower rates of cardiovascular disease and colorectal cancer.

In a separate study of 4,125 older US adults, cereal fibre, but not fibre from other sources, was associated with lower blood levels of inflammatory markers.

Why might whole grains show a stronger signal?

It isn’t entirely clear. They contain a mixture of insoluble bran fibres and more soluble fibres, alongside minerals and phytochemicals that may contribute independently. Some cereal fibres are fermented by gut bacteria; others seem to work through quite different routes, including improving bowel transit and possibly insulin sensitivity.

The stronger associations seen with cereal fibre don’t prove that cereal fibre itself is uniquely protective; whole grains bring along plenty besides fibre. But the broader evidence for fibre, including intervention studies, is strong enough to support a causal effect on cardiovascular health.

When you’re thinking about where to get your fibre, make sure some of it comes from whole grains: oats, barley, wholemeal bread, wholegrain pasta, etc.

What about fibre supplements?

Perhaps it’s a sign of the times that, when something in our diet needs fixing, we’re increasingly inclined to ask whether there’s a pill for it. Or, these days, an injection.

Fibre is no exception. The fibre supplement shelves are certainly well stocked. But now that we’re budding fibre experts, we know enough to assume they’re not all interchangeable.

Psyllium (Metamucil) is the most versatile. Made from the husk of a plantain (the weed in your lawn, not the banana relative), it works as both a bulking agent and a gel-former. In a meta-analysis of 28 studies, about 10g/day of psyllium reduced LDL cholesterol by approximately 0.33mmol/L (~11%) and apoB by 0.05g/L (~6%).

Wheat bran is primarily a bulking agent for bowel regularity, though it can also reduce post-meal blood sugar spikes.

Methylcellulose (Citrucel) and polycarbophil (FiberCon) are water-absorbing, bulk-forming products used mainly for constipation.

Then there’s a broader category: wheat dextrin, inulin, chicory root fibre, partially hydrolysed guar gum and others. These are often marketed as “prebiotics” because they feed gut bacteria and can shift the composition of the gut microbiome. Whether those shifts translate into the kind of meaningful health benefits associated with fibre-rich whole foods is much less certain.

My take is that whole foods should be your default. They provide fibre alongside a host of other beneficial nutrients that supplements can’t replicate. Psyllium has its place, particularly for bowel regularity and LDL reduction. If you do use it, plain, unflavoured psyllium husk added to food is preferable to highly processed versions containing artificial sweeteners, flavourings, and emulsifiers.

What this means for your health

Most of us need a meaningful increase rather than fine-tuning, and, as we saw last week, the evidence suggests benefits continue beyond 30g. So 30g is a useful target to reach, but not a point at which the benefits suddenly stop.

The solution isn’t to find the single “best” fibre source and eat lots of it. Different fibres do different jobs, and different fibre-rich foods bring along different packages of nutrients. A mix of whole grains, legumes, nuts, seeds, fruit and vegetables will serve you better than any one of them alone.

What matters in practice is the fibre you keep eating. Nuts you look forward to, oats you enjoy at breakfast or beans you happily add to chilli will do more for you over time than a bag of wheat bran slowly going stale at the back of the cupboard.

Because my diet is largely plant-based, and full of fruit, vegetables and whole grains, I don’t really need to think about fibre targets. I average 34g a day without trying.

My breakfast is usually muesli. Rolled oats provide the base, then I add nuts, seeds, and dried fruit, plus whatever else appeals that morning: apple, berries, cocoa nibs, or something different. I’m not sitting down to a medicinal bowl of fibre. It’s breakfast I enjoy that happens to contain several good sources of it. Add a slice of seeded, wholegrain bread, and I’m already at 14g of fibre.

The trick is to find your own version of that, a meal or two you genuinely enjoy that does a lot of the fibre work for you.

As always, your responses are anonymous, but they really help me tailor future content to what’s most helpful to you. Please take a moment to click a button.

HEALTH TWEAK OF THE WEEK

There’s convincing evidence that getting enough fibre is linked to major long-term health benefits, including a lower risk of cardiovascular disease and premature death. Most of us, though, are nowhere near recommended intakes: fewer than 10% of US women and just 3% of men reach them, and among UK adults over 65, fewer than 6% get to 30g/day.

So the first job is to get more of it. But fibre isn’t a single substance, and foods don’t all provide the same mix. Whole grains, legumes, nuts, seeds, fruit and vegetables each contribute something a little different, which is why a varied mix makes more sense than relying heavily on one source.

Use 30g/day as a practical target to reach, then keep going if you can. The easiest way to get there is to build more fibre into foods you already enjoy, while adding a few new options that sound appealing enough to become habits.

1. Recheck your baseline. Go back to the 3-day food diary from last week and look at your average daily fibre intake. Work out roughly how far you are from 30g.

2. Choose 2–3 changes that will meaningfully raise your fibre intake. Start from the way you already eat, but give yourself a few different routes in. If you’re well below 30g/day, the aim is to build a noticeably more fibre-rich diet, not just add the occasional virtuous apple.

• Upgrade the staples. Switch white bread, pasta and rice for wholegrain versions. Have baked beans on wholegrain toast for a quick lunch, but avoid versions loaded with added sugar or processed meat. Add canned beans or lentils to soups, stews, sauces or rice.

• Use snacks to your advantage. When you want something between meals, reach for a handful of nuts, some fruit or a bowl of popcorn rather than something with virtually no fibre.

• Add fibre without creating another meal. Toss pumpkin, sunflower, sesame or chia seeds over breakfast, yoghurt or a salad. Stir ground flaxseed into oats. Add a spoonful of nuts or seeds to something you already eat.

• Try one new thing. Make a chia pudding and see whether you like it. Swap rice for quinoa one evening. Open a can of mixed beans, rinse them, add a dressing you enjoy and have them with salad and some crusty wholegrain bread. Try barley or bulgur somewhere you’d normally use rice or pasta.

• If you’re already eating plenty of plants, push the variety and density higher. Add another serving of legumes, use nuts and seeds more deliberately, choose denser whole grains, and look at where another 5–10g could come from without simply eating more food.

Breakfast is still one of the easiest places to make progress. As my muesli shows, oats, wholegrain bread, nuts, seeds and fruit can do a surprising amount of the work before the day has really begun.

The point of the list is that somewhere in it there should be two or three things that make you think, I could do that. Try those this week. If you enjoy them and they fit easily into your life, keep them. Then try something else.

A few changes that stick can shift your fibre intake surprisingly quickly. Get closer to 30g, keep building from there, and you’ve made one more useful change that should pay you back for years to come.

🎧 Prefer to listen while deciding whether your fibre really needs to come from bran?

🎙️ This week’s One Health Tweak a Week podcast picks up where we left off last week. We know most of us need more fibre. The more useful question now is: where should it come from?

You’ll hear:

• Why different fibres do different jobs, from keeping things moving to lowering LDL cholesterol

• Why the fibre in oats, beans, nuts, seeds, fruit and vegetables isn’t nutritionally interchangeable

• Which foods make getting to 30g a day much easier than others

• Why whole grains deserve rather more attention than they usually get

• What psyllium, wheat bran and “prebiotic” fibres can and can’t do

• How to raise your fibre intake without suddenly becoming someone who prepares grain bowls for lunch

👉 Good company for your next walk, commute, or while staring into the cupboard wondering whether there’s anything in there that could quietly add another 5g of fibre to your day.

👉 Listen now!

(Episodes are free for now. Paid subscribers support the deeper research - and unlock practical tools to help you improve your health without turning it into a second job.)

🧭 Before you go

💬 Which of this week’s suggestions are you actually going to try? Wholegrain swaps, nuts for snacks, seeds on breakfast, beans somewhere unexpected, quinoa, chia pudding - or something else entirely?

Leave a comment

📤 Know someone who wants to eat more fibre but would rather not reorganise their entire life around lentils? Forward this to them.

Share

👥 Paid corner - If you did last week’s 3-day fibre check, tell us where you landed and what you’re changing first. I’m particularly interested in the small swaps and additions that feel realistic enough to stick.

Until next Saturday - pick two or three things from the menu and give them a try. A few changes that genuinely suit the way you eat can add up surprisingly quickly.

– Ben

If you missed last week’s issue on the health benefits of eating more fibre, you can find it here:

In this week’s One Health Tweak a Week podcast, we look at why fibre is more complicated than the number on the nutrition label.

We explore:

• Why most adults still fall well short of recommended fibre intakes

• The difference between insoluble, soluble, viscous and fermentable fibres, and why those differences are useful

• Why whole grains seem to have particularly strong links with better long-term health

• Which foods make reaching 30g a day much easier

• Whether fibre supplements such as psyllium, wheat bran and “prebiotic” fibres can do the same job as food

• And, most importantly, practical ways to increase your intake without turning every lunch into a grain bowl

We finish with a menu of simple changes, from switching everyday staples and improving snacks to trying chia, quinoa, beans, nuts and seeds.

The aim is straightforward: find a few changes you genuinely enjoy, get closer to 30g, and make a higher-fibre diet feel like normal eating rather than another nutritional chore.

As a kid, I watched my dad struggle through a bowl of All-Bran every morning. It was a hard watch, and no doubt a harder eat.

Back then, fibre was “roughage”. It kept you regular, and that was pretty much the sales pitch.

It’s no wonder few of us got excited about it. Who wants to sit down to a plate of roughage? If you understood the rationale, it felt l…

Read more

In this episode, we look at why that view is far too narrow.

We explore the evidence linking higher fibre intake with lower risks of cardiovascular disease, type 2 diabetes, colorectal cancer and premature death, and ask the obvious question: is fibre itself helping, or is it simply travelling with an otherwise healthy diet?

We also look at intervention studies showing that specific fibres such as psyllium and oat beta-glucan can lower LDL cholesterol, explain how fibre can affect cholesterol and blood sugar despite the fact that we don’t digest it, and unpack why “fibre” is really a family of substances with different physiological effects.

We also take a more sceptical look at the popular microbiome and short-chain-fatty-acid story, where the human evidence is less tidy than the headlines suggest.

Finally, we look at how much fibre most of us actually eat, why 25–30g/day may be better thought of as a minimum target than an optimum, and the simple first step we’d suggest before trying to change your diet: work out where you’re starting from.

Most people who read One Health Tweak a Week already make a real effort to eat well.

I’m sure you know the broad principles. More vegetables and fruit. More whole grains, beans, nuts and fish. Less processed meat, sugary drinks and heavily processed food.

But knowing the principles isn’t quite the same as being able to look objectively at your…

Read more

You’ve decided a protein supplement might be useful. You’ve done battle with the wall of tubs in the nutrition shop, resisted the one promising some sort of “maximum anabolic matrix”, and finally made it home with something that looks as though it belongs in Arnold Schwarzenegger’s gym locker.

Now what?

How much are you actually supposed to take? Should y…

Read more

In this episode, we look at how to use protein supplements in a practical, targeted way. We follow an active retired couple as they work out their daily protein needs, track what they normally eat and discover that they don’t need more protein at every meal. Breakfast is the main weak spot, lunch is usually fine, and dinner often needs only a small top-up.

We work through the numbers, including why a partial scoop may make more sense than blindly following the serving size on the tub, and explain why leucine becomes more important as we get older. We also tackle a common source of confusion: how a daily target of around 1.2g/kg fits with recommendations to aim for roughly 30–40g of protein at a meal.

Finally, we look at when an evening protein supplement might be useful, why food is often the better answer for smaller gaps, and why resistance exercise still matters if the goal is to preserve muscle and strength.

The aim is to give you a simple blueprint for working out where protein powder genuinely helps, and where it doesn’t.

If you’d like the 10g protein top-up cheat sheet for inside your kitchen cabinet door, you can download it here as a printable PDF:

10g protein top-up cheat sheet - US letter
10g protein top-up cheat sheet - A4

I eat quite a lot of legumes these days. But put me in front of a supermarket wall of kidney beans, chickpeas, lentils, cannellini beans and half a dozen varieties I barely recognise, and I still have a nagging sense that there must be a right one to buy.

What I cook depends more on what happens to be sitting in my kitchen cabinets than any culinary visi…

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In this episode, we take a practical look at how the main legumes compare nutritionally, including calories, protein, fibre and key micronutrients. We’ll see why there probably isn’t a single “best” bean, although lentils, borlotti beans and split peas do have a modest edge in a few areas.

We also look at the one comparison where the differences are more noticeable: dried versus canned beans. We’ll cover what canning does to protein and other nutrients, when that might matter, and why convenience still deserves a place in the decision.

Then we get into the useful bit: which legumes work best in soups, curries, chilli, ragù, salads and creamy dishes, plus how to prepare dried beans safely.

The aim isn’t to optimise your bean cupboard. It’s to help you find a few legume-based meals you genuinely enjoy enough to make again.

Beans are almost universally considered healthy. They feature in every reputable healthy-eating pattern: Mediterranean, DASH, AHEI. And yet they occupy a strangely marginal place in most Western diets.

If your main experience of “eating more beans” involves tipping a tin of something grey and slightly slimy into a saucepan, warming it through and wonderi…

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