It’s very aesthetic. Little glass jars of kefir topped with a sprinkle of seeds. But is it worth the over-complicated addition to a woman’s food prep?

The theory:

The idea is that flax and pumpkin seeds support oestrogen in the follicular phase (the first half of your cycle), while sunflower and sesame seeds support progesterone in the luteal phase (the second half). If you consistently do this over a few months, theoretically, you’ll experience less PMS, more regular cycles, better fertility.

On paper, it could be plausible - these seeds do contain relevant nutrients for hormone health - magnesium, zinc, vitamin E, healthy fats. The trouble is that “contains a nutrient theoretically linked to hormone health” doesn’t mean “eating specific seeds in specific weeks of your cycle will meaningfully shift oestrogen and progesterone.”

The evidence:

… there’s not much, and what does exist doesn’t really support the “different seeds during different weeks” theory. Most of the underlying research uses very large doses of one or two seed types in animals over weeks or months, and even then, hormone changes are only minimal (if at all). One 2025 systematic review did pool ten small human studies and found some encouraging associations between seed intake and PMS symptoms, but there were limitations including small sample sizes and moderate-quality evidence.

The theory, however harmless, is not currently backed by science. This is very similar to a lot of wellness trends – they’re not exactly a ‘scam’ (seeds are healthy after all!) but marketed with far more confidence than justified by the research.

The trend does however open a broader question: Do your micronutrient needs change across your cycle? And if so, should you be eating differently in different weeks?

Iron is the one nutrient with a real and quantifiable extra need.

Every period, you lose blood, and blood carries iron – approximately 15–30mg per cycle, more if your flow is heavy. This is why the recommended daily iron intake for menstruating women is 18mg/day, more than double that for men or postmenopausal women at 8mg/day. It makes complete sense - if you menstruate, you need more dietary iron, BUT no cycle-syncing is required.

Iron isn’t used up and replenished in a tight weekly cycle. It’s stored as ferritin and released gradually, so eating less iron in the weeks after your period would only slow down rebuilding what you lost.

Magnesium and zinc do fluctuate across the cycle:

Blood levels of both micronutrients dip in the luteal phase. But there’s a nuance - a nutrient level changing in your blood isn’t the same as your body suddenly needing more of it from your diet at that exact moment. It might just reflect how your body is turning over what’s already there. What we don’t have is good evidence that deliberately loading up on magnesium or zinc in week three specifically improves anything, compared with simply having enough of both, consistently, as part of your normal diet.

Vitamin E:

Evidence for vitamin E (along with vitamins A and C) across the cycle is sparse and doesn’t really support any specific recommendations, phase-timed or otherwise. There’s some observational data linking higher vitamin E status to milder symptoms in some studies, but it’s a correlation in a population, not proof that timing your intake changes your experience.

A nutrient-dense diet overall > seed cycling.

There’s a well-evidenced case for menstruating women needing more iron overall – and this is reflected in official dietary guidelines. There isn’t a comparable case for timing zinc, magnesium or vitamin E intake around specific weeks of your cycle. A nutrient-dense diet, eaten consistently, will give you more benefits that cycling your seeds!

It’s worth remembering that no nutrient in the human body has just one job. Zinc isn’t only “for hormones,” we also need it for our immune function, wound healing, and taste perception. Magnesium isn’t only “for PMS” - it’s involved in muscle and nerve function, blood sugar regulation, and bone health. Reducing any of them to a single, cycle-related purpose is very limiting. It makes a nutrient sound like a targeted tool for one job, when really you need all of them, all the time.

What to include in your diet, regularly!

Magnesium: leafy greens (spinach, chard), nuts (almonds, cashews), seeds (pumpkin, chia), wholegrains, dark chocolate, legumes.

Zinc: meat, shellfish (oysters in particular), pumpkin seeds, chickpeas and other legumes, cashews, eggs.

Vitamin E: sunflower seeds, almonds, hazelnuts, avocado, wheatgerm, vegetable oils.

Omega-3’s do have interesting hormone-related health evidence:

Menstrual cramps are largely driven by prostaglandins - hormone-like compounds that trigger uterine contractions and drive inflammation. Omega-3s compete with omega-6 fatty acids for the same enzymes involved in making these compounds and tend to produce a less inflammatory version of them. A meta-analysis of eight studies and 676 women found that daily omega-3 supplementation did reduce both the physical and psychological severity of PMS symptoms compared with placebo, with the effect strengthening the longer women took it.

Similarly, in PCOS research, a randomised trial in 78 women found that 3g of omega-3 daily for eight weeks reduced testosterone levels and improved menstrual regularity compared with placebo.

Omega-3 won’t completely cure period pain or hormonal symptoms, and more research is still needed on optimal dosing, but unlike seed-cycling, controlled trials have shown a genuine mechanism of action. This is one of the reasons omega-3 is on my shortlist of recommended supplements (on a need basis), alongside vitamin D and creatine.

Good dietary sources include oily fish (salmon, mackerel, sardines) 2-3 times a week, plus walnuts, chia and flaxseed if you don’t eat fish.

Summary:

Seed cycling isn’t dangerous. Seeds are a great, nutritious addition to the diet. It’s not what is recommended, but more how the idea is sold – that hormonal wellbeing comes down to precisely timed, mini-interventions, when actually, the real evidence is a bit more boring, and much less ‘Instagram’ worthy.

It’s also a bit elitist. Seeds are quite expensive. Everyone can have ‘balanced hormones’ – not just the women who can afford it.

It is important to get your iron intake right (as a menstruating female), eat magnesium, zinc and vitamin E-rich foods consistently rather than to a cycle-schedule, and consider omega-3s for their evidenced anti-inflammatory effects.

Eat well, all month, every month.

Need help? Drop me an email:sayhello@emilynutritioncoach.co.uk

Not all protein powders are created equal – just because one tub might be £85 with beautiful packaging it doesn’t automatically make it superior to the £30 protein in a plastic bag with with an animated figure on it.

So – does protein quality actually matter, and how do you pick a powder that’s worth the money?

How does protein powder compare to food?

Protein powder is a supplement, but it’s the most “food” supplement there is. It’s just the protein that is naturally contained in other, more complex foods. During processing, the protein is isolated from foods like milk (most common), soy, peas, or eggs - most of the fat, carbs, and water are removed, leaving a concentrated protein powder that can be mixed with water, milk, or into food.

Why do I recommend food first? Whole foods are more than just protein. The whole food contains nutrients like fibre, fats, and micronutrients in a food matrix that slows digestion. The slower release allows the whole food protein to digest more gradually, which helps with appetite management, ticking a box for a lot of people.

Whey protein is digested quickly. For gen pop, this isn’t usually necessary. However, the speed of digestion is why whey became the go-to post-workout shake for the fitness industry.

Protein powder isn’t “better” or “worse” than whole food protein, it’s just a different ‘type’ of protein. Powders are a convenient, fast-absorbing top-up. Food gives you the same protein plus everything else your body needs. If you’re already eating enough protein-rich food across the day, you don’t need a protein powder – but it can an easier way to hit your protein target. As with anything nutrition, it comes down to personal preference.

Protein quality is determined by the amino acids.

The amino acid profile separates a good protein powder from an ‘ok’ protein powder.

Proteins are built from 20 amino acids. Nine of these are ‘essential amino acids’ (EAAs) which means your body can’t make them, so they have to come from your diet. Whey is a ‘complete’ protein - it is rich in all of the EAAs, and is particularly high in leucine, which is the specific amino acid needed to build muscle.

You can also buy EAA and BCAA (branched-chain amino acid - just three of the nine essentials: leucine, isoleucine and valine) supplements. If you’re already eating enough total protein, whether from food or a standard protein powder, you’re already getting all the EAAs and BCAAs you need. Isolated BCAAs in particular have pretty weak evidence behind them on their own; they may offer a small edge if you’re training in a calorie deficit, but for most people they’re an expensive way to buy amino acids you’re already consuming.

Whey protein vs plant-based protein.

With a rise in the number of people following a plant-based diet, there are now plenty of different types of protein powder to choose from suitable for every dietary need. Both animal-based and blends of plant-based proteins can be complete in amino acids, so what’s the difference in quality?

Whey wins on raw protein quality. Using DIAAS (Digestible Indispensable Amino Acid Score) whey isolate scores at the top, around 1.09–1.10. Soy protein isolate is the best plant option at around 0.90, while pea and rice proteins sit lower (roughly 0.60–0.82), each missing/falling short on at least one EAA. Blending plant sources e.g., pea & rice, improves the profile of amino acids – so always check to make sure your plant protein powder is a blend, not a single source.

Although whey is highyly bioavailable with fast absorption and digestion, it does contain lactose. For most people, this won’t matter, but for those who don’t tolerate lactose well, a whey protein concentrate might not be the best option. Plant proteins are generally gentler on sensitive stomachs and dairy-free by nature.

Whey is also usually a cheaper option gram-for-gram (although this may change…) since it’s a by-product of cheese-making and produced on a massive scale. Plant proteins, particularly organic or single-source, tend to cost more to produce driving their purchase price up.

If you eat animal-products and are not lactose intolerant, I will always recommend whey – it’s higher-quality, usually cheaper, and better-absorbed. Plant protein is great if you’re vegan, lactose intolerant, or simply prefer it - just check the label for a blended source rather than rice or hemp alone.

“Diet whey” vs standard WPC/WPI

If you are new here and haven’t read one of my previous Substacks, this might be useful to know… whey protein comes in two main forms: whey protein concentrate (WPC), which is 70–80% protein, plus naturally occurring fats and sugar (lactose), and whey protein isolate (WPI), which is filtered further to 90%+ protein so has little fat or lactose. WPI costs more to produce and is easier to digest, but there’s no real evidence to show it’s better for muscle gain than WPC. The extra cost is only justified for higher purity and easier digestion.

“Diet whey” products, like Myprotein Impact Diet Whey, are not the same thing! They are a whey blend (often WPC plus milk protein) with added extras like green tea extract, CLA, and L-carnitine, generally marketed as fat-loss support, alongside a lower calorie and carb count. The protein itself isn’t meaningfully different in quality - you’re paying a bit extra for the added ingredients and the marketing around them, with little to no evidence around their ‘fat-burning’ potential. The need for a calorie deficit to lose body fat still applies. If you’re looking for a lower-calorie protein shake, check the actual ingredients and nutrition values rather than blindly choosing a ‘diet whey’ label.

Whey vs collagen – they’re not actually competitors

Simply put - collagen is not a substitute for whey if your goal is building or maintaining muscle mass. Collagen is a protein rich in glycine, proline and hydroxyproline – these amino acids are great for skin, joints and connective tissue – whether a collagen supplement is digested into its amino acids, absorbed, and re-built into collagen is up for discussion…

… Collagen it’s an incomplete protein and contains under 1% leucine, nowhere near the amount needed for efficient muscle protein synthesis. If you eat enough total (and complete) protein in your day – food or protein powders – there is no need to also have collagen.

Beef and egg protein powders are lesser-known alternatives.

If you can’t tolerate dairy but you still want an animal-based option, you could try beef and egg white protein powders. Egg white protein is an amino acid complete, well-balanced, dairy-free protein. It’s slightly lower in leucine than whey but this shouldn’t matter unless it’s your sole source of protein. Beef protein isolate is also dairy-free but read the label - many beef protein powders are high in collagen-type beef proteins, which pushes the amino acid profile toward glycine and proline rather than the total amino acid spectrum. Look for beef protein isolate, not a beef protein blend.

A red flag. Quality packaging does not equate to quality protein.

If I could have £1 for every client who bought a supplement based on how nice the packaging was…

The “premium wellness” supplement is here to stay. The elegant matte pouches, minimalist branding, wild nutrition and health claims. Some might be genuinely excellent protein powders. Some, maybe not.

Price and packaging tell you nothing about protein quality on their own. There are well-known UK premium brands that are charging around £2.30 per serving vs standard sports brands charging £0.8-1 per serving for effectively the same protein.

So, when you are choosing the type of protein you want check for these:

- What is the protein source? Is it named specifically or is it a blend?

- What is the amount of protein per serving, and what is the price per serving? Don’t go straight for the tub price alone.

- Check any labels for “proprietary blend” or “protein-complex” – what does this actually mean? It might be a fancy way of naming a less complete mix of proteins, or contain other ingredients that are not required.

Which protein powder is for you?

Protein quality does matter - it comes down to the amino acid profile and how it fits your actual needs. Whey isolate or a well-blended plant protein will comfortably cover most people’s muscle protein synthesis needs. Egg white and beef proteins each have their own niche rather than necessarily being straight substitutes. Collagen is pointless and you’d be much better focussing on eating enough total protein.

Taste and textures of different protein types and different brands will always vary, so you might need to try a few to find the ones you enjoy. This might be different if you’re having your protein as a shake or mixing it with your yoghurt or oats.

Shameless plug. You can get samples of Per4m whey protein from www.fullboarsports.co.uk – if you use code DrEm, you’ll also get 10% off.

However, what’s not talked about as much is the effect GLP-1 medications are having on gut health. Nausea is a common side effect, but the change in eating behaviours experienced by people taking GLP-1s also causes a steadier change to the gut microbiome.

What are GLP-1s?

GLP-1 (glucagon-like peptide-1) is a hormone produced naturally by the gut. Specialised ‘L-cells’ in the small intestine release it in response to eating, usually within 15–30 minutes of a meal entering the gut. It’s part of a group of hormones known as “incretins,” which help regulate blood sugar and appetite in response to food.

The roles of GLP-1:

Stimulate insulin release from the pancreas when blood sugar is elevated. This is why it’s such a useful target for managing type 2 diabetes as well as body weight.

Suppress glucagon, the hormone that tells your liver to release stored sugar, helping to keep blood sugar more stable after meals.

Slows gastric emptying so food stays in your stomach for longer, keeping you feel fuller.

Signals to the brain that you’re full, reducing appetite and food intake.

Medications like semaglutide (Ozempic, Wegovy) and tirzepatide (Mounjaro) are GLP-1 receptor agonists - they’re designed to mimic and amplify the natural hormone, binding to the same receptors and producing a stronger and longer-lasting effect than the body’s own GLP-1 would. Tirzepatide goes a step further targeting a second gut hormone receptor (GIP), which one of the reasons why some of the newer medications produce more pronounced results.

The main effect, and the reason behind their success is appetite suppression. Taking them will make you feel fuller quicker, and for longer, which naturally leads to eating less. They make it easier to create and stick to a calorie deficit.

What’s less talked about is the indirect impact these medications have on the gut.

Less food often means less fibre.

The gut microbiome is dependent on what you eat. It’s particularly reliant on fibre from plant foods such as fruit, vegetables, wholegrains, legumes, nuts and seeds. Fibre is essentially the fuel your gut bacteria ferments to produce short-chain fatty acids (SCFAs), which support so many functions and process in your body such as the integrity of the gut lining, immune function, and metabolic health.

Here’s the problem - even in the absence of GLP-1 medications, only around 4% of people in the UK meet the recommended target of 30g fibre a day. Most of us are already under-fuelling our gut bacteria.

Now add a medication that significantly suppresses appetite. When you’re eating less overall, fibre intake is often one of the first things to drop. This is partly due to appetite suppression which tends to blunt interest in bulkier foods, and partly because, when volume is limited, energy-dense, low-effort foods are often picked first.

Over time, chronically low fibre intake can affect:

• Microbiome diversity.

• SCFA production.

• Digestive regularity.

• Overall gut health.

This isn’t me saying “you shouldn’t use GLP-1s” - it’s me saying “you should be conscious and deliberate about what you eat while taking them.”

Why do GLP-1s cause digestive side effects?

Beyond the indirect and longer-term impact of low fibre intakes on digestion, GLP-1s also have a direct mechanical effect on digestion. They slow gastric emptying, meaning food sits in the stomach for longer than usual.

This is one of the reasons you feel full, but it’s also why bloating, constipation, diarrhoea and nausea are common side effects. Your gut must work differently while you’re on the medication.

Diet quality matters, especially in the absence of quantity.

GLP-1s are a genuinely useful tool for weight loss. But if gut health isn’t factored in, you could end up losing weight while quietly under-supporting your microbiome. As a consequence, you’ll be dealing with digestive symptoms that could, at least partially, be eased through food choices.

Weight loss requires a calorie deficit – but it’s important to look beyond just ‘eating less’; what you eat needs to count! You still need dietary inclusivity to ensure you’re getting all the nutrients your body needs to be healthy.

With a supressed appetite, there’s very little room for empty calories.

• Prioritise fibre wherever you can - small, consistent amounts add up when your overall intake is lower.

• Aim for plant diversity, not just plant quantity. Different fibres feed different bacterial species.

• Choose minimally processed foods where possible, since these tend to retain more of their natural fibre and micronutrient content.

These choices won’t eliminate GLP-1 side effects entirely - some come from the mechanism of the drug itself - but they can meaningfully support gut health and reduce the risk of the microbiome declining with the number on the scale.

A side note on food and GLP-1…

There are certain foods that can stimulate your body’s own GLP-1 release, even after a meal has ended. Things like fermentable fibres, unsaturated fats, and protein-rich foods all play a role in this (PMID 25500202). This is a great example of how food and medications don’t operate silos - what you eat is already signalling to the same hormonal pathway that these drugs target.

If you’re on a GLP-1 medication and want support building a way of eating that protects your gut health alongside your weight loss goals, get in touch - this is exactly the kind of thing I work through with my one-to-one coaching clients.

Perimenopause isn’t simply a calorie problem. It’s a metabolic transition driven by changing hormones, muscle biology, and insulin sensitivity. Understanding what’s happening can help you make nutrition and training decisions that actually work with your physiology rather than against it.

Oestrogen is driving change.

I often get clients are struggling with stubborn “meno-belly.” Meno-belly starts to appear due to [the frustrating] redistribution of fat to the abdomen that so many women experience as they enter into menopause. Whilst fat accumulation can only occur in an energy surplus, the redistribution of body fat is a bit more than a consequence of eating more or moving less.

Oestrogen plays a direct role in regulating where your body stores fat. When oestrogen levels are high and stable, fat tends to be stored peripherally - the hips, thighs, bum. As oestrogen declines during perimenopause, that pattern shifts. Fat begins to migrate viscerally - deep abdominal fat that surrounds your organs.

Visceral fat behaves differently from subcutaneous fat - it’s more inflammatory and more strongly associated with insulin resistance, cardiovascular risk, and metabolic disease than fat stored elsewhere.

This is also why the strategies that ‘worked’ in your 30s - a bit less food, a bit more output - can feel less effective now. Calorie balance still matters, but visceral fat is more resistant to calorie restriction alone than subcutaneous fat, and cardio without resistance training doesn't address the muscle loss that can compound the problem. Results may be slower, less visible, or require a slightly different approach.

An important note on HRT: The relationship between oestrogen and body fat is part of the reason why research into HRT continues to grow. A meta-analysis of 17 randomised controlled trials, with over 29,000 total participants, found that HRT significantly improved insulin sensitivity in postmenopausal women without diabetes or cardiovascular disease. HRT isn’t the right choice for everyone, but I do recommend having a conversation with your GP or a hormone specialist to look at options. The evidence base for HRTs metabolic benefits are becoming considerably stronger.

Muscle is an underrated metabolic organ.

Skeletal muscle is the primary driver of whole-body insulin sensitivity. Around 75-90% of insulin-stimulated glucose uptake happens in muscle tissue. When you have more muscle, your body handles blood sugar more efficiently. When you have less, insulin resistance becomes more likely.

Here’s the problem: muscle loss gradually speeds up as you transition to menopause. Oestrogen has a direct anabolic effect, so as it declines, it gets harder to build and preserve muscle mass. This doesn’t mean you can’t - it just requires a bit more patience! The combination of declining oestrogen, rising insulin resistance, and the shift in fat distribution can create a compounding effect. Consequently, it can feel like your body starts to work against you.

The good news is that muscle is highly responsive to the right inputs. You are not at the mercy of your hormones.

How much protein do you actually need?

This is where nutrition becomes so important, and relatively easy to action. Current research is starting to push beyond the standard dietary guidelines - from ‘what you need to survive’ towards ‘it’s time to thrive.’

The UK Reference Nutrient Intake (RNI) sits at 0.75g of protein per kilogram of bodyweight per day. For a 70kg woman, that’s around 52g which is barely enough to maintain basic function, let alone preserve muscle during a hormonally driven period of slightly accelerated loss.

The emerging research consensus suggests that women in midlife need considerably more. A minimum of 1.0–1.2g/kg/day is now widely recommended simply to protect existing muscle mass and bone density during the menopause transition.

But if the goal is to actively build strength and muscle - which has significant implications for long-term health - the research points to a higher range of 1.2–2.2g/kg/day, depending on your training intensity, body composition, and individual goals.

For most women who lift weights (and you should if you don’t), I tend to recommend a practical target somewhere in the middle of this range, aiming for ~1.6g/kg/day.

And why am I so pro eating protein and lifting weights? Because strength and muscle mass are now recognised as powerful predictors of longevity. Grip strength, lean mass, and physical function all correlate strongly with all-cause mortality risk in long-term studies. This means that building and maintaining muscle in midlife is a genuine long-term health investment.

Strength training.

There is overwhelming evidence for the benefits of resistance training during and after perimenopause. It consistently shows up as one of the most powerful interventions available, not just for body composition, but also for insulin resistance and bone density.

Strength training improves insulin sensitivity through several mechanisms: it increases muscle mass (your primary glucose disposal tissue), upregulates GLUT-4 transporters that allow cells to take up glucose more efficiently, and reduces visceral fat over time. These effects are independent of weight loss, so you don’t have to be in a calorie deficit to benefit metabolically from lifting weights.

For bone density, the evidence is also strong. Weight-bearing resistance exercise creates mechanical load on bone, which stimulates bone remodelling and helps offset the accelerated bone loss that occurs as oestrogen declines.

If you can, try at least two resistance training sessions per week. Three can be your “even-better-if”. By ‘progressive’ I mean ‘aim to increase the load over time for adaptation to continue.’

Targeted input.

Perimenopause doesn’t have to be a passive decline that you just have to manage. It’s a phase that can strongly respond to targeted inputs - so when you understand what you can do, you can feel quite empowered.

These are the core points:

• Fat redistribution and insulin resistance during perimenopause are driven by oestrogen decline - the problem is hormonal and metabolic, not a personal failing.

• Prioritise protein. Aim for at least 1.2g/kg/day, and consider going higher (up to 1.6–2.0g/kg) if you’re training consistently and building strength is a goal (it should be).

• Lift weights. Resistance training is one of the most evidence-backed interventions available for insulin sensitivity, bone density, and body composition during this life stage.

• Think long-term. Muscle mass and strength are directly linked to longevity. What you build now has health implications well into your 60s, 70s, and beyond.

If you’re considering whether HRT might be right for you, the metabolic evidence is at least worth discussing with your doctor. It isn’t the whole picture, but I certainly notice a difference with my clients who have found the right HRT for them.

In the 1980’s the first ‘Gluten-Free’ (GF) food products were manufactured for people with coeliac disease – like bread, flour mixes and biscuits.

As a lifestyle trend, the GF product industry really ignited around 2009–2011 and peaked commercially around 2013–2014. Now when you walk through the supermarket there’s no shortage of options for GF bread, pasta, biscuits, cakes, cereals and even beer.

So how are they made?

Removing gluten is not straightforward. Gluten isn’t just a nutrient. It’s functional. An important structural component in a lot of foods. When it’s removed, it needs to be replaced with something that offers equal functionality.

What is gluten?

Gluten is a group of proteins found naturally in wheat, barley and rye. When flour is mixed with water and kneaded, these proteins form an elastic network. It’s the gluten that allows dough to be stretched and allows bread to rise in the oven.

Glutens function in dough gives it:

• Stretch

• Elasticity

• Structure

• An ability to trap carbon dioxide.

Gluten is one of the reasons wheat became such an important crop in human history.

A quick baking lesson…

When you bake a loaf of bread, the yeast produces carbon dioxide as it ferments. Gluten acts like a net, trapping the carbon dioxide (gas) allowing the dough to rise.

Without gluten, the gas escapes resulting in a loaf that’s small, dense and crumbly.

The biggest challenge in gluten-free food manufacturing is replacing the structural component of gluten.

To compensate for the removal of gluten, manufacturers often use a combination of ingredients that mimic some of its properties. These include:

• Xanthan gum

• Guar gum

• Psyllium husk

• Modified starches

• Hydrocolloids

These ingredients do help improve texture, structure and moisture retention of the dough. But none behave exactly like gluten. This is why the texture of GF bread often feels different to regular bread.

Why do Gluten-Free products often taste different?

GF foods tend to be drier, denser, and more fragile/crumblier than their gluten-containing counterparts. In order to create an acceptable texture, food manufacturers need to add in ingredients, resulting in a longer ingredients list, changes in taste, and differences in nutrition profile.

A gluten-free label is not (always) a ‘healthier’ label

One of the biggest misconceptions is that gluten-free automatically means healthier.

To recreate the texture of wheat-based products, manufacturers often use ingredients such like rice flour, potato, corn, or tapioca starch.

These ingredients can work extremely well texturally, but they don’t always provide the same nutritional profile as (particularly) wholegrain wheat flour. As a result, some gluten-free products may contain:

• Less fibre

• Less protein

• More refined starch

In some cases, manufacturers also add extra fat or sugar to improve mouthfeel and flavour.

NOTE: This doesn’t mean gluten-free foods are unhealthy either. It simply means that “gluten-free” describes the absence of gluten, not the overall nutritional quality of a product.

Why are Gluten-Free products more expensive?

It is much more costly to produce GF foods – because gluten is an allergen, manufacturers need to take additional precautions to prevent contamination from gluten-containing grains.

This can involve:

• Dedicated production lines

• Separate storage facilities

• Additional cleaning procedures

• Regular testing

• Certification schemes

These measures increase cost of production. When you buy a GF loaf of bread, you’re not just paying for different ingredients. You’re also paying for the systems that ensure the product remains safe for people who need it.

What about oats?

Oats can be confusing. A common assumption is that oats contain gluten when in fact, oats are naturally gluten-free. Some packets of oats carry a gluten-free label, but others don’t, despite both having the same single ingredient.

This is down to contamination.

Oats are often grown in fields near wheat, barley or rye. They’re frequently transported using the same vehicles and processed in the same facilities on the same lines. As a result, traces of gluten-containing grains can accidentally find their way into oat products.

For most people this isn’t a problem but for someone with coeliac disease, even these small amounts of contamination can cause a reaction.

Certified gluten-free oats are produced using carefully controlled supply chains and undergo testing to ensure gluten levels remain below regulatory limits.

Gluten-Free is a reformulation label not a removal label.

GF foods are reformulations of their gluten-containing counterparts, not the extraction and removal of gluten from a wheat-based food.

GF foods have an entirely different recipe using alternative ingredients. Manufacturers build a completely new product designed to achieve a similar result.

That’s why gluten-free foods can differ in taste, texture, nutrition and cost.

In a world where everyone is banging on about their unprocessed lives…

… take a minute of appreciation for the food technologists that manage to come up with a safe way for coeliacs to enjoy bread – maybe it’s not exactly the same, but when you understand the challenges, you understand that it’s the best it can be!

What is lactose?

Lactose is the naturally occurring sugar found in milk and most dairy products. It’s a disaccharide - a molecule made of two simpler sugars, glucose and galactose - bonded together.

To digest lactose, your body needs an enzyme called lactase, which is produced in the cells lining the small intestine. Lactase breaks the glucose-galactose bond so both sugars can be absorbed into the bloodstream separately.

It’s not uncommon for people produce less lactase as they move through adulthood. This is a normal physiological change called lactase non-persistence (LNP). Lactase non‑persistence is a genetically programmed decline that begins after early childhood, often between ages 2–10, but in some groups first becomes evident in the late teens or early 20’s. The decline continues at the molecular level during adulthood in non‑persistent individuals, leading to the common pattern of reduced lactose digestion in adults, while genetically lactase‑persistent people maintain high activity for life.

In LNP individuals, because lactose isn’t broken down in the small intestine, it passes into the large intestine, where gut bacteria ferment it. This fermentation produces gas, short-chain fatty acids, and draws water into the colon - causing the familiar symptoms of bloating, cramping, flatulence, and diarrhoea that many people associate with dairy.

A note on prevalence: LNP is actually the global norm, not the exception. Estimates suggest around 65–70% of the world’s adult population has reduced lactase activity. The ability to digest lactose into adulthood (lactase persistence) evolved relatively recently and is most common in populations with long histories of dairy consumption, particularly Northern European populations, where prevalence of lactase persistence is around 90%. In East Asian, West African, and many Middle Eastern populations, rates of LNP are considerably higher.

It’s also worth distinguishing lactose intolerance (a digestive issue) from cow’s milk protein allergy (CMPA), which involves the immune system reacting to proteins in dairy — primarily casein and whey. Lactose-free dairy products still contain these proteins, so they are not appropriate for those with CMPA.

Method 1: Lactase is added for “Lactose-Free Dairy”

The most common approach used by manufacturers to produce lactose-free milk, yoghurt, and similar products is to simply add lactase to the product.

When the lactase enzyme is introduced to milk, it does the same job your small intestine would do; it breaks the lactose down into its two component sugars, glucose and galactose. The result is milk with an almost identical nutrition profile to regular milk, but with the lactose already ‘pre-digested.’

This is how brands like Arla Lactofree produce their products and results in a product that is typically 99.9% lactose-free which is sufficient for most people with a lactose intolerance, though individual tolerance thresholds do vary.

There is a sweetness effect…

Lactose-free dairy frequently tastes noticeably sweeter than regular milk even though no sugar has been added and the total sugar content remains virtually the same. This is because glucose and galactose are each individually sweeter than lactose – your taste receptors perceive free glucose and galactose more readily than bound lactose, so the same quantity of sugar registers as sweeter on the palate.

The perceived sweetness is a natural consequence of the enzymatic process, not an ingredient addition.

Method 2: Lactose is removed using filtration technologies.

This is primarily used in the production of whey protein isolate and some specialist dairy products. Whey is the liquid by-product of cheese or yoghurt production. It naturally contains lactose, along with whey proteins, minerals, and water.

Whey protein isolate (WPI) undergoes more extensive filtration than standard whey protein concentrate, most commonly using ultrafiltration or microfiltration (processes that use size-selective membranes to separate components by molecular weight). Because lactose molecules are larger than some of the filtration targets, this process significantly reduces lactose content, often to below 1% so many isolates are effectively lactose-free.

Ion exchange chromatography is another processing method used for some whey isolates, which selectively captures whey proteins and allows other components - including lactose - to be washed away. The result is a very high-purity protein product.

Naturally lactose-free foods

Naturally lactose free foods are categorically different – their role is to completely replace dairy with something that never contained lactose in the first place.

Plant-based milks like oat milk, soy milk, almond milk, and coconut milk are made from plant sources. They contain no lactose because lactose is a mammalian milk sugar so not found in plants.

Common Marketing Confusion

Nutrition literacy is important:

“Lactose-free” does not mean “dairy-free.”

Lactose-free milk, lactose-free yoghurt, and whey isolate are still dairy products. They still contain cow’s milk proteins. This matters for people with CMPA, dairy allergies, or those following a vegan diet.

“Dairy-free” does not mean nutritionally comparable.

Plant-based milks are frequently assumed to be nutritionally comparable to dairy milk. Most are not, particularly for protein. Cow’s milk (and lactose-free cow’s milk) contains approximately 3.4g of protein per 100ml. Oat milk typically provides around 1g per 100ml. Almond milk often contains less, usually under 0.5g per 100ml. Soy milk is the exception, with a protein content closer to dairy at around 3–3.5g per 100ml, and a complete amino acid profile.

If you choose to switch to plant-based milks without adjusting elsewhere in their diet, this can represent a meaningful reduction in protein intake. This is particularly relevant for older adults, those with higher protein requirements, or people already eating lower-protein diets.

“Plant-based” does not mean healthier.

Many plant-based dairy alternatives are heavily processed and contain added sugars, oils, gums, and emulsifiers to replicate the texture and mouthfeel of dairy. I have nothing against processed foods, but this is worth noting before assuming a health benefit. For example, oat milk can contain added rapeseed oil, dipotassium phosphate (acidity regulator), and sometimes around 4g of sugar.

Fermented dairy.

Some traditionally fermented dairy products are naturally lower in lactose without any special manufacturing process. During fermentation, bacteria consume lactose as an energy source, converting it to lactic acid. This is why live yoghurt, kefir, aged hard cheeses, and butter are often better tolerated by people with lactose intolerance than fresh milk. The degree of tolerance varies with fermentation time and the product involved - hard aged cheeses like cheddar or parmesan contain very little residual lactose, while fresh soft cheeses like ricotta or cottage cheese retain considerably more.

Here’s a little summary:

A lactose-free label can mean one of three things:

1. Lactose has been broken down via the addition of lactase enzymes (lactose-free milk, yoghurt).

2. Lactose has been removed via filtration (whey protein isolate).

3. The food never contained lactose like plant-based alternatives (oat milk).

Each has different implications for digestive tolerance, dairy content, protein quality, and overall nutrition.

Note: individual tolerance to lactose varies considerably. Some people with lactose intolerance tolerate small amounts without symptoms; others are more sensitive. If you’re unsure what’s right for you, reach out sayhello@emilynutritioncoach.co.uk, and I can help you identify your personal threshold.

But do you know where it comes from? I’ve lost count of how many parents have asked me “is it safe” for their teenager to take.

So here is everything you need to know about whey protein…

Protein powder began life as a by-product of cheese production. What was once considered a waste product is now a multi-billion-pound industry.

It starts with milk.

Milk contains two main proteins: around 80% is casein, while the remaining 20% is whey.

When cheese is made, enzymes are added to milk causing the casein proteins to coagulate and form solid curds. These curds eventually become cheese. Left behind is the watery liquid that we know as whey. You’ll recognise it as the liquid you normally tip into the sink from the top of your 0% fat Greek yoghurt.

Historically, this liquid was discarded or used as animal feed. But whey contains a significant amount of nutrients, including protein, lactose, minerals and vitamins, so throwing it away seemed uneconomical and environmentally unfriendly.

On realising this, food manufacturers created a “whey” to harness the value and turn it into the whey protein powder that us from the fitness industry can’t live without today.

How does it go from a liquid to a powder?

Because fresh whey is a liquid, to make a powder, manufacturers must first remove the water and separate the protein from other its components. This is done through different filtration techniques.

The liquid is passed through specialised membranes that allow smaller molecules like lactose (the sugar in milk) and minerals to pass through while retaining the larger protein molecules.

The more filtration, the higher the protein concentration. This is how the different types of whey protein are produced.

(1) Whey Protein Concentrate (WPC)

WPC is the least processed form of whey protein and typically contains anywhere from 70-80% protein. The remaining 20-30% is carbohydrates, fats and naturally occurring milk components. Because it undergoes less processing, WPC retains more of the compounds naturally found in whey, and is usually the cheapest option.

For most people, WPC provides more than enough high-quality protein to support muscle growth and recovery.

(2) Whey Protein Isolate (WPI)

WPI undergoes additional filtration to remove most of the lactose, fat and carbohydrate content, increasing the protein concentration to around 90% or higher. As a result, isolates are sold as more premium options (more £).

For people with a lactose intolerance, isolates can suitable because of their lower lactose contents. However, the nutritional difference between concentrate and isolate can be less than you might assume; a scoop of WPC contains around 24g of protein and a scoop of WPI contains 27g protein.

(3) Hydrolysed Whey

Hydrolysed whey is ‘pre-digested’ by adding enzymes to break down some of the protein chains into smaller fragments called peptides. This process is called hydrolysis.

The smaller protein fragments are absorbed more rapidly by the body (theoretically). Practically, the benefit of hydrolysed whey is quite small - muscle growth is determined by total daily protein intake, strength training, recovery and consistency rather than the speed that amino acids are delivered to the bloodstream.

(4) Casein

Casein is the other 80% of milk protein. Unlike whey, it forms a gel-like structure in the stomach, slowing digestion and absorption. Because of this, it’s common for whey protein to be recommended post-training (“fast” digestion), and casein consumed before bed for “slow” digestion overnight.

Whilst the differing digestion rates are correct, total daily protein intake is far more important than the speed of absorption.

Both whey and casein contain all nine essential amino acids and both can support muscle growth effectively so the choice often comes down to personal preference, personal digestive experience and convenience.

Should you be consuming protein powders?

Protein powder is simply a convenient (and cost effective) way of increasing daily protein intake. You can have it as a shake, mix it into your oats or yoghurt. You don’t ‘have’ to use protein powders, nor would I recommend using them as your sole source of protein.

Where a common barrier is ‘time’ protein powders can remove the need for food prep; they are not only useful if your goal is to build muscle, but generally a great way to boost protein intake.

FYI – protein intake is directly linked to muscle mass, which is directly linked to longevity. Regardless of whether you go to the gym!

We’ve been surrounded by messages telling us to cut things out, eat less, and avoid certain foods. “Healthy eating” has so often been framed as deprivation that it’s no surprise so many women grow up believing thinness equals happiness.

But what if we’ve been mis-taught the message entirely?

What if one of the most effective (and liberating) things you could do for your physical and psychological health is to eat more?

The physical side of under-eating

Energy is everything. And energy comes from food.

Your body doesn’t just need fuel for movement or exercise. It needs energy for every heartbeat, every breath, every hormone, every thought.

When you consistently under-eat, your body adapts. Metabolism slows. Hormones shift. Your brain begins rationing resources, which can leave you feeling foggy, irritable, exhausted, and unfocused. Training performance drops. Recovery worsens. Sleep suffers. Even motivation starts to disappear.

Yes, a calorie deficit matters for fat loss, but chronic restriction makes the process far harder than it needs to be.

Side note: you do not always have to want to lose weight.

Diet culture rarely talks about the fact that eating more of the right foods can actually support fat loss more effectively than simply eating less.

Calories in versus calories out still applies. That part doesn’t change. But we are not machines. We are human beings with hunger hormones, stress responses, emotional needs, social lives, and limited willpower reserves.

When you build meals around foods that are filling, nourishing, and satisfying - lean proteins, vegetables, fruit, whole grains, healthy fats - you naturally stay fuller for longer. Energy becomes more stable. Cravings become easier to manage. You’re less likely to find yourself standing in the kitchen at 4pm raiding the biscuit tin because your blood sugar crashed and your body is desperately trying to catch up.

And honestly? What if you allowed yourself to have a biscuit occasionally anyway? Would one biscuit really ruin your health?

Why eating more can help

• Protein and fibre increase satiety, helping you stay fuller for longer.

• Adequate fuel helps preserve muscle mass, which supports metabolic health.

• Stable blood sugar can reduce cravings, bingeing, and energy crashes.

• Consistent nourishment makes movement and exercise feel more achievable, and often more enjoyable.

• Sustainability always wins over perfection.

The best diet is the one you can actually maintain. And very few people can sustain a lifestyle that leaves them exhausted, hungry, and resentful.

Eating more volume by eating well is not a reward for “good behaviour.” It is the behaviour. It’s the foundation of a healthier, more sustainable relationship with food.

The psychological shift

There’s an enormous sense of relief in telling yourself: I can eat that.

How we feel about food may not be measurable in an app or calorie tracker, but it matters just as much as nutrition itself.

Most women can remember the first time someone commented on their body or what they were eating. The first diet. The first time they felt anxious looking at a menu. The first social occasion overshadowed by guilt around food choices.

Food should be one of life’s simplest pleasures (and privileges), but it has become a moral battleground. Every meal feels like a test. Our choices become tied to our identity, our worth, and our “discipline.”

So here it is:

You have unconditional permission to eat. You deserve to be nourished.

That doesn’t mean chaos or a free-for-all. It means shifting your relationship with food away from fear and punishment, and towards trust, nourishment, enjoyment, connection, and culture.

When foods stop being labelled “good” or “bad,” the obsessive thoughts begin to soften. The bingeing that follows restriction often starts to ease. You begin recognising your own hunger and fullness cues again instead of constantly overriding them.

You can go out for dinner and stay present instead of mentally calculating calories. You can eat birthday cake as part of celebration rather than shame. You can travel and enjoy food experiences without trying to “earn” every meal through exercise.

This is what a healthy relationship with food actually looks like.

• Food no longer defines your worth.

• Cravings become information, not character flaws.

• Social eating becomes connection instead of anxiety.

• You stop feeling the need to “start again Monday.”

• Mental energy gets redirected towards things that truly matter to you.

There’s a particular kind of relief in realising you don’t have to spend your life eating less.

That nourishing yourself properly, with satisfying, wholesome food, may actually be the thing that helps you feel healthier, calmer, and more in control.

For many women, that idea feels almost too good to be true.

It isn’t.

This is one of the most important questions in women’s health advocacy, and the evidence strongly suggests the answer is uncomfortable but clear.

The research funding disparity is already documented

We know from Google Trends that PCOS search interest rose consistently over 18 years while research funding fell. Compare that to conditions predominantly affecting men. Erectile dysfunction — which affects quality of life but is rarely life-threatening — receives research funding that dwarfs what PCOS gets, despite PCOS carrying serious long-term risks of diabetes, cardiovascular disease, endometrial cancer, and significant mental health consequences.

Prostate cancer research receives roughly 4–5 times more funding per patient than ovarian conditions. This isn’t a coincidence — it reflects whose experiences have historically been centred in medicine.

Medicine was built on male bodies

Until 1993, the US National Institutes of Health didn’t even require women to be included in clinical trials. For decades, the “default” human body in medical research was male, meaning drug dosages, diagnostic criteria, and treatment protocols were calibrated on men and then applied to women. Heart attack symptoms are a classic example — the “classic” chest-clutching presentation is predominantly male; women more often experience nausea, jaw pain, and fatigue, symptoms that were historically dismissed as anxiety.

If PMOS affected men, it is almost certain it would have been named more accurately from the outset, because the researchers defining it would have been more likely to share the experience of those being diagnosed.

Diagnosis times tell the story

Women with PCOS have historically waited an average of 2 years for a diagnosis, with many reporting being dismissed multiple times before being taken seriously. Conditions predominantly affecting men tend to have far shorter diagnostic pathways. That delay isn’t just frustrating — it allows metabolic complications to develop unchecked.

The “bikini medicine” problem

There’s a term used in medical education circles — “bikini medicine” — which describes the tendency to treat women’s health as only concerning the parts covered by a bikini: reproductive organs, breast cancer. The systemic, metabolic, and cardiovascular dimensions of conditions like PCOS get relatively little attention because women’s bodies have been medicalised primarily through the lens of reproduction rather than whole-body health. If PMOS affected men, it is hard to imagine its metabolic and cardiovascular features being so consistently overlooked.

Where it gets more nuanced

It’s worth acknowledging that some male-dominated conditions have also been under-researched due to stigma — mental health, for instance, has historically been under-diagnosed in men because of cultural pressure not to seek help. So the picture isn’t simply “male conditions get everything”. But when it comes to complex, multi-system chronic conditions, the pattern is fairly consistent: women’s symptoms are more likely to be attributed to anxiety, lifestyle, or “just being a woman”, and funding follows perception.

The hopeful angle

The PMOS rename, if it sticks and drives the systemic changes promised, is part of a broader correction that’s accelerating. The rise of patient advocacy communities online — which the Google search data implicitly captures — has created a groundswell that is harder for institutions to ignore. Conditions like endometriosis, PMDD, and now PMOS are finally getting serious attention partly because women organised, shared experiences, and demanded better.

The uncomfortable truth is that it shouldn’t have taken that level of public pressure. But the pressure is working — slowly.

It affects 170 million (1 in 8) women worldwide, is typically searched for 1-2 million times per month globally and is the subject of thousands of patient communities. And yet, for decades, it’s very name has been misleading, steering patients, doctors, and researchers in the wrong direction.

Why did PCOS need renaming?

“Polycystic” implies the defining feature is multiple cysts on the ovaries. It isn’t - in fact, a related study by the same researchers found no increase in abnormal ovarian cysts in the condition at all. This single mis-framing has led to decades of women being dismissed when their ultrasounds look “normal”, and clinicians focusing on the wrong organ entirely.

PMOS, by contrast, tells a more complete story. It is a condition involving the endocrine system, metabolism, and the ovaries - not as the primary site of pathology, but as one part of a multi-system picture. Women with PMOS commonly experience irregular periods, elevated androgen levels, insulin resistance, increased risk of type 2 diabetes, cardiovascular disease, and significant psychological impacts including anxiety and depression.

Polyendocrine Metabolic Ovarian Syndrome (PMOS)

Polyendocrine: Reflects the multi-hormonal, systemic nature.

Metabolic: Acknowledges insulin resistance, diabetes risk, cardiovascular impact.

Ovarian: Retained to preserve continuity — but reframed in context.

The Consensus.

The process for change involved 56 patient and professional organisations, more than 22,000 survey responses, and multiple international workshops with both patients and multidisciplinary health professionals.

The result?

“Evolutionary rebranding” - preserving some continuity with the existing name and acronym rather than a complete overhaul.

What happens next is just as significant - clinical guidelines, medical curriculum, and international disease classification systems will be updated. It needs to be more than a terminology shift - what follows should be a commitment to change - in teaching, understanding, funding, and treatment.

Will it actually change how women’s health is treated?

This the most important question, and the answer? - let’s hope so!

The optimist in me…

• A more accurate name invites a broader range of specialists like endocrinologists, cardiologists, and mental health professionals into the conversation, rather than leaving care just with gynaecology.

• Better framing tends to attract better research funding and more targeted policy attention.

• The scale of the consensus process — 56 organisations over 14 years — shows (hopefully) genuine institutional commitment, not just performative change.

• Updated classification systems mean the shift will be embedded in how doctors are trained, not just recommended.

…but still be cautious…

• Name changes in medicine have a mixed track record. The underlying problem for women’s health issues being dismissed is cultural, not terminological.

• Adoption across global healthcare systems will take years (possibly decades) and could be inconsistent.

• Some patients who have built communities and identities around the PCOS label may find the transition disorienting or overwhelming.

• Without sustained pressure from advocates and funding commitments, the rename risks becoming just symbolic.

The attention around the renaming highlights how women’s health has been historically under-researched and under-treated. Alongside growing recognition of conditions like endometriosis, perimenopause, and PMDD, this is medicine slowly — sometimes too slowly — catching up with lived experience.

Whether PMOS leads to better consultations, faster diagnoses, and more holistic care will depend on what happens next: in research funding decisions, in medical school, and in the consultation room conversation between doctor and patient - who may have been waiting for years for answers.

Teede HJ, Khomami MB, Morman R, et al. “Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process.” The Lancet. Published online May 12, 2026. DOI: 10.1016/S0140-6736(26)00717-8

But why?

For years, IBS was dismissed as “stress” or labelled as a condition linked to anxiety. We now know it’s far more complex than that. IBS involves changes in gut function, nervous system signalling, hormone activity, immune responses, and the communication between the gut and the brain.

There’s no single reason why women experience IBS more frequently – it’s likely a combination of biology, hormones, pain perception, and social factors.

Hormones play a major role

One of the biggest differences between men and women when it comes to IBS is the influence of hormones. Oestrogen and progesterone don’t just affect reproductive health — they also influence:

• Digestion

• Gut mobility

• Inflammation

• Pain sensitivity

• The gut microbiome

• The gut-brain axis

Many women notice their IBS symptoms fluctuate throughout their menstrual cycle. Bloating, abdominal pain, and diarrhoea often worsen around menstruation, while constipation can become more noticeable in the days after ovulation.

Hormones also influence serotonin - although serotonin is often discussed in relation to mood, around 90–95% of the body’s serotonin is actually produced in the gut, where it helps to regulate bowel function and sensation.

This may help explain why hormonal shifts can have such a noticeable impact on IBS symptoms.

Women may experience gut pain differently.

One of the most common features of IBS is visceral hypersensitivity - essentially, the nerves in the gut become more sensitive to normal digestive processes. Things that wouldn’t normally cause discomfort, such as stretching of the bowel or gas movement, may trigger pain, cramping, or bloating in someone with IBS.

Research suggests women may:

• Perceive gut discomfort more intensely.

• Have heightened nervous system responses to digestive sensations.

• Experience greater sensitivity to abdominal distension

Women are also more likely to experience overlapping chronic pain conditions, which may point towards broader differences in how the nervous system processes pain signals.

The gut-brain axis.

The bi-directional communication between the digestive system and the nervous system is known as the gut–brain axis. This pathway means stress, emotions, sleep, and nervous system activity can directly affect digestion.

When the body is under chronic stress, the gut can become more sensitive and inflamed causing either slower or faster mobility, making it more reactive to foods and (what should be) normal digestive activity.

This does not mean IBS is “all in your head.” The symptoms are very real. However, the nervous system plays an important role in symptom severity.

Women are statistically more likely to experience anxiety disorders, chronic stress, and conditions linked to nervous system sensitisation, which may partly contribute to the higher rates of IBS seen in women.

The immune system and microbiome.

Men and women have important biological differences in immune function and gut bacteria composition. Women generally mount stronger immune responses than men. While this can be beneficial in fighting infections, it may also increase susceptibility to inflammatory and pain-related conditions.

Researchers are also investigating whether women are more prone to developing “post-infectious IBS” - IBS that develops after a stomach bug or food poisoning episode.

Hormones can influence the balance of bacteria within the gut, which may impact inflammation, digestion, and IBS symptom development.

IBS isn’t “just stress”

One of the most important things to understand about IBS is that it is a genuine disorder involving measurable changes in:

• Gut movement

• Nerve sensitivity

• Microbiome function

• Gut–brain signalling

• Immune activity

Stress absolutely does worsen symptoms, but that doesn’t make IBS imaginary, exaggerated, or simply ‘caused by worry.’

For many women, IBS symptoms are deeply intertwined with hormones, nervous system function, and digestive sensitivity - which is why management often needs to go beyond simply changing diet. Understanding the biology behind IBS can help reduce stigma, improve treatment approaches, and remind people that digestive symptoms deserve to be taken seriously.

It is not about willpower or self-discipline. It’s about how our body’s nervous system has adapted in order to survive.

What do we mean by ‘childhood trauma’?

Trauma isn’t just the dramatic, singular events that we tend to picture. While those experiences — abuse, neglect, the loss of a parent, witnessing violence — are absolutely valid, trauma also encompasses the chronic, constant wounds of childhood: emotional unavailability from caregivers, persistent criticism, instability at home, bullying, poverty, or simply never feeling safe or seen.

These are often referred to as ‘Adverse Childhood Experiences’ (ACEs) — a framework that shows how early adversity ripples through a person’s entire life, affecting mental health, physical health, relationships, and of course, eating behaviour.

The higher a person’s ACE score, the greater their risk of disordered eating, obesity, and troubled relationships with food in adulthood.

Our nervous system doesn’t simply forget.

To understand how trauma shapes eating, we first need to understand what trauma does to the body.

When a child experiences repeated stress or threat — whether physical or emotional — their nervous system adapts. The stress response (fight-flight-freeze) becomes hyperactivated. The body learns to stay on high alert, scanning for danger even when none exists.

Over time, this chronic stress state causes dysregulation in appetite signalling — affecting hormones like ghrelin (hunger hormone) and leptin (satiety hormone), the gut microbiome, and the brain’s reward circuitry around dopamine.

This disruption to our natural regulation causes eating to become entangled with emotional states in ways that bypass conscious awareness.

Food as a coping mechanism

For many children in chaotic or threatening environments, food becomes one of the few reliable sources of pleasure, comfort, or control. This makes complete sense. Food is immediate. It works. It soothes the nervous system in a very ‘real’ way.

But the coping strategies we develop as children don’t simply disappear when we grow up. They might bubble under the surface for a bit, but can show up again later, often in ways we don’t recognise as connected to the past.

This can look like:

o Emotional eating — using food to manage feelings of negative emotions such as anxiety, loneliness, sadness, or numbness. The brain learns that eating (particularly high-fat, high-sugar foods) temporarily blunts emotional pain by triggering dopamine release. A learned neurological pattern.

o Binge eating — consuming large amounts of food rapidly and often in secret, frequently followed by feelings of guilt or shame. Binge eating disorder tend to be correlated with childhood emotional neglect, sexual abuse, and chaotic home environments. Food fills a void, if only temporarily.

o Restriction and control — for those who felt powerless or unsafe growing up, controlling food intake becomes a way to exert control over something. This can be a pathway into anorexic behaviour, where rigidity and control over food intake provides a sense of safety and self-determination that wasn’t there in childhood.

o Dissociation during eating — some trauma survivors describe eating as ‘autopilot’, unaware of what or how much they’ve consumed. This is the mind’s way of escaping an unbearable present and it doesn’t switch off just because the original threat is gone.

o Difficulty with hunger and fullness cues — chronic stress dysregulates the hormones that signal hunger and satiation. Many trauma victims report simply not knowing when they are hungry or full. They have lost touch with the body’s internal regulation and feeding signals.

Shame

One of the most significant aspects of trauma’s impact on eating is the shame that accumulates with it.

Adults who struggle with their relationship with food are often told — by diet culture, sometimes by healthcare providers, and by themselves — that they simply lack discipline. They just need to try harder. Eat less. Move more. Simple.

This narrative is not only unhelpful — it is actively harmful, because it treats the symptom while ignoring the root cause. Shame doesn’t heal disordered eating – it worsens it.

When we feel ashamed of our eating behaviour, we are less likely to talk about it, seek help, or approach ourselves with the curiosity needed for genuine change. Instead, we sit in this viscous cyle: eat to cope with pain → feel shame → feel more pain → eat to cope.

The gut-brain axis

Trauma is not just a memory stored in the mind, we hold it in the body – the way we breather and hold tension. We ‘feel’ it in the nervous system and the gut.

The gut-brain axis is particularly relevant - trauma and chronic stress alter the gut microbiome, affecting digestion, immune function, and emotional regulation. Many trauma survivors deal with IBS, chronic nausea, and disordered digestion.

This is why purely cognitive approaches to changing eating behaviour are often not enough for trauma survivors. You can’t simply think your way out of a pattern that lives in your nervous system.

A good first step:

If you recognise yourself in any of this, the most important thing is to understand that the way you learned to relate to food made sense. You did nothing wrong. It was a response to something real. You survived.

We don’t need to shame those responses into submission, but instead we can gently and gradually, build new behaviours and give the nervous system enough safety that food can become (with time) just food.

It won’t happen over-night. It will require patience. It probably won’t be linear progress. But it is possible, and you deserve support in doing it.

If you’re struggling with your relationship to food and want to talk to someone, you can contact me: sayhello@emilynutritioncoach.co.uk, or your GP can refer you to appropriate support. Beat (beateatingdisorders.org.uk) offers a helpline and resources for those in the UK.

But it’s not a very good explanation.

Before we start cutting foods out, it’s worth understanding what that puffiness actually is. Because in most cases, it has very little to do with sugar—and a lot to do with basic physiology.

What’s actually going on?

Morning facial puffiness is mostly fluid. That’s it.

Not fat gain. Not “toxins.” Not your hormones going rogue overnight.

You’ve been lying flat for 6–8 hours:

- Gravity isn’t pulling fluid into your lower body.

- Fluid redistributes more evenly - including into your face.

- You’re not moving, so lymphatic drainage slows right down.

Add in mild dehydration, your sleep position, and maybe some disrupted sleep, and it’s no surprise your face looks slightly puffier when you wake up.

Then you get up, move around, and it resolves.

No need for a ‘detox’ and no ‘food rule’ broken.

So why do we blame sugar?

A few reasons - and none of them are particularly accurate on their own.

1. You’re probably blaming the wrong part of the food.

Think about the foods people point to: pizza, ice cream, late-night snacks.

Yes, they contain sugar. But they’re also often high in sodium.

Sodium is one of the most reliable drivers of fluid retention. It directly influences how much water your body holds onto.

So when someone says “it was the sugar,” there’s a good chance it was actually the salt.

2. Carbs do increase water storage - it’s normal.

Carbohydrates are stored as glycogen in the liver and muscles. And glycogen is stored with water - roughly 3–4g of water per gram. It’s not a problem. It’s literally how your body is designed to function.

That water:

- Supports energy availability.

- Helps with performance.

- Contributes to that “fuller” muscle look people often want.

It’s not localised to your face, it’s not harmful, and it’s not something your body is trying to get rid of.

It’s just physiology doing its job.

3. “Inflammation” obvs. Or is it?

What instagram tells us: “Sugar causes inflammation → inflammation causes puffiness.”

What science tells us: this is massively oversimplified.

Yes, long-term dietary patterns can influence inflammation. But one dessert does not suddenly create visible swelling in your face overnight. And importantly - fluid retention and inflammation are not the same thing.

They get lumped together because it makes for a better headline, not because it’s accurate.

4. Alcohol is conveniently forgotten.

If there is a dietary factor that regularly contributes to waking up puffy, it’s alcohol. Alcohol disrupts sleep quality, affects fluid regulation, and increases dehydration.

So you wake up feeling a bit puffy, a bit flat, a bit off.

But it’s far easier to blame the dessert than the glass (or two) of wine that came with it.

What’s actually worth asking yourself?

If you wake up with a puffy face, more useful questions are:

- Did I sleep well?

- Am I hydrated?

- Was my evening meal particularly salty?

- Did I drink alcohol?

- What position did I sleep in?

Because in most cases, the answer is simple to the puffy face is - ‘it’s just fluid.’

How to minimise fluid (if you care to - you do not have to).

You don’t need to cut sugar. You just need to be mindful of the basics:

- Stay hydrated across the day.

- Be mindful of very high-sodium meals in the evening.

- Moderate alcohol intake.

- Slightly elevate your head when you sleep.

- Move… your body will sort the rest out quickly once you’re upright.

Waking up with a slightly puffy face is normal. It’s not a sign you’ve “done something wrong,” and it’s definitely not a reason to start cutting sugar out of your diet. Your body isn’t reacting, it’s just functioning.

Cortisol is the body’s primary stress hormone. Is it directly causing weight-gain on its own? No.

In fact, on release, cortisol helps to mobilise energy, it increases alertness, regulates blood sugar, and supports you to deal with both physical and psychological stress. Short bursts of cortisol are essential – it protects you.

So, the issue isn’t cortisol itself. It’s the chronic elevation of cortisol which can shift how the body stores and uses fat and can make fat loss harder.

Defining “chronic” stress – the persistent, long-term state of tension lasting weeks, months, or longer, caused by unrelenting pressures e.g., financial struggles, unhappy relationships, or intense work environments. Unlike acute stress, it feels inescapable and keeps the body’s fight-or-flight response constantly activated. Chronic stress results in severe physical and emotional issues.

Does cortisol cause increased belly fat?

Here’s the nuance most information misses - cortisol doesn’t create fat out of nowhere – we can’t override basic energy balance; energy must come from somewhere. But cortisol can influence where fat is stored, shifting it toward the abdomen and trunk.

When cortisol is chronically elevated, the research shows a consistent pattern:

• Fat storage is increased around the abdomen (visceral fat).

• The risk of insulin resistance and metabolic dysfunction is increased.

So yes — there is a real relationship. But fat storage cannot work independently of calories.

Why is fat storage increased around the abdomen?

When we talk about abdominal fat, we are not talking about the fat that hides our 6-packs. Abdominal fat – or visceral fat – is metabolically active fat cells, stored deeply in the abdomen surrounding internal organs like the liver and intestines. Unlike subcutaneous fat which is the fat we see and feel under the skin, visceral fat is correlated to increased risk of diseases like heart disease and diabetes.

Side note: although visceral fat is more harmful to health, it responds faster to exercise compared to subcutaneous – which is why exercise is so important regardless of visible physique changes.

Visceral fat is more cortisol-responsive than other fat stores. When cortisol levels rise, visceral fat cells are primed to store fat more readily and effectively than the fat cells located elsewhere in the body.

Visceral fat can also amplify cortisol exposure locally via specific enzymes. The enzyme regenerates active cortisol from inactive cortisone in the fat cells. This creates localised ‘hypercortisolism’ in the abdominal fat even when circulating cortisol levels are normal – further contributing to visceral fat storage.

So - when cortisol is elevated, visceral fat cells are basically more responsive.

Cortisol doesn’t override energy balance.

This is where there can be a misunderstanding. Even in chronic-stress states, fat gain still requires a calorie surplus. Cortisol can change fat distribution and influences eating behaviour – but it cannot not create fat from nothing.

How cortisol indirectly drives fat gain

Where cortisol does have a powerful effect is through behaviour and physiology:

1. Increased appetite & cravings – during periods of stress (both acute and chronic), cortisol interacts with the main hunger hormone, ghrelin. This can increase appetite and food cravings, especially for high-calorie (highly palatable) foods. It seems that the larger the cortisol spike, the more prone to stress-eating and therefore weight gain. The effects can vary with stress type, whether it’s chronic or acute stress, and by individual differences (e.g., obesity, or whether we are an ‘emotional eater’ or not).

2. Blood sugar disruption - cortisol is designed to raise blood glucose during stress. When cortisol is too high for too long, it disrupts normal glucose control and promotes insulin resistance, increasing risk of diabetes.

3. Sleep disruption – sleep loss is strongly linked to higher body weight and obesity. Poor or insufficient sleep tends to disrupt the normal daily rhythm of cortisol especially by raising levels later in the day and blunting the usual morning-to-evening decline. Higher levels of cortisol worsen hunger regulation, increasing hunger, usually leading to increased snacking. More food = higher calorie intake.

4. Muscle breakdown – cortisol is a catabolic hormone for muscle. Chronic elevation can reduce lean mass mainly by shifting protein metabolism, reducing protein synthesis and enhancing protein breakdown. Over time, this loss in lean tissue (and more body fat) lowers baseline metabolic rate.

It’s a feedback loop…

High stress = higher cortisol = more visceral fat = more inflammation and stress signalling… = high stress. And the cycle continues.

What can we do about it?

If cortisol is playing a role body weight, the solution isn’t extreme dieting. The solution is regulation.

Things to focus on:

• Consistent calorie intake – think ‘inclusive’ not ‘restrictive.’

• Resistance training – to protect muscle from breakdown, and to improve insulin sensitivity.

• Sleep quality – to support appetite management and overall wellbeing.

• Stress management – find something that actually works for you because we are all different.

Cortisol is not the problem, but living in a constant state of stress might be.

From the outside, it looks like success. But is there a point where that discipline stops being helpful? When it starts becoming something else entirely?

Whether you’re an athlete or not, total rigidity around food can be a red flag.

I write this as a bodybuilder, so I would be a hypocrite if I denied that extreme structure doesn’t have a place in certain phases within sports (for example - a bodybuilding prep, which is inherently extreme). But we need to acknowledge that these phases should be time-limited, and balanced with phases of flexibility (e.g., in a bodybuilders “off-season”).

This doesn’t just apply to athletes.

Maybe you’ve been here yourself.

You go out for dinner and, despite a menu full of options, you choose the “safest”, plainest thing. Not because that’s what you truly want — but because anything else feels uncomfortable.

Or you go on holiday and stick to the same familiar foods, avoiding local dishes, new experiences, anything that feels uncertain.

Or — and this is where it often gets missed — you simply… don’t feel that interested in food anymore.

You say things like:
“I’m just not that hungry.”
“I don’t really think about food.”
“I eat because I have to, not because I enjoy it.”

And on the surface, that can sound neutral. Even positive.

But often, it’s not the full story.

Over time, something subtle happens when eating becomes overly controlled.

You start to disconnect from your internal signals — hunger, appetite, cravings, enjoyment. Not because they’ve disappeared, but because they’ve been consistently overridden.

Hunger becomes something to ignore.
Cravings become something to suppress.
Enjoyment becomes something to question.

And eventually, the narrative shifts.

“I’m not hungry” replaces “I’m ignoring hunger.”
“I don’t enjoy food” replaces “I don’t allow myself to.”

Because physiologically, most people don’t just lose their appetite or enjoyment of food without a reason. Appetite is tightly regulated by the body. Pleasure from food is part of human biology — it’s how we survive.

What’s more likely is that the body has adapted.

Chronic under-eating can blunt hunger signals. Stress can suppress appetite. Repetitive, low-variety diets can reduce food interest. And psychologically, if you repeatedly deny yourself certain foods or experiences, your brain learns to stop expecting them.

It’s not that the desire for food is gone. It’s that it’s been quietened — or overridden — for long enough that it feels that way.

In sport, this often gets labelled as discipline.

In the general population, it gets labelled as “being healthy”, “having good habits”, or “just not being that into food”.

But in both cases, it can reflect the same underlying pattern - rigidity.

We call this rigid style of eating ‘orthorexia nervosa’ — an obsessive focus on eating in a way that feels “correct”, “clean”, or “optimal”.

It’s not currently a formally diagnosed eating disorder, but it’s well documented. Research shows that people who exercise regularly — particularly athletes — have a higher prevalence of orthorexic tendencies, driven by perfectionism, performance pressure, and structured routines.

But importantly, it’s not limited to sport.

In non-athletes, it often shows up more quietly:

• Avoiding foods or food groups without medical need.

• Feeling anxious eating food prepared by others.

• Sticking to the same “safe” meals daily.

• Losing interest in food variety or social eating.

• Undereating, but framing it as “just not being hungry.”

For many people, this way of eating becomes part of their identity.

The ‘low maintenance’ food one.
The “good” one who “doesn’t get these cravings”.
The one who “can take or leave eating”.

Or in sport it’s generally labelled as the “disciplined” or “focussed” one who never deviates from the plan.

Identity can be hard to challenge. Because eating differently doesn’t just feel like a change in behaviour — it feels uncomfortable, unfamiliar, even threatening. Not necessarily because something bad will happen, but because it disrupts a sense of control.

It’s not a structure problem – structure can be helpful in supporting performance, energy, and routine. The problem is when flexibility feels impossible. When eating outside of your usual pattern creates anxiety. When you avoid situations rather than adapt to them. When your world subtly shrinks — fewer meals out, fewer shared experiences, less spontaneity.

That’s not discipline. That’s a relationship with food that’s limiting you.

Food is fuel, yes. But it’s also pleasure, culture, connection, and memory.

It’s trying something new on holiday.
It’s sharing meals with other people.
It’s enjoying food without overthinking it.

And when those parts start to disappear — even if everything looks “fine” on the surface — it’s worth paying attention.

If you recognise any of this in yourself, worth asking yourself:

Do I feel free around food?
Can I eat differently when I need to?
Do I actually enjoy what I’m eating — or have I just learned to say that I do?

Maybe it’s time to really start to listen to your body’s needs again and learn to retune into your appetite.

It’s easy to assume it’s psychological — the tradition, nostalgia, the once-a-year indulgence. But it’s actually designed this way!

1. The thin shell changes how it melts in the mouth.

Easter eggs are made from much thinner chocolate than standard bars. The thinness makes the chocolate melt in the mouth quicker. Faster melting = quicker release of cocos butter which carries flavour compounds. So you experience a more rapid burst of intense chocolatey flavour.

2. The curved shape enhances aroma release.

Unlike a normal chocolate bar, Easter eggs aren’t flat — they’re curved and hollow. When you bite/break into them, the shell shatters irregularly. This creates jagged edges and small fragments. These fragments expose more surface area to warmth (the melt), and air (aroma release). Aroma is crucial because flavour is mostly smell.

So compared to a dense chocolate bar, Easter eggs create a kind of “flavour explosion” effect — more aroma compounds hit your nose at once.

3. The ‘snap.’

Texture heavily influences how we perceive flavour. Easter eggs tend to have a cleaner and crisper snap, a more delicate structure, and much less density than bars.

This creates a more satisfying sensory experience, and signals “freshness” and “quality” to your brain. That crisp snap primes your brain to expect something better — and it often delivers (learnt experience for next year).

4. Chocolate composition is slightly different.

Many Easter eggs are formulated differently from standard bars. Cost-dependant, the cocoa butter content is usually higher – this offers a smoother mouthfeel, faster melt, and better flavour dispersion. Tempering of the chocolate is done to a smoother texture to help with moulding into thin shells. Easter eggs are designed to melt evenly rather than hold structure.

5. The hollow egg enhances perceived indulgence.

Because Easter eggs are hollow, you tend to eat larger pieces. Those pieces feel more substantial, but they melt quickly creating the intense flavour. High flavour intensity = greater perceived indulgence.

6. Easter eggs are seasonal and nostalgic.

In addition to food technology, there is also the general psychological effect Easter egg chocolate has on us. It is a seasonal treat not available all year round, it’s often eaten socially, and is associated with childhood happiness (nostalgia).

Your brain is primed to enjoy it more — and the physical properties of the chocolate back this up.

In summary…

Easter egg chocolate tastes better because it’s engineered to maximise flavour delivery:

• Thin structure = faster melting.

• Curved shape = more aroma release.

• Higher cocoa butter = smoother taste.

• Crisp texture = better sensory experience.

It’s a perfect example of how food technology and psychology can be combined to enhance eating pleasure.

But the reality is both simpler—and more nuanced—than that.

Insulin resistance isn’t caused by a single food, nutrient, or meal – not even sugar. It’s something that develops over time, and is shaped by how we eat, move, sleep, and live.

What is insulin resistance?

Insulin is a hormone that helps move glucose (sugar) from your bloodstream into your cells, where it can be used for energy.

When you become insulin resistant, your cells stop responding as efficiently to that signal. This causes your body to compensate by producing more insulin. For a while, this works. But over time, it can lead to higher blood sugar levels and increase the risk of type 2 diabetes and other metabolic conditions.

The biggest driver of insulin resistance is being consistently over-fuelled.

At its core, insulin resistance is strongly linked to a mismatch between: energy coming in (from food) vs. energy being expended (through movement and metabolism).

When we consistently take in more energy than we need, the body has to store the excess somewhere. Initially, it’s stored in fat tissue. But over time, especially when storage capacity is exceeded, fat starts to accumulate in places it shouldn’t - like the liver (non-alcoholic fatty liver disease) and muscles. This is sometimes referred to as lipotoxicity.

This is where the problem begins - these tissues are crucial for managing blood sugar. The excess fat (from consistent excess calorie intake) interferes with how they respond to insulin.

Body fat isn’t just storage – it is metabolically active.

One of the biggest shifts in how we understand metabolism is recognising that body fat isn’t passive – it is metabolically active.

When fat tissue expands (particularly around the abdomen), it can start releasing inflammatory signals into the body. These signals interfere with insulin’s ability to do its job properly. This is often described as chronic low-grade inflammation.

This type of inflammation is not the kind you feel when you’re unwell — it’s silent and ongoing disruption which happens ‘within the body.’

Movement matters!

Your muscles are one of the main places that glucose gets used.

When you move:

• Muscles take up more glucose from the blood.

• Insulin becomes more effective.

• Blood sugar is better regulated.

When you’re inactive, the opposite happens. This is why even short-term increases in activity can improve insulin sensitivity - sometimes even before any noticeable fat loss occurs. This is why exercise is so important regardless of fat loss. *Top tip, go for a 10-minute walk after meals to stimulate glucose uptake into the muscles.

Sleep and stress impact your metabolism.

Two factors that are often overlooked in the context of body fat: sleep and stress.

A few nights of poor sleep can reduce insulin sensitivity. This is partly due to changes in hormones like cortisol, which affect how your body handles glucose.

Chronic stress keeps cortisol elevated, which can increase blood sugar levels and can make cells less responsive to insulin over time.

These aren’t the sole (or main) causes of insulin resistance, but they add to the overall picture.

What about diet?

Diet absolutely matters BUT it’s not about one single nutrient.

There’s no strong evidence that carbohydrates, in isolation, cause insulin resistance.

Instead, dietary patterns that contribute include:

• Regular overeating.

• Diets low in fibre and minimally processed foods.

• Low protein intake (which can affect satiety and body composition).

In other words, it’s the overall dietary pattern that matters, not a single nutrient or ingredient.

Genetics and individual differences.

Some people are more prone to insulin resistance than others. Family history, ethnicity, and where the body tends to store fat (visceral vs subcutaneous) all influence insulin resistance. Two different people can live almost identical lives but have different levels of risk.

In summary…

Insulin resistance is not caused by:

• Eating carbs

• Having sugar

• “Spiking insulin”

It is primarily driven by a long-term mismatch between energy intake and energy use, combined with factors like inflammation, inactivity, poor sleep, and stress.

Insulin resistance isn’t about one meal: it’s the cumulative effect of all the environmental factors that your body lives in. Instead of focusing on avoiding specific foods, it’s more useful to focus on ways to support your body and its environment:

• Eating enough (amount and variety) but not constantly over-consuming.

• Moving regularly (especially resistance training and walking).

• Prioritising sleep.

• Managing stress where possible.

Insulin resistance won’t stop fat loss, but loosing body fat will make you more insulin sensitive.

A final note on PCOS…

The relationship between Polycystic ovary syndrome (PCOS) and insulin resistance is thrown around on social media a lot. Let me explain what we actually know…

PCOS and insulin resistance are deeply intertwined. When cells respond poorly to insulin, the pancreas compensates by producing more — and chronically elevated insulin directly disrupts ovarian function. Unlike most tissues, the ovaries remain highly sensitive to insulin stimulation, responding by overproducing androgens like testosterone, which drives the hallmark features of PCOS: irregular periods, ovulatory dysfunction, acne, and excess hair growth. This is why interventions that improve insulin sensitivity — a high protein, high fibre (lower-glycaemic) diet, regular exercise, or metformin — can improve not just blood sugar, but also menstrual regularity, fertility, and androgen levels simultaneously.

Recently, oxalates have entered the spotlight, with some articles suggesting they cause everything from mineral deficiencies to gut damage and chronic fatigue.

Should we be concerned? Spoiler alert… probably not.

What Are Oxalates?

Oxalates (or oxalic acid) are naturally occurring compounds found in many plant foods. Plants produce them as a defence mechanism against pests and environmental stress.

Foods that contain higher amounts of oxalates include:

• Spinach

• Beetroot leaves

• Swiss chard

• Rhubarb

• Almonds

• Cocoa

• Sweet potatoes

• Buckwheat

Because oxalates can bind to minerals such as calcium, iron and magnesium, they’re often labelled as “antinutrients.” This sounds alarming, but the reality is more nuanced.

Do oxalates block mineral absorption?

Technically, yes — oxalates can bind to minerals and reduce their absorption. But the key point is that this happens within the specific food they’re attached to, not across your entire diet.

Take spinach as an example; spinach contains calcium, but much of that calcium isn’t absorbed because it’s bound to oxalate. However, this doesn’t mean eating spinach will cause a calcium deficiency. Most people get calcium from many other foods throughout the day.

In real-world diets, mineral absorption depends on overall dietary patterns, not individual compounds. If oxalates significantly impaired mineral status, we would expect populations eating lots of vegetables to show widespread deficiencies. This isn’t what we see.

Where oxalates do matter: Kidney stones.

The strongest scientific link between oxalates and health is kidney stones. About 70–80% of kidney stones contain calcium oxalate crystals. For people who are prone to kidney stones, reducing dietary oxalate intake may be recommended alongside other strategies such as:

• Drinking more fluids

• Reducing excessive sodium intake

• Ensuring adequate calcium intake

However, for people with no history of kidney stones, oxalates are generally not considered a major health concern. Clinical guidelines do not recommend widespread oxalate restriction for the general population.

What about claims linking oxalates to fatigue, gut damage or joint pain?

Some [wellness] articles suggest oxalates contribute to issues such as:

• “Leaky gut”

• Joint pain

• Fatigue

• Skin problems

There is no evidence that normal dietary intakes of oxalates cause any of these issues. Much of the evidence comes from case reports, small studies or anecdotal accounts which fail to highlight additional confounding variables. Evidence like this can be useful for generating hypotheses, but they certainly don’t establish causation.

At the population level, there is no clear evidence that dietary oxalates cause systemic inflammatory or metabolic problems in healthy individuals.

Taking the “green smoothies” to an extreme.

There is one scenario where oxalates can become an issue: very large (and I mean, extreme), repetitive intakes of high-oxalate foods. For example, consuming large spinach smoothies every day can significantly increase oxalate intake. There are rare case reports of kidney problems linked to extreme dietary patterns like this. But these situations usually involve:

• Very high daily consumption

• Highly restrictive diets

• Underlying health vulnerabilities

These cases are not representative of typical eating habits.

The Bigger Picture

From a public health perspective, the bigger nutritional challenges most people face are:

• Low fruit and vegetable intake

• Low fibre consumption

• High intake of ultra-processed foods

Discouraging plant foods because they contain oxalates risks creating more problems than it solves. Many oxalate-containing foods — such as leafy greens, beans, nuts and whole grains — are consistently linked with improved health outcomes.

“The poison is in the dose.”

Many beneficial plant compounds exist because plants evolved chemical defences. These include:

• Polyphenols

• Glucosinolates

• Lectins

• Oxalates

At normal dietary levels, these compounds are not harmful and may even stimulate beneficial biological adaptations. This concept is sometimes called hormesis — where small amounts of stress trigger protective responses in the body.

Should you avoid oxalates?

For most people, the answer is no. Instead of focussing on restriction, take a balance approach, and simply:

• Eat a varied diet to ensure multiple sources of different vitamins and minerals

• Rotate different fruits and vegetables

• Avoid extreme dietary patterns

Oxalate restriction may be appropriate for individuals who are prone to calcium oxalate kidney stones, but for everyone else, it’s rarely necessary.

In summary…

Oxalates are a natural component of many plant foods. While they can contribute to kidney stones in susceptible individuals, they are unlikely to pose a health risk for most people eating a balanced diet.

Nutrition headlines often magnify small biochemical effects into widespread dietary fears.

In reality, diet quality, variety and overall lifestyle habits matter far more than the presence of a single compound in food.

Gluten is inflammatory – bye bye bread.
Seed oils are inflammatory – here’s to a boring salad.
Carbohydrates are inflammatory – who needs energy anyway?
Dairy is inflammatory – what is a world without cheese?

But the reality is that much of this conversation is oversimplified, and sometimes misleading.

So, let’s look at what inflammation actually is.

What inflammation really means:

Inflammation is a biological immune response that helps the body repair damage and fight infection. There are two broad types:

Acute inflammation
This is short-term and beneficial. For example, resistance training creates small amounts of muscle damage that trigger inflammatory signalling, which ultimately drives muscle repair and growth.

Chronic low-grade inflammation
This is the type associated with disease. It involves persistent activation of immune signalling pathways and is linked with conditions such as cardiovascular disease, insulin resistance, and type 2 diabetes.

Social media often treats these two things as if they are the same, but they are not.

Our biological goal is to regulated inflammation, not to completely eliminate all inflammatory processes.

The problem with the “anti-inflammation” narrative:

A lot of content has turned inflammation into a catch-all explanation for any uncomfortable physical sensation.

Feeling bloated? You must be inflamed.

Holding water after a salty meal? Inflammation.

Feeling sluggish after a large meal? Inflammation again.

In reality, these experiences are usually explained by normal physiology, including temporary shifts in fluid balance, glycogen storage, normal digestion, fibre intake, and sodium balance.

They are not indicators of systemic inflammation.

Another common issue is the claim that individual foods are inherently inflammatory. While certain foods can cause problems for people with specific intolerances or medical conditions, most healthy individuals do not experience meaningful inflammatory responses to normal foods.

So, we might not want to reduce acute inflammation, but how do we reduce chronic inflammation?

One of the most reliable ways to reduce chronic inflammation is fat loss *(in overweight or obese individuals).

One of the most consistent findings in metabolic health research is that losing excess body fat reduces systemic inflammation.

Obesity is widely recognised as a state of chronic low-grade inflammation.

As fat cells enlarge, they become metabolically stressed and begin to release inflammatory signalling molecules. At the same time, immune cells infiltrate adipose tissue, further increasing the production of inflammatory cytokines such as:

• TNF-α

• IL-6

• C-reactive protein (CRP)

This chronic inflammatory environment is one reason why excess body fat is linked with metabolic disease. The encouraging part is that reducing fat mass generally improves this inflammatory profile.

What the research shows:

Energy-restrictive diets and bariatric surgery consistently reduce inflammatory markers. These interventions typically lead to reductions in circulating levels of the inflammatory cytokines. At the same time, weight loss often increases adiponectin, a hormone produced by fat tissue that:

• Improves insulin sensitivity

• Reduces inflammation

• Increases fatty acid oxidation

A large review of 76 trials involving 6,742 participants found that most weight-loss interventions significantly reduced circulating inflammatory cytokines (Bianchi, 2018).

Long-term dietary trials also suggest that at least 5% body weight loss is typically required to see meaningful reductions in markers such as IL-6 (Bulmer et al., 2025).

The greatest improvements in obesity-related inflammatory markers tend to occur when weight loss reaches 10% or more of body weight (Forsythe et al., 2008).

Some important nuances:

As with most aspects of physiology, the relationship between weight loss and inflammation is not perfectly linear. For example, very rapid or early weight loss can temporarily increase some inflammatory signals. This has been observed following bariatric surgery or during periods of extreme calorie restriction before longer-term improvements occur (Savulescu-Fiedler et al., 2024).

In addition, even after body weight has normalised, inflammation within adipose tissue can persist for some time. Improvements are often gradual rather than immediate (Sougiannis et al., 2020).

These nuances are important, but they do not change the broader pattern seen across the literature.

The bigger picture:

When you see social media chat about reducing inflammation, the conversation often revolves around:

• Turmeric

• Greens powders

• “Detox” protocols

• Eliminating specific foods

Yet the evidence consistently points to something far less glamorous/specific/sellable.

Reducing excess body fat is one of the most reliable ways to lower chronic inflammation.

That doesn’t mean supplements or dietary quality are irrelevant, but their effects are typically much smaller than the impact of sustained changes in body composition and overall lifestyle.

In conclusion…

Inflammation is not something that needs to be “eliminated.” It is a normal and necessary biological process.

The real concern is chronic, dysregulated inflammation, which is strongly associated with metabolic health and body fat levels. While social media often focuses on individual “inflammatory foods,” the evidence suggests that the most consistent improvements occur when people:

• Reduce excess body fat

• Improve overall diet quality

• Sleep well

• Stay physically active

• Manage chronic stressors

In other words, the fundamentals of health still matter far more than any supposed anti-inflammatory superfood.

Is a sprinkle here and half teaspoon there actually giving you a meaningful anti-inflammatory effect?

Firstly, what is turmeric?

Turmeric comes from the root of the plant Curcuma longa. The bright yellow colour comes from curcuminoid compounds, the most important of which is curcumin. Curcumin is the compound most researched for its anti-inflammatory and antioxidant effects.

Turmeric powder is only 2-5% curcuminoids – therefore, most of what you add to food (or coffee apparently) is not curcumin.

What does research focus on?

To experience benefits for things like joint pain, osteoarthritis, metabolic inflammation, exercise recovery, and CRP (marker of inflammation) reduction, research does not use turmeric the kitchen spice.

In general, research uses standardised turmeric extracts containing up to 95% curcuminoids or enhanced curcumin formulations. Studies typically supplement with anywhere between 500-1500mg curcumin per day.

That’s a lot of spice to add to your curry!

And it’s not just about the quantity – absorption matters!

Taking a high dose of curcumin is not enough. It is poorly absorbed, and because it is fat soluble, rapidly metabolised, and quickly eliminated, your body struggles to keep meaningful levels in circulation. So, when you see curcumin supplements on the shelf, you’ll often see that they are combined with absorption enhancers.

The most common of these enhancers is black pepper. Piperine, a compound in black pepper, increases curcumins bioavailability by slowing it’s breakdown. However, piperine works by interfering with liver enzymes involved in drug metabolism, which means it can also affect certain medications, and so it is not suitable for everyone.

There are other options to enhance the bioavailability of curcumin which offer a more therapeutic inflammatory effect:

- Phospholipid complexes: Curcumin is bound to phosphatidylcholine, known as phytosome, which improves the absorption without interfering with drug metabolism.

- Liposomal curcumin: Curcumin is dispersed and encapsulated in tiny spheres that improve uptake by mimicking human cell membranes.

- Taking it with fat: By pairing turmeric extract with a source of fat like olive oil, or full fat yoghurt, absorption is improved – just not to the same level as supplement potency.

Does this make cooking with turmeric pointless?

Not at all! Turmeric, the spice, contributes small amounts of anti-inflammatory compounds and adds a small amount of antioxidant support. It provides flavour, making food choices more exciting and supporting long-term dietary diversity. Just make sure you are separating culinary inclusion from therapeutic dosing.

Final points…

Adding turmeric to meals is a great habit for overall diet quality but expecting it to significantly reduce chronic inflammation in culinary doses is probably unrealistic. If you are looking for targeted anti-inflammatory benefits, you need to focus on a standardised, well-formulated extract supported by scientific evidence.

As always, context matters – so ask yourself, what is this inflammation and what’s driving it? Am I addressing influencing lifestyle factors like stress management and sleep quality? How balanced is my overall diet?

It’s also worth remembering that nutritional supplements work by gently influencing specific biochemical pathways, and they will never replicate the potency or clinical impact of medical anti-inflammatory drugs.