Water is essential for daily functioning and health, and we can only survive a few days without it. Yet we constantly lose water through sweat, urination and even evaporation when we breathe.

This is why we have evolved a way to regulate and maintain water in our bodies. Like other animals, our survival relies on a strong biological drive that tells us to find and drink water to balance fluid loss.

This is thirst – a sensation of dryness in the mouth signalling we need to have a drink. This basic physiological mechanism is controlled mainly by part of the brain’s “control centre”, called the hypothalamus. The hypothalamus receives signals from various regions of the body and in return, releases hormones that act as a messenger to signal the thirst sensation.

What is dehydration?

Staying hydrated (having enough water in our bodies) is important for several reasons, including:

• regulating body temperature through sweat and respiration
• lubricating joints and eyes
• preventing infections
• digesting and absorbing nutrients
• flushing out waste (via the kidneys)
• preventing constipation
• brain function (including memory and concentration)
• mood and energy levels
• physical performance and recovery from exercise
• skin health.

Dehydration occurs when our body doesn’t have enough water. Even slight drops in fluid levels have noticeable consequences, such as headaches, feeling dizzy, lethargy and struggling to concentrate.

Chronic dehydration can pose more serious health risks, including urinary tract infections, constipation and kidney stones.

What does the evidence say?

Despite thirst being one of the most basic biological drivers for good hydration, science suggests our feelings of thirst and subsequent fluid intake don’t always correlate with hydration levels.

For example, a recent study explored the impact of thirst on fluid intake and hydration status. Participants attended a lab in the morning and then later in the afternoon to provide markers of hydration status (such as urine, blood samples and body weight). The relationship between levels of thirst in the morning and afternoon hydration status was negligible.

Further, thirst may be driven by environmental factors, such as access to water. For example, one study looked at whether ample access to water in a lab influenced how much people drank and how hydrated they were. The link between how thirsty they felt and how hydrated they were was weak, suggesting the availability of water influenced their fluid intake more than thirst.

Exercise can also change our thirst mechanism, though studies are limited at this stage.

Interestingly, research shows women experience thirst more strongly than men, regardless of hydration status. To understand gender differences in thirst, researchers infused men and women with fluids and then measured their thirst and how hydrated they were. They found women generally reported thirst at a lower level of fluid loss. Women have also been found to respond more to feeling thirsty by drinking more water.

Other ways to tell if you need to drink some water

While acknowledging some people will need to drink more or less, for many people, eight cups (or two litres) a day is a good amount of water to aim for.

But beyond thirst, there are many other ways to tell whether you might need to drink more water.

1. urine colour: pale yellow urine typically indicates good hydration, while darker, concentrated urine suggests dehydration

2. frequency of going to the toilet: urinating regularly (around four to six times a day) indicates good hydration. Infrequent urination can signal dehydration

3. skin turgor test: gently pinching the skin (for example, on the back of the hand) and observing how quickly the skin returns to its normal position can help assess hydration. Slow return may indicate dehydration

4. mouth and lips: a dry mouth or cracked lips can be early signs of dehydration

5. headaches and fatigue: frequent headaches, dizziness, or unexplained fatigue can be signs of inadequate hydration

6. sweating: in physically active people, monitoring how much they sweat during activity can help estimate fluid loss and hydration needs. Higher levels of sweat may predispose a person to dehydration if they are unable to replace the fluid lost through water intake

These indicators, used together, provide a more comprehensive picture of hydration without solely depending on the sensation of thirst.

Of course, if you do feel thirsty, it’s still a good idea to drink some water.

Lauren Ball, Professor of Community Health and Wellbeing, The University of Queensland and Kiara Too, PhD candidate, School of Human Movement and Nutrition Sciences, The University of Queensland

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Social media and lifestyle magazines have turned gluten – a protein in wheat, rye and barley – into a dietary villain.

Athletes and celebrities have promoted gluten-free eating as the secret to better health and performance.

But our review in The Lancet published today challenges that idea.

By examining decades of research, we found that for most people who think they react to gluten, gluten itself is rarely the cause.

Symptoms but not coeliac

Coeliac disease is when the body’s immune system attacks itself when someone eats gluten, leading to inflammation and damage to the gut.

But people with gut or other symptoms after eating foods containing gluten can test negative for coeliac disease or wheat allergy. They are said to have non-coeliac gluten sensitivity.

We wanted to understand whether gluten itself, or other factors, truly cause their symptoms.

What we did and what we found

Our study combined more than 58 studies covering symptom changes and possible ways they could arise. These included studying the immune system, gut barrier, microbes in the gut, and psychological explanations.

Across studies, gluten-specific reactions were uncommon and, when they occurred, changes in symptoms were usually small. Many participants who believed they were “gluten sensitive” reacted equally – or more strongly – to a placebo.

One landmark trial looked at the role of fermentable carbohydrates (known as FODMAPs) in people who said they were sensitive to gluten (but didn’t have coeliac disease). When people ate a low-FODMAP diet – avoiding foods such as certain fruits, vegetables, legumes and cereals – their symptoms improved, even when gluten was reintroduced.

Another showed fructans – a type of FODMAP in wheat, onion, garlic and other foods – caused more bloating and discomfort than gluten itself.

This suggests most people who feel unwell after eating gluten are sensitive to something else. This could be FODMAPs such as fructans, or other wheat proteins. Another explanation could be that symptoms reflect a disorder in how the gut interacts with the brain, similar to irritable bowel syndrome.

Some people may be truly sensitive to gluten. However, current evidence suggests this is uncommon.

People expected symptoms

A consistent finding is how expecting to have symptoms profoundly shapes people’s symptoms.

In blinded trials, when people unknowingly ate gluten or placebo, symptom differences almost vanished.

Some who expected gluten to make them unwell developed identical discomfort when exposed to a placebo.

This nocebo effect – the negative counterpart of placebo – shows that belief and prior experience influence how the brain processes signals from the gut.

Brain-imaging research supports this, showing that expectation and emotion activate brain regions involved in pain and how we perceive threats. This can heighten sensitivity to normal gut sensations.

These are real physiological responses. What the evidence is telling us is that focusing attention on the gut, coupled with anxiety about symptoms or repeated negative experiences with food, has real effects. This can sensitise how the gut interacts with the brain (known as the gut–brain axis) so normal digestive sensations are felt as pain or urgency.

Recognising this psychological contribution doesn’t mean symptoms are imagined. When the brain predicts a meal may cause harm, gut sensory pathways amplify every cramp or sensation of discomfort, creating genuine distress.

This helps explain why people remain convinced gluten is to blame even when blinded studies show otherwise. Symptoms are real, but the mechanism is often driven by expectation rather than gluten.

So what else could explain why some people feel better after going gluten-free? Such a change in the diet also reduces high-FODMAP foods and ultra-processed products, encourages mindful eating and offers a sense of control. All these can improve our wellbeing.

People also tend to eat more naturally gluten-free, nutrient-dense foods such as fruits, vegetables, legumes and nuts, which may further support gut health.

The cost of going gluten-free

For the approximately 1% of the population with coeliac disease, avoiding gluten for life is essential.

But for most who feel better gluten-free, gluten is unlikely to be the true problem.

There’s also a cost to going gluten-free unnecessarily. Gluten-free foods are, on average, 139% more expensive than standard ones. They are also often lower in fibre and key nutrients.

Avoiding gluten long term can also reduce diversity in your diet, alter your gut microbes and reinforce anxiety about eating.

Is it worth getting tested?

Unlike coeliac disease or a wheat allergy, non-coeliac gluten sensitivity has no biomarker – there’s no blood test or tissue marker that can confirm it.

Diagnosis instead relies on excluding other conditions and structured dietary testing.

Based on our review, we recommend clinicians:

• rule out coeliac disease and wheat allergy first
• optimise the quality of someone’s overall diet
• trial a low-FODMAP diet if symptoms persist
• only then, consider a four to six-week dietitian-supervised gluten-free trial, followed by a structured re-introduction of gluten-containing foods to see whether gluten truly causes symptoms.

This approach keeps restriction targeted and temporary, avoiding unnecessary long-term exclusion of gluten.

If gluten doesn’t explain someone’s symptoms, combining dietary guidance with psychological support often works best. That’s because expectation, stress and emotion influence our symptoms. Cognitive-behavioural or exposure-based therapies can reduce food-related fear and help people safely reintroduce foods they once avoided.

This integrated model moves beyond the simplistic “gluten is bad” narrative toward personalised, evidence-based gut–brain care.

Jessica Biesiekierski, Associate Professor of Human Nutrition, The University of Melbourne

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Winter is here, along with cold days and the inevitable seasonal surge in respiratory viruses.

But it’s not only the sniffles we need to worry about. Heart attacks and strokes also tend to rise during the winter months.

In new research out this week we show one reason why.

Our study shows catching common respiratory viruses raises your short-term risk of a heart attack or stroke. In other words, common viruses, such as those that cause flu and COVID, can trigger them.

Wait, viruses can trigger heart attacks?

Traditional risk factors such as smoking, high cholesterol, high blood pressure, diabetes, obesity and lack of exercise are the main reasons for heart attacks and strokes.

And rates of heart attacks and strokes can rise in winter for a number of reasons. Factors such as low temperature, less physical activity, more time spent indoors – perhaps with indoor air pollutants – can affect blood clotting and worsen the effects of traditional risk factors.

But our new findings build on those from other researchers to show how respiratory viruses can also be a trigger.

The theory is respiratory virus infections set off a heart attack or stroke, rather than directly cause them. If traditional risk factors are like dousing a house in petrol, the viral infection is like the matchstick that ignites the flame.

For healthy, young people, a newer, well-kept house is unlikely to spontaneously combust. But an older or even abandoned house with faulty electric wiring needs just a spark to lead to a blaze.

People who are particularly vulnerable to a heart attack or stroke triggered by a respiratory virus are those with more than one of those traditional risk factors, especially older people.

What we did and what we found

Our team conducted a meta-analysis (a study of existing studies) to see which respiratory viruses play a role in triggering heart attacks and strokes, and the strength of the link. This meant studying more than 11,000 scientific papers, spanning 40 years of research.

Overall, the influenza virus and SARS-CoV-2 (the virus that causes COVID) were the main triggers.

If you catch the flu, we found the risk of a heart attack goes up almost 5.4 times and a stroke by 4.7 times compared with not being infected. The danger zone is short – within the first few days or weeks – and tapers off with time after being infected.

Catching COVID can also trigger heart attacks and strokes, but there haven’t been enough studies to say exactly what the increased risk is.

We also found an increased risk of heart attacks or strokes with other viruses, including respiratory syncytial virus (RSV), enterovirus and cytomegalovirus. But the links are not as strong, probably because these viruses are less commonly detected or tested for.

What’s going on?

Over a person’s lifetime, our bodies wear and tear and the inside wall of our blood vessels becomes rough. Fatty build-ups (plaques) stick easily to these rough areas, inevitably accumulating and causing tight spaces.

Generally, blood can still pass through, and these build-ups don’t cause issues. Think of this as dousing the house in petrol, but it’s not yet alight.

So how does a viral infection act like a matchstick to ignite the flame? Through a cascading process of inflammation.

High levels of inflammation that follow a viral infection can crack open a plaque. The body activates blood clotting to fix the crack but this clot could inadvertently block a blood vessel completely, causing a heart attack or stroke.

Some studies have found fragments of the COVID virus inside the blood clots that cause heart attacks – further evidence to back our findings.

We don’t know whether younger, healthier people are also at increased risk of a heart attack or stroke after infection with a respiratory virus.

That’s because people in the studies we analysed were almost always older adults with at least one of those traditional risk factors, so were already vulnerable.

The bad news is we will all be vulnerable eventually, just by getting older.

What can we do about it?

The triggers we identified are mostly preventable by vaccination.

There is good evidence from clinical trials the flu vaccine can reduce the risk of a heart attack or stroke, especially if someone already has heart problems.

We aren’t clear exactly how this works. But the theory is that avoiding common infections, or having less severe symptoms, reduces the chances of setting off the inflammatory chain reaction.

COVID vaccination could also indirectly protect against heart attacks and strokes. But the evidence is still emerging.

Heart attacks and strokes are among Australia’s biggest killers. If vaccinations could help reduce even a small fraction of people having a heart attack or stroke, this could bring substantial benefit to their lives, the community, our stressed health system and the economy.

What should I do?

At-risk groups should get vaccinated against flu and COVID. Pregnant women, and people over 60 with medical problems, should receive RSV vaccination to reduce their risk of severe disease.

So if you are older or have predisposing medical conditions, check Australia’s National Immunisation Program to see if you are eligible for a free vaccine.

For younger people, a healthy lifestyle with regular exercise and balanced diet will set you up for life. Consider checking your heart age (a measure of your risk of heart disease), getting an annual flu vaccine and discuss COVID boosters with your GP.

Tu Nguyen, PhD Candidate, Department of Paediatrics, University of Melbourne, Murdoch Children’s Research Institute; Christopher Reid, John Curtin Distinguished Professor, cardiovascular epidemiologist and clinical trialist, Curtin University; Diana Vlasenko, Research Assistant, Murdoch Children’s Research Institute; Hazel Clothier, Lead Epidemiologist, Centre for Health Informatics, Murdoch Children’s Research Institute, and Jim Buttery, Professor of Child Health Informatics, Department of Paediatrics, Murdoch Children’s Research Institute

This article is republished from The Conversation under a Creative Commons license. Read the original article.