Category: 8. Health

Glucagon-like-peptide-1 receptor agonists (GLP-1) are being explored in oncology due to their positive effects on glucose, body fat, insulin resistance, and inflammation, all of which influence cancer progression. While the impact of other glucose-lowering drugs on cancer survival is mixed, newer agents like sodium-glucose cotransporter-2 (SGLT2) inhibitors have been reported to improve survival compared to DPP4 inhibitors. Although GLP-1s have been linked to a lower incidence of some cancers, their effect on survival in cancer patients with type 2 diabetes (T2D) is unclear. In a retrospective cohort study published by investigators in JAMA Network, researchers evaluated whether the use of GLP-1s is linked with improved survival among individuals with cancer and T2D.¹

Diabetes and Cancer

According to the CDC, nearly 1 in 5 individuals with cancer also have diabetes. Individuals with diabetes who are newly diagnosed with cancer could experience disrupted diabetes management and eating plans. Cancer treatments, such as chemotherapy, radiation therapy, and hormone therapy, can significantly impact a patient’s ability to manage their blood sugar. Chemotherapy, while effective at targeting cancer cells, can harm healthy cells, leading to side effects, such as mouth sores, nausea, vomiting, and loss of appetite, which in turn can make eating difficult and potentially cause low blood sugar. Radiation therapy, which uses high-energy rays to kill cancer cells, can cause the body to release excess sugar, leading to a spike in blood sugar, and may also cause fatigue that interferes with meal and activity plans. Hormone therapy, commonly used for prostate and breast cancer, can cause nausea and fatigue, which makes it difficult to maintain proper nutrition and stay active. Additionally, other medications, such as steroids, that are commonly administered with chemotherapy to combat nausea, can directly raise blood sugar levels.²

Despite the challenges, effective diabetes management remains crucial during cancer treatment, and remaining in control of blood sugar can help reduce the risk of infections and benefit the overall cancer treatment outcomes. The CDC recommends individuals try eating a balanced meal plan on days that they feel well enough, including foods that are higher in calories or protein but are still healthy, foods that improve appetite, and foods that are enjoyable.²

GLP-1s Use in Diabetes and Cancer

Researchers conducted a retrospective cohort using Medicare data from 2013 to 2020 to evaluate the connection between GLP-1s and all-cause mortality in individuals with T2D and cancer. Included individuals were aged 66 years and older, with T2D and 1 of 9 cancers—thyroid, pancreatic, bladder, colorectal, lung, kidney, breast, endometrial, or prostate.¹

In the cohort comparing GLP-1s with SGLT2 inhibitors, a total of 2553 matched pairs were involved with a median follow-up of 1.65 years from first drug prescription. In the other cohort comparing dipeptidyl peptidase-4 (DPP4) inhibitors, a total of 2564 matched pairs were included with a median follow-up of 1.7 years.¹

The results demonstrated that among older patients with cancer and T2D, GLP-1 use was linked to lower all-cause mortality compared to DPP4 inhibitor use and showed no significant difference when compared to SGLT2 inhibitors. The survival advantage over DPP4 inhibitors was consistent across demographics, including age, sex, non-Hispanic White individuals, obesity status, and several cancers like colorectal, lung, and breast cancer. The study authors noted that although a recent study indicated that the impact of GLP-1 expression on survival varies by cancer type, this study provides new evidence on the comparative effectiveness of GLP-1s.¹

However, this current study has limitations, including potential confounding factors and some underpowered subgroup analyses, emphasizing the need for clinical trials to confirm the role of GLP-1s in cancer survivorship.¹

REFERENCES

1. Radwan RM, Lu Y, Dai H, et al. GLP-1 RA Use and Survival Among Older Adults With Cancer and Type 2 Diabetes. JAMA Netw Open. 2025;8(7):e2521887. doi:10.1001/jamanetworkopen.2025.21887

2. CDC. I Have Diabetes and Cancer. What Can I Eat? News release. May 15, 2024. Accessed July 25, 2025. https://www.cdc.gov/diabetes/healthy-eating/diabetes-and-cancer-what-to-eat.html

A 2023 CDC report tracked more than 200 pool-associated outbreaks over a four-year period. But a few basic precautions can ward off these dangers |Image used for representational purpose only
| Photo Credit: AP

The air we breathe may do more than harm our lungs – it could also be quietly raising our risk of dementia.

A global analysis of data from nearly 30 million people suggests that air pollution – particularly from vehicle exhaust – significantly increases the risk of Alzheimer’s and vascular dementia.

Dementia currently affects over 57 million people. The number is projected to rise to almost 153 million by 2050. Although some areas such as Europe and North America are witnessing minor declines in prevalence, the global view is much less reassuring.

Researchers from the University of Cambridge’s Medical Research Council Epidemiology Unit took a closer look at the connection between pollution and dementia.

By combining results from 51 studies conducted across several continents – 34 of which qualified for meta-analysis – the experts were able to draw on a larger and more dependable data pool.

Which pollutants raise dementia risk?

The analysis focused on three major air pollutants: PM2.5, nitrogen dioxide (NO₂), and soot.

PM2.5, or fine particulate matter, consists of tiny particles small enough to reach deep into the lungs. These particles are generated by sources such as vehicle exhaust, industrial processes, wood burning, and construction dust.

Nitrogen dioxide, a byproduct of burning fossil fuels, is commonly found in vehicle emissions – especially from diesel engines. This gas is known to worsen asthma and reduce lung function.

Soot comes from sources like diesel exhaust and wood fires. It not only harms the environment but can also reach deep into the lungs, contributing to respiratory and heart problems.

Air pollution’s role in dementia

The findings were clear: for every 10 micrograms per cubic meter (μg/m³) increase in PM2.5, the relative risk of developing dementia rose by 17 percent. For the same increase in NO₂, the risk increased by three percent.

For each 1 μg/m³ rise in soot, the relative dementia risk rose by 13 percent. To put that in context, in 2023, the average roadside PM2.5 level in Central London was 10 μg/m³ – the same amount linked to a 17% higher dementia risk.

London’s average NO₂ level stood at 33 μg/m³. Roadside soot levels were 0.93 μg/m³ in London, 1.51 μg/m³ in Birmingham, and 0.65 μg/m³ in Glasgow.

Tackling air pollution for public health

“Epidemiological evidence plays a crucial role in allowing us to determine whether or not air pollution increases the risk of dementia and by how much,” said Dr. Haneen Khreis.

“Our work provides further evidence to support the observation that long-term exposure to outdoor air pollution is a risk factor for the onset of dementia in previously healthy adults.”

According to Dr. Khreis, tackling air pollution can deliver long-term health, social, climate, and economic benefits. “It can reduce the immense burden on patients, families, and caregivers, while easing pressure on overstretched healthcare systems.”

How does air pollution affect the brain?

The health impacts appear to go beyond just Alzheimer’s. The researchers found the association between air pollution and dementia was slightly stronger for vascular dementia, which is caused by reduced blood flow to the brain.

Around 180,000 people in the UK alone are affected by this type of dementia.

How does air pollution impact the brain? Researchers have identified several possible mechanisms.

The most widely supported theories involve inflammation and oxidative stress – both of which can damage cells, proteins, and even DNA. These processes are already linked to other chronic diseases.

Pollutants may enter the brain directly, or indirectly via the bloodstream, after first affecting the lungs or heart. Once in the brain, they can trigger the kind of inflammation known to contribute to dementia.

Equity gap in air pollution studies

The review also highlighted a gap in the current research: most of the studies were conducted in high-income countries and focused on predominantly white populations.

This matters because marginalized communities often face higher exposure to pollution, yet they remain underrepresented in research.

“Efforts to reduce exposure to these key pollutants are likely to help reduce the burden of dementia on society,” said study co-first author Clare Rogowski.

“Stricter limits for several pollutants are likely to be necessary targeting major contributors such as the transport and industry sectors. Given the extent of air pollution, there is an urgent need for regional, national, and international policy interventions to combat air pollution equitably.”

Environmental fixes to fight dementia

The team argues that solutions can’t just come from doctors or healthcare workers. Urban design, environmental policy, and transportation planning all play a role.

“These findings underscore the need for an interdisciplinary approach to dementia prevention,” said Dr. Christiaan Bredell.

“Preventing dementia is not just the responsibility of healthcare: this study strengthens the case that urban planning, transport policy, and environmental regulation all have a significant role to play.”

The message is clear: reducing air pollution isn’t just a public health priority – it’s a critical step toward protecting brain health on a global scale.

The full study was published in the journal The Lancet Planetary Health.

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An international team of researchers has found that obesity prevalence would shift significantly under proposed new criteria that could hinder the prevention and early detection of serious health conditions.

The study, published in Plos Global Public Health, analysed data from 56 countries to compare the prevalence of pre-clinical and clinical obesity using the existing BMI criteria with what the prevalence would be under the proposed criteria that requires at least one health condition to already be present before a person is considered clinically obese, such as diabetes, hypertension, or high cholesterol.

“Obesity is a serious problem and the definitions we use have implications for clinical treatment, health expenditures, disease surveillance, and for peoples’ awareness of their own health risks. So, it is important to understand how much any new definition would impact the prevalence of obesity,” said lead author Rodrigo Carrillo-Larco, assistant professor of global health at Emory University’s Rollins School of Public Health.

The study was authored by researchers from Emory University and Johns Hopkins University in the US, University of Queensland in Australia, Zhejiang University School of Medicine in China, and Universidad Peruana Cayetano Heredia and Universidad Cientifica del Sur in Peru.

When the additional health issues were included into the criteria for obesity, the prevalence dropped significantly among the 142,250 adults surveyed—with some nations seeing a drop of more than 50 per cent—but the results varied by nation and gender.

For example, the East African nation of Malawi had among the highest decreases in obesity prevalence under the proposed definition, but the decline was uneven among men (68 per cent) and women (53 per cent).

While the new definition could be more aligned with current disease risk, the researchers urged caution before considering a shift in obesity surveillance to the proposed standard because doing so would create substantial challenges in terms of measurement, equity, and implementation. And for individuals who would no longer be considered obese, it could provide a dangerous false sense of security.

“At the population level we would expect the prevalence of obesity to drop, but we should be mindful that it’s an artificial drop because the new definition is more strict or complex—that reduction in obesity is not real,” Carrillo-Larco said.

Washington: A groundbreaking study that was recently published is reshaping our understanding of obesity in economically developed societies. The research, which analysed data from over 4,000 adults across 34 diverse populations, suggests that the rising tide of obesity is more closely linked to dietary changes, particularly the consumption of ultraprocessed foods, rather than a simple reduction in physical activity.

The study, titled “Energy expenditure, obesity, and economic development across populations,” published in the Proceedings of the National Academy of Sciences (PNAS), was a collaborative effort by a large team of international researchers, with Herman Pontzer from Duke University’s Department of Evolutionary Anthropology and Amanda McGrosky (now an assistant professor of biology at Elon University and a Duke postdoctoral alumna) identified as lead investigators. The primary objective was to unravel how economic development influences obesity by meticulously examining its relationship with various components of energy expenditure. The researchers gathered and analysed data from 4,213 adults spanning 34 distinct populations, representing a broad spectrum of economic development. These included traditional hunter-gatherer communities, pastoralist groups, farming societies, and highly industrialised communities. By comparing these diverse groups, the team aimed to identify precise patterns and correlations between economic development, energy expenditure, and body composition metrics such as body mass, Body Mass Index (BMI), and body fat.

For years, a common assumption has been that as nations develop economically, their populations become more sedentary, leading to increased rates of obesity. However, this new study presents a more nuanced picture. Researchers found that while economic development is indeed associated with higher body mass, BMI, and body fat, it surprisingly correlates with greater total, basal, and even activity energy expenditure. This finding directly challenges the notion that reduced physical activity is the sole or primary cause of weight gain in modern societies.

“Our findings challenge the simplistic notion that reduced energy expenditure is the primary driver of obesity in developed contexts,” stated Herman Pontzer, principal investigator with the Pontzer Lab. “Instead, we found that people in more economically developed societies tend to expend more energy overall, yet they still experience higher rates of obesity, indicating other powerful factors are at play.” Amanda McGrosky added, “While we saw a marginal decrease in size-adjusted total energy expenditure with economic development, differences in total energy expenditure explained only a fraction of the increase in body fat that accompanied development. This suggests that other factors, such as dietary changes, are driving the increases in body fat that we see with increasing economic development.”

The most significant revelation from the study points to the critical role of diet. The research strongly indicates that the increased consumption of ultraprocessed foods is a more substantial factor contributing to obesity in these populations. This implies that fundamental changes in food availability, accessibility, and composition – particularly the pervasive presence of highly processed items – are playing a more dominant role than previously emphasised.

The implications for public health are profound. While physical activity remains vital for overall well-being, the study underscores the urgent need for public health initiatives to shift their focus towards comprehensive dietary interventions. Efforts to prevent and combat obesity in economically developing and developed nations should prioritise strategies that address the pervasive influence of ultraprocessed foods and promote healthier eating patterns. This research highlights that a holistic approach, tackling both energy intake and expenditure with a strong emphasis on dietary quality, will be essential in addressing the global obesity epidemic. The authors further note that “Diet and physical activity should be viewed as essential and complementary, rather than interchangeable.”

 

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For reasons not fully understood, Parkinson’s disease is the fastest growing neurological disease in the world. That is bad news considering how debilitating the condition is, and that there is no curative treatment available. Fortunately, the future looks brighter, with research in the field adding to our understanding of the disease by the day. But until a cure is finally found, physicians and their patients will have to manage Parkinson’s disease the best way we presently know how.

To give patients the best chance at improving their quality of life, the key is early detection. That is not as easy as it sounds, however. Diagnosis of the disorder is challenging, and requires a physical evaluation by a specially trained neurologist. The time and cost — and in many cases, lack of available specialists — can be a significant barrier standing in the way of someone seeking a diagnosis, especially those that are not yet symptomatic. As such, people are frequently diagnosed only after the disease has already progressed significantly.

But those barriers may disappear in the near future, thanks to the work of a group of researchers at the University of Rochester. They have developed an algorithm that can detect Parkinson’s disease with a high level of accuracy just by listening to a person speak for a few seconds. And they have made this tool available for use via the web, so no trip to the clinic or hefty bill from a neurologist is involved.

Past research has shown that nearly 89% of those with Parkinson’s experience subtle changes in their voice, such as altered speech patterns, reduced clarity, or different breathing and pausing habits before obvious symptoms appear. So the team designed a web-based screening system that prompts users to read two short pangrams (sentences that contain every letter of the alphabet), such as “The quick brown fox jumps over the lazy dog.”

Once the user recites the sentences using a computer’s microphone, an artificial intelligence (AI) model analyzes the recording for speech characteristics associated with Parkinson’s. This model was trained and validated on a dataset collected from more than 1,300 participants, both with and without Parkinson’s. Validation studies showed that the system achieved an accuracy rate of 85.7% in diagnosing the disease.

The team achieved this result by leveraging semi-supervised deep learning models such as Wav2Vec 2.0, WavLM, and ImageBind. These advanced models, trained on millions of audio samples, can detect subtle speech patterns that traditional methods might miss. By fusing multiple speech embeddings into a unified representation, the group created a model that outperformed existing diagnostic techniques.

While this AI-based test is not meant to replace a formal diagnosis, it could serve as an accessible, low-cost way to flag individuals who should seek further evaluation. This is particularly valuable in areas with limited access to neurologists, but can be used by anyone, anywhere. If you would like to take the test for yourself, check out the researchers’ website for more information.

Over the years, the guidance on eating eggs has been wildly inconsistent, with some studies suggesting that the popular breakfast choice is deleterious to one’s health, while other studies prop them up as an excellent source of protein and other nutrients.

Well, a new study adds its voice to the growing body of evidence that eggs are actually really good for you. It’s an examination of the discrete influences of saturated fat and cholesterol on levels of low-density lipoprotein (LPL), or ‘bad’, cholesterol in the body.

“Eggs have long been unfairly cracked by outdated dietary advice. They’re unique – high in cholesterol, yes, but low in saturated fat. Yet it’s their cholesterol level that has often caused people to question their place in a healthy diet,” says exercise scientist Jonathan Buckley of the University of South Australia.

“In this study, we separated the effects of cholesterol and saturated fat, finding that high dietary cholesterol from eggs, when eaten as part of a low saturated fat diet, does not raise bad cholesterol levels. Instead, it was the saturated fat that was the real driver of cholesterol elevation.”

Related: Study Finds Eggs Might Protect Brain Health And Lower Cholesterol

The researchers recruited 61 adults with the same baseline levels of LDL cholesterol, and tasked them with undertaking three different diets, for five weeks each. A total of 48 participants completed all three diets.

The first was a high-cholesterol, low-saturated fat diet that included two eggs per day. The second was a low-cholesterol, high-saturated fat with no eggs. Finally, the third was high in both cholesterol and saturated fat, and included one egg per week.

The results showed that diets high in saturated fat correlated with a rise in LDL cholesterol levels. However, the high-cholesterol, low-saturated fat diet produced a reduction in LDL cholesterol levels – suggesting that eggs are not responsible for bad cholesterol.

“You could say we’ve delivered hard-boiled evidence in defense of the humble egg,” Buckley says. “So, when it comes to a cooked breakfast, it’s not the eggs you need to worry about – it’s the extra serve of bacon or the side of sausage that’s more likely to impact your heart health.”

The research has been published in The American Journal of Clinical Nutrition.

Of all the hormones produced by the body, cortisol is the most misunderstood. It’s essential to any number of biological processes, and yet commonly typecast as “the one to do with stress” – an evolutionary adaptation for different times, wildly unsuited to modern living, something to reduce with meditation, reset with ice baths or regulate with red-light therapy.

Personal trainers will tell you to avoid long runs in case they result in “cortisol belly”, while influencers diagnose “cortisol face” as a sign of too much pressure in the office. To top it all, social media has recently seen the rise of the “cortisol cocktail” – a combination of coconut water, orange juice, salt, and lemon that TikTokers claim can reduce stress and help with weight loss.

But how much of this has any kind of scientific validity – and is worrying about your cortisol levels doing you more harm than good?

The first thing to understand is what cortisol is, and what it actually does: and yes, that does include helping to manage our response to external stressors. In situations that the body perceives as fight-or-flight, it helps the body to produce immediate energy – as well as suppressing non-essential functions such as digestion or repair (we’ll get to whether this is a bad thing or not shortly). “Cortisol plays a vital role in blood-sugar regulation, by prompting the liver to produce glucose and helping ensure a steady supply of fuel to the brain and body,” says Hannah Alderson, a nutritionist, hormone specialist and author of Everything I Know About Hormones. “It also helps modulate inflammation, keeping immune responses in check and preventing them from going into overdrive. It’s key in how we metabolise fat, protein and carbohydrate.” It also regulates blood pressure, can act as a mood buffer, and kicks in to help fight infection if we’re recovering from an acute illness. But one of its most vital roles is also its least talked-about.

“It’s the hormone that gets us out of bed,” says Angela Clow, emeritus professor of psychophysiology at the University of Westminster. “You get this burst of it in the morning, which is called the ‘cortisol awakening response’. That’s not a bad thing or a stress response – it’s the body’s way of waking up and promoting cognitive function. You’ve probably experienced a time when you have an early flight or a busy day ahead, and your body anticipates it and wakes you up without needing an alarm clock. That’s cortisol priming your brain to be more alert and more active, preparing you for the day ahead.”

Research published earlier this year confirmed that cortisol is already increasing from its lowest point about three hours before you wake up – putting to rest any idea that getting up itself is stressful for the body, and suggesting instead that rising cortisol levels are part of what gets us ready for the day. Like every other higher organism on the planet, we’ve evolved to live in an environment that’s dark for (roughly) half of every day, and so our body needs a way to switch from restoration into activity, which seems to be one of cortisol’s key roles.

“A very large proportion of the genes in your body are sensitive to cortisol,” says Stafford Lightman, a professor of medicine at Bristol Medical School and co-author on the recent research. “And so cortisol has a daily rhythm, and that daily rhythm regulates multiple genes in multiple tissues; in your brain, your liver and your immune system.”

As part of this process, cortisol levels gradually decline throughout the day, with periodic bursts approximately every 90 minutes helping to maintain proper bodily function. This certainly isn’t a bad thing, but it does make gauging it difficult: you could take two measurements 30 minutes apart and get two wildly differing numbers. Under laboratory conditions, researchers take cortisol readings from blood or saliva multiple times a day to obtain a general picture of how volunteers’ levels fluctuate and respond to stressors. At-home tests are much less useful: if you’re only testing yourself once or twice a day, the only thing you might notice is that your levels are very high or very low.

So what about the idea that the minor stresses of everyday life are constantly keeping our cortisol levels perilously high? One common characterisation of the way this might work is that our bodies, evolved to deal with sabre-tooth tiger attacks and flash floods, can’t easily distinguish between those sorts of immediate, physical threats and more psychological ones – an argument on the school run, say, or a nasty email from a client. Social stressors, the theory goes, can be insidious: they’re basically ever-present, especially if we’re prone to catastrophise, and if our bodies’ restorative systems switch themselves off every time we encounter them, we’ll never have time for rest and repair.

In baboon troops – which are very social and hierarchical – this effect is visible, with the lower-pecking-order males suffering with worse immunity and shorter lifespans, as their fight-or-flight systems are constantly prioritised over the rest-and-digest ones. But baboon lives tend to be genuinely far more stressful than human ones – if you’re kicked out of the troop or can’t find a mate, you’re facing a genuine, near-immediate threat to your genes’ survival, rather than just feeling a bit put out. There’s speculation, of course, that our bodies can’t make this sort of distinction, and that we still internally respond to having our birthday forgotten at the office like we would to banishment on the savannah. But is that really true?

As it turns out, probably not. To test the effect of short-term bursts of stress, psychologists have developed all sorts of unpleasant laboratory procedures – from cold-water immersion to problem-solving under time pressure, to the Trier Social Stress Test, where volunteers are tasked with delivering a speech and mental arithmetic task in front of an unresponsive panel of evaluators. And the effect isn’t as pronounced as you might have been led to believe.

“Trying to stress a human is really difficult,” says Lightman. “Even plunging your hand into freezing-cold water has very little effect. If you’ve got a really important job interview that is going to govern the rest of your life, then yes, that’s probably going to be stressful. But it’s very subjective – some people, of course, actually like giving presentations in front of a crowd. With things like the Trier test, you might get a reaction the first time, and then you won’t again – just understanding what the test is about is enough to destroy the effect.”

This means you’re unlikely to be suffering spikes in cortisol from the odd snippy Zoom call or altercation at the self-checkout – and, even if your body sees those situations as a threat to your wellbeing, there are other systems that kick in first. “It’s not just cortisol that goes up in stressful situations,” says Dr Thomas Upton, a clinical research fellow who also worked on the recent study. “There are other hormones – like catecholamines, your adrenaline and noradrenaline – that play key roles in the immediate part of the fight-or-flight response. This is what helps you ‘fight the lion’ and get yourself out of the situation, followed up by cortisol release if the stress is strong enough or long enough. What you’re feeling in a very stressful situation like a jump scare is a rush of adrenaline that makes your heart pound and your mouth go dry and all the rest of it.”

Brief, short-term stress is probably not doing you any harm, then. But does this mean heightened cortisol becomes more of an issue when you’re continuously stressed over the long term – for instance, from worrying about a family problem or the mortgage – or even deliberately putting yourself through too many difficult workouts?

“That’s a bit trickier,” says Prof Clow. “If you just have a short burst of perceived stress, you will have a little burst of cortisol. That’s fine: your body will speedily return to normal cortisol secretion. But if you’re chronically stressed, repeatedly getting these bursts, that can affect the regulation of your underlying circadian pattern, which is regulated by your biological clock. So that, instead of having a healthy dynamic pattern of cortisol secretion over each 24 hours, you get ‘flat-lining’, which is not able to regulate other processes adequately.”

Constant stress, then, is probably bad for your cognitive function and health. But cortisol is unlikely to change how you look, unless there are larger problems at play. “If you had Cushing’s syndrome, which is a rare condition where cortisol levels in the body are very high, for example due to a tumour of the adrenal gland, then yes, you might gain extra weight around the stomach, or notice that your face becomes round and puffy,” says Niamh Martin, a professor of endocrinology at Imperial College London. “But that tends to be with very, very high cortisol levels.”

And, while it’s true that something like a long run can elevate cortisol levels over the short term, that doesn’t mean there’s any need to ditch your plans for a new personal best. “Doing, say, a marathon is a massively stressful situation for the body,” says Upton. “You need a cortisol response in that situation, and there’s nothing wrong with it: if you didn’t have that response, the results would probably be terrible. You might actually die.”

The good news, then, is that you can happily ignore the most outlandish advice about keeping cortisol in check with cocktails or cold plunges. Unless you’re suffering from a clear medical issue, you probably also don’t need to worry about how your cortisol’s changing on a daily or hourly basis. Several companies are working on methods for continuously monitoring cortisol levels as you go about your everyday life – but even these could do most people more harm than good. “Something that we’ve seen with glucose monitors is that they create a lot of ‘worried well’ people who put one on, have their breakfast and say, oh hell, my blood sugar’s gone up too much,” says Lightman. “And then they start worrying about doing all sorts of things and make themselves ill. If you’re an Olympic sprinter or something, continuous monitoring might be useful. But, among most people, there’s so much individual variation that the range we call ‘normal’ is huge.”

There’s one more obvious question here, though: if cortisol isn’t the culprit, why does stress seem to go hand in hand with poor health, immune-system disruption and weight gain? “It’s very difficult to unpick,” says Martin. “For instance, many of us have a complex relationship with food – and there are behavioural reasons why we eat besides being hungry – so it’s easy to blame cortisol if we notice that we’re gaining weight, but it might also be that, because we’re stressed, we’re eating in a different way. Similarly, you might be having a tough time at work and that means you don’t have time to exercise, or you’re not sleeping well because you’re stressed and that’s negatively affecting your cortisol levels, rather than the relationship going the other way. Part of the issue is that we still don’t fully understand the chronic stresses that modern life involves and what their impact is on our bodies over a long period of time.”

So what does all this mean for you and your life – stressful or otherwise? “I think the most evidence-backed approach is to treat cortisol as something like a bystander, rather than blaming it for any issues you’re having,” says Martin. “If you’re chronically stressed, that’s something to deal with for health reasons, but it’s not necessarily a question of artificially finding ways to keep your cortisol down – it’s more holistic than that. The most important thing is to look after yourself, rather than reaching for an expensive supplement or a cortisol cocktail or anything like that.”

“There are a few things that seem to help keep cortisol well regulated,” says Clow. “The research suggests, for instance, that the earlier you wake – within reason – promotes a healthy and dynamic cortisol rhythm. So getting plenty of sleep and then getting up relatively early seems to be very good for you. There’s increasing evidence that night-time light exposure inhibits your melatonin secretion, which liberates cortisol and allows it to rise while you sleep.” It’s worth mentioning, though, that getting enough sleep – and on a regular schedule – might be more important.

Physical exercise seems to keep cortisol well regulated but, if you can’t face the gym, that’s not necessarily a bad thing. “Gentle exercise, like walking, stretching or pilates, can regulate cortisol far better than an hour-long Hiit class on an empty stomach,” says Alderson. “Breath work is amazing and you can do it anywhere. Micromoments of joy are a lot simpler to weave in than grand gestures like week-long yoga retreats – and, even if they’re not directly affecting your cortisol, they matter more than people realise. A laugh, a hug, a walk in nature: this stuff really matters.”

Finally, it’s important to remember that, even if modern living does occasionally nudge your hormones outside optimal levels, cortisol is on your side. Your body’s stress response to most things should be good for you. Try to get some exercise every day, sleep on a regular schedule, and eat as sensibly as you can. Don’t worry about the other stuff: you really don’t need the stress.