Walk into any pharmacy in urban India, or scroll through videos from wellness influencers on social media, and you'll find powders, gummies and drinks promising to boost your collagen. When placed conspicuously at billing counters, much like bubble gum and candy used to be a decade ago, customers are prompted to make a last-minute collagen purchase. More protein bars now list it as an ingredient, too, touting its benefits for healthy skin, bones and joints. Propelled by these claims, India’s market for these products stood at nearly $65 million in 2024. Recently, ‘vegan collagen’ has joined the growing list of offerings in this segment of the supplement market. The name, however, can be misleading: plants do not contain collagen.

It is the most abundant protein in the human body, making up about 30% of our total protein. But we don’t simply absorb the collagen that we consume directly (from animal sources). So what actually happens to it inside our bodies—and can consuming it via food items or supplements really help us make more of the bodily protein we’re trying to preserve? 

We don’t simply absorb the collagen that we consume directly.

Molecular mysteries and misnomers

Imagine your body as a suspension bridge. The steel cables aren't glamorous—you notice them only when they fray—but without them, the bridge begins to weaken. Collagen is one of those cables.

Specialised cells in our bodies called ‘fibroblasts’ are responsible for synthesising it. They act like protein factories, linking together amino acids (primarily glycine, proline and hydroxyproline) to make collagen. Collagen molecules are rope-like structures which can withstand a lot of stress. This makes them the perfect scaffolding for our bodies, giving tendons their tensile strength, bones much of their framework, and cushioning cartilage. 

What consumers often get wrong is that this protein is not simply a tank that you can refill. “Collagen is not a single substance but a family of more than 28 classes, each serving different functions in the body,” says Mumbai-based dermatologist Dr. Manasi Shirolikar. Ingested collagen doesn’t travel intact to the dermis; its molecules are too large to pass through the skin’s outer barrier. This fundamental nature is why supplements—vegan, or otherwise—are not the answer to boosting its reserves. Our body cannot digest whole, native collagen ‘as is.’

Natural collagen molecules (from food, or supplements) are enormous and tightly bound. Digestive enzymes like pepsin break them down into individual amino acids and di/tri-peptides (chains of two and three amino acids respectively), says Dr. Shirolikar. This is why most oral supplements are in the form of hydrolysed collagen (or collagen peptides), where the collagen has already been artificially broken down into tiny chains, so your gastrointestinal tract can digest and absorb it much more efficiently. However, even these contain peptides too large for direct absorption into your skin or joints.

Collagen molecules are rope-like structures which can withstand a lot of stress. This makes them the perfect scaffolding for our bodies.

Even though supplements may be marketed as collagen builders, our bodies don’t preserve these distinctions. The acid in our gut denatures these molecules, rerouting them wherever necessary, perhaps to make keratin for our hair. Or the peptides may form collagen that gets deposited in other parts of the body, such as cartilage, bone, muscles, or tendons. It’s not necessarily going to manufacture the collagen that gives us the glowing skin we’re pinching our wallets for. 

Also read: Whey to go: A complete guide to protein

A marketing gimmick

The beauty industry’s fascination with collagen began in the late 1990s and early 2000s, when it first appeared as an ingredient in skin creams and serums, touted to enhance elasticity. However, its effectiveness as a topical (directly on the skin) application was doubted by dermatologists early on, as collagen is not naturally found on the skin’s surface but in the deeper layers. Skincare products containing collagen only temporarily moistened and plumped up skin, appearing to reduce fine lines and wrinkles. People continue to be drawn to these products possibly because a structural protein is marketed as a shortcut to a youthful appearance. These marketing claims are ambitious at best, and ridiculous at worst (some promise to improve skin ‘texture’ by up to 42%!). Elasticity aside, they are promoted as a way to reduce fine lines, improve hydration, brighten the complexion, or even thicken hair.  

Your body doesn't need collagen from food to produce collagen. It needs the raw materials and the right nutrients.

Collagen is found naturally only in animal connective tissue. Foods richest in collagen include tougher cuts of red meat, as well as the skin and bones of freshwater and saltwater fish. Bone broth and gelatin, made by simmering animal bones with a little vinegar for several hours, are often promoted as health foods. ‘Vegan’ collagen then, is largely a marketing gimmick, and has become a buzzword because it promises to cater to India’s large vegetarian demographic.

What slips unnoticed is that these supplements are labelled as ‘boosters’ or ‘builders.’ They contain plant-derived amino acids (glycine, proline, lysine) plus cofactors (helper molecules) like vitamin C, copper, zinc, silica, and at times, hyaluronic acid. “They contain zero actual collagen,” Dr. Shirolikar clarifies. 

So do vegetarians get only limited access to the fountain of youth? “Definitely not,” affirms Dr Shirolikar. "Your body doesn't need collagen from food to produce collagen. It needs the raw materials and the right nutrients." It is always built from scratch inside the body (since both builders and collagen from whole foods are broken down into a common pool of amino acids). To do this, it first needs enough dietary protein to supply amino acids, which can come from legumes, grains, soy, nuts, seeds, dairy or eggs.

To make collagen, the body also depends on vitamin C, an essential cofactor that supports the enzymes stabilising the newly formed collagen fibres by modifying proline and lysine. Without enough vitamin C, collagen is produced but remains weak and unstable—the underlying mechanism behind scurvy. Minerals such as copper, zinc and manganese also support different stages of formation and cross-linking. “As long as you're meeting your protein and micronutrient needs, your body can make perfectly healthy collagen—even if you've never eaten it in your life,” Dr Shirolikar adds. 

Also read: Insulin, explained: The lock-and-key mechanism controlling blood sugar

Youth cannot be bottled 

What justifies a continued interest in supplements, Dr. Shirolkar explains, is this: “Collagen hydrolysate delivers an unusually glycine/proline/hydroxyproline-rich amino acid pool that ordinary dietary protein doesn't replicate as efficiently.”  Some of these peptide chains resist being broken down into individual amino acids and may act as ‘signalling molecules.’ That is, “they may reach dermal fibroblasts in our body and stimulate them to produce more collagen and hyaluronic acid,” she adds. 

Most people forget that a decline in collagen is a natural outcome of aging. Production declines by roughly a percent every year, starting from the mid-twenties. Any pill purporting that it can magically fill that ‘tank’ should be taken with a grain of salt. There’s some early, encouraging research, but a lack of randomised controlled trials (which are the gold standard for testing dietary supplements); in any case, there is not enough knowledge to substantiate the rapidly growing collagen market in India and across the world. Many of these supplements are not vetted by state drug administrations. Moreover, several studies are funded by the very nutraceutical companies who stand to gain by expanding the collagen market. 

Marine collagen supplements (extracted from the skin, scales and bones of fish) also come with safety considerations. Fish in polluted waters store heavy metals in their tissues. Supplements derived from seafood may especially be contaminated by methylmercury, which damages the nervous system. Like other dietary supplements, they are not evaluated for safety or effectiveness before reaching the market. Together, these concerns complicate the idea that collagen supplements are both environmentally benign and inherently risk-free. 

Dr. Shirolikar’s advice is to stick to the basics that keep our bodies well-oiled every day: using sunscreen, getting enough sleep and smoking less. “If there's one intervention with the strongest evidence for preserving collagen, it's broad-spectrum sunscreen. UV exposure activates matrix metalloproteinases (MMPs)—enzymes that break down collagen, making sun protection the single most effective defence against premature skin ageing.” Adequate dietary protein and micronutrients like vitamin C, zinc and copper may be less glamorous, but they're the essential building blocks for collagen synthesis. Without them, nothing else works as well.

Photoprotection and adequate sleep (during which growth hormone pulses drive tissue repair) have better-established effects on slowing down collagen breakdown than any other oral supplement. Supplements are reasonable to try, but evidence to their benefits is modest and inconsistent, Dr. Shirolikar says. They shouldn’t replace the fundamentals! 

The most accurate way to think about collagen supplements is that they don't replace lost collagen or become skin collagen. At best, they may provide some of the ingredients—and perhaps some molecular signals—that support your body's own collagen factory. Everything else still depends on the same fundamentals: protecting collagen from damage, eating enough protein and getting the nutrients needed to build it in the first place.

Also read: In an age of food abundance, why does ‘hidden hunger’ hold India back?

Edited by Anushka Mukherjee and Neerja Deodhar

Slider Credit: NIH Photo Gallery via Wikimedia Commons

For ages, women have learnt to live with inexplicable changes in their bodies in a state of resigned acceptance. They often repress the anxiety that arises from signs of unfamiliarity. Consulting a doctor is an afterthought that comes too late. This is reinforced by social conditions that pay scant attention to women’s health, creating a cascading effect of flawed assumptions about symptoms, late diagnoses and erroneous treatment.

One of the most pronounced examples of this lived medical reality is the Polycystic Ovary Syndrome (PCOS), a hormonal and metabolic disorder that has affected, by global estimates, 170 million women. The all-too-common disorder occurs when the ovaries produce excess hormones called androgens, which manifest in symptoms like irregular menstrual cycles, excessive acne or hair growth, or enlarged ovaries. Worryingly, a patient with no pronounced symptoms can also be diagnosed with the condition.

For a disorder so vastly prevalent, its constellation of physical and psychological symptoms has, for long, hindered a thorough comprehension of its underlying nature. Over nine decades after the term was first coined, a global congregation arrived at the consensus that “PCOS” does little to reflect the range of complications found in persons living with this condition. In May 2026, Polycystic Ovary Syndrome was officially renamed Polyendocrine Metabolic Ovarian Syndrome (PMOS). This new terminology was the result of a 14-year-long process organised by 56 academic, patient and clinical organisations.

What’s in a name?

The engagement involved two global surveys that recorded 14,360 responses from patients and health professionals, group workshops and market analysis to arrive at an agreement as to whether PCOS needed a new name and if it did, to pick a most suitable replacement. Part of the process relied on the Delphi method—questionnaire-based surveys to gather consensus from participants with domain expertise in a given subject—to arrive at a conclusive redefinition. The health professionals who participated in the surveys represented a wide range of disciplines including gynaecology, reproductive endocrinology, nutrition and nursing.

The terms “polyendocrine” and “ovarian” stood out as potential alternatives in the survey results. A workshop held in February 2026 settled on the new term. Only two participants did not support a name change. In a paper detailing the process to rename the condition, The Lancet stated that the transition to the usage of PMOS across the board is estimated to take three years of time. 

“The current name reflects only one organ and fails to capture the disorder’s multisystem nature,” reads the paper authored by the researchers who led the process. A patient with PMOS can show symptoms that concern endocrine, metabolic, reproductive, psychological and dermatological features. The old term gave the misleading idea that the condition should necessarily entail the presence of cysts in ovaries, when in reality, irrespective of the presence of cysts, a patient can be diagnosed with the condition due to the evidence of other symptoms. Besides, the old term resulted in disproportionate emphasis on pregnancy-related concerns. “The reproductive focus of the name can reinforce stigma, particularly in sociocultural contexts where fertility carries high value,” the authors said. 

An evolving perception of PCOS

PMOS patients, and doctors across specialties who have been treating this disorder, have widely welcomed the new terminology. “It helps to specify what exactly is the clinical diagnosis. The ovaries are only one part and not the whole disease on its own,” says Dr. Aakanksha Padma Naik, a Mumbai-based gynaecologist. The term PCOS, she says, suggested that cysts in the ovaries “was the only point that mattered”.

While references to symptoms in the ovaries can be traced back to medical texts of the 19th century, the first significant breakthrough in characterising PCOS is attributed to Irving Freiler Stein and Michael Leo Leventhal, two American gynaecologists. In 1935, at a meeting of the Central Association of Obstetricians and Gynaecologists, Stein and Leventhal described the clinical histories of seven women with symptoms including irregular periods, hirsutism (excessive hair growth in a male pattern) and infertility. They also reported that the seven women had enlarged ovaries. The paper presented by the two doctors was titled “Amenorrhea associated with bilateral polycystic ovaries”, elaborating on the formation of multiple cysts–fluid-filled sacs–in the ovaries, causing them to become enlarged and painful. Amenorrhea denotes the absence of menstruation. 

Besides, the old term resulted in disproportionate emphasis on pregnancy-related concerns.

PCOS has since been a subject of extensive research in modern medicine, evolving to acknowledge that its diagnosis cannot be confined to symptoms in the ovaries. A milestone in the study of this disorder arrived in 2003 when 27 medical experts gathered in Rotterdam, Netherlands for a conference to come up with a revised criteria to diagnose it. The guidelines that are now known as the Rotterdam criteria stipulate that a patient can be diagnosed with PCOS if two of these three features are found: oligo-anovulation, that is infrequent or absent ovulation; hyperandrogenism characterised by an excess production of androgens which are hormones typically associated with male physiological characteristics; polycystic ovaries, that is, the presence of 12 or more follicles–small sacs containing immature eggs–in each ovary measuring 2-9 mm in diameter and/or an ovarian volume exceeding 10 ml. This consensus at Rotterdam expanded the definition of PCOS and became the widely accepted standard to confirm the diagnosis of this condition. 

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Not just a gynaecologist’s concern

The new term—Polyendocrine Metabolic Ovarian Syndrome—decentres the ovaries and represents the disorder’s character as one that affects diverse aspects of the body. The endocrine system is responsible for creating and releasing hormones that regulate various bodily functions. The new name draws focus towards hormonal imbalance and metabolic dysfunction that characterise the condition. 

For instance, resistance to insulin, a hormone that regulates blood sugar, is commonly observed in patients diagnosed with PMOS. This may result in hyperinsulinemia—the body’s response of overproducing insulin to keep blood sugar levels stable. The high-insulin state can stimulate the ovaries to produce excess androgens, which in turn triggers insulin resistance, furthering a vicious cycle that disrupts multiple bodily functions. The new term is meant to reflect such interactions between endocrine and metabolic abnormalities. 

PMOS is not just a gynaecological concern, but a syndrome that needs to be treated by a cross-section of specialists

Dr. Naik says that irrespective of the name change, gynaecologists were already following the practice of referring patients with symptoms such as insulin resistance to doctors specialised in endocrinology. “With the change of name, patients are more likely to see and understand the diagnosis versus just us understanding it,” she says. Earlier, she says, when gynaecologists referred patients to an endocrinologist or recommended that they undergo a series of tests to check hormone levels, patients were often sceptical of its necessity. If they approached a gynaecologist to address their irregular menstrual cycle, they were puzzled as to why they were being asked to test their insulin levels. With the new term, Dr. Naik hopes that patients will comprehend that PMOS is not just a gynaecological concern, but a syndrome that needs to be treated by a cross-section of specialists. 

“When you look at ‘polycystic ovaries’, people think that it is all about cysts in the ovaries,” says Dr. Anurag Lila, an endocrinologist, adding that patients were mainly concerned with the status of the cysts, requesting an ultrasound to see whether they have grown or reduced. “The disease is much beyond that,” Dr. Lila says.

Also read: Insulin, explained: The lock-and-key mechanism controlling blood sugar

The disruption of the Hypothalamic-Pituitary-Gonadal axis, the endocrine system that functions through a complex feedback loop between hormone-producing glands, is a key factor underlying PMOS. To diagnose or rule out PMOS, an endocrinologist examines the hormonal levels which in turn reflect the extent of risk of diabetes, gestational diabetes, and dyslipidemia (abnormal levels of lipids or fats in the bloodstream). 

Dr. Lila opines that there is no reason for a delay in diagnosing PMOS regardless of the specialist consulted by a patient. A gynaecologist, endocrinologist or dermatologist, he says, can identify symptoms associated with the condition. “There are difficulties in managing it because like in any disorder such as obesity or weight gain, it is not easy to make lifestyle changes,” he says. 

PMOS, as Dr. Lila put it, is not owned by any one branch of medicine. “If we try to make a strict compartmentalisation, it will be wrong. It is a team of doctors who manage it.” If the symptoms manifest in hirsutism, for example, a dermatologist steps in to treat it. Likewise, only a mental health professional can address the depression or anxiety that a PMOS patient may be coping with. “It is a multisystem disorder that affects you at multiple levels. The treatment and the modality changes at every stage of its management,” Dr. Lila says.

The role of nutrition

Women live with the symptoms of PMOS for much of their lives, and a balanced diet is critical to keeping them in check. But there is no one-size-fits-all approach, says nutritionist Aditi Prabhu. “Each case has to be handled with care and personalised based on individual goals, current symptoms, health complaints, root cause analysis, medical history, blood reports, lifestyle patterns, sleep habits, stress levels, mental health and their overall relationship with food, especially if they have had any previous experience with dieting,” she says. Broadly, whole grains and pulses, protein sources, a variety of fruits and vegetables, fibre and omega-3-rich foods are part of the diet plan that Prabhu charts for her patients. 

Patients grappling with PMOS can grow conscious of their body image. “A lot of women are constantly under the pressure of losing weight, as they are repeatedly made to believe that losing weight is the only solution,” says Prabhu. Enforcing this as the one-stop solution is a trivialisation of a complex condition that manifests differently in each patient. Even a woman with a regular menstrual cycle and optimal weight, Prabhu points out, can struggle with other PMOS symptoms such as mood swings, insulin resistance or metabolic dysfunction.

This name change will not make a major impact unless it is also accompanied by changes in the way this condition is diagnosed, treated and communicated to patients

Insulin resistance heightens the risk of diabetes in PMOS patients. Irregular diet, poor sleep patterns, inflammation, increased fat percentage, chronic stress accelerates sensitivity to insulin. “Early screening and managing it before it worsens can help reduce the risk of diabetes in the long term,” the nutritionist says. Insulin resistance and other symptoms of this condition can be significantly improved if the patient consistently follows recommended dietary and lifestyle changes. 

Like many healthcare professionals, Prabhu agrees that the new terminology is a “more holistic representation of the condition”. But it can only go so far in translating into positive practical implications. “This name change will not make a major impact unless it is also accompanied by changes in the way this condition is diagnosed, treated and communicated to patients,” she says. 

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What happens to the food we eat, once we’ve devoured it and wiped our plates clean? It gets chewed, swallowed, and pulverized, as it passes through the esophagus, stomach, and small intestine. Here, at long last, the delicious contents of our plates become things the body can use: water, electrolytes, fatty acids, amino acids, and sugars. These components then cross over from the small intestine into the bloodstream, through a variety of processes, to be utilised by different organs.

Given the largely carbohydrate-based Indian diet, the sugars are the largest end product of digestion, and the primary providers of energy. This sugar can be galactose or fructose, but largely, it is glucose.

Glucose lying around in the blood is bad for us.

There's just one tiny problem: our bodies cannot use all that glucose (or other building blocks like amino acids and fatty acids) all at once. While some is consumed by hungry cells immediately, the rest is stored either as glycogen in liver and muscle cells, or as triglyceride in fat cells. This is, in part, a simple rationing exercise; one cannot use up all energy stores in one go.

But it is also a matter of safety. Glucose lying around in the blood is bad for us. Professor and Head of Department of Physiology at Navi Mumbai’s D.Y. Patil Medical College, Dr. Vivek Nalgirkar explains why: "In the short term, the glucose gets converted to fat and causes weight gain. In the long term, it irreversibly binds with protein structures (like skin) in the body, weakening the body and accelerating ageing." So, glucose needs to be packed away safely.

Lock and key

The pancreas, tucked right behind the stomach, is responsible for detecting this excess glucose, and kickstarting the storage process. Gathered in small clusters of the organ are specialised cells called beta cells, which pick up on the high glucose levels in the bloodstream and release insulin. This hormone acts like a key, opening the doors (insulin receptors) of liver, muscle, and fat cells, and ushering glucose inside them. It was first isolated in 1921, and shortly after, in January 1922, it was administered as part of diabetes treatment for the first time.

Naturally, there are times (for example, when you skip lunch) when the body needs to dig into its glucose reserves. For this, the pancreas has a different set of specialised cells called alpha cells. They look out for low glucose levels in the bloodstream (i.e. when glucose is gone) and release a hormone called glucagon. Glucagon opens the doors in the reverse fashion, emptying glucose from the cells they are stored in, and back into the bloodstream.

Together, insulin and glucagon ensure that the blood sugar levels remain constant in the body. Too little (hypoglycemia), and your body—your brain especially—buckles under the lack of energy; too much (hyperglycemia), and the excess energy wreaks havoc on your organs.

The link to diabetes and obesity

Trouble begins to brew when insulin does not work like it is supposed to. Sometimes, the immune system thinks that the beta cells responsible for making insulin are dangerous, and destroys them. This results in Type 1 diabetes and requires patients to take insulin supplements. 

The more common condition, however, is Type 2 diabetes, where the body becomes insulin-resistant. The beta cells continue to make and release insulin, but the hormone is no longer able to open the muscle, fat, or liver cells and pack away the glucose. "Think of it like trying to open a rusted lock," says preventative diabetologist Dr. Jagruti Parikh. "Naturally, the door won't open.” The ‘rusting’ happens because of harmful compounds that form when fats or proteins react with excess blood glucose, and can be triggered due to various factors like excess fat, infections, or stress.

This hormone acts like a key, opening the doors of liver, muscle, and fat cells, and ushering glucose inside them

Insulin resistance contributes to obesity through various ways. Firstly, the beta cells can continue to sense excess glucose in the blood, and release higher quantities of insulin to try to counteract it. This upsets the balance that insulin and glucagon concentrations usually maintain, and this high insulin concentration is linked with obesity. Second, since the cells are starving despite abundant glucose in the bloodstream, the brain sends out hunger signals and we end up eating more. Lastly, the liver can struggle to process this extra energy and starts accumulating excess fat inside its cells, resulting in fatty liver disease. Insulin resistance is also a foundational issue causing PMOS (previously termed PCOS/PCOD). 

Also read: Food fortification 101: Can foods built in with nutrients counter malnutrition, deficiencies?

The emergence of GLP-1 drugs

The miracle drug of recent times, GLP-1 (which includes the likes of Ozempic), was introduced to control diabetes through weight reduction. GLP-1 stands for glucagon-like peptide-1, and it is a hormone that exists naturally in the body. It acts in the small intestine before digestion is complete. GLP-1 receptor agonists are lab-made medications that are meant to mimic the natural hormone. The first GLP-1 drug was cleared for diabetes treatment by the US FDA in early 2005. 

It performs two useful functions for diabetes patients. First, it addresses the issue of excess insulin in blood by restoring the ratio of the hormone to glucagon. "Glucagon is an antagonist (antagonists are substances that block the effect of another substance, or prevent a certain biological response), in a sense. It will normalise the glucagon-to-insulin ratio which is skewed in diabetes patients," says Dr. Nalgirkar. Secondly, GLP-1 reduces hunger at both a biological and psychological level. It affects how the brain ascertains satiety, how quickly the stomach empties food, and even how the liver performs metabolism.

The medication is only prescribed to diabetic patients who match certain diagnostic criteria. "It is never the first line of treatment," says Dr. Parikh. She stresses that GLP-1 drugs are worthless without coordinated changes in lifestyle, otherwise the lost weight will be gained back once the medication is discontinued. Given its prohibitive cost, it is also not a medication most people can afford to take for years together. Dr. Nalgirkar also warns that our understanding of the medication is still in nascent stages.

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GLP-1 drugs find alternate ways to balance blood sugar levels, but there also exists the possibility of reversing insulin resistance. Though the mechanism behind it is not fully understood yet, study after study has proved that exercise and a mindful diet makes our cells more sensitive to insulin, possibly because they increase the number of receptors (locks) on the cell’s surface.

Beneath its 'wonder drug' status, GLP-1 is simply a medication that is prescribed in specific use cases, and approached with the caution of any drug in its early years. In a fat-fearing society such as the one we inhabit, the history and purpose of the medication can serve as an important reminder to not get carried away by its promises of weight loss.

India’s diabetes burden is only growing, with a recent study finding that the country tops the Asia Pacific region in Type 2 diabetes, both in terms of absolute burden and mortality. It is imperative to focus on lifestyle, both diet and exercise, to buck the trend. 

‍Cover art by Pratik Bhide

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June has arrived, and despite the onset of the Southwest monsoons in India, many parts of the country are still waiting for the rains to release us from the clutches of this relentless heat.

It has been a harsh summer for India. On a single day in April 2026, all 50 of the world’s hottest cities were in the country; by May 2026, it housed 97 of the world’s top 100 hottest cities. Andhra Pradesh alone recorded over 300 cases of heatstroke. Though consolidated data on heat-related illnesses are yet to emerge for 2026, India recorded over 7,000 heatstroke cases last year. A 2024 paper also affirmed the prevailing belief that heat-related deaths in India are massively underreported.

Studies suggest that India’s heat events are becoming more frequent and prolonged, though not more intense. From a public health perspective, this means exposure to heat stress for extended periods, without an opportunity to recover from the damage it causes. With recent studies suggesting that heat stress persists in the monsoons as well, it is more important now than ever to understand how the human body responds to heat. 

Heat stress 101

Heat stress occurs when the body cannot adequately dissipate the heat it absorbs from the environment. It is not a single condition but a spectrum. Its earliest manifestations are heat rashes, sunburns, and painful limb cramps. These require only minimal medical intervention, if blisters form on the skin or the cramps become severe. 

A heat stroke is the endpoint of heat stress. It is much harder to treat than to prevent

In the next stages, heat stress progresses to cause fainting, heat exhaustion, and finally, heat stroke. Heat exhaustion presents with heavy sweating, body temperature above 38°C (100.4°F), rapid breathing, blurred vision, a weak pulse, and nausea. While suffering from heat stroke, a person becomes dizzy, weak, and acts strangely; their body temperature rises above 41°C (105.8 °F), and their pulse quickens. Any stage after fainting requires medical attention, and heat stroke cases warrant calling an ambulance. 

“Many people ignore early symptoms until the condition becomes serious. A heat stroke is the endpoint of heat stress. It is much harder to treat than to prevent,” says Dr. Keerthi Varman M, a General Physician and General Secretary of the Tamil Nadu Resident Doctors Association. 

The best way to avoid heat stress is to avoid stepping out or doing strenuous activity during the hottest times of the day, wear loose-fitted clothes, and remain adequately hydrated. In case someone around you is displaying symptoms of heat stress, move the person to a cool area, offer them sips of water, loosen any tight clothing, and fan and spray them with water.

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Why the body’s cooling mechanisms fail

The human body constantly tries to maintain a stable internal temperature, usually between 36.2 C to 36.7 C (97.3 F to 98.2 F). The hypothalamus acts as the brain’s central thermostat, continuously monitoring core temperature via thermoreceptors in the blood and skin to maintain equilibrium. Under normal conditions, it triggers cooling mechanisms like sweating and vasodilation, or the widening of blood vessels, which allows more blood to flow to the skin, from where it is dissipated into the atmosphere. 

When sweating does not work, vasodilation becomes the only way left to cool the body, which puts pressure on the heart vessels.

This system is insufficient in extreme heat events, and becomes inefficient when high temperatures are coupled with high humidity. If the air is already saturated with moisture, sweat will not evaporate. It is this act of evaporation—and not the act of sweating by itself—that cools the body. In just under a decade, India’s average relative humidity has increased from 67.1% to 71.2%, making humidity-related heat stress a rising concern. When sweating does not work, vasodilation becomes the only way left to cool the body, which puts pressure on the heart vessels. This (alongside ozone poisoning) is why excess heat is linked to cardiovascular stress. In fact, a 2025 study found cardiovascular failure to be the cause of most heat-related fatalities. Excessive heat is also linked with impaired kidney function and a worsening of chronic respiratory illnesses and diabetes. 

Though high temperatures are usually associated with the daytime, factors like pollution and urban heat islands have contributed to warmer nights over the past decade. The body usually recovers from heat stress during the night, making warmer nights a compounding factor in heat-related illnesses. As a result, body temperature continues to rise and reaches a point that exceeds the normal temperature range, leading to heat stress. 

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Measuring heat stress

It is this layered understanding of how humans experience heat that led to the development of heat indices. The simplest one is the Heat Index which considers the air temperature and humidity to give a more realistic understanding of how easily the body can cool itself through sweating. 

However, the amount of heat the body absorbs and how easily it cools itself depends on many other environmental factors. So, two more advanced indices were developed: the Wet Bulb Globe Temperature (WBGT), and the Universal Thermal Climate Index (UTCI). The WBGT assesses heat using more parameters, like wind speed and solar radiation, while the UTCI takes a more interdisciplinary approach and integrates areas like thermal physiology, occupational medicine, and mathematical modelling. There are also specialised indices like the Thermal Work Limit (TWL), which is used mainly for workplace safety. It helps determine how much physical work a person can safely do in hot conditions by also considering clothing and air pressure. Though UTCI is fast gaining favour globally, India continues to rely on the Heat Index and WBGT. 

The prevailing understanding is that the human threshold is a wet bulb temperature of 35°C.

All of these indices map the heat stress they measure to the corresponding physiological responses it results in, and the kind of adjustment in activity it might require. Naturally, one might wonder: how hot is too hot?  

The prevailing understanding is that the human threshold is a wet bulb temperature of 35°C. Beyond this limit, even a young, healthy person seated in the shade and having access to enough drinking water would experience a continual increase in core body temperature, which will escalate to heatstroke and death within a few hours. However, some recent studies found minimally active young adults to reach thermoregulatory failure at wet bulb temperatures as low as 26°C or 31°C. More importantly, research scholars from Harvard say that—even from a purely physiological viewpoint—there is no straightforward answer. Factors like age, income, and preexisting health conditions change one’s capacity to withstand heat, posing the question: ‘too hot for whom?’. 

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Prevention and planning

The questions of ‘how hot is too hot?’ and ‘too hot for whom?’ similarly transfer to a sociological study of heat stress. Roughly three-quarters of India’s workforce—about 380 million people—work in occupations like agriculture and construction which have high heat exposure. Over 90 percent of the labour force works in the informal sector, with no guarantee of basic employee protections or employer liability. 

This puts certain sections of society most at risk of heat stress: those who work outdoors, and the rural and urban poor. This includes construction workers, sanitation workers, street vendors, agricultural labourers, salt pan workers, delivery workers, and traffic police personnel. The rural poor, who cook on firewood stoves and walk long distances to fetch water, face prolonged, compounded heat exposure with little relief. A case study in Yavatmal, Maharashtra found that in a district where 64% of houses have tin roofs, indoor temperatures reached up to 45.8°C during peak summer hours, exceeding outdoor temperatures—meaning the home meant to shelter them only worsened their exposure. The urban poor in informal settlements face near identical conditions, where building materials trap heat and make staying indoors as dangerous as working outside. Certain occupations are also inherently more at risk, like those who work in glass or rubber factories, experiencing additional heat stress due to their workplace. Caste-based occupations, similarly, involve higher exposure to heat stress, as quantified by a 2024 IIM-B study.

The rural poor, who cook on firewood stoves and walk long distances to fetch water, face prolonged, compounded heat exposure with little relief.

Without clearly defined employee-employer relationships, it is hard to articulate how best to protect informal workers. But they are also the ones hit hardest by the absence of policies. A 2026 paper by Harvard University’s Salata Institute for Climate and Sustainability proposes coordination between various stakeholders, including worker unions, employers, governments and civil society institutions, to fasten progress. They do emphasise, however, that it would be unreasonable to expect employers to be able to fund and deliver these protections alone, and that sustainable funding mechanisms must be explored.   

Environmental engineer and activist Prabhakaran Veeraarasu points out that these variations in how heat stress affects people does not reflect in the Heat Action Plans (HAPs) that cities prepare. This happens at two levels. India currently relies primarily on absolute temperature thresholds defined by the Indian Meteorological Department (IMD) for its Heat Action Plans (HAPs). Policies built on the cruder surface temperatures are working with incomplete data and will produce incomplete solutions. Notable exceptions are Thane city (since 2024), and Tamil Nadu, since earlier this month, which have both adopted a basic Heat Index instead. 

The more serious concern is structural. Heat Action Plans worldwide have a tendency to lack legislative and financial backing, resulting in committees, but not change. India’s HAPs, specifically, suffer from short-sightedness; immediate measures like water coolers are not accompanied by long-term measures to increase shaded areas. 

Until heat is understood not just as a weather condition but as a lived physiological and social burden, many of its worst effects will continue to go unrecognised and unprevented. 

Though milk and dairy products are cornerstones of Indian cuisines and nutrition, we seldom stop to think about the food and agricultural systems that bring them to our kitchens and dinner plates. The welfare of the animals at the centre of these systems, their ability to walk and loiter freely, to choose when and what they will eat may sound like small freedoms, but they are important determinants of cattle health.

To the still-ambivalent reader, I offer a more personal, selfish reason to care about this aspect of domestication: livestock well-being affects milk composition, and by extension, the health and nutrition of the milk you consume.

The most widely accepted way of measuring this stress is to test for the concentration of cortisol, the dominant stress hormone in cattle.

Like humans, livestock respond to stress through changes in hormones secreted. Hormones secreted into the bloodstream of distressed cattle cross right over into their milk, and consequently, into our stomachs. India is the world's largest milk producer, and the steadily increasing demand for dairy only poses greater risk to cattle, owing to the prevalence of intensive, stress-causing practices.

Measuring stress in tangible ways

Cattle express stress in various ways. For instance, ruminating (the act of regurgitating swallowed food and chewing it again) is a natural behaviour essential for digestion, only undertaken during rest periods. When stressed or unwell, the time spent ruminating reduces. Vocalisations—the various bellows, grunts, and moos of cattle—also reveal their emotional state. Higher frequencies, lower pitches and reduced intensity of vocalisation are all associated with higher stress. The most widely accepted way of measuring this stress is to test for the concentration of cortisol, the dominant stress hormone in cattle.

Like humans, livestock respond to stress through changes in hormones secreted.

Cortisol is a hormone found in most mammals, including humans. Ordinarily, it performs a host of constructive functions to support immunity, reproduction, inflammation, and most famously, the stress response. Chronic stress elevates cortisol levels for extended periods of time. Stress in cattle can stem from factors like heat stress and disease, or management practices like being housed in compact spaces, or not having ready access to drinking water. If not identified and rectified, this stress essentially puts the cattle on survival mode permanently. The protein in their muscles breaks down, bones start decalcifying, and some cattle undergo neural degeneration too. Needless to say, the cattle's productivity falls too.

Also read: Understanding the social behaviour of buffaloes, a sensitive species

Cortisol you didn’t ask for

Stress-free cattle, thus, is in any dairy farmer's best interests. Why should it concern a consumer? It changes the nutritional profile of the milk, markedly reducing its fat, protein, and lactose content.

Unlike bacteria, cortisol is unaffected by sterilisation or pasteurisation. So, with your spoonful of creamy curd, you may be getting a dash of cortisol that you didn't really sign up for.

Also read: Buffalo domestication: How housing conditions in rural, urban India affect welfare

Conscious consumption = prevention?

So, how do we know if the milk we are drinking is cortisol free? Put simply, we don't. The Food Safety and Standards Authority of India (FSSAI) guidelines do not mandate testing milk for cortisol, and most labs do not have the requisite infrastructure to conduct these tests. India does not even have guidelines specifying the maximum safe limit of the hormone in dairy products, unlike countries like Japan.

The only way to ensure that dairy animals are being treated well, is to become conscious of our consumption

The solution, within the existing landscape, is to try and ascertain how cattle are treated in dairy farms. Some responses of cattle to their environment or management are natural, and any milk we consume will have traces of cortisol. While cortisol acts as a litmus test to confirm or deny stress, looking out for good management practices, like not tethering livestock, emerges as a key indicator of well-being.

The only way to ensure that dairy animals are being treated well, is to become conscious of our consumption. But better decisions cannot come from a system that does not make information public and accessible. Conscious consumption can only come after traceability, and the capacity to trace which livestock systems one’s dairy is coming from. 

Also read: Keeping it cool: How to spot signs of heat stress in buffaloes

Far, far away from where I sit in Bengaluru, lies a tranquil sea on the western shores of South America. No matter where one lives, one must care about this coast, and the temperature of the waters there. It impacts us in all sorts of ways, like how hot our summers get, how expensive our vegetables become, and how heavily it will rain in the coming monsoons. If the ocean water is the average (or “neutral”) temperature, all is well. If it is cooler than usual (an event called La Nina), some countries suffer, but India enjoys a bounty. But warm waters on the coasts of Peru (the El Nino) tend to spell drought and distress for us. 

These warm waters affect the flow of winds and how they pick up moisture, resulting in them being framed as the evil that affects weather, lives, and livelihoods. In reality, it is actually a part of the ebbs and flows of natural climatic patterns. Thanks to climate change, both El Nino and its cold counterpart, La Nina, are persisting for longer, becoming more frequent, and possibly more intense. This makes it harder for ecosystems to recover from the disruptions that these phenomena cause—and that is cause for concern. This year, a new term is strewn across the news: the “super El Nino”, a scarier version of everything that the warm seawaters of Peru imply. 

What makes it ‘super’

The premise of the El Nino currents is simple: usually, trade winds (equatorial winds flowing east-to-west) carry warm waters from the Peruvian coast towards Indonesia. In their place, cool water rises up the ocean to occupy Peru’s shores. For reasons science has not yet fully understood, the trade winds weaken at irregular intervals every 2-7 years, and warm water stays back in South America. Without sufficient heat building up at the Indonesian coast, cloud formation is affected, and India’s southwest monsoons are weakened.

The April 2026 update of the World Meteorological Organization (WMO) indicates an increasing likelihood that a strong El Nino event will occur as early as May–July 2026, and peak in 2027 before receding. Ordinarily, an El Nino is declared when the sea surface temperature in the central Pacific Ocean exceeds 0.5°C above the long-term average temperature for a few sustained, consecutive months. While a ‘super’ El Nino is not an official term, it is used when the estimated rise in the sea’s temperature is more than 2°C. The last three super El Niño events occurred in 2015-16, 1997-98 and 1982-83. The 2015-16 El Niño led to a record global annual average temperature at the time, a record that 2027 is now predicted to snatch. 

Thanks to climate change, both El Nino and its cold counterpart, La Nina, are persisting for longer

There are caveats to this declaration of ‘super’: firstly, this forecast is muddied because it is difficult to predict an abnormality like the El Nino when seasonal changes are also causing variations in weather patterns. Moreover, overall global warming trends affect the baselines that are used to calculate if the rise in sea temperature is an abnormality. What is important, though, is that the figure and intensity is disputed–not the fact that El Nino (‘the little boy’) is visiting. 

Also read: In the battle of Alphonso vs Kesar, climate change plays dirty

Strained resources

Most literature on El Nino discusses its impact on the Indian monsoons (and rightfully so), but it begins affecting our weather earlier on, contributing directly to heatwaves. Heatwaves reduce productivity of staple crops, livestock, and commercial fish while simultaneously making working conditions unbearable for farm labour, especially women. The risk extends beyond farm productivity—agricultural workers are 35 times more likely to die from occupational heat exposure than all workers combined in other sectors. 

This harsh summer is followed by a below-normal southwest monsoon, dropping to 92% of the long period average this year according to forecasts by the India Meteorological Department (IMD). The heat has already put soil moisture, groundwater and surface water under stress due to increased evaporation and increased demand for water due to the heat. This reduces the water available for domestic, industrial, and agricultural use. 

While a ‘super’ El Nino is not an official term, it is used when the estimated rise in the sea’s temperature is more than 2°C.

The water required for agriculture is worth dwelling on for many reasons, including its key role in providing employment as well as food security. Rain-fed irrigation accounts for around 50% of India’s net sown area, and around 40% of the total food production. Of the remaining half of the sown area, groundwater sources like tubewells make up a significant chunk. All of these sources, including the moisture the soil itself stores to remain healthy, are compromised by the El Nino. 

This context is important to comprehend what a weak and delayed monsoon means for an Indian farmer. With rain-fed crops, a farmer’s sowing cycle depends on when the monsoons will come—planting too soon and too late both carry consequences, impacting crop quality and yield. 

Findings from a 2025 study add nuance to this conversation: while El Nino reduces net summer rainfall, it paradoxically increases the frequency and intensity of heavy daily rainfall. This means that the little rainfall that farmers receive is hard to harness, and tends to destroy rather than nurture crops. 

Rain-fed irrigation accounts for around 50% of India’s net sown area, and around 40% of the total food production.

This hits farmer incomes, even after the El Nino event passes. An RBI paper studying the 2015-16 super El Nino noted that rural wages remained subdued even after agricultural growth resumed. Data also suggests that more people have moved into agriculture after the COVID-19 pandemic, meaning that the economic distress affects more people. Produce from livestock, like milk and eggs, which often serve as contingent sources of income during times of drought, are also affected by El Nino. The supply crunch created by reduced grain, vegetable, and dairy production increases prices for consumers as well. The RBI’s inflation projections for the year captures this. Its inflation prediction peaks in the third quarter (October to December), which is when the impact of the monsoons on food prices will become most apparent. That said, there is some cautious optimism. An SBI Research statement points out that our stock of foodgrains is sufficient to “thwart any untoward disruption” caused by dips in Kharif production. 

Also read: Climate change in my cup: Why India’s cocoa and coffee production is at risk

Building resilience

The one silver lining with El Nino is that predictive mechanisms are well established, and afford us time to prepare. The most critical of preparatory measures is early warning systems that alert farmers to extreme weather conditions and provide guidance on potential remedial measures. 

The agrometeorological advisory services that the India Meteorological Department (IMD) provides to farmers via television, radio, and SMS are a step in this direction.

Adapting agricultural practices to this changing reality is another way to arrest how badly it affects farmers. This includes shifting to efficient irrigation and water management practices, embracing climate-resilient crop varieties, and practicing multicropping and agroforestry to maintain soil health. A statement by the agricultural ministry shared that, thanks to coordinated efforts on better water management, irrigation, and agricultural practices, the country’s reservoir storage is at 127.01% of the normal level for this period. This water is considered crucial in softening El Nino’s impact on the Kharif crops. 

While these measures can actively combat the damage that El Nino is causing, climatologists urge us to look at the larger picture.

While these measures can actively combat the damage that El Nino is causing, climatologists urge us to look at the larger picture. The oceans are absorbing over 93% of the additional heat generated because of global warming. It is this heat that collects over the East Pacific ocean to cause El Nino. Climatologist James Hansen compares this heat build up to a battery, saying that “human-made warming is decreasing the time needed to recharge the battery” and making El Ninos more and more frequent. The El Nino, thus, is not the disease, but the symptom. How we tackle global warming is going to define our future. 

Read more: A crop for the future: Why India should invest in ragi and its climate resilience