DEMOGRAPHY IS POLITICS
Soon it will be a business issue, too
Kirk Lawless - Ipsos Global Healthcare Monitors June 2025
HEALTHCARE VS EVOLUTION
Can GLP-1s rewrite our evolutionary story?
Kirk Lawless - Ipsos Global Healthcare Monitors May 2025
HEALTHCARE vs EVOLUTION
Can GLP-1s rewrite our evolutionary story?
Kirk Lawless - Ipsos Global Healthcare Monitors May 2025
Nature: The Ruthless Architect
For six million years, human evolution has been guided by the blind hand of natural selection, not with foresight or compassion but with relentless, unfeeling pressure. From our microbial origins four billion years ago, we’ve been playing in nature’s casino, where the game is survival and existence is the prize…
The house deals in fire, famine, drought, predators, and plagues. The only way to win – to bet against extinction – is to adapt. Our ancestors evolved not for comfort but for resilience, and especially for hunger; scarcity of calories was the great driver of change.
In times of ice and ash, when crops failed and plant life diminished, we shifted from vegetarian foragers to opportunistic omnivores. We scavenged bones and sucked marrow, the win being calories, which freed up energy and fuelled brain growth. Then we mastered fire and began to cook – extracting more energy from food, reducing the cost of digestion, and diverting more fuel to our brains.
Soon, we didn’t just survive, we started shaping our environment. Community became our winning hand; divide the labour, multiply the rewards. It was no longer survival of the fittest but survival of the group. Farming turned food from luck into steady supply in most parts of the world. And with that came an explosion in our time, energy, and creativity.
We’d beaten the house. Or so we thought.
Calories: The Gold Standard of Evolution
Our evolutionary formula was simple: find more fuel, win more time, do more thinking. So, we built civilisations around the most calorie-rich foods we could farm. Nature didn’t plan this – she doesn’t plan at all – but the unintended consequence of each successful adaptation was this: we got better at finding calories and worse at resisting them.
Today, we live in towers of glass, wired to the world, able to summon cooked meals without even moving. We don’t chase food, it chases us. And we can’t stop eating – because our biology is still playing the old game, even though the rules have changed.
We may have woken up to this reality, but our knowledge is just a few decades old; nowhere near enough to fight billions of years of evolution. We remain genetically, biochemically and hormonally hardwired to seek out the most calorific resources and consume as much as we can.
That biological pull continues to shape the modern obesity crisis – but not everyone sees it that way. Latest findings from Ipsos’ Consumer Obesity Monitor indicate how divided public perception remains: 45% of respondents saw obesity as a disease, while 41% saw it as the result of ‘bad habits’ᶦ. Strikingly, 40% of those diagnosed with obesity/overweight said they felt personally to blameᶦᶦ.
The science tells a different story – one rooted not in blame but in biology. To understand how we got here, we need to take a closer look at fat itself…
The unintended consequence of each successful adaptation was this: we got better at finding calories and worse at resisting them.
Fat: From Friend to Foe
Fat is our ancient banker, storing every spare calorie for the inevitable hard times ahead – and extremely effectively too. But now, for most of us, the famine never comes. Still the banker keeps on storing, demanding storage space in every corner of our bodies.
Excess fat stops acting like a quiet savings account and starts behaving like a relentless creditor: it turns into pressure. Around the neck and throat, that pressure crowds the upper airway, narrowing the passage so much that it repeatedly collapses during sleep – the hallmark of obstructive sleep apnea (OSA)ᶦᶦᶦ. Each pause in breathing fragments deep-rest cycles, starving brain and body of the overnight repair they depend on.
And evolution is unguided. It just adapts, tests the best solution, and moves to the next adaptation. This has led to some counterintuitive quirks like fat becoming a big player in the immune system. The bigger fat gets, the more out of control our immune system becomes. This can lead to autoimmune manifestations, such as psoriasisᶦᵛ.
This same crushing weight of inflammation can contribute to pulmonary arterial hypertension (PAH)ᵛ, reshaping the vessels of the lungs and overloading the heart. The great pump that keeps the body running begins to strain against rising pressure and, in time, this burden can ripple outward – triggering other physiological breakdowns, including chronic kidney disease (CKD)ᵛᶦ.
However, it's important to note that the relationships between obesity and conditions like psoriasis, PAH, and CKD are complex and multifactorial. While obesity is a significant risk factor, genetic predispositions, immune system dysfunctions, and other environmental factors also play crucial roles in the development and progression of these diseases. Mother Nature has many games at her casino, and we've been playing them all simultaneously for millions of years; sometimes the chips of one spill over into another. We are complex indeed.
The fat-immunity link manifests in other ways too. As fat builds up in the liver, it triggers inflammation and damage which leads to scarring. Once the liver is irreversibly scarred, we get liver failure. This condition is known as metabolic dysfunction-associated steatohepatitis (MASH)ᵛᶦᶦ.
With fat so inextricably linked to the immune system, and inflammation in particular, our bodies become awash with signals of inflammation. These little bad news messages reach the brain. This can cause neuroinflammation, damaging neurons over time – a major factor in the progression of Alzheimer’s Diseaseᵛᶦᶦᶦ.
Yet, it's essential to acknowledge that Alzheimer's Disease is also multifaceted, with inflammation just one factor among many. Recent studies even suggest that viral infections, such as herpes zoster, may play a role in its development. Notably, research indicates that the shingles vaccine could reduce the risk of dementia by approximately 20%, although the exact mechanisms remain under investigationᶦˣ.
The banker’s dark tricks are far more numerous than the losses listed here. Our bodies are brilliant machines, honed for survival, but our evolutionary wiring – built for scarcity – has turned on us in a world of excess. According to Ipsos’ 2024 Global Trends Surveyˣ, a staggering 63% of people would like to lose weight.
Excess fat stops acting like a quiet savings account and starts behaving like a relentless creditor: it turns into pressure.
GLP-1: The Body’s Internal Alarm
Our bodies do have brakes: naturally-occurring hormones like glucagon-like peptide-1 (GLP-1) that tell our brains, “enough”.
But in a world of hyper-available food, where we can consume vast numbers of calories at speed, GLP-1’s signal comes too late. We’ve already eaten well past full by the time it kicks in (with the excess stored by the bank). Then our GLP-1 levels drop again because our systems are still preparing for the next famine that doesn’t arrive. The GLP-1 mechanism is a useful one but a simple one; it doesn’t do math or surveillance.
Enter modern science and the pharmaceutical industry. The new, much-touted GLP-1 receptor agonist drugs (GLP-1s), first developed for type 2 diabetes before their wider benefits became clear, mimic the effects of the GLP-1 hormone. They work by increasing our GLP-1 levels, triggering the “enough” signal faster and keeping it steady for longer, reducing our hunger windowˣᶦ.
GLP-1s are now widely perceived as ‘wonder drugs’ that will change the lives of millions, if not billions. Not just in diabetes and obesity, but in sleep apnea, CKD and potentially MASH, PAH, psoriasis, Alzheimer’s and many more conditions besides. And you can see why. Fat equals physical pressure and inflammation, hormonal havoc, metabolic mayhem, and neurological noise. GLP-1s help reduce fat by amplifying the body’s natural satiety signal.
Our bodies do have brakes: naturally-occurring hormones like glucagon-like peptide-1 (GLP-1) that tell our brains, “enough”.
But that’s not even the whole story. GLP-1 is a remarkably versatile hormone, evolved over hundreds of millions of years and conserved across species from fish to mammals. Beyond regulating appetite, GLP-1 plays roles in insulin secretion, glucagon inhibition, gastric emptying, and even cardiovascular and neurological functions. This multifunctionality – although not yet entirely understood – is also why GLP-1 receptor agonists are being explored for such a vast range of diseases and disorders.
Still, exploration is not approval. We must draw a clear line between what we know and what we're still learning. GLP-1s have proven benefits in obesity, type 2 diabetes, chronic kidney disease (CKD)ˣᶦᶦ, cardiovascular disease, and obstructive sleep apneaˣᶦᶦᶦ, supported by robust Phase 3 trial data and regulatory approvalsˣᶦᵛ.
MASH sits in a unique position. Promising Phase 3 results have already been reportedˣᵛ, with regulatory submissions expected soon. While they have not yet been approved, both semaglutide and survodutide have shown significant histological improvements in large late-stage trialsˣᵛᶦ, setting MASH apart from other conditions still in early stages of investigationˣᵛᶦᶦ.
Other indications – such as PAH, psoriasis, and Alzheimer's Disease – remain under investigation, with varying levels of early clinical and preclinical evidence, and with science still unfoldingˣᵛᶦᶦᶦ. Only time will give us the answers.
Among healthcare professionals, confidence in GLP-1s is growing – but not without nuance. According to a recent survey conducted by Ipsos among 350 HCPs, 52% agreed that the use of GLP-1s will reduce the prevalence of diseases linked to obesity (rising to 68% in the US). However, only 35% believed GLP-1s are the biggest advance in healthcare in recent yearsˣᶦˣ.
Nonethless, the GLP-1 revolution continues to gather speed, with usage levels rising. Towards the end of 2024, Ipsos surveyed 4200 consumers in the US (currently the market with the greatest access) and found that a staggering 12% were taking a GLP-1ˣˣ.
Of course, no drug is without its limitations and this includes GLP-1s. The versatility that makes them so promising is what also makes them unpredictable. Mimicking a hormone that helps regulate metabolism, the brain, the gut, and even parts of our immune system is bound to have effects both welcome and unwelcome. Nausea and gastric discomfort are well-known travellers on this journey. So too is hair loss in some cases, a by-product of rapid weight lossˣˣᶦ.
And GLP-1s are not suitable for all. They are contraindicated in people with a history of certain rare thyroid cancers, discouraged in those with pancreatitis, and not recommended during pregnancyˣˣᶦᶦ. And there’s growing concern about what happens to muscle over time; if weight is lost too quickly, it’s not just fat that melts away. We risk losing strength. What matters isn’t just the number on the scale, but where the weight came fromˣˣᶦᶦᶦ.
For those who are eligible and can manage any side-effects, GLP-1s have one more catch: fat cells stay, and they don’t forget. Even when they shrink, they scream to be refilled. That’s why weight loss is so hard. The cells remain, hungry and loud. If you stop taking GLP-1s too soon, the body – still wired for its former size – pulls you back. Not out of malice but out of ancient instinct.
Time: Our Invisible Ally
The GLP-1 solution isn’t just the injection. It’s time. Time for the brain and body to settle into a new normal. Time for the subconscious to stop fighting weight loss like it’s a threat. Time to shift the settling point – the body’s defended weight range – through patience, consistency, and gentle rewiring.
For some, that rewiring comes through movement – building muscle, walking more, healing better. But not everyone can exercise easily. For those people, GLP-1s offer the first real lifeline: a biochemical pause button.
The reason, and it’s something we’ve neglected to point out thus far, is that you are amazing. Your brain uses a fraction of the energy of current AI systems and outthinks them. Where they need Olympic swimming pools of water to cool them, you need a few litres of water. Your immune system can ultimately beat any threat it encounters; it just needs time to find the right answer.
The Next Chapter: Winning Together?
Obesity is not a personal failure. It’s a global evolutionary trap. One that we’ve all helped build – through food systems, economics, and cultural reward loops that promote consumption above all else.
The pharmaceutical industry has handed us a powerful tool, but with it come some difficult questions. How do we produce enough GLP-1 doses to supply hundreds of millions (soon to be billions) of us, for years? And even if we can, who will fund it? It can’t rest on pharma’s shoulders. GLP-1 production requires raw materials, energy, technology, infrastructure and lots of people – all of whom work for the dollar, not for survival. And these drugs are financially out of scope for most individuals.
What about governments? Few can easily afford them for all eligible citizens – but the real question is, can they afford not to? The cost of treating obesity and all related diseases no doubt outstrips the cost of GLP-1s for all who need them (and remember they are both prevention and cure). That’s to say nothing of lost productivity and personal suffering.
As we stand at this crossroads of biology and technology, we must consider how to make these life-changing treatments accessible to all who need them and are eligible for them (not all of us will be). The potential benefits – improved health outcomes, increased productivity, reduced healthcare costs – could reshape our society. But realising this potential will require unprecedented cooperation between governments, healthcare systems, and pharma.
In the end, GLP-1s are more than just weight loss drugs. They're a chance to rewrite our evolutionary story, to take control of our biology in a way never before possible. As we move forward, we must carefully balance the promise of these medications with ethical considerations and equitable access. The future of human health – and perhaps of our species – may depend on it.
Nature doesn’t care if we win – but, finally, we do. Can we come together and work out how to make it happen?
As we stand at this crossroads of biology and technology, we must consider how to make these life-changing treatments accessible to all who need them
About the Research: Ipsos Consumer Obesity Monitor
Launched in Q1 2025, the Ipsos Consumer Obesity Monitor captures the evolving attitudes, behaviours and perceptions of general consumers and GLP-1 users. The Monitor captures the evolving ways in which consumers are managing their weight, their awareness of/experiences with novel anti-obesity treatments (led by GLP-1s), and the effects of GLP-1s on users’ lifestyles, attitudes and consumption habits. Data are available to multiple clients, but analysis and deliverables are tailored to subscribers’ strategic needs and business questions. The data cited in this article were collected from 8400 consumers in US (4,200), China (1,400), Brazil (1000), UK (900) & Germany (900), providing perceptions online in Q4 2024. Data are © Ipsos 2025, all rights reserved.
COMING SOON: Ipsos’ GLP-1 PersonaBot: ‘Converse’ with AI-enabled personas of GLP-1 consumer segments, based on Consumer Obesity Monitor data, as if they were real people…
Ipsos also runs an Obesity & Cardiometabolic Disease Therapy Monitor, capturing real-world prescribing of GLP-1s (and other therapies) across these indications, layered with the perceptions of treating healthcare professionals.
Contact:
Roberto Cortese Senior Director, Ipsos Obesity & Cardiometabolic Disease Monitors Roberto.Cortese@ipsos.com
References
i. Ipsos Consumer Obesity Monitor: 8400 consumers in US, China, Brazil, UK & Germany providing perceptions online in Q4 2024 (%s reflect Top 2 Box scores on a 7-point scale, where 7 = Completely agree and 1 = Do not at all agree) ii. Ipsos Consumer Obesity Monitor: 2642 consumers in US, China, Brazil, UK & Germany diagnosed with obesity/overweight providing perceptions online in Q4 2024 (%s reflect Top 2 Box scores on a 7-point scale, where 7 = Completely agree and 1 = Do not at all agree) iii. Ryan S et al. “Obesity and obstructive sleep apnoea: pathogenesis and treatment.” Eur Respir Rev 28: 190006 (2019). Available at: https://pubmed.ncbi.nlm.nih.gov/31243096/ (Accessed 28 May 2025) iv. Armstrong AW, Harskamp CT, Armstrong EJ. “Psoriasis and obesity: a systematic review and meta-analysis.” JAMA Dermatol 149: 195-200 (2013). Available at: https://pubmed.ncbi.nlm.nih.gov/23208415/ (Accessed 28 May 2025) v. Zafrir N, Adir Y. “Obesity and pulmonary hypertension: pathogenesis and clinical perspectives.” European Respiratory Review 27 (150): 180097 (2018). Available at: https://pubmed.ncbi.nlm.nih.gov/30291516/ (Accessed 28 May 2025)
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x. Ipsos Global Trends Survey 2024 (50,237 adults aged 18-74 in 50 markets worldwide providing perceptions online between February & April 2024) Ipsos Global Trends – Conscientious Health | Ipsos Global Trends - Methodology
xi. Blundell JE et al. “Once-weekly semaglutide 2.4 mg: appetite control drives weight loss.” Diabetes Obes Metab 19: 1242-1251 (2017). Available at: https://pubmed.ncbi.nlm.nih.gov/28266779/ (Accessed 28 May 2025)
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xv. Sanyal AJ et al. “A Phase 2 randomized trial of survodutide in MASH and fibrosis.” N Engl J Med 391:311-319 (2024). Available at: https://pubmed.ncbi.nlm.nih.gov/38847460/ (Accessed 28 May 2025)
xvi. Ibid
xvii. Blundell JE et al. “Once-weekly semaglutide 2.4 mg: appetite control drives weight loss.” Diabetes Obes Metab 19: 1242-1251 (2017). Available at: https://pubmed.ncbi.nlm.nih.gov/28266779/ (Accessed 28 May 2025) xviii. Drucker DJ. “GLP-1 physiology informs the pharmacotherapy of obesity.” Mol Metab 57: 101447 (2022). Available at: https://pubmed.ncbi.nlm.nih.gov/34626851/ (Accessed 28 May 2025) xix. Ipsos panel survey: 350 HCPs in US, EU4, UK providing perceptions online in Q1 2025 xx. Ipsos Consumer Obesity Monitor: 4,200 consumers in US providing perceptions online in Q4 2024 xxi. Godfrey H et al. “Alopecia associated with semaglutide and tirzepatide: FAERS analysis.” J Eur Acad Dermatol Venereol 39:e153-e154 (2025). Available at: https://pubmed.ncbi.nlm.nih.gov/38925559/ (Accessed 28 May 2025) xxii. U.S. FDA. WEGOVY® (semaglutide) Prescribing Information – rev Mar 2024. Available at: https://www.novo-pi.com/wegovy.pdf (Accessed 28 May 2025) xxiii. Prado CM et al. “Muscle matters: the effects of medically induced weight loss on skeletal muscle.” Lancet Diabetes Endocrinol 12: 785-787 (2024). Available at: https://pubmed.ncbi.nlm.nih.gov/39265590/ (Accessed 28 May 2025)
