DEMOGRAPHY IS POLITICS
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Pieter De Richter - Ipsos Global Healthcare Monitors June 2025
DOES EVERYTHING REALLY CAUSE CANCER?
How our changing world is impacting our cells, and what it means for all of us
Pieter De Richter - Ipsos Global Healthcare Monitors June 2025
DOES EVERYTHING REALLY CAUSE CANCER?
How our changing world is impacting our cells, and what it means for all of us
Pieter De Richter Ipsos Global Healthcare Monitors June 2025
Introduction: the rising burden of cancer mortality
The COVID pandemic was a stark reminder of a fact that was once firmly embedded in the human psyche: infectious diseases can be deadly. Putting aside the pandemic, however, we are fortunate to live in an era where humanity has largely turned the tide on infectious pathogens. Where they were once the primary cause of death for our species, medical advances such as the advent of vaccines and the arrival of potent antibiotics have brought their mortality rates far below those of other conditions¹.
We don’t even have to go all that far back in time to see how much the situation has changed: as a particularly striking example of the changing fates of humankind throughout the 20th century, the chart below shows how the top causes of death in Japan were infectious diseases (tuberculosis and pneumonia) all the way up to 1940s.
By the 1960s, a very different picture had emerged: cerebrovascular diseases, malignant neoplasms (cancer) and heart disease were the leading cause of death at this point. Fast forward to 2019, and these three still feature in the top 4, alongside senility. What stands out the most, however, is that malignant neoplasms have risen so much as a cause of death that they are now responsible for almost as many deaths in Japan as the next three causes combined. Following an upward trajectory that started just around the time that infectious diseases fell off a metaphorical cliff, the rise of cancer has truly been remarkable, and profoundly impactful.
Fig 1: Annual transition of the mortality rate by cause of death (selected) in Japan from 1899 to 2019
Source: Adapted from trends in deaths and death rates (per 100 000 population) by sex and causes of death - Ministry of Health, Labour and Welfare, Japan2
Sadly, Japan is far from an exception: similar trends can be observed in many countries around the world. In the US, cancer overtook pneumonia and influenza as the second leading cause of death in 1938³, and has continued to close the gap on heart diseases ever since: back in 1940, there were about 2.4 heart disease deaths for every cancer death⁴; by 2010, this gap had narrowed to be almost 1:1⁵. Globally, cancer was the second leading cause of death (behind cardiovascular diseases) in 2021⁶.
If the headlines all of us are frequently exposed to are any indication, this seemingly inexorable rise of cancer in the modern age should perhaps not come as a surprise: given the number of - often alarming – stories we are bombarded with on a frequent basis, one could be forgiven for thinking that (nearly) everything causes cancer. How did we get here, and do we have any hope of turning the tide, as a society or individually? Join us on a journey of discovery through the multi-faceted, intertwined, and at times unexpected causes of cancer.
Of genes and inheritance
Cancer is, by definition, the uncontrolled replication of poorly differentiated cells. To put it simply, cancer happens when cells in our body are multiplying when they shouldn’t be. Cell replication is normally a carefully balanced affair that ensures cells divide and multiply precisely as and when required. Any less, and our tissues don’t get renewed when they should, wounds don’t heal, blood cells don’t get replenished etc. Any more, and cancer can happen. Controlling all of this is an extremely complex system of genes, gene switches, signalling molecules and receptors in every single cell in our body. Cancer occurs when this system is destabilised enough to override the many fail-safe mechanisms in our cells and immune system.
How does this destabilisation take place? In essence, through damage to our DNA. Disrupt enough essential pieces of DNA in a single cell (without killing the cell outright), and it will go haywire, potentially replicating out of control and causing tumours to form, ultimately interfering with normal organ function and – if left unchecked – resulting in organ failure and death.
DNA damage can, unfortunately, happen in many different ways. Before looking more closely at some of the main environmental, lifestyle and other causes that can potentially lead to damage to our genetic material, let’s first address another question that comes up frequently in this context: is cancer hereditary?
An oft-quoted statistic is that around 5-10% of cancers are considered to be hereditary in nature⁷. It is easy to misinterpret this statement, however. Here is what this doesn’t mean:
- 5-10% of people with cancer were pre-determined to get cancer as a result of the genes they inherited from their parents
- 5-10% of cancers are completely unrelated to environmental or lifestyle factors
What it does mean is that 5-10% of people with cancer had a (sometimes significantly) increased likelihood of developing cancer due to the genes they inherited from their parents, and went on to develop cancer due to the complex interplay between those (internal) inherited genes and (external) environmental and/or lifestyle factors.
Let’s illustrate this with arguably the most well-known example of hereditary cancer: BRCA-positive breast cancer. Women who inherited certain mutations in one of the two BRCA genes are at significantly increased risk of developing breast (and ovarian) cancer. In fact, the association between these genes and breast cancer risk was found to be so strong that the genes themselves were directly named after BReast CAncer. To quantify this, women carrying mutations in BRCA1 are at an estimated 72% cumulative risk of developing breast cancer by the age of 80⁸ (meaning their total chance of ever developing breast cancer by age 80 is 72%). Two things worth noting here:
- 72% is a very high percentage, but some context is required: the cumulative risk of women with no known risk factors (i.e. no inherited genes associated with breast cancer) of getting breast cancer by age 90 is estimated to be 12-13% in the United States⁹. In other words, women with BRCA1 mutations are about 6 times as likely to develop breast cancer in their lives as those with no inherited risk mutations
- 72% is a very high percentage, but it is not 100%. In other words, almost 3 out of 10 of those women with BRCA1 mutations will not develop breast cancer by age 80
What makes the 28% of these women different from the 72% who do go on to develop cancer? And, indeed, what makes the 87-88% of women in the general population different from the 12-13% who do develop breast cancer despite not having any genes that increase risk?
The answer, it turns out, partly lies in all the things we are exposed to during our lifetimes that increase the risk of developing cancer, as opposed to the genes we inherited.
Smoking kills (but not always)
Smoking kills. This is a fact, plain and simple. Will everyone who smokes die from smoking-related reasons? No. Will everyone who smokes develop lung cancer? Again, no. Are people who smoke more likely to develop lung cancer? Yes: people who smoke are a staggering 15-30 times as likely to get lung cancer as non-smokers¹⁰. It is therefore not surprising that the majority of patients with lung cancer around the world are (current or previous) smokers. Take for example this data from the 2024 Ipsos Oncology Monitor in two different countries in different parts of the world; they show the distribution of non-small cell lung cancer patients (the most common form of lung cancer) and small cell lung cancer patients (the other main form of lung cancer) under active care, based on their smoking history:
Fig 2: Smoking history of reported drug-treated lung cancer patients in 2024
Source: Ipsos Global Oncology Monitor (January – December 2024, physicians reporting on drug-treated NSCLC and SCLC patients in China and Italy; participating physicians were primary treaters and saw a minimum number of patients per month. Sample sizes (number of patients) by cancer type and country as indicated in fig.2. Data collected through pen and paper in China and online in Italy).
Across both types of lung cancer, the majority of patients included in the study were current or ex-smokers, with the highest rates seen in small cell lung cancer patients. To put these numbers in perspective, the smoking rates in the general adult population in China and Italy, respectively, were 24.1%¹¹ and 24.2%¹² (in 2022), much lower than the rates seen among both types of lung cancer patients.
Despite this very strong link between smoking and lung cancer, it should be noted that not all lung cancer patients have a smoking history. As seen in the table above, between 34% and 44% of patients with non-small cell lung cancer included in the study in Italy and China were never-smokers. If not smoking, what caused their lung cancer? The answer is complex but, interestingly, never-smokers who develop non-small cell lung cancer are much more likely to be female, of East Asian descent (hence the comparatively higher never-smoker rates in China), and be diagnosed with tumours that harbour specific mutations in the EGFR (which stands for Epidermal Growth Factor Receptor) gene¹³. In data from the Ipsos Oncology Monitor in China, over 80% of never-smokers with non-small cell lung cancer in the sample were female, with more than half of those having tumours with an EGFR mutation:
Fig 3: Sex and EGFR mutation status among reported drug-treated never-smokers with non-small cell lung cancer in China (2024)
Source: Ipsos China Oncology Monitor (January – December 2024, physicians reporting on n=1,045 drug-treated never-smoker patients with NSCLC; participating physicians were primary treaters and saw a minimum number of patients per month. Data collected through pen and paper).
Unlike BRCA mutations, EGFR mutations aren’t typically inherited; they arise as a result of environmental factors, and as per the chart above these factors are often unrelated to smoking.
The implications are that smoking causes lung cancer through different molecular pathways than those implicated in never-smokers, i.e. they are fundamentally quite different diseases at the cellular level. It is unclear exactly what might be driving these EGFR mutations in never-smokers, but various proposed mechanisms include radon exposure, asbestos, and air pollution. More research remains to be done in this space¹⁴.
Genes and cigarettes
Smoking isn’t just linked to lung cancer, unfortunately. Smokers are more likely to develop a range of different cancer types, including breast cancer¹⁵. Interestingly, this correlation appears to be stronger for patients with inherited BRCA mutations than for those lacking BRCA mutations¹⁶. This is a clear example of the interplay between heritability (genetics) and environment, and helps to answer the earlier question regarding the reason(s) why not all women with BRCA mutations develop breast cancer. The implication is clear: if you are a woman with a BRCA mutation, avoiding smoking is even more important than for the general population.
The data below is taken from the Ipsos Oncology Monitor in the US, and shows the trend over time in the percentage of ever-smokers (current or ex-smokers) among early-stage breast cancer patients (early-stage meaning those with breast cancer that has not yet spread to distant organs), with or without BRCA mutations:
Fig 4. % reported early-stage breast cancer ever-smokers in the US, by BRCA mutation status
Source: Ipsos US Oncology Monitor (January 2021 – December 2024, physicians reporting on drug-treated early breast cancer patients, with or without BRCA mutations; participating physicians were primary treaters and saw a minimum number of patients per month. Sample sizes (number of patients) as indicated on the chart (n=with BRCA mutations; without BRCA mutations). Data collected online).
While the gap appears to have narrowed in the latest data point, during the period of 2021-2023 early breast cancer patients with BRCA mutations were notably more likely to have ever smoked than those without BRCA mutations. It is also worth noting that ever-smoking rates among both patient subsets, but especially among patients with BRCA mutations, were higher than smoking rates in the overall population of women in the US (estimated at 10.1% among adult women in 2022¹⁷). Smoking, therefore, appears to increase the risk of developing breast cancer for all women, but especially for those with BRCA mutations.
The fact remains, however, that a lot of women without BRCA mutations who are diagnosed with breast cancer are never-smokers. What, then, caused their cancer, if not genetics and not cigarette consumption?
We are what we eat, drink, and do
Fig 5: Comparison of selected key risk factors by country vs age-standardised cancer rates (ASR)
Source: See ‘References’ 21-25
There are, of course, a large number of other lifestyle factors that contribute to cancer risk. It has been known for some time, for example, that exercise reduces the risk of cancer²³. Based on self-reported exercise rates as per an Ipsos study conducted in 2021 across a number of countries (see values in column 2), however, there doesn’t seem to be a clear association between mean number of hours of physical exercise per week and overall age-standardised cancer incidence, on a country level.
One of the main postulated mechanisms by which exercise reduces cancer risk is by lowering the risk of obesity, which in itself is associated with the risk of multiple cancers²⁴. Overlaying adult obesity rates with cancer ASR again paints a mixed picture: while some of the countries with the highest levels of obesity (such as Australia, Hungary and the United States) also show very high cancer incidence overall, countries with relatively low obesity rates (such as France and the Netherlands) nevertheless rank very high in terms of overall cancer incidence, and some countries that also have very high adult obesity rates (Chile and Saudi Arabia) show a much lower overall cancer incidence.
What could explain these apparent contradictions? First of all, many different factors influence cancer risks, and it can be very hard to control for those factors when comparing distinct populations, e.g. different countries as in the table above. Several lifestyle factors such as smoking²⁵, alcohol intake²⁶ and red meat intake²⁷ are highly dependent on cultural factors, and those differences may outweigh differences in overall obesity rates or exercise rates. With regards to red meat consumption, for example, a country such as France has a very high red meat intake but a much lower obesity rate compared to Saudi Arabia, which has much more obesity despite much lower consumption of red meat, even though self-reported activity levels are relatively similar in both markets. It is interesting to note that red meat consumption per capita appears to show a stronger association with overall cancer incidence than obesity rates, at least for the set of countries shown in the table. Alcohol consumption appears to show the strongest association with overall cancer incidence by country, with 6 of the top 10 countries in the table consuming more than 10 litres per person per year, compared to just 1 of the bottom 7 countries in the table, and the two with the lowest alcohol consumption showing the lowest overall cancer incidence of the listed countries.
Alcohol, incidentally, is linked to an increased risk of developing many different types of cancer, including breast cancer, liver cancer, colorectal cancer, oesophageal cancer, oral cancer, and more²⁸. The higher an individual’s alcohol consumption, the higher the risk of cancer²⁹; furthermore, alcohol consumption in combination with smoking is particularly bad³⁰, due to (a) alcohol causing changes in cells lining the mouth and throat that make it easier to absorb the cancer-causing molecules in tobacco smoke and (b) alcohol impacting the way in which these cancer-causing molecules in tobacco are metabolised in the body. This is another good example of why individual risk factors should not be considered in isolation.
Despite the seemingly weaker correlation between obesity and overall cancer incidence at the country level, the impact of obesity on risk of developing specific cancer types becomes rather more apparent when the relative prevalence of individual cancer types within countries/regions is considered, as in the chart below:
Fig 6: Distribution of top 5 cancer types* within each BMI segment among reported drug-treated cancer types in China (% patients)
Source: Ipsos US Oncology Monitor (January 2021 – December 2024, physicians reporting on drug-treated early breast cancer patients, with or without BRCA mutations; participating physicians were primary treaters and saw a minimum number of patients per month. Sample sizes (number of patients) as indicated on the chart (n=with BRCA mutations; without BRCA mutations). Data collected online).
Among these reported female patients in China, breast, uterine and ovarian cancers all show clear associations with BMI, with their relative prevalence (out of all the reported drug-treated cancer types) increasing with increasing BMI levels. Among the obese women (BMI greater than 30), these three cancer types together account for 60% of all the drug-treated cancer patients, compared to just 34% of underweight women (BMI below 18.5) with cancer. Non-small cell lung cancer shows the lowest relative prevalence among those who are obese, and stomach/oesophageal cancers show a higher relative prevalence among those who are underweight. We will revisit the relative importance of obesity as a risk factor for these different cancer types later in this paper, but for now it is worth remembering that the association between obesity and overall cancer incidence is complicated by the widely varying impact of BMI on different cancer types.
A malignant lack of sleep
We’ve considered a number of lifestyle factors related to recreational substance use (smoking and alcohol) and dietary choices (obesity and red meat). It’s not all about what we put into our bodies, however. The way we treat our bodies when we are not really doing anything may also have an impact on our probability of developing cancer.
At the surface, a lack of sleep doesn’t seem to be an obvious candidate for leading to uncontrolled cell replication. Whereas cigarette smoke contains harmful chemicals that directly lead to DNA damage, and fat tissue promotes inflammatory pathways that in turn also cause mutations³¹, it is perhaps less conceptually obvious how not sleeping enough leads to cancer. The mechanism by which sleep disruption leads to malignancies seem to be primarily linked to³²:
- Changes to the circadian rhythm, i.e. the regulation of our body clock. This in turn appears to disrupt essential processes such as DNA damage repair
- Weakening of the immune system. As discussed before, the immune system represents a sort of fail-safe system against tumours, by eliminating cancer cells before they can take hold. A weakened immune system diminishes this ability to prevent cancer
- Hormonal imbalances
Lack of sleep (4-5 hours per night) appears to be linked to increased odds of developing breast, colon, ovarian and prostate cancers, with further research into other cancer types pending³³. Interestingly, some studies have also linked long sleep (>9 hours) to increased colorectal and lung cancer risk³⁴.
Risks and organs: taking stock
As we have seen throughout this paper, different cancers are linked, to a greater or lesser extent, to different sets of potential risk factors. The table below summarises which of the main risk factors we have discussed so far – as well as a couple of new ones - are associated with which cancers (out of a selected list of key cancer types). Indicated in the table is the relative strength of association (++ for a strong association, + for a weaker but still notable link or a potentially strong link that requires further study), as well as the most important environmental/lifestyle risk factor for each cancer type, where applicable (in yellow highlights).
Fig 7: Association of selected risk factors with selected cancer types
NB: Values are based on author’s interpretation of numbers in multiple sources (see references 35-93) For specific references per value, click here.
Worth noting is that there are a couple of instances (marked by a -) where the risk of specific cancers actually decreases as a result of being obese or overweight:
- The risk of lung cancer decreases in people with obesity
- The risk of certain oral cancers decreases in people with obesity
- The risk of gastric cancer is highest in people who are underweight, but is also elevated in people who are obese
- Some studies have found an increased risk of prostate cancer in overweight men or men with obesity, whereas others have found a decreased risk, particularly in younger men
This seemingly contradictory effect also helps explain why overall cancer incidence isn’t very strongly associated with obesity rates by country, despite the clear increase in risk of certain cancer types in people with obesity (this is, of course, in addition to the long list of other comorbidities that are linked to being overweight or obese; in other words, it would be a bad idea to pursue obesity as a risk reduction strategy!).
Similarly, while alcohol is a clear and major risk factor for many different cancers, some studies indicate that the risk of kidney cancer and lymphoma is somewhat reduced by alcohol consumption. However, the potential harms from alcohol consumption far outweigh the slight reduction in risk of a small subset of cancers.
In the last column, we’ve added a risk category that we’ve not yet discussed, but is nevertheless strongly associated with several cancer types: pathogens. This is essentially an umbrella term for a varied group of infectious agents, ranging from bacterial H. pylori infections (the most important cause of gastric cancer worldwide) to viral HBV and HCV infections (a major cause of liver cancer), and even parasites (such as Schistosoma, which can cause bladder cancer).
Age and cancer
There is one risk factor, thus far unmentioned, that overshadows all the others: age. The incidence of nearly all cancers increases with increasing age, often at an exponential rate. The chart below shows normalised incidence (normalised by equating 0 to the minimum value and 100 to the maximum value in the dataset) of several key cancer types by age.
Fig 8: Normalised incidence of selected cancer types by age
Source: The importance of aging in cancer research93
Overall, the normalised risk of cancer for those aged 65-69 is around twice as high as those aged 55-59, with risk doubling again by around age 80. Interestingly, however, the risk of several cancers actually peaks around age 75, and then rapidly falls once people hit very advanced ages. Leaving aside this decline in the eldest individuals for now, let’s first dive into the reasons why there is a such a strong link between age and cancer risk.
Mutations drive cancer, but a single mutation is rarely sufficient to lead to a tumour. Cancer typically arises due to the accumulation of mutations: once a certain threshold of a high enough number of mutations in so-called proto-oncogenes (genes that play a role in regulating cell growth) and/or tumour suppressor genes (genes that help prevent uncontrolled cell growth) is reached in a cell, it enables it to escape the various balancing mechanisms and start replicating uncontrollably. While some of these mutations may be inherited, most typically happen at some point after birth (referred to as somatic or sporadic mutations), due to external factors such as smoking, radiation exposure, infection with certain pathogens, alcohol consumption and so on. A simple outcome of probabilities is that the chance of accumulating enough mutations in a single cell for cancer to happen increases with time, by definition: the more time passes (i.e. the older one gets), the higher the likelihood of multiple cancer-causing mutations having arisen in a given cell in the body.
There is more to it, however. When a cell goes rogue after accumulating enough mutations to allow it to multiply uncontrollably, this doesn’t always automatically lead to cancer. Our immune system is constantly on high alert for such rogue cells, and will actively seek out and destroy them before cancer can take hold. As we age, however, our immune system gradually starts losing its edge⁹⁴, and these processes become less and less reliable. The same applies to the cellular machinery inside each of our cells that detects and repairs mutations in our DNA before they can cause damage: such cellular repair mechanisms become less effective as we age. In fact, our chromosomes themselves become less stable and more prone to random mutations with passing age⁹⁵. It is therefore no wonder that we see such an exponential increase in cancer incidence with time: not only do our cells accumulate more mutations as we grow older, but our bodies become less and less able to prevent those mutations from turning our cells into malignant tumours.
In addition, other factors such as chronic inflammation and disruptions in the bacteria that make up our gut flora are linked to both ageing and increased cancer incidence⁹⁶, further amplifying age-related cancer risks.
Why then do certain cancers show such a steep decline in incidence once we get into our eighties or nineties? The reasons are highly complex and beyond the scope of this paper, but in summary certain cellular features of advanced ageing can actually reduce the likelihood of cells turning into malignant cells⁹⁷, once they become dominant enough to outweigh the aforementioned cancer-promoting factors.
What does this all mean for us?
Clearly, there are many things that we can do to reduce our risk of developing cancer. Avoiding alcohol (ideally altogether), red and processed meats, and smoking are key behaviours that are within our control. Similarly, aiming for a healthy weight (not underweight, but certainly not obese), getting in enough exercise, using sun protection, and optimising sleep are also sensible strategies for reducing cancer risk. Reducing the risk of being infected with potentially cancer-causing pathogens, by getting a cervical cancer vaccine, avoiding the use of shared needles, and adopting safe sex behaviours, is also key.
When it comes to other dietary changes, things can get confusing and hard to keep track of: there is a long list of potentially carcinogenic foods out there that require further study to really determine whether they cause a meaningful increase in cancer risk or not. These include things such as ultra-processed foods⁹⁸, artificial sweeteners⁹⁹, acrylamide¹⁰⁰ (which can form from cooking certain foods at high temperatures), and others. If your ultimate goal is to do everything you can to reduce cancer risk, then your best strategy might be to err on the side of caution and avoid – or at least keep to a minimum – your intake of these foods until they are given the all-clear.
What about ageing? Time marches on for all of us, and on the surface of it there seems to be very little we can do to reduce age as a risk factor. However, a distinction should be made between chronological age and biological age. While the former is completely outside of our control, the latter is not. Biological age, as quantified by a number of clinical biomarkers¹⁰¹ (as opposed to merely years on a calendar), is increasingly being linked to increased cancer risk, including in (chronologically) younger individuals¹⁰². Nutrition, physical activity levels, stress and other environmental factors can all contribute to biological age being more advanced than chronological age; therefore, focusing on keeping the body biologically young, rather than stressing over the passing of time, can help keep cancer at bay.
That leaves one factor that we haven’t mentioned yet: luck. We’ve all heard stories of distant relatives who lived into their nineties, smoked like a chimney, started their day with a glass of beer, never did a minute of exercise in their lives, and yet avoided cancer altogether. Or, unfortunately, stories of friends or family who get diagnosed in their forties despite not having a family history of cancer, living a healthy lifestyle, avoiding the sun and processed foods, and never having smoked or drunk. At the end of the day, luck does play a role in all of this. With every cigarette smoked or glass of beer consumed, comes a risk of causing an oncogenic mutation that pushes a cell to go out of control. This risk is however just that: a risk, a statistical percentage that is higher than 0% but never 100%. There are very few things that we can do that are guaranteed to cause cancer, even over prolonged periods of time. Something like 15% of smokers develop lung cancer in their lifetime (compared to just 1% of never-smokers¹⁰³), and if you smoke more than 35 cigarettes a day, your lifetime risk of lung cancer is over 26%. In other words, around three quarters of very heavy smokers never develop lung cancer; whether you feel that is an acceptable risk ultimately depends on your own risk tolerance.
What about those of us who do everything possible to avoid cancer, but still develop it, even at an age where general cancer risk is seen as low, and even without any inherited increase in cancer risk? Ultimately, a significant percentage of cancers (some estimates are as a high as 65%, although this is subject to ongoing debate¹⁰⁴) are due to “bad luck” mutations that occur randomly during cell division, independent of any external factors. Such cancers could not realistically be prevented; all we can do is to focus on the risk factors that are in our control.
How changing risk factors will shape the future of cancer
We started this paper by looking at the past, and how cancer had overtaken the other leading causes of death since the late 1970s in Japan, and has been closing the gap on heart disease in the US ever since the 1940s. This didn’t tell the whole story, however: in many countries, cancer mortality has actually been decreasing since peaking in the 1990s. As stated before, there were almost as many deaths in the US from cancer as from cardiovascular diseases in 2010; however, by 2021, this gap had increased again, with cancer deaths continuing to fall while heart disease deaths have levelled off¹⁰⁵. The age-standardised mortality rate from cancer in Australia dropped by around 50% from the early 1990s to 2020¹⁰⁶. Similar trends could be seen in several European countries¹⁰⁷.
What has caused this recent drop in cancer mortality? There are several reasons: better screening practices allowing for earlier detection and earlier intervention, significant advances in drug treatments and molecular diagnostics, as well as changes in lifestyle factors.
Perhaps the most well-known of the latter is the decline in cigarette smoking in many countries around the world¹⁰⁸, thanks to growing awareness of the link to cancer, as well as government interventions. More recently, alcohol usage has started declining in several regions of the world¹⁰⁹. The HPV vaccine has led to significant declines in cervical cancer¹¹⁰. Hepatitis C infections have been declining since the introduction of novel antivirals¹¹¹. There are of course country-specific nuances: in China, for example, cigarette smoking rates only started declining much more recently than in the West, leading to a much later peak in lung cancer mortality in both genders. In fact, after a period of decline, cigarette sales have recently started increasing again in China¹¹².
There are other words of caution among the positivity, and chief amongst those is the impact of the global obesity pandemic. In 1980, around 5% of men around the globe were obese (defined as BMI ≥ 30 kg/m²). By 2008, this had increased to 10%¹¹³, climbing up to 14% by 2022¹¹⁴. In women, an increase from 8% in 1980, to 13% in 2008, to almost 19% in 2022 was observed. In other words, whereas only about 1 in 20 men and 1 in 12 women were obese back in 1980, the most recent data shows a staggering 1 in 7 men and almost 1 in 5 women around the world now dealing with obesity. Furthermore, as these are global averages, the situation in several individual countries is notably worse, with nearly 42% of adults being obese in the US as of March 2020¹¹⁵.
As we saw before, obesity is linked to an increased risk in a number of cancers, and indeed the age-standardised rates for e.g. uterine cancer and breast cancer have both increased against this background of increasing global obesity rates:
- Globally, the age-standardised rate (ASR) for uterine cancer has increased from 8.67 per 100,000 in 1990 to 9.99 per 100,000 in 2019¹¹⁶. This trend was most pronounced in high Socio-demographic Index (SDI) regions, where an increase from approximately 14 per 100,000 to almost 20 per 100,000 was observed between 1990 and 2016. High SDI regions are also those with the highest prevalence of, and fastest uptake of, obesity over this period¹¹⁷
- Globally, the breast cancer ASR increased from 16.42 per 100,000 in 1990 to 26.88 per 100,000 in 2021¹¹⁸
While it is impossible to determine to what extent the increase in obesity has driven the above increases as compared to all the other risk factors we discussed earlier, it is probably a safe assumption that obesity did meaningfully contribute to this increase. Extrapolating from this, and in the absence of any other major changes in risk factors, we can reasonably expect the ASR for these cancers with a strong link to obesity to continue increasing, assuming that global obesity rates do continue their upward trend.
That in itself may turn out to be a big assumption: while most projections do predict a continued increase in obesity (for example, a 2019 paper stated that adult obesity rates are likely to reach 48.9% by 2030 in the US), there is a major caveat here. The recent approval and uptake of GLP-1 (glucagon-like peptide 1) agonists for weight loss¹¹⁹ has the potential to halt or even reverse the trend in increasing obesity rates - the machinations of which are detailed in a current PoV written by my colleague, Healthcare vs Evolution (June 2025). With it, comes the potential to lower the ASR of obesity-linked cancer types, though it is still too early to tell.
Closing thoughts
While it may sometimes indeed seem like everything causes cancer, there are plenty of things within our control that we can do to significantly lower our individual risk. Some of the data is confusing, and at times even contradictory. The phrase “requires further research” is commonplace in this field (as illustrated by this very paper). Nevertheless, our knowledge of cancer risks continues to advance incrementally with each study, and as we – as a society and as individuals – learn more about how to manage these risks, we become better equipped to prevent cancer. Governments have a key role to play in this through awareness campaigns (e.g. the famous Slip, Slop, Slap campaign in Australia¹²⁰ to reduce the risk of skin cancer), regulations (e.g. introducing smoke-free zones in public places) and taxation (e.g. sugar taxes), but ultimately our individual choices are key as well.
What about the part we cannot control, that dreaded element of bad luck? Apart from hoping and waiting for paradigm-shifting advances in total cancer prevention at the cellular level (e.g. see the Ipsos paper Mastering Complexity¹²¹), one thing we can all do is to stay informed of, and follow, international and local screening guidelines. Regardless of whether it’s due to lifestyle factors, inherited genes or simply bad luck, catching cancer early is often key to ensuring a good prognosis. With the advent of blood-based multi-cancer early detection tests, it is becoming increasingly possible to detect cancers before symptoms take hold, allowing for early intervention and treatment.
Being human is wonderfully complex. Our multi-cellular nature means that the tiny cells that make up our body are constantly maintaining an intricate balance between stability and replication. Every single day, an estimated two trillion cells in our body undergo cell division. That’s over 20 million divisions per second. In the time it’s taken you to read this paper, about 50 billion cells will have divided in your body. Each of those events, just through sheer bad luck, can lead to errors that have the potential to result in cancer. Even in non-dividing cells, a stray UV ray could hit your DNA in just the wrong way, or a carcinogen from cigarette smoke (even through secondary inhalation) could cause a catastrophic mutation. Considering those numbers for a minute, and ending on a positive note, perhaps the most amazing statistic of this paper is that 70-75% of us will go through life without ever developing cancer at all.¹²²
About the Research
The Ipsos Global Oncology Monitor is a physician-reported multi-client patient record database, capturing prescribing of anti-cancer and supportive care agents. Participating physicians are screened for specialty, level of seniority and number of drug-treated cancer patients seen per study wave and must be the primary decision-maker for their patients. Each wave, participants provide demographic information and de-identified information on a predefined quota of oncology patients (across solid and liquid tumours) seen in consultation, retrospectively. Data used in this article were collected online in the US, Italy and China; sample sizes are provided with the charts.
Data are © Ipsos 2025, all rights reserved.
References
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