New Research Shows Obesity May Reshape How Breast Cancer Spreads
Key Takeaways:
- Obesity may alter how early, non-invasive breast lesions progress into invasive cancer, a University of Oklahoma study suggests.
- In women with obesity, progression was linked to inflammation, immune cell activity, metabolic changes and raised levels of the enzyme SULF2 – not the rapid cell division seen in women without obesity.
- The findings could improve risk prediction for women with DCIS and help reduce overtreatment.
A different route to invasive disease
Obesity may change how early-stage breast cancer becomes invasive, according to a study by University of Oklahoma researchers published in The American Journal of Pathology.
Obesity is already recognised as a risk factor for invasive breast cancer, but researchers have not fully understood how it helps early, non-invasive breast lesions develop into invasive cancer. A clearer picture of this process could strengthen physicians’ ability to predict and treat the disease.
In the study, breast cancers in women without obesity displayed the typical signs of turning invasive, including rapid cell division and an increased ability to invade neighbouring tissue. In women with obesity, however, the researchers identified a different set of biological changes that appeared to help the cancer become invasive.
The cancer environment became more inflamed, with the arrival of immune cells that advanced the growth of the tumour. The tumour cells also appeared better able to survive under stress, and there were changes in cellular metabolism – how the cells use nutrients for energy.
“This could be why women with obesity are at higher risk for invasive breast cancer,” said Bethany Hannafon, Ph.D., co-lead author of the study and an assistant professor in the Department of Obstetrics and Gynecology at the OU College of Medicine. “The changes that the cancer cells are undergoing are allowing them to survive and thrive.”
A cooperative cancer “neighbourhood”
The researchers also found differences in the “neighbourhood” of cells and tissues surrounding the cancer. Epithelial cells, where the tumour originally develops, co-opt other cells around them to create an environment that is even more conducive to cancer growth.
“In women with obesity, there is cooperation between all the cell types, not just the cancer cells, which helps an early pre-cancer to become an invasive breast cancer,” said co-lead author Elizabeth Wellberg, Ph.D., assistant professor in the Department of Pathology at the OU College of Medicine. “That may be an area of future study – can a drug or intervention that targets only one cell type interrupt the whole network of progression toward invasive cancer?”
The role of the enzyme SULF2
The research team additionally discovered higher levels of an enzyme called Sulfatase 2 (SULF2) in the tumour cells of women with obesity, suggesting that it may play an important part in cancer progression. SULF2 will be a further focus of future studies.
Why better DCIS risk prediction matters
Understanding what causes early, non-invasive tumours – known as ductal carcinoma in situ, or DCIS – to become invasive is important because not all women will go on to develop invasive cancer, yet they currently receive the same treatment.
“In women diagnosed with DCIS, about half will later develop invasive ductal carcinoma (IDC) that spreads into surrounding breast tissue. But we currently have no way of determining which women are most at risk. As a result, many women with DCIS receive the same treatments used for IDC, including surgery, radiation and sometimes hormone therapy. Overtreatment is a major concern, but if we had better ways of determining risk, unnecessary treatments could potentially be reduced,” Hannafon said.
While breast cancer survival rates have improved over the past two decades, the number of women diagnosed with invasive breast cancer has not declined – underscoring the need for better ways to predict and prevent disease progression.
A growing public health concern
The rising prevalence of obesity gives the findings added weight.
“Obesity is on the rise – 50% of Americans are expected to be obese by 2030,” said the paper’s first author, Cole Hladik, Ph.D., who worked in Hannafon’s lab while earning his doctorate. “That statistic further highlights the importance of considering a patient’s metabolic health alongside the biology of the tumor itself.”
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Obesity Identified as Key Driver of Rising Cancer Rates in Younger Adults
Key Takeaways:
- A major new study has found that overweight and obesity are likely to be significant contributors to rising cancer rates among younger adults in England.
- Researchers found that many traditional behavioural cancer risk factors – including smoking, alcohol consumption and physical inactivity – have remained stable or improved over the past two decades, making them unlikely to fully explain the increase in early-onset cancers.
- Although excess weight appears to play an important role, researchers say it cannot entirely account for the rise in cancers such as bowel cancer, suggesting that additional biological, environmental and early-life factors may also be involved.
Study highlights growing concern over early-onset cancer
Being overweight or living with obesity may be a key driver behind rising cancer rates in younger adults in England, according to a major new study led by researchers at The Institute of Cancer Research, London, and Imperial College London.
The analysis, published in BMJ Oncology, examined trends in cancer incidence alongside changes in known behavioural cancer risk factors over nearly two decades. Researchers found that while rates of several cancers among younger adults have continued to increase, many established lifestyle-related risk factors have either improved or remained stable during the same period.
These findings led researchers to conclude that obesity is likely to be one of the most important contributors to the increase in cancer incidence among younger generations in England.
At the same time, the researchers stressed that rising body mass index (BMI) alone does not fully explain the growing number of cancer cases, indicating that additional factors may also be contributing to the trend.
Researchers analysed cancer trends across England
The research team used national cancer registry data from England covering the years 2001 to 2019. The study was conducted by scientists from the Cancer Epidemiology and Prevention Research Unit (CEPRU) at both The Institute of Cancer Research (ICR) and Imperial College London.
Researchers examined incidence trends across:
- 22 cancer types in women
- 21 cancer types in men
From this analysis, they identified 11 cancers that are increasing among adults aged between 20 and 49 years and are associated with known behavioural risk factors.
All of the cancers identified – except oral cancer – are recognised as being linked to excess weight.
For most cancer types, increases seen in younger adults mirrored trends observed in adults aged over 50, where the overall disease burden remains considerably higher. However, bowel cancer and ovarian cancer stood out as notable exceptions because rates were increasing only among younger age groups.
Most traditional risk factors have improved
The study examined trends in several well-established behavioural cancer risk factors, including:
- Smoking
- Alcohol use
- Overweight and obesity
- Physical inactivity
- Red and processed meat consumption
- Low fibre intake
Together, these risk factors accounted for an estimated 40–50 per cent of bowel, endometrial, oral and liver cancer cases in 2019.
However, researchers found that trends for most of these risk factors have either remained stable or improved over time, making them unlikely to substantially explain the recent rise in cancer incidence among younger adults.
According to the analysis:
- Smoking among younger adults has fallen by approximately two per cent annually over the past two decades.
- Alcohol consumption has largely stabilised or declined.
- Physical inactivity has decreased.
- Consumption of red and processed meat has reduced.
- Fibre intake, while still below recommended levels, has gradually improved.
In contrast, rates of overweight and obesity have steadily increased since 1995.
The largest increases in obesity were observed among younger women, where obesity prevalence rose by approximately 2.6 per cent relative increase per year.
Obesity linked to rising bowel cancer rates
The researchers found evidence linking rising BMI to increasing bowel cancer rates among younger adults.
Among younger women, bowel cancer rates associated with BMI rose from 0.9 to 1.6 cases per 100,000 people. In comparison, bowel cancer rates not attributable to BMI increased from 6.4 to 9.6 cases per 100,000 people.
Similar patterns were also observed in men.
However, the authors emphasised that the total number of BMI-linked bowel cancer cases remained lower than the number of cases not linked to BMI. This suggests that although obesity is an important contributor, it cannot fully explain the scale of the increase in bowel cancer among younger adults.
Additional causes may be contributing
The study points to the likelihood that multiple interacting factors are contributing to rising cancer rates in younger generations.
Several suspected contributors have previously been proposed, including:
- Ultra-processed foods
- Antibiotic use
- Air pollution
However, researchers noted that many of these exposures have also shown relatively stable or declining trends in the UK, complicating efforts to identify the main drivers of early-onset cancers.
The authors also highlighted emerging evidence suggesting that obesity-related mechanisms not fully captured by BMI may influence cancer risk. These include:
- Metabolic dysfunction
- Chronic inflammation
- Alterations in the gut microbiome
Further research is needed to determine whether these mechanisms directly contribute to the development of bowel cancer and other cancers in younger adults.
Experts say more research is urgently needed
The researchers called for large-scale, long-term studies capable of tracking exposures across the entire life course in order to better understand what is driving rising rates of early-onset cancers.
Professor Marc Gunter, Co-Director of the Cancer Epidemiology and Prevention Research Unit at Imperial College London, said:
“The changes we’re seeing in cancer incidence, particularly the rates of some cancers in younger adults, don’t have a single cause or a simple answer. They reflect a complex mix of generational effects, gaps in long-term exposure data, and shifts in diagnosis and detection, and show how much more scientists still need to understand about when and how cancer develops across the life course. While rising rates in younger adults are concerning, it remains crucial not to lose sight of cancer trends in older adults, where the absolute burden of disease is still far greater.”
Professor Montserrat García-Closas, Co-Director of the Cancer Epidemiology and Prevention Research Unit and Group Leader in Integrative Cancer Epidemiology at The Institute of Cancer Research, London, said the findings indicate that behavioural changes alone cannot explain current trends.
She said:
“Our findings show that while cancer rates are rising in younger adults, the trends are unlikely to be explained by changes in most known behavioural risk factors. Smoking, alcohol and other behaviours have been stable or improving for two decades, yet early-onset cancers continue to increase – particularly bowel cancer.
“Excess weight is an important contributor, although it cannot fully account for the scale of the rise in bowel and other cancers. This tells us that multiple factors – including early-life exposures – may be acting together. Understanding these patterns is essential for identifying what is truly driving cancer risk in today’s generations. We now need deeper research, better measurement and continued surveillance to uncover the causes behind these worrying trends.
“However, we cannot wait to act. Tackling obesity across all ages, particularly in children and young people, through stronger public health policies and wider access to effective interventions, could slow the rise in cancer and prevent many cancers – and must become a national priority.”
Calls for stronger prevention and public health action
The findings have prompted renewed calls for stronger public health measures aimed at preventing obesity and improving cancer prevention strategies across all age groups.
Professor Kristian Helin, CEO of The Institute of Cancer Research, London, said the study highlights an urgent public health challenge requiring coordinated action across research, prevention and policy.
He said:
“This work highlights a growing public health challenge and the need for urgent action across research, prevention and policy. Although rising cancer rates in younger adults are concerning, the burden remains overwhelmingly higher in older people, which means prevention efforts must span all ages.
“This study makes clear that traditional lifestyle risks alone cannot explain current trends – pointing to the importance of investigating other exposures such as the potential role of the microbiome, while strengthening strategies to address obesity and other established risks. To protect future generations, we must invest in understanding the causes of cancer at all ages and ensure that early diagnosis, screening and prevention strategies keep pace with a changing population.”
CCH insights:
The outcomes of this study are concerning but not entirely surprising, given that obesity rates in children and young people are still rising and obesity is a significant risk factor for many cancers. It adds further support for the call to treat obesity at the earliest opportunity, regardless of the age of the individual. The longer obesity goes untreated the greater the risk of individuals developing serious chronic diseases such as cancer, type 2 diabetes and heart disease.
Larger Organs, More Cells – New Study Clarifies How Obesity May Increase Cancer Risk
Key Takeaways:
- A new study suggests that larger organ size in people living with obesity increases cancer risk due to a higher number of cells
- Organ growth appears to be driven largely by an increase in cell number rather than simply larger cells
- Findings indicate that organ size may be a more precise predictor of cancer risk than BMI alone
A longstanding question in obesity and cancer
For many years, researchers have recognised a clear association between obesity and an increased risk of cancer, particularly in organs such as the liver, kidneys and pancreas. However, the biological mechanism underpinning this relationship has remained uncertain.
A research team from City of Hope and its Translational Genomics Research Institute, known as TGen, has now provided a clearer explanation. Their findings suggest that the relationship may be explained by a straightforward principle – larger bodies tend to have larger organs, and larger organs contain more cells.
This increase in cell number creates more opportunities for mutations and, consequently, cancer development.
Study design and key findings
The study, presented in Cancer Research, analysed data from 747 adults across a broad spectrum of body mass index (BMI), ranging from underweight at 18.5 kg/m² to severe obesity above 40 kg/m².
Researchers examined the pancreas, kidneys and liver, identifying a consistent pattern: as body weight increased, organ size increased proportionally.
For every 5-point rise in BMI:
- The liver increased in size by 12%
- The kidneys increased by 9%
- The pancreas increased by 7%
These findings demonstrate a measurable and progressive relationship between BMI and organ enlargement.
More cells, not just bigger cells
To better understand how organs grow, the research team analysed kidney tissue from autopsies and biopsy samples from living individuals. This allowed them to distinguish between two biological processes:
- Hypertrophy – where existing cells grow larger
- Hyperplasia – where the number of cells increases
First author Sophie Pénisson, PhD, explained the importance of this distinction:
“When an organ increases in size, the question is to know whether it’s because the cells in it become bigger or whether there are more of them [that are] the same size,” Pénisson said. “And the first case is we call hypertrophy, with bigger cells, and hyperplasia is when we have more cells.”
The results showed that approximately 60% of kidney growth was due to hyperplasia, meaning an increase in the number of cells, while the remainder was due to hypertrophy.
A simple but powerful explanation for cancer risk
These findings support the idea that a greater number of cells increases the likelihood of cancer simply by increasing the number of opportunities for mutations to occur.
Senior author Cristian Tomasetti, PhD, illustrated this concept with a simple analogy:
“Think of playing the lottery: The more tickets you buy, the greater your chances of winning,” Tomasetti said. “Similarly, the more cells in an organ, the more mutations and the greater the risk of one cell going awry during division and becoming cancerous.”
Importantly, this mechanism does not replace existing explanations such as inflammation or hormonal disruption. Instead, it works alongside them.
Pénisson elaborated on this interaction:
“If more cells is like having more raffle tickets, she said, ‘if on top of that, there is inflammation – it means you play more often. With greater frequency, again, you increase your risk of developing cancer.’”
Rethinking BMI as a predictor of risk
The study also raises important questions about the use of BMI as a measure of cancer risk.
Although BMI is widely used in clinical practice, the researchers observed considerable variation in organ size among individuals with similar BMI values. Some individuals within a “healthy” BMI range had organ sizes typically seen in severe obesity, while others with higher BMI did not.
The authors wrote:
“We…observe substantial interindividual variation in organ size among people with similar BMI: For example, some individuals in the healthy BMI range have organ sizes expected only in severe obesity, and vice versa. This large variability suggests that organ size itself may be a better predictor of cancer risk than BMI, a possibility we believe warrants further investigation.”
They further concluded:
“Taken together, these findings establish organ hyperplasia as a previously unrecognized contributor to obesity-related kidney, liver, and pancreatic cancer risk, complementing known mechanisms including inflammation, hormonal changes, and metabolic dysfunction.”
Pénisson reinforced this point:
“When an organ doubles in size, it is expected to roughly double its risk of developing cancer,” Pénisson said, noting that BMI does not distinguish between fat mass and lean tissue. “Our work suggests that, at least for some organs, their dimensions may predict cancer risk better than BMI.”
Can weight loss reverse the risk?
An important question arising from these findings is whether reducing body weight can reverse organ enlargement and lower cancer risk.
Tomasetti indicated that this is an active area of research:
“It’s actually something we are working on right now,” Tomasetti said. “But yes, preliminary data seem to indicate that essentially, you are reverting back according to the same process” that caused the weight gain.
He also referenced emerging evidence presented at the American Society of Clinical Oncology, suggesting a link between GLP-1 receptor agonists and reduced cancer risk, although further research is needed to confirm this relationship.
Implications for treatment and prevention
Given the global scale of obesity, affecting more than 2 billion people, these findings may have important implications for prevention strategies and treatment approaches.
Tomasetti suggested that therapies such as GLP-1 receptor agonists could play a broader role:
GLP-1 RAs “are something that should be given to people as a treatment option to reduce the cancer risk, among other things,” including heart disease.
While further research is needed, this study provides a clearer mechanistic link between obesity and cancer risk and highlights the potential importance of organ size as a clinical marker.
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GLP-1 Receptor Agonists Unlikely to Meaningfully Influence Obesity-Related Cancer Risk, Review Suggests
Key Takeaways:
- Evidence from randomised trials suggests GLP-1 receptor agonists are unlikely to meaningfully increase or reduce the risk of most obesity-related cancers.
- For several cancer types, including colorectal, liver and endometrial cancer, the certainty of evidence remains low due to limited follow-up.
- Researchers emphasise the need for longer-term studies with cancer-specific outcomes to fully understand potential risks or protective effects.
A comprehensive systematic review published online on 8 December in Annals of Internal Medicine suggests that glucagon-like peptide-1 receptor agonists, commonly known as GLP-1 RAs, have little or no effect on the risk of developing cancers associated with obesity.
The review was led by Albert Ko, MD, of the Harvard T.H. Chan School of Public Health in Boston, and examined data from randomised, placebo-controlled trials involving people treated with GLP-1 RAs for type 2 diabetes or overweight and obesity. While these medications have transformed metabolic care in recent years, concerns have persisted about their long-term safety, including potential cancer risk.
Scope and purpose of the review
GLP-1 receptor agonists are widely prescribed for glycaemic control and weight management, yet their association with cancer has remained uncertain. To address this gap, the researchers conducted a systematic review and meta-analysis to assess whether treatment with GLP-1 RAs is associated with an increased or reduced risk of obesity-related cancers.
The review focused on cancers known to have strong links with excess adiposity, including thyroid, pancreatic, colorectal, gastric, oesophageal, liver, gallbladder, breast, ovarian, endometrial and kidney cancers. It also included multiple myeloma and meningioma.
Data sources and study selection
The authors searched PubMed, Embase, Web of Science, Scopus and the Cochrane Central Register of Controlled Trials from database inception through to August 2025. Only randomised, placebo-controlled trials reporting at least one of the specified cancer outcomes were eligible for inclusion.
In total, 48 trials met the inclusion criteria, encompassing 94,245 participants. None of the trials had been specifically designed to evaluate cancer outcomes, and follow-up durations were generally short.
Methods and quality assessment
Risk of bias across the included trials was assessed using the Cochrane Risk of Bias 2 tool. The certainty of evidence for each outcome was evaluated using the GRADE framework, which considers factors such as study limitations, consistency of results and precision of estimates.
Pooled odds ratios were calculated using random-effects meta-analysis to account for variation between studies.
Main findings by cancer type
The analysis found that GLP-1 receptor agonists probably have little or no effect on the risk of several common obesity-related cancers, based on evidence of moderate certainty.
Specifically:
- Thyroid cancer showed no clear association with GLP-1 RA use, with an odds ratio of 1.37 (95% CI, 0.82 to 2.31), corresponding to between one fewer and nine more cases per 10,000 people treated.
- Pancreatic cancer risk was similarly unaffected, with an odds ratio of 0.84 (95% CI, 0.53 to 1.35), equating to nine fewer to six more cases per 10,000 people.
- Breast cancer showed an odds ratio of 0.95 (95% CI, 0.60 to 1.49), indicating no meaningful difference in risk.
- Kidney cancer also demonstrated no significant association, with an odds ratio of 1.12 (95% CI, 0.78 to 1.60).
For other cancers, including colorectal, oesophageal, liver, gallbladder, ovarian and endometrial cancer, as well as multiple myeloma and meningioma, the evidence suggested little or no effect. However, the certainty of this evidence was rated as low.
For gastric cancer, the findings were described as very uncertain, reflecting sparse data and wide confidence intervals.
Consistency across analyses
The results remained consistent across multiple sensitivity and subgroup analyses. These included analyses restricted to trials with a low risk of bias, studies involving newer agents such as semaglutide or tirzepatide, and comparisons across different follow-up durations, populations, GLP-1 RA classes, doses, weight-loss profiles and durations of action.
This consistency strengthens confidence that the observed lack of association is not driven by a specific drug, dose or patient group.
Limitations of the evidence
The authors highlight important limitations that temper the conclusions. Most notably, the included trials were not designed to detect cancer outcomes and generally had relatively short follow-up periods. As a result, rare cancers or effects that emerge only after prolonged exposure may not have been captured.
Implications and next steps
Summarising the findings, the authors conclude that GLP-1 receptor agonists “may have little or no effect on risk for obesity-related cancers,” while emphasising the need for further research. As they write, “These findings offer important insights into the safety of GLP-1 RAs but highlight the need for longer-term studies with cancer-specific end points to clarify potential risks or protective effects.”
For clinicians and people considering or already using GLP-1 receptor agonists, the review provides a degree of reassurance regarding cancer risk in the short to medium term. However, ongoing surveillance and dedicated long-term studies will be essential as use of these medications continues to expand globally.
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Obesity-Linked Lipids Drive Aggressive Breast Cancer Growth in Mouse Models
Key Takeaways:
- New research from the University of Utah reveals that lipids – fat molecules elevated in people living with obesity – can accelerate tumour growth in aggressive forms of breast cancer.
- The findings suggest that lipid-lowering therapies may slow cancer progression and that high-fat diets such as ketogenic regimens may worsen outcomes in some patients.
- Researchers caution that weight loss without addressing lipid levels is insufficient protection against obesity-associated cancers like triple-negative breast cancer.
Lipids identified as key driver in obesity-related breast cancer
A new study from the University of Utah’s Huntsman Cancer Institute (HCI) has found that lipids, a hallmark of obesity, play a significant role in fuelling tumour growth in an aggressive form of breast cancer. The research, funded by the National Cancer Institute and conducted using preclinical mouse models, highlights how lipid metabolism may be a crucial therapeutic target for individuals living with obesity who have or have survived breast cancer.
The findings suggest that breast cancer patients and survivors with obesity could benefit from therapies that lower lipid levels. Conversely, high-fat dietary approaches, such as the ketogenic diet, may have unintended adverse effects by increasing lipid availability to cancer cells.
“The key here is that people have underestimated the importance of fats and lipids in the all-encompassing term that is obesity,” explained Dr Keren Hilgendorf, assistant professor of biochemistry and investigator at HCI. “But our study shows that breast cancer cells are really addicted to lipids, and the abundance of lipids in patients with obesity is one of the reasons that breast cancer is more prevalent and more aggressive in these patients.”
Focus on triple-negative breast cancer
The study focused on triple-negative breast cancer (TNBC) – a fast-growing and difficult-to-treat subtype that lacks receptors for oestrogen, progesterone, and HER2. TNBC is more common in women under 40 and in Black women, and it accounts for approximately 10 to 15 per cent of all breast cancer cases. This form of cancer is particularly prone to recurrence and metastasis.
A high level of lipids in the blood, known as hyperlipidaemia, is a frequent feature of obesity. Dr Hilgendorf and her colleagues, Dr Amandine Chaix and Dr Greg Ducker, both from HCI, examined how lipid levels influence tumour growth using specialised mouse models.
Lipid levels alone drive tumour growth
The researchers used two sets of models: one group of mice was fed high-fat diets, while another was genetically engineered to develop hyperlipidaemia without other typical markers of obesity, such as elevated blood glucose or insulin levels. In both cases, tumours grew faster when lipid levels were high.
“The idea is that lipids, which form the surface membrane of the cell, are like building blocks,” explained Dr Chaix, assistant professor of nutrition and integrative physiology. “If a cell receives the signal to proliferate and more building blocks are available, the tumour is going to grow more easily. We see that a high amount of lipids enables this proliferation.”
Importantly, when lipid levels were lowered – even in the presence of high glucose and insulin – breast cancer cell growth slowed down.
Potential implications for treatment and prevention
While the research was conducted in mice, the results point to potential therapeutic strategies for people with obesity and breast cancer.
“We think this has therapeutic implications, because if you could just lower the lipids – which we already know how to do in patients, for example, with lipid-lowering medication – that could be a way to decelerate breast cancer growth,” said Dr Hilgendorf. “If we can target these high levels of fat in the blood, the cancer sufferers, because the lipids are no longer feeding the cancer. But while our results in mice were striking, there are clear limitations in directly projecting these findings onto human patients. More research using human samples and patients will be necessary to confirm our hypotheses.”
Rethinking weight management in cancer care
These findings may also influence how clinicians guide people with obesity and breast cancer in managing their weight. While weight loss is commonly recommended to reduce recurrence risk, there is limited guidance on the best dietary approaches.
Some individuals turn to ketogenic diets, which are high in fat and low in carbohydrates, to induce ketosis – a state where the body uses fat rather than carbohydrates for energy. However, the new findings raise concerns about such diets in this patient group.
“For patients who are diagnosed with breast cancer and have an elevated BMI [body mass index], we would advise them to consult their physician and develop a weight-loss plan as part of their treatment,” said Dr Ducker, assistant professor of biochemistry. “If you have high cholesterol levels to start with, think about a weight-loss plan or potential pharmaceuticals that could lower your lipid levels. As our study shows, diets like keto that are very high in fat can have serious unintended side effects – even causing the tumour to grow.”
Beyond breast cancer: Broader implications
The research team believes that lipid-driven tumour growth may not be limited to breast cancer alone. Elevated lipid levels could also contribute to tumour progression in other cancers linked to obesity, such as ovarian or colorectal cancers.
The next stage of the research will investigate how anti-lipid drugs could improve the effectiveness of chemotherapy and explore the mechanisms through which lipids feed cancer cells.
Dr Chaix, Dr Ducker and Dr Hilgendorf emphasised that their results apply specifically to triple-negative breast cancer, and that ketogenic diets might still hold benefits for other forms of cancer. Nevertheless, their findings underscore the need for careful, evidence-based dietary guidance for people with obesity affected by cancer.
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Many People with Severe Obesity Face Medical Discrimination, Study Finds
Key Takeaways:
- A new study reveals that over 40% of clinics in the United States refused to schedule an appointment for a hypothetical patient with severe obesity.
- More than half of practices surveyed lacked the basic facilities or equipment required to provide appropriate care to patients with a body mass index (BMI) of 60 or greater.
- Researchers warn that discrimination and inadequate resources may contribute to poorer health outcomes, including delayed cancer detection, among people living with severe obesity.
Widespread discrimination in clinical settings
People living with severe obesity frequently encounter discrimination and barriers when seeking medical care, according to a new study published in the Annals of Internal Medicine. Researchers reported that about 2 in 5 (41%) clinics refused to schedule an appointment for a hypothetical patient weighing 465 pounds.
One receptionist at an orthopaedic surgeon’s office stated: “We’ve reached our limit for bariatric patients at this site,” without offering further explanation.
The study highlights a critical issue in access to care: beyond outright refusals, more than half of clinics (52%) did not have the equipment or facilities necessary to provide basic medical care for patients with very high body weights. Severe obesity is defined as a BMI of 40 or higher, with extremely severe obesity considered a BMI of 60 or greater.
Lack of facilities and equipment
Many clinics lacked essential infrastructure, including examination tables or chairs that could safely support higher weights, wide enough doorways and hallways for patient mobility, and appropriately sized medical gowns.
Dr Tara Lagu, senior author of the study and adjunct lecturer of medicine and medical social sciences at Northwestern University Feinberg School of Medicine in Chicago, emphasised the harmful impact of such deficiencies:
“Patients living with severe obesity are likely already struggling with shame and difficulty navigating the world. To tell a patient that they can’t be examined on a table, or can’t wear a gown, or need to stand during an appointment makes what should be a safe place and the experience of seeing a doctor humiliating and degrading. We need to acknowledge, as a profession, that all people deserve better than this.”
Affected population and health risks
According to the researchers, approximately 1 in every 270 Americans – close to 1 million adults – lives with extremely severe obesity (BMI ≥ 60). These individuals are two to three times more likely to experience significant health problems compared with the general population.
Despite this increased risk, previous studies have shown that people with obesity are less likely to receive preventive health services such as cancer screenings. Dr Lagu explained:
“Obesity affects cancer screenings, and failure to screen can result in later cancer detection. We’re always attributing worse outcomes in higher-weight patients to weight itself, but more and more studies are now pointing to worse care, lack of care or being care avoidant as possible reasons for these delays.”
Study design and findings
To investigate barriers to care, researchers used a “secret shopper” approach, in which callers attempted to schedule an appointment for a hypothetical patient weighing 465 pounds. They contacted 300 clinics across four metropolitan areas – Boston, Cleveland, Houston, and Portland, Oregon. The study covered five specialties: dermatology, endocrinology, obstetrics and gynaecology, orthopaedic surgery, and ear, nose, and throat (ENT).
Lead researcher Dr Molly Hales, a physician at University of Chicago Medicine, noted that the caller questions were intentionally designed to suggest possible urgent medical needs:
“We designed some of the questions our callers asked to be red flags for a receptionist to think, ‘I should really schedule this person,’ because the questions suggested the patient might have cancer and need an urgent workup.”
Despite this, only 59% of clinics overall were willing to schedule the appointment. ENT specialists were least likely to agree, with only 48% offering an appointment, while endocrinologists were most likely to accept and to have suitable facilities.
Humiliating workarounds
Even among clinics that agreed to see the hypothetical patient, around 1 in 6 (16%) suggested workarounds that could be humiliating, such as requiring the patient to stand during the exam or to use a sheet instead of a gown.
Dr Hales observed:
“Our numbers likely underestimate the magnitude of the problem. Likely, very few high-weight patients who are scheduling appointments know to even ask if they can be accommodated based on their weight, and they might be hesitant to ask these questions or advocate for themselves because of the social stigma.”
Potential solutions
The researchers highlighted that a Clinical Environment Checklist has been developed to guide outpatient clinics in ensuring they can provide appropriate care for patients with obesity. However, it has not been widely adopted.
Dr Hales noted:
“They designed the checklist to be used by general outpatient clinics and tested it in both primary care and subspecialty settings, so it’s a good resource for clinics in determining where there are opportunities for improvement.”
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