Obesity Care

Dietary Melatonin Intake Linked to Lower Rates of Obesity and Depression

Key Takeaways: 

• Higher intake of melatonin from foods was associated with lower prevalence of obesity and depression in a large cohort of Brazilian university graduates.
  
• No significant associations were found between dietary melatonin intake and most cardiometabolic outcomes, including hypertension, metabolic syndrome or type 2 diabetes.
  
• The strongest associations were observed at moderate rather than very high levels of dietary melatonin intake, highlighting the complexity of diet–health relationships.
  
  
  

Background and study context

In a study published in the Journal of Human Nutrition and Dietetics, researchers examined the melatonin content of commonly consumed foods and explored how dietary melatonin intake was associated with a range of health outcomes. The analysis used cross-sectional data from a large cohort of Brazilian university graduates.

Melatonin is a hormone best known for regulating circadian rhythms and sleep–wake cycles. Beyond its endogenous production, melatonin is also present in both animal-based and plant-based foods. Experimental, observational and supplementation studies have linked melatonin to sleep regulation, mood, and metabolic health. Although the concentration of melatonin in foods is considerably lower than in supplements, diets rich in melatonin-containing foods have been shown to increase circulating melatonin levels within physiological ranges.

Previous evidence suggests that increasing melatonin intake through food may deliver doses that align more closely with natural circadian rhythms than pharmacological supplementation, potentially avoiding suprapharmacological exposure. On this basis, dietary melatonin has attracted interest as a marker of broader dietary patterns rather than as a direct therapeutic intervention.

Rationale for examining dietary melatonin

Obesity, depression and sleep disorders represent a substantial and growing public health burden. Prior observational and experimental studies have suggested that melatonin may have protective effects against inflammatory, metabolic and neurobehavioural outcomes. In addition, observational research has reported inverse associations between melatonin exposure and outcomes such as liver cancer incidence and all-cause mortality.

Despite this, relatively few studies have investigated habitual dietary melatonin intake or its associations with chronic conditions in adult populations. The present study aimed to address this gap by estimating melatonin intake from the diet and examining its relationship with multiple health outcomes in a large cohort.

Study design and population

The analysis drew on data from the Cohort of Universities of Minas Gerais (CUME+) study. CUME+ is an open, prospective cohort designed to assess the impact of dietary patterns and nutrition transition on noncommunicable diseases.

At baseline, participants completed a questionnaire administered in two parts. The first part collected information on sociodemographic characteristics, clinical history, lifestyle factors, anthropometric measures and self-reported morbidity.

Dietary assessment and estimation of melatonin intake

The second part of the baseline assessment included a food frequency questionnaire (FFQ), alongside questions on dietary habits, supplement use and cooking practices. Nutrient intake was estimated using established food composition tables.

Dietary melatonin content was estimated based on values reported in the scientific literature for individual food items. These estimates were then adjusted for total energy intake to account for differences in overall food consumption between participants.

Health outcomes and definitions

The health outcomes assessed in the study included obesity, obstructive sleep apnoea (OSA), hypertension, metabolic syndrome (MetS), type 2 diabetes (T2D), sleep duration, dyslipidaemia and depression.

Obesity was defined as a body mass index of 30 kg/m² or higher. Depression and OSA were identified based on self-reported medical diagnoses.

Dyslipidaemia was defined as the presence of at least one abnormal lipid parameter, including total cholesterol of 200 mg/dL or higher, triglycerides of 150 mg/dL or higher, high-density lipoprotein cholesterol below 40 mg/dL for males or below 50 mg/dL for females, or low-density lipoprotein cholesterol of 130 mg/dL or higher.

Cardiometabolic criteria

Metabolic syndrome was defined as central obesity plus any two of the following criteria: elevated triglycerides or treatment for hypertriglyceridaemia, reduced high-density lipoprotein cholesterol or treatment, elevated blood pressure or treatment for hypertension, and elevated fasting plasma glucose or a diagnosis of type 2 diabetes.

Hypertension was defined by the use of antihypertensive medication, a physician diagnosis, systolic blood pressure of 140 mmHg or higher, or diastolic blood pressure of 90 mmHg or higher. Type 2 diabetes was defined as a self-reported or physician diagnosis, use of antidiabetic medication, or fasting plasma glucose of 126 mg/dL or higher.

Sleep duration was categorised as short if participants reported sleeping less than seven hours per day, and normal if they reported seven hours or more per day.

Statistical analysis

Associations between dietary melatonin intake and health outcomes were estimated using logistic and Poisson regression models. Analyses were adjusted for a wide range of potential confounders, including age, sex, family income, binge drinking, smoking status, screen time, physical activity, medication use and sleep duration.

Participant characteristics

The final analysis included 8,320 participants with a mean age of 35.9 years. Most participants were female and reported that they did not smoke. Around one third of the cohort reported short sleep duration.

Dyslipidaemia, depression, obesity and hypertension were the most commonly reported health conditions within the study population.

Melatonin content of foods and dietary sources

Melatonin content was estimated for 119 of the 144 food items included in the FFQ. Reported concentrations ranged from 0 to 169.9 ng per gram of food. Mean daily melatonin intake was estimated at 25,554.7 ng and was significantly higher in males than in females.

The main dietary sources of melatonin in this population were coffee, lentils and beans, and rice. Higher melatonin intake was associated with lower intake of protein, cholesterol, and saturated and monounsaturated fats, alongside higher intake of fibre and carbohydrates. These patterns suggest that dietary melatonin intake may reflect broader differences in dietary composition.

Associations with health outcomes

After full adjustment, no significant associations were observed between dietary melatonin intake and obstructive sleep apnoea, hypertension, metabolic syndrome or type 2 diabetes. Initial associations with sleep duration and dyslipidaemia were attenuated after adjustment for age and sex and did not remain statistically significant.

In contrast, dietary melatonin intake showed an inverse association with both obesity and depression. Participants with daily melatonin intakes between approximately 14,900 and 34,400 ng were less likely to have obesity, while intakes between approximately 14,900 and 25,000 ng were associated with a lower likelihood of depression.

Notably, the strongest associations were observed in intermediate intake quintiles rather than among those with the highest melatonin intake, suggesting a non-linear relationship.

Conclusions and implications

In this cohort of Brazilian university graduates, higher dietary melatonin intake was associated with lower prevalence of obesity and depression, while no significant associations were identified for most other cardiometabolic outcomes or sleep duration.

The findings support existing hypotheses that dietary melatonin may play a role in metabolic and neurobehavioural regulation, potentially through anti-inflammatory pathways. However, the cross-sectional design of the study means that causal relationships cannot be established.

Further longitudinal and experimental research is needed to confirm these associations, determine whether dietary melatonin has an independent effect beyond overall dietary patterns, and clarify the biological mechanisms that may underlie the observed relationships.

CCH insights:

This is an interesting study, but it is difficult to see where this research leads to. If a person is suspected of having obesity, depression or some other condition due to a lack of melatonin, the solution is surely likely to be supplementation of melatonin, not an increase in melatonin-rich foods – because dietary changes are notoriously difficult to adhere to and when we are looking at just one nutrient, supplementation is a much easier option.

Read More

Almost a Quarter of UK GPs Report Obesity in Children Aged Four and Under

Key Takeaways:

• Nearly one in four UK GPs report seeing children aged four and under where obesity is a clinical concern, with cases identified even in infancy.
• Most GPs find conversations about weight with children and parents difficult, citing fear of distress, stigma and complaints.
• The survey also raises concerns about inappropriate private access to GLP-1 weight loss medicines among adults who do not meet eligibility criteria.
  
  
  

Growing concern among family doctors

Almost a quarter of UK general practitioners report seeing children aged four or under who are living with obesity, according to a new survey of family doctors. The findings point to what respondents described as an “alarming” escalation of childhood obesity presenting at ever younger ages.

The research found that almost half of GPs, 49 per cent, have seen boys and girls up to the age of seven with obesity, including a small number of children younger than one year old. These early presentations raise concerns about long-term health consequences and the pressures faced by primary care clinicians in addressing weight sensitively and effectively.

Survey scope and headline findings

The survey, conducted by MDDUS, asked 540 family doctors about their experiences of managing obesity, the rapid growth in the use of weight loss medications, and the implications of widespread overweight and obesity for the NHS.

Almost one in four respondents, 23 per cent, said they had seen children aged zero to four where obesity was a clinical concern. Across childhood more broadly, 81 per cent of doctors reported seeing obesity in children between the age of 12 months and 11 years.

Dr John Holden, chief medical officer at MDDUS, said:
“These findings are an alarming confirmation of the growing crisis of childhood obesity across the country and the very real difficulties this creates in everyday GP consultations.”

Challenges of discussing weight with families

Despite the scale of the issue, most GPs reported significant difficulty in raising concerns about weight with children and their families. Four in five doctors, 80 per cent, said they find it somewhat or very challenging to talk to the parents of a child under 16 living with obesity about their weight and health. Only 10 per cent said they found such conversations easy.

Nearly two thirds of respondents, 65 per cent, also reported difficulty speaking directly with young people themselves about weight, with just 20 per cent describing those discussions as easy.

Doctors cited multiple reasons for this hesitation. Conversations with parents are often constrained by concerns that parents may become upset, reported by 72 per cent, angry, reported by 47 per cent, or may make a complaint, reported by 24 per cent. A further 74 per cent worried that such discussions could cause shame or stigma. Similar concerns were reported when speaking with children, including fears that conversations about weight could contribute to disordered eating behaviours.

Building confidence in these delicate conversations is the focus of professional training such as the College of Contemporary Health’s Behaviour Change Skills: Person-Centred Communication, a CPD-accredited online short course.

The wider determinants of childhood obesity

Respondents highlighted that obesity is shaped by complex and interrelated factors, including poverty, limited access to nutritious food, and fewer safe or affordable opportunities for children to be physically active. These realities, the survey suggests, shape how GPs approach discussions about weight.

Dr Holden said GPs therefore approach these conversations “with care and empathy for families under pressure”. He added:
“When parents feel judged or blamed, conversations can quickly become emotionally charged and, as our members tell us, can lead to complaints from distressed or angry parents.”

Calls for stronger prevention measures

Katharine Jenner, executive director of the Obesity Health Alliance, said the findings underline a failure to protect children early in life.

She said that the high numbers of GPs seeing infants and very young children with obesity “is another sign we’re letting children down before they even start school. If we’re serious about prevention, it has to begin in the earliest years, otherwise the damage follow them through life.”

Jenner called for a stronger focus on prevention, including reformulation of food and drink products to improve their nutritional quality, tighter restrictions on the marketing of products high in fat, salt and sugar, and better support for families facing structural and financial barriers to healthy eating.

Concerns over private access to weight loss drugs

Alongside childhood obesity, the survey also explored GP experiences of adult patients using weight loss medications inappropriately. Doctors reported that some adults who should not be using GLP-1 weight loss drugs are obtaining them through deception from private pharmacies.

These include people with eating disorders, such as anorexia or bulimia, and people already taking other medications that could interact adversely with so-called “fat jabs” and pose risks to their health.

It is estimated that around 1.5 million people in Britain are using GLP-1 medicines for weight loss, the majority having obtained them privately rather than through the NHS, where eligibility criteria are strict.

One GP told the survey that GLP-1s are being “accessed privately pretty indiscriminately by many people whose body mass index is not in the obese category”. Another described a patient with a history of anorexia nervosa who had also obtained the drugs privately. Overall, 67 per cent of family doctors said they had seen patients using GLP-1s despite not meeting eligibility rules.

These findings raise questions about how rigorously private pharmacies are carrying out appropriate checks, including assessments of medical history and potential drug interactions, before supplying weight loss medications.

Implications for the NHS and future care

The vast majority of GPs surveyed said obesity is likely to be a defining public health challenge during their careers, with 92 per cent agreeing with that statement. An even higher proportion, 95 per cent, believe obesity will significantly affect the NHS’s ability to deliver care.

However, views on weight loss injections were more mixed. While 59 per cent of respondents believe such medications will ultimately save the NHS money, 22 per cent disagreed.

Government response

The Department of Health and Social Care did not comment directly on the survey findings. A spokesperson said:
“Every child deserves the best possible start in life, which is why this government is taking decisive action to tackle childhood obesity.

“We are restricting junk food advertising on television before 9pm and online, a move expected to remove up to 7.2bn calories per year from children’s diets; while giving local authorities new powers to stop fast food shops opening outside schools.

“Through our ten-year health plan, we’re shifting the focus from sickness to prevention to create a healthier nation.”

CCH insight:

This study highlights the considerable challenges that primary care practitioners face in addressing obesity in young children. It is a very sensitive issue, and there may also be cultural attitudes that see overweight children as beautiful or healthy. Unfortunately, healthcare professionals in the UK are not trained to deal with obesity and the unique challenges it presents. It requires a very sensitive approach, communicating with parents in a non-judgemental way, highlighting the role of the obesogenic environment and finding ways to support behaviour change at a family level. On the positive side, if this can be achieved, an entire family can benefit from these interventions, not just the child with excess weight an entire family can benefit from these interventions, not just the child with excess weight. Because so much rests on how these conversations are handled, CCH’s Behaviour Change Skills: Person-Centred Communication CPD short course (2 CPD hours, fully online, CPD-accredited) gives healthcare professionals a practical, evidence-based foundation in person-centred communication – helping them raise sensitive issues like weight with patients and families supportively and without judgement.

Explore Person-Centred Communication →

Read More

Genetic Study Establishes Causal Link Between Obesity and Dementia

Key Takeaways: 

• New genetic evidence suggests that higher body weight and elevated blood pressure play a direct causal role in the development of dementia.
  
• The findings indicate that addressing obesity and high blood pressure earlier in life may offer an important opportunity for dementia prevention.
  
• Much of the increased dementia risk associated with higher body weight appears to be driven by high blood pressure, highlighting a potentially modifiable pathway.
  
  
  

Obesity, blood pressure and dementia risk

People living with obesity and high blood pressure may face a higher risk of developing dementia, according to a new study published in The Journal of Clinical Endocrinology & Metabolism. The research adds to a growing body of evidence linking cardiovascular and metabolic health to long-term brain health.

Dementia represents a major and escalating global public health challenge. There is currently no cure, and people living with dementia experience a progressive decline in mental abilities, including memory, thinking and reasoning. Over time, this decline can significantly impair daily functioning and independence.

The most common forms of dementia include Alzheimer’s disease, vascular dementia and mixed dementia. Although these conditions vary in their underlying pathology, all involve progressive damage to nerve cells in the brain, leading to worsening problems with memory, language, problem-solving and behaviour.

Study identifies a causal relationship

The study was led by Ruth Frikke-Schmidt, M.D., Ph.D., Professor and Chief Physician at Copenhagen University Hospital – Rigshospitalet and the University of Copenhagen.

“In this study, we found high body mass index (BMI) and high blood pressure are direct causes of dementia,” said Frikke-Schmidt. “The treatment and prevention of elevated BMI and high blood pressure represent an unexploited opportunity for dementia prevention.”

Researchers analysed genetic and health data from participants in Copenhagen and the UK. Their analysis revealed a clear causal link between higher body weight and an increased risk of dementia.

How Mendelian randomisation strengthened the findings

The researchers were able to establish a direct causal relationship by using a Mendelian randomisation study design, which closely mimics the structure of a randomised controlled trial.

In Mendelian randomisation, naturally occurring genetic variants associated with higher BMI are used as proxies for lifelong exposure to higher body weight. Because these genetic variants are randomly inherited from parents to offspring, their distribution is not influenced by lifestyle, socioeconomic status or other confounding factors.

This process mirrors the random assignment of participants to treatment or placebo groups in drug trials. As a result, any differences in dementia outcomes between individuals with BMI-increasing genetic variants and those without can be more confidently attributed to body weight itself, rather than to external influences.

Using this approach, the researchers were able to demonstrate that higher BMI plays a direct causal role in increasing the risk of dementia.

Blood pressure emerges as a key driver

Further analysis suggested that much of the increased dementia risk associated with higher body weight was driven by elevated blood pressure. This finding points to a potential pathway through which obesity may contribute to cognitive decline.

By implication, preventing or effectively treating obesity and high blood pressure could help reduce the risk of dementia, particularly forms linked to vascular damage in the brain.

“This study shows that high body weight and high blood pressure are not just warning signs, but direct causes of dementia. That makes them highly actionable targets for prevention,” said Frikke-Schmidt.

Implications for prevention and future research

The findings also raise important questions about the timing of weight management interventions. While weight-loss medications have recently been tested in people with early-stage Alzheimer’s disease, these trials have not shown clear benefits for halting cognitive decline once symptoms are established.

“Weight-loss medication has recently been tested for halting cognitive decline in early phases of Alzheimer’s disease, but with no beneficial effect,” Frikke-Schmidt said. “An open question that remains to be tested is if weight-loss medication initiated before the appearance of cognitive symptoms may be protective against dementia. Our present data would suggest that early weight-loss interventions would prevent dementia, and especially vascular-related dementia.”

Together, the results reinforce the importance of addressing obesity and high blood pressure not only to protect cardiovascular health, but also as part of a broader strategy to reduce the long-term risk of dementia.

Read More

Genetic Links Between Obesity and Autoimmune Diseases Identified in Large European Study

Key Takeaways:

• Large-scale genetic analyses have identified a substantial shared genetic basis between obesity and several autoimmune disorders in people of European ancestry.
  
• Dozens of shared genetic loci and genes appear to influence both body weight regulation and immune system function, particularly pathways involved in immune homeostasis.
  
• The findings suggest potential causal links between obesity and certain autoimmune conditions, with implications for future therapeutic strategies.
  
  
  

Overview of the study

A recent study published in the Journal of Translational Medicine has identified important genetic links between obesity and autoimmune disorders, shedding new light on why these conditions often co-occur. The research, led by Jiang and colleagues, focused on individuals of European ancestry and used large-scale genomic datasets to explore how shared genetic factors may influence both excess body weight and immune-mediated disease.

Obesity and autoimmune disorders represent a significant comorbidity burden, yet until now their shared genetic architecture has remained poorly understood. By applying advanced cross-trait genome-wide association study (GWAS) methods, the researchers aimed to uncover pleiotropic genetic variants – genes or loci that influence more than one trait – that may contribute to both conditions.

Study methods and analytical approach

The researchers conducted a comprehensive cross-trait analysis using GWAS summary data for obesity and 17 autoimmune diseases. Genetic correlations between traits were assessed using LD score regression and high-definition likelihood methods, allowing the team to quantify the extent to which obesity and autoimmune conditions share inherited risk.

To identify specific shared genetic loci, the team employed Stratified Pleiotropic Locus Mapping (PLACO), followed by Bayesian colocalization analyses to confirm whether obesity and autoimmune diseases truly shared the same causal genetic variants. Further analyses examined gene-level effects and tissue-specific heritability, while potential drug targets were prioritised using summary-based Mendelian randomisation (SMR).

In addition, immune co-localization techniques and bidirectional Mendelian randomisation were used to explore immunological mechanisms and to clarify potential causal relationships between obesity and autoimmune diseases.

Key genetic findings

The analysis identified eight autoimmune diseases with significant genetic correlations to obesity. In total, researchers discovered 10,324 pleiotropic single-nucleotide polymorphisms (SNPs), which mapped to 52 independent risk loci. Of these, nine loci were confirmed as shared causal variants through colocalization analysis.

Gene-level investigations revealed 133 unique pleiotropic genes. Notably, genes such as CLN3, SH2B1, and MMEL1 were highlighted and found to be enriched in biological pathways related to hematopoietic cell differentiation and immune homeostasis. These pathways are central to both metabolic regulation and immune function, reinforcing the biological plausibility of a shared genetic basis.

Tissue and immune cell involvement

Tissue-specific heritability analyses showed that shared genetic effects were most prominent in immune-related tissues, particularly the spleen, whole blood, and Epstein–Barr virus (EBV)-transformed lymphocytes. This finding further supports the role of immune system regulation in the overlap between obesity and autoimmune disease risk.

Immune co-localization analyses implicated six traits related to IgD+ CD38− B cell subsets as key pathological conduits. These immune cells may represent an important link between metabolic dysfunction and autoimmune processes.

Evidence of causal relationships

Using bidirectional Mendelian randomisation, the study provided evidence that obesity may play a causal role in the development of certain autoimmune conditions, including hypothyroidism, psoriasis, and multiple sclerosis. Conversely, an inverse causal association was observed between type 1 diabetes and obesity risk, suggesting a more complex and condition-specific relationship.

Implications and conclusions

In their conclusions, the authors state:

“This study demonstrates a robust shared genetic foundation between obesity and multiple autoimmune diseases, pinpointing specific pleiotropic loci, genes, and immune cell subsets.”

By identifying shared genetic mechanisms, the research provides a clearer mechanistic framework for understanding why obesity and autoimmune disorders frequently coexist. Importantly, these findings also highlight potential molecular and immunological targets for future therapeutic intervention, with the potential to address both metabolic and autoimmune disease pathways simultaneously.

Overall, the study represents a significant step forward in understanding the complex interplay between body weight regulation and immune system dysfunction, and it opens new avenues for research into integrated prevention and treatment strategies.

Read More

Obesity Independently Associated With Higher Rates of Tinnitus in US Adults, Large Population Study Suggests

Key Takeaways: 

• Adults living with obesity were significantly more likely to report tinnitus than those without obesity, even after accounting for demographic, behavioural and psychological factors.
  
• Around one in five adults with obesity reported tinnitus, compared with approximately one in seven adults without obesity.
  
• The findings highlight metabolic health and body weight as potentially relevant, modifiable factors in the broader management of tinnitus.
  
  
  

A growing public health question

Obesity appears to be independently associated with a higher prevalence of tinnitus, according to a large, nationally representative study of adults in the United States published online on 2 November in Cureus. 

The research was led by Ashir Ahtsham of Lahore General Hospital in Pakistan and examined whether obesity contributes to tinnitus prevalence beyond the influence of age, sex, mental health and other known risk factors. The analysis drew on data from the National Health and Nutrition Examination Survey (NHANES), a long-running survey designed to reflect the health of the US population.

Tinnitus, commonly described as ringing, buzzing or other sounds perceived in the absence of an external auditory stimulus, affects a substantial proportion of adults worldwide. While its causes are multifactorial and not fully understood, increasing attention has been given to the role of systemic and metabolic health in its development and persistence.

How the study was conducted

The researchers performed a cross-sectional analysis using de-identified data from the NHANES 2015–2016 and 2017–2018 survey cycles. These two cycles were combined in line with established analytic guidance to improve statistical power.

After excluding individuals under the age of 20 and those with missing data on body mass index or tinnitus, the final analytic sample included 5,452 adults aged 20 years and older. Obesity was defined using standard criteria, with a body mass index of 30 kg/m² or higher.

Tinnitus was assessed through self-report. Participants were classified as having tinnitus if they reported experiencing ringing, buzzing or other noises in their ears lasting five minutes or more in the absence of an external sound.

To isolate the association between obesity and tinnitus, the researchers adjusted their analyses for a range of potential confounders, including age, sex, race and ethnicity, smoking status, sleep duration and symptoms of depression, assessed using the Patient Health Questionnaire-9. Hearing loss data were not included, as this would have substantially reduced the available sample across both survey cycles. Readers interested in the detailed methodology can refer directly to the journal article.

Tinnitus was common, particularly among people with obesity

Across the full sample, 863 participants reported tinnitus, corresponding to a weighted prevalence of 17.2 percent. Tinnitus was more frequently reported by older adults, men and individuals living with obesity or depression.

Notably, the prevalence of tinnitus differed markedly by obesity status. Around 20.3 percent of adults with obesity reported tinnitus, compared with 15.0 percent of adults without obesity. This difference remained statistically significant at the population level.

Age was also a strong factor. Tinnitus prevalence increased steadily with age, rising from just over 10 percent in adults aged 20–39 years to nearly one quarter of those aged 60 years and older. Differences were also observed across racial and ethnic groups, with non-Hispanic White adults reporting the highest prevalence.

Obesity remained a significant predictor after adjustment

In unadjusted analyses, obesity was associated with a 44 percent higher likelihood of reporting tinnitus. Importantly, this association persisted even after accounting for demographic characteristics, lifestyle factors and depression.

After full adjustment, adults living with obesity still had approximately 41 percent higher odds of reporting tinnitus than adults without obesity. The strength and consistency of this association suggest that obesity may contribute to tinnitus prevalence independently, rather than simply reflecting shared risk factors such as age or mental health.

As the authors note, “These findings underscore the potential role of body weight and metabolic health in the development or progression of tinnitus.” They add that, “The substantial burden of obesity in recent years and its association with tinnitus highlight the importance of considering modifiable metabolic risk factors as part of comprehensive tinnitus management.”

Why might obesity and tinnitus be linked?

Although the study was not designed to explore biological mechanisms directly, the authors outline several plausible pathways supported by existing research.

Obesity is characterised by chronic low-grade inflammation, metabolic dysregulation and vascular dysfunction. These processes may impair microcirculation within the cochlea and disrupt normal auditory signalling. Excess adipose tissue is also known to produce pro-inflammatory cytokines, which may contribute to oxidative stress and neural inflammation affecting auditory pathways.

In addition, obesity is frequently associated with metabolic syndrome, insulin resistance and sleep disorders, all of which have been independently linked to tinnitus severity and distress. Together, these factors may help explain why people living with obesity experience tinnitus more frequently, even in the absence of measured hearing loss.

Strengths and limitations

A key strength of this study is its use of a large, nationally representative dataset with appropriate weighting to reflect the US population. The analysis also accounted for a wide range of demographic, behavioural and psychological variables.

However, the authors emphasise that the cross-sectional design means causality cannot be inferred. Tinnitus was self-reported, which may introduce recall or reporting bias. Important factors such as occupational noise exposure, medication use and audiometric hearing thresholds were not included, and these may partially mediate the observed association.

For readers seeking detailed statistical outputs or subgroup analyses, the original journal article provides comprehensive tables and supplementary information.

Implications for clinical practice and future research

The findings suggest that obesity is independently associated with tinnitus among US adults, reinforcing the view that tinnitus should be considered within a broader framework of systemic and metabolic health.

While weight reduction cannot currently be recommended as a specific treatment for tinnitus, the results support the inclusion of metabolic risk assessment as part of holistic tinnitus care. Building the confidence to assess and manage excess weight as part of that broader, whole-person picture is the focus of professional training such as the College of Contemporary Health’s Obesity Essentials, a CPD-accredited online short course. Further longitudinal studies, particularly those incorporating objective hearing measures, are needed to clarify causal pathways and to determine whether improvements in metabolic health could reduce tinnitus risk or severity.

As the burden of both obesity and tinnitus continues to rise globally, understanding how these conditions intersect may help inform more comprehensive and person-centred approaches to prevention and management.

CCH insight

Findings like these are a reminder that obesity rarely acts in isolation – its metabolic and inflammatory effects can reach into unexpected areas of health. CCH’s Obesity Essentials CPD short course (10 CPD hours, fully online, CPD-accredited) helps healthcare professionals understand these wider systemic effects and build the practical skills to assess and manage patients with overweight and obesity as part of holistic, person-centred care.
Explore Obesity Essentials →

Read More

Abdominal Obesity Identified as a Key Risk Factor for Migraine in Young Adults, Large South Korean Study Finds

Key Takeaways:

• A nationwide cohort study of more than six million young adults found that obesity is associated with an increased risk of developing migraine over time
  
• Abdominal obesity, measured by waist circumference, was a stronger and more consistent predictor of migraine risk than overall body mass index
  
• The association was particularly pronounced in younger adults and appeared to be influenced by lifestyle factors such as alcohol consumption
  
  
  

A large longitudinal study conducted in South Korea has found that obesity, particularly abdominal obesity, is associated with a higher risk of developing migraine in young adulthood. The research suggests that fat distribution around the abdomen is a more important predictor of migraine onset than overall body weight as measured by body mass index. The findings were published in the medical journal Neurology.

Migraine is a disabling neurological disorder that places a substantial burden on individuals, healthcare systems, and society. While genetic predisposition plays a significant role in determining who develops migraine, environmental and lifestyle factors are also recognised contributors. In clinical practice, managing coexisting conditions is widely regarded as an important component of migraine care.

Obesity is already known to increase the severity and frequency of migraine attacks in people who live with the condition, a process often described as chronification. However, whether obesity contributes to the initial development of migraine in people without a prior history has remained less certain. Much of the existing evidence has been based on cross-sectional studies, which capture data at a single point in time and cannot establish the direction of cause and effect.

Moving beyond cross-sectional evidence

To address this limitation, the authors of the new study designed a large prospective cohort analysis to examine whether obesity precedes and increases the risk of migraine onset. Their primary objective was to assess the association between obesity and incident migraine, and to determine whether migraine risk increased in line with the severity of obesity. A further aim was to compare the predictive value of general obesity with that of abdominal obesity.

The researchers drew on data from the Korean National Health Insurance Service, which provides healthcare coverage for approximately 99 percent of the South Korean population. The analysis focused on adults aged 20 to 39 who underwent routine health examinations between 2009 and 2012.

The initial dataset comprised more than six million individuals. To ensure that only new cases of migraine were captured, the researchers applied rigorous exclusion criteria. Individuals with a prior diagnosis of migraine were removed, as were those with missing information on body measurements or lifestyle factors. To reduce the risk of including people with undiagnosed migraine at baseline, anyone diagnosed within the first year of follow-up was also excluded.

After these exclusions, the final study population included 6,106,560 participants. The average age was approximately 30 years, and around 39 percent of participants were female.

Long-term follow-up and detailed health data

Participants were followed from the date of their health examination until the end of 2018. New cases of migraine were identified using medical claims data, specifically the International Classification of Diseases code G43. The average follow-up period was seven years, allowing for robust assessment of long-term risk.

During health examinations, trained medical staff measured height, weight, and waist circumference while participants wore light clothing. Body mass index was calculated as weight in kilograms divided by height in metres squared. Body mass index was categorised into five groups, ranging from underweight to stage 2 obesity. Waist circumference was divided into six categories using 5 centimetre increments, enabling a detailed assessment of abdominal obesity.

The dataset also included extensive information on potential confounding factors. Participants completed questionnaires covering smoking status, alcohol consumption, physical activity, and income level. Blood tests provided measurements of cholesterol, glucose, and other metabolic markers, allowing for comprehensive statistical adjustment.

Abdominal fat emerges as a stronger predictor than body mass index

The analysis showed a clear association between obesity and the risk of developing migraine. In models that adjusted for age and sex, migraine risk increased progressively with higher body mass index, with individuals living with stage 2 obesity showing a higher likelihood of receiving a migraine diagnosis compared with those in the normal weight range.

However, the association was even more pronounced when abdominal obesity was examined. Waist circumference demonstrated a dose-dependent relationship with migraine risk, meaning that each incremental increase in waist size was associated with a stepwise rise in risk. This pattern persisted even after adjustment for a wide range of demographic, lifestyle, and metabolic factors.

When the researchers adjusted their models to account for waist circumference, the association between body mass index and migraine weakened. In contrast, the relationship between waist circumference and migraine remained strong even after body mass index was taken into account. This indicates that abdominal obesity functions as an independent risk factor for migraine, more influential than overall body weight.

Participants with the largest waist measurements had significantly higher hazard ratios for migraine, while those with the smallest waist circumferences showed a reduced risk.

Underweight status and the role of muscle mass

The study also explored the relationship between being underweight and migraine risk. Initial analyses suggested that underweight individuals might have an increased risk of migraine. However, this association disappeared after full statistical adjustment, indicating that low body weight alone is unlikely to be a direct cause of migraine.

More nuanced findings emerged when waist circumference was controlled for. Extremely low body mass index was associated with higher migraine risk, which the authors suggest may reflect low skeletal muscle mass rather than low fat mass. Skeletal muscle plays a role in modulating inflammatory processes, and reduced muscle mass may contribute to a pro-inflammatory state.

Inflammation as a plausible biological mechanism

Inflammation is widely considered a key biological link between obesity and migraine. Adipose tissue, particularly visceral fat stored deep within the abdominal cavity, is metabolically active and releases a range of pro-inflammatory cytokines and adipokines.

Visceral fat is known to produce higher levels of inflammatory mediators than subcutaneous fat. This distinction may explain why waist circumference was a more reliable predictor of migraine risk than body mass index. Chronic low-grade inflammation associated with excess abdominal fat could lower the threshold for migraine development and increase susceptibility to neurological sensitisation.

Differences by age and lifestyle factors

Subgroup analyses revealed that age modified the observed associations. The link between abdominal obesity and migraine was stronger in adults under 30 years of age than in those in their thirties. This suggests that younger adults may be particularly vulnerable to the neurological effects of excess abdominal fat.

Lifestyle factors also influenced the strength of the association. The relationship between abdominal obesity and migraine was more pronounced in non-smokers than in smokers, and stronger in people who consumed alcohol heavily. Alcohol is known to have vasodilatory effects and is a recognised migraine trigger.

The researchers proposed that alcohol use and obesity may have synergistic effects, with alcohol-related vascular changes interacting with obesity-driven inflammation to further increase migraine risk.

Study limitations and future directions

Several limitations should be considered when interpreting the findings. Because migraine cases were identified using health insurance claims, only individuals who sought medical care were included. Many people live with migraine without receiving a formal diagnosis, which may have led to an underestimation of true incidence.

The study population was limited to South Korea, and patterns of body composition and fat distribution vary across ethnic groups. As a result, the waist circumference and body mass index thresholds used in this study may not be directly applicable to other populations. The gender distribution was also uneven, reflecting the characteristics of the national screening programme.

As an observational study, the analysis cannot definitively establish causation. Although the temporal relationship between obesity and migraine onset was clear, unmeasured factors may still have influenced the results despite extensive statistical adjustment.

Future research is needed to confirm these findings in other populations and to explore the underlying biological pathways in greater detail. Studies examining specific inflammatory mediators and adipokines may help clarify how abdominal obesity contributes to migraine development.

Implications for migraine prevention

Despite its limitations, this large-scale study provides compelling evidence that maintaining a healthy body composition may play a role in preventing migraine, particularly in young adults. The findings emphasise that fat distribution, not just overall weight, is clinically relevant. For clinicians, assessing abdominal obesity may offer additional insight when evaluating migraine risk and discussing preventive strategies with patients.

Developing that assessment skill set – including looking beyond BMI to measures such as waist circumference – is the focus of professional training such as the College of Contemporary Health’s Obesity Essentials, a CPD-accredited online short course covering the assessment and management of overweight and obesity.

The study, Association Between Obesity and the Risk of Migraine: A Nationwide Cohort Study in South Korea, was authored by Soo-Im Jang, Namoh Kim, Kyungdo Han, and Mi Ji Lee.

CCH insight:

Yet another inflammatory condition linked to obesity! It is interesting to note that this study found waist circumference to be a much better predictor of migraine risk than BMI. This is because waist circumference is a better indicator of excess visceral fat, which produces high levels of pro-inflammatory mediators. So this is a reminder of the limitations of BMI and the importance of considering waist circumference or waist:height ratio when assessing the extent and impact of excess body weight when assessing the extent and impact of excess body weight. For practitioners wanting to sharpen that assessment skill set, CCH’s Obesity Essentials CPD short course (10 CPD hours, fully online, CPD-accredited) covers how to assess and manage patients with overweight and obesity using a rounded, evidence-based approach that goes beyond a single number on the scale.

Explore Obesity Essentials →

Read More

Bottle Feeding Toddlers to Sleep Linked to Tooth Decay and Excess Weight in Early Childhood

Key Takeaways: 

• More than three in ten toddlers were still being bottle fed to sleep at two years of age
  
• Bottle feeding to sleep at age two was linked to almost double the risk of overweight in early childhood
  
• Continuing the practice at age three was associated with nearly twice as many teeth affected by decay
  
  
  

Parents and carers are being urged to avoid using bottles to help toddlers fall asleep, after new research found clear links between the practice, early childhood tooth decay, and excess weight gain.

The study, published in the Australian and New Zealand Journal of Public Health, was led by researchers at the University of Sydney and drew on data from more than 700 toddlers participating in Western Sydney University’s Healthy Smiles Healthy Kids (HSHK) cohort study. The long running study follows children from birth to examine factors influencing oral health and broader health outcomes.

Study design and data sources

Researchers analysed information collected through surveys completed by mothers, alongside clinical dental examinations and measurements of children’s height and weight. Importantly, the analysis also accounted for a range of other factors known to influence dental health and body weight, allowing the researchers to better isolate the impact of bottle feeding to sleep.

What the researchers found

The findings showed that bottle feeding to sleep remains common well beyond infancy and is associated with measurable health risks:

• More than 30 percent of children were still bottle fed to sleep at two years of age
  
• Children who were bottle fed to sleep at age two were almost twice as likely to have overweight in early childhood
  
• Children who were bottle fed to sleep at age three had nearly double the number of teeth affected by dental decay
  
  
  

Why bottle feeding to sleep matters

Lead author Heilok Cheng, a PhD candidate in the Susan Wakil School of Nursing and Midwifery at the University of Sydney, emphasised that most parents and carers are acting with good intentions but may not be fully aware of the longer term risks.

“Australian recommendations advise parents to start introducing cups at 6 months of age and stop using baby bottles at 12 months. Bottle feeding in bed is not recommended at any age. Our research now provides a much more robust evidence base for that advice.”

She explained that many commonly used drinks for toddlers can increase the risk of dental decay.

“Common toddler drinks, including cow’s milk and formula, often contain either natural or added sugars, increasing the risk of tooth decay. When a bottle is offered at bedtime it’s often being used by carers to calm an unsettled child or encourage the child to drift off to sleep. Because the bottle isn’t being offered in response to hunger, it can lead to overfeeding, putting children at risk of unhealthy weight gain.”

Cheng also highlighted the need for better support for families navigating infant and toddler feeding practices.

“We need to do more to support families and help them avoid getting into the habit of putting a child or baby to bed with a bottle, so that our future generations are set up with a healthy future from the start.”

Wider implications for policy and prevention

The authors note that the findings reinforce the importance of coordinated public health action to reduce childhood obesity and improve oral health. They also point to the potential value of universal dental care as part of a broader strategy to prevent avoidable dental disease in early life.

About the Healthy Smiles Healthy Kids study

The Healthy Smiles Healthy Kids (HSHK) cohort study is led by Associate Professor Amit Arora from Western Sydney University, in collaboration with Sydney Local Health District, South Western Sydney Local Health District, the University of Sydney, the University of Queensland, the University of Technology Sydney, and Curtin University.

The study is funded by the Australian National Health and Medical Research Council, NSW Health, the Australian Dental Research Foundation, and the Oral Health Foundation. The full paper, “Bottle feeding to sleep beyond 12 months is associated with higher risk of tooth decay and overweight in Australian children: Findings from the Healthy Smiles Healthy Kids cohort study”, was published in the Australian and New Zealand Journal of Public Health.

CCH insight:

This is an interesting study, which provides very strong evidence for avoiding bedtime bottle-feeding to help infants get to sleep. It would be interesting to know if the excess weight gain resulting from bedtime bottle-feeding is due simply to the extra calories provided by the bedtime milk, or if it also encourages increased emotional eating – it is believed that emotional eating, which is a common cause of overeating in adults, has its behavioural origin in the soothing effect we experience when suckling as a baby, so we come to associate fatty sugary food (like breast or formula milk) with bringing relief from anxiety and stress.

Read More

Maternal Obesity Linked to Early Changes in Infant Gut Microbiome, Study Suggests

Key Takeaways: 

• Infants born to mothers with obesity show distinct differences in gut bacteria during the first six months of life, including reduced microbial diversity.
  
• These early microbial changes are associated with pathways linked to fat metabolism, particularly in the first three months after birth.
  
• Researchers suggest that early-life interventions targeting the gut microbiome may help reduce longer-term metabolic risks for children.
  
  

Maternal obesity and the infant gut microbiome

Babies born to mothers with obesity may begin life with a markedly different gut microbiome, a factor that could influence their metabolism and long-term health, according to new research from Nazarbayev University (NU).

The study, led by researchers Almagul Kushugulova and Samat Kozhakhmetov, explored how maternal obesity may shape the early development of the gut microbiome in infants. The research team followed 24 mothers and their babies from birth to six months of age, analysing stool samples using advanced DNA sequencing techniques.

By comparing infants born to mothers with obesity with those born to mothers without obesity, the researchers identified clear differences in the composition and diversity of gut bacteria during early life.

Reduced microbial diversity and altered metabolic pathways

The analysis showed that infants of mothers with obesity had significantly lower gut microbial diversity. In addition, these infants had a higher abundance of bacterial species associated with fat metabolism.

These differences were most pronounced during the first three months of life, a period widely recognised as critical for the establishment of the gut microbiome and for metabolic programming.

“During the first three months of life, we observed what appears to be a shift in how gut bacteria process nutrients – with a tendency toward fat storage pathways rather than breaking down carbohydrates for energy,” Kozhakhmetov explained.

He noted that this early metabolic pattern may have implications for how energy balance is regulated later in life.

Opportunities for early intervention

The researchers suggest that their findings open the door to preventive strategies during infancy. Kozhakhmetov highlighted that understanding these early microbial shifts could inform interventions aimed at promoting healthier metabolic outcomes.

This discovery, he said, “opens up possibilities for early intervention”, including approaches such as targeted probiotics or tailored dietary guidance designed to support a more balanced gut microbiome and potentially reduce future metabolic risk.

Beyond metabolism – immune and appetite regulation

The implications of the findings may extend beyond metabolism alone. The researchers propose that maternal obesity could also influence immune system development and appetite regulation in children through microbial transmission.

“We tend to think that we only pass on our genes to our children. But our research suggests that we may also pass on our bacteria – and the type of bacteria a child inherits could have important effects on their long-term health, potentially influencing their health trajectory as they grow,” Kushugulova said.

This perspective reinforces the idea that early-life exposures play a significant role in shaping health across the life course.

Placing the findings in context

The study, published in the journal Biomedicines, adds to a growing body of research highlighting the importance of the early-life microbiome. Previous studies have linked maternal weight status and gut dysbiosis to disrupted nutrient metabolism, inflammation, and changes in immune, metabolic, or neurodevelopmental outcomes in children.

As obesity during pregnancy becomes increasingly common worldwide, the authors argue that maternal health should be viewed as a key determinant not only of pregnancy outcomes, but also of a child’s longer-term metabolic health.

Implications for future research and practice

The researchers conclude that interventions targeting the gut microbiota during early infancy may represent a promising avenue for reducing health risks associated with maternal obesity. Further research will be needed to determine which strategies are most effective, when they should be implemented, and how they can be integrated into routine maternal and child healthcare.

Taken together, the findings underline the importance of addressing obesity before and during pregnancy, while also highlighting the potential of microbiome-focused approaches to support healthier outcomes for future generations.

CCH insight:

Evidence for the role of the gut microbiome in obesity and metabolic health continues to grow. This study is ground-breaking in demonstrating that maternal obesity influences the new-born child’s microbiome, potentially priming the child for health challenges later in life right from their first few weeks of life. On the positive side, this offers the potential to identify babies at risk of metabolic diseases from a very early stage of life, and also the opportunity for early interventions though diet, pre- and probiotics.

Read More

Internalised Weight Stigma Places Heavy Emotional Burden on People Seeking Bariatric Care, Indian Study Finds

Key Takeaways:

• More than 71 percent of participants preparing for metabolic and bariatric surgery reported high levels of internalised weight bias, with many expressing self-blame, shame, and reduced self-worth.
  
• Younger individuals and those with a higher BMI reported stronger internalised stigma, which affected emotional well-being, social relationships, and readiness to seek treatment.
  
• Researchers and clinicians stress that obesity is a chronic disease, not a personal failing, and warn that stigma significantly harms mental health and delays access to appropriate care.
  
  

Introduction

A new study has highlighted the profound emotional and psychological toll experienced by people living with obesity who are preparing for metabolic and bariatric surgery. The research found that internalised weight bias is widespread among individuals seeking specialist care, with many reporting depressive symptoms, reduced self-esteem, and deep feelings of self-criticism linked to their weight.

The pilot study, titled The Burden from Within—An Indian Pilot Study on Weight Bias Internalisation, was published in Obesity Surgery, the international journal of the International Federation for the Surgery and Other Therapies for Obesity (IFSO).

Weight stigma beginning in childhood and persisting into adulthood

Lead author Dr Aparna Govil Bhasker, a Mumbai-based bariatric surgeon at the MetaHeal Laparoscopy and Bariatric Surgery Centre, told The Indian Express that stigmatising experiences often begin early in life. She explained that weight-related bullying is common during childhood and continues into adulthood for many people.

“People living with obesity are frequently judged as lazy or lacking willpower. Negative media portrayals, especially weight-based memes and stigmatising content, only deepen these harmful beliefs. Post-pandemic trends show that online negativity toward obesity has grown even stronger,” she said.

Study design and participant profile

To assess the emotional impact of obesity on people seeking surgical intervention, the research team evaluated 142 participants using the validated Weight Bias Internalization Scale (WBIS). Of the total cohort, 78.9 percent were women, and all participants had a body mass index of at least 27.5 kg/m².

Researchers examined total WBIS scores, associations with age, and correlations with BMI to understand how internalised stigma manifests in individuals preparing for metabolic and bariatric surgery.

High prevalence of internalised weight bias

The study revealed striking levels of internalised stigma:

• More than 71.1 percent of participants scored above the neutral benchmark on the WBIS, indicating widespread internalisation of negative weight-based beliefs.
  
• Around 74.6 percent reported feeling depressed about their weight.
  
• More than half felt less attractive because of their weight.
  
• More than one-third questioned their own competence.

The findings indicate that weight stigma does not simply come from external sources. Many participants had come to believe the negative stereotypes directed at them.

Self-judgement, self-hate, and social avoidance

The report found that more than half of the individuals surveyed expressed intense self-criticism, including feelings of self-hatred related to their weight. Many participants described weight as a defining measure of their personal worth.

Social relationships were also severely affected. Approximately 45.8 percent of participants questioned why anyone they considered attractive would want to date them. Half believed they did not deserve a fulfilling social life until they lost weight.

The data also showed that younger participants experienced stronger internalised bias, while those with higher BMI levels demonstrated deeper self-directed stigma.

“This shows that obesity status and internalisation of weight bias affect social interactions, connections, and relationships, which can have a long-lasting impact on the life course of an individual’s personal, emotional, occupational, and financial trajectory,” Dr Govil Bhasker said.

Obesity rising rapidly in India but not recognised as a disease

The researchers noted that obesity rates in India have nearly doubled since 2005. Data from the fifth National Family Health Survey (2019–21) show that 24 percent of women and 22.9 percent of men aged 15 to 49 years live with overweight or obesity.

Despite this rapid rise, obesity is not officially classified as a disease in India. Dr Govil Bhasker argued that the findings underline the deep societal stigma embedded in attitudes toward obesity.

“Patients often feel ashamed, guilty, and discouraged. They endure years of negative comments, judgment, and misinformation, and over time, these negative experiences become internalized. This affects their self-worth and mental health and can delay their decision to seek proper treatment. Obesity is a chronic disease, not a personal failure, and supporting patients emotionally is just as important as helping them medically,” she said. She added that targeted interventions are urgently needed.

Stigma’s broad impact on mental and physical health

Dr Vishakha Jain, Professor of Medicine at AIIMS BibiNagar and one of the study’s co-authors, emphasised that stigma infiltrates every aspect of daily life.

She explained that persistent stigma affects physical health, mental well-being, occupational performance, and social relationships. It can contribute to unhealthy eating patterns and biological stress responses, including increased inflammation.

“Together, these pressures create a cycle of self-blame and prejudice, often making individuals feel undeserving of care,” Dr Jain said.

Conclusion

The study provides compelling evidence that internalised weight stigma is highly prevalent among people preparing for bariatric care in India and that it carries profound psychological, social, and behavioural consequences. The authors urge greater recognition of obesity as a chronic disease and call for emotional as well as medical support for individuals affected.

Read More

Early-life Exposure to Fat-related Food Odours May Shape Lifelong Obesity Risk

Key Takeaways: 

• Early exposure to fat-related food odours during development may prime the brain and body for heightened metabolic responses to high-fat foods later in life.
  
• Sensory cues from a maternal diet, independent of nutritional content or maternal metabolic status, can influence thermogenesis, gene expression, and susceptibility to obesity in adult mice.
  
• Findings suggest a previously underappreciated mechanism of metabolic programming, in which food odours encountered during gestation and lactation can affect lifelong dietary preferences and obesity risk.
  
  

Introduction

A recent study published in Nature Metabolism explores how non-nutritive sensory cues from foods rich in fat, particularly odours, influence the developing brain and metabolic pathways. The research investigates how these early sensory inputs may shape central responses to food cues, metabolic health, and the risk of obesity in adulthood. The findings expand on a substantial body of work showing that early-life nutritional exposure influences later metabolic outcomes, but highlight the specific and previously overlooked contribution of fat-related odours.

Maternal obesity and early nutritional exposure

How maternal diet affects offspring

Developmental exposure to a maternal diet high in calories and fat is a well-recognised risk factor for obesity and metabolic disorders throughout life. Numerous studies have linked maternal high-fat diet (HFD) consumption with outcomes such as excess gestational weight gain, insulin resistance, and increased adiposity in mothers, all of which may contribute to lifelong metabolic vulnerability in offspring.

Despite these strong associations, the specific components of HFDs that drive metabolic programming remain only partly understood. While nutrients themselves contribute directly to energy balance and metabolic pathways, foods also contain non-nutritive sensory elements, including volatile odours. Fetuses and newborns experience these odours during development, meaning that sensory exposure is layered on top of nutritional exposure.

Sensory memories formed early in life

Perinatal olfactory experiences contribute to the formation of sensory memories that influence food preferences and eating habits into adulthood. The authors emphasise that understanding how non-nutritive cues from a maternal HFD influence long-term dietary preferences and metabolic responses is crucial for clarifying early-life drivers of obesity risk.

Study approach

Separating nutritional and sensory influences

To distinguish nutritional caloric components from sensory components, the researchers designed an isonutritional model using a standard normal chow diet (NCD) infused with fat-related odours. This bacon-flavoured diet (BFD) enabled researchers to expose mice to fat-related sensory cues without increasing calorie content.

• BFD: NCD enriched with bacon odours, designed to mimic the odour profile of a standard lard-based high-fat diet (HFDlard).
  
• HFDbutter: A butter fat-based HFD used to represent a non-pork, high-fat option.
  

This design allowed the researchers to isolate the effect of fat-related sensory exposure during development, independent of maternal metabolic changes such as insulin resistance, weight gain, or altered lipid levels.

Odour profile analysis

A detailed chemical characterisation identified 155 volatile compounds across the diets, including aldehydes, ketones, and alcohols. Hierarchical clustering revealed:

• HFD and HFDlard shared high sensory similarity
  
• Both differed significantly from HFDbutter and NCD
  
• BFD’s odour profile closely matched HFDlard, yet its nutritional profile remained identical to NCD
  

These findings confirmed that BFD was an appropriate tool for studying sensory-specific metabolic programming.

Sensory cues and neural activation

Experimental analyses showed that fat-related food odours induced phosphorylation of S6 in olfactory sensory neurons (OSNs), demonstrating that the odours elicited detectable neural activation. Mice perceived BFD as more similar to HFDlard than to NCD, reinforcing that the sensory model accurately represented fat-related olfactory cues.

Early exposure and adult metabolism

Developmental exposure primes obesogenic responses

Control mice exposed only to NCD during development (NCDdev) showed no changes in interscapular brown adipose tissue (iBAT) thermogenesis or hepatic mechanistic target of rapamycin (mTOR) phosphorylation when later exposed to HFDlard odours. In contrast, mice developmentally exposed to BFD (BFDdev) displayed significant increases in both iBAT temperature and hepatic p-mTOR when encountering these odours for the first time in adulthood.

This indicates that early exposure to fat-related odours enhances metabolic responsiveness to high-fat sensory cues later in life.

Independent of maternal obesity

Importantly, these heightened responses occurred without maternal insulin resistance, adiposity, or weight gain. This demonstrates that sensory exposure alone, rather than changes in maternal metabolism, can programme obesity risk.

Sex-specific sensitivity

• Females: Lactation appeared to be the most sensitive developmental window for programming effects.
  
• Males: Required exposure throughout the entire developmental period to exhibit similar heightened metabolic responses.
  
  
  

Responses to different high-fat diets

Eight-week-old BFDdev and NCDdev mice were also exposed to HFDbutter. The aim was to test whether heightened susceptibility required precise sensory matching or whether vulnerability generalised across high-fat diets.

Findings showed that early exposure to fat-related sensory cues increased obesity susceptibility even when adult exposure involved a high-fat diet with different sensory characteristics. This suggests that early sensory programming affects broad metabolic pathways rather than specific flavour-diet associations.

While a perfect sensory match between early and later exposure was not necessary, some degree of sensory similarity still appeared relevant in shaping metabolic outcomes.

Changes in the maternal environment

The study found that feeding mothers BFD altered the volatile odour profile of both amniotic fluid and milk. These changes exposed developing offspring to fat-related sensory information during gestation and lactation, influencing their early sensory learning and shaping later responses to food.

Impairments in thermogenesis and metabolic flexibility

BFDdev mice demonstrated reduced iBAT thermogenesis compared with NCDdev controls. They also exhibited lower expression of thermogenic-related genes in iBAT, including:

• Cidea
• Pparg
  

These findings indicate that developmental exposure to fat-related odours impairs metabolic flexibility and weakens homeostatic responses to hypercaloric diets in adulthood.

Altered neuronal responses to fat

The researchers reported a specific impairment in Agouti-related peptide (AgRP) neuronal responsiveness to dietary fat in BFDdev mice. These neurons help regulate hunger and energy balance. Despite this, responses to major hormonal signals remained unaffected, suggesting that sensory-specific pathways were selectively disrupted.

Conclusion

The study provides compelling evidence that early-life exposure to fat-related food odours can contribute to long-term obesity risk by shaping metabolic and neuronal responses long before an individual consumes high-fat foods. These sensory cues act independently of calorie exposure and maternal metabolic health, highlighting a novel pathway through which obesity susceptibility may be programmed. Although the research was conducted in mice, it underscores the potential importance of early sensory environments in influencing metabolic health across the lifespan.

CCH insights:

This is fascinating research. We already know that the diet of a pregnant woman can influence the dietary preferences and health outcomes of her child, but now it appears odours of certain foods during pregnancy may have similar affects. It adds an intriguing new line of investigation in terms of the Developmental Origins of Health and Disease. However, we must remember this study was in mice, using bacon odours to mimic a lard-based high fat diet, so we are a long way from being able to draw conclusions about real world implications for pregnant women.

Read More

Mice Study Connects Soybean Oil Intake to Liver Changes and Obesity

Key Takeaways: 

• New research in mice suggests that weight gain linked to soybean oil is driven by the metabolic products of linoleic acid rather than the oil itself.
  
• Genetically engineered mice resistant to obesity on a high-fat soybean oil diet produced fewer oxylipins and showed healthier liver function.
  
• Scientists believe differences in human genetics, enzyme levels, and metabolic stress may influence people’s susceptibility to soybean-oil-related metabolic effects.
  
  

A closer look at soybean oil and obesity

Soybean oil is the most widely consumed cooking oil in the United States and is a key ingredient in many processed foods. A growing body of research has associated high intake of soybean oil with weight gain in animals. A new study from the University of California, Riverside (UCR), published in the Journal of Lipid Research, provides fresh insight into why this may occur.

Researchers found that mice consuming a high-fat diet rich in soybean oil gained considerable weight. However, a separate group of genetically engineered mice did not, despite eating the same diet. These altered mice carried a slightly different version of a liver protein that affects the expression of hundreds of genes involved in fat metabolism.

The findings point toward a metabolic mechanism that may help explain differences in weight gain among individuals exposed to similar diets.

“This may be the first step toward understanding why some people gain weight more easily than others on a diet high in soybean oil,” said Sonia Deol, a UCR biomedical scientist and corresponding author of the study.

The role of HNF4α in fat metabolism

In humans, both forms of the liver protein known as HNF4α occur naturally. However, the alternative version typically appears only under certain conditions, such as chronic illness, prolonged fasting, metabolic stress, or alcoholic fatty liver disease. These variations, combined with factors such as age, sex, medication use, and underlying genetics, may influence how different people respond to high levels of soybean oil in their diet.

The UCR team believes that the altered form of HNF4α in genetically engineered mice changes how the body processes linoleic acid, a major fatty acid in soybean oil.

Building on earlier research

The study adds to previous findings from the same research group.

“We’ve known since our 2015 study that soybean oil is more obesogenic than coconut oil,” said Frances Sladek, a UCR professor of cell biology. “But now we have the clearest evidence yet that it’s not the oil itself, or even linoleic acid. It’s what the fat turns into inside the body.”

One of the major metabolic products of linoleic acid is a group of molecules called oxylipins. These compounds are associated with inflammation, fat accumulation, and other metabolic changes.

Oxylipins and their link to weight gain

Mice engineered to produce the alternative form of HNF4α showed markedly lower levels of oxylipins in their livers, despite consuming a high-fat soybean oil diet. They also had healthier liver profiles and enhanced mitochondrial function. Improved mitochondrial activity may help explain their resistance to weight gain.

Researchers pinpointed specific oxylipins derived from both linoleic acid and alpha-linolenic acid (another fatty acid found in soybean oil) that appeared necessary for weight gain in regular mice.

However, the picture is complex. Even though transgenic mice on a low-fat diet showed elevated oxylipin levels, they did not become obese. This suggests that while these molecules contribute to weight gain, they are unlikely to be the sole drivers. Other metabolic conditions must also play a role.

Genetic variation in enzyme levels

Further analysis revealed that the modified mice had far lower levels of two key enzyme families responsible for converting linoleic acid into oxylipins. These enzymes are highly conserved across all mammals, including humans, and can vary significantly from person to person based on factors such as genetics and diet.

The scientists also observed that oxylipin levels in the liver, rather than in the bloodstream, were correlated with body weight. This indicates that standard blood tests may not reliably detect early metabolic disturbances linked to diet.

Soybean oil’s rise in the American diet

Soybean oil consumption in the United States has risen dramatically over the past century. It has increased from around 2 percent of total daily calories to almost 10 percent. Although soybeans provide protein and the oil contains no cholesterol, modern diets deliver far greater quantities of linoleic acid than the body is likely evolved to manage.

In line with this, the UCR study found that soybean oil intake was associated with increased cholesterol levels in mice despite the oil containing no dietary cholesterol. This reflects the complex interplay between dietary fats and internal metabolic pathways.

Questions for future research

The team now aims to understand precisely how oxylipin formation leads to weight gain and whether oils with similarly high linoleic acid content – including corn, sunflower, and safflower oils – trigger comparable effects.

“Soybean oil isn’t inherently evil,” said Deol. “But the quantities in which we consume it is triggering pathways our bodies didn’t evolve to handle.”

Although the researchers have no plans for human trials, they hope the findings will inform future studies and guide public health policy.

“It took 100 years from the first observed link between chewing tobacco and cancer to get warning labels on cigarettes,” Sladek noted. “We hope it won’t take that long for society to recognise the link between excessive soybean oil consumption and negative health effects.”

Read More

Scientists Discover Key Protein Triggering Inflammation Linked to Obesity and Type 2 Diabetes

Key Takeaways:

• Researchers have identified FAM20C as a protein that triggers inflammation and insulin resistance in fat cells, a process linked to type 2 diabetes.
  
• Blocking or removing the FAM20C gene in mice improved insulin sensitivity and reduced inflammation, even without weight loss.
  
• High levels of FAM20C in human fat tissue are associated with insulin resistance, suggesting a potential new therapeutic target.
  
  

Early trigger identified in obesity-related inflammation

Investigators at Weill Cornell Medicine have uncovered an early step in the chain of events that links obesity to inflammation and insulin resistance – key contributors to the development of type 2 diabetes.

Their findings, published on 28 October in the Journal of Clinical Investigation, identify a protein known as FAM20C as a critical “switch” that initiates inflammation within fat cells. The study, conducted in mice, shows that when this protein is removed or blocked, metabolic health improves markedly, even without weight loss.

“By inhibiting or getting rid of FAM20C in fat cells, the mice became healthier even at the same body weight,” said senior author Dr James Lo, the Rohr Family Clinical Scholar and an Associate Professor of Medicine in the Division of Cardiology at Weill Cornell Medicine. “Their fat becomes metabolically healthier, reducing harmful inflammation in fat cells that can lead to chronic diseases like type 2 diabetes, fatty liver disease and heart disease.”

FAM20C: A molecular switch for inflammation

The research team, led by first author Dr Ankit Gilani, a Research Associate in Medicine at Weill Cornell Medicine, discovered FAM20C while screening genes that were switched on in the fat cells of mice with obesity and inflammation. FAM20C belongs to a class of enzymes known as kinases, which work by adding phosphate groups to other proteins – a process that can alter their activity and influence gene expression.

When the researchers increased the production of FAM20C in fat cells, the cells began releasing inflammatory molecules and became resistant to insulin. In contrast, blocking or deleting the gene in mice with obesity had the opposite effect – it reduced inflammation, improved insulin sensitivity, and decreased the accumulation of visceral fat (fat surrounding internal organs), even when total body weight remained unchanged.

“During obesity, when this gene is switched on in the adipose tissue, it causes inflammation,” Dr Gilani explained. “It drives the expression of other inflammatory genes, and then it causes insulin resistance, which can lead to type 2 diabetes.”

Evidence from human fat tissue

To determine whether the same mechanism operates in humans, the researchers analysed visceral fat tissue samples from individuals living with obesity. They found that higher levels of FAM20C were associated with insulin resistance – a key driver of type 2 diabetes – while people with lower FAM20C levels tended to exhibit better metabolic health despite having overweight or obesity.

These findings suggest that the FAM20C pathway could play a pivotal role in determining whether fat tissue becomes inflamed and metabolically harmful or remains relatively benign.

Next Steps: Targeting FAM20C and its downstream pathways

The research team now plans to investigate how FAM20C influences other tissues involved in metabolism and metabolic disease. They are particularly interested in a protein called CNPY4, which is activated by FAM20C and appears to be central to the inflammatory process.

“CNPY4 is going to be a major focus of future research to see how strongly it affects insulin resistance, and whether it could be a target for therapies to treat or prevent insulin resistance,” said Dr Lo, who is also a member of the Weill Center for Metabolic Health and the Cardiovascular Research Institute at Weill Cornell Medicine, and a cardiologist at NewYork-Presbyterian/Weill Cornell Medical Center.

Ultimately, the team hopes to develop small-molecule drugs that can block FAM20C or CNPY4 activity. Such therapies could reduce inflammation, lower visceral fat levels, improve insulin sensitivity, and help prevent or treat type 2 diabetes. Dr Lo noted that these treatments might one day be used alongside weight loss medications, or to support people who continue to experience metabolic inflammation and cardiovascular risk even after losing weight.

Funding and support

This research was supported in part by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health (NIH), through grants R01DK121140 and R01DK121844.

CCH insights

For a long time now we have known that inflammation in visceral adipose tissue is a major factor in insulin resistance, but it is still unknown why some people with obesity experience this adipose tissue inflammation and subsequent metabolic dysfunction, while other people with obesity do not. This research suggests that the FAM20C protein may contribute to this switch from healthy adipose tissue to inflamed, dysfunctional adipose tissue, and could offer an exciting new therapeutic pathway for type 2 diabetes and other cardiometabolic conditions.

Read More