Parental Weight Before Pregnancy Linked to Higher Risk of Fatty Liver Disease in Adult Offspring, UK Study Finds
Key Takeaways:
- Pre-pregnancy overweight or obesity in either parent is associated with a significantly increased risk of metabolic dysfunction associated steatotic liver disease (MASLD) in their children by early adulthood.
- When both parents were living with overweight or obesity prior to conception, the likelihood of MASLD in offspring by age 24 was more than three times higher.
- Much of this increased risk appears to be mediated by excess weight accumulated during childhood and adolescence.
Rising concern over MASLD across generations
Parental weight status before pregnancy may play an important role in shaping long-term liver and metabolic health in the next generation, according to new research published online in Gut. The findings suggest that overweight and obesity in both mothers and fathers prior to conception are linked to a heightened risk of metabolic dysfunction associated steatotic liver disease (MASLD) in their children as young adults.
MASLD, previously known as non-alcoholic fatty liver disease, is now recognised as the most common chronic liver condition worldwide. Researchers note that the disease affects approximately 15% of children and more than 30% of adults globally. The condition is characterised by excess fat accumulation in the liver alongside cardiometabolic abnormalities and may progress to cirrhosis or liver failure in some individuals.
While earlier studies have primarily focused on maternal obesity, uncertainty has remained regarding the contribution of paternal weight and the role of childhood weight trajectories in determining future disease risk.
Large UK birth cohort provides long-term insight
To investigate these questions, researchers analysed data from 1,933 participants enrolled in the UK Avon Longitudinal Study of Parents and Children (ALSPAC), a long-running population study tracking health outcomes across generations.
The study examined associations between parental body mass index (BMI) before pregnancy and the likelihood that offspring would develop MASLD by the age of 24.
MASLD was defined as the presence of elevated liver fat together with at least one cardiometabolic risk factor, such as raised cholesterol levels or elevated fasting glucose.
Both parents provided information on height, weight, BMI and waist circumference before pregnancy. They also completed detailed questionnaires during pregnancy and following childbirth covering a wide range of potential influencing factors, including:
- Age at delivery
- Smoking during early pregnancy
- Weekly alcohol consumption prior to pregnancy
- Employment status
- Educational attainment
Mothers additionally reported physical activity levels and whether they had previously been diagnosed with diabetes or hypertension at study enrolment.
Tracking early life and adolescent risk factors
Extensive information was also collected about the children, allowing researchers to examine developmental influences across childhood and adolescence. Recorded factors included:
- Sex
- Mode of delivery
- Gestational age and birthweight
- Antibiotic exposure during the first six months of life
- Duration of breastfeeding
Participants underwent repeated measurements of BMI and waist circumference between the ages of 7–9, 10–12 and 13–17 years. Lifestyle factors in early adulthood, including alcohol and tobacco use, were also assessed.
One in ten young adults developed MASLD
By age 24, MASLD was identified in 201 participants, representing approximately one in ten individuals in the cohort. The remaining 1,732 participants had normal liver findings.
Those living with MASLD were more likely to be male and to have a higher BMI compared with peers without the condition.
After adjusting for multiple potential confounding factors, both maternal and paternal overweight or obesity before conception were independently associated with increased odds of MASLD in offspring.
Each additional kilogram per square metre of maternal BMI increased the likelihood of MASLD by 10%, while each equivalent increase in paternal BMI was associated with a 9% rise in risk.
Most notably, offspring whose parents were both living with overweight or obesity prior to pregnancy had more than three times the odds of developing MASLD compared with those whose parents had a normal BMI.
Childhood weight plays a central role
Further analysis suggested that much of this association operates through weight gain during childhood and adolescence. Researchers estimated that 67% of the increased risk linked to parental overweight or obesity was explained by cumulative excess BMI between the ages of 7 and 17.
Additional analyses incorporating maternal and offspring sugar intake, as well as genetic susceptibility to MASLD, produced similar results, strengthening confidence in the observed associations.
Observational findings with important limitations
The authors emphasise that the study was observational and therefore cannot establish direct causation. Several limitations were also acknowledged.
Parental weight data prior to pregnancy were self-reported, and information was unavailable regarding parental MASLD status or certain underlying health conditions before and during pregnancy. In addition, physical activity levels of offspring in early adulthood were not captured, which may have influenced outcomes.
Implications for preconception health
Despite these limitations, the researchers conclude that their findings highlight the potential importance of parental metabolic health before conception in shaping long-term outcomes for future generations.
They state that the results “lend support to an early life influence of biparental obesity on offspring metabolic health, suggesting efforts to mitigate excess adiposity of both mothers and fathers before conceiving may confer longitudinal benefits to the metabolic outcomes of their future offspring.“
The study adds to growing evidence that prevention of metabolic disease may need to begin not only in childhood, but even before pregnancy, with both parents playing a meaningful role in influencing lifelong health trajectories.
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New Cochrane Review Finds Intermittent Fasting Offers No Clear Weight Loss Advantage
Key Takeaways:
- A major Cochrane review found intermittent fasting did not lead to clinically meaningful weight loss compared with standard dietary advice or no structured diet.
- Evidence on safety and long-term outcomes remains limited due to small trials, inconsistent reporting, and short follow-up periods.
- Experts caution against overinterpreting social media claims and emphasise the need for individualised, long-term approaches to weight management.
Intermittent fasting under scrutiny
Intermittent fasting has become one of the most widely promoted dietary strategies for weight loss, often presented as a superior alternative to conventional calorie reduction. However, a new Cochrane review suggests that these claims may not be supported by robust evidence.
According to the review, intermittent fasting does not appear to deliver greater weight loss than standard dietary advice or even no specific diet plan. The findings challenge the widespread perception that structured fasting schedules offer a unique or clinically meaningful advantage for people who are overweight or living with obesity.
Obesity remains a global public health challenge
Obesity continues to represent a major public health concern worldwide and is now among the leading causes of death in high-income countries. Data from the World Health Organization show that global adult obesity rates have more than tripled since 1975. By 2022, an estimated 2.5 billion adults were classified as overweight, including around 890 million adults living with obesity.
Against this backdrop, intermittent fasting has gained substantial attention. Eating patterns such as alternate-day fasting, periodic fasting, and time-restricted feeding are widely promoted across social media platforms, often accompanied by claims of rapid weight loss and metabolic benefits.
What the review examined
To assess whether intermittent fasting truly offers an advantage, researchers analysed 22 randomised clinical trials involving 1,995 adults across North America, Europe, China, Australia, and South America. The studies evaluated a range of fasting approaches, including alternate-day fasting, periodic fasting, and time-restricted feeding. Most trials followed participants for up to one year.
When outcomes were compared with those of traditional dietary advice or no dietary intervention, intermittent fasting did not result in a clinically meaningful difference in weight loss. In practical terms, fasting-based approaches did not outperform more conventional strategies.
Limited evidence on safety and long-term outcomes
The review also highlighted substantial limitations in the available evidence. Reporting of side effects varied widely between studies, and many trials were relatively small. Inconsistent data collection made it difficult to draw firm conclusions about safety or potential long-term effects.
As a result, the overall certainty of the evidence was judged to be limited.
“Intermittent fasting just doesn’t seem to work for overweight or obese adults trying to lose weight,” said Luis Garegnani, lead author of the review from the Universidad Hospital Italiano de Buenos Aires Cochrane Associate Centre.
Social media enthusiasm outpaces the evidence
Garegnani also warned against the level of enthusiasm surrounding intermittent fasting online. “Intermittent fasting may be a reasonable option for some people, but the current evidence doesn’t justify the enthusiasm we see on social media.”
A further concern is the lack of long-term research. Few studies have examined outcomes beyond relatively short trial periods. “Obesity is a chronic condition. Short-term trials make it difficult to guide long-term decision-making for patients and clinicians,” Garegnani added.
Generalisability remains uncertain
Most of the studies included in the review primarily involved white participants living in high-income countries. Given that obesity prevalence is rising rapidly in low and middle-income countries, the findings may not fully reflect outcomes in more diverse global populations.
The authors note that responses to intermittent fasting could vary depending on sex, age, ethnic background, underlying health conditions, or existing eating behaviours and eating disorders.
Implications for clinical practice
Given the current state of evidence, the review’s authors advise caution when recommending intermittent fasting as a weight loss strategy.
“With the current evidence available, it’s hard to make a general recommendation,” said Eva Madrid, senior author from the Cochrane Evidence Synthesis Unit Iberoamerica. “Doctors will need to take a case-by-case approach when advising an overweight adult on losing weight.”
Overall, the findings reinforce the need for personalised, sustainable approaches to weight management rather than reliance on highly promoted dietary trends.
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Big Breakfast Study Shows Protein Reduces Appetite While Fibre Supports Gut Microbiome Health
Key Takeaways:
- Within a calorie-restricted big-breakfast eating pattern, a higher-protein breakfast improved satiety, while a higher-fibre breakfast produced more favourable gut microbiota and short-chain fatty acid profiles.
- Both dietary approaches led to clinically meaningful short-term weight loss and improvements in metabolic markers, but with distinct physiological effects.
- Fibre-rich breakfasts were linked to greater abundance of beneficial butyrate-producing bacteria, whereas protein-rich breakfasts may better support appetite control and dietary adherence.
Background and rationale
A recent study published in the British Journal of Nutrition examined how breakfast composition influences appetite regulation, energy balance and markers of gut microbiota health when consumed as part of a calorie-restricted, big-breakfast weight-loss diet.
There is growing evidence that meal timing, in addition to dietary composition, plays an important role in healthy weight management. Previous research has shown that people who eat earlier in the day tend to lose more weight than those who eat later. Morning calorie intake has also been associated with improved blood glucose control and lower hunger levels compared with evening intake.
Larger breakfasts have been shown to improve appetite control, while late eating patterns have been linked to increased hunger and greater fat storage. Despite public health advice emphasising the importance of breakfast for weight management, relatively little is known about what people typically consume in the morning. Moreover, evidence explaining how meal timing, calorie distribution and macronutrient composition interact to influence appetite remains limited.
Study design and dietary interventions
The researchers used a randomised crossover design to compare two calorie-restricted weight-loss diets with identical big-breakfast calorie distribution but differing macronutrient profiles. The primary outcomes were appetite, energy balance and gut microbiota composition and metabolites, rather than clinical gastrointestinal outcomes.
Healthy adults with overweight or obesity, aged 18–75 years, were recruited. The protocol consisted of:
- a four-day ad libitum diet
- a four-day maintenance diet
- a 28-day high-fibre weight-loss diet or high-protein weight-loss diet
These phases were separated by a washout period, with participants acting as their own controls. Resting metabolic rate was measured by indirect calorimetry during screening.
The maintenance diet provided 15% of energy from protein, 55% from carbohydrate and 30% from fat, and was set at 1.5 times resting metabolic rate to maintain body weight. Both weight-loss diets were set at 100% of resting metabolic rate to induce a calorie deficit.
Participants consumed three meals per day, with 45% of daily calories at breakfast, 20% at lunch and 35% in the evening. Lunch intake was allowed ad libitum within the provided calorie allowance.
- High-fibre weight-loss diet – 50% carbohydrate, 15% protein and 35% fat, incorporating both soluble and insoluble fibre sources such as lentils, fava beans, buckwheat and wheat bran.
- High-protein weight-loss diet – 30% protein, 35% carbohydrate and 35% fat, using foods including fish, poultry, eggs, red meat and dairy.
Measurements and outcomes assessed
Body density, waist and hip circumference, resting metabolic rate, total body water and blood pressure were measured. The thermic effect of food was assessed every 30 minutes for four hours after breakfast. Subjective appetite was evaluated using visual analogue scales.
Blood samples collected after an overnight fast were used to assess glucose, lipid profile and insulin as metabolic biomarkers rather than clinical disease outcomes. Insulin and glucose values were used to calculate HOMA-IR, HOMA-β and the insulin-to-glucose ratio. Total body water was measured using deuterium dilution, and faecal samples were collected to analyse gut microbiota composition.
Weight loss, energy expenditure and metabolic markers
Nineteen participants completed the study, including two women. The mean age was 57.4 years and the mean body mass index was 33.3 kg/m², indicating a predominantly male cohort and limiting generalisability to broader populations.
Energy intake did not differ significantly between the two weight-loss diets. Average weight loss was 4.87 kg with the high-fibre diet and 3.87 kg with the high-protein diet. Both diets significantly reduced fat mass and fat-free mass compared with the maintenance diet, although loss of fat-free mass was greater with the high-fibre approach.
Total body water was reduced following the high-fibre diet but not after the high-protein diet. Waist and hip circumferences, as well as waist-to-hip ratio, were significantly reduced with both weight-loss diets compared with the maintenance diet.
The high-protein breakfast maintained postprandial satiety, whereas the high-fibre breakfast was associated with reduced satiety after meals. Resting metabolic rate declined significantly after both weight-loss diets. The thermic effect of food was lower following the high-fibre diet than after the high-protein or maintenance meals.
Both weight-loss diets improved lipid profiles relative to baseline, with no significant difference between the two approaches. Fasting and postprandial glucose levels were reduced by around 10% following the high-fibre diet and by 8–7% following the high-protein diet compared with the maintenance diet. Fasting insulin, HOMA-IR and the insulin-to-glucose ratio were significantly lower after both weight-loss diets.
HOMA-β decreased significantly more after the high-protein diet than after the maintenance diet, with no significant change observed after the high-fibre diet.
Gut microbiota composition and short-chain fatty acids
Total bacterial load in faecal samples did not differ significantly between the two weight-loss diets. However, microbial diversity was lower following the high-protein diet compared with the high-fibre diet.
Distinct differences in microbiota composition were observed between the dietary patterns, although individual variation remained a major determinant of microbiota profiles and diet explained only part of the observed variability.
The high-fibre diet was associated with a greater abundance of butyrate-producing bacteria, including Anaerostipes hadrus, Roseburia faecis and Faecalibacterium prausnitzii. At the genus level, Bifidobacterium, Faecalibacterium and Roseburia were linked to the high-fibre diet, while Streptococcus was associated with the high-protein diet.
Total short-chain fatty acids and key faecal short-chain fatty acids, including acetate, butyrate and propionate, were significantly lower with the high-protein diet compared with the high-fibre diet.
Interpretation and clinical implications
Overall, the findings suggest that within a calorie-restricted big-breakfast eating pattern, breakfast composition meaningfully influences short-term weight loss, metabolic health markers and gut microbiota characteristics.
Both dietary approaches led to significant weight reduction and metabolic improvements. The high-protein breakfast produced greater satiation, which may support long-term adherence in some people. In contrast, the high-fibre breakfast promoted a more favourable gut microbiota profile and higher short-chain fatty acid production, which may be beneficial for long-term gut health, although this was inferred from microbial and metabolic markers rather than direct clinical outcomes.
The authors emphasised that longer-term studies are needed to determine whether these differences are sustained over time and how they translate into long-term health outcomes.
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Obesity Associated With Higher Risk of Severe Infectious Disease, Large Study Finds
Key Takeaways:
- People living with obesity face a substantially higher risk of hospitalisation or death from a wide range of common infections, with risk increasing alongside body weight.
- Weight change matters – moving out of obesity is associated with fewer severe infections, while progression into obesity increases risk.
- Global estimates suggest that around one in ten infectious disease deaths worldwide may be linked to obesity.
Obesity and severe infection risk across multiple pathogens
A large population-based study has examined the relationship between obesity and the risk of severe infectious diseases, finding that people living with obesity are significantly more likely to be hospitalised or die from common infections. These include influenza, Covid-19, pneumonia, and gastrointestinal and urinary tract infections. For people living with morbid obesity, the risk was approximately three times higher than for people of healthy weight.
“During the pandemic, obesity was widely linked to a higher likelihood of severe Covid-19. We set out to investigate how broadly this link applies across different types of infections and whether any underlying factors contribute to it. Our findings extend beyond any single pathogen, with similar associations observed for bacterial, viral, parasitic and fungal infections,” says one of the article’s lead authors, Solja Nyberg of the University of Helsinki and the Finnish Institute of Occupational Health.
Notably, HIV and tuberculosis were exceptions, with no evidence that obesity increased the risk of severe disease for these infections. The researchers also found that comorbidities, socioeconomic status, and lifestyle factors such as alcohol consumption and physical activity did not explain the increased infection risk associated with obesity.
Weight matters for infection outcomes
Participants were followed for an average of 13–14 years, with body mass index (BMI) measured at baseline. People living with obesity, defined as a BMI of 30 kg/m² or higher, had a 70% greater risk of hospitalisation or death from any infectious disease compared with people of healthy weight, defined as a BMI of 18.5–24.9. The risk increased progressively with higher body weight.
People living with morbid obesity, defined as a BMI of 40 kg/m² or higher, experienced a risk of severe infection three times that of people of healthy weight.
Importantly, changes in body weight over time were also associated with changes in risk. Participants who lost weight and moved from obesity to overweight or healthy weight experienced 20% fewer severe infections compared with those whose obesity persisted. In contrast, weight gain from overweight to obesity was linked to a 30% higher risk of severe infection.
Possible links with immune system dysfunction
“Obesity is a well-known risk factor for diabetes and other chronic diseases. The links now identified indicate that severe infectious diseases should be added to the same list,” says Mika Kivimäki of the University of Helsinki and University College London, who led the study.
“Obesity seems to weaken the immune system’s ability to manage infections, raising the risk of severe disease,” he explains.
Kivimäki also notes that experimental evidence from studies of weight-loss drugs supports a link between obesity and immune function. Reductions in body weight appear to lower the risk of severe infections alongside other health benefits. However, he emphasises that further research is needed to confirm the biological mechanisms underlying these associations.
Obesity and global infectious disease mortality
The researchers analysed data from large Finnish cohorts and the UK Biobank, tracking participants through national health registers. They also incorporated infectious disease mortality data from the Global Burden of Disease study to assess how obesity contributes to infectious disease deaths across countries and regions.
Their analysis suggests that approximately 0.6 million of the 5.4 million infectious disease deaths recorded worldwide in 2023, equivalent to around 11% or one in ten, were associated with obesity.
In the Nordic countries, the estimated proportions of infectious disease deaths linked to obesity were:
- Finland – 19%
- Sweden – 13%
- Norway – 11%
- Denmark – 12%
Among high-income countries, the United States recorded the highest proportion in 2023, at 26%.
Importance of vaccination and prevention
The researchers stress that adults living with obesity should ensure their vaccinations are up to date and take up booster doses when offered to groups at higher risk of severe infection.
They also highlight several limitations of the study. As an observational analysis, it cannot establish causality. In addition, participants in the Finnish cohorts and the UK Biobank are not fully representative of the general population, meaning the findings should be generalised with caution.
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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.
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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.
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.
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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.
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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.
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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. 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.
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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.
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.
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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.
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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.
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