The National Health and Nutrition Examination Survey (NHANES), overseen by the Centers for Disease Control and Prevention, employs a stratified, multistage, probabilistic method to representatively survey the US civilians. This survey assesses their health and nutritional status through household interviews, physical examinations at mobile examination centers, and lab tests performed by certified health professionals. All the procedures were conducted according to the Declaration of Helsinki principles, and the protocol was reviewed and approved by the NHANES Center for Health Statistics Ethics Review Board, with written consent obtained from all participants.
Our research analyzed data from five 2 − year NHANES cycles from 2007 to 2016, focusing on coffee intake (total, caffeinated, and decaffeinated) and SαKl levels. We included 50,588 participants from these cycles, restricting our analysis to those aged 40 − 79 who consented to allow their surplus serum to be used for future studies. Initially, 19,344 participants were eligible; however, exclusions were made for missing α-Klotho data (n = 5,580), incomplete coffee intake data (n = 804), pregnancy (n = 8), cancer (n = 1,536), and other missing covariates like demographic and behavioral factors or disease history (n = 1,531). Additional exclusions were made for females with total energy intakes of less than 500 or more than 5000 kcal/day (n = 53) and males with less than 500 or more than 8000 kcal/day (n = 21), resulting in a final sample of 9,811 participants.
Exposure assessments
We assessed total coffee intake—disaggregated into caffeinated and decaffeinated varieties—and quantified dietary caffeine using the Food and Nutrient Database for Dietary Studies, which was developed by the US Department of Agriculture specifically for dietary research. This database provides details on nutrient composition for a wide array of foods and is frequently employed in analyzing NHANES survey data. From 24-h dietary recall interviews, we extracted data on total coffee, caffeinated coffee, and decaffeinated coffee intake, using information reported on the first day to maximize the inclusion of dietary data. Coffee consumption was precisely calculated using food codes flagged with 921. In our study, the primary exposure variable was the daily total coffee consumption (g/day), and the secondary was caffeinated and decaffeinated coffee consumption (g/day).
Outcomes
According to the NHANES Laboratory/Medical Technologists Procedures Manual [17], SαKl levels were analyzed using samples collected for the NHANES cycles from 2007 to 2016 and processed between 2019 and 2020. These samples were maintained at − 80 °C and assessed with an enzyme-linked immunosorbent assay kit from IBL International, Japan. Each sample was tested twice to ensure accuracy, and the average of these two measurements was used. The kit’s sensitivity was 6.0 pg/mL. On average, SαKl levels were 698.0 pg/mL, with a range of 285.8 to 1638.6 pg/mL [18].
Assessment of covariates
We considered multiple potential confounders in our analysis, including race/ethnicity (classified as Mexican American, other Hispanic, non-Hispanic White, non-Hispanic Black, and Others), body mass index (BMI) (categorized as normal: < 25 kg/m2, overweight: 25 to 30 kg/m2, obese: ≥ 30 kg/m2), the ratio of family income to poverty (PIR) (segmented as < 1.30, 1.30 − 2.99, and ≥ 3.00) [19], education level (classified as less than high school, high school or GED, above high school), and smoking status (defined as never: < 100 cigarettes in lifetime, former: ≥ 100 cigarettes but not currently smoking, current: ≥ 100 cigarettes while currently smoking). Alcohol consumption was categorized based on previously published criteria [20] (categorized as never drinker, former drinker, light-to-moderate drinker, heavy drinker). Total energy intake was sourced from the 24-h dietary recall. Physical activity (PA) levels were categorized as inactive, moderate, or vigorous. Hypertension was identified by a systolic blood pressure value ≥ 140 mmHg, diastolic blood pressure ≥ 90 mmHg, or habitual use of blood pressure medication [21]. A combination of diagnostic criteria and patient history determined COPD. The presence of CVD was identified based on doctor-diagnosed conditions.
Statistical analysis
All statistical analyses were conducted using R software (The R Foundation; version 4.3.2). We set the significance threshold at P < 0.05. To accommodate the survey’s nonresponse and differential sampling, we utilized NHANES survey weights as per the analytical guidelines provided. We assessed baseline characteristics using weighted linear regression for continuous variables and weighted chi-square tests for categorical variables. The results were presented as numbers (weighted percentages) for categorical data and weighted means ± Standard Error (SE) for continuous data. Our multivariate linear regression models explored the relationships between total coffee, caffeinated coffee, decaffeinated coffee intake and SαKl levels. The analysis was structured according to the STROBE guidelines: Model 1 was adjusted for demographic factors (age, sex, and race/ethnicity); Model 2 further included all variables (BMI, marital status, education level, PIR, smoking status, alcohol consumption, physical activity, energy intake, eGFR, hypertension, CVD, and COPD). To assess nonlinear relationships, we used generalized additive models (GAM) and restricted cubic splines (RCS). Based on the smoothing curve, the turning point was calculated through a recursive algorithm, followed by two-piecewise linear regression models. Furthermore, subgroup analyses were conducted to explore variations in the relationship between coffee consumption and SαKl levels across different demographics, including age (≥ 60 years) and sex.
Yvonne Hughes was 19, and attending the funeral of a friend with cystic fibrosis, when she realised: “Oh shit, I’m going to die of this.” She had met him during shared hospital stays in childhood, and although Hughes had always known she had CF, she had never understood her illness as terminal until that day in 1992, when she stood at the back of the crowded chapelin Glasgow. For three days afterwards, she couldn’t stop crying. “I had a kind of meltdown. That’s probably the first time I thought that this thing I had was going to kill me.”
Over the next few months, Hughes, who was studying at the University of Glasgow, listened to her mum, dad and older sister chatting during family meals as if she was a ghost at the table. “I pulled back from them. I deliberately didn’t talk or include myself,” she says. “I wanted them to get used to sitting and chatting without me, so that when I died, they wouldn’t notice I wasn’t there.”
It’s a harrowing responsibility for a teenager to take, but self-erasure must have felt like a way to pre-empt death, perhaps to resist it. When she was growing up, cystic fibrosis was considered “a childhood disease” – because about half of those diagnosed did not survive their teens. A genetic condition in which the body creates thick, sticky mucus, it makes digestion difficult, damages lung function and can lead to respiratory failure. It affects about 160,000 people globally.
Now 52, and enjoying what she calls a “second chance” at life more than 30 years later, Hughes has emerged as a comedian. We are speaking on a video call before her one-hour show, Absolutely Riddled, which she is performing at the Edinburgh fringe, based on her experiences of living with the condition. “I want to be true to myself and my story,” she says. Why does she think she survived when so many didn’t?
‘My mum said: “We thought you were going to die, every day”’ … Hughes, far right, with her hospital friends on a day trip in 1984. Photograph: Jeremy Sutton-Hibbert/The Guardian
For most of her childhood, Hughes, who works as a community development worker in Renfrewshire, didn’t regard herself as struggling for survival. Her parents didn’t sit her down in childhood to explain her illness; she had been diagnosed at six weeks old. But there were hospital visits and tablets and eating often made her vomit. Gradually, she says, she “put together those two words, cystic and fibrosis, with something that I had”.
At school, she kept her illness hidden, taking her medication at home. She was popular; joined the Brownies, then Guides. “I’m a very level-headed person, but I keep a lot in my mind. I remember when I was younger thinking: ‘There’s no point telling people about this because everyone is dealing with something. I’m nothing special.’ I just got on with it.”
Roughly one in every 2,500 people are born with cystic fibrosis in the UK, Australia and the US. Hughes’s older sister does not have the illness and the family had no idea what it meant for their lives, or for Hughes herself.
Only as she grew older did Hughes build a sense of the precariousness of her life. “My mum said to me: ‘We thought you were going to die, every day. We just didn’t know.’ It became their new normal to keep me alive.”
If she got a chest infection, pleurisy or pneumonia, she would go into hospital, and over the years made friends on the CF ward, a fragile community. When the curtains were closed around a bed for a long time, Hughes and the other children knew not to go past. She reasoned with herself, to allay her fears: “People were dying around me but I put it down to: ‘Maybe they had a really bad infection, maybe they were worse than me.’” In childhood, she developed “a lot of level-headed thought processes around why those people died”.
‘I thought there was no point telling people because everyone was dealing with something. I was nothing special.’ Photograph: Jeremy Sutton-Hibbert/The Guardian
She found solace in the Cystic Fibrosis Trust magazine, and dreamed of attending one of the advertised camps. “Luckily, I didn’t,” she says, because in the early 1990s, scientists discovered that the camps were a hotbed for the spread of bacteria, present in the lungs and phlegm of children with CF. Many cross-infected each other, some with fatal consequences.
Did Hughes struggle to accept that sense of herself, as both vulnerable and a threat? “Absolutely,” she says. Hospitals implemented a policy of segregation, according to bacteria carried. Hughes has the pseudomonas bacteria, and after her friend’s funeral in 1992, she stopped seeing people with cystic fibrosis in case they had different bacteria or bugs that might lead to cross-infection.
She has stayed in touch by phone with one old friend. “We shared growing up in the hospital ward and I do love speaking to him.” But after that funeral, “I became reckless,” she says. “I thought: ‘Well, life’s for living. I’m just going to do what I want.’ I didn’t care very much for myself. I thought: ‘What’s the point?’ I spiralled.”
Her 20s and 30s passed in a blur of “festivals, partying, travelling when I could, flying by the seat of my pants … ” She had hoped to meet someone, and to have children. “I thought it would happen. And it never did.” In her 30s, her lung function got so low – 45%, then 36% – that she wouldn’t have been able to sustain a pregnancy anyway. “That was something I tried to grieve. But over the course of a year, I thought: ‘I’d rather be alive.’ My mantra became: ‘I’d rather have a full and short life than a long and unhappy one.’ These kinds of philosophical things got me through.”
Hughes doesn’t have a mantra now – “other than trying to be funny”. The frequency of her performances range from three times a week to every few weeks, depending on her health needs. But even in her reckless phase, she embodied a stoicism, too. She worked throughout – at a call centre, a radio station, the CF Trust. “I just had to keep going, pay my bills and mortgage.”
Did she ever wonder: “Why me?” She has had years of spitting out and swallowing mucus – “constant, constant” – hankies everywhere, non-stop sterilising of stuff, endless medication and pain, unable to take the next breath for granted. As a child, when she went into hospital, there was a faint sense of privilege at being given Lucozade and new slippers, things her sister didn’t get. But no one else in her family has the illness. Didn’t she feel aggrieved?
“It’s a difficult question,” she says. “I’ve thought about ‘Why me?’ in a positive sense – that it was me because I could handle it. Or, I’m glad … because this has made me the way I am.” She has also thought, “Why at all? Why did cystic fibrosis come into being? Why have this weird disease that just kind of ruins lives?”
‘I just got on with it.’ Photograph: Yvonne Hughes/PA
While Hughes survived childhood by reminding herself that she wasn’t special, the differences between her life and others’ sharpened as she entered her 40s. She became an aunt, and bore close witness to her peers’ life transitions while she kept on being “just Yvonne – the one that never reached any potential”.
“I couldn’t have a career because I would always get ill. I never moved social class. I always remained working class.” Her dad was a welder, her mother a GP receptionist. “Everything I did, I did myself. But it was day by day, week by week. There was never a plan. I always felt I could never get ahead of myself.”
In 2018, aged 45, with deteriorating health, Hughes took redundancy from her job as public affairs officer at the CF Trust.Eating was difficult. Her weight hovered around 7 stone. She braced herself for the possibility of a lung transplant, but as her lung capacity dropped to 30%, she was deemed too ill for the waiting list. “I was like: ‘OK, that door’s closed. At this point, there isn’t anything else on the horizon to keep me alive.’” She completed an end-of-life form, and met the palliative care team. She thought: “I’ll see my days out with my parents, make memories and know I did well to get to 48.”
Then, in 2020, the UK government granted access to a new drug, Kaftrio. Hughes had read about its worldwide trials. When the delivery driver knocked on the door, she told him: “You’re going to save my life.” At that point, her lung function was down to 26%.
Within an hour or two of the first tablet, she started coughing. “They call it the purge,” she says. There was so much mucus – dark, watery and horribly fascinating – she captured it in a cup, put a lid on it, and stowed it in a drawer in her bedroom. “I kept that cup for a long time,” she says. Maybe she already knew it was a relic.
The Kaftrio turned Hughes’s life “a whole 180, literally overnight”. There are side-effects – insomnia, weight gain, which have brought other challenges – but before long, she says, “I could breathe again without coughing. I went back to work within the year. I could run, I could dance, I could speak, I could stand up straight and cook. I used to always be bent over, catching my breath. And then all of a sudden that was gone. It was a miracle.”
Energised, she decided to enrol in an evening course. Acrylic painting, maybe, or playing the keyboard? But at the University of Strathclyde’s Centre for Lifelong Learning, it was the flyer for comedy that caught her eye. “I had always loved going to gigs. Something clicked and I enrolled.”
She performed a five-minute set for the course finale – and immediately wanted to do it again. “I started applying for clubs, Monkey Barrel and the Stand Comedy Club [both in Edinburgh]. I got Red Raw [the Stand’s beginners’ slot] and went from there. I want to change my life,” she says, “and I am doing comedy to see if I can change my life.”
‘Comedy was the one thing that was for me’ … Hughes performing at Monkey Barrel, Edinburgh. Photograph: Yvonne Hughes/PA
Nearly four years ago, Hughes met her partner, Alan, online. Having spent a lifetime feeling unable “to rely on a future”, she has had to learn to picture one – and to override her old instinct to absent herself to mitigate later losses. Sometimes, this means catching herself in the act of “pulling back” from Alan, and letting the pleasure she takes in his company teach her to quiet her mind.
Life now is so different, it requires a conscious effort to remember how hard it was from one moment to the next. “I used to breathe so shallowly that I had to take a – haa! – sharp intake of breath – to feel I was breathing,” she says. The sound punctuated even the simplest actions – after getting into a car, for instance, after reaching for her seatbelt, after pulling it across her, after fastening it.
“Now I can get in the car, pull the seatbelt over and go. I can walk and talk. I can laugh without wetting myself or going into a convulsion of coughing, pulling a muscle or breaking a rib,” she says. “It is a horrible, horrible disease. It suffocates you. It takes every inch of your breath away. And now it is something I can live with and not die from. I’ll probably live to get my pension.”
Comedy has brought “fun, joy and laughter” back into Hughes’s life. But it has also given her something that nothing else has. “I had never found anything for me in my life. I’d never married. I had no children. So I had no community. Nothing,” she says. “There were people getting their careers and their lives sorted. Comedy was the one thing that was for me. And it still is. Just for me.”
But the search for such a pill—or indeed any treatment as effective as CPAP—has proved challenging. Dozens of drugs have failed to show efficacy in clinical trials, and while HGNS was first approved by the US Food and Drug Administration in 2014, Miller says that its rollout has been limited, as many doctors are uncertain about the risk-to-benefit trade-off. “The device is quite costly, and the implantation requires a surgical procedure,” he explains, which comes with added risk to the patient. “As with any new technology, there is often a lag in acceptance from both the medical community and insurers.”
It’s unlikely that a single therapy will be found as an alternative to CPAP, Gaisl argues, because sleep apnea isn’t one single disease—rather, a diverse cluster of conditions. Obesity is known to be one of the major risk factors—and the weight-loss drug tirzepatide has recently been licensed as a sleep apnea therapy—because excess fat around the neck and upper body can obstruct the airway and cause pauses in breathing. But there are many other causes, some of which are only recently coming to light. Researchers are now beginning to understand the impact of ethnicity on sleep apnea, for example, with patients in Asia at heightened risk.
Sleep apnea is resultant of “a mosaic of different things, not just obesity,” says Gaisl. “We’re increasingly seeing that different subgroups benefit most from more personalized approaches.”
This recognition has led researchers to focus more on the EDS population. Gaisl estimates that simply having EDS is equivalent to increasing your BMI by 11 points in terms of the likelihood of developing sleep apnea. That’s because the genes linked to EDS affect the structure of so-called “matrix proteins” like collagen and elastin, which provide the framework for the body’s connective tissues—everything from skin to tendons, muscles, and ligaments.
“Collagen is an integral part of almost all tissues, including those which form the airway,” says Karim Ghobrial-Sedky, an adjunct professor at Drexel University and a sleep specialist who has treated EDS patients with sleep apnea. “In EDS, it’s this abnormality in collagen which makes the airway more prone to collapsing when the person is taking a breath.”
Because of this, researchers believe that EDS sleep apnea patients are especially suited to treatments targeting muscles in the tongue and throat—like Miller’s HGNS, or a newer drug combination under development by a company called Apnimed. Based on the discovery that two compounds, atomoxetine and aroxybutynin, could work in synergy to improve upper airway muscle tone and reduce airway muscle relaxation during sleep, Apnimed has been shown in a clinical trial to reduce instances of sleep apnea by 56 percent. “People with hypermobility are a prime target cohort for these kinds of therapies,” says Gaisl.
While EDS was long considered rare, recent studies suggest genetic hypermobility may affect as many as 1 in 500 people, with women disproportionately affected. Gaisl believes the underlying biology behind these conditions also offers clues for explaining other subtypes of sleep apnea. In his view, the genetics of EDS actively mirrors the damage which other people are inadvertently inflicting on their matrix proteins through behaviors and environmental stresses like smoking, chronic inflammation, excessive dietary sugar and the aging process itself, heightening their risk of sleep apnea through midlife.
“EDS is a kind of natural experiment which is giving us insights into some of the key biological mechanisms behind sleep apnea that are masked in the general population,” says Gaisl.
Such individuals could benefit more from targeted therapies like HGNS or Apnimed’s drug combination, compared with patients whose apnea is primarily driven by weight gain or underlying breathing abnormalities. Newer diagnostics are applying AI algorithms to patients’ sleep data, pinpointing key patterns that suggest a specific type of airway collapse. In the future, these tools could help clinicians to identify such people both faster and more accurately, as well as individuals with undiagnosed hypermobility. These insights could then be used to tailor their treatment.
As researchers learn more about the role of matrix proteins in EDS-related sleep apnea, it could even pave the way for entirely new treatments in future.
Matrix proteins “really point to the importance of collagen in maintaining the airway during sleep,” says Gaisl. “This opens up a new avenue for therapeutics which perhaps target how the connective tissues are impacted over time, causing sleep apnea—treatments which could ultimately benefit a much broader range of patients.”
It may not be about boosting testosterone or self-control; new research suggests the decision to participate in the viral challenge says more about your personality than its potential health benefits.
Study: No Nut November, temporary abstinence, and sexual wellbeing: a study of the short-term abstinence-based internet trend. Image Credit: NeelRong / Shuttertock
In a recent study in The Journal of Sexual Medicine, researchers investigated the psychological and sexual wellbeing impacts of “No Nut November” (NNN). NNN is a challenge that involves a month of abstinence from masturbation and/or ejaculation, and is gaining mainstream internet popularity, yet its effects on sexual wellbeing remain unknown. The present study makes a direct comparison of sexual pleasure, desire, or function metrics between NNN participants and non-participants before and after the challenge.
Study findings revealed no significant differences between participants and non-participants across all measured metrics, revealing no scientific evidence backing up the internet hype surrounding NNN. However, the study observed that individuals who had previously participated in the NNN challenge reported higher levels of sexual flexibility, suggesting a potential predisposing factor that may draw them to such trends.
Background
Several internet trends, including the “ice bucket challenge” and “planking,” have periodically captured global attention and witnessed astounding participation, with little consideration given to their psychological or health impacts.
One of the most popular internet trends that, unlike most of its peers, has withstood the test of time is “No Nut November” (NNN). In this yearly challenge, participants (predominantly but not exclusively men) attempt to abstain from masturbation and ejaculation for the entire month. However, the study found participants defined the rules variably: 44.5% as “no ejaculation” (allowing sexual activity without orgasm), while 33.3% banned all sexual activity. Born from the dark depths of online forums, NNN is now a mainstream phenomenon, with some of its growing participant cohort claiming benefits ranging from improved self-control and sexual pleasure to increased testosterone and reduced fatigue. The current research did not assess physiological claims, such as changes in testosterone levels.
Interestingly, while these claims have never been scientifically verified, extreme variants of the challenge (like the NoFap community promoting lifelong abstinence) have been found to result in generally adverse outcomes, such as increased participant anxiety and even erectile dysfunction. The study authors emphasize that NNN is distinct from NoFap as a short-term, social challenge rather than a lifelong commitment. These confounding lines of evidence, alongside NNN’s ever-growing participation, make methodologically robust investigations of the trend’s psychological and sexual health impacts essential.
About the study
As the first systematic and empirical evaluation of NNN’s impacts on sexual health, the current study aimed to address gaps in scientific understanding of a rapidly growing global trend with potentially widespread consequences. It comprised an online survey designed to characterize NNN participants and measure the trend’s effects on sexual wellbeing. Study participants were recruited via online platforms (subreddits, Facebook advertisements, Instagram/Twitter/X posts, etc.) in October 2023.
Based on their NNN participation history (previous or prospective NNN participants versus NNN non-participants), volunteers were categorized into ‘cases’ and ‘controls’. The study collected data at two time points: Time 1 (T1) in October 2023, before NNN, and Time 2 (T2) in December 2023/January 2024, following the challenge’s conclusion. Study data comprised participants’ demographic and medical histories, NNN participation information, and a custom questionnaire evaluating different aspects of sexual wellbeing.
Specifically, the questionnaire included: 1. Sexual Pleasure Scale (SPS) – pleasure from sexual activities, 2. Sexual Desire Inventory-Solitary (SDI-SD) – desire for solo sexual activity, 3. Arizona Sexual Experience Scale (ASEX) – overall sexual functioning and dysfunction, 4. SexFlex Scale (SFS) – psychological flexibility regarding sexual matters, and 5. Sexual Excitation Scale-Short Form (SES-SF) – a measure of arousal and sexual excitation at baseline only (T1).
Statistical analyses included Analysis of Covariance (ANCOVA) to compare sexual wellbeing at T1 between those who had previously participated in NNN and those who hadn’t. Repeated-measures Analysis of Variance (ANOVA) models were also used to track changes from T1 to T2 between a group actively participating in NNN 2023 versus the controls.
Study findings
The final study dataset comprised 435 individuals who completed the T1 survey, and only 114 who completed the T2 follow-up. Demographic data revealed that NNN participants were predominantly white (62.9%), heterosexual (54.0%), and male (66.7%), but also included women (20.6%) and gender-diverse individuals (10.6%). An eye-opening and potentially alarming finding was that 57.1% of participants reported first participating in NNN before adulthood (18 years), suggesting the trend has a significant reach among adolescents and may have implications for sexual development.
Analysis revealed:
No statistically significant differences in sexual wellbeing between participants and non-participants across T1 and T2
Higher baseline sexual flexibility in NNN participants (adjusted mean = 18.07 vs. 16.14, ηp² = .030, p = .008)
At T1, men reported significantly higher solitary desire (p = .011), lower sexual dysfunction (p < .001), and higher sexual excitation (p < .001) than women/gender-diverse individuals
Conclusions
This pioneering study provides the first scientific evidence evaluating the psychological and sexual wellbeing impacts of the “No Nut November” phenomenon, finding that the month-long period of abstinence from ejaculation has no cost or benefit to participants’ sexual wellbeing. These findings counter strong yet unfounded claims made by both proponents and critics online, and while limited by their reliance on self-report data and a 74% attrition rate between timepoints, they lay crucial groundwork for future research.
Perhaps the study’s most intriguing outcome was the association between NNN participation and sexual flexibility. Rather than abstinence causing a change, it appears that a pre-existing characteristic (being more sexually open and flexible) may instead predispose individuals to participate in such challenges.
Could everyday plastic chemicals in pregnancy quietly influence your child’s brainpower? New Canadian research uncovers subtle links between prenatal phthalate exposure and preschool IQ, with boys especially at risk.
Study: Prenatal exposure to phthalates and preschool children’s intellectual scores: Effect modification by child sex. Image Credit: Sibirian sun / Shutterstock
In a recent study published in the journal Environment International, a group of researchers tested whether prenatal phthalate metabolites, individually and as a mixture, forecast preschool Full Scale Intelligence Quotient (FSIQ), Performance Intelligence Quotient (PIQ), and Verbal Intelligence Quotient (VIQ), and whether these links vary by child sex and specific cognitive domains.
Background
Picture a daycare circle where plastics may whisper into growing brains. Phthalates (plasticizers used in flooring, food wrappers, and cosmetics) cross the placenta and disrupt thyroid and sex steroid signals that guide neurodevelopment. Canadian surveys show almost every expectant mother carries these chemicals, yet studies on child intelligence report mixed results and seldom evaluate mixtures.
Meta-analytic hints of greater male susceptibility in specific cognitive domains, uncertain mechanisms, and shifting phthalate replacements deepen the puzzle. Because IQ shapes lifelong achievement and equity, the stakes are societal.
Robust cohort studies that use repeated biomonitoring and advanced mixture modeling are essential. Ongoing research should track phthalate exposures in modern, diverse populations.
About the study
The present analysis used 511 singleton mother–child pairs from the Maternal-Infant Research on Environmental Chemicals (MIREC) study, which recruited women before 14 weeks’ gestation in ten Canadian cities between 2008 and 2011 and followed children to age four.
Spot urine collected at 6–13 and 16–21 weeks was assayed via ultra-performance liquid chromatography–tandem mass spectrometry for 20 phthalate metabolites detected in at least 40 percent of samples. Concentrations were specific-gravity corrected and averaged; molar sums represented parent compounds such as di-isodecyl phthalate (DiDP). Intraclass correlation coefficients gauged stability between trimesters.
Intelligence was assessed with the Wechsler Preschool and Primary Scale of Intelligence, Third Edition (WPPSI-III), yielding FSIQ, PIQ, and VIQ normed to 100. Multiple linear regression quantified the change in each IQ domain per doubling in metabolite concentration, adjusting for site, maternal age, country of birth, smoking, socioeconomic status (SES), and Home Observation Measurement of the Environment (HOME) score; interaction terms explored modification by child sex.
Weighted Quantile Sum (WQS) regression with repeated holdout validation and bidirectional indices summarized the joint influence of nine correlated metabolites. Sensitivity checks incorporated maternal Body Mass Index (BMI) and restricted analyses to metabolites detected in ≥ 70 percent of samples, while replacing ΣDiDPm with its dominant metabolite (MCiNP).
Study results
Mothers averaged 33 years, 83 percent were Canadian-born, and only 4 percent fell below the low-income threshold; HOME scores (mean = 47/55) reflected enriched caregiving. Children tested at a mean age of 3.4 years scored slightly above the population norm (FSIQ = 106.9, PIQ = 103.2, VIQ = 109.3).
Detection frequencies ranged from 42 percent to 99 percent, and geometric means for summed phthalate groups spanned 0.27 µg/L for the sum of DiDP metabolites (ΣDiDPm), driven primarily by MCiNP (89 percent detection), to 59.9 µg/L for the sum of di-n-butyl phthalate metabolites (ΣDnBPm). Intraclass correlations between trimesters were modest (0.14–0.38), indicating within-person variability.
In single-metabolite regression, every doubling in ΣDiDPm was associated with lower scores in all domains (FSIQ = −0.6, PIQ = −0.6, VIQ = −0.5 points). Monomethyl phthalate (MMP) showed the opposite pattern, predicting gains of 1.6–1.7 points across domains, while mono-benzyl phthalate (MBzP) correlated with a 1.0-point rise in PIQ. No other parent-compound sums or individual metabolites were significant.
Striking sex–domain interactions emerged: the inverse ΣDiDPm–VIQ association was exclusive to boys (−1.1 points per doubling) and statistically significant (p interaction = 0.04), whereas the positive MMP–PIQ link appeared only in girls (+3.2 points per doubling, p interaction = 0.024). Similar but non-significant heterogeneity emerged for MEP–VIQ (p interaction = 0.099).
Bidirectional WQS regression, integrating nine correlated metabolites into positive and negative indices, yielded no significant mixture effects on any IQ scale, and heterogeneity tests showed no sex-specific mixture vulnerability. Trimester-specific models echoed the main findings but lost statistical significance, likely owing to reduced precision from single-spot samples.
Sensitivity checks that adjusted for maternal BMI or substituted ΣDiDPm with MCiNP amplified the negative PIQ association (−1.35 points), confirming robustness. Notably, ΣDiDPm showed effects despite the lowest exposure levels (0.27 µg/L) among measured phthalates.
When geometric means were stratified by fetal sex, mothers carrying boys had significantly higher urinary concentrations of the sum of di-iso-butyl phthalate metabolites (ΣDiBPm, p = 0.02) and mono-3-carboxypropyl phthalate (MCPP, p = 0.03), mirroring patterns reported in other birth cohorts.
Across analyses, mixture coefficients hovered near zero, suggesting that opposing effects of individual metabolites (e.g., MMP↑ vs. ΣDiDPm↓ IQ) may cancel composite impacts.
Collectively, the data point to DiDP as a potential developmental neurotoxicant and highlight the need for sex-stratified risk assessment. Although point changes appear modest, a one-point population shift in FSIQ can push thousands of children above or below educational thresholds, underscoring public health relevance.
Conclusions
To summarize, results indicate prenatal DiDP exposure may slightly lower preschool FSIQ, with boys showing VIQ vulnerability, whereas MMP and MBzP show small positive links requiring confirmation. Caution is warranted as DiDP effects largely reflect its MCiNP metabolite, and low exposure levels (0.27 µg/L) suggest heightened neurotoxicity potential.
Even minor IQ shifts influence classroom placement, lifetime earnings, and population health, underscoring the need for prevention. Simply swapping plasticizers is not inherently safer; regulators and industry should reassess DiDP neurotoxicity and expedite truly benign substitutes.
Parents can curb phthalate uptake by limiting food-contact plastics and fragranced items. Cohort research employing repeated biomarkers, diverse populations, and mixture-aware models is essential to clarify causality and guide evidence-based policy.
Worldwide, reducing phthalate burdens remains a public health priority.
Journal reference:
C.V. Goodman, C. Till, S. Berghuis, J.M. Braun, G. Muckle, A. Chen, Y. Oulhote, B. Lanphear, J. Ashley-Martin, T.E. Arbuckle. (2025). Prenatal exposure to phthalates and preschool children’s intellectual scores: Effect modification by child sex. Environment International. DOI: 10.1016/j.envint.2025.109701 https://www.sciencedirect.com/science/article/pii/S0160412025004520
Sweetened dairy is a source of added sugar in the diet, so opt for unsweetened when you can.
Dairy contains protein, calcium, phosphorus and potassium to support overall health.
Use dairy in a variety of recipes from smoothies and desserts, to main dishes and sandwiches.
If you’ve ever eaten a spoonful of flavored yogurt, you know just how sweet it can be. Most dairy products contain some sugar because lactose—aka milk sugar—is a sugar. However, naturally occurring lactose is considered a natural sugar. But some varieties of dairy products—yogurts, ice cream, kefir, cottage cheese—might also contain added sugars if they’re flavored. After all, sweetened dairy products are one of the top sources of added sugar in our diet, but unsweetened dairy provides many essential vitamins and minerals. “Dairy is a fantastic source of micronutrients that support bone health, including calcium, vitamin D and phosphorus,” says Kerry Conlon, M.S., RD, a dietitian specializing in gastrointestinal diseases and disorders. If you’re looking to reduce your intake of added sugar, you don’t have to give up dairy. Instead, opt for dairy foods that are free of added sugar. That way you’ll get all of the protein and bone-fortifying and muscle-growing nutrients minus the sweet stuff. Here are six dairy foods that are low in sugar—and delicious ideas for incorporating them into your routine.
1. Plain Greek Yogurt
Nonfat or low-fat plain strained Greek-style yogurts are high in protein and are lower in saturated fat. “It’s a great substitute for sour cream and can easily be added to a variety of meals and snacks to increase protein and calcium intake,” says Eliza Whitaker, M.S., RDN, a registered dietitian and medical nutrition advisor at Dietitian Insights. Protein in dairy is important for growth, immunity, tissue repair and hormone production. Studies show that regularly consuming dairy products positively impacts muscle mass in middle-aged and older adults. That’s especially important because muscle mass declines with age, which is linked to reduced physical function.
What’s more, most Greek yogurts contain probiotics that support gut health. “Probiotics can help reduce inflammation and bloating and promote regular bowel movements,” says Conlon.
Research suggests that consuming yogurt and other fermented milk products is associated with a reduced risk of colorectal cancer, breast cancer and type 2 diabetes, along with improved bone, gastrointestinal and cardiovascular health.
One container (150 grams) of unsweetened nonfat plain Greek yogurt contains 5 grams of natural sugar and 15 grams of protein. Rather than buying a flavored yogurt, mix in your favorite fresh fruit at home for added fiber and vitamins.
2. Kefir
It’s time to pour yourself a glass of this probiotic sip. “Kefir is a nutrient-dense, fermented dairy product offering several scientifically backed health benefits,” says Julia Trifan, M.S., RD, a research dietitian at Children’s Hospital Los Angeles.
Kefir is rich in probiotics and also has anti-inflammatory properties. According to research, kefir can reduce the production of several proinflammatory proteins in the body, helping decrease inflammation and reduce the risk of complications from viruses, Trifan explains.
One cup of plain kefir contains 7 grams of natural sugar and 10 grams of protein. Try it by itself or use it as the base of a smoothie.
3. Cottage Cheese
“Another versatile, low-sugar dairy product is cottage cheese,” says Whitaker. One cup of low-fat cottage cheese contains 9 grams of natural sugar and 24 grams of protein.
Protein is used in the body for muscle building and maintenance, as well as enzyme and hormone production, proper immune system function, and fluid and electrolyte balance. “It’s also satiating and can leave you feeling full for longer. Plus, increasing protein intake above the recommended daily allowance may be beneficial for maintaining a healthy weight,” Whitaker adds. You can calculate how much protein you need to eat every day using our handy tool.
4. Milk
Milk is one of the most nutrient-dense and balanced foods there is. It contains protein, carbohydrates and dietary fat. (Unless you buy skim milk, of course.)
One 8-ounce glass of 1% milk provides about 8 grams of protein and 12 grams of sugar and provides calcium, vitamin D and potassium. “Potassium found in dairy products supports heart health, adequate hydration and fluid balance and helps prevent hypertension, stroke and kidney stones. Low potassium intake may contribute to impaired glucose tolerance and increase the risk of developing type 2 diabetes,” says Whitaker.
While the sugar content might seem high, all of the sugar in milk is from naturally occurring lactose, and there are no added sugars in unflavored milk.
5. Ricotta Cheese
Ricotta cheese is naturally low in sugar, making it a great choice for those looking to reduce their sugar intake while still enjoying rich and creamy textures.
Ricotta cheese is made from whey, the liquid by-product of cheese production, so it only has small amounts of lactose, the natural sugar found in milk. Ricotta is also packed with high-quality protein and calcium. One ½-cup serving of low-fat ricotta cheese has 12 grams of protein and 6 grams of natural sugar.
Incorporating ricotta into your diet can enhance both sweet and savory dishes, adding nutritional value without the extra sugar.
6. Hard Cheeses
Hard cheeses like Cheddar, Swiss and Parmesan are also excellent low-sugar dairy options that can be enjoyed regularly. They undergo a longer aging process that breaks down most of their lactose. This not only may make them suitable for individuals with lactose intolerance, but it also makes them lower in sugar. A 1-ounce (about ¼ cup grated) serving of Parmesan contains 8 grams of protein and 0 grams of sugar.
Hard cheeses also provide protein and calcium, along with other essential nutrients like phosphorus and vitamin A. They make a great addition to many meals and can be added to fruit or crackers to make a balanced snack.
Low-Sugar Dairy Recipes to Try
Our Expert Take
Dairy products are a great source of protein, calcium, vitamin D and other nutrients, and there are health benefits of eating dairy every day. While dairy contains lactose, a sugar naturally found in milk, you can easily find low-sugar dairy products to incorporate into meals and snacks. Enjoy plain varieties of strained Greek-style yogurt, cottage cheese, kefir, ricotta, milk and hard cheeses. There’s a lot of internet chatter claiming that dairy is inflammatory, with recommendations to avoid it. However, there’s evidence that eating dairy may help reduce inflammation. “The only reason one should avoid dairy is if they have a milk protein allergy or lactose intolerance, and even people with lactose intolerance can still enjoy some dairy products,” says Conlon.
Samoa’s Ayres Ava on attack against the Cook Islands during the OFC 2024 Under-16 Women’s Championship in Fiji. Photo: Kirk Corrie / Phototek.nz
Samoa’s football federation (SFA) says they have taken measures to ensure players and officials participating in the upcoming Oceania Football Conferderation (OFC) 2025 Under-16 Women’s Championship is not affected by the recent dengue fever outbreak in the the country.
A statement from SFA said officials have worked with hotels that will house teams to assess their preparedness for safeguarding guests.
“In light of the recent dengue fever outbreak in Samoa, we proactively visited each hotel where our team will be staying over the weekend to assess their preparedness for safeguarding guests against this health concern,” it stated on Monday.
“We were pleased to discover that the hotels have implemented several comprehensive measures.
“They have already conducted thorough spraying to eliminate potential mosquito breeding grounds, each room is equipped with repellent, ensuring guests have easy access to protection while they relax.
“Hand sanitisers will be readily available throughout the premises, promoting good hygiene practices and the hotels are committed to maintaining a clean and safe environment, offering peace of mind to everyone staying with them.
“These proactive steps reflect a strong commitment to guest safety and well-being during our visit.”
The OFC Under-16 tournament kicks off in Apia on Friday, with eight teams competing. They include Fiji, American Samoa, Samoa, New Zealand, New Caledonia, Tahiti, Solomon Islands and Tonga.
The OFC is expected to update teams on Wednesday about the risks and status.
Local media Taumua Online reported on Tuesday that schools have closed this week as close to 16,000 dengue fever cases have been recorded so far.
The online website said a fumigation operation resumed this week covering all Samoa schools along with other high-risk areas as part of a nationwide dengue response.
This is in addition to a national clean-up campaign last Saturday, mobilising villages and communities to clean their surroundings and eliminate mosquito breeding grounds as part of the nationwide dengue response.
Deputy Director of the Pediatric Ward at the Tupua Tamasese Meaole (TTM) hospital Ulugia Dr Tito Kamu confirmed cases continue to rise and the most vulnerable age group is from 1 to 15 years old, the outlet reported.
He said that the hospital is managing and they have to pull-in public health doctors and call-in senior doctors on call to assist.
A study published in Thorax looks at ultra-processed food (UPF) consumption and the risk of lung cancer.
Prof Kevin McConway, Emeritus Professor of Applied Statistics, The Open University, said:
“I have to confess that my heart rather sank when I got the request from SMC to comment on this study. That’s not because it’s complicated, and not even because it’s a particularly bad study of its type. It’s just that it’s yet another of a class of studies about ultra-processed foods (UPFs) that, in my view, are doing nothing much to advance what is known about associations between the consumption of UPFs and human health. I’m well aware that studies with other kinds of methodology are going on – I just wish that researchers would concentrate more on those other types of research, instead of repeatedly cranking the handle of doing studies like this one.
“The type of study that I’m getting sick of seeing goes like this. The researchers find an existing large observational study, that involves a cohort of people, and for which the data have been made available to other researchers on application. Many of the cohort studies involved took place in the UK or the USA. Of course it’s generally a good thing that data from big studies is made available for other research, but that doesn’t mean that all the research you can do with this secondary data is necessarily very useful.
“Typically, the researchers wouldn’t have been involved in the original study whose data they are using, and often are based in an entirely different country. In this case, the original study was in the USA, and all but one of the researchers is based in China (with one being at Harvard).
“To be useable for a study aiming to examine the association between consumption of UPFs and some health outcome, the original study has to have recorded information on what the participants eat, and then has to follow them up reasonably systematically, and record the health outcome. It also has to record other potentially relevant information about the participants.
“The outcome – in this case a diagnosis of lung cancer, but in other studies it might be death from a particular cause or from all causes – typically might take a long time to develop, so the participants have to be followed up for a long time. (In the case of this new study, the average length of follow-up was over 12 years.)
“Make no mistake – although the cohort used in this new study comes from a randomised trial of cancer screening, the so-called PLCO Cancer Screening Trial, the new study is observational. That’s because the exposure of interest – how many UPFs the participants said they consumed – wasn’t allocated to them at random. The participants themselves chose what to eat and drink.
“The trouble with observational studies like this is that each one of them, on its own, might find an association, that is, a correlation between what people eat in the way of UPFs, and the risk of the health outcome of interest. But it can’t tell you whether that association is one of cause and effect. That’s because there will typically be many other factors that differ between the groups that consume different amounts of UPFs. These are called potential confounders or potential confounding factors – if one or more of them happens to be associated also with people’s risk of the health outcome, then the potential confounders might be the cause of the association with the health outcome, and not the participants’ UPF consumption at all.
“It’s possible to make statistical adjustments to try to allow for potential confounders, but that process isn’t definitive – you can never be sure that you have adjusted for all the potential confounders, so you can never be sure about cause and effect. That’s why this study, like any decent study of this general type, points out that it can’t establish what is causing what.
“In this particular new study, for instance, although the researchers made adjustments for participants’ smoking status (that is, whether they were current smokers, past smokers, or never smoked), they did not adjust for the amount that people smoked, and they point out that this is a limitation of the study and may potentially lead to biases. (Actually it seems strange that they did not make that adjustment, since my reading of the information about the underlying clinical trail (at https://cdas.cancer.gov/plco/) indicates that information on the amount people smoked was collected and available.) And we certainly can’t assume that no other potential confounders were omitted from the adjustments. (See also point 1 in Further Information below.)
“If there were lots of other studies looking at associations between UPF consumption and lung cancer risk, including studies on the actual mechanisms by which the cancer might be caused by the foods, we might eventually get to a conclusion about cause and effect. But the researchers on the new study are proud to point out its novelty, so we’re clearly nowhere near that position yet.
“The new study certainly doesn’t rule out the possibility that eating larger quantities of UPFs cause increases lung cancer risk, but it doesn’t come near to establishing that this cause and effect really exist. That’s why I feel it has told us rather little.
“Studies of this general type very often have two other important limitations, to do with the measurement of people’s consumption of different foods and drinks, and they both apply to this new study (and indeed are mentioned as limitations by the researchers). Because a long follow-up period is needed, and because the definition of ultra-processed foods did not emerge until 2009, the questionnaires used to measure people’s consumption of foods and drinks used in the underlying cohorts were very often not designed to measure UPF consumption. That certainly applies to the PLCO Cancer Screening Trial that provided data for this new study. It recruited participants between 1993 and 2001, and recorded their diets between 1998 and 2001. (See also point 2 in Further Information below.) Also, often, and certainly in this case, the participants’ diets were recorded only once during their participation, so the new study cannot take account of any changes of diet.
“I have done some calculations (using https://realrisk.wintoncentre.uk/) to give what, I hope, is a clearer view of the actual size of the risk associated with consuming greater amounts of UPFs. A relevant point is that, despite the fact that the new study uses data from over 100,000 participants in the underlying PLCO Trial, most of them were not diagnosed with lung cancer during the 12 years of follow-up. Somewhere between 1 and 2 in every 100 of them got lung cancer during follow-up. Thus the estimates of difference in lung cancer risk between the groups that consumed different amounts of UPFs are subject to quite large statistical margins of error.
“In a group of 1,000 people who are just like the quarter of participants that consumed the lowest levels of UPFs, less than one serving per day on average, about 11 would get a lung cancer diagnosis in a 10-year period. Now consider another group of 1,000 people, who are just like the first 1,000 in terms of all the factors used for statistical adjustment in the researchers’ calculations, except that they all consumer UPFs at a rate like those of the highest quarter in the study (so more than 3.7 servings per day, on average). If the differences in lung cancer risk are due to the higher UPF consumption, and I repeat that this study just can’t establish that, then we’d expect about 15 cases of lung cancer in the second, high-UPF group of 1,000. That’s just 4 more than in the low-UPF group, despite the large difference in UPF consumption between the groups. The statistical uncertainty means that that number could plausibly be greater or smaller – between 3 and 6 more lung cancer cases in the high-UPF group than the low-UPF group of 1,000 people. So even if the higher UPF consumption was somehow known to be what causes the increased risk (and, remember, this can’t be known from this type of study), arguably the increase isn’t all that large anyway.
“Studies of this kind also usually can do little or nothing directly to investigate how high UPF consumption might possibly cause an increase in health risk, and that’s the case in this new study. The authors make suggestions on how high UPF consumption could potentially increase the risk of lung cancer, but these suggestions are based on other previous studies at best, and don’t come from the new data analysis.
“The press release repeats the suggestion in the research paper that the compound acrolein is known to be a toxic component of cigarette smoke, and that (of course) it is well known that cigarette smoke increases lung cancer risk. It also mentions that acrolein is found in grilled sausages and caramel sweets, which would generally be counted as UPFs. But it appears* that acrolein is found in many food substances, including some that would not be counted as UPFs. In any case, the data behind the new research did not make any measurements of acrolein.”
Further information
The following points are more technical.
The researchers calculated what’s called an E-value, to give a measure of how strong the effect of a single potential confounder, not included in their adjustments, would have to be in order to wipe out the observed association between UPF consumption and lung cancer risk. They point out that the E-value implies that a single potential confounder would need to have a stronger effect than smoking status to overturn their observed association. However, you have to remember that they left out smoking amount as a factor to adjust for, and that might have a strong effect in addition to smoking status. Also E-values look only at the effect of one omitted confounder at a time – there could be several of them, whose combined effect could be great enough to overturn the observed association. We simply can’t tell.
The new research paper reports that the Diet History Questionnaire (DHQ) used in the underlying study to measure diet, was validated in four 24-hour dietary recalls. But the study on the 24-hour recalls, reference 16 in the new research paper, was not part of either the underlying PLCO Cancer Screening Trial nor the new research. It was based on research carried out in 1997, before the PLCO trial began to collect diet information from the DHQ, and its aim was to investigate how closely DHQ results matched those from detailed 24-hour food recalls, which were considered more accurate. That study found that the correlation between food components measured by the DHQ and by the dietary recalls was only about 0.5, meaning that the DHQ results explained only roughly a quarter of the variability in the more accurate dietary recalls. However, I am no expert on dietary measurement and you’d need to check with dietitians to check this concern.
* ‘Origin and fate of acrolein in foods’, Jiang et al. https://www.mdpi.com/2304-8158/11/13/1976 , though my own expertise does not extend to knowing how dangerous (if at all) these amount of acrolein would be to health.
Prof Sam Hare, Consultant Chest Radiologist, Royal Free London NHS Trust, said:
“A quarter of lung cancer cases occur in non-smokers so we do need research exploring whether other factors are associated with lung cancer. We also know immunity is linked to cancer biology so it is a good idea to do research into factors like diet.
“However, further work is needed to establish direct causation between UPFs and lung cancer. Crucially, whilst the study does make some adjustments for smoking status, the amount of smoking is not factored in, which is known to be directly related to lung cancer development. Dietary habits also change considerably over the course of such long term studies. As such, it is difficult to directly conclude that lung cancer is related to the level of UPF consumption alone given it was only declared at the start of the study.
“That said, given the relative dearth of information on non-smoking related risk factors in lung cancer, it is important that the scientific community conducts more studies like this – we need genuine evidence-based advancement in the early diagnosis of lung cancer in non-smokers, but this study isn’t quite able to give us the answers yet.”
Rachel Richardson, Acting Head of Methods Support, The Cochrane Collaboration, said:
“This is a well-conducted observational study, but there are some important factors to bear in mind when considering any wider implications.
“Firstly, this study uses data from a series of trials of screening conducted amongst older adults living in the USA. It is very likely that regulations governing food (for example, permitted additives) are different from those in the UK, which means that American diets are likely to be different from ours in the UK. The fact that this study only included people aged 55-74 also limits the extent to which the findings may be relevant to younger people.
“Secondly, because this study uses data that were originally collected for a different purpose, the information they have is limited in terms of the research question they are trying to answer. A significant limitation is that information on food intake was only collected once which does not reflect the fact that diets change over time. The authors also do not seem to have had information on other factors that are related to lung cancer, for example, exposure to air pollution or second-hand smoke – these are likely to be confounding factors.”
Dr Adam Jacobs, Executive Director and Strategic Consultant, Biostatistics, Ergomed, said:
“Wang et al found a statistically significant association between ultra-processed food (UPF) consumption and lung cancer. This association was strong enough to be clinically relevant, with a 41% increased risk of lung cancer in the highest quartile of UPF consumption compared with the lowest – owever, the important question is whether this association is causal, in other words whether it is the UPF consumption itself that drives the risk of lung cancer or whether people with high UPF consumption are more likely to be at increased risk of lung cancer for other reasons.
“The most obvious confounding factor here is smoking, which is well known to cause a greatly increased risk of lung cancer. If people with high UPF consumption smoked more than people with low UPF consumption, then that difference in smoking could easily lead to the observed results. Although Wang et al attempted to adjust for smoking in their analysis, their adjustment was very crude: they categorised participants into only 2 categories: current or former smokers, and non-smokers (assessed by self report). If people in the high UPF consumption group were more likely to be current smokers rather than former smokers, or smoked more cigarettes per day, or were more likely to have claimed to be non-smokers when in fact they were smokers, then none of these factors would have been captured in the analysis. Wang et al correctly identify this limitation themselves in the paper.
“Without more detailed adjustment of their statistical model for smoking intensity, it seems unsafe to conclude that the observed association between UPF consumption and lung cancer risk was a causal effect of the UPF consumption, and confounding by smoking also seems a plausible explanation of the results.”
Prof Tom Sanders, Professor emeritus of Nutrition and Dietetics, King’s College London, said:
“This an analysis of data collected in the United States comparing diet and lifestyle and subsequent development of lung cancer. The authors claim to find about a 0.4 fold increase in risk of lung cancer associated with the highest ultraprocessed after adjusting for other risk factors. This could be entirely due to residual confounding due to poorly recorded exposure to tobacco as well as occupational exposure to inhaled carcinogens.
“Other studies show that smoking is an enormous cause of lung cancer, increasing risk 12 fold. The statistical analysis only includes current/previous smokers without detail in terms of number of pack years of smoking. It also does not ascertain properly current smokers because individuals are known to lie about smoking habit. A test such as plasma or urinary cotinine is needed to check for smoking status. Unhealthy diets often go hand in hand with smoking habit and low socioeconomic status. But there appears to be no plausible mechanism to explain why ultraprocessed food should affect risk of lung cancer.”
‘Association between ultra-processed food consumption and lung cancer risk: a population-based cohort study’ by Kanran Wang et al. was published in Thorax at 23:30 UK time on Tuesday 29 July 2025.
DOI: 10.1136/thorax-2024-222100
Declared interests
Prof Kevin McConway: “I don’t have any relevant interests to declare.”
Prof Sam Hare: “No conflicts of interest directly relevant to this work. I am a past National Specialty Adviser to NHS England for Imaging. I am CEO and co-founder of the HLH Imaging Group Limited.”
Rachel Richardson: “I have no interests to declare.”
Dr Adam Jacobs: “No competing interests to declare.
Ergomed is a contract research organization: https://ergomedcro.com/.”
Prof Tom Sanders: “I have received grant funding for research on vegans in the past. I have been retired for 10 years but during my career at King’s College London, I formerly acted as consultant for companies that made artificial sweeteners and sugar substitutes.
“I am a member of the Programme Advisory Committee of the Malaysia Palm Oil Board which involves the review of research projects proposed by the Malaysia government.
“I also used to be a member of the Scientific Advisory Committee of the Global Dairy Platform up until 2015.
“I did do some consultancy work on GRAS affirmation of high oleic palm oil for Archer Daniel Midland more than ten years ago.
“My research group received oils and fats free of charge from Unilever and Archer Daniel Midland for our Food Standards Agency Research.
“I was a member of the FAO/WHO Joint Expert Committee that recommended that trans fatty acids be removed from the human food chain.
“Member of the Science Committee British Nutrition Foundation. Honorary Nutritional Director HEART UK.
“Before my retirement from King’s College London in 2014, I acted as a consultant to many companies and organisations involved in the manufacture of what are now designated ultraprocessed foods.
“I used to be a consultant to the Breakfast Cereals Advisory Board of the Food and Drink Federation.
“I used to be a consultant for aspartame more than a decade ago.
“When I was doing research at King’ College London, the following applied: Tom does not hold any grants or have any consultancies with companies involved in the production or marketing of sugar-sweetened drinks. In reference to previous funding to Tom’s institution: £4.5 million was donated to King’s College London by Tate & Lyle in 2006; this funding finished in 2011. This money was given to the College and was in recognition of the discovery of the artificial sweetener sucralose by Prof Hough at the Queen Elizabeth College (QEC), which merged with King’s College London. The Tate & Lyle grant paid for the Clinical Research Centre at St Thomas’ that is run by the Guy’s & St Thomas’ Trust, it was not used to fund research on sugar. Tate & Lyle sold their sugar interests to American Sugar so the brand Tate & Lyle still exists but it is no longer linked to the company Tate & Lyle PLC, which gave the money to King’s College London in 2006.”
