Matthew Broberg-Moffitt, 37, remembers the first Christmas clearly. He was 16 years old and was helping his grandmother cook in the kitchen of their home in Nebraska, US. She asked him to taste the gravy she was making and tell her whether it needed seasoning. But he couldn’t bring himself to put the spoon in his mouth. Two decades later, he still has that feeling. Last year, when his mother-in-law took over a stuffing he was making, he felt so upset he had to leave the festivities for the day.
Broberg-Moffitt has had a non-specified eating disorder since late childhood and says, like many with disordered eating, that the festive period – with its intense focus on food, alcohol, treats and overindulging – is particularly difficult. In order to deal with it he tries to be involved in the preparation of food, so he can control what goes into the dishes. Pretending to snack while cooking is also an excuse he uses if he doesn’t want to eat later.
Daniela Beck, from Woking, was diagnosed with anorexia in 2017 and also makes sure she is in charge of cooking at Christmas to manage her food-related anxiety. “I find it easier that way,” she says. The 23-year-old also practices eating the components of her Christmas meal in the weeks before, and asks family not to gift her any food or clothes. But the hardest bit? The narrative of over-indulging and then dieting in January. “You have to participate and then a week later are told to go on a diet because you were ‘naughty’ at Christmas,” she says.
Download the new Indpendent Premium app
Sharing the full story, not just the headlines
There are approximately 1.25 million people in the UK with an eating disorder, according to BEAT, the UK’s largest dedicated charity. The disorders affect predominantly girls and young women between the ages of 12-20, but men also make up 25 per cent of sufferers. Recent research from the NHS information centre showed up to 6.4 per cent of the population displayed signs of an eating disorder.
Although eating disorders can be triggered at any time in the year, many with conditions like anorexia or bulimia – which the NHS says are characterised by people to try and restrict their weight – can find Christmas particularly challenging. “With such an intense focus on food and family, Christmas can be an understandably difficult time for people managing an eating disorder,” Sarah Murphy, associate director for advice at Rethink Mental Illness, tells The Independent.
Caroline Price, director of services at BEAT says she often sees people particularly struggling in December. “The Christmas period can be extremely difficult for people with all kinds of eating disorders. The pressure to eat large amounts can be triggering for people with binge eating disorder and bulimia, as well as causing anxiety for people with anorexia.”
“Christmas itself doesn’t trigger my eating disorder but the opportunity to be triggered is much more than usual because of all the things that are associated with the holiday,” says Jason Fisher from Manchester who has had binge eating disorder since he was 10. Although the 20-year-old loves Christmas – “I put my tree up on 1 November” – his coping techniques, like meal prepping, are hard to maintain with lots of spontaneous meals out and abnormal treats like advent calendars. “I find myself sneaking extra food during the holidays, and one Christmas I just spent lying on the floor night after night full of nothing but hatred for what I was,” he says. “I desperately wanted some help and support for how I was feeling.”
Some people find the period so hard they create ways to remove themselves from the festivities entirely.
Sophie Smith, 28, from London, who suffers from periodic anorexia and recurrent bulimia says she would purposefully ask for more shifts in her bar job in the weeks leading up to Christmas, so that she could avoid socialising and therefore reduce her calorie intake. She would also spend long parts of Christmas Day in bed asleep for the same reason. “It was a safe way to remove myself from these situations without being judged or questioned,” she explains.
Others find that they are unable to cope at home and are admitted to hospital or a treatment programme over the period. Rebecca Quinlan, 31, from Chelmsford in Essex, who was diagnosed with anorexia in 2008, had to spend several Christmases in hospital because of how extreme her eating disorder became around the holiday period.
Before she was admitted she remembers getting up at 5am on Christmas morning to exercise in the kitchen for two hours, before anyone woke up. She worried having one extra Brussels sprout would make her gain weight, and would even stop herself smelling the food in case she “inhaled calories”. One year she got so angry at the portion of turkey served by her mum she threw the plate across the room in front of her family.
“[Christmas] was a stark reminder that while I thought I had been doing well and my eating disorder was getting smaller, actually it was still very much there,” she says. “I was so down the whole time because I was obsessing about what I was eating and how I could burn calories.”
Similarly, Hope Virgo, 29, from London, who was diagnosed with anorexia 16 years ago, says she remembers a Christmas that really showed her how far her illness had come to taking over her life. She was so determined to avoid eating she caused a scene at the dinner table and used the distraction to hide food in her pockets.
“I would shove it in to my pockets then empty it out later on when I had the chance. It was horrid looking back there was meat and gravy in the pockets of my jacket, dripping through. But I felt like it was the only way. Up until that point it had been fairly easy to go under the radar, but my family were on eggshells around me that Christmas.”
Ms Quinlan says what triggers her eating disorder at Christmas, more than food, is the perception that it is the “most wonderful time of the year”. She says: “I feel so far removed from this so Christmas heightens my feelings of sadness and loneliness.”
Ms Price, from BEAT, says this is common among those with eating disorders. “People with eating disorders often try to hide their illness and at Christmas when eating is a social occasion – often with people who they do not see frequently – they may feel ashamed and want to isolate themselves from others,” she says.
This emotional impact cannot be underestimated. Jodie, who did not want her surname to be used, 24, from Hertfordshire, was diganosed with anorexia in 2019 and says getting ready to spend her first Christmas with the eating disorder diagnosis is “terrifying”. “This year I don’t just feel stressed. I don’t just feel anxious. I feel absolutely terrified. I feel full of dread.”
Cara Sturgess, 29, from Hampshire, who has had anorexia for 17 years, also says that one of the most misunderstood parts of eating disorders is that it cannot be “switched off” just because the social calendar requires you eat and drink. She says: “We can’t pretend that everything is okay for the sake of Christmas.”
So how can the festive period be managed best for those managing eating disorders? Ms Price says for the sufferer themselves there are a few things they can do, including planning ahead and sharing concerns with those closest to them. “It’s important to plan ahead and openly discuss when and how food will be involved over the Christmas period.
“It can help to steer attention away from food, so once meals are over, find activities that focus on something else, such as a family walk, playing board games, or watching a funny film together.”
But more importantly, for family and friends, avoid comments such as ”don’t you look healthy?” or “haven’t you done well eating your dinner?” as these could be misinterpreted and cause more harm than good.
Ms Quinlan says people should try not to talk about over-eating. “This triggers my ED into panic mode and I [feel] I must never ever do that.”
Rebecca Lindley, 26, from Sheffield, who has had anorexia for 12 years, says: “Stop talking about the diet you’re going to go on in January and don’t use words like ‘bad’ or ‘naughty’ around food. This whole mentality makes people with ED feel that they can’t enjoy themselves around Christmas without making up for it later.”
Ms Murphy recommends that the most important thing for friends and family to do is show patience, love and understanding. “Accept that you might not understand everything that a loved one is going through. Instead positively reinforce your relationship with them as much as possible.”
If you have been affected by any of the issues mentioned in this article, you can contact the following organisations for support: the BEAT helpline on 0808 801 0677 or Mind on 0300 123 3393.
Brain aging differs with cognitive ability regardless of education | Scientific Reports – Nature.com
Higher general cognitive ability (GCA) is associated with lower risk of neurodegenerative disorders, but neural mechanisms are unknown. GCA could be associated with more cortical tissue, from young age, i.e. brain reserve, or less cortical atrophy in adulthood, i.e. brain maintenance. Controlling for education, we investigated the relative association of GCA with reserve and maintenance of cortical volume, -area and -thickness through the adult lifespan, using multiple longitudinal cognitively healthy brain imaging cohorts (n = 3327, 7002 MRI scans, baseline age 20–88 years, followed-up for up to 11 years). There were widespread positive relationships between GCA and cortical characteristics (level-level associations). In select regions, higher baseline GCA was associated with less atrophy over time (level-change associations). Relationships remained when controlling for polygenic scores for both GCA and education. Our findings suggest that higher GCA is associated with cortical volumes by both brain reserve and -maintenance mechanisms through the adult lifespan.
Does higher intelligence protect against brain atrophy in aging? Numerous findings motivate this question: General cognitive ability (GCA) is positively associated with brain volume and cortical characteristics at various life stages, including young adulthood and older age1,2,3,4,5. GCA is consistently associated with all-cause mortality and health, with higher GCA related to lower risk of diseases and lifestyle factors known to negatively affect brain health4. In part, associations are still found after controlling for factors such as educational attainment, suggesting that contemporary GCA in itself is of importance4. While higher education has been posited as a protective factor against neurodegenerative changes6,7, we recently documented in a large-scale study of multiple cohorts that education is not associated with rates of brain atrophy in aging8. A more promising candidate influence on brain aging may thus be GCA independently of education. Whether GCA level is predictive of longitudinal cortical change has primarily been investigated in older cohorts, and with mixed results9,10,11. The relationship of GCA level and cortical changes through the adult lifespan has to our knowledge hitherto not been investigated.
In this context, the lifespan perspective is critical and has implications for understanding functional loss in older age. Several studies indicate that people with higher GCA in young adulthood may be at lower risk of being diagnosed with neurodegenerative disorders in older age4,12,13. Recent findings from large datasets point to a relationship between family history of Alzheimer´s Disease (AD) and cognitive performance level four decades before the typical age of onset of AD14. However, GCA-AD risk associations have not been consistently observed, and mechanistic factors are poorly understood15. Possible explanations include both a brain reserve, i.e. “threshold model”16, as well as a brain maintenance17 account. The brain reserve model would entail that higher GCA as a trait is related to greater neuroanatomical volumes early in life, young adulthood inclusive, thus delaying the time when people fall below a functional threshold of neural resources in the face of neurodegenerative changes with age. This would happen even if such changes in absolute terms are of similar magnitude across different ability levels, i.e. slopes are parallel, indicating “preserved differentiation”18, where initial differences in young are upheld with age16,19. The brain maintenance17, or “differential preservation”18 account would on the other hand predict less brain change in adulthood for people of higher ability, and therefore a smaller risk of cognitive decline and dementia19. The brain reserve and maintenance accounts of the relationships between GCA, brain characteristics and clinical risk are not mutually exclusive, but their relative impact through the adult lifespan is unknown. Collectively, the current findings indicate a need to understand whether there is a relationship between GCA as a trait and brain changes, independently of education, over the adult lifespan.
We tested whether GCA predicted brain aging as indexed by cortical volume, area and thickness change measured longitudinally in 7002 MRI scans from several European cohorts covering the adult lifespan in the Lifebrain consortium20 and the UK Biobank (UKB)21,22 (n = 3327, age range 20–88 years at baseline, maximum scan interval of 11 years, see Online Methods for details). To disentangle possible environmental and genetic influences on the relationship between GCA and brain aging, we controlled for educational attainment in the main analyses, and in a second step for polygenic scores (PGSs) for education and GCA23,24. Established PGSs are only moderately predictive of GCA23, but in view of evidence that the polygenic signal clusters in genes involved in nervous system development23, we did expect such scores to explain part of the intercept effect, with no or weaker effects on brain aging. We expected any effects of GCA on cortical changes to apply to all ages, but in view of recent findings of greater relationships between brain and cognitive function in older than younger individuals3, we also tested the age interaction. Based on previous findings, including from broader cross-sectional Lifebrain cohorts25, and mixed results from smaller longitudinal older cohorts9,10,11, we hypothesized that GCA would be positively related to anatomically widely distributed cortical characteristics through the adult lifespan (intercept effect), but that associations with differences in cortical aging trajectories (slope effects) may be observed to a lesser extent. We expected effects of GCA to be at least partially independent of education8, both for intercept and slope associations.
The main models of associations of GCA with cortical characteristics, and their change, were run separately for samples within the Lifebrain consortium (n = 1129, 2606 scans)20 and the UK Biobank (UKB, n = 2198, 4396 scans)21,22, and then meta-analyses were run on the results, using the metafor package26. Using the estimate and standard error at each vertex, random effects meta-analyses were conducted at each vertex separately. In all main models, sex, baseline age, scanner, time (interval from baseline) and education were entered as covariates. In modeling the effects of GCA on cortical characteristics (level-level analyses), GCA was entered as the predictor (explanatory variable), whereas in modeling the effects of GCA on brain aging (level-change analyses), the interaction term of GCA × time was entered as the predictor, and education × time was entered as an additional covariate along with GCA and education. Since brain aging (i.e. change) was of chief interest, we did not include intracranial volume (ICV), which is stable, in the main analyses. For direct comparison, we also then present level-level analyses without controlling for ICV. This was also chosen given the paucity of evidence for region-specific associations, and previous studies indicating that neuroanatomical volume in and of itself, when controlling for sex, may be associated with GCA9,25. Results from models including ICV, as well as models without education, as covariates, can be found in the Supplementary Information (SI). Additional analyses included the interaction term baseline age × time as a covariate, and in one set of analyses we entered the interaction term baseline age × time × GCA as predictor (with relevant two-way interaction terms as covariates), to test if effects differ reliably across the lifespan.
GCA level: brain level analyses
Cluster p-value maps across Lifebrain and UKB for the relationship of GCA and cortical characteristics controlled for education, are shown in Fig. 1. For cortical volume and area, there were widespread positive associations of GCA bilaterally across the cortical mantle seen in all lobes. For area, significant effects were seen across 47.6% and 44.2% of the left and right hemisphere surface, respectively. For volume, similar numbers were 37.4% and 19.5% for left and right, respectively.
For cortical thickness, only minor positive effects were seen, in proximity of the left central sulcus, covering only 1.1% of the surface.
Results of analyses per sample, controlling and not controlling for education are shown in Supplementary Figs. 1 and 2. Effects were largely similar, though slightly more restricted spatially, when controlling, than when not controlling for education. When adding ICV as a covariate, the intercept effects for cortical volume and area in the meta-analysis shown in Fig. 1 became non-significant, with only a very small effect on cortical thickness in the left hemisphere remaining (see Supplementary Fig. 3), pointing to these being broad effects grounded in greater neuroanatomical structures in general, rather than being region-specific.
To show effect sizes, we calculated the effect of 1 SD increase in GCA on cortical volume. Across Lifebrain and UKB, 1 SD higher GCA was associated with 1.0% larger cortical volume. Effect size maps for level-level analyses showing the regional variation in effect sizes for each sample separately are shown in Supplementary Fig. 4. Effect sizes were numerically smaller in Lifebrain (0.6%) than in UKB (1.3%). Restricting the analyses to regions where significant effects were seen, 1 SD increase in GCA was associated with 2.0% larger cortical volume in Lifebrain and 1.6% larger volume in UKB, but please note that these latter effect sizes are inflated by being within significant regions. Similar analyses for cortical area showed that 0.8% larger area was associated with 1 SD higher GCA across the cortex, with effects being 0.6% in Lifebrain and 0.9% in UKB. Restricting the analyses to regions where significant effects were seen, 1 SD increase in GCA was associated with 1.6% larger cortical volume in Lifebrain and 1.2% larger volume in UKB, with the same caveat as above. For thickness, effects were minute: 0.06% across studies (Lifebrain 0.04%; UKB 0.08%). Within significant clusters (UKB only), the effects of 1 SD higher GCA was 0.8%.
GCA level: brain change analyses
Having confirmed the expected positive relationships between GCA and cortical volume and area controlled for education in terms of an intercept effect, we investigated the question of slope effects. Associations of GCA level at baseline and change in cortical characteristics, controlled for education, are shown in Fig. 2. As expected, effects were more spatially limited than those seen for intercept models, with only restricted regions showing significant relationships: Higher baseline GCA was associated with less regional cortical volume reduction in the left middle cingulate gyrus, a medial area around the central sulcus and a part of the lingual gyrus. The most extensive effects were seen for thickness change, where higher baseline GCA was associated with less thinning in regions corresponding to the volume effects, in addition to parts of the right anterior and lateral temporal cortex and an area in the most medial part of the intersection between the central sulcus and the superior frontal cortex. No associations with area change were observed Taken together, this means that the observed positive associations of GCA with volume change primarily reflect less cortical thinning with higher GCA. (See Supplementary Fig. 5 for result for each subsample separately).
Associations of GCA with cortical change were essentially unaffected by adding ICV as a covariate (Supplementary Fig. 6).
In order to illustrate the GCA-cortical change relationships, and to characterize consistency of effects across samples (UKB and Lifebrain), we plotted the generalized additive mixed model (GAMM) for the different GCA quintiles, from lowest to highest (Fig. 3), depicting change trajectories for average cortical volume and thickness within the regions showing significant GCA x time associations. Across samples, subgroups with higher GCA started with higher volume and had less volume loss over time. For instance, on average, people with maximum cognitive score in UKB are expected start out with a regional average cortical volume of 1.72 mm3 that would be maintained for the next three years, whereas those with the lowest GCA would on average start out with 1.64 mm3 and decrease to 1.61 mm3 over the next three years. Thus, the greatest GCA-associated differences in cortical volume are found in the intercepts (level), whereas differences in slope (change) are smaller in the follow-up period. For cortical thickness, the change trajectories were also very consistently ordered, but those with higher GCA did not uniformly have thicker cortex at first timepoint in these areas. Rather, differential rates of cortical thinning over time were critical in creating cortical thickness differences in these regions in aging. This was evident in both samples, but especially pronounced in UKB.
To further assess effect sizes, we created histograms of the vertex-wise distribution of effects of one SD higher GCA for each metric for absolute volume, area and thickness as well as their change, shown in Fig. 4. (For cortical distributions of such effect sizes per sample, see Supplementary Fig. 7). As can be seen, almost all vertices show positive level–level relationships between GCA and volume and area. For thickness, the distribution is only slightly shifted to the right of zero, confirming the weak GCA-thickness relationships. As for GCA level-brain change, the histograms showed that for area, effects were distributed almost perfectly around zero. For volume, there was a clear shift rightwards, meaning that higher GCA tended to be related to less volume reductions, but substantially less than for the offset effects. Cortical thickness showed the most rightward skewness of the distribution, much larger than for the offset results. Inspecting all histograms, it is clear that higher GCA is related to larger cortical volume and area, and less thickness change.
Influence of polygenic scores (PGSs) for GCA and education on the level-level and level-change associations
Next, we investigated whether effects were maintained when covarying for established PGSs for GCA and education in the UKB23,24. Fifty-two participants in the main models were excluded due to missing genetic data. In these analyses, we regressed out the first ten genetic ancestry factors (GAFs) from the GCA variable prior to analysis. The intercept associations of GCA and cortical characteristics that were observed in the main model (Fig. 1) largely remained when controlling for the PGSs, but the extent of the significant regions were somewhat reduced for cortical volume and area (Supplementary Fig. 8). The associations of GCA and cortical change largely remained and were only slightly attenuated when controlling for PGSs for GCA and education (Fig. 5; compare to UKB results in Supplementary Fig. 5).
Influence of age on the level-change associations
We next tested the three-way interaction baseline GCA × baseline age × time, to see whether the level-change associations differed reliably across the lifespan. Significant interaction effects were seen for change in small regions of the left hemisphere, mostly laterally for volume, and for slightly more extended regions, for cortical thickness (see Fig. 6).
The positive three-way interactions of baseline GCA × baseline age × time indicates that higher level of GCA is associated with less atrophy at distinct ages. To visualize these interaction effects, we divided the cohorts according to whether participants were above or below age 60 years. This division point was chosen in view of it being an approximate age at which select cognitive and regional cortical volume and thickness changes have been reported to accelerate in longitudinal studies27,28. In order to explore how GCA level related to cortical thickness change over time across the two age groups, we plotted the expected cortical change trajectories, within the significant regions shown in Fig. 6, as a function of GCA, with each sample divided into quintiles, from lowest to highest GCA. The plots are shown in Fig. 7. While GCA level was weakly, and in Lifebrain even inversely related to atrophy in these regions in the younger group, the expected trajectories for the older group were relatively consistently ordered so that persons with a higher GCA level had less decline, especially of cortical thickness. The GCA quintile differences are more pronounced in the older group, suggesting the latter half of the lifespan is driving the interaction. As one outlier in the older group in Lifebrain was noted as having a high cortical thickness value for age at the first timepoint in the region of interest, we carefully checked this segmentation, but found no sign of flawed segmentation, and thus decided to keep this person in analyses.
The current study provides novel findings on GCA not only as a marker of brain characteristics, but also of brain changes in healthy aging. The finding that higher GCA level is associated with larger neuroanatomical structures to begin with, i.e. greater brain reserve, confirms findings in previous studies of various age groups1,2,3,4,25,29. While level of GCA has been associated with cortical change in some older groups10,11, but not others9, the current demonstration of an association of GCA levels, controlled for education, on cortical volume and -thickness declines through the lifespan in multiple cohorts across a relatively long follow-up time, constitutes a novel finding. Also, the finding of an age-interaction with pronounced effects of GCA on cortical thinning and volume changes only in older ages in select regions, is novel.
The association of GCA level and cortical change appears relatively moderate. This may explain why such associations have not previously been consistently found. The “effect” of GCA on cortical change must be viewed in relation to the intercept effects, which, as shown here, constitute a major source of GCA-related cortical volume variation through the lifespan: Those with higher GCA have greater cortical area to begin with, yielding higher cortical volumes in young adulthood. We have previously found that cortical area seems in part determined neuro-developmentally early on, is associated with GCA, and shows parallel trajectories for higher and lower GCA groups1. As there is a relatively minor age change in area, compared to thickness28, slope effects on cortical volume are chiefly caused by moderately different rates of cortical thinning for people of differential cognitive ability. Differences in cortical thinning are thus key to the maintenance effects of GCA, whereas early differences in cortical area drive the intercept effect. Through the adult lifespan, both will affect cortical volume.
It is of interest that these GCA-brain change associations were found when education was controlled for, suggesting that the contemporary GCA level may not only be related to brain reserve16 to begin with, and preserved differentiation18, but also brain maintenance17, and differential preservation18. This is evident from the—across samples—consistently steeper slopes of regional cortical decline with lower GCA (as illustrated in Fig. 3). With our recent findings on the variable nature of education-brain-cognition relationships, as well as education not being associated with atrophy rates in aging25,30, this points to the component of GCA not being associated with education variance as a more promising candidate for predictive or potentially protective effects on brain aging. There is evidence that education may serve to increase GCA31,32. However, while GCA level may be impacted, slope, i.e. cognitive decline, is likely not32,33. There is also evidence to suggest that education, without mediation through adult socioeconomic position, cannot be considered a modifiable risk factor for dementia34.
While one would then think the underlying mechanism in the observed GCA-brain change relationships may be genetic, known genetic factors only partially explained relationships, as effects remained after controlling for PGSs for general cognitive ability and education. However, the PGSs are known to be only moderately predictive of GCA23, and genetic pleiotropic effects on GCA and cortical characteristics and their change may still likely be part of the underlying mechanism. While it has been suggested that GCA may associate with differences in epigenetic age acceleration, it was recently reported that such epigenetic markers did not show associations with longitudinal phenotypic health change35. While it is possible that individual differences in epigenetic age acceleration in older age could be caused by e.g. behaviors associated with intelligence differences over the life course, differences in epigenetic markers and GCA could also both be the result of a shared genetic architecture or some early, including in-utero, environmental event35,36.
A significant three-way interaction of baseline GCA by baseline age by time on regional cortical thickness changes was observed by meta-analysis across cohorts. These effects indicated that higher level of GCA is more associated with less atrophy at older ages. However, as these regional interaction effects were highly restricted, and also seemed to rest in part on unexpected, albeit weakly, inverse direction of smaller effects in younger28 age in Lifebrain, we consider them tentative until replicated. The higher baseline age of the UKB sample, also may make it less suitable to study adult lifespan interactions. Moreover, greater power would be desired to study three-way interactions of possibly smaller effect size.
Some further limitations to the present study should also be noted: The samples included are heterogeneous and may have varying degrees of representativeness of the populations of origin, indeed, lack of population representativity is known37. Data from relatively short time periods were used. Changing exposure trends over time, in health, education, and welfare, may thus relate to age at baseline, and could have effects that could not readily be studied in isolation here. Furthermore, as cognitively healthy participants were recruited, sample representativity may vary with age. Since persons with known neurodegenerative disorders were excluded, results cannot readily be generalized to persons suffering from various types of dementia. To shed light on the potential genetic contribution to the observed GCA-cortical change relationships, we controlled for PGSs for GCA and educational attainment. While these results indicated negligible genetic contributions, direct investigation of the genetic relations using standard methods, e.g. linkage disequilibrium score regression38, may be better suited to investigate this, when large-scale GWAS for longitudinal cortical changes in adulthood becomes available. Finally, change-change relationships between GCA and cortical characteristics could not readily be addressed in the present samples with similar models, due to variability in availability of comparable test data across timepoints. In a lifespan perspective, we know that such relationships do exist, in that both brain and cognition increase in development and decline in aging17,27,28,39. However, to what extent individual differences in GCA change are related to individual differences in cortical trajectories in the present samples, is beyond the scope of this study.
In conclusion, the present study shows that with higher GCA, primarily brain reserve, but also brain maintenance yield higher cortical volumes through the adult lifespan. These effects were seen when controlling for effects of education. As there is otherwise scarce evidence so far that human behavioral traits are associated with differential brain aging trajectories, this is of great interest to investigate further. While controlling for known polygenetic markers for GCA and education did not substantially diminish the effects, the underlying mechanisms may still be related to genetic pleiotropy. However, this leaves open the possibility that factors associated with increased GCA other than education, and possibly genes, could serve to diminish cortical atrophy in aging. Such factors affecting normal individual differences in GCA are not known with certainty, but as childhood GCA is highly predictive of GCA in aging40, they likely work at developmental, rather than adult and senescent stages.
Materials and methods
The UK Biobank (UKB)22 and the Lifebrain samples are described in Table 1. The samples from the European Lifebrain (LB) project (http://www.lifebrain.uio.no/)20 included participants from major European brain studies: the Berlin Study of Aging II (BASE II)41, the BETULA project27, the Cambridge Centre for Ageing and Neuroscience study (Cam-CAN)42, Center for Lifebrain Changes in Brain and Cognition longitudinal studies (LCBC)1, and the University of Barcelona brain studies (UB)43,44,45.
GCA was measured by partially different tests in the different cohorts. National versions of a series of batteries and tests were used, see SM for details. These included the UKB Fluid Intelligence test46, tests from the Wechsler batteries47,48,49 combined with the National Adult Reading Test (NART)50, the Cattell Culture Fair Test51 combined with the Spot The Word task52, as well as local batteries, for which procedures are described in SM and elsewhere53,54. It is clearly a limitation that content and reliability of the GCA measures may vary, but there is reason to assume that the measures index partally similar abilities. For instance, the UKB fluid intelligence measure has been shown to have moderate to high reliability, and correlated > 0.50 with a measure of GCA created using 11 reference tests, including NART and Wechsler measures55. See SM for further details.
MRIs were processed using FreeSurfer, version 7.1 for Lifebrain, and version 6.0 for UKB (https://surfer.nmr.mgh.harvard.edu/https://surfer.nmr.mgh.harvard.edu)56,57,58,59. We ran vertex-wise analyses to assess regional variation in the relationships between cortical structure and the measures of interest, i.e. GCA and the interaction of GCA × time. Cortical surfaces were reconstructed from the same T1-weighted anatomical MRIs, yielding maps of cortical area, thickness and volume. Surfaces were smoothed with a Gaussian kernel of 15 mm full-width at half-maximum. Spatiotemporal linear mixed models60,61 were performed running on MATLAB R2017a (using FreeSurfers ST-LME package https://surfer.nmr.mgh.harvard.edu/fswiki/LinearMixedEffectsModels), for each of the samples separately, with GCA, and then additionally with the interaction term of GCA and time in turn as predictors, and sex, baseline age, scanner, time (interval since baseline scan) and education were entered as covariates unless otherwise noted. These models also account for the spatial correlation between residuals at neighboring vertices and the temporal correlation of residuals within repeated measurements of single participants. Surface results were tested against an empirical null distribution of maximum cluster size across 10 000 iterations using Z Monte Carlo simulations, yielding results corrected for multiple comparisons across space (p < 0.01 corrected)62.
All studies were conducted, and all methods performed, in accordance with relevant guidelines and regulations as set forth by the relevant authorities, including the Declaration of Helsinki, all participants gave informed consent, and subprojects were approved by the relevant ethical review boards. UK Biobank has approval from the North West Multi-centre Research Ethics Committee as a Research Tissue Bank approval. The Lifebrain project was approved by Regional Committees for Medical Research Ethics–South East Norway. For additional details, see SM. Screening criteria were not identical across studies, but participants were recruited to be cognitively healthy and did not suffer from neurological conditions known to affect brain function, such as dementia. All samples consisted of community-dwelling participants, some were convenience samples, whereas others were contacted on the basis of population registry information. Further details on samples, GCA measures, MRI acquisition and processing and statistical analyses, are presented in SM. The Lifebrain data supporting the results of the current study are available from the PI of each sub-study on request (see SM), given approvals. UK Biobank data requests can be submitted to http://www.ukbiobank.ac.uk. Computer code used for the analyses is available on github: https://github.com/Lifebrain/p032-gca-brain-change.
Walhovd, K. B. et al. Neurodevelopmental origins of lifespan changes in brain and cognition. Proc. Natl. Acad. Sci. USA. 113, 9357–9362. https://doi.org/10.1073/pnas.1524259113 (2016).
Fjell, A. M. et al. High-expanding cortical regions in human development and evolution are related to higher intellectual abilities. Cereb. Cortex 25, 26–34. https://doi.org/10.1093/cercor/bht201 (2015).
Cox, S. R., Ritchie, S. J., Fawns-Ritchie, C., Tucker-Drob, E. M. & Deary, I. J. Structural brain imaging correlates of general intelligence in UK Biobank. Intelligence 76, 101376. https://doi.org/10.1016/j.intell.2019.101376 (2019).
Deary, I. J., Hill, W. D. & Gale, C. R. Intelligence, health and death. Nat. Hum. Behav. 5, 416–430. https://doi.org/10.1038/s41562-021-01078-9 (2021).
Deary, I. J., Cox, S. R. & Hill, W. D. Genetic variation, brain, and intelligence differences. Mol. Psychiatry https://doi.org/10.1038/s41380-021-01027-y (2021).
Livingston, G. et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. Lancet 396, 413–446. https://doi.org/10.1016/S0140-6736(20)30367-6 (2020).
Livingston, G. et al. Dementia prevention, intervention, and care. Lancet 390, 2673–2734. https://doi.org/10.1016/S0140-6736(17)31363-6 (2017).
Nyberg, L. et al. Educational attainment does not influence brain aging. Proc. Natl. Acad. Sci. USA 118, 18. https://doi.org/10.1073/pnas.2101644118 (2021).
Jancke, L., Sele, S., Liem, F., Oschwald, J. & Merillat, S. Brain aging and psychometric intelligence: A longitudinal study. Brain Struct. Funct. 225, 519–536. https://doi.org/10.1007/s00429-019-02005-5 (2020).
Ritchie, S. J. et al. Brain volumetric changes and cognitive ageing during the eighth decade of life. Hum. Brain Mapp. 36, 4910–4925. https://doi.org/10.1002/hbm.22959 (2015).
Raz, N. et al. Neuroanatomical correlates of fluid intelligence in healthy adults and persons with vascular risk factors. Cereb. Cortex 18, 718–726. https://doi.org/10.1093/cercor/bhm108 (2008).
Yeo, R. A., Arden, R. & Jung, R. E. Alzheimer’s disease and intelligence. Curr. Alzheimer Res. 8, 345–353. https://doi.org/10.2174/156720511795745276 (2011).
Nyberg, J. et al. Cardiovascular and cognitive fitness at age 18 and risk of early-onset dementia. Brain 137, 1514–1523. https://doi.org/10.1093/brain/awu041 (2014).
Talboom, J. S. et al. Family history of Alzheimer’s disease alters cognition and is modified by medical and genetic factors. Elife 8, 4619. https://doi.org/10.7554/eLife.46179 (2019).
Rodriguez, F. S. & Lachmann, T. Systematic review on the impact of intelligence on cognitive decline and dementia risk. Front. Psychiatry 11, 658. https://doi.org/10.3389/fpsyt.2020.00658 (2020).
Katzman, R. et al. Clinical, pathological, and neurochemical changes in dementia: A subgroup with preserved mental status and numerous neocortical plaques. Ann. Neurol. 23, 138–144. https://doi.org/10.1002/ana.410230206 (1988).
Nyberg, L., Lovden, M., Riklund, K., Lindenberger, U. & Backman, L. Memory aging and brain maintenance. Trends Cogn. Sci. 16, 292–305. https://doi.org/10.1016/j.tics.2012.04.005 (2012).
Salthouse, T. A., Babcock, R. L., Skovronek, E., Mitchell, D. R. D. & Palmon, R. Age and experience effects in spatial visualization. Dev. Psychol. 26, 128–136. https://doi.org/10.1037/0012-16220.127.116.11 (1990).
Tucker-Drob, E. M. Cognitive aging and dementia: A life span perspective. Annu. Rev. Dev. Psychol. 1, 177–196. https://doi.org/10.1146/annurev-devpsych-121318-085204 (2019).
Walhovd, K. B. et al. Healthy minds 0–100 years: Optimising the use of European brain imaging cohorts (“Lifebrain”). Eur. Psychiatry 50, 47–56. https://doi.org/10.1016/j.eurpsy.2017.12.006 (2018).
Alfaro-Almagro, F. et al. Image processing and quality control for the first 10,000 brain imaging datasets from UK Biobank. Neuroimage 166, 400–424. https://doi.org/10.1016/j.neuroimage.2017.10.034 (2018).
Nobis, L. et al. Hippocampal volume across age: Nomograms derived from over 19,700 people in UK Biobank. Neuroimage Clin. 23, 101904. https://doi.org/10.1016/j.nicl.2019.101904 (2019).
Hill, W. D. et al. A combined analysis of genetically correlated traits identifies 187 loci and a role for neurogenesis and myelination in intelligence. Mol. Psychiatry 24, 169–181. https://doi.org/10.1038/s41380-017-0001-5 (2019).
Lee, J. J. et al. Gene discovery and polygenic prediction from a genome-wide association study of educational attainment in 1.1 million individuals. Nat. Genet. 50, 1112–1121. https://doi.org/10.1038/s41588-018-0147-3 (2018).
Walhovd, K. B. et al. Education and income show heterogeneous relationships to lifespan brain and cognitive differences across European and US cohorts. Cereb. Cortex https://doi.org/10.1093/cercor/bhab248 (2021).
Viechtbauer, W. Conducting meta-analyses in R with the metafor package. J. Stat. Softw. 36, 1–48. https://doi.org/10.18637/jss.v036.i03 (2010).
Nyberg, L. et al. Biological and environmental predictors of heterogeneity in neurocognitive ageing: Evidence from Betula and other longitudinal studies. Ageing Res. Rev. 64, 101184. https://doi.org/10.1016/j.arr.2020.101184 (2020).
Storsve, A. B. et al. Differential longitudinal changes in cortical thickness, surface area and volume across the adult life span: Regions of accelerating and decelerating change. J. Neurosci. 34, 8488–8498. https://doi.org/10.1523/JNEUROSCI.0391-14.2014 (2014).
Walhovd, K. B. et al. Cortical volume and speed-of-processing are complementary in prediction of performance intelligence. Neuropsychologia 43, 704–713. https://doi.org/10.1016/j.neuropsychologia.2004.08.006 (2005).
Raz, N., Rodrigue, K. M., Kennedy, K. M. & Acker, J. D. Vascular health and longitudinal changes in brain and cognition in middle-aged and older adults. Neuropsychology 21, 149–157. https://doi.org/10.1037/0894-418.104.22.168 (2007).
Lager, A., Seblova, D., Falkstedt, D. & Lovden, M. Cognitive and emotional outcomes after prolonged education: A quasi-experiment on 320 182 Swedish boys. Int. J. Epidemiol. 46, 303–311. https://doi.org/10.1093/ije/dyw093 (2017).
Lovden, M., Fratiglioni, L., Glymour, M. M., Lindenberger, U. & Tucker-Drob, E. M. Education and cognitive functioning across the life span. Psychol. Sci. Public Interest 21, 6–41. https://doi.org/10.1177/1529100620920576 (2020).
Seblova, D., Berggren, R. & Lovden, M. Education and age-related decline in cognitive performance: Systematic review and meta-analysis of longitudinal cohort studies. Ageing Res. Rev. 58, 101005. https://doi.org/10.1016/j.arr.2019.101005 (2020).
Seblova, D. et al. Does prolonged education causally affect dementia risk when adult socioeconomic status is not altered? A Swedish natural experiment in 1.3 million individuals. Am. J. Epidemiol. 190, 817–826. https://doi.org/10.1093/aje/kwaa255 (2021).
Stevenson, A. J. et al. Childhood intelligence attenuates the association between biological ageing and health outcomes in later life. Transl. Psychiatry 9, 323. https://doi.org/10.1038/s41398-019-0657-5 (2019).
Li, S. et al. Genome-wide average DNA methylation is determined in utero. Int. J. Epidemiol. 47, 908–916. https://doi.org/10.1093/ije/dyy028 (2018).
Stamatakis, E. et al. Is cohort representativeness passe? Poststratified Associations of lifestyle risk factors with mortality in the UK biobank. Epidemiology 32, 179–188. https://doi.org/10.1097/EDE.0000000000001316 (2021).
Bulik-Sullivan, B. K. et al. LD Score regression distinguishes confounding from polygenicity in genome-wide association studies. Nat. Genet. 47, 291–295. https://doi.org/10.1038/ng.3211 (2015).
Walhovd, K. B. et al. Long-term influence of normal variation in neonatal characteristics on human brain development. Proc. Natl. Acad. Sci. U.S.A. 109, 20089–20094. https://doi.org/10.1073/pnas.1208180109 (2012).
Deary, I. J., Whalley, L. J., Lemmon, H., Crawford, J. R. & Starr, J. M. The stability of individual differences in mental ability from childhood to old age: Follow-up of the 1932 Scottish Mental Survey. Intelligence 28, 49–55. https://doi.org/10.1016/S0160-2896%2899%2900031-8 (2000).
Bertram, L. et al. Cohort profile: The Berlin aging study II (BASE-II). Int. J. Epidemiol. 43, 703–712. https://doi.org/10.1093/ije/dyt018 (2014).
Shafto, M. A. et al. The Cambridge Centre for Ageing and Neuroscience (Cam-CAN) study protocol: A cross-sectional, lifespan, multidisciplinary examination of healthy cognitive ageing. BMC Neurol. 14, 204. https://doi.org/10.1186/s12883-014-0204-1 (2014).
Rajaram, S. et al. The Walnuts and Healthy Aging Study (WAHA): Protocol for a nutritional intervention trial with walnuts on brain aging. Front. Aging Neurosci. 8, 333. https://doi.org/10.3389/fnagi.2016.00333 (2016).
Uribe, C. et al. Patterns of cortical thinning in nondemented Parkinson’s disease patients. Movement Disord. 31, 699–708. https://doi.org/10.1002/mds.26590 (2016).
Vidal-Pineiro, D. et al. Task-dependent activity and connectivity predict episodic memory network-based responses to brain stimulation in healthy aging. Brain Stimul. 7, 287–296. https://doi.org/10.1016/j.brs.2013.12.016 (2014).
Sudlow, C. et al. UK biobank: An open access resource for identifying the causes of a wide range of complex diseases of middle and old age. PLoS Med. 12, e1001779. https://doi.org/10.1371/journal.pmed.1001779 (2015).
Wechsler, D. Wchsler Abbreviated Scale of Intelligence (The Psychological Corporation, 1999).
Wechsler, D. Wechsler Adult Intelligence Scale (WAIS-III): Administration and Scoring Manual 3rd edn. (The Psychological Corporation, 1997).
Wechsler, D. Wechsler Adult Intelligence Scale: Fourth Edition (WAIS-IV) (Pearson Education Inc., 2008).
Nelson, H. & Willison, J. The National Adult Reading Test (NART) (Windsor NFER-Nelson, 1991).
Cattell, R. B. & Cattell, H. E. P. Measuring Intelligence with the Culture Fair Tests (The Institute for Personality and Ability Testing, 1973).
Baddeley, A., Emslie, H. & Nimmosmith, I. The spot-the-word test: A robust estimate of verbal intelligence based on lexical decision. Br. J. Clin. Psychol. 32, 55–65. https://doi.org/10.1111/j.2044-8260.1993.tb01027.x (1993).
Duzel, S. et al. The subjective health horizon questionnaire (SHH-Q): Assessing future time perspectives for facets of an active lifestyle. Gerontology 62, 345–353. https://doi.org/10.1159/000441493 (2016).
Nilsson, L. G. et al. The Betula prospective cohort study: Memory, health, and aging. Aging Neuropsychol. Cogn. 4, 1–32. https://doi.org/10.1080/13825589708256633 (1997).
Fawns-Ritchie, C. & Deary, I. J. Reliability and validity of the UK Biobank cognitive tests. PLoS ONE 15, e0231627. https://doi.org/10.1371/journal.pone.0231627 (2020).
Dale, A. M., Fischl, B. & Sereno, M. I. Cortical surface-based analysis I. Segmentation and surface reconstruction. Neuroimage 9, 179–194. https://doi.org/10.1006/nimg.1998.0395 (1999).
Fischl, B. et al. Whole brain segmentation: Automated labeling of neuroanatomical structures in the human brain. Neuron 33, 341–355 (2002).
Reuter, M., Schmansky, N. J., Rosas, H. D. & Fischl, B. Within-subject template estimation for unbiased longitudinal image analysis. Neuroimage 61, 1402–1418. https://doi.org/10.1016/j.neuroimage.2012.02.084 (2012).
Jovicich, J. et al. Brain morphometry reproducibility in multi-center 3T MRI studies: A comparison of cross-sectional and longitudinal segmentations. Neuroimage 83, 472–484. https://doi.org/10.1016/j.neuroimage.2013.05.007 (2013).
Bernal-Rusiel, J. L. et al. Statistical analysis of longitudinal neuroimage data with linear mixed effects models. Neuroimage 66, 249–260. https://doi.org/10.1016/j.neuroimage.2012.10.065 (2013).
Bernal-Rusiel, J. L. et al. Spatiotemporal linear mixed effects modeling for the mass-univariate analysis of longitudinal neuroimage data. Neuroimage 81, 358–370. https://doi.org/10.1016/j.neuroimage.2013.05.049 (2013).
Hagler, D. J. Jr., Saygin, A. P. & Sereno, M. I. Smoothing and cluster thresholding for cortical surface-based group analysis of fMRI data. Neuroimage 33, 1093–1103. https://doi.org/10.1016/j.neuroimage.2006.07.036 (2006).
The Lifebrain project is funded by the EU Horizon 2020 Grant Agreement Number 732592 (Lifebrain). In addition, the different sub-studies are supported by different sources: LCBC: The European Research Council under grant agreements 283634, 725025 (to A.M.F.) and 313440 (to K.B.W.), as well as the Norwegian Research Council (to A.M.F., K.B.W.), The National Association for Public Health’s dementia research program, Norway (to A.M.F). Betula: a scholar grant from the Knut and Alice Wallenberg (KAW) foundation to L.N. Barcelona: Partially supported by an ICREA Academia 2019 grant award; by the California Walnut Commission, Sacramento, California. BASE-II has been supported by the German Federal Ministry of Education and Research under Grant Numbers 16SV5537/ 16SV5837/ 16SV5538/ 16SV5536K /01UW0808/ 01UW0706/ 01GL1716A/ 01GL1716B, the European Research Council under grant agreement 677804 (to S.K.). The Cambridge Centre for Ageing and Neuroscience (Cam-CAN) was supported by a programme grant from the UK Biotechnology and Biological Sciences Research Council (Grant Number BB/H008217/1) and by continued intramural funding from the UK Medical Research Council to the Cognition & Brain Sciences Unit in Cambridge. Part of the research was conducted using the UK Biobank resource under Application Number 32048.
The authors declare no competing interests.
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
About this article
Cite this article
Walhovd, K.B., Nyberg, L., Lindenberger, U. et al. Brain aging differs with cognitive ability regardless of education.
Sci Rep 12, 13886 (2022). https://doi.org/10.1038/s41598-022-17727-6
Received: 04 March 2022
Accepted: 29 July 2022
Published: 16 August 2022
Polio booster campaign – The Hippocratic Post
Polio booster campaign: Last month an unvaccinated man in Rockland county, New York contracted and became parylised by Poliomyelitis (Polio). This was the first recorded case of the disease for almost a decade in the United States.
The Polio virus, is a highly infectious disease which is transmitted person-to-person spread mainly through the faecal-oral route or, sometime less frequently, by contaminated water or food. The virus then multiplies in the intestine, from where it can invade the nervous system and cause paralysis.
Typically the virus attacks children, causing muscle weakness and paralysis, but in some cases patients will suffer permanent disability or death.
Once prevalent in the 1950’s, the virus was brought under control in the US by a national vaccination roll out in the mid 1950’s which led to its eradication by 1979, when the US was declared polio free. In the UK the last case was recorded in 1984.
Originally the vaccine for polio was a weakened version of the polio virus delivered in the form of drops, and those people of a certain age will recall being given a polio sugar cube as children, the method invented by Dr. Albert Sabin, of the Children’s Hospital Research Foundation in Cincinnati, Ohio.
Today most countries in the developed world use “inactivated Polio” injections as opposed to oral drops, because the “live” weakened virus in the drops causes a mild stomach infection which whilst it builds host immunity, the weakened “live” virus is also expelled in faeces into the environment. This in turn can lead to further mild infections within the community. The oral drops are still used by many countries in the developing world as a cheap way of responding to outbreaks and creating herd immunity.
The strain of polio virus which has been detected in sewerage in New York and London has been identified as a mutated form of vaccine-derived poliovirus brought into the respective cities by overseas travelers. Given vaccine reticence in recent years to follow health advice regarding immunisations, this new strain of polio could make a resurgence if left unchecked and current infections are projected to far greater than the case detected in Rockland County.
Dr Patricia Schnabel Ruppert, health commissioner for Rockland County, said she was worried about polio circulating in her state undetected.
“There isn’t just one case of polio if you see a paralytic case. The incidence of paralytic polio is less than 1%,” she told the BBC. ‘Most cases are asymptomatic or mildly symptomatic, and those symptoms are often missed. So there are hundreds, perhaps even thousands of cases that have occurred in order for us to see a paralytic case.’
As the polio vaccine continues to be included in the Centers for Disease Control and Prevention’s (CDC) standard child immunization schedule, those already vaccinated are not considered at significant risk.
Whilst there is a low risk posed from the emergence of the Polio virus in waste water, there is an easy solution to its elimination both here in the UK and across the pond. Health officials are sending a clear message to check that you are up to date with your own vaccinations and ensure that children’s routine vaccinations have not been neglected during the disruption of the covid pandemic. In addition, children aged 1 to 9 years old in London are being offered a dose of polio vaccine by the UK Government’s Polio booster campaign.
Rapid Polio Spread In New York: All You Need To Know – TheHealthSite
Polio is a disease that causes children to be crippled early. The polio virus detection in New York City’s sewage indicates that the disease is secretly spreading among people who are not vaccinated. The New York State Health Department and city said the poliovirus detection in its wastewater noted that it was likely to spread locally. Provincial Health Commissioner Dr Mary T. Bassett said the poliovirus discovery in wastewater samples in New York City was terrifying but not startling.
Different Polio Strains
- There are mainly two strains of the polio virus. One highly lethal and contagious variant has now disappeared, while the other vaccine-derived polio (vaccine-derived polio) has been reported to be rare. This second strain has been found in the wastewater of the UK capital London and the US city of New York. In Israel’s Jerusalem, a genetically similar virus has been found in London and New York.
- In places like London and New York, cases of vaccine-derived polio have not been reported in the past. However, it is widespread in other countries. In 2021 alone, 415 cases infected with this variant have been reported in Nigeria. The live virus, which reached the body of children as a vaccine, comes out through their faeces after a few weeks. In countries where vaccination has been reduced, this virus can spread again and mutate to become harmful.
The vaccine containing this live virus is no longer used in countries like Britain and America. Especially now that after covid-19, the restrictions related to travel are over again.
Why Is Polio Spreading Now?
Derek Ehrhardt, global polio lead at the Centers for Disease Control and Prevention (CDC) in the US, says experts agree that vaccine-derived and wild polio strains are still present among low-vaccination populations. According to the United Nations, 1081 vaccine-derived polio cases were reported in 2020, compared to three times fewer cases in the previous year, i.e. 2019. However, even in the year 2022, 177 cases have been reported so far.
This is a matter of even more concern, especially for developing countries like India, because our neighbouring countries, Pakistan and Afghanistan, are still battling polio infection.
Total Wellness is now just a click away.
Follow us on
China’s premier urges pro-growth policies as economy sputters – Al Jazeera English
Spreading roots: City of Charlottetown calling for art proposals for tree appreciation program – Saltwire
Canada's largest women's festival, Kingston Women's Art Festival, returns – Kingstonist
Silver investment demand jumped 12% in 2019
Europe kicks off vaccination programs | All media content | DW | 27.12.2020 – Deutsche Welle
Global Media Markets, 2015-2020, 2020-2025F, 2030F – TV and Radio Broadcasting, Film and Music, Information Services, Web Content, Search Portals And Social Media, Print Media, & Cable – GlobeNewswire
News13 hours ago
Baskin-Robbins signs its largest franchise development agreement in 51 years in Canada
Health13 hours ago
Why it’s crucial to say that monkeypox is predominately affecting gay and bisexual men – Broadview Magazine
Health12 hours ago
Rapid Polio Spread In New York: All You Need To Know – TheHealthSite
News12 hours ago
Hip Hop Icon Maestro Fresh Wes Takes Scarborough Back To School!
Sports4 hours ago
Schneider: 'Everything is on the table' for struggling Kikuchi – TSN
News3 hours ago
Ageism: Does it Exist or Is It a Form of ‘I’m a Victim!’ Mentality? [ Part 3 ]
Politics22 hours ago
Politics Briefing: One year after Afghanistan fell to the Taliban – The Globe and Mail
Sports16 hours ago
Series preview: Blue Jays look to turn things around vs. Orioles – Sportsnet.ca