Body mass index but not genetic risk is longitudinally associated with altered structural brain parameters

Abstract

Evidence from previous studies suggests that elevated body mass index (BMI) and genetic risk for obesity is associated with reduced brain volume, particularly in areas of reward-related cognition, e.g. the medial prefrontal cortex (AC-MPFC), the orbitofrontal cortex (OFC), the striatum and the thalamus. However, only few studies examined the interplay between these factors in a joint approach. Moreover, previous findings are based on cross-sectional data. We investigated the longitudinal relationship between increased BMI, brain structural magnetic resonance imaging (MRI) parameters and genetic risk scores in a cohort of n = 502 community-dwelling participants from the Study of Health in Pomerania (SHIP) with a mean follow-up-time of 4.9 years. We found that (1) increased BMI values at baseline were associated with decreased brain parameters at follow-up. These effects were particularly pronounced for the OFC and AC-MPFC. (2) The genetic predisposition for BMI had no effect on brain parameters at baseline or follow-up. (3) The interaction between the genetic score for BMI and brain parameters had no effect on BMI at baseline. Finding a significant impact of overweight, but not genetic predisposition for obesity on altered brain structure suggests that metabolic mechanisms may underlie the relationship between obesity and altered brain structure.

Cardiovascular risk factors in secondary progressive multiple sclerosis: A cross‐sectional analysis from the MS‐STAT2 randomized controlled trial

“…There is established literature supporting the relationship between higher BMI and aspects of MS severity, including cross‐sectional and longitudinal changes in grey matter volumes [34–39]. This is not necessarily an MS‐specific effect, as similar results, particularly between higher BMI and lower grey matter volumes, have been found in people without MS [40–48]. Interestingly, given our finding of a relationship between greater prematurely achieved CVR or higher lipid ratios and worse verbal working memory performance, one previous study of predominantly RRMS found that higher FRS is also associated with poorer CVLT‐II performance [49].…”

“…There is established literature supporting the relationship between higher BMI and aspects of MS severity, including cross-sectional and longitudinal changes in grey matter volumes [34][35][36][37][38][39]. This is not necessarily an MS-specific effect, as similar results, particularly between higher BMI and lower grey matter volumes, have been found in people without MS [40][41][42][43][44][45][46][47][48].…”

Higher Dietary Inflammatory Index scores are associated with brain MRI markers of brain aging: Results from the Framingham Heart Study Offspring cohort*

“…Missing data were excluded from analysis (Apolipoprotein ε4[ APOE ε4 ; n = 41], body mass index [BMI; n = 5], physical activity [ n = 122], smoking status [ n = 1], total to high‐density lipoprotein [HDL] cholesterol ratio [ n = 10], anti‐cholesterol medication [ n = 1], prevalent diabetes [ n = 7], cardiovascular disease [CVD; n = 1], adiponectin [ n = 342], CD40 [ n = 18], CRP [ n = 17], 8‐EPI‐isoprostane [ n = 281], fibrinogen [ n = 16], IL‐6 [ n = 18], IL‐18 [ n = 91], intercellular adhesion molecule [ICAM; n = 16], resistin [ n = 335], and TNF‐α [ n = 488]). Confounders were selected based on the published literature (Table S4 in supporting information) 36–42 . Model 1 was adjusted for age, age squared, sex, and the time interval between examination cycle 7 (i.e., baseline FFQ and covariates assessment) and the measurement of MRI outcomes.…”

A Case for Estradiol: Younger Brains in Women with Earlier Menarche and Later Menopause

“…To determine if our results remain stable and significant when accounting for potential confounds known to affect brain health, we repeated the aforementioned cross-sectional and longitudinal analyses for reproductive span, menarche, and menopause using additional parameters. More specifically, we removed the variance associated with the number of live births 58 (UK Biobank data field #2734), hormone replacement therapy 7 (#2814), hysterectomy 59 (#3591), bilateral oophorectomy 59 (#2834), body mass index 60 (#21001), diastolic and systolic blood pressure 61 (#4079 and #4080), diabetes 62 (#2443), education 63 (#6138), income 64 (#738), and a composite lifestyle factor 65 . The latter was expressed as a general lifestyle score that was calculated based on a number of factors (see Supplemental Table 4), known to increase / decrease the risk of adverse cardiovascular events.…”

“…7 (#2814), hysterectomy59 (#3591), bilateral oophorectomy 59 (#2834), body mass index60 (#21001), diastolic and systolic 15 blood pressure *…”