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The End of the Obesity Epidemic
Despite apocalyptic predictions from a vocal alliance of health professionals, politicians and social commentators that rising obesity levels would lead to a global health crisis, the crisis has not materialised. In this provocative follow up to his classic work of obesity scepticism, The Obesity Epidemic, Michael Gard argues that we have entered into a new, and perhaps terminal, phase of the obesity debate.
Evidence suggests that obesity rates are levelling off in Western societies, life expectancies continue to rise in line with rising obesity rates, and across the world policy-makers have remained largely indifferent and inactive in the face of this apparently deadly threat to our health and well-being. Dissecting and dismissing much of the over-blown rhetoric and ideological bias found on both sides of the obesity debate, Gard demonstrates that the science of obesity remains radically uncertain and that it is impossible to establish an objective ‘truth’ on which to base policy. His powerful and inescapable conclusion is that we should now mark the end of the obesity epidemic.
Offering a road map through the maze of claims and counter-claims, while still holding to a sceptical standpoint, this book provides an unparalleled anatomy of obesity as a scientific, political and cultural issue. It is essential reading for anybody with an interest in the science or sociology of health and lifestyle.
eBook
FTO Obesity-risk Allele Influences Brain Structure in Children
Background: Variants on the FTO gene increase obesity risk. FTO has been previously associated with alterations in brain structure, but less is known about the influence of FTO on brain structure in children. Methods: We examined differences in grey matter volume (GMV) and cortical thickness (CT) between FTO SNP rs9939609 allele carriers in 2 to 15 year old children. Structural MRI data were drawn from a longitudinal study of healthy brain development (Resonance). We cross-sectionally analyzed differences in GMV and CT in typically developing children grouped by FTO risk alleles: AA [high risk], n = 53, age = 7.4 ± 2.9 y, 26M,27F, BMIz = 0.32 ± 1.13; AT [moderate risk], n = 142, age = 7.31 ± 2.98 y, 77M,65F, BMIz = 0.25 ± 1.21; TT [low risk], n = 89, age = 7.26 ± 3.1 y, 56M,33F, BMIz = -0.0035 ± 1.38. GMV and CT measurements were obtained using FreeSurfer. Preliminary multivariate GLM analysis was performed in SPSS to assess group differences (Bonferroni corrected for multiple comparisons, P < 0.05), where GMV and CT were adjusted for age, sex and BMIz, with additional total intracranial volume adjustments for GMV. Results: The AT vs. TT group demonstrated alterations in left amygdala, right cerebellum, left superior temporal sulcus and left fusiform gyrus (lower GMV); right superior parietal cortex (higher CT). The AA vs. TT group showed alterations in left caudal anterior cingulate cortex and right cerebellum (lower GMV), right frontal pole (higher GMV+CT), and left lateral occipital cortex (higher CT). Conclusions: Structural brain alterations associated with FTO risk alleles could predict future obesity. Future longitudinal analyses will examine effects of FTO variants on brain development and weight trajectories, with potential implications for neurobehaviorally targeted obesity prevention.
Journal Article
Frequency of MC4R Pathway Variants in a Large US Cohort of Patients with Severe Obesity
Background: The melanocortin 4 receptor (MC4R) pathway is critical for the regulation of energy balance. Variants within genes comprising this pathway, including POMC, PCSK1, LEPR, SH2B1, and SRC1, have a well-established association with severe obesity. However, the frequency of variants in these genes have not been assessed systematically in a clinically relevant US population. Methods: We sequenced POMC, PCSK1, LEPR, SH2B1, and SRC1 exons and intron-exon boundaries in 35,276 US individuals with severe obesity (<18 years old, >97th percentile BMI for age; >18 years old, BMI >40kg/m2). This cohort is comprised of individuals sequenced across multiple initiatives, including the Uncovering Rare Obesity (URO) diagnostic genetic testing program. In the current analysis, we included rare variants classified as pathogenic/likely pathogenic (P/LP) or as a variant of uncertain significance (VUS) according to ACMG criteria. We additionally included one non-rare variant, PCSK1 p.N221D, which for which published functional and population studies suggests a potential contribution to obesity. Results: 10.2% of individuals with severe obesity carried >1 rare variants in >1 of the 5 studied genes, including 0.7% who carry a P/ LP variant and 9.5% who carry a VUS variant. An additional 5.4% carried the PCSK1 p.N221D variant. Within the context of a community focused clinical diagnostic tool, URO demonstrated a slightly higher frequency of P/LP and PCSK1 N221D genotypes, 1.2% and 6.9%, respectively, and a 9.8% frequency of VUS genotypes. Conclusions: Overall, in our large US-based cohort of individuals with severe early-onset obesity, 15.6% of individuals carry a potentially clinically relevant variant in the MC4R pathway genes POMC, PCSK1, LEPR, SH2B1, and SRC1. Understanding the role of these variants in the pathophysiology of obesity may improve the clinical care of individuals living with these rare genetic diseases of obesity.
Journal Article