Clinical Obesity in Adults and Children. Группа авторов

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coatings for textiles, non‐stick cookware, food containers, floor polish, fire‐fighting foam, and industrial surfactants. The strong carbon‐fluorine chemical bond makes PFAS extremely resistant to thermal, chemical, and biological degradation, which results in bioaccumulation and persistence in human tissues for years. Four PFAS – perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), perfluorononanoic acid (PFNA), and perfluorohexane sulfonate (PFHxS) – are almost universally detected in the serum of pregnant women, neonates, and children worldwide, which indicates that exposure is ubiquitous. Furthermore, these chemicals can cross the placenta [71]. A substantial body of evidence exists suggesting that prenatal exposure to PFAS could adversely affect fetal growth. In a systematic review and meta‐analysis, greater prenatal PFOA exposure was associated with a 19 g decrement in birth weight (95% CI: −8 to −30 g) [72]. These results in humans are similar to those observed in rodent studies [73]. Some human observational studies indicate an association of higher circulating concentrations of certain PFAS with weight gain or obesity in children and adults [74,75]. Additionally, some prospective cohort data show that prenatal PFAS exposure is associated with alterations in infant or child growth, increased adiposity during childhood and adulthood [76–78], although others have not shown associations [79,80].

      Infant growth patterns and timing

      Just like fetal growth, early postnatal growth is a strong predictor of later size. Because weight gain accompanies linear growth, weight gain in excess of linear growth is more interesting than weight gain alone. Obtaining accurate length measures is crucial for this effort [81]. Many studies, unfortunately, do not have accurate lengths and therefore resort to examining weight gain alone.

      Independent of birth size, greater postnatal weight gain predicts later adiposity and related cardiometabolic risk [82,83]. Meta‐analyses have found that accelerated weight gain during the first weeks or months of life is associated with higher BMI or obesity later in life [84,85]. For example, Baird et al. [84] reviewed 10 studies that assessed the relationship of infant growth with subsequent obesity. Compared with other infants, among infants with more rapid growth the ORs and relative risks of later obesity ranged from 1.17 to 5.70. Associations were consistent for obesity at different ages and for people born over a period from 1927 to 1994.

      Despite the seeming consistency of these studies, counterexamples exist. Among Finnish men, those who eventually developed coronary heart disease, compared with the cohort as a whole, appeared to have experienced declining height, weight, and BMI during the first year of life before increasing dramatically after the age of 2 years [86]. Gain in BMI in the first 2 years of life was associated with adult lean mass but not fat mass [87]. In contrast, BMI gain from 2 to 7 years was associated with higher fat as well as lean mass. Indian men and women who developed impaired glucose tolerance or type 2 diabetes in young adulthood appeared to follow the same pattern of slower early growth followed by faster growth in later childhood [88]. These discrepancies in the role of infant weight gain may be due to differing measurements or participant experiences across time or geography, but the true explanations are as yet unclear. In addition, the apparent cardiometabolic harms of rapid infant weight gain need to be balanced against its potential benefit for neurocognitive outcomes, especially in babies born preterm.

      Infant diet quality and eating behaviors

      One predictor of infant weight gain is infant feeding. In observational studies, having been breastfed at all or for a longer duration predicts a lower risk for subsequent obesity. In a meta‐analysis of 25 studies with a total of 226,508 participants from 12 countries, breastfeeding was associated with a significantly reduced risk of obesity in children (AOR 0.78; 95% CI: 0.74, 0.81). Categorical analysis of 17 studies revealed a dose‐response effect between breastfeeding duration and reduced risk of childhood obesity [89]. However, other data do not support a causal relationship between breastfeeding and lower obesity risk. It may be that infant growth predicts breastfeeding success, rather than the other way around, i.e. “confounding by indication” [90]. Furthermore, follow‐up of children in a large cluster‐randomized trial of breastfeeding promotion in the Republic of Belarus showed no intervention effect on anthropometric outcomes, obesity, or cardiometabolic risk factors through adolescence [91–93]. One should note, however, that all children in the Belarussian trial were initially breastfed, and the rates of obesity in the population overall were quite low.

      Another group of investigators compared observational results from cohorts from high‐income with low‐ or middle‐income countries (LMIC), where confounding structures differ. They applied standardized approaches for assessing the confounding structure of breastfeeding by socio‐economic position to the British Avon Longitudinal Study of Parents and Children (ALSPAC) (N ≃ 5000) and Brazilian Pelotas 1993 cohorts (N ≃ 1000). Although a higher socio‐economic position was strongly associated with breastfeeding in ALSPAC, there was little such patterning in Pelotas. In ALSPAC, breastfeeding was associated with lower blood pressure (BP), lower BMI, and higher intelligence quotient (IQ), adjusted for confounders, but in the directions expected if due to socio‐economic patterning. In contrast, in Pelotas, breastfeeding was not strongly associated with BP or BMI but was associated with higher IQ. The authors concluded that reported associations of breastfeeding with child BP and BMI are likely to reflect residual confounding.

      Other behaviors in infancy

      It is worth noting that there is likely to be substantial confounding in relation to studies of childhood sleep. For example, in one analysis, 1‐year‐old children’s sleep characteristics such as bedtime, sleep latency, and sleep efficiency were predicted by maternal and paternal BMI [101]. Race/ethnicity and other sociodemographic factors associated with childhood obesity also strongly predicted child sleep habits [102]. Nonetheless, some emerging data from interventions suggest that improving sleep in infancy may promote healthier weight gain [103]. Although many children have poor sleep hygiene [104], sleep quality and possibly duration appear modifiable even in infancy [105].

      Despite extensive studies addressing the potential relationship between events in early life and long‐term health, including obesity risk, there is still limited understanding of the mechanisms by which this may arise (reviewed in [106]).

      Epigenetics

      Much attention has been directed towards the role of epigenetic mechanisms. Epigenetics is a term used to describe mechanisms that alter gene activity without changing the DNA sequence. The most common mechanisms include changes in DNA methylation, histone modifications, and small noncoding RNAs. To date, the most frequently studied has been DNA methylation.

      Most studies in humans addressing epigenetic mechanisms have focused on changes in DNA methylation

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