OBJECTIVE
To identify factors in childhood which might influence the development of obesity in adulthood.


BACKGROUND
The prevalence of obesity is increasing in the UK and other developed countries, in adults and children. The adverse health consequences of adult obesity are well documented, but are less certain for childhood obesity. An association between fatness in adolescence and undesirable socio-economic consequences, such as lower educational attainment and income, has been observed, particularly for women. Childhood factors implicated in the development of adult obesity therefore have far-reaching implications for costs to the health-services and economy.


SEARCH STRATEGY
In order to identify relevant studies, electronic databases--Medline, Embase, CAB abstracts, Psyclit and Sport Discus-were searched from the start date of the database to Spring 1998. The general search structure for electronic databases was (childhood or synonyms) AND (fatness or synonyms) AND (longitudinal or synonyms). Further studies were identified by citations in retrieved papers and by consultation with experts.


INCLUSION CRITERIA
Longitudinal observational studies of healthy children which included measurement of a risk factor in childhood (<18 y), and outcome measure at least 1 y later. Any measure of fatness, leanness or change in fatness or leanness was accepted. Measures of fat distribution were not included. Only studies with participants from an industrialized country were considered, and those concerning minority or special groups, e.g. Pima Indians or children born preterm, were excluded.


FINDINGS
Risk factors for obesity included parental fatness, social factors, birth weight, timing or rate of maturation, physical activity, dietary factors and other behavioural or psychological factors. Offspring of obese parent(s) were consistently seen to be at increased risk of fatness, although few studies have looked at this relationship over longer periods of childhood and into adulthood. The relative contributions of genes and inherited lifestyle factors to the parent-child fatness association remain largely unknown. No clear relationship is reported between socio-economic status (SES) in early life and childhood fatness. However, a strong consistent relationship is observed between low SES in early life and increased fatness in adulthood. Studies investigating SES were generally large but very few considered confounding by parental fatness. Women who change social class (social mobility) show the prevalence of obesity of the class they join, an association which is not present in men. The influence of other social factors such as family size, number of parents at home and childcare have been little researched. There is good evidence from large and reasonably long-term studies for an apparently clear relationship for increased fatness with higher birth weight, but in studies which attempted to address potential confounding by gestational age, parental fatness, or social group, the relationship was less consistent. The relationship between earlier maturation and greater subsequent fatness was investigated in predominantly smaller, but also a few large studies. Again, this relationship appeared to be consistent, but in general, the studies had not investigated whether there was confounding by other factors, including parental fatness, SES, earlier fatness in childhood, or dietary or activity behaviours. Studies investigating the role of diet or activity were generally small, and included diverse methods of risk factor measurement. There was almost no evidence for an influence of activity in infancy on later fatness, and inconsistent but suggestive evidence for a protective effect of activity in childhood on later fatness. No clear evidence for an effect of infant feeding on later fatness emerged, but follow-up to adulthood was rare, with only one study measuring fatness after 7y. Studies investigating diet in childhood were limited and inconc

Childhood predictors of adult obesity: a systematic review.

Context Research has implicated an addictive process in the development and maintenance of obesity. Although parallels in neural functioning between obesity and substance dependence have been found, to our knowledge, no studies have examined the neural correlates of addictive-like eating behavior. Objective To test the hypothesis that elevated“food addiction” scores are associated with similar patterns of neural activation as substance dependence. Design Between-subjects functional magnetic resonance imaging study. Setting A university neuroimaging center. Participants Forty-eight healthy young women ranging from lean to obese recruited for a healthy weight maintenance trial. Main Outcome Measure The relation between elevated food addiction scores and blood oxygen level–dependent functional magnetic resonance imaging activation in response to receipt and anticipated receipt of palatable food (chocolate milkshake). Results Food addiction scores (N = 39) correlated with greater activation in the anterior cingulate cortex, medial orbitofrontal cortex, and amygdala in response to anticipated receipt of food (P  Conclusions Similar patterns of neural activation are implicated in addictive-like eating behavior and substance dependence: elevated activation in reward circuitry in response to food cues and reduced activation of inhibitory regions in response to food intake.

/pdf/neural-correlates-of-food-addiction-3bfqfaadfe.pdf

Neural Correlates of Food Addiction

Obesity is a growing problem worldwide and is associated with a range of comorbidities, including cognitive dysfunction. In this review we will address the evidence that obesity and high fat feeding can lead to cognitive dysfunction. We will also examine the idea that obesity-associated systemic inflammation leads to inflammation within the brain, particularly the hypothalamus, and that this is partially responsible for these negative cognitive outcomes. Thus, obesity, and high fat feeding, lead to systemic inflammation and excess circulating free fatty acids. Circulating cytokines, free fatty acids and immune cells reach the brain at the level of the hypothalamus and initiate local inflammation, including microglial proliferation. This local inflammation likely causes synaptic remodeling and neurodegeneration within the hypothalamus, altering internal hypothalamic circuitry and hypothalamic outputs to other brain regions. The result is disruption to cognitive function mediated by regions such as hippocampus, amygdala, and reward-processing centers. Central inflammation is also likely to affect these regions directly. Thus, central inflammation in obesity leads not just to disruption of hypothalamic satiety signals and perpetuation of overeating, but also to negative outcomes on cognition.

Obesity and neuroinflammation: a pathway to cognitive impairment.

Physiology of Behavior

Stress as a common risk factor for obesity and addiction.

Behavioral studies reveal that obese vs. lean individuals show attentional bias to food stimuli. Yet research has not investigated this relation using objective brain imaging or tested whether attentional bias to food stimuli predicts future weight gain, which are important aims given the prominence of food cues in the environment. We used functional magnetic resonance imaging (fMRI) to examine attentional bias in 35 adolescent girls ranging from lean to obese using an attention network task involving food and neutral stimuli. BMI correlated positively with speed of behavioral response to both appetizing food stimuli and unappetizing food stimuli, but not to neutral stimuli. BMI correlated positively with activation in brain regions related to attention and food reward, including the anterior insula/frontal operculum, lateral orbitofrontal cortex (OFC), ventrolateral prefrontal cortex (vlPFC), and superior parietal lobe, during initial orientation to food cues. BMI also correlated with greater activation in the anterior insula/frontal operculum during reallocation of attention to appetizing food images and with weaker activation in the medial OFC and ventral pallidum during reallocation of attention to unappetizing food images. Greater lateral OFC activation during initial orientation to appetizing food cues predicted future increases in BMI. Results indicate that overweight is related to greater attentional bias to food cues and that youth who show elevated reward circuitry responsivity during food cue exposure are at increased risk for weight gain.

https://onlinelibrary.wiley.com/doi/pdf/10.1038/oby.2011.168

Attentional bias to food images associated with elevated weight and future weight gain: an fMRI study.

http://zaldlab.psy.vanderbilt.edu/resources/Publications2/relationofobesity.pdf

Relation of obesity to consummatory and anticipatory food reward

Prospective studies have identified factors that increase risk for eating pathology onset, including perceived pressure for thinness, thin-ideal internalization, body dissatisfaction, dietary restraint, and negative affect. Research also suggests that body dissatisfaction and dietary restraint may constitute prodromal stages of the development of eating disorders. Prevention trials indicate that interventions that reduce pressure to be thin, thin-ideal internalization, body dissatisfaction, and negative affect significantly reduce eating disorder symptoms. Further, there is evidence that selective prevention programs that target young women at elevated risk for eating pathology by virtue of thin-ideal internalization, body dissatisfaction, and negative affect produce significant larger intervention effects than do universal programs offered to unselected populations. Thus, research on risk factors and prodromal stages of eating pathology has assisted in the design of efficacious prevention programs and the identification of high-risk individuals to target with these interventions; additional research in this area may lead to even more effective prevention programs.

Risk factors and prodromal eating pathology

Relation of regional gray and white matter volumes to current BMI and future increases in BMI: a prospective MRI study

Janet Ng

Papers

Attentional bias to food images associated with elevated weight and future weight gain: an fMRI study.

Relation of obesity to consummatory and anticipatory food reward

Risk factors and prodromal eating pathology

Relation of regional gray and white matter volumes to current BMI and future increases in BMI: a prospective MRI study

An fMRI study of obesity, food reward, and perceived caloric density. Does a low-fat label make food less appealing? ☆