Sucrose Exposure in Early Life Alters Adult Motivation and Weight Gain

Sucrose Exposure in Early Life Alters Adult Motivation and Weight Gain
Christianne R M Frazier et al., 2008
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0003221


Abstract

The cause of the current increase in obesity in westernized nations is poorly understood but is frequently attributed to a ‘thrifty genotype,’ an evolutionary predisposition to store calories in times of plenty to protect against future scarcity. In modern, industrialized environments that provide a ready, uninterrupted supply of energy-rich foods at low cost, this genetic predisposition is hypothesized to lead to obesity. Children are also exposed to this ‘obesogenic’ environment; however, whether such early dietary experience has developmental effects and contributes to adult vulnerability to obesity is unknown. Using mice, we tested the hypothesis that dietary experience during childhood and adolescence affects adult obesity risk. We gave mice unlimited or no access to sucrose for a short period post-weaning and measured sucrose-seeking, food consumption, and weight gain in adulthood. Unlimited access to sucrose early in life reduced sucrose-seeking when work was required to obtain it. When high-sugar/high-fat dietary options were made freely-available, however, the sucrose-exposed mice gained more weight than mice without early sucrose exposure. These results suggest that early, unlimited exposure to sucrose reduces motivation to acquire sucrose but promotes weight gain in adulthood when the cost of acquiring palatable, energy dense foods is low. This study demonstrates that early post-weaning experience can modify the expression of a ‘thrifty genotype’ and alter an adult animal's response to its environment, a finding consistent with evidence of pre- and peri-natal programming of adult obesity risk by maternal nutritional status. Our findings suggest the window for developmental effects of diet may extend into childhood, an observation with potentially important implications for both research and public policy in addressing the rising incidence of obesity.

[Maybe a low-sugar diet in childhood is a good way to prevent obesity in the adult life.]

Food and drug reward: overlapping circuits in human obesity and addiction

Food and drug reward: overlapping circuits in human obesity and addiction
Volkow ND et al., 2012
https://www.bnl.gov/isd/documents/77781.pdf


Abstract

Both drug addiction and obesity can be defined as disorders in which the saliency value of one type of reward (drugs and food, respectively) becomes abnormally enhanced relative to, and at the expense of others. This model is consistent with the fact that both drugs and food have powerful reinforcing effects –partly mediated by dopamine increases in the limbic system- that, under certain circumstances or in vulnerable individuals, could overwhelm the brain’s homeostatic control mechanisms. Such parallels have generated significant interest in understanding the shared vulnerabilities and trajectories between addiction and obesity. Now, brain imaging discoveries have started to uncover common features between these two conditions and to delineate some of the overlapping brain circuits whose dysfunctions may explain stereotypic and related behavioral deficits in human subjects. These results suggest that both obese and drug addicted individuals suffer from impairments in dopaminergic pathways that regulate neuronal systems associated not only with reward sensitivity and incentive motivation, but also with conditioning (memory/learning), impulse control (behavioral inhibition), stress reactivity and interoceptive awareness. Here, we integrate findings predominantly derived from positron emission tomography that investigate the role of dopamine in drug addiction and in obesity and propose an updated working model to help identify treatment strategies that may benefit both of these conditions.

Dysfunction of the prefrontal cortex in addiction

Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications
R Z Goldstein & Nora D Volkow, 2011
http://www.nature.com/nrn/journal/v12/n11/full/nrn3119.html


Abstract

 

The loss of control over drug intake that occurs in addiction was initially believed to result from disruption of subcortical reward circuits. However, imaging studies in addictive behaviours have identified a key involvement of the prefrontal cortex (PFC) both through its regulation of limbic reward regions and its involvement in higher-order executive function (for example, self-control, salience attribution and awareness). This Review focuses on functional neuroimaging studies conducted in the past decade that have expanded our understanding of the involvement of the PFC in drug addiction. Disruption of the PFC in addiction underlies not only compulsive drug taking but also accounts for the disadvantageous behaviours that are associated with addiction and the erosion of free will.

Addiction, reward sensitivity and expectation sensitivity

Addiction: Decreased reward sensitivity and increased expectation sensitivity conspire to overwhelm the brain's control circuit
Nora D Volkow et al., 2010
http://europepmc.org/articles/PMC2948245?pdf=render

Abstract

Based on brain imaging findings, we present a model according to which addiction emerges as an imbalance in the information processing and integration among various brain circuits and functions. The dysfunctions reflect (a) decreased sensitivity of reward circuits, (b) enhanced sensitivity of memory circuits to conditioned expectations to drugs and drug cues, stress reactivity, and (c) negative mood, and a weakened control circuit. Although initial experimentation with a drug of abuse is largely a voluntary behavior, continued drug use can eventually impair neuronal circuits in the brain that are involved in free will, turning drug use into an automatic compulsive behavior. The ability of addictive drugs to co-opt neuro transmitter signals between neurons (including dopamine, glutamate, and GABA) modifies the function of different neuronal circuits, which begin to falter at different stages of an addiction trajectory. Upon exposure to the drug, drug cues or stress this results in unrestrained hyperactivation of the motivation/drive circuit that results in the compulsive drug intake that characterizes addiction.

Social Isolation in America

Social Isolation in America: Changes in Core Discussion Networks over Two Decades
Miller Mc Pherson et al., 2006
http://sites.duke.edu/theatrst130s02s2011mg3/files/2011/05/McPherson-et-al-Soc-Isolation-2006.pdf


Abstract

Have the core discussion networks of Americans changed in the past two decades? In 1985, the General Social Survey (GSS) collected the first nationally representative data on the confidants with whom Americans discuss important matters. In the 2004 GSS the authors replicated those questions to assess social change in core network structures. Discussion networks are smaller in 2004 than in 1985. The number of people saying there is no one with whom they discuss important matters nearly tripled. The mean network size decreases by about a third (one confidant), from 2.94 in 1985 to 2.08 in 2004. The modal respondent now reports having no confidant; the modal respondent in 1985 had three confidants. Both kin and non-kin confidants were lost in the past two decades, but the greater decrease of non-kin ties leads to more confidant networks centered on spouses and parents, with fewer contacts through voluntary associations and neighborhoods. Most people have densely interconnected confidants similar to them. Some changes reflect the changing demographics of the U.S. population. Educational heterogeneity of social ties has decreased, racial heterogeneity has increased. The data may overestimate the number of social isolates, but these shrinking networks reflect an important social change in America.

Individual Differences in Aging

Trajectories of brain aging in middle-aged and older adults: Regional and individual differences
Naftali Raz et al., 2011 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879584/

Abstract

The human brain changes with age. However, the rate and the trajectories of change vary among the brain regions and among individuals, and the reasons for these differences are unclear. In a sample of healthy middle-aged and older adults, we examined mean volume change and individual differences in the rate of change in 12 regional brain volumes over approximately 30 months. In addition to the baseline assessment, there were two follow-ups, 15 months apart. We observed significant average shrinkage of the hippocampus, entorhinal cortex, orbital–frontal cortex, and cerebellum in each of the intervals. Shrinkage of the hippocampus accelerated with time, whereas shrinkage of the caudate nucleus, prefrontal subcortical white matter, and corpus callosum emerged only at the second follow-up. Throughout both assessment intervals, the mean volumes of the lateral prefrontal and primary visual cortices, putamen, and pons did not change. Significant individual differences in shrinkage rates were observed in the lateral prefrontal cortex, the cerebellum, and all the white matter regions throughout the study, whereas additional regions (medial–temporal structures, the insula, and the basal ganglia) showed significant individual variation in change during the second follow-up. No individual variability was noted in the change of orbital frontal and visual cortices. In two white matter regions, we were able to identify factors associated with individual differences in brain shrinkage. In corpus callosum, shrinkage rate was greater in persons with hypertension, and in the pons, women and carriers of the ApoEε4 allele exhibited declines not noted in the whole sample.

Increased longevity evolves from grandmothering

Increased longevity evolves from grandmothering
Peter S Kim, 2012
 http://home.utah.edu/~u0552264/Kim%20et%20al%202012.pdf


Abstract

 

Postmenopausal longevity may have evolved in our lineage when ancestral grandmothers subsidized their daughters’ fertility by provisioning grandchildren, but the verbal hypothesis has lacked mathematical support until now. Here, we present a formal simulation in which life spans similar to those of modern chimpanzees lengthen into the modern human range as a consequence of grandmother effects. Greater long-evity raises the chance of living through the fertile years but is opposed by costs that differ for the sexes. Our grandmother assumptions are restrictive. Only females who are no longer fertile themselves are eligible, and female fertility extends to age 45 years. Initially, there are very few eligible grandmothers and effects are small. Grandmothers can support only one dependent at a time and do not care selectively for their daughters’ offspring. They must take the oldest juveniles still relying on mothers; and infants under the age of 2 years are never eligible for subsidy. Our model includes no assumptions about brains, learning or pair bonds. Grandmother effects alone are sufficient to propel the doubling of life spans in less than sixty thousand years.

[Under modern circumstances women live quite a few years longer than men. Maybe the "selection for longevity" did really primarily act on women.]