Abstract
Over the past decade, a great deal of research has established the importance of cognitive processes in the control of energy intake and body weight. The present paper begins by identifying several of these cognitive processes. We then summarize evidence from human and nonhuman animal models, which shows how excess intake of obesity-promoting Western diet (WD) may have deleterious effects on these cognitive control processes. Findings that these effects may be manifested as early-life deficits in cognitive functioning and may also be associated with the emergence of serious late-life cognitive impairment are described. Consistent with these possibilities, we review evidence, obtained primarily from rodent models, that consuming a WD is associated with the emergence of pathophysiologies in the hippocampus, an important brain substrate for learning, memory, and cognition. The implications of this research for mechanism are discussed within the context of a “vicious-cycle model,” which describes how eating a WD could impair hippocampal function, producing cognitive deficits that promote increased WD intake and body weight gain, which could contribute to further hippocampal dysfunction, cognitive decline, and excess eating and weight gain.
Highlights
The ability to maintain energy balance and to control one’s body weight involves much more than monitoring bodily energy reserves and the detection of physiological signals that tell when we are hungry or food sated
We (1) describe how memory, expectancies, decision making, reward valuation, inhibition, and other cognitive processes can contribute to food intake and body weight regulation; (2) consider evidence from nonhuman and human animals, which indicate that excess food intake and body weight gain negatively impact those processes; (3) review findings, which link this negative impact of diet and obesity to pathophysiologies in brain substrates for learning and memory processes that may contribute to the control of intake; and (4) discuss the possibility that some of these pathophysiological changes may increase the risk of cognitive deficits early in life and for Alzheimer’s disease (AD) and AD-like dementias in late adulthood
The DIO, but not DR rats, showed impaired performance on a discrimination problem that depends on the hippocampus. Neither of these groups was impaired on a hippocampalindependent discrimination. These results show that selective increases in blood-brain barrier (BBB) permeability and selective impairment in hippocampal-dependent cognitive functioning co-occur in rats that become obese when maintained on a Western diet (WD)
Summary
The ability to maintain energy balance and to control one’s body weight involves much more than monitoring bodily energy reserves and the detection of physiological signals that tell when we are hungry or food sated. The decision to obtain and consume food depends on our knowledge and expectations about food availability, quality (e.g., hedonic, nutritive), the cost and effort required to obtain it, and the potential short-term (e.g., fullness, malaise) and long-term consequences (e.g., on health) of eating it, among other factors Much of this information resides in memory, and our ability to retrieve the memories of previous experiences with food and eating is an important determinant of our current and future appetitive and consummatory behavior. The purpose of this article is to summarize the role of cognitive processes in the control of energy intake and body weight by providing an overview that integrates data and theory from several broad research domains. The article concludes with the description of a vicious-cycle model that links both obesity and dietary factors to impairments in cognitive processes that are dependent, directly or indirectly, on the functioning of the hippocampus
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