On learning predictive relationships between sweet tastes and calories
It is likely that one of the earliest associations formed by humans and other animals is that based on the signaling relationship between sweet taste in the mouth and the subsequent arrival and absorption of calories in the gut. This type of signaling relationship is thought to enable sweet taste to evoke physiological responses that anticipate and promote the efficient utilization of the energy contained in foods and fluids. Therefore, if consuming non-caloric sweeteners weakens this relationship, the ability to regulate intake of sweet, high calorie foods and beverages could also be degraded (from Davidson, Martin, Clark, & Swithers, 2011).
Why do we eat or why can’t we refrain from eating?
“When food and stimuli associated with food are encountered, these cues may evoke vigorous appetitive and consummatory responding on some occasions and little or no responding at other times. A common interpretation of this pattern of behavior is that animals engage in appetitive and eating behavior until they become satiated and then refrain from making these responses until satiety wanes. How does satiety inhibit, and the absence of satiety promote, appetitive responding? The answer to this question may depend on an animal’s ability to resolve a predictable ambiguity by learning that satiety signals predict when food cues will not be followed by an appetitive postingestive outcome” (Davidson, Kanoski, Schier, Clegg, & Benoit, 2007).
On the role of motivational concepts in theories of feeding behavior
“ While our analysis refers to terms such as “sweet taste”, “satiety signals”, and “appetitive” and “aversive postingestive consequences”, we used these terms descriptively—not as explanations of behavior in their own right. That is, in our model sweet taste refers to a sensory rather than a hedonic property of food; satiety signals refer to sensory events of internal origin that suppress behavior, without ascribing that suppressive effect to any motivational property of satiety itself; appetitive and aversive consequences refer to outcomes of intake that promote or suppress, respectively, behavior that is instrumental to obtaining and consuming food, without the additional claims that those outcomes incentivize or reward the behaviors that are associated with them” (From Davidson, Sample, & Swithers, 2013).
Linking western diet consumption to obesity and cognitive disorders
“It may be that the ability of a Western diet to interfere with hippocampal-dependent learning and memory processes is causally linked to its capacity to promote excessive energy intake and obesity. Research from our laboratory and elsewhere has shown that Western diet-induced learning and memory impairments can precede the development of diet-induced obesity. It may be the case that impairments in hippocampal-dependent processes promote intake and body weight gain by interfering with learned control of energy regulation” (from Kanoski & Davidson, 2011).
On potential links between obesity and Alzheimer’s Disease (AD)
“Obesity and Alzheimer’s Disease are two of the most serious health challenges facing Western cultures. At present, there are no effective therapies for either disease. Although most clinicians and scientists view these disorders as having distinct etiologies and underlying pathologies, the present findings suggest that both may have common dietary origins and brain substrates. Our results join with other recent findings in pointing to the need for a more integrative research approach that could help describe shared neuronal and behavioral mechanisms that may underlie obesity and AD and help identify effective new treatments to prevent or ameliorate both of these serious threats to well-being”. (Kanoski, Zhang, Zheng, & Davidson, 2010).
On early-life cognitive deficits and late-life cognitive dementias
“The results of human studies suggest that obesity is associated with cognitive decline across the lifespan, from relatively mild deficiencies early in life to severe dementia in old age Furthermore, the hippocampus and structures comprising the larger hippocampal formation have been identified as early targets of brain pathologies that give rise to progressive deterioration of cognitive function as such pathologies spread to additional medial temporal lobe structures and then to other areas of the brain. It may be that consuming diets high in saturated fat and carbohydrate produces changes in the brain that impair hippocampal-dependent cognitive functioning; these changes precede and perhaps contribute to overeating, leading not only to obesity and metabolic disease, but also to further interference with the hippocampus and perhaps other substrates for cognitive functioning. From this perspective, early detection of mild forms of hippocampal-dependent cognitive dysfunction and early therapeutic interventions that effectively treat these forms of cognitive disorder should also help to prevent subsequent weight gain and stop the initiation of a vicious-cycle of obesity and cognitive decline” (From Davidson, Hargrave, Swithers, Sample, Fu, Kinzig, & Zheng, 2013).