Rats that binge eat fat-rich food do not show somatic signs or anxiety associated with opiate-like withdrawal: Implications for nutrient-specific food addiction behaviors

Abstract

Previous studies suggest that binge eating sugar leads to behavioral and neurochemical changes similar to those seen with drug addiction, including signs of opiate-like withdrawal. Studies are emerging that show multiple neurochemical and behavioral indices of addiction when animals overeat a fat-rich diet. The goal of the present study was to utilize liquid and solid diets high in sugar and fat content to determine whether opiate-like withdrawal is seen after binge consumption of these diets in Sprague Dawley rats. Control groups were given ad libitum access to the sweet-fat food or standard chow. All rats were then given a battery of tests to measure signs of opiate-like withdrawal, which included somatic signs of distress, elevated plus-maze anxiety, and locomotor hypoactivity. Neither naloxone-precipitated (3 mg/kg) nor deprivation-induced withdrawal was observed in rats that were maintained on a nutritionally complete pelleted sweet-fat diet, a sweet, high-fat diet supplemented with standard rodent chow, or a liquid sweet-fat food. Further, body weight reduction to 85%, which is known to potentiate the reinforcing effects of substance of abuse, did not affect naloxone-precipitated signs of opiate-like withdrawal. Thus, unlike previous findings reported regarding rats with binge access to a sucrose solution, rats that binge eat sweet-fat combinations do not show signs of opiate-like withdrawal under the conditions tested. These data support the idea that excessive consumption of different nutrients can induce behaviors associated with addiction in different ways, and that the behaviors that could characterize “food addiction” may be subtyped based on the nutritional composition of the food consumed.

“Eating addiction”, rather than “food addiction”, better captures addictive-like eating behavior

“…For example, repeated 12 h food deprivation followed by 12 h intermittent access to normal food and a sugar solution leads to sugar "binging" (defined operationally as an increased intake compared to rats offered unrestricted access over the same time period). Furthermore, there is evidence that endogenous opioid signaling is active during sugar (but not fat; Bocarsly et al, 2011) binging, as i.p. administration of the opioid receptor antagonist, naloxone, results in somatic effects reminiscent of a withdrawal syndrome (Colantuoni et al, 2002).…”

Obesity and the Neurocognitive Basis of Food Reward and the Control of Intake

“…Rats allowed intermittent access to high-sugar and high-fat foods develop escalating, binge-like eating (117,118). Enforced abstinence from sugar and administration of the opioid antagonist naloxone results in a withdrawal syndrome with a behavioral (enhanced anxiety, teeth chattering, forepaw tremor, and head shakes) (119) and neural profile (low levels of dopamine and high levels of acetylcholine in NAcc) similar to that seen in drug withdrawal (119,120).…”

Etiology of Food Addiction

“…Aşırı miktarda tüketilen şekerin madde bağımlılığında gözlenen davranışsal ve nörokimyasal değişikliklere neden olduğunu destekleyen araştırmaların yanı sıra son zamanlarda yapılan hayvan deneylerinde aşırı miktarda şekerli veya yağlı besinlerin alımının tam olarak opiyat çekilme belirtileri ile örtüşmediğini gösteren olumsuz bulgular da elde edilmiştir. [40] …”