Intense Sweetness Surpasses Cocaine Reward

Abstract

BackgroundRefined sugars (e.g., sucrose, fructose) were absent in the diet of most people until very recently in human history. Today overconsumption of diets rich in sugars contributes together with other factors to drive the current obesity epidemic. Overconsumption of sugar-dense foods or beverages is initially motivated by the pleasure of sweet taste and is often compared to drug addiction. Though there are many biological commonalities between sweetened diets and drugs of abuse, the addictive potential of the former relative to the latter is currently unknown.Methodology/Principal findingsHere we report that when rats were allowed to choose mutually-exclusively between water sweetened with saccharin–an intense calorie-free sweetener–and intravenous cocaine–a highly addictive and harmful substance–the large majority of animals (94%) preferred the sweet taste of saccharin. The preference for saccharin was not attributable to its unnatural ability to induce sweetness without calories because the same preference was also observed with sucrose, a natural sugar. Finally, the preference for saccharin was not surmountable by increasing doses of cocaine and was observed despite either cocaine intoxication, sensitization or intake escalation–the latter being a hallmark of drug addiction.ConclusionsOur findings clearly demonstrate that intense sweetness can surpass cocaine reward, even in drug-sensitized and -addicted individuals. We speculate that the addictive potential of intense sweetness results from an inborn hypersensitivity to sweet tastants. In most mammals, including rats and humans, sweet receptors evolved in ancestral environments poor in sugars and are thus not adapted to high concentrations of sweet tastants. The supranormal stimulation of these receptors by sugar-rich diets, such as those now widely available in modern societies, would generate a supranormal reward signal in the brain, with the potential to override self-control mechanisms and thus to lead to addiction.

Reward comparison: the Achilles’ heel and hope for addiction

“…In general, it appears that all natural rewards can be protective. Drug self-administration is reduced by the availability of a sweet such as saccharin or a glucose + saccharin mixture [83][84][85]. Drug self-administration is reduced by the availability of a running wheel, particularly in females [86].…”

“…Environmental enrichment also is protective in rats when provided during adulthood alone [90]. Sweets and even chow are protective when presented in adulthood concurrent with the opportunity to self-administer drug [83][84][85]. Finally, the sweets need not be concurrently available to be protective in adult rats.…”

Epigenetic Mechanisms on Food Addiction

“…The recent tendency to eat over the necessary, with significant imbalances of the nutrients of the diet, has induced a higher incidence of eating disorders (ED). Especially, the excessive consumption of sugar-based foods has contributed, together with other environmental risk factors (dieting, media exposure, body image dissatisfaction, and weight-related teasing), to an increase of cases of over-eating diseases, such as obesity, binge-eating disorder, and bulimia nervosa [1][2][3][4]. Neuroscience focused the research strategies on the possibility that a maladaptive eating behavior can characterize some eating disorders as well as maladaptive drug intake characterizes drug addiction.…”

“…It has been recognized that the resemblance may reflect the involvement of the same neural systems, including those implicated in regulatory self-control and reward in both groups of disorders. It has been widely demonstrated that the DAergic "meso-limbic" reward system has a crucial role not only in the passage from an occasional use to an abuse of drugs, but also in the transition from a normal feeding to a maladaptive compulsive eating behavior [1,3,[6][7][8]. Human studies showed that DAergic release correlates with the reward from both drug and food use [9,10].…”

“…Recently, because drug-and food-seeking behavior share similar brain areas and neurotransmission systems, it has been suggest the possibility to produce animal model of maladaptive over-eating disorders [1,6,8,[23][24][25] using the same, adapted paradigms used to investigate drug addiction [8,24,26]. Furthermore, genetic animal models, such as transgenic mice and conditional knock-out mice have been used to investigate the possible role of epigenetic mechanisms underlying drug and food addiction [27][28][29].…”