Binge-drinking alcohol and then heading to the nearest fast food restaurant can feel so natural it seems as if it’s wired into the brain. Now, early-stage research presented at the Experimental Biology Meeting in Orlando on Monday suggests that the impulse to binge booze and food really does have a neurological basis, revealing a troubling connection that may explain even more types of uncontrollable binge habits.
At the meeting, Caitlin Coker, a graduate student at Penn State School of medicine, presented preliminary research showing that bingeing alcohol and fatty foods are part of a “vicious cycle” of brain activity that uses the same underlying neurocircuitry. She developed this concept using the results of her study on mice, which she conducted under the guidance of Yuval Silberman, Ph.D., an assistant professor of neural and behavioral sciences. The results, which are not yet peer reviewed, suggest that mice who binge on fatty food can’t help but binge on alcohol too.
“Over the short term, for example within a single meal in people or a single exposure session in rodent models, fats intake can increase alcohol intake and vice versa,” Silberman tells Inverse. “As far as we can tell, while the brain regions involved in binge eating or binge drinking behaviors appear to be very similar, there have been no published studies that have directly examined the relationship of such binge behaviors over a long term period.”
Spring Break For Mice
In their experiment, they exposed a group of mice to both high-fat diets and alcohol over a “long-term” period of eight weeks. One group of mice was given intermittent access to a high-fat diet only once per week — so when they got the chance, they mice really went for it, simulating a binge eating scenario. Another group of mice had constant access to high-fat chow, and another group had constant access to normal mouse chow.
All the mice had limited access to alcohol too, which allowed the researchers to see whether the mice would binge drink when they got the chance. In an experimental setup that bears an uncanny similarity to a typical spring break trip, the mice got a chance to binge for four hours a day, four days a week, before they were cut off for three days.
At the end of eight weeks, the team found that the mice who had only limited access to a high-fat diet — that is, those who would binge eat when given the opportunity — also tended to binge drink when presented with alcohol. In the abstract to the presentation, Coker reports that binge drinking mice drank significantly more alcohol than mice on either diet.
More Than Just Drunk Munchies
The results suggest that drunk munchies are a very real thing. But Silberman believes that the relationship between binge eating and binge drinking indicates something even more complicated going on in the brain, even if the current data set, which included no neuroimaging, can’t prove just yet.
“What we think is happening is that the high fat diet binges are modulating intake neurocircuitry to be sensitized to subsequent modulation by alcohol to further increase intake,” he posits. “There are a number of brain regions that may be involved in these behaviors, such as the hypothalamus, ventral tegmental area, nucleus accumbens, and prefrontal cortex.”
In other words, bingeing may change the way the brain processes intake; this, in turn, may lead to alcohol abuse, which may lead to food binging, and so the vicious cycle continues. Silberman doesn’t think it’s just fatty foods that drive a change in intake neurocircuitry. He and Coker believe that the same neurological effects that drive someone to binge on fatty food may apply to other compulsive binge behaviors, like gambling.
“In this case, binge eating, but many similar behavioral issues — say gambling issues — could also be a symptom of underlying binge behaviors that may be risk factors for alcohol use disorders,” he says.
Though we do know that overeating has roots in certain brain regions, it’s far from certain whether there truly is a single neurological impulse that drives us to both pound shots and seek the comfort of unhealthy hangover food in a never-ending cycle. The work may be in its early stages, but it’s an important first step to finding an explanation for why some impulses feel impossible to control.
Abstract: Obesity and alcoholism, two of the most common chronic conditions in the United States, may be behaviorally linked as binge intake of palatable diets, such as diets high in fat (HFD), and binge alcohol (EtOH) intake may utilize similar neurocircuitry. We hypothesized that binge intake of one modality (i.e. HFD) may sensitize the shared neurocircuitry to further activation by another modality (i.e. EtOH). Therefore, we combined a binge HFD intake model in mice where HFD access is limited to one 24hr session per week (Limited Access HFD: LAH) with a patterned EtOH access schedule that also promotes binge-like intake in a two-bottle choice model (Limited Access EtOH: LAE; 4hrs/day, 4days/wk). Control mice were given the same EtOH access schedule but were given continuous ad libitum access to HFD (60% calories from fat) or control Chow diet (10% calories from fat). Six-week old male C57Bl/6J mice were weight matched, individually housed, and assigned to HFD+LAE, Chow+LAE, or LAH+LAE groups (n=10 per group). All groups of mice were given increasing EtOH concentrations over the course of the study (10% EtOH for three weeks, 15% EtOH for two weeks, and 20% EtOH for two weeks). Body mass was measured daily while EtOH/water intake and EtOH preference were assessed after every drinking session. Over the course of the study, HFD+LAE mice gained significantly more weight than Chow+LAE or LAH+LAE mice (p=0.001; one-way ANOVA). While weight gain was predominantly linear in HFD+LAE and Chow+LAE mice, LAH+LAE mice showed weight cycling indicating a binge-like eating pattern. LAH+LAE mice consumed significantly more EtOH than Chow+LAE or HFD+LAE mice (p=0.001, repeated measures two-way ANOVA), suggesting that binge intake of HFD led to increased binge EtOH intake patterns in LAH mice. LAH+LAE and Chow+LAE mice showed higher preference towards EtOH than HFD+LAE mice (p=0.001, repeated measures two-way ANOVA). Together, these results suggest limited access to palatable diets induce binge-like eating patterns that further cross-sensitize to binge alcohol intake and mitigates the loss of alcohol preference in mice given continuous HFD.