Obesity and drug addiction rates have skyrocketed across the globe within the past two decades and showing no sign of slowing down. One reason these epidemics have been allowed to proliferate is due to how society interacts with them. Both diseases are viewed with scrutiny and disdain as a byproduct of western philosophy that centers on the individual and their agency in making choices. As a result, many hold the notion that these afflicted individuals should pull themselves up by the bootstraps and curb their behavior. While it may be easy to pin the blame on the individuals lack of will, current research regarding the role of neurochemical modulation suggests that individuals are wired to engage in these activities. Specifically, researchers have been exploring the effects of leptin upon the brain reward circuit and how it modulates food related behavior and drug consumption.
In their paper, “ A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila”, Dr. Beshel and her team explored the effects of mammalian leptin homolog, upd1 and how it effects obesity linked behavior. By manipulating upd1 in drosophila, flies exhibited commonly associated symptoms of mammalian obesity such as increased attraction to food cues, increased food intake, and increased weight. It was discovered that these symptoms were the result of mediation by dome-less receptors expressing Drosophila neuropeptide F, a homolog to mammalian neuropeptide Y. Within the NPY circuits, which is functionally conserved, upd1 inhibits npf neurons until the flies have eaten after which npf activity increases and upd1 secretion decreases. Dr. Beshel’s research effectively highlights the role leptin has in the brain reward mechanisms as it inhibits hunger and also showcases that obesity is an etiologically diverse condition with no singular cause.
Given that leptin has a distinct role in modulating the reward circuit in the brain via inhibition of hunger, researchers in Brazil have taken an interest in leptins role in modulating drug use, specifically with crack cocaine. In Dr. Escobar and her teams’ paper “Leptin levels and its correlation with crack-cocaine use severity: A preliminary study”, their main priority was to discover a possible correlation between leptin concentration and the severity of crack use. The paper cites that given the role of food and illicit drugs in the brain reward circuit, it can be expected to see a sharing of neurochemicals among drug seeking behavior and food consumption. Using this logic, the researchers hypothesized that leptin has a role in modulating the drug seeking behaviors. By taking blood samples and surveys from crack users, the researchers were able to measure leptin levels and severity of crack use. It was found that leptin concentration yielded an inverse correlation with the severity of crack use, with higher severity crack users displaying lower levels of leptin. Given the results, the researchers postulated that leptin may have a role in regulating crack intake. These findings also suggest that leptin could be used as a neurochemical marker in the regulation of crack use and highlights leptin’s role within the brain’s reward circuit. The paper cites previous human clinical studies have found lower concentrations of leptin in cocaine users as compared to non-users and also reported cocaine dependent users having higher intake of fat and carb rich foods. This phenomenon seems to support the researcher’s assumptions that the sympathetic effects of cocaine inhibit leptin and stimulate overeating. The study however did have some short comings, as it included a cross sectional design, lacked female participants and a control group. However, the study discovered a possible link between leptin and the modulation of food intake and drug use which opens up room for further investigation.
Obesity and drug addiction are seen as afflictions resulting from the weakness of one’s will and only require a simple solution, stop partaking in their respective vices. The research from Dr. Beshel’s lab and Dr. Escobar have been integral steps forward in the investigation of how leptin operates in the brain reward circuits. Both papers highlight the complex mechanisms behind food seeking behavior and also accentuate the notion that these conditions hold varied etiologies. The information gleaned from this research paves the way not only for a more complete understanding of how leptin works but also allows for the removal of the stigma associated with these conditions. If society doesn’t engage in a cultural revolution in how they view epidemics like obesity and drug addiction, they will continue to wreak havoc upon their victims.
Citations
Beshel, J., Dubnau, J., & Zhong, Y. (2017). A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila. Cell metabolism, 25(1), 208–217. https://doi.org/10.1016/j.cmet.2016.12.013
Escobar, M., Scherer, J. N., Ornell, F., Bristot, G., Soares, C. M., Guimarães, L. S., . . . Pechansky, F. (2018). Leptin levels and its correlation with crack-cocaine use severity: A preliminary study. Neuroscience Letters, 671, 56-59. doi:10.1016/j.neulet.2018.02.009
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