For the individual, obesity bears consequences on their short and long-term health, in addition to crippling their overall well-being. For the nation, it translates into incredible losses in productivity and profit, as an increasingly overwhelming majority of the population in the United States fall into the category of either overweight or obese. Bordering upon epidemic, the rising weight problem has ignited a barrage of investigating bodies of scientific studies and inquiries, all curious as to how it works and how it can be stopped.
Using fruit flies (Drosophila melanogaster) to examine feeding pathways in the brain, Jen Beshel and colleagues studied molecular modulators and behaviors of obesity related to it in A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila. Notable mechanisms important to the study were those of the circuit involving upd1, domeless receptors, and npf (a nonmammalian neuropeoptide that regulates food odor valuation and stimulates appetite), and the circuit involving leptin, leptin receptors, and npy (a mammalian neuropeptide that is a homolog of npf). Upd1, a leptin analog, is a ligand that bears similar weight-regulating functions. Through the manipulation of neural circuits and knockout of upd1, the study found that upd1 linked to domeless receptors on npf-positive cells affected satiety, and that obesity traits are mediated by the leptin analog in the brain, rather than fat tissues. The neural circuit studied in in fruit flies is functionally conserved with that in mammals; thus, the study offers a good prediction as to what would happen in mammals undergoing similar obesogenic or anorexigenic conditions.
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| From Obesity alters brain structure and function. |
In 2016, a story published in the Guardian went on to investigate what obesity, in turn, does to the brain. Using the results from a study in the University of Cambridge, it highlighted links between obesity and memory loss, raising flags as to whether another consequence of the lifestyle is a potential contribution to dementia. Supporting this notion is Lucy Cheke and her colleagues, who in this study found a clear relationship between BMI (Body Mass Index, a measure of weight relative to height) and memory deficits. This furthers an ever-expanding body of knowledge suggesting obesity may contribute to neurodegenerative diseases including Alzheimer's. Another study cited in the article showed a correlation between healthy, middle-aged adults with raised abdominal fat and lower brain volume, a loss especially prominent in the hippocampus. As this part of the brain is crucial in learning and memory, this finding can help explain the eating behaviors individuals struggling with obesity as well as form the basis of proposed memory damage, a growing concern. Going along with Beshel's focus on neural-hormonal correlates in the brain rather than the fat body, this illustrates the importance of the association between brain function and obesity.
A year after the story was published, a review by Chelsea Stillman and colleagues (Body-Brain Connections: The Effects of Obesity and Behavioral Interventions on Neurocognitive Aging) provided yet another examination of obesity's effect on neurocognitive function by comparing and contrasting it with the effects physical activity and fitness have on the brain. On a cellular and molecular level, there are several emerging mechanisms that offer to explain the pathways for obesity’s negative impact on brain function and structure – areas the pathways of physical activity and energy restriction positively impact. Decrease in gray matter volume is one such negative structural change. According to the review, the areas of the brain affected by obesity and aging are shown to increase in neurocognitive health with the introduction of physical activity interventions – one such area being the hippocampus, crucial for episodic and relational memory as mentioned in the Guardian article. The review went on to say that though obesity and physical activity do not simply cause inverse effects (the review states their effects of limbic and reward-related brain networks as one example of where they diverge), there is substantial overlap between the mechanisms of the two. The existence of lifestyles that reduce obesity have always been known; however, this notion that such lifestyles can also improve neurocognitive health exponentially raises their benefit and provides key insight into effective solutions or mediators of obesity beyond the externally physical results.
These are glimpses into only a few studies from the vast body of rising knowledge that continues to shed further light on the health crisis that is gripping the US and spreading to other westernizing countries. As we raise our understanding of its severity, hopefully we come closer towards a means of mediating the consequences of obesity and moving towards a future where it rampage is but a scientific and historical memory.
References
Beshel, J, et al. “A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila.” Cell Metabolism., U.S. National Library of Medicine, 10 Jan. 2017
www.ncbi.nlm.nih.gov/pubmed/28076762
Costandi, Mo. “Obesity alters brain structure and function.” The Guardian, 23 November 2016. https://www.theguardian.com/science/neurophilosophy/2016/nov/23/obesity-alters-brain-structure-and-function
Stillman, Chelsea M. et al. “Body–Brain Connections: The Effects of Obesity and Behavioral Interventions on Neurocognitive Aging.” Frontiers in Aging Neuroscience 9 (2017): 115. PMC. Web. 18 Oct. 2018.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5410624/
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