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/
