Obesity
is rapidly becoming one of the leading health problems in the U.S. paralleling
cardiovascular disease. The number of obese adolescents is staggering, with a
three-fold increase since the 1970’s, where 18.5 percent of adolescence
population is obese. Not only are we seeing an increasing in adolescents with
obesity but in babies and children as well, with an increase from 32 million in
the 90’s to 41 million in 2016 (Robertson, 2019).
A recent study using imaging
techniques suggests that obesity could be causing inflammation in the nervous system
(Robertson, 2019). With today’s advancements in technology scientist have been
able to get a deeper look at the white matter of the brain. High amounts of
both leptin and insulin were correlated with increased inflammation in the
brains of obese adolescents (Robertson, 2019). The increase in inflammation was
seen with higher amounts of white matter damage. The damage was found in the
corpus callosum (connection point between the left and right hemispheres) and
in the orbitofrontal gyrus (emotion and reward center) in the obese adolescents.
What are leptin and Insulin? Leptin is a
hormone that signals satiety. This signal tells the body you are in a
high-energy state and do no need to consume more. The resistance to leptin
causes a dysfunction in the negative feed back loop. This signals to fat cells to
release more leptin. This high leptin is associated with an increased
inflammatory response (Ferrier, & Harvey, 2011). Obese adolescents were
also seen to have increase levels of insulin, the hormone responsible for
controlling glucose levels in the blood, indicating a problem in receptors
associated with insulin (Robertson, 2019). Prolonged insulin resistance can eventually
lead to type II diabetes.
There have been various studies that indicate
adolescent is a critical time for brain development especially in areas that
regulate behavior, cognition, and adaptation. This sensitive time of brain
development is highly susceptible to damaging effects by drugs, hormones, and
so forth (Konrad et al., 2013). This may be why inflammation during adolescents
can have more serious consequences then if experienced later in life.
A preliminary study showed that
adolescents with type II diabetes performed worse in a variety of cognitive
tasks (Yau et al., 2010). If prolonged inflammation brought on by obesity can
be indicative of poor health and reduced learning ability, more research should
be done to see exactly how these hormones are influencing inflammation, why
only certain brain regions are being affected, and if the affects are
reversible. Based on the biomedical principle non-maleficence childhood obesity
should be a priority not only in healthcare but also for parents and the food
industry.
References
Ferrier,
D. R., & Harvey, R. (2011). Lippincotts illustrated reviews: biochemistry
5th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
Konrad,
K., Firk, C., & Uhlhaas, P. J. (2013). Brain development during
adolescence: neuroscientific insights into this developmental period. Deutsches
Arzteblatt international, 110(25), 425–431. doi:10.3238/arztebl.2013.0425
Robertson, S. (2019, November 25). MRI
reveals signs of brain damage among obese adolescents. Retrieved from https://www.news-medical.net/news/20191125/MRI-reveals-signs-of-brain-damage-among-obese-adolescents.aspx.
Yau, DC Javier, CM Ryan, et al.
Preliminary evidence for brain complications in obese adolescents with type 2
diabetes mellitus Diabetologia, 53 (2010), pp. 2298-2306
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ReplyDeleteErin, I am very interested and invested in the topic of pediatric obesity (it is what I am doing my independent project over) and I particularly like your focus on mental performance. It is somewhat common sense at this point that obesity is related to health disparities such as metabolic syndrome, but I feel as though the impact on mental development is a lesser known potential outcome. I reviewed your resource from Robertson (2019) and I am curious as to what inflammatory markers they used to identify inflammation in the nervous system. I know we have discussed briefly in class the role of different cytokines, so I am curious if they are responsible for an inflammatory cascade in the nervous system as well.
ReplyDeleteI am also curious if they thought about looking into the function of microglia in the white matter. Microglia play a prominent role in the immune response in the nervous system and are typically dormant in a mature nervous system (Bazan, N. G., et al). Another future direction for research on mental functioning and obesity could look at the activity of the microglia where an increase in activity could potentially indicate brain tissue damage as the microglia are working as macrophages.
Bazan, N. G., Halabi, A., Ertel, M., & Petasis, N. A. (2012). Neuroinflammation. Basic Neurochemistry (8th ed.). 610-620.
Thank you for a great read, Erin. In addition to the processes you mentioned, insulin and leptin also cause deregulation of the hormone ghrelin. Ghrelin is produced in the stomach, promotes hunger, and regulates glucose homeostasis by decreasing insulin production (Pradhan, Samson & Sun, 2013). So once the body is thrown into disarray through obesity it had mechanisms that perpetuate this cycle and make the issue worse. Hormone dysfunction in a developing brain is problematic. This topic is especially apropos in our current obesity epidemic. Tackling this issue is complicated, because implementing policy against obesity-contributing factors is often viewed as infringing upon one's rights. However, when children are involved, and their brain development is on the line, I believe that autonomy of the parents needs to be seriously questioned.
ReplyDeleteReferences:
Pradhan, G., Samson, S. L., & Sun, Y. (2013). Ghrelin: Much more than a hunger hormone . Current Opinion in Clinical Nutrition and Metabolic Care, 16(6). doi: 10.1097/mco.0b013e328365b9be