Write a 5-6 page paper double space using the information below: In your paper: Describe one other field (such as biology or medical sciences) that studies your topic. Summarize your flawed source, in

Write a 5-6 page paper double space using the information below:

In your paper:

Describe one other field (such as biology or medical sciences) that studies your topic.

Summarize your flawed source, including any evidence provided.

Provide evidence from your three peer-reviewed journal articles.

Relate the actions of the mind and body to psychological and physical health.

Describe one of the psychological or behavioral theories that explain your topic.

Construct your own explanation to explain the cause of your topic.

Using one of the following controversial statements:

Obesity is caused by a lack of willpower.

Topic of your choice related to the content in the chapters on Motivation, Sex, Gender, or Emotion in your course text, Brain and Behavior: An Introduction to Behavioral Neuroscience. Remember that this book is available in the VitalSource bookshelf in the courseroom. What the textbook says is below:

Because obesity is dangerous to the person’s health as well as an occasion for social and career discrimination, it is important to ask why people become overweight and why obesity rates are rising so dramatically. Although the causes have been difficult to document, most authorities believe that the global increase in obesity has a simple explanation: People are eating more and richer foods and exercising less (J. O. Hill, Wyatt, Reed, & Peters, 2003). The cause of obesity seems straightforward enough, then: Energy in exceeds energy out, and the person gains weight. But we would miss the point entirely if we assumed that people become obese just because they cannot resist the temptation to overeat. Research has not supported the popular opinion that obesity is completely under voluntary control (Volkow & Wise, 2005) or that it can be characterized simply as lack of impulse control, inability to delay gratification, or maladaptive eating style (Rodin, Schank, & Striegel-Moore, 1989). In fact, as we will see later, obesity has a number of features in common with drug addiction.

Another popular belief is that obese children learn overindulgence from their family. Obesity does run in families, and BMI and other measures are moderately related among family members. However, the evidence consistently points to genetic rather than environmental influences as more important (Grilo & Pogue-Geile, 1991). To the extent that environment does play a role, it is mostly from outside the family.

Find one flawed source of information on the Internet. To find a flawed source, look for one with a substantial number of errors.

https://www.reddit.com/r/TalkTherapy/comments/11iahuh/therapist_told_me_weight_loss_is_about_selfcontrol/

“I had a first session with someone was supposed to be my own mental health counselor, and she stated this in response to my proclaimed goals of wanting to lose weight. She said “Well, you know PairEfficient, weight loss is really just about self-control” in this very chastising tone with an almost critical, condescending side-eye look. In an instant, my stomach dropped and I knew I should start looking for another therapist.

I mean, how reductive and judgmental was that statement? I found it to be very harmful because it’s overlooking the many factors that contribute to this apparent lack of “self control”: increased appetite and uncontrollable need from fatigue, emotional conflict, trauma response, comorbid with other mental health disorders (ADHD, depression, which she knows I have both), a coping mechanism, etc.

I proceeded to tell her all of the above and how most of those reasons applied to me directly, and she said okay, so then it’s an issue of finding you new coping mechanisms. Yes, I mean sure, but she stated that after the fact without even trying to ask about my struggles with weight loss. There was also a mixup of sending me the intake form so she did not see that I struggle with binge eating, but did she really need to in order not to make such a dismissive statement?”

Peer review article 1: Medawar, E., & Witte, A. V. (2022). Impact of obesity and diet on brain structure and function: a gut–brain–body crosstalk. The Proceedings of the Nutrition Society, 81(4), 306-316. https://doi.org/10.1017/S0029665122002786

Most societies witness an ever increasing prevalence of both obesity and dementia, a scenario related to often underestimated individual and public health burden. Overnutrition and weight gain have been linked with abnormal functionality of homoeostasis brain networks and changes in higher cognitive functions such as reward evaluation, executive functions and learning and memory. In parallel, evidence has accumulated that modifiable factors such as obesity and diet impact the gut–brain axis and modulate brain health and cognition through various pathways. Using neuroimaging data from epidemiological studies and randomised clinical trials, we aim to shed light on the underlying mechanisms and to determine both determinants and consequences of obesity and diet at the level of human brain structure and function. 

Peer review 2:  Kim, C. Y., Park, Y., Namgung, J. Y., Park, Y., & Park, B. Y. (2024). The macroscale routing mechanism of structural brain connectivity related to body mass index. Human brain mapping, 45(13), e70019. https://doi.org/10.1002/hbm.70019

Understanding the brain's mechanisms in individuals with obesity is important for managing body weight. Prior neuroimaging studies extensively investigated alterations in brain structure and function related to body mass index (BMI). However, how the network communication among the large‐scale brain networks differs across BMI is underinvestigated. This study used diffusion magnetic resonance imaging of 290 young adults to identify links between BMI and brain network mechanisms. Navigation efficiency, a measure of network routing, was calculated from the structural connectivity computed using diffusion tractography. The sensory and frontoparietal networks indicated positive associations between navigation efficiency and BMI. The neurotransmitter association analysis identified that serotonergic and dopaminergic receptors, as well as opioid and norepinephrine systems, were related to BMI‐related alterations in navigation efficiency. The transcriptomic analysis found that genes associated with network routing across BMI overlapped with genes enriched in excitatory and inhibitory neurons, specifically, gene enrichments related to synaptic transmission and neuron projection. Our findings suggest a valuable insight into understanding BMI‐related alterations in brain network routing mechanisms and the potential underlying cellular biology, which might be used as a foundation for BMI‐based weight management.

Peer review 3: Ravichandran, S., Sood, R., Das, I., Dong, T., Figueroa, J. D., Yang, J., Finger, N., Vaughan, A., Vora, P., Selvaraj, K., Labus, J. S., & Gupta, A. (2024). Early life adversity impacts alterations in brain structure and food addiction in individuals with high BMI. Scientific reports, 14(1), 13141. https://doi.org/10.1038/s41598-024-63414-z

Obesity and food addiction are associated with distinct brain signatures related to reward processing, and early life adversity (ELA) also increases alterations in these same reward regions. However, the neural mechanisms underlying the effect of early life adversity on food addiction are unknown. Therefore, the aim of this study was to examine the interactions between ELA, food addiction, and brain morphometry in individuals with obesity. 114 participants with high body mass index (BMI) underwent structural MRIs, and completed several questionnaires (e.g., Yale Food Addiction Scale (YFAS), Brief Resilience Scale (BRS), Early Traumatic Inventory (ETI)). Freesurfer 6 was applied to generate the morphometry of brain regions. A multivariate pattern analysis was used to derive brain morphometry patterns associated with food addiction. General linear modeling and mediation analyses were conducted to examine the effects of ELA and resilience on food addiction in individuals with obesity. Statistical significance was determined at a level of p < 0.05. High levels of ELA showed a strong association between reward control brain signatures and food addiction (p = 0.03). Resilience positively mediated the effect of ELA on food addiction (B = 0.02, p = 0.038). Our findings suggest that food addiction is associated with brain signatures in motivation and reward processing regions indicative of dopaminergic dysregulation and inhibition of cognitive control regions. These mechanistic variabilities along with early life adversity suggest increased vulnerability to develop food addiction and obesity in adulthood, which can buffer by the neuroprotective effects of resilience, highlighting the value of incorporating cognitive appraisal into obesity therapeutic regimens.