Metabolic Signals and Feeding Patterns

Question 1

Human survival is greatly dependent on their ability to consume food to facilitate metabolism. Food may also generate excessive energy that is converted to fat tissues for storage and use during fasting (Leidy, et al., 2011). The stored reserves meet the metabolic requirements of the body during times of food deprivation. Food consumption patterns are influenced by personal cravings and the normal feelings of hunger. These habits are also influenced by homeostatic processes in the human body, in addition, to other hedonic sensations. Proper energy balance in the human body is achieved when the brain detects the level of bodily energy reserves and regulates the extent of energy expenditure and intake in the body (Leidy, et al., 2010). If you are a student, psychology dissertation help can be invaluable in understanding these complex interactions. Various scholars have proposed hypotheses to explain metabolic signals that convey messages to the human brain. One such theory, called the ‘Glucostatic Hypothesis’ posits that meal initiation is triggered by reduction in blood glucose levels and terminated by increased blood glucose levels. Numerous scientific experiments on animals buttressed this theory. Other scholars disagree with the notion that glucose is the primary instigator of human metabolism. This divergent opinion emerges from the reality that the body strictly regulates its blood glucose levels in plasma (Ortinau, Culp, Hoertel, Douglas, & Leidy, 2013). It is also supported by the reality of limited glycogen storage capacity in body muscles and the liver. Consequently, it becomes difficult for the body to rely on blood glucose alone as an initiator for feeding processes because it is designed to contain and preserve limited glucose levels. The human and animal bodies store excess energy in the adipose tissue, which is commonly called ‘fat tissue.’ It has been observed that human beings and animals retain standard levels of body weight and body fat regardless of the noteworthy fluctuations in their feeding patterns and food intake quantities . This observation encouraged scholars to propose the ‘adipostatic model’, where fat-controlled elements influence the brain, helping it to control feeding patterns, hence weight regulation. The theory received support from the discovery of leptin and other metabolic hormones, together with their receptors. These hormones act on the fat stores to regulate body weight by affecting body energy use and feeding patterns.

Connection between the Stomach and the Brain

The gastrointestinal tract plays a critical role during digestion and nutrient absorption. It is also the only food conduit in the body. Ingesting meals stimulates receptors that coordinate the repeated contraction and distention of to propel food across the digestive system to facilitate absorption of nutrients. Sensory nerves transmit signals from the gastrointestinal tract to the brain. These signals induce the brain to commission various reactions in the body. For example, chemoreceptors send signals showing the composition of nutrients in the food, while the mechanoreceptors induce the propulsion and distension movements in the intestinal tract. The gastrointestinal tract also releases hormones that regulate feeding tendencies in human beings (Wood et al, 2018). It releases peptides that communicate with the brain through the postrema area. The postrema is a circular organ at the top of the fourth ventricle in the brain. It allows neurons to produce responses to gastrointestinal hormones that circulate in the brain. These hormones further relay the appropriate signals to other circuits in the brain.

Interaction between the Brain and Leptin

Leptin plays a critical role in facilitating communication between the energy stores in the body and the brain. The adipose tissue expresses this hormone. Consequently, obese persons have higher leptin levels, which reduce concurrently with weight loss. The changes in in leptin levels are regulated by insulin levels in the body (Theilade et al, 2021). Environmental factors and other polygenic components, including sedentary lifestyles and high-energy foods determine whether persons can contract obesity. High body leptin levels often infers a reduction in reduced leptin transport to the brain. This reality means leptin cannot affect the hypothalamus (Sihag & Jones, 2018). Studies have also shown that restoring proper leptin circulation in the body corresponds weight loss initiatives in the body. This mean normalized activity patterns in the brain and regulation of leptin levels corresponds to normal weight levels in the body.

Peripheral factors Regulating Feeding and Metabolism

The body secretes insulin whenever the body receives meals. It helps the body to store proteins, fat and glycogen. Studies conducted where insulin is injected in the brain impedes food intake into the bloodstream. The adipocytes secrete the adiponectin which circulate in the plasma to promote weight loss. This hormone shows contrary characteristics to leptin. It is significantly reduced in cases of obesity in the human body. Adipocyte deficient persons show increased insulin resistance levels. This condition increases susceptibility to atherosclerosis and other vascular injuries (Ramos, 2021).

Hedonic Approaches to controlling Satiety and Hunger

Eating encourages metabolism and provides energy. This reality means it is regulated by homeostatic controls. It is also noteworthy that human appetite is susceptible to the control of factors beyond physiological considerations. For example, food can arouse desire by acting on different human senses. This stimulating effect can override the rationality and compel humans to feed. Leptin hormones can also impact on taste perceptions by increasing response to sweet tastes. Psychotropic drugs also impact on feeding habits, hence human weight (Panda & Shinde, 2017). This reality exists because food offers similar neuronal rewards as drugs. Leptin reduces the urgency to eat by activating dopamine.

Summarily, eating plays a critical role in energy acquisition by the body. The stomach works with the brain to regulate human appetite by releasing the appropriate hormones and neural signals. Whenever nutrients enter the small intestines, it promotes the release of peptides that encourages a person to stop feeding. The peripheral organs release cytokine and other hormones, which regularize body energy levels by controlling food intake and energy release. The brainstem and hypothalamus contain neurons that maintain homeostatic nature by regulating feeding habits (Emilien & Hollis, 2017). The limbic system also has neurons that control the rewards derived from food intake and the motivation to eat. Brain imaging provides information provides information about the interaction between metabolic signals and the brain. This information can also be received by studying various phenomena, including animal models (Jain & Singh, 2018). Human behavior, and other physiological and genetic components of the digestive system can also provide additional information about the connection between eating and satiety. Overall, information about the mental and biological reasons for eating encourage understanding of human interaction with food.

References

Emilien, C., & Hollis, J. H. (2017). A brief review of salient factors influencing adult eating behaviour.

Nutrition research reviews, 30(2), 233-246.

Gómez-Martínez, D. G., Ramos, M., del Valle-Padilla, J. L., Rosales, J. H., Robles, F., & Ramos, F.

(2021). A bioinspired model of short-term satiety of hunger influenced by food properties in virtual creatures. Cognitive Systems Research, 66, 46-66.

Jain, S., & Singh, S. N. (2018). regulation of Food Intake: a complex Process. Def. Life Sci. J, 3, 182- 189.

Leidy, H. J., Leidy, H. J., Armstrong, C. L., Tang, M., Mattes, R. D., & Campbell, W. W. (2010). The influence of higher protein intake and greater eating frequency on appetite control in overweight and obese men. Obesity, 18(9), 1725-1732. Retrieved 5 5, 2021, from https://ncbi.nlm.nih.gov/pubmed/20339363

Leidy, H. J., Leidy, H. J., Tang, M., Armstrong, C. L., Martin, C. B., & Campbell, W. W. (2011). The effects of consuming frequent, higher protein meals on appetite and satiety during weight loss in overweight/obese men. Obesity, 19(4), 818-824. Retrieved 5 5, 2021, from https://ncbi.nlm.nih.gov/pubmed/20847729

Ortinau, L. C., Culp, J. M., Hoertel, H. A., Douglas, S. M., & Leidy, H. J. (2013). The effects of increased dietary protein yogurt snack in the afternoon on appetite control and eating initiation in healthy women. Nutrition Journal, 12(1), 71-71. Retrieved 5 5, 2021, from https://nutritionj.biomedcentral.com/articles/10.1186/1475-2891-12-71

Panda, V., & Shinde, P. (2017). Appetite suppressing effect of Spinacia oleracea in rats: involvement of the short term satiety signal cholecystokinin. Appetite, 113, 224-230.

Sihag, J., & Jones, P. J. H. (2018). Oleoylethanolamide: the role of a bioactive lipid amide in modulating eating behaviour. Obesity Reviews, 19(2), 178-197.

Theilade, S., Christensen, M. B., Vilsbøll, T., & Knop, F. K. (2021). An overview of obesity mechanisms

in humans: Endocrine regulation of food intake, eating behaviour and common determinants of body weight. Diabetes, Obesity and Metabolism, 23, 17-35

Wood, A. C., Momin, S., Senn, M., & Hughes, S. O. (2018). Pediatric eating behaviors as the intersection of biology and parenting: lessons from the birds and the bees. Current nutrition reports, 7(1), 1-9.

Effects of Psychoactive Drugs on Transmission

Neurotransmission is a cyclic process which happens in several stages and makes use of several components within the human body. Different drugs affect various steps of transmission, which then disrupts normal human functionality (Brandt et al, 2020). Some drugs alter the neurotransmission cycle by imitating the neurotransmitters. Prescription opioids and heroin fall under this category. The chemical composition of these drugs resembles that of enkephalin and endorphin, which are the natural opioids that reside in the brain. This reality means the drugs can stipulate the specialized receptors that respond to these opioids in the body (Lopez et al, 2019). Consequently, heroin and prescription opioids induce stronger reactions from these receptors that the natural opioids would have.

References

Brandt, S. D., Walters, H. M., Partilla, J. S., Blough, B. E., Kavanagh, P. V., & Baumann, M. H. (2020). The psychoactive aminoalkylbenzofuran derivatives, 5-APB and 6-APB, mimic the effects of 3, 4-methylenedioxyamphetamine (MDA) on monoamine transmission in male rats. Psychopharmacology, 237(12), 3703-3714.

Lopes, J. P., Pliássova, A., & Cunha, R. A. (2019). The physiological effects of caffeine on synaptic transmission and plasticity in the mouse hippocampus selectively depend on adenosine A1 and A2A receptors. Biochemical pharmacology, 166, 313-321.

Potential Effects of Inattentional Blindness

Drew et al. (2013) concluded that inattentional blindness is not a preserve of a specific segment in the community. All people, including very highly trained professionals are susceptible to this occurrence. Their study exposed 24 radiologists to samples lung nodules. An abnormally large gorilla lung nodule was introduced into the specimen under review and 83% of the highly qualified radiologists could not identify it. The study further established that a significant majority of those who missed the strange specimen looked directly at its location. This outcome means that inattentional blindness is a common phenomenon that can affect anyone, including the most experienced of persons. This negates the common belief that inattentional blindness typically affects amateurs in a certain field.

Reference

Drew, T., Võ, M. L. H., & Wolfe, J. M. (2013). The invisible gorilla strikes again: Sustained inattentional blindness in expert observers.

Psychological science, 24(9), 1848-1853.

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