The adverse effects of obesity reduce the body’s natural potential of optimal physical, mental health and cognitive function. Obesity is associated with a greater risk of health problems such as hypertension, stroke, diabetes, and sleep apnea. These issues attribute to an increased risk of dementia and cognitive dysfunction.

Glucose homeostasis plays a key role in the neural mechanisms of the brain. Insulin signals nutrients by circulating within the body in proportion to body fat mass. In addition to other regulatory mechanisms, this allows the brain to control feeding behavior by stimulating energy storage and metabolic homeostasis. Metabolic imbalances modify insulin sensitivity and lead to impaired glucose output inhibition [Qatanani and Lazar et al., 2007 (1)].

Free radicals are formed when weak molecular bonds are split. Their instability causes them to attack neighboring stable molecules and lead to a chain reaction of disturbing living cells. Antioxidants, such as vitamins C and E, defend the body from the damaging effects of free radicals by acting like scavengers. They protect cells from tissue damage that can potentially lead to disease.

Moreover, insulin resistance links oxidative stress, which is the continuous imbalance between free radical production and the body’s antioxidant defenses to detoxify its harmful effects. Enhanced oxidative stress is a result of accumulated fat, which impairs the secretion of insulin and damages glucose uptake in muscle and fat. Increased oxidative stress is the underlying cause of pathogenesis in vascular cell walls that lead to the development of cardiovascular problems, plaque formation. Data suggests, in a study conducted by Dr. Convit (2) in 2002, that management of blood sugar levels may enhance memory and possibly decrease the risk of Alzheimer’s disease.

In congruence with these findings, added stress due to excess weight can negatively affect the anatomy and physiology of the body. A study in 2010, led by Dr. Thompson (3), concluded that obesity is associated with “atrophy in brain areas targeted by neurodegeneration: hippocampus, frontal lobes, and thalamus” [Raji et al., 2010 (3)]. These brain regions play a critical role in the maintenance of memory, executive function, and sensory interpretation, respectively.

Central respiratory function is also disrupted by the mechanical effects of obesity. Reduced lung expansion is especially destructive during sleep. Obstructive sleep apnea is a disorder where breathing stops for brief periods because of an obstructed upper airway. Excess weight and increasing body mass index (BMI) restricts expansion of the chest wall and increases airway resistance, which decreases lung volume [Zammit et al. 2010 (4)]. This boosts respiratory muscle workload for consistent breathing. Complications of sleep apnea include fatigue, heart problems, metabolic syndrome, and more.

Cognitive impairments lead to deficits in executive function, response, reflex time, planning, and memory [Spitznagel et al. 2013 (5)]. Blood sugar levels, oxidative state, respiration and other mechanisms influence our cognitive abilities. Weight loss from bariatric surgery may reduce the comorbidities of an obese patient. The primary outcomes are improvements with diabetes, blood pressure, glucose levels, sleep apnea, BMI, and excess weight resolutions.

Weight loss surgery reverses the stressors of the body to permit the development and preservation of cognitive function. By improving anatomical aspects of physical health, the overall mental well-being of patients is remarkably enhanced.

A number of studies have looked at the short [Gunstad 2011(6)] and intermediate  [Alosco 2013, (7)] term improvement in memory function after weight loss surgery

Thank you to Contributor: Mariam Michelle Gyulnazaryan

References for Cognitive Function

1. Qatanani M, Lazar MA. Mechanisms of obesity-associated insulin resistance. Genes & Dev. 2007; 21: 1443-1455.
2. Convit A, Wolf OT, Tarshish C, de Leon MJ. Reduced glucose tolerance is associated with poor memory performance and hippocampal atrophy among normal elderly. PNAS. 2013; 100 (4): 2019-2022.
3. Raji CA, Ho AJ, Parikshak N, Becker JT, Lopez OL, Kuller LH, Hua X, Leow AD, Toga AW, Thompson PM. Brain structure and obesity. Hum Brain Mapp. 2010; 31(3): 353-364.
4. Zammit C, Liddicoat H, Moonsie I, Makker H. Obesity and respiratory diseases. Int J Gen Med. 2010; 3:335-343.
5. Spitznagel MG, Alosco M, Strain G, Devlin M, Cohen R, Paul R, Crosby RD, Mitchell JE, Gunstad J., Cognitive function predicts 24-month weight loss success following bariatric surgery. Surg Obes Relat Dis. 2013; 9(5): 765-770.
6. John Gunstad, Gladys Strain, Michael J. Devlin, Rena Wing, Ronald A. Cohen, Robert H. Paul, Ross D. Crosby, James E. Mitchell, 2011, ‘Improved memory function 12 weeks after bariatric surgery’, Surgery for Obesity and Related Diseases, vol. 7, no. 4, pp. 465-472
7. Michael L. Alosco, Mary Beth Spitznagel, Gladys Strain, Michael Devlin, Ronald Cohen, Robert Paul, Ross D. Crosby, James E. Mitchell, John Gunstad, 2013, ‘Improved memory function two years after bariatric surgery’, Obesity, vol. 22, no. 1, pp. 32-38
8. Furukawa S, Fujita T, Shimabukuro M, Iwaki M, Yamada Y, Nakajima Y, Nakayama O, Makishima M, Matsuda M, Shimomura I. Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest. 2004; 114(12): 1752-1761.
9. Mitchell JE, de Zwaan M. Psychosocial assessment and treatment of bariatric surgery patients. 2011;6: 103-109.
10. Nguyen JCD, Killcross AS, Jenkins TA. Obesity and cognitive decline: role of inflammation and vascular changes. Front Neurosci. 2014; 8: 375.
11. Chan JSY, Yan JH, Payne VG. The impact of obesity and exercise on cognitive aging. Front Aging Neurosci. 2013; 5: 97.