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      Weight gain as a consequence of living a modern lifestyle: a discussion of barriers to effective weight control and how to overcome them

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          Abstract

          Objective

          The purpose of this commentary is to discuss modern lifestyle factors that promote weight gain and to suggest methods for clinicians to more effectively educate patients about weight management.

          Discussion

          Most adults in the United States are overweight or obese. Multiple factors related to the modern lifestyle appear to play causal roles. In general, the population maintains sedentary lives and overconsumes calorie-dense foods. In particular, refined carbohydrates negatively impact metabolism and stimulate neural addiction mechanisms, which facilitate weight gain. As adipose tissue mass accumulates, satiation centers in the hypothalamus become resistant to insulin and leptin, which leads to increased caloric consumption. Several behavior issues further augment weight gain, such as eating too quickly, a lack of sleep, high stress levels, and a lack of exercise. Finally, adipose tissue accumulation alters the body weight set point, which leads to metabolic changes that function to resist weight loss efforts. Each of these factors may work together to augment weight gain and promote obesity. Health care providers, such as chiropractic physicians, who educate patients on wellness, prevention, and lifestyle changes are well positioned to address these issues.

          Conclusion

          People need to be educated about the modern lifestyle factors that prevent effective weight management. Without this knowledge and the associated practical application of lifestyle choices that prevent weight gain, becoming overweight or obese appears to be an unavoidable consequence of living a modern lifestyle.

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          Most cited references75

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          Addiction-like reward dysfunction and compulsive eating in obese rats: Role for dopamine D2 receptors

          We found that development of obesity was coupled with the emergence of a progressively worsening brain reward deficit. Similar changes in reward homeostasis induced by cocaine or heroin is considered a critical trigger in the transition from casual to compulsive drug-taking. Accordingly, we detected compulsive-like feeding behavior in obese but not lean rats, measured as palatable food consumption that was resistant to disruption by an aversive conditioned stimulus. Striatal dopamine D2 receptors (D2R) were downregulated in obese rats, similar to previous reports in human drug addicts. Moreover, lentivirus-mediated knockdown of striatal D2R rapidly accelerated the development of addiction-like reward deficits and the onset of compulsive-like food seeking in rats with extended access to palatable high-fat food. These data demonstrate that overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuitries and drives the development of compulsive eating. Common hedonic mechanisms may therefore underlie obesity and drug addiction.
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            The metabolic consequences of sleep deprivation.

            The prevalence of diabetes and obesity is increasing at an alarming rate worldwide, and the causes of this pandemic are not fully understood. Chronic sleep curtailment is a behavior that has developed over the past 2-3 decades. Laboratory and epidemiological studies suggest that sleep loss may play a role in the increased prevalence of diabetes and/or obesity. Current data suggest the relationship between sleep restriction, weight gain and diabetes risk may involve at least three pathways: (1) alterations in glucose metabolism; (2) upregulation of appetite; and (3) decreased energy expenditure. The present article reviews the current evidence in support of these three mechanisms that might link short sleep and increased obesity and diabetes risk.
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              Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk.

              We sought to investigate the effects of sleep loss on high-sensitivity C-reactive protein (CRP) levels. Concentrations of high-sensitivity CRP are predictive of future cardiovascular morbidity. In epidemiologic studies, short sleep duration and sleep complaints have also been associated with increased cardiovascular morbidity. Two studies were undertaken to examine the effect of acute total and short-term partial sleep deprivation on concentrations of high-sensitivity CRP in healthy human subjects. In Experiment 1, 10 healthy adult subjects stayed awake for 88 continuous hours. Samples of high-sensitivity CRP were collected every 90 min for 5 consecutive days, encompassing the vigil. In Experiment 2, 10 subjects were randomly assigned to either 8.2 h (control) or 4.2 h (partial sleep deprivation) of nighttime sleep for 10 consecutive days. Hourly samples of high-sensitivity CRP were taken during a baseline night and on day 10 of the study protocol. The CRP concentrations increased during both total and partial sleep deprivation conditions, but remained stable in the control condition. Systolic blood pressure increased across deprivation in Experiment 1, and heart rate increased in Experiment 2. Both acute total and short-term partial sleep deprivation resulted in elevated high-sensitivity CRP concentrations, a stable marker of inflammation that has been shown to be predictive of cardiovascular morbidity. We propose that sleep loss may be one of the ways that inflammatory processes are activated and contribute to the association of sleep complaints, short sleep duration, and cardiovascular morbidity observed in epidemiologic surveys.
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                Author and article information

                Contributors
                Journal
                J Chiropr Humanit
                J Chiropr Humanit
                Journal of Chiropractic Humanities
                National University of Health Sciences
                1556-3499
                22 October 2013
                December 2013
                : 20
                : 1
                : 27-35
                Affiliations
                Professor, Department of Clinical Sciences, National University of Health Sciences, Pinellas Park, FL
                Author notes
                [* ]Corresponding author. David R. Seaman, DC, MS, Professor, National University of Health Sciences, SPC-Health Education Center, 7200 66th St N, Pinellas Park, FL 33706. Tel.: + 1 727 803 6129; fax: + 1 727 329 8494. dseaman@ 123456nuhs.edu
                Article
                S1556-3499(13)00003-X
                10.1016/j.echu.2013.08.001
                4111078
                0039a0ae-212d-4219-bc9d-7d24daf55d01
                © 2013 National University of Health Sciences. All rights reserved.
                History
                : 5 July 2013
                : 27 August 2013
                : 28 August 2013
                Categories
                Original Article

                Complementary & Alternative medicine
                obesity,inflammation,weight loss,body mass index,diet, reducing,chiropractic,public health

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