Lifestyle determinants of the drive to eat: A meta-analysis

Department of Neuroscience, Uppsala University, Uppsala, Sweden.
American Journal of Clinical Nutrition (Impact Factor: 6.77). 07/2012; 96(3):492-7. DOI: 10.3945/ajcn.112.039750
Source: PubMed


Obesity is emerging as the most significant health concern of the 21st century. Although this is attributable in part to changes in our environment-including the increased prevalence of energy-dense food-it also appears that several lifestyle factors may increase our vulnerability to this calorie-rich landscape. Epidemiologic studies have begun to show links between adiposity and behaviors such as television watching, alcohol intake, and sleep deprivation. However, these studies leave unclear the direction of this association. In addition, studies that investigated the acute impact of these factors on food intake have reported a wide variety of effect sizes, from highly positive to slightly negative.
The purpose of this article was to provide a meta-analysis of the relation between lifestyle choices and increases in acute food intake.
An initial search was performed on PubMed to collect articles relating television watching, sleep deprivation, and alcohol consumption to food intake. Only articles published before February 2012 were considered. Studies that took place in a controlled, laboratory setting with healthy individuals were included. Studies were analyzed by using 3 meta-analyses with random-effects models. In addition, a 1-factor ANOVA was run to discover any main effect of lifestyle.
The 3 most prominent lifestyle factors-television watching, alcohol intake, and sleep deprivation-had significant short-term effects on food intake, with alcohol being more significant (Cohen's d = 1.03) than sleep deprivation (Cohen's d = 0.49) and television watching (Cohen's d = 0.2).
Our results suggest that television watching, alcohol intake, and sleep deprivation are not merely correlated with obesity but likely contribute to it by encouraging excessive eating. Because these behaviors are all known to affect cognitive functions involved in reward saliency and inhibitory control, it may be that they represent common mechanisms through which this eating is facilitated.

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    • "This mechanism is linked with altered gene expression secondary to epigenetic mechanisms (in particular hypomethylation of the Il13ra2 gene) [62]. Thus, genetic, epigenetic and lifestyle factors as well as the presence of toxic agents in the environment have a main role in the pathogenesis of obesity [63] [64] [65], and the pancreas can be considered a key organ in this process. "
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    ABSTRACT: The worldwide obesity epidemic is paralleled by a rise in the incidence of pancreatic disorders ranging from "fatty" pancreas to pancreatitis and cancer. Body fat accumulation and pancreatic dysfunctions have common pathways, mainly acting through insulin resistance and low-grade inflammation, frequently mediated by the epigenome. These mechanisms are affected by lifestyle and by the toxic effects of fat and pollutants. An early origin is common, starting in pediatric age or during the fetal life in response to nutritional factors, endocrine disruptor chemicals (EDCs) or parental exposure to toxics. A "fatty pancreas" is frequent in obese and is able to induce pancreatic damage. The fat is a target of EDCs and of the cytotoxic/mutagenic effects of heavy metals, and is the site of bioaccumulation of lipophilic and persistent pollutants related with insulin resistance and able to promote pancreatic cancer. Increased Body Mass Index (BMI) can act as independent risk factor for a more severe course of acute pancreatitis and obesity is also a well-known risk factor for pancreatic cancer, that is related with BMI, insulin resistance, and duration of exposure to the toxic effects of fat and/or of environmental pollutants. All these mechanisms involve gene-environment interactions through epigenetic factors, and might be manipulated by primary prevention measures. Further studies are needed, pointing to better assess the interplays of modifiable factors on both obesity and pancreatic diseases, and to verify the efficacy of primary prevention strategies involving lifestyle and environmental exposure to toxics
    European Journal of Internal Medicine 12/2014; 25(10):865-873. DOI:10.1016/j.ejim.2014.10.012 · 2.89 Impact Factor
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    • "Obesity rates have more than doubled since 1980, and in 2008 more than 1.4 billion adults were categorically overweight or obese [1]. There are a variety of lifestyle factors that have been proposed to contribute to this obesity pandemic [2]–[4]. For example, several epidemiological and laboratory studies have linked television (TV) watching to both increases in acute food intake, and subsequent weight gain and adiposity [2], [5]–[7]. "
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    ABSTRACT: Obesity is a serious and growing health concern worldwide. Watching television (TV) represents a condition during which many habitually eat, irrespective of hunger level. However, as of yet, little is known about how the content of television programs being watched differentially impacts concurrent eating behavior. In this study, eighteen normal-weight female students participated in three counter-balanced experimental conditions, including a ‘Boring’ TV condition (art lecture), an ‘Engaging’ TV condition (Swedish TV comedy series), and a no TV control condition during which participants read (a text on insects living in Sweden). Throughout each condition participants had access to both high-calorie (M&Ms) and low-calorie (grapes) snacks. We found that, relative to the Engaging TV condition, Boring TV encouraged excessive eating (+ 52 % g, P=0.009). Additionally, the Engaging TV condition actually resulted in significantly less concurrent intake relative to the control ‘Text’ condition (- 35 % g, P=0.05). This intake was driven almost entirely by the healthy snack, grapes; however, this interaction did not reach significance (P=0.07). Finally, there was a significant correlation between how bored participants were across all conditions, and their concurrent food intake (beta= 0.317, P=0.02). Intake as measured by kcals was similarly patterned but did not reach significance. These results suggest that, for women, different TV programs elicit different levels of concurrent food intake, and that the degree to which a program is engaging (or alternately, boring) is related to that intake. Additionally, they suggest that emotional content (e.g. boring vs. engaging) may be more associated than modality (e.g. TV vs. text) with concurrent intake.
    PLoS ONE 07/2014; 9(7):e100602.. DOI:10.1371/journal.pone.0100602 · 3.23 Impact Factor
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    • "It is established that various biological functions benefit from a restful night's sleep – e.g. memory consolidation, problem solving, and clearance of toxic substances from the brain (Wagner et al., 2004; Rasch et al., 2007; Chapman et al., 2012; Xie et al., 2013; Herzog et al., 2013). In addition, sleep appears to be crucial for the functioning of the human immune system (Bryant and Curtis, 2013; Bryant et al., 2004; Besedovsky et al., 2012). "
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    ABSTRACT: Lack of sleep greatly affects our immune system. The present study investigates the acute effects of total sleep deprivation on blood neutrophils, the most abundant immune cell in our circulation and the first cell type recruited to sites of infection. Thus, the population diversity and function of circulating neutrophils were compared in healthy young men following one night of total sleep deprivation (TSD) or after 8 h regular sleep. We found that neutrophil counts were elevated after nocturnal wakefulness (2.0±0.2×109/l vs. 2.6±0.2×109/l, sleep vs. TSD, respectively) and the population contained more immature CD16dim/CD62Lbright cells (0.11±0.040×109/l [5.5±1.1%] vs. 0.26±0.020×109/l [9.9±1.4%]). As the rise in numbers of circulating mature CD16bright/CD62Lbright neutrophils was less pronounced, the fraction of this subpopulation showed a significant decrease (1.8±0.15×109/l [88±1.8%] vs. 2.1±0.12×109/l [82±2.8%]). The surface expression of receptors regulating mobilization of neutrophils from bone marrow was decreased (CXCR4 and CD49d on immature neutrophils; CXCR2 on mature neutrophils). The receptor CXCR2 is also involved in the production of reactive oxygen species (ROS), and in line with this, total neutrophils produced less ROS. In addition, following sleep loss, circulating neutrophils exhibited enhanced surface levels of CD11b, which indicates enhanced granular fusion and concomitant protein translocation to the membrane. Our findings demonstrate that sleep loss exerts significant effects on population diversity and function of circulating neutrophils in healthy men. To which extent these changes could explain as to why people with poor sleep patterns are more susceptible to infections warrants further investigation.
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