LEGISLACIÓN TRIBUTARIA DE CHILE

obesity (Pérusse et al., 2005). Research has revealed inconsistent results, indicating that between 30-80% of weight problems are attributable to genetic factors (Harvey & Withers, 2008). Family studies demonstrate that obesity is correlated with family genealogy (Maes et al., 1997; Sørensen, Rasmussen, & Magnusson, 2007). Twin and adoption studies have found that the BMIs of monozygotic twins are more similar than those of dizygotic twins (Maes et al., 1997; Sørensen et al., 2007; Wansink & Kim, 2005). However, this correlation has been shown to decrease gradually with age, which may be attributable to environmental and lifestyle influences. This phenomenon is less clear for dizygotic twins.

While some studies maintain that genetic factors play a large role in the development of overweight and obesity, no consensus has been reached concerning the true extent of the role of genetics in overweight and obesity (Harvey & Withers, 2008; Maes et al., 1997). A systematic review by Silventoinen, Rokholm, Kaprio, and Sørensen (2010) indicates that both genetic and environmental factors contribute to increased BMI in children.

2.5.2 Neurological and biological causes. Research into the relationship between obesity and neurobiology has significantly increased in recent years (Harvey & Withers, 2008). Numerous neurotransmitters, neural pathways, and hormones have been identified as significant contributors to the regulation of weight and energy intake (Harvey & Withers, 2008). For example, neuropeptides at the hypothalamic level are essential for the regulation of energy expenditure, feeding behaviour, and neuroendocrine function (Grill & Kaplan, 2002).

Suriel (2013) proposes that people who are naturally thin – that is, people who have always been thin and are able to maintain a healthy weight without strict dietary and exercise regimes – experience increased levels of dopamine when eating, compared to obese people. Due to the role of dopamine in pleasure and reward, Suriel (2013) concludes that overweight and obese people experience less pleasure when eating, and therefore need to consume more food in order to experience pleasure. MRI studies reveal that overweight and obese people concurrently experience similar levels of reward, when presented with highly desired foods, as those of people

addicted to drugs who are presented with images of the substance to which they are addicted (Suriel, 2013).

Suriel (2013) found that there are physiological differences between people who are naturally thin and overweight people. Naturally thin people are found to eat only in response to hunger, and are not preoccupied with food. This lack of obsession with food means that the neurotransmitters that respond to the constant anticipation of food are not released in naturally thin people.

Serotonin has been identified as contributing to the development of obesity, Since low serotonin levels are closely linked to depression, depression and obesity are considered to share a common pathophysiology (Rosmond, 2004). Depression has been found to be predictive of developing obesity (Luppino et al., 2010) and is associated with an 18% increased risk of being obese (De Wit et al., 2010). Depression and obesity have been found to increase cardiovascular disease. Stunkard, Faith and Allison (2003) discovered that major depression among adolescents predicted a greater body mass index in adult life than in adolescents who had not been depressed.

Obesity was found to be positively correlated with major depression among women, but inversely related to depression among men (Stunkard et al., 2003). Gender was also found by Luppino et al. (2010) to be a moderating variable. Rosmond (2004) proposes that obesity and depression may represent different manifestations of the same neurobiological disease process. However, it is not clear whether depression or obesity is the first causal factor. It is considered possible that the psychological implications of perceiving oneself as overweight or obese could lead to social isolation, unhappiness, and stigmatisation (Rogge, Greenwald, & Golden, 2004), all of which may contribute to the development of depression. Depression, in turn, then exacerbates overweight and obesity. This explanation offers an alternative to the neurobiological explanation.

Gender is also considered a causal factor in the development of overweight and obesity (Brown, 1991; Del Mar et al., 2009). Men typically have a higher total body mass than women, whereas women have more subcutaneous fat, measured by skinfold thickness. Women also have much more peripheral fat in the legs and hips than men (Kissebah, Freedman, & Peiris, 1989).

Parity has been highly correlated with overweight and obesity in women (Arroyo, Avila-Rosas, Fernandez, Casanueva, & Galvan, 1995; Coitinho, Sichieri, & D'Aquino Benício, 2001; Ölin & Rössner, 1996; Weng, Bastian, Taylor Jr, Moser, & Ostbye, 2004). The Health and Retirement study by Weng et al. found that for each

additional birth, women face a 7% increase in the risk of obesity (Weng et al., 2004). However, since a 4% increase in risk of obesity was also found in men, it is plausible that the increased risk of developing overweight and obesity after childbirth could also be attributable to lifestyle changes for both men and women (Weng et al.,

2004). The Stockholm Pregnancy and Weight Development Study found that women who retained more weight postpartum demonstrated a larger increase in reported lifestyle changes, such as changes in diet, exercise, and meal patterns, than women who retained less postpartum weight (Rössner & Öhlin, 1995). This suggests that postpartum weight gain influences lifestyle changes that contribute to overweight and obesity. Research also indicates that the BMI of women prior to pregnancy (Coitinho et al., 2001), being of a young age at menarche, the time period between menarche and first birth, maternal age, and high gestational weight gain, are considered important in determining the risk of becoming overweight after pregnancy (Gunderson, Abrams, & Selvin, 2000).

Brain physiology and biochemistry have also been found to contribute to the development of overweight and of obesity by causing the problematic behaviours associated with obesity. The inability to modify these problematic behaviours, and to reduce the intake of dietary fat and sugar when individuals are consciously aware of the medical benefits of reducing these substances, has been attributed to brain physiology and biochemistry (Wurtman & Wurtman, 1987, as cited in Brown, 1991).

2.5.3 Environmental factors. Research into the causal factors of overweight and