**3. Obesity is a complex and multi-factorial disease**

Obesity is a multifactorial, chronic, and progressive disease whose pathogenesis is tied to a strong genetic component as well as a multitude of hormonal, metabolic, psychological, cultural and behavioral factors.

Physiologically, the path to weight gain is defined by a positive energy balance which occurs when consumed calories (energy intake) exceeds used calories (energy expenditure) in the performance of basic biological functions, daily activities, and exercise [3]. A positive energy balance can be caused by overeating or by not getting enough physical activity. In addition, there are other conditions that affect energy balance and fat accumulation which do not involve excessive eating or sedentary behavior. These include:

Chronic sleep loss.

Chronic stress and psychological distress.

Consumption of foods that, independent of caloric content, cause metabolic/ hormonal changes that can increase body fat – foods high in sugar or high fructose corn syrup, processed grains and meats, and fats.

Low intake of fat-fighting foods such as fruits, vegetables, legumes, nuts, seeds, quality protein.

Various medications – such as steroids and anti-depressants. Various pollutants.

Weight gain is self-perpetuating, which is a reason why obesity is considered a progressive disease. Weight gain causes hormonal, metabolic and molecular changes that increase the potential for even greater fat accumulation. Obesity-associated biological changes reduce the body's ability to oxidize fat for energy, increase the conversion of glucose/carbohydrates to fat, and increase the body's capacity to store fat. This means that more calories consumed will end up being stored as fat. To worsen matters, obesity affects appetite and hunger regulators in a way that can decrease satiety, increasing portion size and eating frequency. Weight gain, therefore, changes the biology of the body in a manner that favors further weight gain and obesity [3].

#### *Long Term Success and Follow-Up after Bariatric Surgery DOI: http://dx.doi.org/10.5772/intechopen.107177*

Dieting to reduce caloric intake is a primary treatment for obesity, but it can also contribute to obesity progression. Dietary weight-loss causes biological responses that can persist long-term and end up contributing to weight regain. Weight loss can lead to reduced energy expenditure and calorie conservation if the body 'thinks' it is starving. A reduction in energy expenditure with dietary weight-loss requires that, to maintain weight-loss, an individual eat even fewer calories compared with someone of equal body size who has never dieted before. Eating less can be especially difficult with dieting, since there can be associated long-term changes in appetite regulation which increase hunger and food consumed. Such diet-induced changes favor a positive energy balance and weight regain. Since the conditions responsible reduced energy expenditure and increased appetite can persist long-term, an individual often will not only regain their lost weight, but even more [3].

Changes in fat metabolism are another biological response that occurs with dieting. Dietary weight-loss can lead to reduced oxidation of dietary fat by approximately 50 percent [4]. This includes reduced fat burning during low-grade activity such as walking, house chores, or working on a computer. This reduction in fat oxidation following a dietary weight-loss increases the amount of fat available for storage. In fact, dieting increases the capacity for fat depots to store even more fat than before a diet. These changes lead to a progressive increase in fat accumulation even if the individual is not overeating.

As a heritable trait, obesity is influenced by the interplay of genetics, epigenetics, metagenomics and the environment. Genetic predisposition to obesity is well studied and described [5, 6]. An example of this is a classic study of obesity within Danish adopted individuals, which demonstrated a high degree of correlation of body mass index (BMI) between adoptees and their biological parents, instead of their adoptive parents [5]. Another study by the same authors demonstrated that twins raised separately had similar BMI with each other, regardless of the environment in which they were raised [7]. Epigenetic changes may be involved as mediators of environmental influences and provide future opportunities for intervention [8].

Obesity can be associated with several endocrine alterations due to changes in the hypothalamic–pituitary hormones axis. These include hypothyroidism, Cushing's disease, hypogonadism, and growth hormone deficiency. Besides its role in energy storage, adipose tissue has several other important functions that can be mediated through hormones or substances synthesized and released by adipocytes, which include leptin and adiponectin. Additionally, obesity is also a common feature of polycystic ovarian syndrome with hyperinsulinemia being the primary etiological factor [9].

Metabolic syndrome is a condition characterized by a specific constellation of reversible major risk factors for cardiovascular disease and type 2 diabetes. The main diagnostic components are reduced HDL-cholesterol, raised triglycerides, blood pressure and fasting plasma glucose, all of which are related to weight gain, specifically intra-abdominal/ectopic fat accumulation and a large waist circumference. Metabolic syndrome is directly related to advancing age, affecting 30–40% of people by age 65. This seems to be driven mainly by progressive adult weight gain, and by a genetic or epigenetic predisposition to intra-abdominal/ectopic fat accumulation. Metabolic syndrome can also be associated with conversely, a lack of subcutaneous adipose tissue, low skeletal muscle mass and anti-retroviral drugs. Reducing weight even by only 5–10% substantially lowers all metabolic syndrome components, and the risk of type 2 diabetes and cardiovascular disease [10].

Culture also has a substantial association with BMI. This association is important for understanding the pattern of obesity across different cultures and countries. It is also important to recognize the importance of the association of culture and BMI in developing public health interventions to reduce obesity [11].

### **4. Psychology and behavior**

Numerous studies support a strong link between obesity and mental health. This relationship is a two-way street; while mental health disorders increase the risk for obesity, having obesity also increases the risk of mental health disorders, especially in certain populations. Mental health disorders can increase the risk for obesity for various reasons. Medications used to treat psychiatric illnesses, such as anti-depressants, can themselves cause weight gain and insulin resistance. Additionally, mental illnesses are correlated with behaviors such as chronic sleep loss, poor eating behaviors, and sedentary behavior, which can contribute to obesity development.

Obesity increases the risk for depression. This is likely due to numerous complex factors, including poor self-esteem and depressed mood in response to weight bias and stigma, decreased activity and impaired mobility from joint and back pain associated with excess weight, and biological disruptions caused by adipocyte secretion of chemicals during obesity [12]. Obese patients overall have higher levels of stress, anxiety, depression, food craving, and emotional and behavioral disturbance [EBD] symptoms, with lower levels of self-esteem and quality of life compared with normalweight individuals. Additionally, the severity of psychological disorders is directly related to the degree of obesity [12].

It is important that patients with mental health disorders are monitored for weight disorders, and that obese individuals are screened for mental health disorders. Treatment of obesity is associated with a significant improvement of anxiety, depression, and general psychopathology, and a similar pattern of reduction of binge eating symptomatology. Pre-treatment emotional eating severity has been found to be a significant outcome modifier, supporting the importance of a pre-treatment careful psychological assessment to supervise the post-surgical outcome [13].

Evaluation for underlying eating disorders such as food addiction and binge eating can be important assessment criteria for patients looking to undergo bariatric surgery, as well as for ongoing assessment afterwards. There are multiple surveys, questionnaires, and assessment tools that can be used to evaluate psychopathology before and after bariatric surgery. Examples include the Yale Food Addiction Scale (YFAS), Emotional Eating Scale, Beck Depression Inventory-Second Edition (BDI-II), Hospital Anxiety and Depression Scale, and the Short-Form Health Survey-36 (SF-36). These disorders share overlapping and non-overlapping features; the presence of both may represent a more severe obesity subgroup among treatment-seeking samples. Loss-of-control (LOC) eating, a key marker of binge eating, is one of the few consistent predictors of suboptimal weight outcomes post-bariatric surgery [14].

The presence of food addiction without binge eating has mixed results in terms of impact on weight loss after bariatric surgery. While some studies do not appear to show an impact [15], others show a correlation between higher number of food addiction symptoms and less weight loss [16]. Patients with emotional eating diagnosed pre-operatively, such as in response to anger/frustration, anxiety, or depression, are

more likely to miss follow-up appointments and have poorer weight loss outcomes at 1-year post-op [16]. Evidence like this supports screening for these behaviors during the pre-surgical psychosocial evaluation, which would allow opportunities for psychotherapy and potential improvement in weight loss outcomes.

Psychiatric symptoms may not be related to weight loss outcomes [16]. Depressive disorders, as opposed to anxiety disorders, have been shown to decrease significantly after bariatric surgery. Importantly however, the presence of depressive disorders after bariatric surgery significantly predicts post-surgical outcomes and may signal a need for heightened clinical attention [17].
