This book on obesity has been written in a very different way — not those typical book type — which preaches high and mighty things. Obesity is most commonly caused by a combination of excessive food intake, lack of physical activity, and genetic susceptibility. A few cases are caused primarily by genes, endocrine disorders, medications, or mental illness. Evidence to support the view that obese people eat little yet gain weight due to a slow metabolism is not generally supported. On average, obese people have a greater energy expenditure than their thin counterparts due to the energy required to maintain an increased body mass. Obesity is mostly preventable through a combination of social changes and personal choices. Changes to diet and exercising are the main treatments. Diet plays an important role in the genesis of obesity. Personal choices, advertising, social customs and cultural influences, as well as food availability and pricing all play a role in determining what and how much an individual eats. This book has been written not in the usual format of cause-effect-treatment. When we are in the house we get to eat only what is in the kitchen but when we go to a cafeteria, we can get whatever we want, and of there is also the advantage of self-service.
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Obesity: An Introduction
Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have a negative effect on health.
People are generally considered obese when their body mass index (BMI), a measurement obtained by dividing a person's weight by the square of the person's height, is over 30 kg/m2, with the range 25–30 kg/m2 defined as overweight. Some East Asian countries use lower values.
Obesity increases the likelihood of various diseases, particularly heart disease, type 2 diabetes, obstructive sleep apnea, certain types of cancer, and osteoarthritis.
Obesity is most commonly caused by a combination of excessive food intake, lack of physical activity, and genetic susceptibility. A few cases are caused primarily by genes, endocrine disorders, medications, or mental illness.
Evidence to support the view that obese people eat little yet gain weight due to a slow metabolism is not generally supported. On average, obese people have a greater energy expenditure than their thin counterparts due to the energy required to maintain an increased body mass.
Obesity is mostly preventable through a combination of social changes and personal choices. Changes to diet and exercising are the main treatments.
Diet quality can be improved by reducing the consumption of energy-dense foods, such as those high in fat and sugars, and by increasing the intake of dietary fiber. Medications may be taken, along with a suitable diet, to reduce appetite or decrease fat absorption.
If diet, exercise, and medication are not effective, a gastric balloon or surgery may be performed to reduce stomach volume or bowel length, leading to feeling full earlier or a reduced ability to absorb nutrients from food.
Obesity is a leading preventable cause of death worldwide, with increasing rates in adults and children.
In 2014, 600 million adults (13%) and 42 million children under the age of five were obese.
Obesity is more common in women than men. Authorities view it as one of the most serious public health problems of the 21st century.
Obesity is stigmatized in much of the modern world (particularly in the Western world), though it was seen as a symbol of wealth and fertility at other times in history and still is in some parts of the world.
In 2013, the American Medical Association classified obesity as a disease.
BMI (kg/m) Classification
Obesity and BMI
A "super obese" male with a BMI of 53 kg/m2: weight 182 kg (400 lb), height 185 cm (6 ft 1 in)
Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health. It is defined by body mass index (BMI) and further evaluated in terms of fat distribution via the waist–hip ratio and total cardiovascular risk factors.
BMI is closely related to both percentage body fat and total body fat. In children, a healthy weight varies with age and sex. Obesity in children and adolescents is defined not as an absolute number but in relation to a historical normal group, such that obesity is a BMI greater than the 95th percentile.
BMI is usually expressed in kilograms per square metre, resulting when weight is measured in kilograms and height in metres. To convert from pounds per square inch multiply by 703 (kg/m2)/(lb/sq in).
The most commonly used definitions, established by the World Health Organization (WHO) in 1997 and published in 2000, provide the values listed in the table.
Some modifications to the WHO definitions have been made by particular organizations. The surgical literature breaks down class II and III obesity into further categories whose exact values are still disputed.
Any BMI ≥ 35 or 40 kg/m2 is severe obesity.
A BMI of ≥ 35 kg/m2 and experiencing obesity-related health conditions or ≥ 40–44.9 kg/m2 is morbid obesity.
A BMI of ≥ 45 or 50 kg/m2 is super obesity.
As Asian populations develop negative health consequences at a lower BMI than Caucasians, some nations have redefined obesity; Japan have defined obesity as any BMI greater than 25 kg/m2 while China uses a BMI of greater than 28 kg/m2.
EFFECTS ON HEALTH
Excessive body weight is associated with various diseases, particularly cardiovascular diseases, diabetes mellitus type 2, obstructive sleep apnea, certain types of cancer, osteoarthritis and asthma. As a result, obesity has been found to reduce life expectancy.
Obesity is one of the leading preventable causes of death worldwide. A number of reviews have found that mortality risk is lowest at a BMI of 20–25 kg/m2 in non-smokers and at 24–27 kg/m2 in current smokers, with risk increasing along with changes in either direction. This appears to apply in at least four continents. In contrast, a 2013 review found that grade 1 obesity (BMI 30-35) was not associated with higher mortality than normal weight, and that overweight (BMI 25-30) was associated with "lower" mortality than was normal weight (BMI 18.5-25). Other evidence suggests that the association of BMI and waist circumference with mortality is U- or J-shaped, while the association between waist-to- hip ratio and waist-to-height ratio with mortality is more positive. In Asians the risk of negative health effects begins to increase between 22–25 kg/m2. A BMI above 32 kg/m2 has been associated with a doubled mortality rate among women over a 16-year period. In the United States obesity is estimated to cause 111,909 to 365,000 deaths per year, while 1 million (7.7%) of deaths in Europe are attributed to excess weight. On average, obesity reduces life expectancy by six to seven years, a BMI of 30–35 kg/m2reduces life expectancy by two to four years, while severe obesity (BMI > 40 kg/m2) reduces life expectancy by ten years.
Obesity increases the risk of many physical and mental conditions. These comorbidities are most commonly shown in metabolic syndrome, a combination of medical disorders which includes: diabetes mellitus type 2, high blood pressure, high blood cholesterol, and high triglyceride levels.
Complications are either directly caused by obesity or indirectly related through mechanisms sharing a common cause such as a poor diet or a sedentary lifestyle. The strength of the link between obesity and specific conditions varies. One of the strongest is the link with type 2 diabetes. Excess body fat underlies 64% of cases of diabetes in men and 77% of cases in women.
Health consequences fall into two broad categories: those attributable to the effects of increased fat mass (such as osteoarthritis, obstructive sleep apnea, social stigmatization) and those due to the increased number of fat cells (diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease). Increases in body fat alter the body's response to insulin, potentially leading to insulin resistance. Increased fat also creates a proinflammatory state, and a prothrombotic state.
Although the negative health consequences of obesity in the general population are well supported by the available evidence, health outcomes in certain subgroups seem to be improved at an increased BMI, a phenomenon known as the obesity survival paradox. The paradox was first described in 1999 in overweight and obese people undergoing hemodialysis, and has subsequently been found in those with heart failure and peripheral artery disease (PAD).
In people with heart failure, those with a BMI between 30.0 and 34.9 had lower mortality than those with a normal weight. This has been attributed to the fact that people often lose weight as they become progressively more ill. Similar findings have been made in other types of heart disease. People with class I obesity and heart disease do not have greater rates of further heart problems than people of normal weight who also have heart disease. In people with greater degrees of obesity, however, the risk of further cardiovascular events is increased. Even after cardiac bypass surgery, no increase in mortality is seen in the overweight and obese. One study found that the improved survival could be explained by the more aggressive treatment obese people receive after a cardiac event. Another found that if one takes into account chronic obstructive pulmonary disease (COPD) in those with PAD, the benefit of obesity no longer exists.
At an individual level, a combination of excessive food energy intake and a lack of physical activity is thought to explain most cases of obesity. A limited number of cases are due primarily to genetics, medical reasons, or psychiatric illness. In contrast, increasing rates of obesity at a societal level are felt to be due to an easily accessible and palatable diet, increased reliance on cars, and mechanized manufacturing.
A 2006 review identified ten other possible contributors to the recent increase of obesity: (1) insufficient sleep, (2) endocrine disruptors (environmental pollutants that interfere with lipid metabolism), (3) decreased variability in ambient temperature, (4) decreased rates of smoking, because smoking suppresses appetite, (5) increased use of medications that can cause weight gain (e.g., atypical antipsychotics), (6) proportional increases in ethnic and age groups that tend to be heavier, (7) pregnancy at a later age (which may cause susceptibility to obesity in children), (8) epigenetic risk factors passed on generationally, (9) natural selection for higher BMI, and (10) assortative mating leading to increased concentration of obesity risk factors (this would increase the number of obese people by increasing population variance in weight). While there is substantial evidence supporting the influence of these mechanisms on the increased prevalence of obesity, the evidence is still inconclusive, and the authors state that these are probably less influential than the ones discussed in the previous paragraph.
A 2016 review supported excess food as the primary factor. Dietary energy supply per capita varies markedly between different regions and countries. It has also changed significantly over time. From the early 1970s to the late 1990s the average food energy available per person per day (the amount of food bought) increased in all parts of the world except Eastern Europe. The United States had the highest availability with 3,654 calories (15,290 kJ) per person in 1996. This increased further in 2003 to 3,754 calories (15,710 kJ). During the late 1990s Europeans had 3,394 calories (14,200 kJ) per person, in the developing areas of Asia there were 2,648 calories (11,080 kJ) per person, and in sub-Saharan Africa people had 2,176 calories (9,100 kJ) per person. Total food energy consumption has been found to be related to obesity.
The widespread availability of nutritional guidelines has done little to address the problems of overeating and poor dietary choice. From 1971 to 2000, obesity rates in the United States increased from 14.5% to 30.9%. During the same period, an increase occurred in the average amount of food energy consumed. For women, the average increase was 335 calories (1,400 kJ) per day (1,542 calories (6,450 kJ) in 1971 and 1,877 calories (7,850 kJ) in 2004), while for men the average increase was 168 calories (700 kJ) per day (2,450 calories (10,300 kJ) in 1971 and 2,618 calories (10,950 kJ) in 2004). Most of this extra food energy came from an increase in carbohydrate consumption rather than fat consumption. The primary sources of these extra carbohydrates are sweetened beverages, which now account for almost 25 percent of daily food energy in young adults in America, and potato chips. Consumption of sweetened drinks such as soft drinks, fruit drinks, iced tea, and energy and vitamin water drinks is believed to be contributing to the rising rates of obesity and to an increased risk of metabolic syndrome and type 2 diabetes. Vitamin D deficiency is related to diseases associated with obesity.
As societies become increasingly reliant on energy-dense, big-portions, and fast-food meals, the association between fast-food consumption and obesity becomes more concerning. In the United States consumption of fast- food meals tripled and food energy intake from these meals quadrupled between 1977 and 1995.
Agricultural policy and techniques in the United States and Europe have led to lower food prices. In the United States, subsidization of corn, soy, wheat, and rice through the U.S. farm bill has made the main sources of processed food cheap compared to fruits and vegetables. Calorie count laws and nutrition facts labels attempt to steer people toward making healthier food choices, including awareness of how much food energy is being consumed.
Obese people consistently under-report their food consumption as compared to people of normal weight. This is supported both by tests of people carried out in a calorimeter room and by direct observation.
A sedentary lifestyle plays a significant role in obesity. Worldwide there has been a large shift towards less physically demanding work, and currently at least 30% of the world's population gets insufficient exercise. This is primarily due to increasing use of mechanized transportation and a greater prevalence of labor-saving technology in the home. In children, there appear to be declines in levels of physical activity due to less walking and physical education. World trends in active leisure time physical activity are less clear. The World Health Organization indicates people worldwide are taking up less active recreational pursuits, while a study from Finland found an increase and a study from the United States found leisure-time physical activity has not changed significantly. A 2011 review of physical activity in children found that it may not be a significant contributor.
In both children and adults, there is an association between television viewing time and the risk of obesity. A review found 63 of 73 studies (86%) showed an increased rate of childhood obesity with increased media exposure, with rates increasing proportionally to time spent watching television.
Like many other medical conditions, obesity is the result of an interplay between genetic and environmental factors. Polymorphisms in various genes controlling appetite and metabolism predispose to obesity when sufficient food energy is present. As of 2006, more than 41 of these sites on the human genome have been linked to the development of obesity when a favorable environment is present. People with two copies of the FTO gene (fat mass and obesity associated gene) have been found on average to weigh 3–4 kg more and have a 1.67-fold greater risk of obesity compared with those without the risk allele. The differences in BMI between people that are due to genetics varies depending on the population examined from 6% to 85%.
Obesity is a major feature in several syndromes, such as Prader–Willi syndrome, Bardet–Biedl syndrome, Cohen syndrome, and MOMO syndrome. (The term "non-syndromic obesity" is sometimes used to exclude these conditions.) In people with early-onset severe obesity (defined by an onset before 10 years of age and body mass index over three standard deviations above normal), 7% harbor a single point DNA mutation.
Studies that have focused on inheritance patterns rather than on specific genes have found that 80% of the offspring of two obese parents were also obese, in contrast to less than 10% of the offspring of two parents who were of normal weight. Different people exposed to the same environment have different risks of obesity due to their underlying genetics.
The thrifty gene hypothesis postulates that, due to dietary scarcity during human evolution, people are prone to obesity. Their ability to take advantage of rare periods of abundance by storing energy as fat would be advantageous during times of varying food availability, and individuals with greater adipose reserves would be more likely to survive famine. This tendency to store fat, however, would be maladaptive in societies with stable food supplies. This theory has received various criticisms, and other evolutionarily-based theories such as the drifty gene hypothesis and the thrifty phenotype hypothesis have also been proposed.
Certain physical and mental illnesses and the pharmaceutical substances used to treat them can increase risk of obesity. Medical illnesses that increase obesity risk include several rare genetic syndromes (listed above) as well as some congenital or acquired conditions: hypothyroidism, Cushing's syndrome, growth hormone deficiency, and the eating disorders: binge eating disorder and night eating syndrome. However, obesity is not regarded as a psychiatric disorder, and therefore is not listed in the DSM-IVR as a psychiatric illness. The risk of overweight and obesity is higher in patients with psychiatric disorders than in persons without psychiatric disorders.(Continues…)
Excerpted from "Basic Health Care Series Obesity"
Copyright © 2017 Juliann Moen.
Excerpted by permission of Vij Books India Pvt Ltd.
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Table of ContentsObesity: An Introduction; Diet and Obesity; Social Determinants of Obesity; Management of Obesity; Fat Acceptance Movement; Social Stigma of Obesity; Causes of Obesity; Obesity Treatment; Obesity Care and Fitness