Obesity and type 2 diabetes
Obesity is an excess of body fat that may impair health, and it is the main cause of the insulin resistance from which type 2 diabetes develops. Both diseases have risen worldwide since the 1980s, driven by changes in diet and physical activity acting on a susceptibility that varies between people, and their consequences run from the mechanical and metabolic effects of excess fat to the psychological burden of a chronic disease and its cost to health systems.
Definition and measurement of obesity
The World Health Organization defines obesity as an abnormal or excessive accumulation of fat that may impair health. It counts a body mass index (BMI) of 30 kg/m² or more as obese. Overweight lies in the transition zone between that threshold and the normal weight limit of 25 kg/m², and the normal range runs from 18.5 to 25 kg/m².
BMI is weight in kilograms divided by the square of height in metres, and it is the measure most frequently used in epidemiological studies to classify body condition. Adolphe Quetelet proposed BMI in 1835, basing it on average measurements from a population of Scottish soldiers. A major limitation is that it does not distinguish fat mass from lean mass. BMI has been reported to undercount obese people by 39%. Abdominal obesity, measured by waist circumference or waist-to-hip ratio, is considered a more reliable predictor of the risk of metabolic complications of obesity.
Diabetes and type 2 diabetes
Diabetes is a chronic disease in which either insulin production is impaired or the body uses insulin inefficiently. Insulin is a hormone released by pancreatic β-cells in response to a rise in plasma glucose after food. Diabetes mellitus is the most common disease resulting from impaired release of a pancreatic hormone. Diabetes is a metabolic disease that leads to secondary microvascular and macrovascular complications, such as nephropathy, neuropathy and cardiovascular disease.
In type 2 diabetes the body does not release enough insulin or becomes insensitive to it, which is called insulin resistance. Type 2 diabetes results from a combination of insufficient insulin production and insulin resistance, and it is frequently associated with obesity and lack of exercise. At first the pancreas can still produce insulin and the problem is insulin action. As the pancreas works harder and harder, a relative insulin deficiency becomes an absolute one. As the disease progresses, the β-cells can no longer produce insulin, which eventually leads to a deficiency.
In 2012, type 2 diabetes was put at 90% of diabetes cases. Accounts from 2011 and 2013 put it at about 95%. It most often affects people from ethnic and racial minority populations and is linked to excess adiposity.
How obesity leads to type 2 diabetes
Although genetic factors influence the risk of developing diabetes, obesity is well established as the main cause of type 2 diabetes. Obesity is a key risk factor because it is the main cause of insulin resistance. An obese, insulin-resistant person does not necessarily develop diabetes, because the β-cells compensate by producing more insulin. Type 2 diabetes occurs when the β-cells are damaged and can no longer compensate, which leads to hyperglycaemia. The release of increased amounts of free fatty acids from adipose tissue in obese people is a crucial factor linking obesity, insulin resistance and impaired β-cell function. Obesity-induced tissue inflammation also releases pro-inflammatory cytokines and activates protein kinases known to take part in the development of insulin resistance.
Type 2 diabetes is caused by the body's ineffective use of insulin brought on by excess body weight and too little physical exercise. Its causes are generally a sedentary lifestyle and the consumption of more fats and sugars. The risk of type 2 diabetes increases with the level and the duration of overweight and with the amount of visceral fat, the fat deposited around the abdominal organs. As the body accumulates fat, the likelihood of type 2 diabetes developing increases dramatically, and abdominal fat is the most dangerous. A study of the association between diabetes and BMI found that at a BMI of 35 kg/m² the relative risk of type 2 diabetes rose by 40%. Even thin people are at risk if they lead a sedentary or unhealthy life, with low physical activity, irregular eating, a poor diet or emotional stress, because these build up "invisible" visceral fat. Type 2 diabetes usually appears after the age of 40, but in South Asian and African-Caribbean people it often appears after 25.
The interlocking epidemics of obesity and type 2 diabetes are called "diabesity". Obesity behaves less like a twin of diabetes than like an older sibling leading the way, with diabetes following closely behind. In the late 1980s and early 1990s the prevalence of diabetes in the United States rose dramatically, and 75% of the increase occurred in the part of the population who were obese or very overweight. The worldwide rise in obesity explains the outbreak of diabetes in recent decades. Diabesity was described in 2010 as a major international public health problem.
Prevalence of obesity and diabetes
Obesity is associated with many chronic diseases, and the dramatic rise in its prevalence worldwide has become a major health concern. According to the WHO, obesity worldwide has more than doubled since 1980. Its prevalence had risen dramatically over the two decades before 2012, with serious consequences for healthcare and financial systems. Fifty years before 2012 there were no statistics on obesity.
In 2012 half a billion people, 12% of the world's population, were considered obese, and the prevalence kept rising, fuelled by a lifestyle of bad diet and inactivity. Another 2012 account put the average prevalence of obesity worldwide at 33%. In 2008, 1.4 billion people were overweight, with a BMI of 25 kg/m² or more, and 500 million of them were obese, with a BMI of 30 kg/m² or more. Almost a billion adults were overweight in 2012 and one-third of them clinically obese, and the age-adjusted prevalence of obesity in the USA was 33.8%.
Obesity was at first a problem of high-income countries and seen only in adults, but it has spread to middle- and low-income countries and to children and adolescents. In 2010, 44.2% of men and 48.3% of women in the USA were obese, and 26.3% of women in the UK. In 2012, 39.1% of women in Chile, 52.7% in Trinidad and Tobago and 36.8% in South Africa were considered obese. Figures were creeping up in Southeast Asia and the Middle East, where the population had historically been thin. In China, 1% of men were overweight in 2002 and 4.1% obese in 2010, yet 45% of men were considered overweight, with a BMI of 25 kg/m² or more. Africa was dealing with the double burden of undernutrition and obesity, the latter a particular problem in large African towns. The worst affected region was the Pacific Islands, where 84.6% of men in Nauru were overweight in 2010.
In the UK, a 2011 prediction had the obesity rate rising from 25% to 40% by 2030. On average, people in the UK in 2012 were 19 kg heavier than they had been in the mid-1960s.
In 2012 type 2 diabetes had become a burden for society and its incidence continued to increase, and diabetes had become a pandemic of the twenty-first century. In 2011, 366 million people worldwide had diabetes, and 4.6 million died from the consequences of high blood sugar. Eighty per cent of those deaths occurred in low- and middle-income countries, where the burden of diabetes had increased at a dramatic rate. In 2012 the WHO estimated that one adult in ten had diabetes. Another 2012 estimate gave 346 million people with diabetes worldwide, a number still increasing, and attributed the increase to changes in diet and lifestyle.
In 2012 diabetes was estimated to affect more than 32 million citizens of the European Union, nearly 10% of its population, and a further 32 million were not yet diagnosed or had pre-diabetes. Rates were expected to rise further as the population aged, and the European Parliament considered diabetes an epidemic. The complications of type 2 diabetes are preventable through early diagnosis and lifestyle change, but type 2 diabetes is frequently diagnosed too late, and 50% of all people with diabetes were unaware of their condition.
In the United States in 2011, almost 10% of the adult population had diabetes: 24 million Americans had diabetes and 79 million had pre-diabetes, and 25% of those with either were unaware of their condition. In 2013 an estimated 23 million people in the United States had diabetes mellitus, approximately 5 million of them undiagnosed.
Seventeen years of nationally representative survey data from the Centers for Disease Control and Prevention put the chance of diabetes developing in the average person born in the United States in 2000 at one in three, rising to one in two for certain minority populations, such as Black and Latino populations. Experts likewise estimated that diabetes would develop during the lifetime of one in three children born in 2000. One doomsday scenario for the future has diabetes developing in 75% of adults worldwide.
Obesity and type 2 diabetes in children
What used to be called adult-onset diabetes is increasingly being diagnosed in children. Children, some as young as seven, are more often being diagnosed with type 2 diabetes. The rise was first noticed among the Pima Indians of Arizona, in children as young as seven, and a few years later in children from other Native American tribes. The CDC began to study the situation in the 1980s, setting up large registries in Arizona, Texas and Ohio to search for diabetes in youth. In 1996, 30% of the cases of diabetes in children were type 2, against just 5% a decade earlier. Type 2 diabetes traditionally accounted for less than 2% of cases in children, and by 2011 it had risen to more than 25%, likely because of the growing obesity epidemic in children.
An ageing population and diagnosis in more people through greater awareness are not the whole answer to the rise. Data implicate both behavioural and environmental causes. Studies indicate that children's average daily calorie intake rose by 200 calories over a seven-year period. Adding 500 calories a day adds a pound of body weight in two weeks, and a slice of pizza is at least 500 calories and a basic burger almost twice that. Wherever economic growth increases, diabetes begins to increase, and the increase in diabetes and obesity is evident everywhere there are data.
By 2005 the number of overweight children in the United States had tripled since 1970. By 2007 the prevalence of childhood obesity in the United States had increased more than three-fold over 30 years, accompanied by significant increases in the incidence of type 2 diabetes in children and adolescents. A US report found the prevalence of obesity to be 17% in the age group 2–19 years. By 2011 genes, epigenetic modifications and environmental influences had led to a high BMI in one-third of children, and approximately 15% of the overweight and 25% of the obese among them had pre-diabetes.
Childhood obesity leads to an increased risk of obesity later in life. Diabetes-related complications often appear after about 20 years with the disease, so the overweight and obese teenagers of 2011 would face them by the age of 35. One 2011 forecast held that the epidemic would impair the ability of that year's children to raise their own children and would reduce the productivity of the future American workforce, and that the next generation might be the first to live shorter lives than its parents. Children may now be the first generation to be sicker and die younger than their parents.
Causes of obesity
Obesity is a gradual process resulting from an energy imbalance, in which the energy taken in from food and drink exceeds the energy used by physiological and physical activity. The excess energy is stored as body fat, and too much fat is a major risk factor for many diseases. This seemingly simple imbalance is driven by a complex mixture of genetic, environmental, psychosocial and cultural factors.
Apart from specific endocrine and neurological disorders, the cause of overweight is more calorie intake than calorie expenditure. People becoming obese are therefore eating more, or eating foods and drinks with more calories, or being less active, or both. In theory the solution is equally clear: eat less or eat less caloric foods, become more active, or both. Possible answers to why obesity is nonetheless becoming a global epidemic include that people do not know exactly what they are eating, that they know and eat it anyway, that they cannot change a sedentary lifestyle because they lack the time or the will, and that they do not care about their body weight, being unaware of the health risks of obesity or unconcerned about their health. Overweight seems not to be simply the result of a mathematical equation: genetic, epigenetic, endocrine, neurological and environmental factors contribute to its genesis, and there are many psychological, social, cultural and economic aspects to gaining, maintaining and losing weight.
Over the centuries people have become taller, heavier and stronger, and one of the major reasons is the increasing supply of calories in the diet. Weight gain was once extremely beneficial for health, well-being and lifespan, but by 2012 it had gone too far and become detrimental, in an epidemic of overeating. Centuries ago obesity was a synonym of wealth, and this perception still holds in some cultures where undernourishment is present. In past centuries and even decades, excess weight was a sign of health and wealth. Today overweight and obesity are highly prevalent across all social classes. The energy balance changed immensely after the Second World War with the introduction of cars, television and prepared foods, along with changes in the idea of a portion and reduced physical activity.
The prevalence of obesity began to increase drastically from the mid-1980s. Since genomes have remained mainly unchanged for generations, lifestyle changes over the past few decades seem to have had a major role in the rise. The childhood obesity epidemic has grown so quickly that it is most likely due to changes in culture and not to genetics. Globally, consumption of unhealthy foods high in sugar, fats and salt and low in nutrients and vitamins has increased enormously. Intake of sugary drinks has also increased globally, and they are considered to make up a large part of the increased calorie intake leading to obesity. Portion sizes have increased, and so has the consumption of processed and convenience foods high in sugar and fat. Lifestyles have become more inactive and jobs more sedentary: people use transport instead of walking, spend long hours in front of computers and televisions for work and leisure, and spend little energy because everything is nearby and on hand. One account holds that people in the UK were not exercising less in 2012 but needed to exercise more to counteract their change in diet. It attributes the increase in obesity mainly to the consumption of large quantities of high-fructose corn syrup, introduced into the diet by the food industry in the 1970s.
In the United States the obesity epidemic is fuelled by increasing food intake coupled with decreasing physical activity. The "super-size" serving is one change in the American diet that may be affecting the health of the country's young people, and daily inactivity may be another factor. A small restaurant soda held 6 ounces in the 1950s against 16 ounces in 2005, and supersized portions of French fries had become the norm. Children ate 40% more at a heavily advertised fast-food meal than at home, few walked or cycled to school, and American children watched an average of four hours of television a day. Fewer than 10% of US schools had daily mandatory physical education programmes in 2007. Fewer than 20% of US middle and high schools provided physical education classes in 2005.
Although obesity is considered self-inflicted, the social and economic changes that come with development also influence lifestyle choices. Many towns have been built without pavements or enough space for children to play actively, and healthy foods may be inaccessible or too expensive. Obesity is closely related to socio-economic status, with a higher prevalence among poorer and less-educated people. School cafeterias may not offer healthy menus, and parents may not teach healthy lifestyles. The agricultural and food industries have often selected food options for their customers on profit rather than health. In the USA between 1985 and 2000, prices for fruit and vegetables rose 118%, against 35% for fats, 46% for sugars and 20% for carbonated soft drinks.
Chemicals in the environment may add to the problem, as certain chemicals have been shown to cause metabolic changes. Endocrine-disrupting chemicals from packaging and food processing, such as bisphenol A, can be detected in foods and in the urine and serum of most humans. Experimental studies in animals have found an association between low-dose foetal exposure to bisphenol A and obesity at puberty, and an American study observed the same in humans. Early antibiotic use in infants under six months of age has been linked to obesity. Other possible factors include lack of sleep and certain medications and illnesses: BMI is inversely correlated with sleep duration, and obesity is associated with some psychological problems and with smoking cessation.
One researcher holds that humans are still adapted to the ancestral hunter-gatherer diet and lifestyle, in which people survived by gorging when food was abundant, preferring energy-rich foods and minimising energy expenditure to necessary physical activity. An obesogenic society, with energy-dense food abundant, easily available, effortless and cheap, is exactly what hunter-gatherers would have needed to survive, and without the periods of famine between, this biological adaptation to hunger results in the global epidemic of obesity and related habits. Diabesity is a global epidemic resulting from the collision of ancient genes, designed to aid survival in an austere environment, with a modern environment in which people need not spend most of their time procuring food. Consuming the most calories while expending the least energy is no longer the goal, and the question has become how to consume the proper amount of calories and bring physical activity back into daily life.
Genetics of obesity
In a population exposed to the same obesogenic environment, some people remain thin while some of the overweight cannot lose weight, which suggests inter-individual variation in susceptibility to obesity, with biological mechanisms or genes influencing it. Obesity runs in families, and family and twin studies have shown BMI to be 40–60% heritable. Abdominal obesity is 45–60% heritable.
In the mid-1990s several studies examined genes suspected to be involved in obesity because of their expression in extreme or early-onset obesity and evidence from transgenic animal models. Mutant mice accumulating five times the normal amount of body fat were found to lack the single ob gene, which is active in fat cells and produces a protein that reaches the brain through the bloodstream to signal satiety. The protein was named leptin, from the Greek leptos, thin. Mice of a second obesity model, db mice, lack the gene for the leptin receptor and so cannot receive the satiety message. Several conditions of childhood obesity have been linked to mutations in these genes, and mutations in the melanocortin receptor gene cause severe early-onset obesity. Obesity is a common phenotype of several syndromes, including Prader-Willi syndrome, Bardet-Biedl syndrome, a sub-phenotype of Fragile X syndrome and WAGR syndrome. These single-gene defects are rare, and all their cases together come nowhere near the prevalence of obesity.
Genome-wide linkage studies towards the end of the 1990s revealed approximately 300 chromosomal loci associated with obesity, but no single causal gene or variant. Genome-wide association studies (GWAS), begun in 2005, have been more successful, testing two million genetic variants for association in extremely large samples of unrelated people. GWAS of obesity-related traits, namely BMI, waist circumference, waist-to-hip ratio, body fat percentage and extreme early-onset obesity, found 52 robust loci. For BMI, 32 loci reaching genome-wide significance have been identified in white European-type adults, of which eight are strongly linked to an adjacent common missense single-nucleotide polymorphism and 15 contain genes that may be linked biologically to obesity. The established loci explain only a fraction of the heritability, approximately 2–4%. In 2012, knowing a person's genotype at all eight of those loci did not provide a clinically viable test for obesity risk. Childhood obesity and parental obesity, the two traditional predictors, appear to be the only reliable predictors of obesity risk in adult life.
GWAS have been extremely useful in identifying genes in the susceptibility loci, allowing new hypotheses about the biology of common obesity. FTO was the first obesity-associated gene described and is expressed in the feeding regions of the hypothalamus. It may affect food intake, as carriers of the risk allele have been shown to prefer energy-dense and more palatable foods. Some of the genes found, such as MCR4, POMC and BDNF, were already known to be involved in monogenic obesity, and SH2B1 causes obesity when knocked out in mice and appears to be involved in leptin signalling. Many of these genes are highly expressed in the brain, particularly the hypothalamus, which suggests a central role for the brain in the predisposition to obesity. One of the most recent variants maps within GIPR, which encodes an incretin receptor thought to play a role in nutrient sensing and insulin secretion in the periphery, suggesting that variation in insulin secretion may be involved in the development of obesity. An estimated 250 common variant loci for human obesity remain to be discovered, and many more loci with smaller effects will probably be identified. These might be found through more extensive searches and by broadening searches to children, adolescents and adults of non-European descent.
Environment and genetic disposition both appear to take part in the development of obesity, and the Pima Indians are the classic example of a gene–environment interaction. Sixty-nine per cent of Pima Indians living in the obesogenic environment of Arizona are obese, against about 30% of white Americans in the same environment. In the restrictive environment of Mexico only 13% become obese, suggesting that something in the Pima Indians' genetic makeup predisposes them to obesity. A number of studies report that physical activity attenuates the association between the FTO locus and obesity traits, and such gene–physical activity interactions carry the public-health message that genetic susceptibility to obesity may be modifiable. Research points towards the possibility of changing gene function without changing genomic sequences, and perinatal metabolic programming appears to influence early-life obesity through epigenetic effects. Assortative mating for obesity is estimated to have increased the prevalence of obesity in the population by about 5%.
Consequences of obesity and diabetes
Overweight and obesity are associated with a variety of chronic diseases, including musculoskeletal problems, type 2 diabetes mellitus, cardiovascular diseases and cancer. As body weight rises to the level defined as obese, several pathologies appear. The increased mass of adipose tissue leads to disability and to effects on quality of life such as shame, depression, physical discomfort, sexual problems and social isolation. Excess fat may also lead to sleep apnoea, through increased abdominal pressure on the diaphragm and reduced lung volume, and to osteoarthritis through stress on the joints. The metabolic changes of obesity, as pathogenic products are released from larger and more numerous fat cells, increase the risk of a second set of diseases: type 2 diabetes, coronary heart disease, hypertension, endometrial, breast and colon cancers, metabolic syndrome, dyslipidaemia, stroke, non-alcoholic fatty liver disease, gallbladder disease, and gynaecological problems such as abnormal menses and infertility. Metabolic syndrome is a combination of high blood sugar, high blood pressure, high triglycerides and high cholesterol, and dyslipidaemia includes high total cholesterol or triglycerides. Obesity may also accelerate cognitive decline and increase deficits in academic achievement. The risks of all these problems are greater with overweight as well as with obesity.
Most of the diseases associated with obesity are deadly. On average obesity reduces life expectancy by 6–7 years, and it has become one of the leading preventable causes of death in the world. By 2007 obesity had quickly begun to rival tobacco use as the major preventable cause of disease and death in the United States. Overweight and obesity are linked to more deaths worldwide than underweight. The Centers for Disease Control and Prevention estimate that 112,000–365,000 excess deaths a year in the United States can be attributed to obesity, more than 80% of them among people with a BMI over 30 kg/m².
Obesity is a burden in most aspects of life: to health, to quality of life, and socially, professionally and economically. It also affects psychological dimensions such as self-acceptance, self-esteem, mood, social interaction and sexuality. Overweight and obesity have been linked to lower educational status and professional achievement, and consequently lower incomes, a relation whose direction of causality is a chicken-and-egg dilemma. A small experimental study in Germany found that human-resources professionals more often disqualified obese applicants, especially women, from being hired and less often nominated them for a supervisory position, while non-ethnic normal-weight individuals were favoured. The study suggests that weight-related stigmatisation is a social and economic problem as well as a public-health one.
Obesity is the leader of a wealthy market that incessantly demands new products, such as weight-management programmes, diets, drugs and surgical approaches, fostered not least by the ideal of beauty. Most women's magazines carry many diet recipes, often with details of which diets worked for which prominent people, and the food industry has long recognised the huge market potential of diet products. A "diet" version of an unhealthy product, such as diet potato chips, may act as a licence to consume it, or to eat twice the amount at half the calories each.
Diabetes complications are numerous, including cardiovascular disease, stroke and microvascular complications that can lead to blindness and renal failure, so people with diabetes have a reduced quality of life and life expectancy. The microvascular complications impair patients' daily activities and productivity and shorten their life expectancy. Diabetes is a chronic illness with serious and expensive consequences: diabetes-induced kidney damage, for example, may need treating with dialysis or ultimately transplantation. Properly controlling blood sugar, blood pressure and cholesterol can stave off severe loss of function such as amputation, kidney failure and blindness. In 2011 only 7% of the diabetic population was able to control all three, and up to nine medications may be needed to control diabetes properly, so patient adherence is difficult to achieve.
Psychological aspects of diabetes
People with diabetes have to cope with an incurable chronic disease that threatens their lives, and depression, anxiety and eating disorders are very common among them. These can usually be treated effectively but tend to recur. Apart from its psychological impact, diabetes directly affects brain function and structure, bringing further psychological and neurological challenges. People with type 1 or type 2 diabetes show cognitive impairments whose pathophysiology has not been completely elucidated, the hypotheses involving hypoglycaemia, hyperglycaemia, insulin resistance or vascular disease.
Diabetes-related depression, anxiety disorders, eating disorders, and psychotic and bipolar disorders are relevant to diabetes treatment. One-third of people with diabetes encounter a psychological diagnosis such as depression or an eating disorder at some stage of their illness, and these diagnoses also affect their cooperation in managing the disease. Psychological disorders sometimes develop at later stages of diabetes, and diabetes is also more prevalent in people with certain psychological disorders. The prevalence of type 2 diabetes is higher in people with bipolar disorder and schizophrenia than in the general population, which could be due to the side effects of antipsychotic medication or to physiological or socioeconomic abnormalities accompanying mental disorders.
Successful diabetes treatment requires a range of lifestyle changes as well as medication, and good mental health is vital for effective treatment, so diabetes management should always include psychological care. Psychological care is acknowledged to be a necessary part of effective diabetes care. Psychological care can be regarded as support for a sustained pro-diabetic lifestyle. Psychological consultancy in diabetes care is used to promote healthy behaviour through direct contact with the patient or through services to other caregivers such as nurses. Non-adherence to therapy is one of the leading reasons for psychological referral. The International Society for Pediatric and Adolescent Diabetes published recommendations in 2009 for psychological care in young people with diabetes, based on 40 years of paediatric experience, which also address family dynamics and social support. A survey by Diabetes UK, a UK diabetes charity, found that about 85% of people with diabetes did not have access to adequate psychological support and that only 3% of the services provided complied with current recommendations.
Costs of obesity and diabetes
In the USA in 2005 the medical costs of obesity totalled about $190.2 billion, 20.6% of all medical expenses. In the UK the National Health Service spends about £5.1 billion a year on obesity-associated medical costs, and with people living longer the costs are expected to keep rising. A 2011 prediction put the extra cost of UK obesity to the National Health Service at £2 billion a year by 2030.
In 2007 diabetes cost the United States alone $174 billion. The WHO estimated that China would lose $551 billion in income between 2006 and 2015 to heart disease, stroke and diabetes. In the poorest countries, people with diabetes and their families bear most of the cost of medical care. Diabetes is responsible for over 10% of healthcare expenditure in most EU member states, and average healthcare costs for an EU citizen with diabetes are estimated at €2100 a year. A study of the direct and indirect cost burden of diabetes in five EU countries estimated a total of €188 billion for 2010, and linear extrapolation suggests about €300 billion for the EU that year.