Obesity is a condition in which the natural energy reserve, stored in the fatty tissue of humans and other mammals, is increased to a point where it is associated with certain health conditions or increased mortality. It is a form of malnuitrition.

Obesity is both an individual clinical condition and is increasingly viewed as a serious public health problem. Excessive body weight has been shown to predispose to various diseases, particularly cardiovascular diseases, diabetes mellitus type 2, sleep apnea, and osteoarthritis.

Causes of Obesity

Overeating

Obesity results when the lifetime energy intake exceeds lifetime energy expenditure by more than it does for individuals of “normal weight”.

When food energy intake exceeds energy expenditure, fat cells (and to a lesser extent muscle and liver cells) throughout the body take in the energy and store it as fat.

Other Factors

There are other factors that contribute to obesity. Some of these are beyond your control.

• Your genes and some genetic disorders
• Underlying illness (e.g. hypothyroidism – The Thyroid Glands produces insufficient hormone (thyroxine).
• Eating disorders (e.g., binge eating disorder as in bulimia)
• Certain medications (e.g., some antipsychotics, some fertility medication)
• Sedentary lifestyle – The individual sits or lies down most of the day.
• A high glycemic diet (i.e., a diet that consists of meals that give high blood sugar)
• Weight cycling, caused by repeated attempts to lose weight by dieting
• Stressful mentality
• Insufficient sleep
• Smoking cessation

Poverty
When you look around your country, you would find that there is a relationship between obesity and economic status. For example, in a study conducted in 2004, it was discovered that obese American subjects are approximately half as wealthy as thin ones.

Poor Diet and Poverty

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Is there a relationship between Poverty and Obesity

• Yes there is a relationship as fast foods are usually less expensive and therefore more accessable to the poor.
• Through education and the understanding that thry can prepare meals at home from simple unexpensive foods of high nutritional values. They do not have to buy the fast foods which generally have high calorific value and contribute to obesity.

• Poorer people are often fatter than their richer counterparts. Research has revealed that even when the differences in income were removed from the equation, the inequity persisted — thin subjects were richer than fat ones because of inherited wealth.
• A lower level of education and the tendency to rely on cheaper fast foods might contribute to these results.
• Another study finds women who married into higher status are usually thinner than women who married into lower status.

Measuring Obesity

Measuring Obesity

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• The figure at the far right is most obese.
• the measure used here is waist circumference.

Another way of measuring obesity is to determine the amount of body fat. Doctors and scientists generally agree that men with more than 25% body fat and women with more than 30% body fat are obese. However, it is difficult to measure body fat precisely. The most accepted method has been to weigh a person underwater, but underwater weighing is a procedure limited to laboratories with special equipment. Two simpler methods for measuring body fat are the skinfold test, in which a pinch of skin is precisely measured to determine the thickness of the subcutaneous fat layer.

Life Style Diseases are diseases you get as a result of the way you live. Many of these diseases are related to the social, cultural, religious and ethnic norms of your community and also its economic status. This list includes the deficiency diseases. Others may be described as self inflicted diseases as get them as a result of choices you make. Examples of these are eating disorders such as Anorexia Nervosa and Bulimia and Obesity.

Anorexia nervosa … anorexia nervosa, bulimia, … Bulimia nervosa, … anorexia nervosa and bulimia … Anorexia Nervosa Anorexia Nervosa, … Anorexia (nervosa); Bulimia (nervosa … … on to develop anorexia nervosa. Anorexia Nervosa And Bulimia … Following anorexia nervosa Anorexia Nervosa · Bulimia Nervosa … as anorexia nervosa or bulimia … ANOREXIA NERVOSA & BULIMIA NERVOSA. … for anorexia nervosa or bulimia … Anorexia Nervosa; Bulimia Nervosa … … anorexia nervosa and bulimia … … with anorexia nervosa, bulimia … … anorexia nervosa and bulimia … … for Anorexia Nervosa and Bulimia … of Anorexia Nervosa and Bulimia … ANOREXIA NERVOSA OBESITY

The Ebola virus was first identified in a western equatorial province of Sudan and in a nearby region of Zaire (now Democratic Republic of the Congo) in 1976 after significant epidemics in Yambuku, northern Zaire, and Nzara, southern Sudan.

Ebola haemorrhagic fever (EHF) is one of the most virulent viral diseases known to humankind, causing death in 50-90% of all clinically ill cases. Several different species of Ebola virus have been identified.

The Ebola virus is transmitted by direct contact with the blood, body fluids and tissues of infected persons.Transmission of the Ebola virus has also occurred by handling ill or dead infected chimpanzees.

The term diabetes, without qualification, usually refers to diabetes mellitus, which is associated with excessive sweet urine (known as “glycosuria”) but there are several rarer conditions also named diabetes. The most common of these is diabetes insipidus in which the urine is not sweet (insipidus meaning “without taste” in Latin); it can be caused by either kidney (nephrogenic DI) or pituitary gland (central DI) damage.

The principal two idiopathic forms of diabetes mellitus are known as types 1 and 2. The term “type 1 diabetes” has universally replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes (IDDM). Likewise, the term “type 2 diabetes” has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and non-insulin-dependent diabetes (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature. Various sources have defined “type 3 diabetes” as, among others,gestational diabetes, insulin-resistant type 1 diabetes (or “double diabetes”), type 2 diabetes which has progressed to require injected insulin, and latent autoimmune diabetes of adults (or LADA or “type 1.5″ diabetes.) There is also maturity onset of the young (MODY) which is a group of several single gene (monogenic) disorders with strong family histories that present as type 2 diabetes before 30 years of age.

Type 1 diabetes mellitus

Type 1diabetes mellitus is characterized by loss of the insulin-producing beta cells of the Islets of Langerhans in the pancreas, leading to a deficiency of insulin. The main cause of this beta cell loss is a T-cell mediated autoimmune attack. There is no known preventive measure which can be taken against type 1 diabetes; it is about 10% of diabetes mellitus cases in North America and Europe (though this varies by geographical location), and is a higher percentage in some other areas. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults but was traditionally termed “juvenile diabetes” because it represents a majority of the diabetes cases in children.

The principal treatment of type 1 diabetes, even from its earliest stages, is replacement of insulin combined with careful monitoring of blood glucose levels using blood testing monitors. Without insulin, diabetic ketoacidosis often develops which may result in coma or death. Treatment emphasis is now also placed on lifestyle adjustments (diet and exercise) though these cannot reverse the progress of the disease. Apart from the common subcutaneous injections, it is also possible to deliver insulin by a pump, which allows continuous infusion of insulin 24 hours a day at preset levels, and the ability to program doses (a bolus) of insulin as needed at meal times. An inhaled form of insulin, Exubera was approved by the FDA in January 2006, although Pfizer discontinued the product for business reasons in October 2007. Non-insulin treatments, such as monoclonal antibodies and stem-cell based therapies, are effective in animal models but have not yet completed clinical trials in humans.

Type 1 treatment must be continued indefinitely in essentially all cases. Treatment need not significantly impair normal activities, if sufficient patient training, awareness, appropriate care, discipline in testing and dosing of insulin is taken. However, treatment is burdensome for patients, insulin is replaced in a non-physiological manner, and this approach is therefore far from ideal. The average glucose level for the type 1 patient should be as close to normal (80–120 mg/dl, 4–6 mmol/l) as is safely possible. Some physicians suggest up to 140–150 mg/dl (7-7.5 mmol/l) for those having trouble with lower values, such as frequent hypoglycemic events. Values above 400 mg/dl (20 mmol/l) is sometimes accompanied by discomfort and frequent urination leading to dehydration. Values above 600 mg/dl (30 mmol/l) usually require medical treatment and may lead to ketoacidosis, although they are not immediately life-threatening. However, low levels of blood glucose, called hypoglycimia, may lead to seizures or episodes of unconsciousness and absolutely must be treated immediately.

Type 2 diabetes mellitus

Type 2 diabetes mellitus is characterized differently due to insulin resistance or reduced insulin sensitivity, combined with reduced insulin secretion. The defective responsiveness of body tissues to insulin almost certainly involves the insulin receptors in cell membranes. In the early stage the predominant abnormality is reduced insulin sensitivity, characterized by elevated levels of insulin in the blood. At this stage hyperglycemia can be reversed by a variety of measures and medication that improve insulin sensitivity or reduce glucose production by the liver. As the disease progresses the impairment of insulin secretion worsens, and therapeutic replacement of insulin often becomes necessary.

There are numerous theories as to the exact cause and mechanism in type 2 diabetes. Central obesity(fat concentrated around the waist in relation to abdominal organs, but not subcutaneous fat) is known to predispose individuals for insulin resistance. Abdominal fat is especially active hormonally, secreting a group of hormones called adipokines that may possibly impair glucose tolerance. Obesity is found in approximately 55% of patients diagnosed with type 2 diabetes. Other factors include aging (about 20% of elderly patients in North America have diabetes) and family history (type 2 is much more common in those with close relatives who have had it). In the last decade, type 2 diabetes has increasingly begun to affect children and adolescents, likely in connection with the increased prevalence of childhood obesity seen in recent decades in some places. Environmental exposures may contribute to recent increases in the rate of type 2 diabetes. A positive correlation has been found between the concentration in the urine of bisphenol A, a constituent of polycarbonate plastic, and the incidence of type 2 diabetes.

Type 2 diabetes may go unnoticed for years because visible symptoms are typically mild, non-existent or sporadic, and usually there are no ketoacidic adipose . However, severe long-term complications can result from unnoticed type 2 diabetes, including renal failure due to diabetic nephropathy, vascular disease (including coronary artery disease), vision damage due to diabetic retinophathy , loss of sensation or pain due to diabetic neurophathy, and liver damage from non alcoholic stestohepetitis.

Type 2 diabetes is usually first treated by increasing physical activity, decreasing carbohydrates intake, and losing weight. These can restore insulin sensitivity even when the weight loss is modest, for example around 5 kg (10 to 15 lb), most especially when it is in abdominal fat deposits. It is sometimes possible to achieve long-term, satisfactory glucose control with these measures alone. However, the underlying tendency to insulin resistance is not lost, and so attention to diet, exercise, and weight loss must continue. The usual next step, if necessary, is treatment with oral Anti diabetic drugs. Insulin production is initially only moderately impaired in type 2 diabetes, so oral medication (often used in various combinations) can be used to improve insulin production (e.g.,sulfonylureas), to regulate inappropriate release of glucose by the liver and attenuate insulin resistance to some extent (e.g., metformis), and to substantially attenuate insulin resistance (e.g.,thiazolidinediones). According to one study, overweight patients treated with metformin compared with diet alone, had relative risk reduction of 32% for any diabetes endpoint, 42% for diabetes related death and 36% for all cause mortality and stroke. Oral medication may eventually fail due to further impairment of beta cell insulin secretion. At this point, insulin therapy is necessary to maintain normal or near normal glucose levels.

Gestational diabetes

Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable but requires careful medical supervision throughout the pregnancy. About 20%–50% of affected women develop type 2 diabetes later in life.

Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal sufactant production and cause respiratory distress syndrome. hyperbilirubinemia may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental profusion due to vascular impairment. induction may be indicated with decreased placental function. A cesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomial, such as shoulder dystocia.

A 2008 study completed in the U.S. found that more American women are entering pregnancy with preexisting diabetes. In fact the rate of diabetes in expectant mothers has more than doubled in the past 6 years. This is particularly problematic as diabetes raises the risk of complications during pregnancy, as well as increasing the potential that the children of diabetic mothers will also become diabetic in the future.

Other types

There are several rare causes of diabetes mellitus that do not fit into type 1, type 2, or gestational diabetes; attempts to classify them remain controversial. Some cases of diabetes are caused by the body’s tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organisation when the current taxonomy was introduced in 1999.

Signs and symptoms

The classical triad of diabetes symptoms is polyuria, polydipsia and polyphagia, which are, respectively, frequent urination, increased thirst and consequent increased fluid intake, and increased appetite. Symptoms may develop quite rapidly (weeks or months) in type 1 diabetes, particularly in children. However, in type 2 diabetes symptoms usually develop much more slowly and may be subtle or completely absent. Type 1 diabetes may also cause a rapid yet significant weight loss (despite normal or even increased eating) and irreducible fatigue. All of these symptoms except weight loss can also manifest in type 2 diabetes in patients whose diabetes is poorly controlled.

When the glucose concentration in the blood is raised beyond its renalthresholds , reabsorption of glucose in the proximal renal tubuli is incomplete, and part of the glucose remains in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst.

Prolonged high blood glucose causes glucose absorption, which leads to changes in the shape of the lenses of the eyes, resulting in vision changes; sustained sensible glucose control usually returns the lens to its original shape. Blurred vision is a common complaint leading to a diabetes diagnosis; type 1 should always be suspected in cases of rapid vision change, whereas with type 2 change is generally more gradual, but should still be suspected.

Patients (usually with type 1 diabetes) may also initially present with diabetic ketoacidosis (DKA), an extreme state of metabolic dysregulation characterized by the smell of acetone on the patient’s breath; a rapid, deep breathing known as Kussmaul breathing;polyuria; nausea; vomiting and abdominal pain; and any of many altered states of consciousness or arousal (such as hostility and mania or, equally, confusion and lethargy). In severe DKA,coma may follow, progressing to death. Diabetic ketoacidosis is a medical emergency and requires immediate hospitalization.

A rarer but equally severe possibility is hyperosmolar nonketotic state, which is more common in type 2 diabetes and is mainly the result of dehydration due to loss of body water. Often, the patient has been drinking extreme amounts of sugar-containing drinks, leading to a visious cycle in regard to the water loss.

Pathophysiology

Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending release, via exocytosis, which is primarily triggered by food, chiefly food containing absorbable glucose. The chief trigger is a rise in blood glucose levels after eating

Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Therefore deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus.

Most of the carbohydrates in food are converted within a few hours to the monosaccerides glucose, the principal carbohydrate found in blood and used by the body as fuel. Insulin is released into the blood by beta cells (β-cells), found in the Islets of Langerhans in the pancreas, in response to rising levels of blood glucose after eating. Insulin is used by about two-thirds of the body’s cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone glucagon which acts in an opposite manner to insulin. Glucose thus recovered by the liver re-enters the bloodstream; muscle cells lack the necessary export mechanism.

Higher insulin levels increase some anabolic (“building up”) processes such as cell growth and duplication,protein synthesis, and fat storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction, and vice versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat burning metabolic phase).

If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resestance), or if the insulin itself is defective, then glucose will not be absorbed properly by those body cells that require it nor will it be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidocis.

Diagnosis

The diagnosis of type 1 diabetes, and many cases of type 2, is usually prompted by recent-onset symptoms of excessive urination (polyurea) and excessive thirst (polydipsia), often accompanied by weight loss. These symptoms typically worsen over days to weeks; about a quarter of people with new type 1 diabetes have developed some degree of diabetic ketoacidosis by the time the diabetes is recognized. The diagnosis of other types of diabetes is usually made in other ways. These include ordinary health screening; detection of hyperglycemia during other medical investigations; and secondary symptoms such as vision changes or unexplainable fatigue. Diabetes is often detected when a person suffers a problem that is frequently caused by diabetes, such as a heart attech, strok, neuropathy, poor wound healing or a foot ulcer, certain eye problems, certain fungal infectios or delivering a baby with macrosomia or hypoglycemia.

Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:

• fasting plasma glucose level at or above 126 mg/dL (7.0 mmol/l).
• plasma glucose at or above 200 mg/dL (11.1 mmol/l) two hours after a 75 g oral glucose load as in a glucos terelance test.
• random plasma glucose at or above 200 mg/dL (11.1 mmol/l).

A positive result, in the absence of clinical symptoms of diabetes, should be confirmed by another of the above-listed methods on a different day. Most physicians prefer to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete. According to the current definition, two fasting glucose measurements above 126 mg/dL (7.0 mmol/l) is considered diagnostic for diabetes mellitus.

Patients with fasting glucose levels between 110 and 125 mg/dL (6.1 and 7.0 mmol/l) are considered to have impaired fasting glycemia. Patients with plasma glucose at or above 140 mg/dL or 7.8 mmol/l two hours after a 75 g oral glucose load are considered to have impaired glucos terelance. Of these two pre-diabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus as well as cardiovascular diseases.

While not used for diagnosis, an elevated level of glucose irreversibly bound to haemoglobin (termed glycosylated haemoglobin or HbA1c) of 6.0% or higher (the 2003 revised U.S. standard) is considered abnormal by most labs; HbA1c is primarily used as a treatment-tracking test reflecting average blood glucose levels over the preceding 90 days (approximately). However, some physicians may order this test at the time of diagnosis to track changes over time. The current recommended goal for HbA1c in patients with diabetes is <7.0%, which is considered good glycimic control, although some guidelines are stricter (<6.5%). People with diabetes who have HbA1c levels within this range have a significantly lower incidence of complications from diabetes, including retinopathy diabetic nephropathy

Prevention

Type 1 diabetes risk is known to depend upon a genetic predisposition based on H types (particularly types DR3 and DR4), an unknown environmental trigger (suspected to be an infection, although none has proven definitive in all cases), and an uncontrolled autoimmune response that attacks the insulin producing beta cells. Some research has suggested that breastfeeding decreased the risk in later life; various other nutritional risk factors are being studied, but no firm evidence has been found.  Giving children 2000 IU of Vitamin D during their first year of life is associated with reduced risk of type 1 diabetes, though the causal relationship is obscure.

Children with antibodies to beta cell proteins (ie, at early stages of an immune reaction to them) but no overt diabetes, and treated with vitamin B-3 (niacin), had less than half the diabetes onset incidence in a 7-year time span as did the general population, and an even lower incidence relative to those with antibodies as above, but who received no vitamin B3.

Type 2 diabetes risk can be reduced in many cases by making changes in diet and increasing physical activity. The American Diabetes Assosiation (ADA) recommends maintaining a healthy weight, getting at least 2½ hours of exercise per week (several brisk sustained walks appear sufficient), having a modest fat intake, and eating sufficient fiber (eg, from whole grains). The ADA does not recommend alcohol consuption as a preventive, but it is interesting to note that moderate alcohol intake may reduce the risk (though heavy consumption absolutely and clearly increases damage to bodily systems significantly); a similarly confused connection between low dose alcohol consumption and heart disease is termed the Frecnh Paradox.

There is inadequate evidence that eating foods of low glycemic index is clinically helpful despite recommendations and suggested diets emphacizing this approach.

There are numerous studies which suggest connections between some aspects of Type II diabetes with ingestion of certain foods or with some drugs. Some studies have shown delayed progression to diabetes in predisposed patients through prophylactic use of metformin, rosiglytazone, or valsartan. In patients on hydroxychloroquine for rheumatoid arthritis, incidence of diabetes was reduced by 77% though causal mechanisms are unclear. Breastfeeding may also be associated with the prevention of type 2 of the disease in mothers. Clear evidence for these and any of many other connections between foods and supplements and diabetes is sparse to date; none, despite secondary claims for (or against), is sufficiently well established to justify as a standard clinical approach.

Demography is today widely taught in many universities across the world, attracting students with initial training in social sciences, statistics or health studies. Being at the crossroads of several disciplines such as geography, economics, sociology or epidemiology, demography offers tools to approach a large range of population issues by combining a more technical quantitative approach that represents the core of the discipline with many other methods borrowed from social or other sciences. Demographic research is conducted in universities, in research institutes as well as in statistical departments and in several international agencies. Population institutions are part of theCicred (International Committee for Coordination of Demographic Research) network while most individual scientists engaged in demographic research are members of the International union for Scientific Study of Population -IUSSP or, in the United States, in the Population association of America.