Also known as PCOS. More than 50% of women with PCOS are obese. Even in the absence of obesity, insulin resistance is often seen. Which came first, the chicken or the egg? Whether Poly Cystic Ovarian Syndrome is a cause or consequence of obesity is controversial. Typically, women with PCOS have irregular menses, hirsutism, insulin resistance, and elevated levels of testosterone and luteinizing hormone. So, if obesity causes PCOS at least in some cases, aren’t these symptoms another good reason to want to minimize or eliminate obesity?

Medical science has long been asking the question, is obesity due to nature or nurture? It is estimated that genetic factors are responsible for 30-40% of the variability in adult weight. Endocrine or metabolic disorders account for less than 1% of cases of obesity. When someone has Hypothyroidism (low thyroid) that person rarely has only weight gain. Typically the person’s symptoms will include cold intolerance, fatigue, constipation, and hair loss along with some weight gain. Then that leaves nurture or environment responsible for 60-70% of obesity in adults. In some cases, behavioral-based approaches have been found to be helpful with weight loss.

Central obesity is defined as obesity in the belly section as opposed to peripheral obesity which is obesity in arms, legs, hips, etc. Central obesity is believed to be the result of increased androgenic affects, and is more common in men than women. When central obesity is seen in women, it is often related to hyperandrogenic states such as PCOS (polycystic ovarian syndrome). With central obesity a person is more at risk for heart disease and heart attack. Obesity may also be an independent risk factor for congestive heart failure and cardiomyopathy.

Obesity is a well-established risk factor for hypertension; weight loss has been found to be the most effective lifestyle change to decrease blood pressure.

Obesity is associated with elevated triglycerides and low high-density lipoprotein cholesterol levels; weight loss will improve these levels. Some – but not all – studies have found obesity to be an independent risk factor for coronary artery disease.

Up to 80% of cases of type 2 diabetes can be attributed to overweight and obesity. Overweight women are at a 40-fold increased risk for the condition, whereas overweight men are at a 60-fold increased risk. There is a delay of about 10 years between the onset of being overweight and the development of diabetes; over time, insulin resistance surpasses the body’s ability to increase insulin production and blood glucose rises.

Ghrelin is a peptide that is produced in the stomach and the duodenum that stimulates eating. Leptin is a protein that is produced in adipose tissue, and it provides negative feedback to appetite-control centers. Central nervous system neurotransmitters are involved in appetite control, and they may be modulated with medication.

Antidepressants, antipsychotics, anticonvulsants, and hypoglycemic agents can all contribute to weight gain.

Metabolic syndrome increases the risk of type 2 diabetes, coronary artery disease, and cerebrovascular disease.

Smoking is the largest avoidable cause of cancer, and obesity is the second largest. An increased risk of death from several cancers is seen among obese patients, including esophageal, colon, kidney, gallbladder, and pancreatic cancer as well as non-Hodgkin’s lymphoma and multiple myeloma; there is also a trend toward an increased risk of prostate, gastric, ovarian, and endometrial cancer. Breast cancer has been most closely associated with central obesity.

Being overweight is a major risk factor for Obstructive Sleep Apnea.

Fatty liver disease is the most common cause of elevations in liver enzymes, and it affects 20% of the U.S. population.

The association between obesity and degenerative joint disease among adults is most often seen in weight-bearing joints such as the hips and knees.

The U.S. Preventative Services Task Force recommends screening for obesity in adults; this can be done with three simple steps: measuring BMI, measuring waist circumference, and identifying comorbidities.

In a study that compared four different popular diets, all were equally effective with regard to resultant weight loss, but at 1 year the maintained weight loss was only 2 Lbs.

Low- carbohydrate diets may be difficult to adhere to long term, and they may adversely affect nutritional status.

Very-low-calorie diets may produce more rapid initial weight loss, but they produce similar results as other diets over time. A low-calorie diet is most often employed. When the patient chooses less energy-dense food, the volume of food eaten may stay about the same.

To qualify for bariatric surgery, a patient should have a BMI of more than 40 and weight-related complications.

The United States is the epicenter of a global obesity pandemic. Driven by advances in food production that have made palatable, economical calories in excess of need readily available to almost the entire population almost all the time and by comparable advances in labor-saving technologies, obesity and overweight now engulf some 65% to 80% of adults in the United States, as well as a steadily rising proportion of children.

With rates rising to unprecedented levels with each passing year, obesity is rightly referred to as an epidemic and is, arguably, the most poorly controlled and potentially dire health threat facing the United States. Obesity is the major modifiable risk factor for type 2 diabetes (itself now epidemic) and a major contributor to most predominant causes of premature death and disability, including but not limited to cardiovascular disease, cancer, stroke, obstructive pulmonary disease, and degenerative arthritis. Secular trends are similar in most other developed countries. Cultural transitions in developing countries are associated with a rapid rise in the rate of obesity as well, even while historical public health scourges such as microbial diseases persist. Obesity thus constitutes a global health crisis. At the 10th International Congress on Obesity in Sydney, Australia, in September 2006, it was announced that for the first time in history, the planet-wide population of overweight (over 1 billion) outnumbered the hungry (roughly 600 to 700 million).

An inability to curtail the spread of obesity has resulted in a tendency to exaggerate the complexities, if not the difficulties, of the challenges involved. While the investigation of obesity rightly subsumes metabolism, genetics, lipidology, endocrinology, and even newly emerging disciplines such as nutrigenomics, it must be conceded that human physiology is much the same as it ever was and thus cannot house the explanation for suddenly skyrocketing obesity rates. That answer resides in an environment that is not the same as it was before, rendering human adaptations to a world of caloric scarcity and a high demand for physical exertions largely obsolete. In short, our patients (and we) are getting fat in record numbers for the simple reason that they (and we) can do so- for the first time in history. It is scarcely an exaggeration to say that human intelligence, since it first evolved, has been dedicated to making obesity possible by establishing a reliable supply of palatable food and by inventing technologies to reduce the physical ardors required for survival. We have become, in the fullness of time, victims of our own resourcefulness and success.

But while accounting for the obesity epidemic is simple, reversing it will be anything but easy-and from this derives the false and even harmful perspective that complexity impedes our progress. This view is false because a reduction in caloric intake to the level required for maintenance of a healthful weight is all that is universally needed for weight control. This view is harmful because it shifts attention and resources from the demanding but potentially rewarding task of pursuing what we know, to the often-frivolous task of parsing what we do not.

The role of clinicians in contending with this challenge is itself subject of debate. The US Preventive Services Task Force has expressed ambivalence about the utility of clinical counseling for weight control. We are accustomed in medical research to some degree of reductionism, the study of active ingredients. Thus, when obesity interventions are studied, they are generally examined discretely, independently of societal trends. When such interventions fail to make appreciable differences in the outcome(s) of interest- generally some measure of weight-we conclude that they are ineffective. Or, at best, we fail to conclude that they are effective.

But the “mass” against which we are working is daunting. The world is powerfully, and ever more, obesigenic. Even interactions that apply an effective counterforce may fail to move this massive and ever-accumulating resistance. The implications are that for there to be any hope of curtailing the obesity epidemic, we must apply all reasonable countermeasures concurrently.

The predominant measure used to characterize weight at the population level is body mass index (BMI), generally expressed as weight (mass), in kilograms, divided by the height, in meters squared (kg per m2 ). This measure of weight adjusted for height offers the benefits of simplicity and convenience for assessing weight in large populations and for monitoring trends over time. BMI, however, is a notoriously crude measure of adiposity (body fat stores), both of which are of more importance to health than weight, per se. BMI cannot distinguish between fat and muscle mass, nor between peripherally versus centrally distributed fat mass.

Despite its limitations when applied to an individual, BMI performs well at the population level for several reasons. BMI trends reflect trends in adiposity, not muscularity. There is nothing to suggest that increasing legions of the muscular and fit are responsible for consistent increases in BMI in the United States and other countries; there is much to suggest that rising BMI is indicative of increasing adiposity. The distinction between excess body fat and muscularity is easily made at the individual level, and thus the use of the BMI is unlikely to generate clinically relevant confusion. Finally, such crude measures as the BMI, and even casual inspection, correlate fairly well with costly and sophisticated measures of adiposity.

Overweight in adults is defined as BMI at or above 25kg per m2.

Adult obesity is defined in stages.

Stage 1 obesity is a BMI of 30 to 34.9. Stage 2 obesity is a BMI of 35 to 39.9; and. Stage 3 obesity is a BMI of 40 or higher.

A BMI of 25 to 29.9 is “overweight.”

Stage 3 obesity was formerly known as “morbid obesity.” Current Definitions of Overweight and obesity in Adults. BMI

Category < 18     Underweight 18 to < 25     Healthy Weight 25 to < 30     Overweight 30 to < 35     Stage I Obesity 35 to < 40     Stage II Obesity > 40     Stage III Obesity (formerly “morbid” obesity)

The name change is appropriate and important for two reasons.

First, although a BMI of 40 is quite high, it is not invariably associated with morbidity.

Second, and of greater importance epidemiologically, morbidity is often induced by obesity at a BMI well below 40. The risks of complications of excess adiposity may, in general, be considered low, moderate, and high as BMI rises through overweight to stage III obesity, but the actual risk in an individual will vary.