Almost everyone knows someone who has diabetes. An estimated 18.2 million Americans and 2 million Canadians, over 6% of each nation’s population, have been diagnosed with diabetes.1,2 Millions more have the disease and are unaware of it.
The World Health Organization estimates that by 2025, the number of people with diabetes will reach 300 million—a staggering 122% increase in less than 30 years.3 At the dawn of the third millennium and 83 years after the discovery of insulin, “we are still grappling with the enormous complexity of a disease process in which almost every aspect of the body’s metabolism goes awry.”4
Diabetes is now recognized as the sixth leading cause of death and disability in the US. Its associated health care costs have spiked dramatically, more than doubling from $44 billion to $92 billion from 1997 to 2002. In Canada, diabetes treatment now consumes 15% of the national health care budget. Today, diabetes accounts for 28% of all new cases of kidney disease in Canada, and is a primary cause of adult blindness, non-trauma-related limb amputations, and major cardiovascular events.5
The disease exhibits a strong ethnic bias: Native Americans, Hispanic-Latino Americans, and African-Americans show an increased prevalence compared to the non-Hispanic white population. Unknown in Canada’s aboriginal community until recently, type II diabetes has undergone exponential growth. Within the next two decades, 27% of Canada’s First Nations (native) peoples are expected to develop the disease.5
Epidemiological data from elsewhere mirror the North American situation. Within the next 30 years, diabetes is projected to soar by almost 50% in Great Britain, 72-78% in New Zealand and Australia, and a staggering 184% in Mexico.6
Diabetes is often misunderstood as a simple sugar imbalance that can be readily corrected through medical intervention. In truth, it is a complex metabolic disorder in which a confluence of social, behavioral, dietary, and lifestyle factors unmask an underlying genetic susceptibility. The disease has serious implications for vision, cardiovascular health, and kidney and neural functions. Its expression largely depends on lifestyle issues, including diet, weight management, and physical exercise—a multifaceted combination of factors that makes treatment complex and
The Driver: Type II Diabetes
The predominant form of diabetes is type II or non-insulin-dependent diabetes, a disease highly correlated with family history, physical inactivity, obesity, and ethnicity. Traditionally associated with middle age, the incidence of type II diabetes among younger adults and children is rising dramatically. More common in women, especially those with a history of gestational (pregnancy-related) diabetes, its prevalence in America has tripled in the last 30 years. While increasing across all age and ethnic groups, its ascendance among children and adolescents is most worrisome.
Over 90% of diabetics are type II, and it is the rapid increase in this form of the disease that is propelling the global increase in all diabetes cases. While diabetes exhibits a strong hereditary component, its rate of increase is too great to be a consequence of increased gene frequency. Instead, evidence points toward the combined influences of lifestyle, dietary, and environmental factors.7
An Emerging Epidemic: Diabetes and Children
Virtually unknown in children until recently, type II diabetes is now appearing with alarming regularity in overweight and sedentary young people. During the last three decades, the number of overweight children in the US has more than doubled. With this has come a dramatic rise in type II diabetes. In major US urban centers, the percentage of children with newly diagnosed type II diabetes has ballooned from less than 5% in 1994 to 30-50% in recent years.8
Obesity is a hallmark of the disease. A predisposition toward visceral obesity (deposition of abdominal fat) is associated with increased insulin resistance and contributes to its early onset.9 This may explain why 85% of American children who develop type II diabetes are overweight or obese at the time of diagnosis. According to Dr. Arlan Rosenbloom, chair of the American Diabetes Association Consensus Panel, “Type II diabetes in children is an emerging epidemic.”
Insulin Resistance: the Silent Stalker
Syndrome X is the dark force behind type II diabetes. Also known as metabolic syndrome, it is a preclinical stage of the disease, believed to affect up to 25% of North American adults. A constellation of metabolic changes that progress silently over a period of years, Syndrome X is characterized by increased resistance to insulin, the regulatory hormone that suppresses hepatic (liver) glucose output and removes excess glucose from the blood.
The onset of insulin resistance is characterized by a host of related symptoms, including:
- hypertension (high blood pressure)
- elevated blood triglycerides (fats)
- elevated LDL (“bad”) cholesterol
- reduced HDL (“good”) cholesterol
- accelerated hardening of the arteries
- proliferation of cells in the arterial walls
- development of abdominal obesity
- glycosylation (cross-linking of fats and proteins with glucose)
- hyperinsulinemia (high-blood insulin levels).
The syndrome is particularly alarming in children and adolescents because the changes, which in adults are usually spread over a number of years, are compressed into a few short years in young teens.10 The longer a person has the disease, the greater the likelihood of developing long-term disabilities. Unfortunately, physicians are now seeing more young people prematurely develop these life-threatening complications.
The prognosis is not encouraging: approximately one-third to one-half of those diagnosed with insulin resistance will develop diabetes. Of those, two-thirds will eventually die of cardiovascular complications. Compared to non-diabetics, adult diabetics are almost twice as likely to have asthma, three times more likely to have hypertension and heart disease, and four times more likely to suffer a stroke.11
Clearly, early detection of the disease is paramount.
A Delicate Balance
Insulin is produced by highly specialized beta cells in the pancreas, a lobular gland located behind the stomach. The hormone is secreted into the blood in response to elevated blood-sugar levels. Insulin helps the body utilize blood sugar by binding to specialized receptor sites on the cellular surfaces, much like a key fits into a lock. Insulin “unlocks” the receptor and glucose (a molecule too large to pass through) is transported into the cell. Once inside, glucose is used for cellular fuel, and any excess is stored as glycogen (a form of animal starch) or converted to glycerol for the formation of fat.
When blood sugar levels are low, or during times of stress, liver glycogen stores are quickly converted back to glucose by the action of glucagon, another pancreatic hormone. Glucagon also encourages the breakdown of fat in adipose tissue to glycerol and fatty acids. The liver reconverts these to glucose, releasing it into the blood. Through this intricate balancing act, insulin and glucagon perform a central role in regulating the body’s blood-sugar level.
Rising insulin resistance disrupts this balance when the normal levels of insulin no longer unlock the cellular “doors.” The beta cells of the pancreas, in a futile attempt to restore homeostasis, shift into “overdrive” and begin pumping out ever-increasing amounts of insulin. Chronically high levels of insulin further “desensitize” the cellular receptors, leading to even greater insulin resistance. A vicious and damaging cycle ensues—the genesis of type II
|Photomicrograph of human pancreas magnified 125x. |
The Mechanism of Onset
What defies explanation is what causes insulin resistance in the first place. We know that virtually everyone who develops type II diabetes starts with insulin resistance. We also know that the risk of developing type II diabetes is strongly correlated with central body obesity and the ectopic (abnormal) accumulation of fat. It appears that insulin resistance may not be determined so much by the amount of body fat as by where the fat is located.4 In fact, one of the best predictive markers for insulin resistance is excess body weight, in particular weight around the waist.
McGarry presents a compelling case that the ectopic accumulation of fat in muscle and other peripheral tissues is intimately involved with the onset of insulin resistance and the gradual collapse of pancreatic beta cell function.4 Insulin sensitivity can fall dramatically without the appearance of diabetes, as long as the pancreatic beta cells compensate. It is their inevitable demise (possibly due to lipotoxicity) that leads to increased hyperglycemia, a further rise in blood lipids, and an ever-greater accumulation of fat in the muscle cell. Increasing hyperlipidemia (high blood lipids) in turn exacerbates insulin resistance and degrades liver function.