By Lyle MacWilliam, BSc, MSc, FP
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
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
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
The onset of insulin resistance is characterized by a host of related symptoms, including:
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
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
The Mechanism of Onset
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.