THE ART OF medicine is quite peculiar. Once in a while, medical treatments become established that don’t really work. Through sheer inertia, these treatments get handed down from one generation of doctors to the next and survive for a surprisingly long time, despite their lack of effectiveness. Consider the medicinal use of leeches (bleeding) or, say, routine tonsillectomy.
Unfortunately, the treatment of obesity is also one such example. Obesity is defined in terms of a person’s body mass index, calculated as a person’s weight in kilograms divided by the square of their height in meters. A body mass index greater than 30 is defined as obese. For more than thirty years, doctors have recommended a low-fat, calorie-reduced diet as the treatment of choice for obesity. Yet the obesity epidemic accelerates. From 1985 to 2011, the prevalence of obesity in Canada tripled, from 6 percent to 18 percent.1 This phenomenon is not unique to North America, but involves most of the nations of the world.
Virtually every person who has used caloric reduction for weight loss has failed. And, really, who hasn’t tried it? By every objective measure, this treatment is completely and utterly ineffective. Yet it remains the treatment of choice, defended vigorously by nutritional authorities.
As a nephrologist, I specialize in kidney disease, the most common cause of which is type 2 diabetes with its associated obesity. I’ve often watched patients start insulin treatment for their diabetes, knowing that most will gain weight. Patients are rightly concerned. “Doctor,” they say, “you’ve always told me to lose weight. But the insulin you gave me makes me gain so much weight. How is this helpful?” For a long time, I didn’t have a good answer for them.
That nagging unease grew. Like many doctors, I believed that weight gain was a caloric imbalance—eating too much and moving too little. But if that were so, why did the medication I prescribed—insulin—cause such relentless weight gain?
Everybody, health professionals and patients alike, understood that the root cause of type 2 diabetes lay in weight gain. There were rare cases of highly motivated patients who had lost significant amounts of weight. Their type 2 diabetes would also reverse course. Logically, since weight was the underlying problem, it deserved significant attention. Still, it seemed that the
health profession was not even the least bit interested in treating it. I was guilty as charged. Despite having worked for more than twenty years in medicine, I found that my own nutritional knowledge was rudimentary, at best.
Treatment of this terrible disease—obesity—was left to large corporations like Weight Watchers, as well as various hucksters and charlatans mostly interested in peddling the latest weight-loss “miracle.” Doctors were not even remotely interested in nutrition. Instead, the medical profession seemed obsessed with finding and prescribing the next new drug:
But all along, we needed to treat obesity. We were trying to treat the problems caused by obesity rather than obesity itself. In trying to understand the underlying cause of obesity, I eventually established the Intensive Dietary Management Clinic in Toronto, Canada.
The conventional view of obesity as a caloric imbalance did not make sense. Caloric reduction had been prescribed for the last fifty years with startling ineffectiveness.
Reading books on nutrition was no help. That was mostly a game of “he said, she said,” with many quoting “authoritative” doctors. For example, Dr. Dean Ornish says that dietary fat is bad and carbohydrates are good. He is a respected doctor, so we should listen to him. But Dr. Robert Atkins said dietary fat is good and carbohydrates are bad. He was also a respected doctor, so we should listen to him. Who is right? Who is wrong? In the science of nutrition, there is rarely any consensus about anything:
To discover the answers, we need to turn to evidence-based medicine rather than vague opinion.
Literally thousands of books are devoted to dieting and weight loss, usually written by doctors, nutritionists, personal trainers and other “health experts.” However, with a few exceptions, rarely is more than a cursory thought spared for the actual causes of obesity. What makes us gain weight? Why do we get fat?
The major problem is the complete lack of a theoretical framework for understanding obesity. Current theories are ridiculously simplistic, often taking only one factor into account:
But all chronic diseases are multifactorial, and these factors are not mutually exclusive. They may all contribute to varying degrees. For example, heart disease has numerous contributing factors—family history, gender, smoking, diabetes, high cholesterol, high blood pressure and a lack of physical activity, to name only a few—and that fact is well accepted. But such is not the case in obesity research.
The other major barrier to understanding is the focus on short-term studies. Obesity usually takes decades to fully develop. Yet we often rely on information about it from studies that are only of several weeks’ duration. If we study how rust develops, we would need to observe metal over a period of weeks to months, not hours. Obesity, similarly, is a long-term disease. Short-term studies may not be informative.
While I understand that the research is not always conclusive, I hope this book, which draws on what I’ve learned over twenty years of helping patients with type 2 diabetes lose weight permanently to manage their disease, will provide a structure to build upon.
Evidence-based medicine does not mean taking every piece of low-quality evidence at face value. I often read statements such as “low-fat diets proven to completely reverse heart disease.” The reference will be a study of five rats. That hardly qualifies as evidence. I will reference only studies done on humans, and mostly only those that have been published in high-quality, peer- reviewed journals. No animal studies will be discussed in this book. The reason for this decision can be illustrated in “The Parable of the Cow”:
Two cows were discussing the latest nutritional research, which had been done on lions. One cow says to the other, “Did you hear that we’ve been wrong these last 200 years? The latest research shows that eating grass is bad for you and eating meat is good.” So the two cows began eating meat. Shortly afterward, they got sick and they died.
One year later, two lions were discussing the latest nutritional research, which was done on cows. One lion said to the other that the latest research showed that eating meat kills you and eating grass is good. So, the two lions started eating grass, and they died.
What’s the moral of the story? We are not mice. We are not rats. We are not chimpanzees or spider monkeys. We are human beings, and therefore we should consider only human studies. I am interested in obesity in humans, not obesity in mice. As much as possible, I try to focus on causal factors rather than association studies. It is dangerous to assume that because two factors are associated, one is the cause of the other. Witness the hormone replacement therapy disaster in post-menopausal women. Hormone replacement therapy was associated with lower heart disease, but that did not mean that it was the cause of lower heart disease. However, in nutritional research, it is not always possible to avoid association studies, as they are often the best available evidence.
Part 1 of this book, “The Epidemic,” explores the timeline of the obesity epidemic and the contribution of the patient’s family history, and shows how both shed light on the underlying causes.
Part 2, “The Calorie Deception,” reviews the current caloric theory in depth, including exercise and overfeeding studies. The shortcomings of the current understanding of obesity are highlighted.
Part 3, “A New Model of Obesity,” introduces the hormonal theory of obesity, a robust explanation of obesity as a medical problem. These chapters explain the central role of insulin in regulating body weight and describe the vitally important role of insulin resistance.
Part 4, “The Social Phenomenon of Obesity,” considers how hormonal obesity theory explains some of the associations of obesity. Why is obesity associated with poverty? What can we do about childhood obesity?
Part 5, “What’s Wrong with Our Diet?,” explores the role of fat, protein and carbohydrates, the three macronutrients, in weight gain. In addition, we examine one of the main culprits in weight gain—fructose—and the effects of artificial sweeteners.
Part 6, “The Solution,” provides guidelines for lasting treatment of obesity by addressing the hormonal imbalance of high blood insulin. Dietary guidelines for reducing insulin levels include reducing added sugar and refined grains, keeping protein consumption moderate, and adding healthy fat and fiber. Intermittent fasting is an effective way to treat insulin resistance without incurring the negative effects of calorie reduction diets. Stress management and sleep improvement can reduce cortisol levels and control insulin.
The Obesity Code will set forth a framework for understanding the condition of human obesity. While obesity shares many important similarities and differences with type 2 diabetes, this is primarily a book about obesity.
The process of challenging current nutritional dogma is, at times, unsettling, but the health consequences are too important to ignore. What actually causes weight gain and what can we