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AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS 6 Diabesity: The Causes of Our Modern Plague Mark Hyman, MD Epidemiology The global prevalence of overweight and obesity of 1 billion people now exceeds that of malnutrition. In 1980 there were no states with obesity rates over 15%. In 2008 there were no states with obesity rates under 15%, and all except Colorado have obesity rates over 20%. i Recent NHANES data show that nearly three quarters of Americans are now overweight. ii Childhood obesity has increased 3-4 fold since the 1960’s. iii The prevalence of type-2 diabetes in America has tripled since the 1980s. From 1983 to 2008, the number of people in the world with diabetes increased seven-fold, from 35 to 240 million. The problem is expanding globally. In China 92 million have diabetes, 60% of which are undiagnosed and 148 million have metabolic syndrome, 100% of which are undiagnosed. iv In just three years, from 2008 to 2011, we added another 110 million diabetics to our global population. Obesity also places a large economic burden on our society. Direct health care costs in the U.S. over the next decade attributable to diabetes and 44 pre-diabetes will be $3.4 trillion, or one in every ten health care dollars spent. The direct and indirect costs of diabetes in America in 2007 amounted to $174 billion. The cost of obesity is also significant, and amounts to $113 billion every year. From 2000 to 2010, these two conditions have already cost us a total of $3 trillion. That’s three times the estimated cost of fixing our entire health care system! 12 Overweight and obesity are for the majority, markers of a single unifying metabolic dysfunction - insulin resistance. Rather than discrete risk stratification based on ideal body weight, overweight (BMI 30) or diabetes (fasting glucose < 126), it is more useful to consider the metabolic dysfunction as a continuum of dysfunction from optimal insulin sensitivity to end stage diabetes. Risk increases progressively with increasing BMI, even below the overweight level of 25. This spectrum has been referred to as ‚diabesity‛ and is a more useful clinical concept focusing on mechanism rather than phenotype for obesity. Mortality and Morbidity 2012
AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS Obesity will take nine years off the life of the average person, v and obesity in adolescents creates the same risk of premature death as heavy smoking. vi Diabesity, along the entire continuum of metabolic dysfunction, is the main driver of cardiovascular disease, vii diabetes, dementia, viii cancer ix and most chronic disease mortality, x and our decreasing life expectancy. A recent 40-year prospective study of 4857 Pima Indian children found that the most important predictor of premature death was insulin resistance, not hypertension or hyperlipidemia. Those in the highest quartile of glucose intolerance had a 73% increased death rate compared to those in the lowest quartile. xi Risk Factors or Causes: Changing the Focus of Clinical Intervention Focus has been on pharmacologic or bariatric surgical approaches to correct downstream risk factors to address this epidemic and its chronic disease sequelae (heart disease and diabetes) at great cost and little or no benefit. The recent ACCORD xii and NAVIGATOR trials documented that aggressive pharmacologic intervention for lipids, xiii glucose xiv and blood pressure xv did not decrease cardiac or overall mortality, and in some cases increased adverse cardiac events and mortality. Surgical approaches of cardiac bypass xvi or angioplasty xvii fared no better. However despite a rich evidence base, xviii little attention has been placed on the lifestyle, biological, social and policy drivers of obesity and overweight. Network or systems medicine, of which the best clinical model is Functional Medicine, provides a new framework for addressing the causes, rather than the risk factors of this epidemic. The dynamic interaction of the social, business and policy systems, lifestyle and environmental toxins drives our expanding phenotype. Chronic disease and obesity is the result of a complex network of biological disturbances driving systemic neuroendocrineimmune dysregulation induced by the effects of diet, levels of stress, our social environment, physical activity and exposure to environmental toxins affecting gene expression. Isolating one risk factor, or even separately treating multiple risk factors, will fail until it is 45 done in the context of addressing the upstream drivers of disease. Distinguishing between risk factors and causes is necessary for effective primary prevention and treatment of chronic disease. xix Treatment must focus on the system, not the symptom. Obesity and its chronic disease consequences, commonly referred to as ‚risk factors‛, dyslipidemia, hyperglycemia and hypertension are only downstream symptoms of upstream biological causes. They are the smoke, not the fire. Unless medicine refocuses on treating the system rather then symptoms (risk factors) through a comprehensive clinical and social systems approach that addresses diet, exercise, stress management and treatment of environmental toxic exposures, medicine will fail to stem the impending tsunami of obesity and chronic disease. Whole systems approaches of lifestyle interventions reduce incidence of cardiovascular disease xx and diabetes by over 90%. xxi These studies are part of a large evidence base documenting how lifestyle intervention is often more effective in reducing cardiovascular disease, hypertension, heart failure, stroke, cancer, diabetes, and deaths from all causes than almost any other medical intervention. xxii Despite the difficulty of behavior change and lifestyle and environmental treatment, it is the only proven model for preventing chronic disease. Risk factor treatment must be replaced with elimination of the drivers, triggers and causes of chronic disease based on the network model of disease and obesity. Metabolic, disease and social networks predict disease and outcomes more effectively than risk factors. xxiii A person's chances of becoming obese increased by 57% if he or she had a friend who became obese in a given interval. Among pairs of adult siblings, if one sibling became obese, the chance that the other would become obese increased by 40%. If one spouse became obese, the likelihood that the other spouse would become obese increased by 37%. Newer tools supporting behavior change with regular feedback metrics and social networks have proven successful and should be widely adopted in policy and medical practice. xxiv 2012
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