A Decade of Commitment: More to Come
FOOD, MEDICINE & HEALTH
A decade ago, the inaugural article of this column addressed evidence associated with the glycemic index (GI). This topic was controversial in 2004, and it remains of questionable clinical value in dietary management. Even the 2010 Dietary Guidelines indicated there was strong evidence that glycemic index and glycemic load (GL) studies were not associated with body weight, and inconsistent or weak evidence related to GI or GL relative to type 2 diabetes or cardiovascular disease (CVD). Obviously, our article was six years ahead of its time. In the years that followed, Food, Medicine & Health has explored a wide array of diet and health issues and the science behind them, with topics ranging from malnutrition to obesity.
Recently, the column initiated dialogue on the food-brain connection and the controversial topic of addiction. Within the neurosciences realm, the current data suggest the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), criteria are not always met relative to food craving or even substance abuse (Volkow & O’Brien, 2007). Clearly, a better understanding of neurocircuitry is necessary for clinical interventions, public policy development, and, more importantly, personal behaviors that may be consideredin disorders such as autism, ADHD, and binge eating. The drug addiction model applied to compulsive food intake and obesity has been challenged (Ziauddeen et al., 2012), although others support the hypothesis (Avena et al.,2012).
Contributing factors to obesity include food environment, energy expenditure, physical environment, environmental influences, personality and reward circuitry, individual predisposition, and appetite and satiety. As noted in a recent review of the biology and genetics of obesity and a history of marketing interventions, such options have ranged from La Parle Obesity Soap (1903) that washed away extra pounds to the Tapeworm Diet (1950s) for those who were not uneasy about swallowing a long parasite. Multiple hypotheses have been advanced, including exogenous and endogenous types, which segued to dietary excess and lack of exercise. Yet, as demonstrated by Jules Hirsch and others, excess caloric intake may not yield increased body weight, and caloric restriction may not produce weight loss. Molecular genetics, such as the phenotypic presentations of fat-mass and obesity-associated (FTO) gene (Yang et al., 2012; Frayling et al., 2007) and DYRK1B mutations (Keramati et al., 2014), may alter our understanding of obesity (Jou, 2014).
The controversy about the impact of sugar on health is ongoing. Fueled by the March 2014 World Health Organization “free sugar” recommendations and incorrect reporting by the media and some CVD risk modeling conveyed as a clinical intervention study, consumer confusion increased and policy makers and “added sugar” labeling proponents were elated. Careful examination of the supporting documents (Moynihan & Kelly, 2014; Te Morenga et al., 2013) indicates the following: a) the 5%en free sugar figure to reduce dental caries is weakly supported with low-quality data; and b) the 10%en free sugar figure only parrots the 10–15%en figure adopted by more than 60 countries. This figure was emphasized by a recent nutrition epidemiologic model regarding sugar intake and CVD risk (Yang et al., 2014). However, the meta-analysis of 13 randomized controlled trials indicated an isocaloric exchange with other carbohydrates showed no change in body weight (Te Morenga et al., 2013), which is the same position noted by the 2010 Dietary Guidelines. The same group also reported inconsistent evidence of a causal relation between sugars and cardiometric risk factors, including serum triglycerides, cholesterol, LDL, HDL, and blood pressure among populations consuming isocaloric energy diets (Te Morenga et al., 2014).
Within the fray are saturated fats and CVD risk. Over the past 50 years, the dynamics of fat and health outcomes shifted from cholesterol and atherosclerosis as advanced by epidemiologist Ancel Keys in the ‘60s to the tropical oil culprits identified in the ‘80s by health-crusading businessman Phil Sokolof and the banishment of industrial trans fats. Two meta-analyses (Siri-Tarino et al., 2010; Chowdhury et al., 2014) suggest saturated fats may not be culpable, however. During these transition periods, the food industry has developed and marketed myriad products consistent with contemporary research. At the same time, molecular genetics research indicated considerable individual variability in response to dietary interventions, including changes in fat profiles (Lopez-Miranda et al., 1994; Ahn et al., 2004).
Recently, the column initiated dialogue on the food-brain connection and the controversial topic of addiction. Within the neurosciences realm, the current data suggest the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), criteria are not always met relative to food craving or even substance abuse (Volkow & O’Brien, 2007). Clearly, a better understanding of neurocircuitry is necessary for clinical interventions, public policy development, and, more importantly, personal behaviors that may be consideredin disorders such as autism, ADHD, and binge eating. The drug addiction model applied to compulsive food intake and obesity has been challenged (Ziauddeen et al., 2012), although others support the hypothesis (Avena et al.,2012).
Contributing factors to obesity include food environment, energy expenditure, physical environment, environmental influences, personality and reward circuitry, individual predisposition, and appetite and satiety. As noted in a recent review of the biology and genetics of obesity and a history of marketing interventions, such options have ranged from La Parle Obesity Soap (1903) that washed away extra pounds to the Tapeworm Diet (1950s) for those who were not uneasy about swallowing a long parasite. Multiple hypotheses have been advanced, including exogenous and endogenous types, which segued to dietary excess and lack of exercise. Yet, as demonstrated by Jules Hirsch and others, excess caloric intake may not yield increased body weight, and caloric restriction may not produce weight loss. Molecular genetics, such as the phenotypic presentations of fat-mass and obesity-associated (FTO) gene (Yang et al., 2012; Frayling et al., 2007) and DYRK1B mutations (Keramati et al., 2014), may alter our understanding of obesity (Jou, 2014).
The controversy about the impact of sugar on health is ongoing. Fueled by the March 2014 World Health Organization “free sugar” recommendations and incorrect reporting by the media and some CVD risk modeling conveyed as a clinical intervention study, consumer confusion increased and policy makers and “added sugar” labeling proponents were elated. Careful examination of the supporting documents (Moynihan & Kelly, 2014; Te Morenga et al., 2013) indicates the following: a) the 5%en free sugar figure to reduce dental caries is weakly supported with low-quality data; and b) the 10%en free sugar figure only parrots the 10–15%en figure adopted by more than 60 countries. This figure was emphasized by a recent nutrition epidemiologic model regarding sugar intake and CVD risk (Yang et al., 2014). However, the meta-analysis of 13 randomized controlled trials indicated an isocaloric exchange with other carbohydrates showed no change in body weight (Te Morenga et al., 2013), which is the same position noted by the 2010 Dietary Guidelines. The same group also reported inconsistent evidence of a causal relation between sugars and cardiometric risk factors, including serum triglycerides, cholesterol, LDL, HDL, and blood pressure among populations consuming isocaloric energy diets (Te Morenga et al., 2014).
Within the fray are saturated fats and CVD risk. Over the past 50 years, the dynamics of fat and health outcomes shifted from cholesterol and atherosclerosis as advanced by epidemiologist Ancel Keys in the ‘60s to the tropical oil culprits identified in the ‘80s by health-crusading businessman Phil Sokolof and the banishment of industrial trans fats. Two meta-analyses (Siri-Tarino et al., 2010; Chowdhury et al., 2014) suggest saturated fats may not be culpable, however. During these transition periods, the food industry has developed and marketed myriad products consistent with contemporary research. At the same time, molecular genetics research indicated considerable individual variability in response to dietary interventions, including changes in fat profiles (Lopez-Miranda et al., 1994; Ahn et al., 2004).
Food, Medicine & Health articles will continue to examine the quantity and quality of evidence, particularly on controversial topics, while engaging a spectrum of established and emerging scientists. Thank you for a decade of support and encouragement. Stand by for Food Medicine & Health 2.0.
Roger Clemens, Dr.P.H., CFS
Contributing Editor
Chief Scientific Officer,
Horn Company, La Mirada, Calif.
[email protected]
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