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Physical Activity Does not Influence Obesity Risk: Time to Clarify the Public Health Message

ByCrossFitFebruary 26, 2020

This 2016 commentary argues increased rates of obesity in the United States and other Western nations are not due to a decrease in physical activity.

First, observational data does not indicate there are any meaningful differences in physical activity levels between populations with varying rates of obesity. Public health authorities have argued that mechanization, motorization, and other factors have led modern Western populations to move less than previous generations (1). The development of the obesity epidemic, however, fails to parallel this shift. Obesity rates began to rise in the mid-1960s, long after technology and culture supported these modern conveniences (2) (Figure 1). Similarly, studies using doubly labeled water, the most rigorous tool used to measure energy expenditure in free-living populations, have shown no difference in mean activity levels between modern agrarian/hunter-gatherer populations and Westerners of similar age and weight. Similarly, there is no relationship between economic development and (decreased) physical activity (3).

Figure 1: Prior to the 1960s, decreases in energy expenditure (due to various social and technological factors) likely drove a small decrease in energy intake. Since the 1960s, however, energy intake has increased without a compensatory increase in energy expenditure.

Second, it is biologically implausible for a decrease in physical activity to lead to weight gain or an increase in physical activity to prevent it. Our appetite and inclination to move are both tightly regulated across a variety of organ systems. These systems are sufficiently sophisticated to keep a healthy adult, prior to current Western societies, at a stable weight throughout adulthood without requiring any deliberate attention to be paid to either energy intake or expenditure. Clinical trials have demonstrated that an increase in physical activity is generally met with an increase in food intake, and vice versa, with this compensatory response visible over a period of weeks rather than days (4). In fact, the effectiveness of these regulatory systems indicates foods that resist these appetite-regulating mechanisms, such as added sugars and especially beverage sugars, may uniquely promote obesity.

Epidemiological evidence within Western populations is difficult to interpret, given well-known fatal flaws in the tools used to assess both dietary intake and energy expenditure, particularly with regard to obese individuals (6). To the extent this data can be interpreted, however, it does not suggest decreased physical intake increases future weight, nor that increased physical activity prevents weight gain. The estimated amount of calories burned by the average American due to deliberate energy expenditure is likely trivial, with men averaging 35 minutes and women averaging 21 minutes per day in “moderate or vigorous” physical activity, a category that can include walking, gardening, and golf (7).

The authors strongly emphasize these claims in no way undermine the established relationships between exercise and disease prevention, and similarly encourage Americans to exercise as much as they are willing and able (8). Specifically, the authors conclude the data clearly indicates the cause of the current obesity epidemic was not a decrease in physical activity within the U.S. population. Instead, they argue, the cause lies in changes to our diet.


  1. What is food addiction?
  2. The Changing Body: Health, Nutrition and Human Development in the Western World Since 1700
  3. Energy expenditure and adiposity in Nigerian and African-American women; Activity, energy expenditure and adiposity among black adults in Nigeria and the United States; Hunter-gatherer energetics and human obesity; Energy expenditure in adults in developing vs. industrialized countries: A meta-analysis of doubly labeled water studies
  4. Changes in weight, waist circumference and compensatory responses with different doses of exercise among sedentary, overweight postmenopausal women; Body fat loss and compensatory mechanisms in response to different doses of aerobic exercise: A randomzied controlled trial in overweight sedentary males; Effects of a 16-month randomized controlled exercise trial on body weight and composition in young, overweight men and women: The Midwest Exercise Trial; Individual variability following 12 weeks of supervised exercise: Identification and characterization of compensation for exercise-induced weight loss; The effect of an incremental increase in exercise of appetite, eating behavior and energy balance in lean men and women feeding ad libitum; Exercise, appetite and appetite-regulating hormones: Implications for food intake and weight control
  5. Calories from soft drinks – Do they matter; A trial of sugar-free or sugar-sweetened beverages and body weight in children
  6. Dietary reporting errors on 24 h recalls and dietary questionnaires are associated with BMI across six European countries as evaluated with recovery markers for protein and potassium intake; OPEN about obesity: Recovery biomarkers, dietary reporting and BMI; Estimating activity energy expenditure: How valid are physical activity questionnaires?; Physical activity in the United States measured by accelerometer
  7. Assessing physical activity and its relationship to cardiovascular risk factors: NHANES 2003-2006
  8. Effects of physical activity on cardiovascular disease; Physical activity and cardiovascular risk factors in children

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