Tweet
I just finished this last night Could you fine people look it over for me?
Young adults (18-22 years of age) are less physically active than adolescents (12-18 years of age).1 As reported by Gordon-Larsen, in a multi-ethnic longitudinal study, the majority of adolescents (61.5%) fail to achieve 5 or more bouts of moderate to vigorous physical activity (MVPA) in a week. Moreover, as adolescents move into young adulthood the percentage of those who do not achieve adequate physical activity (PA) levels rises to 74.1%.1 While it is interesting to note that some ethnic and gender groups achieved less PA than others the largest differences in PA were observed between adolescents and young adults. These findings appear to be in line with those of Raitakari and Anderssen. Raitakari who, in a 6 year study of Finnish youth, tracked the PA of 3, 6, 9, 12, 15 and 18 year olds over a 6 year period found that sedentary rates rose on average from 33.9% in 1980 to 45.5% in 1986.2 In addition Anderssen concluded from both his own studies and his analysis of several smaller cross-sectional studies that "Leisure-time physical activity seems to decline in the late adolescent and young adult years."3
While many researchers tend to focus on race, the concept of the birth cohort as a distinct group within a society has been recognized for more than 45 years. Ryder asserted that each age cohort is differentiated by changes in formal education, peer-group socialization, technological advances and historical events. He further states, "Conceptually the cohort resembles most closely the ethnic group [and] should be used as a group defining variable in its own right… Comparison of such composite cohort biographies would yield the most direct and efficient measurement of the consequences of social change."4 This notion of a birth cohort was revisited by Hogan when he claimed, "…each cohort is characterized by a unique history that is reflected in its behavior and in the production of social change."5 Television and other activities involving screen use is recognized as a powerful and pervasive influence in today's society and warrants research based on year of birth and age of subjects rather than ethnic ancestry.
Increased time spent viewing television and movies, and time spent playing computer games or surfing the Internet (screen time) is gaining acceptance as a leading cause of inactivity in people as they move from childhood to young adulthood. As people age they engage in larger amounts of screen time.1 It is important to note that this pattern of decreasing activity as one ages has been accepted for some time. It is believed that the increased availability of screen time activities in society will have an affect on current and future generations unlike those of the past. In sum, the increase in sedentary activity among a given birth cohort is on the rise and this rise is due to increased screen time.
The recent proliferation of screen time has many consequences. Correlations in; increased aggressive behavior6, decreased school performance7, greater frequency in between-meal snacking8, ingestion of high-density caloric foods6, greater incident of obesity9 and increased attempts by children to influence parents shopping10 have all been documented to varying degrees. It is plausible to presuppose that increases in screen time negatively affect time spent engaged in PA.
Dietz observed that actual rates of obesity corresponded to a 2% increase in fatness for every hour of television watched, clearly showing a dose response relationship. He also found that children who watched >5 hours of television a day at age 6-11 years were twice as likely to be obese at age 12-17 years.9 This lag in onset of obesity is consistent with increases in adiposity due to inactivity. Pate found that subjects who had higher levels of screen time had a lower level of performance in a 1-mile run/walk activity.11 Pate's results were reproduced by Tucker after he observed that light viewers of television performed better in composite fitness tests.12 Robinson concluded that minor yet significant (p = .026) negative associations exist between screen time and PA.13 These findings were also noted among young white males.14
Klesges observed that the more television a person watched, the lower their resting metabolic rates (RMR) were. RMR's dropped from >1600 kilocalories to just over 1350 kcals in obese individuals and from 1400 to 1250 in lean subjects.14 This is consistent with data which shows that RMR increases with PA and therefore points to reversibility.15 It has been observed that while 3-5 year olds actually become more active while watching TV, due to imitating the actions of TV characters, this mimicking behavior is not seen in older viewers, once again illustrating a decline in PA during screen time among older subjects.16
While there are many studies that support the notion of screen time negatively affecting PA as subjects pass into adulthood, much of the data compiled in this paper stems from cross-sectional studies which only observed small, selective samples based on race and or gender, with some relying on self-reported data. Until it can be shown that a specific age cohort does in fact engage in more or less screen time than its counter-part from another era and that the engagement in screen time is a cause of inactivity, interventions should be targeted to as wide a population as possible.
Decreasing the screen time of adolescents and young adults should be of concern to public policy makers as it has been shown that activities adopted in adolescence tend to stay with an individual for the rest of their life. It has already been well established that regular PA will decrease the risk of contracting cardiovascular disease (CVD). Studies are now revealing that physical activity also modifies biological risk factors in adolescents just as they do in adults.[2,17] With approximately 1.1 million Americans suffering a heart attack each year it is reckless for our society to continue to ignore the negative effects of screen time on its youth.
CVD comes in many forms and may have several inter-related causes for each of these forms. Research is currently being conducted which points to an underlying cause of the many forms of CVD. Hypertension, atherosclerosis, left ventricular (LV) hypertrophy and LV remodeling have all been linked to arterial stiffness. [18-20]
Physical activity has been shown to reduce arterial stiffness or increase arterial compliance. Regular aerobic-endurance exercise has favorable effects on the compliance of large elastic arteries despite imparting no positive benefit to age induced LV remolding.[20, 21] In canines, modest exercise training altered the elastic properties of epicardial coronary arteries by 30%, thus improving flow of blood to the heart.[22] Similar findings showing a correlation between habitual exercise and increased arterial compliance have been documented in women, men, young and old subjects.[20,21,23,24] These same studies showed that the sedentary counterparts of the aforementioned groups showed increased measurers of arterial stiffness.
While it is quickly being established that physical inactivity is a predictor of arterial stiffness, the root cause of CVD, there appears to be a point of no return. Older subjects with established atherosclerosis and hypertension are resistant to the adaptations of exercise on arterial compliance.[20, 25] If one looks at the mechanism of arterial hardening this is not surprising.
Over time, elastic fibers undergo a process of fatigue-induced degradation. In the obese, collagen accumulates and forms fibrous caps. These caps are subject to calcification. The formation of atherosclerostic lesions then follows. [26] This process takes considerable time. It would be unreasonable to assume that a state of disease, which takes decades to develop, could be reversed by exercise in a matter of months.
Some observations show that even after three years of weight loss epicardial arterial distress is still present within patients who were morbidly obese [27]. Moreover, the weight status of men in their late teens and early twenties is related to blood pressure when middle age is reached, [28] and VO2 max levels in adolescence are associated with pre-clinical signs of atherosclerosis 24 years later [29]. This provides clear evidence that engaging in PA at a young age offers the most effective method for preventing arterial stiffness [25].
In the body, arterial compliance is achieved through the promotion and restriction of many compounds. Cyclic guanosine monophosphate (cGMP) seems to exert the greatest relaxing effect upon arteries.[22] However, cGMP generation is receptor based and therefore not meditated by mechanical process thought to be necessary if its action were to be considered based on PA.[22] The exogenous substances used to facilitate the production of cGMP carry sever side-effects and therefore used sparingly. Until such time that medical science can fabricate a drug that allows the expression of cGMP without generating intense headaches, exercise appears to be the best alternative.
In regard to physical activity, the force exerted on the inner surface of the arterial wall (shear stress) is the most commonly accepted exercise induced mechanism for epicardial arterial distensibility.[22,8,13,22] Shear stress, a non-receptor mediated stimulus, causes the release of nitric oxide (NO) and prostacyclin (PGI2) from endothelial cells which line the inner surface of arteries. Shear stress is also partly responsible for the restriction of a vasoconstrictor, endothelin-1 (ET-1).[30] The additive affects of having two vasodilators while reducing the amount of vasoconstrictor provides great benefits to the compliance of the vascular system. While the mediation of these three compounds, through PA, does not equal the effect caused by cGMP [22], the use of PA provides a more reliable, consistent and safer means of controlling arterial distensibility.
Today America is experiencing the largest teen population of its young history. With over 33 million people between the ages of 12 and 20, it is of paramount importance to alter the screen time habits of America's youth. The increasing epidemic of obesity in today's youth has many causes. If nothing is done to increase and maintain the levels of physical activity in our young population, our medical system will become overburdened as an influx of new obesity related disease manifests over the next four decades.
William Shakespeare was aware of the dangers of obesity when he wrote…”Make less thy body hence and more thy grace, leave gormandizing; Know thy grave doth gape for thee wider than other men.” We have possessed scientific knowledge of what happens to the body when it becomes obese for more than 75 years. We have the means to change obesity in the vast majority of the population. Through public policy we have the power to affect that change. The only question left is, do we have the will and foresight act?
Young adults (18-22 years of age) are less physically active than adolescents (12-18 years of age).1 As reported by Gordon-Larsen, in a multi-ethnic longitudinal study, the majority of adolescents (61.5%) fail to achieve 5 or more bouts of moderate to vigorous physical activity (MVPA) in a week. Moreover, as adolescents move into young adulthood the percentage of those who do not achieve adequate physical activity (PA) levels rises to 74.1%.1 While it is interesting to note that some ethnic and gender groups achieved less PA than others the largest differences in PA were observed between adolescents and young adults. These findings appear to be in line with those of Raitakari and Anderssen. Raitakari who, in a 6 year study of Finnish youth, tracked the PA of 3, 6, 9, 12, 15 and 18 year olds over a 6 year period found that sedentary rates rose on average from 33.9% in 1980 to 45.5% in 1986.2 In addition Anderssen concluded from both his own studies and his analysis of several smaller cross-sectional studies that "Leisure-time physical activity seems to decline in the late adolescent and young adult years."3
While many researchers tend to focus on race, the concept of the birth cohort as a distinct group within a society has been recognized for more than 45 years. Ryder asserted that each age cohort is differentiated by changes in formal education, peer-group socialization, technological advances and historical events. He further states, "Conceptually the cohort resembles most closely the ethnic group [and] should be used as a group defining variable in its own right… Comparison of such composite cohort biographies would yield the most direct and efficient measurement of the consequences of social change."4 This notion of a birth cohort was revisited by Hogan when he claimed, "…each cohort is characterized by a unique history that is reflected in its behavior and in the production of social change."5 Television and other activities involving screen use is recognized as a powerful and pervasive influence in today's society and warrants research based on year of birth and age of subjects rather than ethnic ancestry.
Increased time spent viewing television and movies, and time spent playing computer games or surfing the Internet (screen time) is gaining acceptance as a leading cause of inactivity in people as they move from childhood to young adulthood. As people age they engage in larger amounts of screen time.1 It is important to note that this pattern of decreasing activity as one ages has been accepted for some time. It is believed that the increased availability of screen time activities in society will have an affect on current and future generations unlike those of the past. In sum, the increase in sedentary activity among a given birth cohort is on the rise and this rise is due to increased screen time.
The recent proliferation of screen time has many consequences. Correlations in; increased aggressive behavior6, decreased school performance7, greater frequency in between-meal snacking8, ingestion of high-density caloric foods6, greater incident of obesity9 and increased attempts by children to influence parents shopping10 have all been documented to varying degrees. It is plausible to presuppose that increases in screen time negatively affect time spent engaged in PA.
Dietz observed that actual rates of obesity corresponded to a 2% increase in fatness for every hour of television watched, clearly showing a dose response relationship. He also found that children who watched >5 hours of television a day at age 6-11 years were twice as likely to be obese at age 12-17 years.9 This lag in onset of obesity is consistent with increases in adiposity due to inactivity. Pate found that subjects who had higher levels of screen time had a lower level of performance in a 1-mile run/walk activity.11 Pate's results were reproduced by Tucker after he observed that light viewers of television performed better in composite fitness tests.12 Robinson concluded that minor yet significant (p = .026) negative associations exist between screen time and PA.13 These findings were also noted among young white males.14
Klesges observed that the more television a person watched, the lower their resting metabolic rates (RMR) were. RMR's dropped from >1600 kilocalories to just over 1350 kcals in obese individuals and from 1400 to 1250 in lean subjects.14 This is consistent with data which shows that RMR increases with PA and therefore points to reversibility.15 It has been observed that while 3-5 year olds actually become more active while watching TV, due to imitating the actions of TV characters, this mimicking behavior is not seen in older viewers, once again illustrating a decline in PA during screen time among older subjects.16
While there are many studies that support the notion of screen time negatively affecting PA as subjects pass into adulthood, much of the data compiled in this paper stems from cross-sectional studies which only observed small, selective samples based on race and or gender, with some relying on self-reported data. Until it can be shown that a specific age cohort does in fact engage in more or less screen time than its counter-part from another era and that the engagement in screen time is a cause of inactivity, interventions should be targeted to as wide a population as possible.
Decreasing the screen time of adolescents and young adults should be of concern to public policy makers as it has been shown that activities adopted in adolescence tend to stay with an individual for the rest of their life. It has already been well established that regular PA will decrease the risk of contracting cardiovascular disease (CVD). Studies are now revealing that physical activity also modifies biological risk factors in adolescents just as they do in adults.[2,17] With approximately 1.1 million Americans suffering a heart attack each year it is reckless for our society to continue to ignore the negative effects of screen time on its youth.
CVD comes in many forms and may have several inter-related causes for each of these forms. Research is currently being conducted which points to an underlying cause of the many forms of CVD. Hypertension, atherosclerosis, left ventricular (LV) hypertrophy and LV remodeling have all been linked to arterial stiffness. [18-20]
Physical activity has been shown to reduce arterial stiffness or increase arterial compliance. Regular aerobic-endurance exercise has favorable effects on the compliance of large elastic arteries despite imparting no positive benefit to age induced LV remolding.[20, 21] In canines, modest exercise training altered the elastic properties of epicardial coronary arteries by 30%, thus improving flow of blood to the heart.[22] Similar findings showing a correlation between habitual exercise and increased arterial compliance have been documented in women, men, young and old subjects.[20,21,23,24] These same studies showed that the sedentary counterparts of the aforementioned groups showed increased measurers of arterial stiffness.
While it is quickly being established that physical inactivity is a predictor of arterial stiffness, the root cause of CVD, there appears to be a point of no return. Older subjects with established atherosclerosis and hypertension are resistant to the adaptations of exercise on arterial compliance.[20, 25] If one looks at the mechanism of arterial hardening this is not surprising.
Over time, elastic fibers undergo a process of fatigue-induced degradation. In the obese, collagen accumulates and forms fibrous caps. These caps are subject to calcification. The formation of atherosclerostic lesions then follows. [26] This process takes considerable time. It would be unreasonable to assume that a state of disease, which takes decades to develop, could be reversed by exercise in a matter of months.
Some observations show that even after three years of weight loss epicardial arterial distress is still present within patients who were morbidly obese [27]. Moreover, the weight status of men in their late teens and early twenties is related to blood pressure when middle age is reached, [28] and VO2 max levels in adolescence are associated with pre-clinical signs of atherosclerosis 24 years later [29]. This provides clear evidence that engaging in PA at a young age offers the most effective method for preventing arterial stiffness [25].
In the body, arterial compliance is achieved through the promotion and restriction of many compounds. Cyclic guanosine monophosphate (cGMP) seems to exert the greatest relaxing effect upon arteries.[22] However, cGMP generation is receptor based and therefore not meditated by mechanical process thought to be necessary if its action were to be considered based on PA.[22] The exogenous substances used to facilitate the production of cGMP carry sever side-effects and therefore used sparingly. Until such time that medical science can fabricate a drug that allows the expression of cGMP without generating intense headaches, exercise appears to be the best alternative.
In regard to physical activity, the force exerted on the inner surface of the arterial wall (shear stress) is the most commonly accepted exercise induced mechanism for epicardial arterial distensibility.[22,8,13,22] Shear stress, a non-receptor mediated stimulus, causes the release of nitric oxide (NO) and prostacyclin (PGI2) from endothelial cells which line the inner surface of arteries. Shear stress is also partly responsible for the restriction of a vasoconstrictor, endothelin-1 (ET-1).[30] The additive affects of having two vasodilators while reducing the amount of vasoconstrictor provides great benefits to the compliance of the vascular system. While the mediation of these three compounds, through PA, does not equal the effect caused by cGMP [22], the use of PA provides a more reliable, consistent and safer means of controlling arterial distensibility.
Today America is experiencing the largest teen population of its young history. With over 33 million people between the ages of 12 and 20, it is of paramount importance to alter the screen time habits of America's youth. The increasing epidemic of obesity in today's youth has many causes. If nothing is done to increase and maintain the levels of physical activity in our young population, our medical system will become overburdened as an influx of new obesity related disease manifests over the next four decades.
William Shakespeare was aware of the dangers of obesity when he wrote…”Make less thy body hence and more thy grace, leave gormandizing; Know thy grave doth gape for thee wider than other men.” We have possessed scientific knowledge of what happens to the body when it becomes obese for more than 75 years. We have the means to change obesity in the vast majority of the population. Through public policy we have the power to affect that change. The only question left is, do we have the will and foresight act?
Comment