Download Chapter 9 Physical Activity and Obesity

Chapter 9
Physical Activity and Obesity
MORE DIE IN THE UNITED STATES OF TOO MUCH FOOD THAN OF
TOO LIT TLE”
― JOHN KENNETH GALBRAITH
Overweight & Obesity
P-198
Energy Balance Equation
Obesity now co-occurs with undernutrition in many developing nations.
The WHO has coined the term “globesity” to refer to the global epidemic of overweight &
obesity.
Obesogenic-
“Thrifty genes”-evolved in humans to defend against fat loss.
“Hungry brain”-motivated to increase energy intake and reduce energy expenditure through
decreased activity.
Obesity experts say weight gain is more attributable to overeating than to being sedentary..
Energy gap—the change in energy expenditure relative to energy intake needed to reverse excess
body weight in a population.
Originally estimated to be 100 calories.
Lose fat—NOT muscle. Physical activity is key to this—not just caloric restriction.
Our prehistoric ancestors (hunters, gatherers) burned about 1200 calories in activity while
consuming about 2900 (22 cal/kg). Today—we eat about 2030 and burn about 580 (activity) (9
cal/kg).
Ancestors had RMR about 15% higher than us.
Sedentary adults in the US have RMR of about 1450.
Jean Mayer research—P-198.
Higher RMR—more body density (more muscle, less fat)—and/or elevated SNS activity.
RMR naturally DECREASES as people get smaller—so you must INCREASE activity as one gets
SMALLER (loses body weight).
Obesity is a chronic disease developing from a persons genotype, the environment along with diet and
activity habits.
Problems develop mostly in adulthood---obese children are often healthy and fairly fit—these
problems (CVD, hypertension, diabetes) take into young adulthood to manifest. This leads to chronic
but reversible conditions.
Overweight or obese: (adult) higher risk of hypertension, hypercholesterolemia, type 2 diabetes,
CHD, stroke, gallbladder disease, osteoarthritis, and certain cancers. Adolescents—3 x risk of high
blood sugar, BP, triglycerides and low HDL’s. Young children—2-3x risk of hypertension, and low
HDL’s.
Obese people are more likely to die from ANY AND ALL CAUSES compared to normal weight
people.
Magnitude of the Problem
1.6 billion 15 and older overweight and 400 million obese (2005).
About 20 million children (under 5) were overweight.
In 2008 205 million men and 297 million women worldwide said to be obese.
The past decade was the first time in recorded history that the number of people who were overweight
equaled the number of people who were underfed and underweight worldwide.
In the US 68% of adults (20+) are overweight including 34% obese---15% of children (6-11) and 18%
of youths (12-19) are obese.
Between 2008-2010 only 1 state (Colorado) had obesity less than 20%.
Obesity highest among people with less education, lower income and in some minority groups.
Childhood obesity tracks into adulthood. P-203.
The economic burden of obesity is $147 billion a year in the US—nearly 10% of the national health
care budget.
Why We Must Exercise Today
1760: The Industrial Revolution
1900-1913: Henry Ford: Automobile & Assembly Line
1920-1940’s: TV & Mechanized farm equipment
1950’s: TV remote control
1960’s: Power tools
1970’s: Silicon Valley
1980’s: MTV, Computer games
1990’s: DVD players, Cell Phones, MP3 players
New Millennium: iPod, iPhone, Wireless Internet, All things electronic
Food Portion Inceases
Look at the evolution of Coca-Cola
1960’s: 8 oz glass bottle (96 calories)
1970’s: 12 oz can (146 calories)
1980’s: 16 plastic bottle (192 calories)
1990’s: 20 oz ‘Big Gulp” (240 calories)
New Millennium: 40 oz drinks (480 calories)
Not to mention: ALL places offer free refills in today’s society!
FAST FOOD
In 1972, we spent $3 billion a year on fast food—today we spend more than
$110 billion
French Fries are the most eaten vegetable in America
Each day, 1 in 4 Americans eats at a fast food restaurant
McDonald’s feeds more than 46 million people a day: More than the entire
population of Spain!
These facts taken from the website of SUPERSIZE ME A Film of Epic Portions: www.supersizeme.com
SUGAR
Simple sugar intake today represents more than the yearly equivalent of 70
pounds of table sugar (18 teaspoons of sucrose a day) and 50 pounds of corn syrup.
100 years ago, the yearly intake of simple sugars averaged only 4 pounds per
person!
Sports & Exercise Nutrition, 2nd edition: McArdle, Katch & Katch
Why Mississippians Top the Obesity List
Southern Culture
Lack of P.E. in schools (and vending/lunch foods)
Low Socioeconomic Status
Lack of Education of Citizens (%)
Weather (heat, humidity, direct sun, cold, rain)
Poor city planning (roads, parks, sidewalks)
Mindset (Think San Diego)
Failure to Face Reality (energy equation)
Treatment of Overweight & Obesity
P-204
Interactions (some unknown) between genes, behaviors and the environment influence obesity.
Most though, is the result of overeating and too little physical activity.
Improvements in chronic disease risk factors can occur with a 2% -3% reduction in excess body
weight (fat).
Obese people may lose weight but many regain the weight back within 3-5 years.
Clinical trials show obesity treatment drugs are only effective when used in combo with diet and
exercise and only with about 5lbs of additional loss than with diet and exercise alone!
Without sustained activity the average weight loss after dieting only is about 22 lbs and 1/3 of
that is gained back within 3-5 years.
Quetelet’s Body Mass Index (BMI)
Patterning of Body fat & Disease Risk: Android and Gynoid patterns; Waist circumference; Waist
to hip ratio; The dangers of abdominal fat.
Table 9.3 on P-206.
Metabolic Syndrome: Metabolic syndrome is a combination of the medical disorders that, when
occurring together, increase the risk of developing cardiovascular disease and diabetes.[1] Some
studies have shown the prevalence in the USA to be an estimated 25% of the population,[2] and
prevalence increases with age.
Metabolic syndrome is also known as metabolic syndrome X, cardiometabolic syndrome,
syndrome X, insulin resistance syndrome, Reaven's syndrome (named for Gerald Reaven),
and CHAOS (in Australia).[3]
Metabolic Syndrome (identified by 3 or more of the following)-Waist: men 40” +; women 35 \” +
Triglycerides: = 150 or +
Reduced HDL: men<40; women<50
BP: = 130/85 or +
Glucose (fasting): = 100 or +
Etiology of Overweight & Obesity: Set Point or Settling Point?
These are 2 common theories about the etiology of being overweight and obesity.
Set Point Theory:Set point theory is a theory that the body maintains its normal weight and body fat
level with internal regulatory controls that dictate how much fat one has. According to the set point
theory, some individuals have a high setting, meaning they tend to have a naturally higher weight as a
set point, and others have a low set point, and therefore a naturally lower body weight.The set point
theory suggests that despite dieting efforts, the body tends to return to its set point weight, however
regular, consistent exercise may help to adjust the natural set point.
Some refer to the set point theory as an internal "thermostat" that regulates body fat.
The Settling Point Theory was proposed by obesity researcher James Hill of the University of
Colorado to help explain why overweight and obesity are more than problems of metabolism (Hill,
Pagliassotti, and Peters 1994). His idea is that weight loss and gain in most humans are more related to
the patterns of diet and physical activity that people “settle” into as habits based on the interaction of
their genetic dispositions, learning, and environmental cues to behavior. Evidence suggests that obese
people are more sensitive to food-related stimuli in the social and physical environment, which
influence their energy intake, than to the stimuli for energy expenditure.
The Role of Physical Activity
Physical activity has an important role in the prevention and treatment of overweight and obesity,
even if that role is not yet completely understood.
One study suggests that prevention of obesity in children should focus on increasing vigorous
physical activity rather than restricting energy intake (Gutin 2008).
The American College of Sports Medicine (ACSM) recommends that adults participate in at least
150 min/week of moderate-intensity physical activity to protect against excessive weight gain and
reduce chronic disease risk factors, especially in adults with a BMI ≥25 or a waist circumference
above 88 cm (35 in.) in women and 102 cm (40 in.) in men.
Even among people who are considered sedentary during their work or leisure, there can be
meaningful differences in daily energy expenditure that results from the routine activities of daily
living, maintaining an upright posture (e.g., standing rather than sitting), and spontaneously
arising movements (e.g., pacing or fidgeting), which has been termed nonexercise activity
thermogenesis, or NEAT (Levine, Eberhardt, and Jensen 1999).
Evidence shows that regular physical activity or physical fitness can (1) reduce health risks in
people who are overweight, (2) protect against excessive weight gain, (3) help overweight and
obese people lose weight, and (4) help people maintain stable weight after they lose it.
Physical Activity & Fitness and the Health Risks of Obesity: The Evidence: P-209.
The mortality risk of obesity may not be eliminated by activity but usually reduced substantially
in those who do not have a chronic disease.
Physical Fitness: P-212.
Are Overweight & Obesity Risk Factors Independent of Physical Activity?: Some challenge the
view that being thin guarantees health and that being fat is life threatening. Perhaps anyone can
have good health regardless of body weight by achieving and maintaining metabolic fitness—
”Metabolic fitness is when the body has improved insulin sensitivity and is achieved when people
eat healthfully and increase their level of regular exercise. Metabolic fitness doesn’t have
anything to do with how much a person weighs.”
Moderate activity can help lower BP among those overweight & obese even when they do not
lose weight.
High body fat contributes to impaired glucose tolerance and diabetes risk by impairing insulin
receptor function in muscle, liver and fat cells. Physical activity can improve insulin sensitivity
and glucose tolerance in people who are overweight or obese.
P-215
An increase of 3% + of bodyweight in adults is excess weight gain and more than 5% is
considered risky for health.
Studies: P-215-219.
Exercise Training Studies (P-220): Are people exercising enough?
Additional studies: P-220-222.
Behavioral Factors: P-222. When someone starts exercise they may eat more (to offset the extra
caloric expenditure through exercise) OR become less active than normal throughout the day
(ADL’s)---one bran muffin and an OJ can more than replenish the 200 or 300 calories burned in a
typical exercise session. Some people may not eat extra. On the other hand---when active people
become sedentary—they usually do NOT eat less to balance off the decrease in energy
expenditure expenditure..
Exercise & Appetite: P-223. The brain senses levels of glucose and insulin and regulated hunger
between meals. Low glucose stimulates hunger while high levels of glucose and insulin inhibit
hunger.
Exercise lowers insulin & glucose. Exercise usually suppresses hunger acutely.
Leptin & Ghrelin
Leptin and ghrelin are two hormones that have been recognized to have a major influence on energy balance.
Leptin is a mediator of long-term regulation of energy balance, suppressing food intake and thereby inducing
weight loss. Ghrelin on the other hand is a fast-acting hormone, seemingly playing a role in meal initiation. As a
growing number of people suffer from obesity, understanding the mechanisms by which various hormones and
neurotransmitters have influence on energy balance has been a subject of intensive research. In obese subjects the
circulating level of the anorexigenic hormone leptin is increased, whereas surprisingly, the level of the orexigenic
hormone ghrelin is decreased. It is now established that obese patients are leptin-resistant. However, the manner in
which both the leptin and ghrelin systems contribute to the development or maintenance of obesity is as yet not
clear.
The hypothalamus (in the brain):The hypothalamus, a part of the brain, is the main regulatory organ for the human
appetite. Appetite is the desire to eat food, felt as hunger. Appetite exists in all higher life-forms, and serves to
regulate adequate energy intake to maintain metabolic needs. It is regulated by a close interplay between the
digestive tract, adipose tissue and the brain. Appetite has a relationship with every individual's behavior. Appetitive
and consummatory behaviours are the only processes that involve energy intake, whereas all other behaviours
affect the release of energy. When stressed, appetite levels may increase and result in an increase of food intake.
Decreased desire to eat is termed anorexia, while polyphagia (or "hyperphagia") is increased eating. Dysregulation
of appetite contributes to anorexia nervosa, bulimia nervosa, cachexia, overeating, and binge eating disorder.
Genetic Factors
P-224
At least 22 genes have been supported in descriptive studies as influences on obesity—but they each account for a
small portion (less than 1%) of variation among people.
A stronger association has been found for the FTO (fat mass & obesity associated) gene.
The population attributable risk of obesity from variations in the FTO gene has been shown to be about 20%.
Fat mass and obesity-associated protein also known as alpha-ketoglutarate-dependent dioxygenase FTO is an
enzyme that in humans is encoded by the FTO gene located on chromosome .
Association with obesity:
A study of 38,759 Europeans for variants of FTO identified an obesity risk allele.[2] In particular, carriers of one
copy of the allele weighed on average 1.2 kilograms (2.6 lb) more than people with no copies. Carriers of two
copies (16% of the subjects) weighed 3 kilograms (6.6 lb) more and had a 1.67-fold higher rate of obesity than
those with no copies. The association was observed in ages 7 and upwards. This gene is not directly associated
with diabetes however increased body-fat also increases the risk of developing Type 2 Diabetes.[27]
Children & Adolescents
P-225
Restricting Caloric Intake & Increasing Physical Activity: P-226—The pro’s and con’s of each or
together..
Physical Activity & Weight Maintenance: The Evidence: Lost body weight is usually regained when
diets are used alone, but diet combined with increased exercise seems to yield better maintenance of
weight loss, especially if the exercise program is maintained after the diet ends.
Strength of Evidence: P-228.
Temporal Sequence
Strength of Association
Consistency
Dose Response
Biological Plausibility
Resistance Exercise
Weight loss after resistance training is usually less than 1kg but that can be misleading when the
training program produces an increase in fat-free mass—This increases energy expenditure—i.e.,
metabolism.
Because the energy needs of internal organs exceed that of skeletal muscles it remains unclear
whether increases in muscle mass explain the increase in RMR reported after resistance training.
Resistance training can increase BMR by an extra 50-75 calories. Most of the increase is
explained by increased LBM—not by extra use of protein as fuel.
As insulin resistance appears to be a key catalyst that induces the cascade of risks associated with
metabolic syndrome the demonstrated protective role of activity against impaired glucose
tolerance assumes special importance for people who are overweight.
The mechanism for this is metabolic change from increased insulin sensitivity due to
upregulation of receptors on muscle and liver (hepatic) cells.
Weight loss or Risk Reduction: P-231
Summary: 100,000 deaths per year in the USA are attributed to obesity—which mainly results
from overeating and inactivity.
Weight loss is not always necessary to achieve health results.