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BMS College of ENGINEERING
(autonomous institute, affiliated with VTU)
Department of Electronics and telecommunication
Topic- obesity disorder
SFH course code:21BT2AESFH
ASSIGNMENT SUBMITTED ON THE PARTIAL FULFILLMENT OF THE AAT
OF SEMESTER ||
SUBMITTED BY-SHRIYANSH THAKUR
AYUSH SHARMA
VIVEK KUMAR
SHASHANK KASHAYUP
Submitted To –PRASHANTH KUMAR H P
DEPARTMENT OF SCIENTIFIC FOUNDATION OF HEALTH
Date Of Submission-17-09-22
OBESITY
DISORDERS
BY:-
SHRIYANSH THAKUR
AYUSH SHARMA
VIVEK KUMAR
SHASHANK KASHAYUP
BMI = weight [kg]/(height [m])2
• At a given BMI, women, on average, have more body fat.
• Morbidity and mortality increase with BMI similarly for men and women.
• Risk at a given BMI can vary between populations.
Body Mass Index (BMI): Medically Significant Adiposity
Adipocyte Hypertrophy and/or Hyperplasia
1. Subcutaneous
2. Intra-abdominal (independent morbidity risk factor)
3. Muscles (particularly in older people)
Health Risks Associated with Obesity
1. Type 2 Diabetes (NIDDM)
2. Cardiovascular Disease
a. Hypertension
b. Dyslipidemia (high total cholesterol, low HDL, high LDL, high triglycerides)
3. Sleep-Breathing Abnormalities
a. difficulty breathing
b. obstructive apnea
4. Gallstones
5. Menstrual irregularity, difficulty getting pregnant
6. Osteoarthritis
7. Cancer (colon, endometrial, breast)
8. Mice lacking insulin receptors in adipose tissue live longer!
Science 299: 572-4 (2003)
Women: RR is 18.1 for BMI ≥ 31 Men: RR is 50.7 for BMI ≥ 35
• WHO estimates BMI < 25 would prevent 64% of Type 2 DM in US men and 74% in
US women.
• Framingham study estimates BMI < 25 would reduce coronary heart disease by 25%
and strokes and congestive heart failure by 35%.
Magnitude of Risk
PREVALENCE OF OBESITY AMONG U.S. ADULTS, BRFSS
<10% 10-15% >15%
1985
1986
1987
1988
1989
1990
1991
1992
1993
1994
1995
1996
1997
1998
Trends in Prevalence Worldwide
OBESITY
Genes
Monogenic syndromes Susceptibility genes
(many genes, each with small effect)
Physical activity Food intake
Environment/Lifestyle
50%-90% of variation in BMI in twin studies
A. Eat more:
Increased food availability
calories/person/day has increased 15% since 1970
% of food $ spent outside the home has doubled since 1970
Increased portion size
in the 1950’s a 12 oz soda at McDonalds was king-sized; now it’s child size
Increased energy density (kcal/g)
high fat foods; low fat/low cal foods
B. Do less:
Increased sedentary leisure time activities
TV, computers, video games; cutbacks in mandatory PE
Decreased occupational physical activity
Increased use of automobiles
“Obesogenic” Environment
Energy Balance
Basal metabolism: energy expenditure of a subject relaxed and at rest, at thermoneutrality, 8–
12 hours after last food ingestion.
Adaptive thermogenesis: energy dissipated as heat in response to environmental changes.
• There are very effective mechanisms to defend against body weight loss but less
effective mechanisms to defend against body weight gain.
• Energy stores (adipose mass) are maintained at a set point.
• Weight loss leads to compensatory response: decreased energy expenditure,
hyperphagia, and eventual restoration of body weight.
• A formerly obese person requires about 15% fewer calories to maintain a “normal’
weight than someone who has not been obese because of the compensatory
decrease in energy expenditure.
Energy Homeostasis
Therapeutic Consequences:
1. Current interventions target energy balance and fat, not the set point.
2. Treatment plateaus: treating obesity results in ~10% weight loss.
3. Recurrence when treatment stops.
THANK YOU

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SFH PROJECT.pptx

  • 1. BMS College of ENGINEERING (autonomous institute, affiliated with VTU) Department of Electronics and telecommunication Topic- obesity disorder SFH course code:21BT2AESFH ASSIGNMENT SUBMITTED ON THE PARTIAL FULFILLMENT OF THE AAT OF SEMESTER || SUBMITTED BY-SHRIYANSH THAKUR AYUSH SHARMA VIVEK KUMAR SHASHANK KASHAYUP Submitted To –PRASHANTH KUMAR H P DEPARTMENT OF SCIENTIFIC FOUNDATION OF HEALTH Date Of Submission-17-09-22
  • 3. BMI = weight [kg]/(height [m])2 • At a given BMI, women, on average, have more body fat. • Morbidity and mortality increase with BMI similarly for men and women. • Risk at a given BMI can vary between populations. Body Mass Index (BMI): Medically Significant Adiposity
  • 4. Adipocyte Hypertrophy and/or Hyperplasia 1. Subcutaneous 2. Intra-abdominal (independent morbidity risk factor) 3. Muscles (particularly in older people)
  • 5. Health Risks Associated with Obesity 1. Type 2 Diabetes (NIDDM) 2. Cardiovascular Disease a. Hypertension b. Dyslipidemia (high total cholesterol, low HDL, high LDL, high triglycerides) 3. Sleep-Breathing Abnormalities a. difficulty breathing b. obstructive apnea 4. Gallstones 5. Menstrual irregularity, difficulty getting pregnant 6. Osteoarthritis 7. Cancer (colon, endometrial, breast) 8. Mice lacking insulin receptors in adipose tissue live longer! Science 299: 572-4 (2003)
  • 6. Women: RR is 18.1 for BMI ≥ 31 Men: RR is 50.7 for BMI ≥ 35 • WHO estimates BMI < 25 would prevent 64% of Type 2 DM in US men and 74% in US women. • Framingham study estimates BMI < 25 would reduce coronary heart disease by 25% and strokes and congestive heart failure by 35%. Magnitude of Risk
  • 7. PREVALENCE OF OBESITY AMONG U.S. ADULTS, BRFSS <10% 10-15% >15% 1985 1986 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998
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  • 10. OBESITY Genes Monogenic syndromes Susceptibility genes (many genes, each with small effect) Physical activity Food intake Environment/Lifestyle 50%-90% of variation in BMI in twin studies
  • 11. A. Eat more: Increased food availability calories/person/day has increased 15% since 1970 % of food $ spent outside the home has doubled since 1970 Increased portion size in the 1950’s a 12 oz soda at McDonalds was king-sized; now it’s child size Increased energy density (kcal/g) high fat foods; low fat/low cal foods B. Do less: Increased sedentary leisure time activities TV, computers, video games; cutbacks in mandatory PE Decreased occupational physical activity Increased use of automobiles “Obesogenic” Environment
  • 12. Energy Balance Basal metabolism: energy expenditure of a subject relaxed and at rest, at thermoneutrality, 8– 12 hours after last food ingestion. Adaptive thermogenesis: energy dissipated as heat in response to environmental changes.
  • 13. • There are very effective mechanisms to defend against body weight loss but less effective mechanisms to defend against body weight gain. • Energy stores (adipose mass) are maintained at a set point. • Weight loss leads to compensatory response: decreased energy expenditure, hyperphagia, and eventual restoration of body weight. • A formerly obese person requires about 15% fewer calories to maintain a “normal’ weight than someone who has not been obese because of the compensatory decrease in energy expenditure. Energy Homeostasis Therapeutic Consequences: 1. Current interventions target energy balance and fat, not the set point. 2. Treatment plateaus: treating obesity results in ~10% weight loss. 3. Recurrence when treatment stops.