2. TEXT
LEARNING OBJECTIVES
▸Apply counseling strategies to promote behavior change in
patients with obesity
▸Learn about new guidelines for management of Obesity
▸Select adequate obesity medications taking into account
patient’s Comorbidities
4. OBESITY
DEFINITIONS
▸Obesity: Body Mass Index (BMI) of 30 kg/m2 or higher.
▸Body Mass Index (BMI): A measure of an adult’s weight in
relation to his or her height, calculated by using the adult’s
weight in kilograms divided by the square of his or her height
in meters.
6. OBESITY
OBESITY PREVALENCE MAPS
▸Adult obesity prevalence by state and territory using self-reported information from the Behavioral
Risk Factor Surveillance System.
▸Obesity is common, serious, and costly
▸The prevalence of obesity was 39.8% and affected about 93.3 million of US adults in 2015~2016.
▸Obesity-related conditions include heart disease, stroke, type 2 diabetes and certain types of
cancer that are some of the leading causes of preventable, premature death. [Read
guidelinesExternal
]
▸The estimated annual medical cost of obesity in the United States was $147 billion in 2008 US
dollars; the medical cost for people who have obesity was $1,429 higher than those of normal
weight
CDC National Center for Health Statistics (NCHS) data briefCdc-pdf
PDF-603KB
7. TEXT
OBESITY
▸Hispanics (47.0%) and non-Hispanic blacks (46.8%) had the
highest age-adjusted prevalence of obesity, followed by non-
Hispanic whites (37.9%) and non-Hispanic Asians (12.7%).
▸The prevalence of obesity was 35.7% among young adults
aged 20 to 39 years, 42.8% among middle-aged adults aged
40 to 59 years, and 41.0% among older adults aged 60 and
older.
8. Prevalence¶ of Self-Reported Obesity Among U.S. Adults by State
and Territory, BRFSS, 2011
*Sample size <50 or the relative standard error (dividing the standard error by the prevalence) ≥ 30%.
¶ Prevalence estimates reflect BRFSS methodological changes started in 2011. These estimates should
not be
compared to prevalence estimates before 2011.
9. Prevalence¶ of Self-Reported Obesity Among U.S. Adults by
State and Territory, BRFSS, 2012
*Sample size <50 or the relative standard error (dividing the standard error by the prevalence) ≥ 30%.
¶ Prevalence estimates reflect BRFSS methodological changes started in 2011. These estimates should
not be
compared to prevalence estimates before 2011.
10. Prevalence¶ of Self-Reported Obesity Among U.S. Adults by
State and Territory, BRFSS, 2013
*Sample size <50 or the relative standard error (dividing the standard error by the prevalence) ≥ 30%.
¶ Prevalence estimates reflect BRFSS methodological changes started in 2011. These estimates should
not be
compared to prevalence estimates before 2011.
11. Prevalence¶ of Self-Reported Obesity Among U.S. Adults by State
and Territory, BRFSS, 2014
*Sample size <50 or the relative standard error (dividing the standard error by the prevalence) ≥ 30%.
¶ Prevalence estimates reflect BRFSS methodological changes started in 2011. These estimates should
not be
compared to prevalence estimates before 2011.
12. Prevalence¶ of Self-Reported Obesity Among U.S. Adults by
State and Territory, BRFSS, 2015
*Sample size <50 or the relative standard error (dividing the standard error by the prevalence) ≥ 30%.
¶ Prevalence estimates reflect BRFSS methodological changes started in 2011. These estimates should
not be
compared to prevalence estimates before 2011.
13. Prevalence¶ of Self-Reported Obesity Among U.S. Adults
by State and Territory, BRFSS, 2016
*Sample size <50 or the relative standard error (dividing the standard error by the prevalence) ≥ 30%.
¶ Prevalence estimates reflect BRFSS methodological changes started in 2011. These estimates should
not be
compared to prevalence estimates before 2011.
14. Prevalence¶ of Self-Reported Obesity Among U.S. Adults
by State and Territory, BRFSS, 2017
¶ Prevalence estimates reflect BRFSS methodological changes started in 2011. These estimates should not be
compared to prevalence estimates before 2011.
*Sample size <50 or the relative standard error (dividing the standard error by the prevalence) ≥
30%.
15. Prevalence¶ of Self-Reported Obesity Among U.S. Adults
by State and Territory, BRFSS, 2018
¶ Prevalence estimates reflect BRFSS methodological changes started in 2011. These estimates should not be
compared to prevalence estimates before 2011.
*Sample size <50 or the relative standard error (dividing the standard error by the prevalence) ≥
30%.
31. OBESITY
NUTRITION
▸Reduced-calorie meal plan and macronutrient
composition.Reducing total energy (caloric) intake should be
the main component of any weight-loss intervention.
▸Modifying macronutrient composition may be considered to
optimize adherence, eating patterns, weight loss, metabolic
profiles, risk factor reduction, and/or clinical outcomes
35. OBESITY
PHYSICAL ACTIVITY
▸Aerobic physical activity training should be prescribed to patients with overweight or
obesity as a component of lifestyle intervention; the ultimate goal should be ≥150
min/week of moderate exercise performed during 3 to 5 daily sessions per week
▸Behavioral lifestyle intervention and support should be intensified if patients do not
achieve a 2.5% weight loss in the first month of treatment, as early weight reduction is a
key predictor of long- term weight-loss success
▸Promote fat loss while preserving fat-free mass; the goal should be resistance training 2
to 3 times per week consisting of single-set exercises that use the major muscle groups
▸Behavioral lifestyle intervention should be tailored to a patient’s ethnic, cultural,
socioeconomic, and educational background
▸Reduce sedentary behavior
AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY COMPREHENSIVE CLINICAL PRACTICE GUIDELINES FOR MEDICAL CARE OF PATIENTS
WITH OBESITY W. Timothy Garvey, Jeffrey I. Mechanick, Elise M. Brett, Alan J. Garber, Daniel L. Hurley, Ania M. Jastreboff, Karl Nadolsky, Rachel Pessah-Pollack, Raymond Plodkowski, and Reviewers of the
AACE/ACE Obesity Clinical Practice Guidelines. Endocrine Practice 2016 22:Supplement 3, 1-203
39. OBESITY
BEHAVIOR THERAPY
▸Self-monitoring of weight, food intake, and physical activity
▸Clear and reasonable goal-setting
▸Education pertaining to obesity, nutrition, and physical activity
▸Face-to-face and group meetings
▸Stimulus control
▸Systematic approaches for problem solving
▸Stress reduction
56. OBESITY
HCG - 500 KCAL
DIET
▸ HCG is a hormone that is produced
by the human placenta during
pregnancy.
▸ Products that claim to contain HCG
are typically marketed in connection
with a very low calorie diet, usually
one that limits calories to 500 per
day.
▸ “reset your metabolism,”
▸ change “abnormal eating patterns”
64. OBESITY
OBESITY + CARDIOVASCULAR DISEASE
Use agents without cardiovascular signals (increased blood
pressure and pulse):
▸Orlistat
▸ Lorcaserin
• Lower risk of increased blood pressure than
phentermine/topiramate
65. OBESITY
SUMMARY
▸ First guideline that specifically names anti-obesity medications and recommended doses
Patient selection criteria:
▸ BMI >27 kg/m2 with one comorbidity
▸ BMI >30 kg/m2 with no comorbidities
▸ Diet, exercise and behavior modification is the foundation of any weight management plan
▸ Provides a blueprint on medications that cause weight gain and their alternatives
▸ New paradigm: treat weight first, then comorbid condition(s
66. OBESITY
SUMMARY
▸Medications can drive weight gain and they can also help patients lose weight and keep it
off
▸Before prescribing, review current medications and try to d/c those causing gain
▸KNOW drug profiles - prescribe the right medication for the right patient
▸Always encourage patient to follow lifestyle changes
▸Evaluate response at ~ 12 weeks on drug and change or increase if weight loss is < 5%
▸MOTIVATE your patient
▸BE AN EXAMPLE
Signaling in the brain of adolescents in response to glucose or fructose: schematic representation of changes in the periphery and brain after the ingestion of glucose or fructose. Subjective responses using variable analog scales (VAS) are shown in the lower-left corner for hunger, fullness, and satiety where differences were detected. Both glucose and fructose are absorbed, but fructose is largely cleared in the liver, where it stimulates de novo lipogenesis. Glucose is taken up by many tissues and stimulates insulin release from the pancreas more so in the adolescents with obesity than in lean adolescents. Both monosaccharides reduce circulating acyl-ghrelin concentrations. Effects of glucose and fructose on cerebral blood flow relative to baseline are shown by arrows in major regions of the brain: the prefrontal cortex, which has major executive functions; the hypothalamus, which modulates appetite; and the limbic system and striatum-thalamus, which encompass the reward feature of food. Solid lines represent neural connections and dashed lines circulating connections. ‡Adjusted for acyl-ghrelin and insulin. ACC, anterior cingulate cortex; F, fructose; Fru, fructose; G, glucose; GLP-1, glucagon like peptide 1; L, lean adolescents; N. accumbens, nucleus accumbens; Ob, adolescents with obesity; OXM, oxyntomodulin; PP, pancreatic polypeptide; PYY, polypeptide YY; TG, triglyceride.