Integrative and Natural approaches toward treating obesity. This is for the practioner but may also be helpful to the general public.

1. Integrative Medicine Approaches
for
Overweight and Obesity
By
Adam Rinde, ND
University House, Seattle, WA
May 24, 2007

2. Purpose of Today
• Obesity is not commonly taught as an exclusive condition in medical
school
• Establish a framework of understanding
• Understand sub-populations of overweight and obese patients
• Develop an awareness of competing schools of thought
• Gain understanding of the psychosocial elements and experience of
the overweight and obese patient
• Learn integrative approaches for management and treatment

3. Clinical Scenario
• You are working as an Naturopathic Physician in a licensed state
and today .
• You are seeing a 35 year-old Hispanic woman who has come to
you complaining of her weight.
• She has been overweight for the past 10 years. She is married and
having trouble getting pregnant.
• She is concerned because she has heard weight can get in the way
of fertility.
• She is also very insecure of her weight and tired of getting dirty
looks from everyone when she is at the supermarket. She notices
rude comments at work
• What background information is pertinent in the
evaluation and management of obesity?

4. Prevalence
– World Health Organization estimates that around one billion
people throughout the world are overweight and that over 300
million of these are obese and if current trends continue, the
number of overweight persons will increase to 1.5 billion by
2015(Kouris-Blazos and Wahlqvist 2007)
– NHANES estimates 61% of the U.S population is overweight or
obese. Obesity is being pegged for 6.8% of total medical costs in
the U.S.
• Estimates state that only 27% to 42% of obese patients seeking
medical help are suggested to lose weight by their medical
professional (Orzano and Scott 2004)
– Percentage of Obesity has increased from 15.3% in 1995 to
23.9% in 2005.
– Those with BMI over 40 is 4.8% of the U.S. Population

5. Obesity Trends* Among U.S. Adults
BRFSS, 1990, 1995, 2005
(*BMI ≥30, or about 30 lbs overweight for 5’4” person)
1995
1990
2005
No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

6. Morbidity and Obesity
• Morbidity associated with overweight and obesity
• Above BMI of 20 Morbidity rates increase in:
– hypertension
– dysplipidemia
– type II diabetes
– coronary artery disease
– stroke
– gall bladder disease
– Gastroesophagael Reflux
– Non-Alcoholic Steatohepatitis (NASH)
– osteoarthritis
– sleep apnea
– Asthma
– certain cancers (endometrial, breast, prostate, and ovarian)
– Also associated other disorders
• Pcos, stress incontinence, menstrual irregularities, infertility, depression

7. Mortality and Obesity (National Heart 1998)
• The relationship between obesity and mortality is unresolved and it is
generally accepted that a BMI related U-curve exists for all-cause
mortality .
• Apparently many studies looking at weight loss and mortality have not
controlled for smoking and unintentional weight loss (Orzano and Scott
2004)
• there is modest increase in mortality until a BMI of 30 kg/m2 where the
mortality rates for CVD increases by 50-100% above that with BMIs in
the range of 20-25 kg/m2
• mortality at BMI >25 relative risk is 1.1, >30 is relative risk 1.5, greater
then 35 BMI increases by factor of 2.5 (diastolic BP increase mortality by
factors of 2 and 5 respectively), with BMI>35 cholesterol of 236 and 290
mg/dl respectively increase mortality factors by
1. 8 and 4 )(Orzano and Scott 2004)

8. Severity of Obesity
Mortality
• BMI related mortality also increases under 20 BMI (u-curve)
• BMI association with mortality weakens with age especially
older then 75
– BMI in Older Adults
• A 20-year prospective study of age groups 55-74 suggests that the lowest
mortality occurs in the BMI age group of 25-30, after adjusting for
smoking, and pre-disposing illness the lowest mortality was: 24.5 in white
men, 26. 5 in white women, 27. 0 in black men, and 29. 8 in black women
– Race/Gender Differences
• Most BMI associated mortality trends are in whites. Some racial/ethnic
groups tend to have a more BMI-resistant mortality (this includes American
Indians, Blacks, Hispanics, Pacific Islanders, and Asian Americans)
• The lowest rate of mortality among Pima Indian males is at a BMI of 35-40
• However Diabetes associated mortality is high in Native American Popn.’s

9. What Are The Underlying Causes?
• Genetic
– suggest that about 25 to 40 percent of the individual differences in body
mass or body fat may depend on genetic factors.(National Heart 1998).
– Adipokines
• Environmental
– Sedentary lifestyle (TV, Commuting, Lack of Exercise, Dining Out).
– Obesogenic Environments .
• Diet
– Over-consumption of energy dense foods.
– Larger portion sizes.

10. Obesogenic Environment
(Heatherington 2007)
• The presence of the following factors influence eating
patterns:
– variety of foods
– Portion size
– availability of highly-palatable energy dense foods
– the presence of others
– Distraction
• all of these influence impact obesity
– within a meal when energy density and portion size are
introduced simultaneously their effects are independent and
additive to increase energy intake. (Kral 2004)
• Think of cafeterias today in urban high schools! And you’ll
find an obesogenic environment.

11. Diet and Lifestyle Factors of
leaness
• Children television watching 2-hours or
more 2x as likely to be obese
• Low fat dairy consumption associated with
less abdominal adiposity. B Brooks et al. Journal of the American
College of Nutrition 25 (6), 523-32 (Dec 2006)

12. Portion Distortion
SPAGHETTI AND MEATBALLS
20 Years Ago Today
500 calories 1,025 calories
1 cup spaghetti with sauce 2 cups of pasta with sauce
and 3 small meatballs and 3 large meatballs
Calorie Difference: 525 calories
Courtesy of National Heart, Lung, and Blood Institute

13. Portion Distortion Coffee
Today
20 Years Ago Mocha Coffee
(with steamed whole milk and
mocha syrup)
Coffee
(with whole milk and sugar)
45 calories 350 calories
8 ounces 16 ounces
Calorie Difference: 305 calories

14. Etiology (cont.)
Psychologic Disorder
 Up to 10% of mildly obese have binge eating disorders
 More common in morbidly obese
 Ghrelin lower in binge-eating disorder subjects PMID: 15867334
– In BED, there is a hyperactive HPA axis related to abdominal obesity that
persists even after treatment, suggesting that cortisol might be a primary factor in
the disorder. PMID: 15677411
Health Conditions
 Polycystic ovarian syndrome (result or cause)
 Cushings disease
 Sleep Disorders/Apnea (result or cause)
 Type II diabetes (result or cause)
 Hypothyroidism
 Insulinoma
 Craniopharyngioma or other traumas/inflammation to hunger/satiety centers
of the brain.

15. Etiology (cont.)
• Drugs
– Primarily corticosteroids and some antidepressants
• Smoking cessation:
– 42% quitters gained >/= 5 cm of waist
circumference and 41% gained at least 5 kg after 1
year of cessation (n=250) PMID: 17222450
– Smoking cessation generally amounts to 100
kcal/day reduction in expenditure
• Other
– Sarcopenia:
• Aging decrease in fat-free body mass

16. Etiology (cont.)
• Right Brain Hypothesis of Obesity:
– (Alonso-Alonso M 2007)
– The Prefrontal Cortex is crucial in regulating food
intake
• It may play a role in regulating reflexive eating in coordination
with the limbic system and hypothalmus. It is essential in top-
down decisions. (example)
• Obese subjects have less PFC activity then lean subjects
• Chronic psychosocial stress, by threat to self-esteem and
anticipation of impending and lasting challenge, may
disinhibit reflexive circuits through a cortisol induced right
PFC dysfunction that is caused by prolonged activity of the
HPA axis.

17. Brain Areas Involved in the Regulation of Food Intake and Schematic Representation of Their
Interactions in the Proposed Model
Alonso-Alonso, M. et al. JAMA 2007;297:1819-1822.
Copyright restrictions may apply.

18. Pathogenesis of Obesity
• Most research centers on the regulation of blood sugar
and insulin dysregulation (including-PPAR-gamma)
• Other components include involvement of the HPA-axis,
adrenal hormones, growth hormone, insulin growth factor,
and endocannabinoid system
• Emerging areas in obesity pathogenesis involve the study
of protein peptides of adipose cells called Adipokines
especially Leptin and Adiponectin (see appendix
Adipokines)
• Adipocytes are highly active and interactive with functions
of the neuroendocrine and immune systems
• Term “obesitis” has been coined to explain the
upregulation of immune/inflammatory markers in obesity
states

20. DDX For Overweight and Obesity
• DDX: (Purnell 2005)
• secondary causes of obesity
– Hypothyroidism, Hypercortisolemia, Cushing’s
Disease, Growth Hormone Deficiency,
Hypogonadism, and Menopause
• Medications:
– corticosteroids-long-term, neurospychotropic
drugs (anti-psychotic and anti-seizure
medications)

21. Patient Experience/Psychosocial Impact
• Social Stigmatism
– Google Results 1,260,000 for obesity epidemic. (0.09 seconds)
– Google Results 19,800,000 for Body Acceptance
• Psychopathology
• Binge Eating Disorder
– Est. 20-50% of those who seek obesity related treatment
• Body Image Distortions/Disorders
• The Fat Acceptance Movement
• The Fit and Fat Movement
• See Appendix for details

23. Psychosocial Impact of Obesity
• 2003 Youth Risk Behavior Surveillance System
of the Centers for Disease Control and
Prevention
• Over 59% of female and 29% of male adolescents in
grades 9 to 12 were trying to lose weight during the 30
days preceding the survey.
• Over 18% of girls and 8% of boys had gone without
eating for 24 hours or more to lose weight.
• In female adolescents, 11.3% had used diet pills and
8.4% had vomited or taken laxatives to lose weight in
the past 30 days(Shapira, Lessig et al. 2005)
• What is the long-term impact of this mindset?

24. Healthy Body Image

25. Evaluation and Management

26. Clinical Scenario
back to your patient
• Clinical Scenario
• What we now understand about obesity:
– Prevalence
– etiology/contributing factors
– Complications of obesity
– Co-morbidities
– Differential diagnosis for obesity
– Secondary causes
– Psychosocial experience impact of obesity
• What History and ROS questions are pertinent?
• What are relevant clinical findings?

27. Clinical Presentation of Obesity
• Seven Attributes
• Questions for contributing risk factors?
• Diet and exercise recall.
• ETOH, RX, Smoking.
• Current Mhx
– check for co-morbidities (established CHD, Asthma, Sleep
Apnea, Type II diabetes, PAD, Aortic Aneurysm, Cancer,
Osteoarthritis, Gallstones, and Gynecologic conditions)
• Family hx.
– Screen for risk factors
• ROS: screen for symptoms relevant to obesity and your
overall DDX

28. Clinical Scenario
Back to Your Patient
Patient
• Onset 10-years ago;weight has steadily increase each year. Weight
seems to be in belly area and back.
– Diet: eats large portions, likes to cook, snacks, eats out a lot, eats at
desk and sometimes in car, does not binge, eats different foods daily,
has tough time recalling foods.
– Exercise: every week she’ll go for a walk 1 or 2 times. Says “no time for
exercise”
– Habits: light ETOH drinker, non-smoker, non-rec drug user.
• Rx: no medications, MVM without Iron daily
• Shx: married, accountant-stressful, no kids-wants kids.
• Mhx: PCOS (diagnosed 3 years ago), Hx. Of severe ankle sprain,
Oligomenorrhea , no history of diabetes
• Fhx: mom: Type II diabetes (alive), Dad (deceased): PRCA

29. Clinical Scenario
Back to Your Patient
• Pertinent ROS:
– Gen: energy (5/10), Sleep poor-interupted..thinks she snores
– CV: slightly elevated blood pressure:
– Pulm: SOB with exercise:
– GI: no abdominal pain, no masses, no constipation, normal BM daily
– MSKTL: pain in right hip and neck, better with exercise/heat , denies weakness
– SKIN: denies fat hump on neck, denies purple streaking on stomach, notices discoloration in underarms
(darkened), notices strange skin mass on knee, some hair growth on face and abdomen.
– Neurologic: denies parasthesias, denies weakness
– Endocrine: denies cold-intolerance
– Psych: some depression and anxiety, denies binging
– GU: Last menstrual period 6 weeks ago, cycles every 6 weeks or longer for the last 6 years, has occasional
cyst rupture
• Last Labs:
– Cholesterol: 2 years ago…think it was elevated
– Glucose: 2 years ago, said it was high, but not diabetes
– Thyroid: tested 2 years ago, said it was normal
• Which physical exams are pertinent to your DDX? What findings
would confirm your diagnosis?

30. Clinical Findings
• Establish Risk via Measuring BMI and Waist
Circumference
• Blood Pressure reading using appropriate size cuff
• Skin:
– screen for acanthosis nigrans on surfaces of the hands and
elbows, axial or neck, sign of insulin resistance
– Screen for Xanthoma’s indicates the presence of chylomicrons
(eruptive xanthoma), type III hyperlipidemia (palmar or
tuberoeruptive xanthoma), or familial hypercholeseterolemia
(tendon xanthoma)
• HEENT, CV, Pulmonary, Abdominal, Msktl, Neuro, Psych
based on complaints

31. Clinical Findings
Physical exam (Purnell 2005)
• BMI (weight/height squared) X 703 when
recorded in pounds in weight and height for inches
– The NHLBI recommends combining BMI with
waist circumference take measurement at
Iliac crest for the most accurate
measurement.
– BMI alone is a controversial measurement for
obesity and overweight

32. Proper Waist Measurement From
NHANES 3 Protocol
• Just above the uppermost
lateral border of the right iliac
crest, a horizontal mark is
drawn then crossed with a
vertical mark on the midaxillary
line.
• The measuring tape is placed
in a horizontal plane around
the abdomen at the level of
this marked point on the right
side of the trunk. The plane of
the tape is parallel to the floor
and the tape is snug but does
not compress the skin.
• The measurement is made at
a normal minimal respiration

33. Clinical Findings:
Fat Distribution

34. Clinical Presentation
Acanthosis Nigricans

35. Clinical Presentation
Xanthomas
• Raised, waxy,
frequently yellow-
colored skin lesions
Eruputive
Xanthoma Knee Xanthoma

36. Clinical Scenario
• P/E:
• Vitals: Height 5’ 4 “ 175 pounds, (BMI= 30.10), BP 140/90 seated, HR 78 bpm
seated
• Temp: 98.6 degrees F. RR: 14brpm
• Waist Circumference: 34 inches
• HEENT: thyroid non-tender, no-thyromegaly
• SKIN: darkened skin pigmentation in b/l ventral region wrist region (1x4 cm)
and on posterior region of neck(2x3 cm). One waxy, raised, yellowish non-
pustular lesion on l. knee. No lipodistrophy in posterior neck, no striae on
abdomen, abdominal fat distribution,
• CV: S1, S2 present, no rubs no murmurs ,Abdominal Aorta <3 cm
• Pulm: Lungs clear x 4 quadrants, no wheezing, no crackles
• MSKTL: Normal Range of motion in cervical region with some crepitus, Normal
mange of motion in hip jt. b/l with crepitus and some tenderness to palp in right
hip joint, positive faber.
• Psych NAD Ox3 slight affect
• Which labs would be useful in the diagnosis and or
management of this patient?

37. Diagnostic Testing for Evaluation
and Screening.
– Screening code for diabetes (277.22)
– Chemistry Panel
• Liver Enzymes
• Fasting Blood Glucose
• Fasting Lipids
• TSH

38. Clinical Scenario
• Lab Results:
– Liver Enzymes: normal
– Fasting Glucose: 96
– Fasting Lipids: Total Cholesterol 265 mg/dl
• HDL: 35 mg/dl (low): LDL 130 mg/dl (borderline
H): Triglycerides: 100 mg/dl
– TSH: 2.3
– What is your diagnosis and classification?

39. Combined BMI/waist circumference risk
Adapted from NHLBI guidelines 1998
Classification BMI Obesity Class Associated Associated disease
disease risk risk
Waist Waist
Circumference Circumference
<40 in male >40 in male
<35 in female >35 in female
Underweight <18
Normal 19-24
Overweight 25-30 Overweight Increased High
Obesity 30-35 I High High
Obesity 35-40 II Very High Very High
Extreme 40> III Extremely Extremely High
Obesity High

40. How is Obesity Classified?
Obesity Markers
Waist Circumference
Overweight and Obesity by BMI
• Men > 40 inches (102 cm)
Obesity Class BMI (kg/m2)
• Women >35 (88cm)
• Underweight < 18.5
• Are classified as High Risk
• Normal 18.5 – 24.9
• Associated with increased risk of CV
• Overweight 25.0 – 29.9 disease, hypertension, Type II
diabetes, dyslipidemia in patients with
• Obesity I 30.0 – 34.9
a BMI of 24.9-34.9
• Obesity II 35.0 – 39.9
• Extreme Obesity III ³ 40
– * Pregnant women who, on the
basis of their prepregnant weight,
would be classified as obese may
encounter certain obstetrical risks.
– However, the inappropriateness of
weight reduction during pregnancy
is well recognized. Hence, this
guideline specifically excludes
pregnant women.

41. ICD-9 Codes/CPT Codes
• Obesity (Not normally covered by Insurance)
– 278.0 Obesity
– Excludes: adiposogenital dystrophy (253.8)
• obesity of endocrine origin NOS (259.9)
– 278.00 Obesity, unspecified
• Obesity NOS
– 278.01 Morbid obesity
– Often co-morbidities are covered
• CPT codes
– V65.3 Dietary surveillance and counseling
– V65.41Exercise counseling

42. Back to Your Patient
• Obesity Stage I: (BMI 30, Waist <35)
– Secondary to:?
• Insulin dysregulation, excess calories, sedentary lifestyle,
poor sleep, stress. What else?
– Problem List: Stage I hypertension,
hypercholesterolemia, high normal glucose,
Oligomenorrhea, Osteoarthritis, PCOS, Stress,
depression?, Apnea/Sleep disorder? acanthosis
nigricans, xanthosis…others? Fhx of Type II diabetes.
– What treatments are best for the patient? What
treatments do more harm then good? Review the
literature, talk with colleagues, consult with experts.

43. Therapeutic Interventions
For
Overweight and Obesity

44. What harm is associated with
treatment?
Morbidity factors
• In the nurses health study, The BMI associated risk for cholecystectomy with un-removed
gallstones was 1.97 for those losing 22lb or more in the previous 2 years.
• In white women weight loss beginning at age 50 was found to increase the risk of hip fracture
(Orzano and Scott 2004)
• Effect of weight cycling controversial
• Weight cycling (a.ka. Yo-Yo dieting)has been shown to be predictive and not predictive of type II
diabetes (Field). The National task force on the prevention of obesity concluded that evidence here
was insufficient to override moderate weight loss in obese subjects.
• Intentional weight loss in of any amount in men over a 13 year period was shown to have a
reduction of 25% in the rate of developing diabetes. In Women with obesity-related health
conditions intentional weight loss of any amount was associated with a 20% reduction in all-cause
mortality, primarily due to a 40-50% reduction in mortality from obesity-related cancers; diabetes-
associated mortality was also reduced by 30-40% in those who intentionally lost weight.
 Remember the difference between intentional weight loss and
weight loss due to illness

45. What harm is associated with
treatment?
Mortality Factors
• Unexplained weight loss associated with increased mortality
• Self reported weight loss associated with lower morality and unintentional
weight loss is associated with higher mortality (Gregg)
• Willamson et. Al. 1995.
– In women with obesity-related health conditions (n = 15,069), In women
with no preexisting illness (n = 28,388), intentional weight loss of > or =
20 lb (> or = 9.1 kg) that occurred within the previous year was
associated with about a 25% reduction in all-cause, cardiovascular, and
cancer mortality.
– however, loss of < 20 lb (< 9.1 kg) or loss that occurred over an
interval of > or = 1 year was generally associated with small to
modest increases in mortality (Weight Cycling Condition)
– REMEMBER WEIGHT LOSS MAY MEAN A SERIOUS
UNDERLYING CONDITION

46. Does dietary modification lead to weight loss?
Which dietary interventions result in long-term weight loss
and reduction of co-morbidities?
• Low Calorie Diet (1000-1200 kCal/day)
– Reduces total body weight by an average of 8% over 3-12 months
• long term loss and maintenance interventions lasting 3-4.5 years reported an average
weight loss of 4% over the long term
• Reduces abdominal fat/waist circumference on average of 1.4 cm to 9.5 cm after 6-12
months
• Very low Calorie Diet (400-500 kcal/day)
• Weight loss is greater in 1 year then LCD but after year weight loss is not better then
LCD. On average VLCD’s resulted in 4-12 kg greater then LCD in the active phase in
the trial. After 1 year these results equalized.
• Lower Fat Diets (20-30%) of calories from fat
• Reducing fat to 20-30% of diet contributes to overall lower caloric intake even
when that is not the focus of the intervention
• However, evidence states weight reduction on a LFD is only efficacious if at the targeted
caloric intake reduction.
– Most studies looking at LFD induced weight loss have looked at a caloric intakes ranging from
1200-2300 calories/day
• Step I, Step II, Exchange, TLC , or Dash diet may be incorporated if co-
morbidities exist

47. Do exercise interventions lead to weight loss?
Which exercise techniques result in the largest amount of weight loss and
greatest adherence?
Cochrane Met analysis (Shaw 2006)
– Exercise with or without diet intervention.
– combined effect faired better then exercise monotherapy in lowering
BMI and body weight.
– Exercise: high intensity vs. low intensity.
• Effect of high intensity exercise was 1.5 kg more weight loss
compared to low intensity
• Compared with diet alone, exercise alone would require treating
17 patients to successfully have 1 patient lose 10 lbs(Orzano
and Scott 2004)
• Parameters of weigh loss benefits are 3-7 sessions per/week of
30-60 minutes of exercise. Intensity varied from 60-85% of
maximum Heart rate.
• Initial recommendations are moderate levels of exercise 3-5
days of week

48. Leptin and Adiponectin Responses in Overweight inactive Elderly following
Resistance Training and Detraining Are Intensity Related Fatouros et al. J Clin
Endocrinol Metab, November 2005, 90(11):5970–5977
• N=50, 3 groups Low Intensity (LI), Mod. Intensity, High Intensity(HI)
• 24 week trial,/ 3 xs per /week
• Subjects executed eight resistance exercises (Universal Machines)
• Selected to stress the major muscle groups in the following order:
– chest press, leg extension, shoulder press, leg curls, latissimus pull down, leg
press, arm curls, and triceps extension:
• two sets per exercise(wk 1–8) and three sets per exercise thereafter
(training intensity was maintained at 45–50% of 1RM in LI, at 60–65% of
1RM in MI, and at 80–85% of 1RM in HI)
• Participants also performed abdominal crunches and lower back exercises:
one set/six repetitions (wk 1–4), two sets/eight repetitions (wk 5–12), three
sets/10 repetitions (wk 13–20), and four sets/10–12 repetitions (wk 21–24
• Results
– Leptin levels fell in all groups
– Adiponectin went up only in the High Intensity Group
– % Leptin decrease associated with RMR increase and BMI decrease
– %Adiponectin increase associated with BMI decrease

49. Are behavioral Interventions effective for weight loss?
Which forms of behavioral interventions are most effective?
• Research states
– Cognitive Behavioral Therapy and
Motivational Interviewing are the strongest
techniques for weight loss
– Favorable outcome directly related to intensity
of intervention

50. Dietary and physical activity behaviors among adults successful
at weight loss maintenance Kruger, et al. International Journal of
Behavioral Nutrition and Physical Activity 2006, 3:17
• Number of Respondents=1958. Population-based survey
on behavioral factors found to be important for successful
weight loss maintenance among adults.
• 31.0% had been unsuccessful at both losing weight and
maintenance after weight loss. Successful weight loss
status differed by sex, age, and current weight status.
• NOTE: this survey was cross-
sectional, amounts of weight loss or
maintained was not recorded nor was
the intensity of exercise performed

51. Dietary and physical activity behaviors among adults successful
at weight loss maintenance Kruger, et al. International Journal of
Behavioral Nutrition and Physical Activity 2006, 3:17 continued
• Assessment of reported weight loss strategies, found that exercising 30 minutes/day
and adding physical activity to daily life were significantly higher among successful
versus unsuccessful weight losers.
• Individuals who were successful at weight loss and maintenance were less likely to
use over-the-counter diet products than those who were unsuccessful at weight loss.
• Significantly more successful versus unsuccessful weight losers reported that on
most days of the week they planned meals (35.9% vs. 24.9%), tracked calories
(17.7% vs. 8.8%), tracked fat (16.4% vs. 6.6%), and measured food on plate (15.9%
vs. 6.7%). Successful losers were also more likely to weigh themselves daily (20.3%
vs. 11.0%).
• There were a significantly higher proportion of successful losers who reported lifting
weights (19.0%) versus unsuccessful (10.9%).
• The odds of being a successful weight loser were 48%-76% lower for those reporting
exercise weight control barriers were influencing factors (e.g., no time, too tired to
exercise, no one to exercise with, too hard to maintain exercise routine) compared to
those who reported little or no influence of exercise;
• similarly, the odds were 48-64% lower for those who found certain dietary barriers to
be influential (e.g., eat away from home too often, diet/health food costs too much).

52. Neutraceutical Interventions
with some research
• Soluble Fiber (Oat Beta Glucan, Guar Gum, Pectin before meals increases
satiety)
• Garcinia cambogia extract Hydrocytic Acid HCA (2800 mg QD HCA),
Gynemna Sylvestre extract, Niacin-bound Chromium. PMID: 15056124
• Green Tea Extract reportedly increases thermogenesis by prolonging
norepinephrines activity in the synaptic clept by degrading catechol-o-
methyltransferase PMID: 17201629
• Citrus aurantium as a thermogenic, weight-reduction replacement for
ephedra , many questions about safety
• Coleus forskohlii (Kerry Bone) –may activate cAmp. Many small studies
exist. modulates weight gain,8-week, 50 mg/day of forskolin to six women
BMI.25, resulted in reduction of body weight and fat content
• Others that have weak evidence or conflicting results: Hoodia, Pyruvate, L-
Carnitine, conjugated linoleic acid.
• Consider: AOX’s to reduce inflammation ,Multivitamin for Very Low Calorie
Diet

53. Reduction of adipose tissue and body weight: effect of water
soluble calcium hydroxycitrate in Garcinia atroviridis on the short
term treatment of obese women in Thailand
• Reduction of adipose tissue and body weight: effect of water soluble calcium hydroxycitrate in Garcinia
atroviridis on the short term treatment of obese women in Thailand.
Roongpisuthipong C, Kantawan R, Roongpisuthipong W.
Division of Nutrition and Biochemical Medicine, Department of Medicine, Ramathibodi Hospital, Faculty of Medicine,
Mahidol University, Bangkok 10400, Thailand. racrp@mahidol.ac.th
Fifty obese women with a body mass index (BMI) over 25 kg/m(2) were randomly allocated into two groups, 25 in
each. Group 1, with a mean (+/-SEM) age of 40.0+/-2 years, received water soluble calcium hydroxycitrate (HCA)
as Garcinia atroviridis. Group 2, with a mean age of 35.6+/-1.8 years, received placebo. All subjects were
recommended a similar diet with 1000 Kcal/day. The trial lasted for 2 months. At baseline the means BMI of Group
1 and Group 2 were 27.5+/-0.2 kg/m(2) and 26.7+/-0.5 kg/m(2), respectively. Group 1 lost significantly more weight
(2.8 vs. 1.4 kg, p<0.05) and at a greater rate than Group 2 throughout the study. The decrease in their body weight
was due to a loss of fat storage as evidenced by a significant decrease in the triceps skin fold thickness. On a short-
term basis, HCA in Garcinia atroviridis was an effective for weight management.
The decrease in their body weight was due to a loss
of fat storage as evidenced by a significant decrease
in the triceps skin fold thickness. On a short-term
basis, HCA in Garcinia atroviridis was an effective for
weight management.
HCA has been proposed to block conversion of
simple sugars to fat, Best used with low-fat diet

54. Pharmaceutical Txt’s For Obesity
• Pharmacologic Therapy
• Since 1995, the use of the prescription drugs fenfluramine
or dexfenfluramine for weight loss had increased greatly
to 14 million prescriptions in 1½ years
• In 1997 the FDA requested voluntary withdrawal of
fenfluramine and dexfenfluramine due to a reported
association with valvular heart disease with drugs of
dexfenfluramine and fenfluramine alone or combined with
phenterimine.
• In 1997 the drug sibutramine hydrochloride monhydrate
was approved for the management of obesity
• Other drugs include orlistat

55. Pharmaceutical Rx
• General recommendations are that Obesity
Rx can be useful as adjunctive therapies in
patients who are > then 30 BMI or those >27
BMI with concomitant obesity related risk
factors
• None of the drugs have shown to reduce
abdominal obesity or improve
cardiorespiratory fitness
• No long-term studies exist on obesity drugs
impact on mortality and obesity and/or long-
term side effects from use of drugs.

56. Pharmaceutical Txts For Obesity
• Subutramine Hydrocholoride
– Is a Serotonine Norepinephrine Reuptake Inhibitor
– Generally works as an appetite suppressant
– Sibutramine dispensed at does of 10-15 mg/day have been shown to
optimize weight loss vs. adverse effects. The NNT was 8 and 4 for
10-15 mg. doses respectively (Orzano and Scott 2004) although the
NNH (number needed to harm) attributable to dry mouth was NNH=7.
– There is strong advise against using sibutramine in patients with
hypertension, heart disease, arrhythmia, and stroke survivors (there
have been deaths in patients on sibutramine
– In large meta-analysis the results from the most of the major drugs
resulted in a weight loss after 1 year of 2- 12 lbs depending dose and
type of Rx. One study with sibutramine, showed a weight loss after 24
weeks of 20 lbs. Most of these trials included dietary/lifestyle
modifications.

57. Pharmaceutical Txts For Obesity
• Orlistat
– Inhibits pancreatic lipase and is responsible
for blocking the absorption of approximately
30% of ingested fat calories.
– It has been shown to induce 6.6 to 8.8 pounds
in 1 yr. compared to placebo. NNT=4 and
NNH=6
– Main side effects: flatus, spotting, fecal
urgency, and incontinence.

58. Pharmaceutical Txt for Obesity
• Rimonabant (also known as SR141716,
Acomplia, Riobant, Slimona, Rimoslim,
and Zimulti)[1] is an anorectic
anti-obesity drug. It is a CB1 cannabinoid
receptor inverse agonist. Its main avenue
of effect is reduction in appetite.
• Recent reports of depression and anxiety
as a side effect.
• updated November 19, 2007

59. Surgical Interventions for Obesity
• Surgery
– Bariatric Surgery
– Types: gastric bypass, gastroplasty (vertical
banded and horizontal banded)
– Be familiar with risks associated with these
surgeries (Demaria, NEJM;356,21.)

60. Surgical Interventions
– Most recommendations for surgery are for
individuals >35 BMI with co-morbidities or> 40
BMI
– In large meta-analysis patients who had a BMI
of 40 kg/m2 or above, or a BMI of 35 to 40 kg/
m2 with comorbidity; most of the study
participants were women. Weight loss due to
surgical intervention such as the gastric
bypass ranged from 50 kg (110 lb) to as much
as 100 kg (220 lb) over a period of 6 months
to 1 year.

61. Types of Bariatric Surgery
Procedures
• Roux-en-y gastric bypass: (RYGP)
– generates weight loss by limiting gastric capacity and causing
mild malabsorption
• Biliopancreatic bypass:
– combines a limited gastrectomy with a long Roux limb intestinal
bypass (generates weight loss primarily through malabsorption)
• Laparoscopic Adjustable Band
– (band placed on the uppermost portion of the stomach restricting
capacity). Band is adjustable to an individuals needs. Weight is
loss through meal volume restriction.
• Vertical Banded Gastrosplasty:
– involves stapling the upper stomach to create limited gastric
capacity

62. Types of Surgeries

63. Complications Of Bariatric Surgery
• Dumping Syndrome
– The dumping syndrome, a complex of neurohormonally
mediated symptoms that include facial flushing,lightheadedness,
palpitations, fatigue, and diarrhea, occurs in as many as 70% of
patients after Roux-en-Y gastric bypass.
• Nutrient Deficiencies
– Deficiencies of iron, calcium, folate, vitamin B12, and other
nutrients occur after procedures with a component of
malabsorption, such as gastric bypass.
– Bileopancreatic Diversion
• protein malnutrition and deficiencies of the fat-soluble vitamins (A,
D, E,and K) may occur.

64. Other Treatment Concerns
• Sleep Quality. Decreased sleep increases
Ghrelin=increased appetite
• GI flora balance: recent reports of link
between certain gut flora strains and
increased caloric absorption.
• Emerging therapies?
– HCG Injections
– GH injections
– Mesotherapy

65. Integrative Treatment
For
Overweight and Obesity

66. Back to Your Patient
• Obesity Stage I: (BMI 30, Waist <35)
– Secondary to:
• Insulin dysregulation, excess calories, sedentary lifestyle,
poor sleep, others?
– Problem List: Dtage I hypertension,
hypercholesterolemia, high normal glucose,
Oligomenorrhea, pcos, stress, depression. Sleep
Apnea/Sleep disorder?, Acanthosis Nigricans,
Xanthosis…others? Fhx of Type II diabetes.
• What are goals, strategies, and treatments for
this patient?

67. Treatment: Assess Your Patient
Behavioral Readiness Assessment
adapted from NHLBI guidelines 1998
• Has the individual sought to lose weight on their
own initiative?
• What events lead the patient to lose weight
now?
• What are the patients stress level and mood?
• Does the individual have an eating disorder?
• Does the individual understand the commitment
required from the treatment?
• How much weight does the patient expect to
lose?

68. Contraindications For Weight Loss
Interventions
• Exclusion From Weight Loss Therapy
– most pregnant or lactating woman
– persons with a serious uncontrolled psychiatric illness
such as a major depression
– patients who have a variety of serious illnesses and for
whom caloric restriction might exacerbate the illness.
– Patients with active substance abuse
– and those with a history of anorexia nervosa or bulimia
nervosa should be referred for specialized care.

69. Treatment Goals
• Safely lower body weight at reasonable rate
– 10% reduction in body weight in 6 months
• Reduce risk factors for disease progression
– Decrease waist circumference, normalize glucose levels,
normalize blood pressure, and lower dyslipidemia.
• Reduce co-morbidities
– Prevent hypertension, prevent diabetes.
• Decrease obesogenic behaviors
– Decrease T.V. time, sedentary time, decrease eating out, and
decrease large serving size
• Develop healthy body image
• Maintain or prevent further weight gain
– Prevent weight cycling or regression

70. Treatment Strategy
• Dietary interventions:
– to restore energy balance and reduce fat body mass and other risk factors (i.e..
hypertension, hyperlipidemia, etc.)
• Exercise intervention:
– to restore energy balance, reduce weight, increase aerobic capacity, modify
adipocytokines, decrease waist circumference, modify body composition and
lower co-morbidities (i.e.. dysglycemia, hypertryglicerdimia, hypertension)
• Behavioral Counseling/Motivational Interviewing
– to reduce obesogenic behavior, confront body image concerns, and provide
support and reinforcement
• Group counseling as needed
• Neutraceutical interventions as needed especially with co-morbidities
• Stress reduction techniques
• Pharmaceutical intervention (consider in morbid obesity)
• Surgical Intervention (consider in morbid obesity)
• Follow-up reinforcement strategies

71. Treatment Implementation
• Low calorie/low caloric density/fiber rich diet (1000-1500kcal/day)
– Consider incorporating volumetric eating strategy (salad or soup) or a SOLUBLE
FIBER SOURCE at beginning of each meal (VOLUMETRICS)
– Serving size recommendations
– Tailor other parameters of diet according to co-morbidities (i.e.. DASH, Step I/II,
TLC diet, Exchange Diet, Mediterranean Diet, Low Glycemic Load diet)
• Moderate increasing to high intensity exercise (30 minutes a day, starting at
3 days/week and increasing to 6 days/week)
– Preferably incorporating resistance training minimal 8 main mover exercises
3/week x 2 -3sets @ 70-85% of 1RM to near muscle failure. Increasing
incrementally
• Twice monthly counseling/cognitive behavioral therapy focusing on reducing
biogenic behavior, positive image, and stress reduction. Include journaling;
goal setting, and commitment reinforcement.
• Group therapy session are an alternative for financial barriers

72. Treatment Implementation
• 10-20 minute mindful meditation daily for
stress reduction.
• Sleep: average of 8 hours of quality sleep/
night. Consider sleep study in apnea
• Other: consider supplementation
• Consider referral to endocrinologist in
morbid obesity

73. Appendix

74. Summary
• Obesity is a complex multi-factorial condition
that required a thorough diagnostic approach.
• It is not as straightforward as calories in vs.
Calories out!
• Treating obesity successfully requires a
multimodality treatment strategy.
• We must stay aware to the experience and
diversity of the overweight and obese patient.
• Questions/comments
email: arinde@bastyr.edu

75. Appendix:
Alternative Perspective to Obesity
The Obesity Myth by Paul Campos
•
Big Fat Lies, by Glenn A. Gasser PHD
•
• Fat by Kulick and Menely
• Feeling Good About the Way You Look. A
Program for Overcoming Body Image
Problems by Sabine Wilhelm PHD
• Others
– The Last Well Person, by Hadler

76. Appendix:
Psychosocial Impact of Obesity
• social stigmatization
– impacts: employment, relationships, salary, discrimination
• Michigan is the only state in the union that prohibits discrimination on the basis of body
weight through the Elliott-Larsen Civil Rights Act of 1977 (Gasser 2002)
– Fat people are routinely described as “ugly, “disgusting”, “sloppy”, “gross”, week-
willed, “self-indulgent”, “lacking self-respect”, “emotionally disturbed”, and
“possibly sick” (Gasser 2002)
– Medical Condemnation of fat exists strongly
– Nearly 116 Million adults are dieting at a given time representing 55% of the total
adult population (Gasser 2002)
– Research has been primarily based on white people and has lacked data
reflecting degree of obesity, physical attractiveness, or the situational context
(National Heart 1998)
• Thinness is not a desirable attribute in some cultural backgrounds
• some evidence exists showing that certain racial and ethnic groups have less stigmatism
about weight then caucasian populations
• While the average weight of Americans is increasing, so is the average life
expectancy (Hadler 2004

77. Appendix
Psychosocial Impacts of Obesity
• Binge Eating Disorder (BED)
– Estimated to occur in 20-50% of those who seek
obesity related treatment
– Characterized by eating large volumes of food within a
discrete time period (for example 2 hours) and
demonstrating a lack of control while these eating
episodes are taking place
– Compared to obese non-bingers; obese bingers are
more likely to be
• a) heavier
• b) have a more likely to report emotional distress
• c) and more likely to have psychiatric illness.

78. Appendix
Psychosocial Impacts of Obesity
• Body Image
– Obese people are more likely to have a degree of body
image distortion
• Binge eaters are at greater risk for body image distortion
• Disordered eaters are more likely to over-estimate weight
• Black women less concerned generally about weight then
white women
• Weight ay be seen as a positive feature in some culture or
subcultures
– Feeling Good About the Way You Look. A Program for
Overcoming Body Image Problems by Sabine Wilhelm
PHD

79. Appendix
Psychosocial Impact of Obesity
• Psychopathology
– Those with childhood/lifetime related obesity report
more emotional distress then those who have acquired
obesity later in life
– in general it is hard to say whether obesity is
associated with more emotional distress then lean
subjects
– However those obese populations seeking treatment
have shown to be in more distress then obese patients
who don’t seek treatment (National Heart 1998)

80. Appendix:
Obesogenic Environment
• F is for Fat
– A movement to improve U.S. obesity policies
and reduce obesogenic environments.
– http://healthyamericans.org/reports/obesity2006/O

81. Appendix
Psychosocial Impact of Obesity
• 2003 Youth Risk Behavior Surveillance System
of the Centers for Disease Control and
Prevention , over 59% of female and 29% of
male adolescents in grades 9 to 12 were trying
to lose weight during the 30 days preceding the
survey. Over 18% of girls and 8% of boys had
gone without eating for 24 hours or more to lose
weight. In female adolescents, 11.3% had used
diet pills and 8.4% had vomited or taken
laxatives to lose weight in the past 30
days(Shapira, Lessig et al. 2005)

82. Appendix: Adipokines
Adipokine Inducers Supressors Physiologic Effect Correlatoin with obesity
Feeding, pertussis toxin,CAMP,
Leptin Leptin may inhibit acetyl-coA Lower in obese subjects,
Glucocorticoids, B-receptor agonist, carboxylase activity, the rate Obese subjects may resistant toLeptin
Cytokines, Obesity Thiazolidinediones, limiting enzyme in fatty-acid
melatonin (exogenous
Glucocorticoids, synthesis. Limits food intake by
and endogenous).
cytokines, and endotoxins mainly down-regulating
Insulin, sympathetic
induce Leptin despite a endocannabinoids
nervous system
reduction in body weight
(Sandoval)
(Auwerx, 739)
sleep disruption
Insulin, HPA axis
(sandoval)
Adiponectin Conjugated linoleic acid in Down regulation of Effects glucose flux, glucose Lower in obese subjects
rats (N. Inoue, et al) chromosome 3p27, clearance, beta-oxidation,
angiotensin II AT1 Body Mass endothelial dysfunction (anti
receptor antagonists atherogenic), tryglyceride
(theoretical) clearande, insulin sensitivity,
thiazolIdinedione weight loss
Reduces macrophage induced
insulin resistance
Anti-inflamatory cytokine
Resistin Weight gain Weight reduction Involved in pro-inflammatory Higher in obese subjects
cascade, may be associated
with chronic inflammation of
obesity that leads to insulin
resistance
Others: being
evaluated
visfatin, TNF-
alpha, retinol
binding factor

83. Appendix: Exercises
Some Favorites
Squat-curl-shoulder press
•
Dumbbell Squats to curl-to press
•
• Walking Dumbbell Lunges
• Walking Lunge-Row
• Cable Row
Gravitron Dips, Gravitron Pull-ups
•
Dumbbell incline bench
•
• Core Stability Exercises

84. Appendix:
Calories Per Exercise/Activity
• High Yield Activities
– Some High Yield
exercises of Daily living
• Basketball-full court
– Shoveling
• Stationary Bike 15-20
– Yard work/mowing,
MPH
Gardening
• Skating (Inline/Ice)
• Skiing Cross-
– Cleaning the house
country/Downhill
especially scrubbing,
• Tennis
vacuuming
• Swimming 20-60
yards/minute – Taking the Stairs
• Jogging 5 MPH
– Walking to the store
• Running 8 MPH
for grocery shopping
• Stair climbing
• Aerobic Dancing

85. Appendix:
Economic Costs of Obesity
• In 1995 some estimates state that Obesity cost
the U.S. $99.2 billion in medical care and
disability costs.
– Approximately $51.6 billion of these dollars were said
to be direct obesity related costs
– And the $47.6 billion remaining cost are indirectly
related
• Published estimates of the economic costs of
obesity such as those noted above use the
prevalence-based approach, assuming that
obesity is causally related to a range of chronic
illnesses.

86. Additional References
• . quot;Obesity Education Initiative Electronic Textbook--Introduction.quot; from http://www.nhlbi.nih.gov/guidelines/obesity/e_txtbk/intro/intro.htm
•
• Alonso-Alonso M, P.-L. A. (2007). quot;The right brain hypothesis for obesity.quot; JAMA : the journal of the American Medical Association 297(16): 1819-22.
•
• Blundell, J. E. and N. A. King (1996). quot;Over consumption as a cause of weight gain: behavioral-physiological interactions in the control of food intake
(appetite).quot; Ciba Foundation symposium 201: 138-54.
•
• Ello-Martin, J., J. Ledikwe, et al. (2005). quot;The influence of food portion size and energy density on energy intake: implications for weight management.quot;
The American journal of clinical nutrition 82(1 Suppl): 236-41.
•
• Gasser, G. A. (2002). Big Fat Lies: The Truth About Your Weight And Your Health. Carlsbad, CA, Gurze Books.
•
• Gautier, J. F., K. Chen, et al. (2000). quot;Differential brain responses to satiation in obese and lean men.quot; Diabetes 49(5): 838-46.
•
• Hadler, N. M. (2004). The Last Well Patient: How to Stay Well Despite The Health-Care System. Quebec, McGill-Queen's University Press.
•
• Hainerova (2006). quot;Association between neuromedin U gene variants and overweight and obesity.quot; J. Clin Endocrinol Metab. 91(12): 5057-63.
•
• Heatherington, N. (2007). quot;Cues to Overeat: psychological factors influencing over consumption.quot; Proc Nutr Soc. 66(1): 113-23.
•
• Kouris-Blazos, A. and M. Wahlqvist (2007). quot;Health economics of weight management: evidence and cost.quot; Asia Pacific journal of clinical nutrition 16
Suppl 1: 329-38.
•
• Kral, T. a. B. R. (2004). quot;Energy Density and Portion Size: their independent and combined effects on energy intake.quot; Physiol Behav 82: 121-8.
•
• Levitsky, D. (2002). quot;Putting behavior back into feeding behavior: a tribute to George Collier.quot; Appetite 38(2): 143-8.
•
• Migrenne, S., C. Magnan, et al. (2007). quot;Fatty acid sensing and nervous control of energy homeostasis.quot; Diabetes Metab.
•
•

87. Additional References
• National Heart, L., and Blood Institute (1998). Guidelines on Overweight and Obesity: Electronic Textbook
•
• NIDDK. (2007). quot;Other statistics related to overweight and obesity.quot; Retrieved May 18, 2007, 2007, from http://win.niddk.nih.gov/statistics/#whydodiffer
.
•
• Oelschlager, B. (2005). quot;Gastrointestinal Complications of Bariatric Surgery.quot; Medscape Gastroenterology Retrieved May 15, 2007, 2007, from
http://www.medscape.com/viewarticle/502881.
•
• Orzano, A. and J. Scott (2004). quot;Diagnosis and treatment of obesity in adults: an applied evidence-based review.quot; The Journal of the American Board
of Family Practice / American Board of Family Practice 17(5): 359-69.
•
• Pignatti, R., L. Bertella, et al. (2006). quot;Decision-making in obesity: a study using the Gambling Task.quot; Eating and weight disorders : EWD 11(3): 126-32.
•
• Purnell, J. Q. (2005). quot;Obesity.quot; Retrieved May,18, 2007, 2007, from http://www.mescape.com/viewarticle/501298.
•
• Reuters (2007). Being stressed out at work can make you fat, a new study suggest. Rheuters Health Information.
•
• Shapira, N. A., M. C. Lessig, et al. (2005). quot;Satiety dysfunction in Prader-Willi syndrome demonstrated by fMRI.quot; Journal of neurology, neurosurgery,
and psychiatry 76(2): 260-2.
•
• Shaw, K., Gennat H, O'Rourke, P, Del Mar C. (2006). quot;Exercise for Overweight Or Obesity.quot; Cochrane Database of Systematic Reviews 2006(4): 99.
•
• Shaw, K., O'Rourke, P, Del Mar C, Kenardy J. (2005). quot;Psychological interventions for overweigth or obesity.quot; Cochrane Database of Systematic
Reviews 2005(2): 62.
•
• Snow, V., et. all (2005). quot;Pharmacologic and Surgical Management of Obesity in Primary Care: A clinical practice guideline from the American College
of Physicians.quot; Annals of internal medicine 142: 525-531.
•
• Trenell, M., Marshall NS, Rogers NL (2007 ). quot;Sleep and metabolic control: waking to a problem?quot; Clin Exp Pharacol Physiol 34(1-2): 1-9.
•
• Wolk R, S. V. (2007). quot;Sleep and the metabolic syndrome.quot; Exp Phsiol 92(1): 67-78.