Integrative Management Of Obesity


Published on

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

No Downloads
Total Views
On Slideshare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide
  • <number>
  • Recent studies of individuals with awide range of BMIs, together with information obtained on their parents, siblings, and spouses stte that 25-40% of body mass or bmi may be geneticSleep disruption is associated with 1) alterations in glucose metabolism; (2) upregulation of appetite; and (3) decreased energy expenditure. these three mechanisms that might link short sleep and increased obesity a PMID: 17442599, PMID: 17308390
  • in my words...people's perceptions of unattainable success
  • The regulation of food intake in humans involves 3 hierarchical levels of control: cognition, homeostasis, and reward. Information on nutritional status is transmitted from theperiphery to lower brain centers by neural and humoral signals. Indirect evidence suggests that peripheral mediators may also act on the cerebral cortex (dotted line). Extensiveinterconnectivity between these regulatory pathways allows precise and integrated control of food intake according to internal and external factors. These interactions arecomplex and may be inhibitory or facilitatory. Homeostatic and reward circuits (reflexive eating mode) tend to favor food intake. Brain areas involved in cognition (reflectiveeating mode), especially the right prefrontal cortex (PFC), tend to decrease food intake. Under normal circumstances, reflective areas can override and suppress reflexive areas(thick arrows). When activity of the right PFC is diminished, however, cognitive control of food intake decreases, favoring obesogenic habits.
  • Body composition/not body weight is more important in determining health riskBMI apparently has a high specificity (98-99%) and this combined with the prevalence of 43%-67% obese patients in a primary care setting, gives it a Postive predictive value of 97%On other hand BMI has a low sensitivity for BMI ranging from 13%-55%A patient with a BMI <30 has a negative predicitive value of 67% tends to misclassify overweight patients as normalAs BMI passes 30 the negative predictive value improves up 84%
  • Research now being done regarding diet/lifestyle vs. surgery effect on morbidity and mortality in the severely obese.
  • chromiumHCA-SX has been shown to reduce appetite, inhibit fat synthesis and decrease body weight without stimulating the central nervous system. NBC has demonstrated its ability to maintain healthy insulin levels, while GSE has been shown to regulate weight loss and blood sugar levels
  • ie. Hyperlipidemia, hypertension, dysglycemia
  • in 1994 Surgeon C. Everett Koop initiated “shape up America” campaign and stated that obesity is responsible for almost 1000 deaths a day in the U.S.(Gasser 2002)Dieting has become a 30 billion dollar industry
  • Integrative Management Of Obesity

    1. 1. Integrative Medicine Approaches for Overweight and Obesity By Adam Rinde, ND University House, Seattle, WA May 24, 2007
    2. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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
    19. 19. 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)
    20. 20. 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
    21. 21. 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?
    22. 22. Healthy Body Image
    23. 23. Evaluation and Management
    24. 24. 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?
    25. 25. 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
    26. 26. 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
    27. 27. 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?
    28. 28. 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
    29. 29. 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
    30. 30. 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
    31. 31. Clinical Findings: Fat Distribution
    32. 32. Clinical Presentation Acanthosis Nigricans
    33. 33. Clinical Presentation Xanthomas • Raised, waxy, frequently yellow- colored skin lesions Eruputive Xanthoma Knee Xanthoma
    34. 34. 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?
    35. 35. Diagnostic Testing for Evaluation and Screening. – Screening code for diabetes (277.22) – Chemistry Panel • Liver Enzymes • Fasting Blood Glucose • Fasting Lipids • TSH
    36. 36. 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?
    37. 37. 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
    38. 38. 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.
    39. 39. 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
    40. 40. 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.
    41. 41. Therapeutic Interventions For Overweight and Obesity
    42. 42. 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
    43. 43. 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
    44. 44. 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
    45. 45. 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
    46. 46. 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
    47. 47. 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
    48. 48. 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
    49. 49. 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).
    50. 50. 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
    51. 51. 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. 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
    52. 52. 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
    53. 53. 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.
    54. 54. 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.
    55. 55. 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.
    56. 56. 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
    57. 57. 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.)
    58. 58. 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.
    59. 59. 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
    60. 60. Types of Surgeries
    61. 61. 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.
    62. 62. 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
    63. 63. Integrative Treatment For Overweight and Obesity
    64. 64. 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?
    65. 65. 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?
    66. 66. 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.
    67. 67. 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
    68. 68. 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
    69. 69. 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
    70. 70. 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
    71. 71. Appendix
    72. 72. 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:
    73. 73. 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
    74. 74. 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
    75. 75. 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.
    76. 76. 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
    77. 77. 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)
    78. 78. Appendix: Obesogenic Environment • F is for Fat – A movement to improve U.S. obesity policies and reduce obesogenic environments. –
    79. 79. 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)
    80. 80. 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
    81. 81. 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
    82. 82. 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
    83. 83. 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.
    84. 84. Additional References • . quot;Obesity Education Initiative Electronic Textbook--Introduction.quot; from • • 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. • •
    85. 85. 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 . • • Oelschlager, B. (2005). quot;Gastrointestinal Complications of Bariatric Surgery.quot; Medscape Gastroenterology Retrieved May 15, 2007, 2007, from • • 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 • • 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.