Obesity Algorithm ® 2017-2018 - PowerPoint Presentation

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Obesity Algorithm 20172018 Obesity Medicine Association Disclaimer and Permissions Disclaimer The Obesity Algorithm guidelines were originally presented by the Obesity Medicine Association OMA in 2013 and have since been updated yearly to include the latest treatments and trends in ID: 816457

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Slide1

Obesity Algorithm®2017-2018

Slide2

Disclaimer and PermissionsDisclaimer

The Obesity Algorithm

guidelines were originally presented by the Obesity Medicine Association (OMA) in 2013 and have since been updated yearly to include the latest treatments and trends in the field of obesity medicine. They were developed to assist health care professionals in the management and care for patients with overweight and obesity. The Obesity Algorithm is not intended to be a substitute for a medical professional's independent judgment and should not be considered medical advice. The content herein is based on medical literature and the clinical experiences of obesity medicine specialists. In areas regarding inconclusive or insufficient scientific evidence, the authors used their professional judgment. The Obesity Algorithm is a working document that represents the state of obesity medicine at the time of publication. OMA encourages medical professionals to use this information in conjunction with, and not as a replacement for, their best clinical judgment. The presented recommendations may not be appropriate in all situations. Any decision by practitioners to apply these guidelines must be made in light of local resources and individual patient circumstances.PermissionsThe Obesity Medicine Association owns the copyright to the Obesity Algorithm but invites you to use the slide set. Access to the Obesity Algorithm content and/or permission for extensive quoting or reproducing excerpts and for the reproduction and use of copyrighted text, images, or entire slides will not be granted until the requestor has signed the copyright consent and permission agreement available at www.ObesityAlgorithm.org. OMA reserves the right to deny a request for permission to use the Obesity Algorithm.

Slide3

Peer ReviewSince its original release in 2013, the Obesity Algorithm has undergone peer review by medical professionals and providers, facilitated by:

Public posting on the web with free access and free download

Presentations and discussions at OMA meetings

Presentations and discussions at other scientific sessions and conferencesCitations in medical literatureThroughout the year, OMA receives comments based on widespread exposure amongst world-wide colleagues (e.g., scientific and clinical peers), as well as via online public access. OMA members are encouraged to provide feedback. This 2017-2018 version of the Obesity Algorithm incorporates worldwide input, as well as interim scientific and clinical trial data.Obesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Slide4

Major Updates Included in the 2017-2018 VersionGeneral updates and text editsSuggested core

slides – Clinical

application

and staff trainingSuggested core slides – Review for the American Board of Obesity Medicine examObesity prevalenceLipodystrophyExpansion of obesity paradoxClinical interpretation of Dual Energy X-Ray Absorptiometry (DXA) resultsGreater detail on the importance of non-exercise activity thermogenesis (NEAT)Anti-obesity drug updates and

summary

Functional foods, supplements & over-the-counter therapies

Investigational anti-obesity

pharmacotherapy

Updated

references

Slide5

Authors and CitationCore Authors: Bays HE,

Seger

, J, Primack C, Long J, Shah NN, Clark TW, McCarthy W.

Contributing Authors: Horn DB, Westman, ECitation: Bays HE, Seger, J, Primack C, Long J, Shah NN, Clark TW, McCarthy W. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2017-2018. www.obesityalgorithm.org (Accessed = Insert date)Obesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Slide6

PurposeTo provide clinicians with an overview of principles important to the care of patients with increased and/or dysfunctional body fat, based upon scientific evidence, supported by medical literature, and derived from the clinical experiences of members of the Obesity Medicine Association.

Slide7

ProcessThe Obesity Algorithm was derived from input by volunteer OMA members consisting of:CliniciansClinical trialists

Researchers

Academicians

Slide8

Intent of UseThe Obesity Algorithm is intended to be a “living document” updated once a year (as needed). It is intended to be an educational tool used to translate the current medical science and the experiences of obesity specialists to better facilitate and improve the clinical care and management of patients with overweight and obesity.

This algorithm

is not

intended to be interpreted as “rules” and/or directives regarding the medical care of an individual patient.While the hope is many clinicians may find this algorithm helpful, the final decision regarding the optimal care of the patient with overweight and obesity is dependent upon the individual clinical presentation and the judgment of the clinician who is tasked with directing a treatment plan that is in the best interest of the patient.The Obesity Algorithm is listed by the American Board of Obesity Medicine as a suggested resource and study-aid for the obesity medicine certification exam. (abom.org/exam-resources)Obesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Slide9

Author-Suggested Abbreviated Subset SlidesAll slides may be useful; however, the following are author suggestions of core slides for specific educational purposes regarding obesity:

Illustrative Core Slides for Clinical Care and Staff Training:

11, 13, 16, 17, 33, 34, 36, 37, 39, 40, 92, 93, 94, 99, 100, 101, 102, 103, 105, 107, 108, 109, 110, 114, 126, 127, 128, 137, 139, 141, 142, 143, 144, 145, 146, 147, 155, 156, 157, 159, 160, 161, 163, 175, 177, 178, 179, 185, 197, 217, 218, 219, 220, 211, 223, 226, 228, 229, 266, 267, 268, 279, 280, 282, 293, 294, 295, 296, 297, 298, 299, 321, 322, 323, 335, 337, 338

Illustrative Core Slides for American Board of Obesity Medicine Review:20-31, 54-63, 65-90, 92-96, 112-123, 125

135

141

147, 159-

172

, 180,

183

198

200

221

226

247

249-261, 270-277, 279-292, 293-298, 299-323, 324-333

Slide10

Table of ContentsObesity Algorithm . . . . . . . . . . . . . . . . . . . . . . .

Obesity Defined as a Disease . . . . . . . . . . . . . .

12Obesity as a Multifactorial Disease . . . . . . . . . . 18Overall Obesity Management Goals . . . . . . . . .

Obesity Classification . . . . . . . . . . . . . . . . . . . .

Fat Mass Disease . . . . . . . . . . . . . . . . . . . . . . .

Adiposopathy (Sick Fat Disease) . . . . . . . . . . .

Obesity Paradox . . . . . . . . . . . . . . . . . . . . . . .

Stress and Obesity: Both Cause and Effect . . .

Patient Evaluation: History . . . . . . . . . . . . . . . .

Patient Evaluation: Physical Exam . . . . . . . . . .

104

Patient Evaluation: Laboratory and Diagnostic

Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

106

Body Composition . . . . . . . . . . . . . . . . . . . . . .

111

Energy Expenditure . . . . . . . . . . . . . . . . . . . . .

124

Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . .

136Concomitant Medications . . . . . . . . . . . . . . . . 140General Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148Nutritional Therapy for Obesity . . . . . . . . . . . . . . . . . . .154Physical Activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173Motivational Interviewing . . . . . . . . . . . . . . . . . . . . . . . 182Behavior Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . .199Technologies for Weight-management . . . . . . . . . . . 222Anti-obesity Medications . . . . . . . . . . . . . . . . . . . . . . . . 224Functional Foods, Supplements, & Over-the-counter Therapies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 248Investigational Anti-obesity Pharmacotherapy . . . . . . . 262Early Versus Late Weight-management Intervention . . 265Bariatric Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 269Executive Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . 334References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339Disclosures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 378Historic Acknowledgement . . . . . . . . . . . . . . . . . . . . . . 380

Slide11

Nutritional Intervention

Physical Activity

Pharmaco-therapy

Bariatric Procedures

Behavior Therapy

Motivational Interviewing

Management Decisions

Evaluation and

Assessment

Obesity Algorithm

Obesity as a Disease

Data Collection

Reference/s: [1]

Slide12

Obesity Defined as a Disease

Slide13

The Obesity Medicine Association’s Definition of Obesity“Obesity is defined as a chronic, relapsing, multi-factorial, neurobehavioral disease, wherein an increase in body fat promotes adipose tissue dysfunction and abnormal fat mass physical forces, resulting in adverse metabolic, biomechanical, and psychosocial health consequences.”

Reference/s: [1]

Slide14

Obesity Is a Disease When…The patient has excessive body fat, as assessed by reliable measures

Excessive body fat is caused by genetic or developmental errors, infections, hypothalamic injury, adverse reactions to medications, nutritional imbalance, and/or unfavorable environmental factors

Multiple pathogenic adipocyte and/or adipose tissue endocrine and immune dysfunctions contribute to metabolic disease (adiposopathy or “sick fat” disease)

Multiple pathogenic physical forces from excessive body fat cause stress damage to other body tissues (fat mass disease)The adverse health consequences of increased body fat are not simply “co-morbidities” or “associated risk factors”

Reference/s: [1]

Slide15

Obesity PrevalenceIn 2015 – 2016, the prevalence of obesity is estimated to be ~ 40% in US adults, and 18.5% of youths

The prevalence of obesity is higher among non-Hispanic black and Hispanic adults than among non-Hispanic white and non-Hispanic Asian adults and youth

At least since 1999, the trend towards an increase in prevalence in obesity continues to increase among adults and youths

Slide16

Obesity Terminology

“People-first”

language recognizes the potential hazards of referring to or labeling individuals by their disease. Thus,

“patient who is overweight or has obesity” or “patient with overweight or obesity” are preferred over “obese patient.” This is similar to the standard with other diseases, such as diabetes mellitus, wherein “patient with diabetes” is preferred over “diabetic patient.”Encouraged TermsWeight

Unhealthy weight

Overweight

Body mass index

Affected by obesity

Discouraged Terms

Morbidly obese

Obese

Fat

Reference/s: [3] [4]

Slide17

Obesity Health Care Office Environment

Clinicians and staff should be trained to avoid hurtful comments, jokes, or being otherwise disrespectful, as patients with obesity may be ashamed or embarrassed about their weight.

Positive Office SpaceSturdy‚ armless chairs and high‚ firm sofas in waiting rooms

Sturdy‚ wide exam tables that avoid or prevent tipping

Sturdy stool or step with handles to help patients climb onto the exam table

Tables/chairs/toilet seats should sustain higher body weights

Extra-large patient gowns

Split toilet seat; provide a specimen collector with a handle

Reading materials in the waiting room that focus on healthy habits‚ rather than physical looks or being “thin”

Appropriate Medical Devices

Large adult blood pressure cuffs or thigh cuffs on patients with an upper-arm circumference greater than 34 cm

Extra-long needles to draw blood

Large vaginal specula

Weight scales with the capacity to measure patients who weigh more than 400 pounds

Reference/s: [5] [6]

Slide18

Slide19

Obesity as a Multifactorial Disease

Reference/s: [1]

Slide20

Multifactorial Inheritance Factors Contributing to Obesity

Mother

Father

Genetic inheritance

Epigenetic inheritance

Familial/cultural/societal inheritance

Obesity and its complications

Reference/s: [7]

Slide21

Genetics: Melanocortin 4 Receptor Deficiency

Clinical Presentation

Obesity, especially in families

Hyperphagia and obesity early in childhoodInsulin resistanceIncrease in bone mineral density (“big boned”)Accelerated linear growthReduced sympathetic nervous activity

Genetic Abnormality

Autosomal dominant or recessive

Most common known genetic defect predisposing to obesity

Polymorphism of gene localized to chromosome 18q22

Reference/s: [7] [8]

Slide22

Genetics: Prader–Willi Syndrome

Clinical Presentation

Obesity, often hyperphagic

Short statureWeak muscle tonePoor growthSmall hands/feetDelayed development

Underdeveloped genitals (often with infertility)

Behavioral/emotional challenges

Mild to moderate intellectual impairment

Insatiable appetite

Narrow forehead

Almond-shaped eyes

Triangular mouth

Often with fair skin and light-colored hair

Genetic Abnormality

Not inherited

Most cases involve loss of function of a portion of chromosome 15

Often reported as the most common human genetic "obesity syndrome"

Reference/s: [7] [8]

Slide23

Genetics: Albright’s Hereditary Osteodystrophy

Clinical Presentation

Obesity

Short statureRounded faceSkeletal defects: shortened fourth metacarpals and other bones of the hands and feetDental hypoplasiaSoft-tissue calcifications/ossifications

Pseudohypoparathyroidism (hypocalcemia, hyperphosphatemia)

Genetic Abnormality

Associated with molecular defect in the gene (GNAS1), which encodes for the alpha subunit of the stimulatory G protein

Reference/s: [7]

Slide24

Genetics: Bardet–Biedl Syndrome

Clinical Presentation

Obesity

Metabolic abnormalities (e.g., type 2 diabetes mellitus,high blood pressure, dyslipidemia)Blindness (retinal dystrophy and pigmentary retinopathy)AnosmiaHearing loss

Dysmorphic extremities: polydactyly and short or fused fingers and toes

Poor coordination

Dental abnormalities

Intellectual disability

Behavioral/emotional challenges

Hypogonadism (with infertility)

Renal cystic disease; renal insufficiency, which may lead to end-stage renal disease

Genetic Abnormality

Autosomal recessive

Mutations of at least 16 genes (BBS genes) applicable to cilia involved in:

Cell movement

Chemical signaling

Sensory input (sight, hearing, and smell)

Reference/s: [7] [8]

Slide25

Genetics: Cohen Syndrome

Clinical Presentation

Obesity

Developmental delayIntellectual disabilitySmall head sizeNarrow hands and feet with slender fingersWeak muscle tone

Retinal dystrophy

Joint hypermobility

Thick hair and eyebrows

Thick eyelashes

“Open mouth” expression with incisoral prominence

Low white blood cell count

Overly friendly behavior

Genetic Abnormality

Typically auto recessive

Mutation of the VPS13B gene (COH1 gene)

Reference/s: [7]

Slide26

Genetics: Borjeson-Forssman-Lehmann Syndrome

Clinical Presentation

Mainly in males

Intellectual disabilitySeizure disordersLarge earlobesShortened toesSmall genitalia

Gynecomastia

Genetic Abnormality

X-linked disorder

Mutation of the zinc finger gene PHF6 (located on the X chromosome)

Reference/s: [7]

Slide27

Genetics: Other Genetic Syndromes Associated with Obesity

Leptin deficiency (due to gene mutation)

Leptin receptor deficiency

Src homology 2 B adapter protein 1 (SH2B1) mutationsCarboxypeptidase E mutationsProhormone convertase-1 deficiencyProopiomelanocortin deficiencyProprotein convertase subtilisin kexin 1/3 deficiency

Brain derived neurotrophic factor (BDNF) deficiency

TrkB deficiency

Sim1 deficiency

Maternal uniparental disomy of chromosome 14

Trisomy 21 (Down’s Syndrome)

Fragile X syndrome

Turner’s syndrome

Alstrom syndrome

Carpenter syndrome

Macrosomia, Obesity Macrocephaly Ocular abnormalities (MOMO) syndrome

Rubinstein-Taybi syndrome

Rapid-onset Obesity with Hypothalamic dysfunction

Hypoventilation and Autonomic Dysregulation (ROHHAD syndrome)

Deletions/mutations of various other gene loci 17 and polymorphisms of fat mass and obesity associated (FTO) gene located on chromosome 16.

Reference/s: [7]

Slide28

Genetics: Lipodystrophy

Clinical Presentation

Lipodystrophy is a congenital or acquired limitation in the proliferation and differentiation of fat cells

HyperphagiaMuscular appearance and prominent peripheral veins from birth due to lack of adipose tissueCongenital (autosomal recessive congenital generalized lipodystrophy and autosomal dominant familial partial lipodystrophy)Acquired (acquired generalized lipodystrophy & acquired partial lipodystrophy)

Human Immunodeficiency Virus lipodystrophy is a common cause of acquired partial lipodystrophy

Leptin levels are reduced

Insulin resistance

Hypertriglyceridemia

Hepatic steatosis

Reference/s: [9] [10]

Slide29

Genetics: Lipodystrophy

Familial Partial Lipodystrophy (

FPLD

)Type 1 = Kobberling lipodystrophy (FPLD1)Primarily in womenLipodystrophy of arms, legs, and sometimes breasts

Increase abdominal and trunk fat deposition (central obesity)

Type 2 = Dunnigan lipodystrophy (FPLD2)

Lipodystrophy of arms, legs, buttocks, abdomen, and chest

Increased subcutaneous adipose tissue to back, face and chin

Cushingoid appearance

Type 3 = Mutations in peroxisome proliferator activated receptor gamma

Clinical presentation similar to FPLD2

Leptin levels are decreased

Diabetes and hypertriglyceridemia

Treatment = nutrition, physical activity,

metreleptin

, gastric bypass

Reference/s: [9] [10]

Slide30

Obesity: Extragenetic Etiology/CausesExtrageneticEnvironment (family, home, geographic location)

Culture

Lack of optimal nutrition and physical activity

Disrupted sleep (e.g., poor quality, too little, or too much)Adverse consequences of medicationsMental stressNeurologic dysfunction (central nervous system trauma, hypothalamic inflammation, leptin resistance) Viral infectionsGut microbiota neurologic signaling and transmission of pro-inflammatory stateObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [7]

Slide31

Obesity: Epigenetic Etiology/CausesEpigenetics: Alterations in gene expression without alteration in the genetic code

Pre-pregnancy

Pre-conception paternal or maternal overweight/obesity may influence epigenetic signaling during subsequent pregnancy:

Increased risk of overweight/obesity in offspringIncreased risk of other diseases (e.g., cardiovascular disease, cancer, diabetes mellitus, etc.) in offspring PregnancyEspecially in the presence of gestational diabetes mellitus, unhealthy maternal nutrition in women who are pregnant and overweight or with obesity may increase placental nutrient transfer to fetal circulation:GlucoseLipids and fatty acidsAmino acidsIncreased maternal nutrient transport may alter fetal gene expression:

Covalent modifications of deoxynucleic acid and chromatin

May impact stem cell fate

May alter postnatal biologic processes involved in substrate metabolism

May increase offspring predisposition to overweight/obesity and other diseases

Post-pregnancy

Adverse effects of epigenetic pathologies may help account for generational obesity

Improvement in generational obesity in offspring will likely require generational change in

nutrition and physical activity in prior generations of parents

Reference/s: [7] [11] [12]

Slide32

Slide33

Within Subsets of Patients with Overweight and/or ObesityDeranged endocrine and immune responses

Sick Fat Disease (SFD) (Adiposopathy)

Endocrine/metabolic:

Elevated blood glucose

Elevated blood pressure

Dyslipidemia

Other metabolic diseases

Abnormal and pathologic

physical forces

Fat Mass Disease (FMD)

Biomechanical/structural:

Stress on weight-bearing joints

Immobility

Tissue compression (i.e., sleep apnea, gastrointestinal reflux, high blood pressure, etc.)

Tissue friction (i.e., intertrigo, etc.)

Reference/s: [13] [14] [15]

Slide34

Overall Management Goals

Adult patient with overweight or obesity

Improve patient health

Improve quality

of life

Improve body weight and composition

Reference/s: [1]

Slide35

Slide36

Body Mass Index: Increase Body Fat (Adiposity)

Body mass index (BMI) in kilograms per meters squared (kg/m

)*Normal Weight18.5-24.9Overweight

25.0-29.9

Class I Obesity

30.0-34.9

Class III Obesity

*Different BMI cut-off points may be more appropriate based upon gender, race, ethnicity, and menopausal status

Normal Weight

18.5-24.9

Overweight

25.0-29.9

Class I Obesity

30.0-34.9

Class II Obesity

35.0-39.9

Reference/s: [16] [17] [18] [19]

Slide37

Percent Body Fat: American Council on Exercise Classification

American Council on Exercise Classification:

Percent body fat*

Essential FatWomen: 10-13%Men: 2-5%

Athletes

Women: 14-20%

Men: 6-13%

Fitness

Women: 21-24%

Men: 14-17%

Acceptable

Women: 25-31%

Men: 18-24%

Obesity

Women: ≥ 32%

Men: ≥ 25%

*Based on “expert opinion;” cut-off points not scientifically validated

Reference/s: [20]

Slide38

Percent Body Fat: U.S. Army Regulations

U.S. Army regulations:

Percent body fat (%BF)

Men %BF Calculator(Age, height, & tape measure of neck and waist)Maximum allowable %BF to join ArmyAge 17-20 24%

Age 21-27 26%

Age 28-39 28%

Age 40+ 30%

Maximum allowable %BF after entry

Age 17-20 20%

Age 21-27 22%

Age 28-39 24%

Age 40+ 26%

Women %BF Calculator

(Age, height, & tape measure of neck, waist, and hip)

Maximum allowable %BF to join Army

Age 17-20 30%

Age 21-27 32%

Age 28-39 34%

Age 40+ 36%

Maximum allowable %BF after entry

Age 17-20 30%

Age 21-27 32%

Age 28-39 34%

Age 40+ 36%

Reference/s: [21] [22]

Slide39

Waist Circumference: Increased Body Fat (Adiposity)

Obesity classification:

Waist circumference (WC)*

Abdominal Obesity - Men> 40 inches> 102 centimeters

Abdominal Obesity - Women

35 inches

88 centimeters

*Different WC abdominal obesity cut-off points are appropriate for different races (i.e.,

90 centimeters for Asian men and

80 centimeters for Asian women)

Reference/s: [23] [24] [25] [26]

Slide40

Obesity: Summary Diagnostic Metrics and Diagnostic Codes

Body Mass Index

30 kg/m2Percent Body fatWomen: ≥ 32%Men: ≥ 25%

Abdominal Obesity: Women

35 inches

88 centimeters

Abdominal Obesity: Men

40 inches

102 centimeters

Overweight and Obesity E66

Code first obesity complicating pregnancy, childbirth and the puerperium, if applicable (O99.21-)

Use additional code to identify body mass index (BMI), if known (Z68.-)

Excludes:

Adiposogenital

dystrophy (E23.6)

Lipomatosis NOS (E88.2)

Lipomatosis dolorosa [Dercum] (E88.2)

Prader-Willi syndrome (Q87.1)

E66.0 Obesity Due to Excess Calories

E66.01 Morbid (severe) obesity due to excess calories

E66.09 Other obesity due to excess calories

E66.1 Drug-induced obesityE66.2 Morbid (severe) obesity with alveolar hypoventilationE66.3 OverweightE66.8 Other obesityE66.9 Obesity, unspecifiedReference/s: [27]

Slide41

Body Mass Index (BMI)AdvantagesIncreased BMI generally correlates with metabolic and fat mass diseases in population studies

Commonly used

Reasonably reproducible

Low costAdequate measure for epidemiological studiesAdequate screening metric for most patientsDisadvantagesMay not correlate with metabolic and fat mass diseases in an individual patientDoes not account for muscle massMay over-diagnose obesity in muscular individuals, under-diagnose patients with sarcopeniaBMI cut-off points do not distinguish between men and women, nor ethnic and racial considerations Should be used as part of the clinical evaluation, and not the sole measure

of obesity for all patients

Reference/s: [16] [17] [18]

Slide42

Percent Body FatAdvantagesMore specific assessment of body fat

May be a reasonable longitudinal measure, especially in patients who may not be losing weight, but engaged in resistance exercise training, and thus may be losing body fat, and increasing muscle

Disadvantages

Some measurement techniques are not always accurate, nor easily reproducible (i.e., single site skinfold calipers)Electronic body fat measurements may be expensive, and as with calipers, the accuracy and reproducibility is dependent upon the equipment and software, as well as the expertise of the technicianCut-off points not validated to correlate to metabolic diseaseObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [20] [28]

Slide43

Waist CircumferenceAdvantages Well-correlated to metabolic disease

Direct anatomical measure of adipose tissue deposition, with an increase in waist circumference reflective of adipose tissue dysfunction

Low cost

DisadvantagesMeasurement not always reproducibleWaist circumference is not superior to BMI in correlating to metabolic disease in patients with BMI > 35 kg/m2Racial/ethnic differences Obesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [24] [25] [26]

Slide44

Which Is the “Best” Measure of Obesity?Population AssessmentBody mass index (BMI), waist circumference (WC), and percent body fat (%BF) similarly correlate with prevalence of metabolic syndrome

Individual Assessment

BMI is a reasonable initial screening measurement for most patients

WC provides additional information regarding adipose tissue function/dysfunction and predisposition to metabolic disease among individuals with BMI<35 kg/m2%BF may be more useful in patients with extremes in muscle mass (i.e., individuals with sarcopenia or substantial increases in muscle mass), and thus may be a more accurate measure of body composition when assessing the efficacy of interventions directed towards change in muscle massObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [1]

Slide45

Fat Mass Disease:Abnormal and Pathologic Physical Forces

Slide46

Clinical Manifestations: Fat Mass DiseaseCardiovascular

Congestive heart failure and cor pulmonale

Varicose veinsThromboembolic events (i.e., pulmonary embolus, stroke)Hypertension (i.e., compression of kidney)Pulmonary Dyspnea

Obstructive sleep apnea

Hypoventilation/Pickwickian syndrome

Asthma

Neurologic

Intracranial hypertension (pseudotumor cerebri

)

due to increased intra-abdominal pressure and sleep apnea, with impaired central venous return.

Stroke (see “cardiovascular”)

Nerve entrapment (i.e., meralgia paresthetica, carpal tunnel syndrome)

Reference/s: [29] [30] [31]

Slide47

Clinical Manifestations: Fat Mass DiseaseMusculoskeletal

Immobility

Osteoarthritis (e.g. knees, hips) Low back pain Myalgias Altered center of gravity Impaired balanceGastrointestinalGastroesophageal refluxHerniasIntegumentStriae distensae (skin stretch marks)

Stasis pigmentation

Venous stasis ulcers

Cellulitis

Skin tags

Intertrigo (i.e. bacterial, fungal skin fold infections)

Carbuncles

Reference/s: [29] [30] [31]

Slide48

Clinical Manifestations: Fat Mass DiseasePsycho-SocialDepression

Hopelessness

Low self-esteem

Body-image dissatisfactionDiminished sex drive Impaired intimacy and sexual relationshipsDecreased work productivity Increased work absenteeismBiasesSociety FamilyWorkplace Harassment

Bullying

Negative Self or External Perceptions

“Unmotivated”

“Weak-willed”

“Less intelligent”

“Less attractive”

“Unsuccessful”

“Overindulgent”

“Lazy”

Weight bias internalization

Increased body fat can contribute to self-stigmatization

Weight stigma may also contribute to mental stress, leading to adiposopathic stress responses and metabolic disease

Reference/s: [29] [30] [31] [32]

Slide49

HistorySnoring (usually loudly)Insomnia

Restless sleep

Sudden wakening with choking or gasping

HeadachesDaytime sleepinessFatigue Increased risk of motor vehicle accidentsForgetfulness Mood changes Lack of interest in sexual behaviorGastroesophageal reflux

*Other sleep disorders associated with obesity include insomnia and restless leg syndrome.

Sleep Disorders and Obesity: Obstructive Sleep Apnea*

Reference/s: [33] [34]

Slide50

Physical Findings

Increased neck circumference

Men > 17 inches

Women > 16 inchesHead abnormalitiesModified Mallampati score of 3 or 4RetrognathiaLateral peritonsillar narrowing

Macroglossia

Tonsillar hypertrophy

Enlarged uvula

High arched/narrow palate

Nasal abnormalities

Overbite

Cardiopulmonary abnormalities

Peripheral edema

Cardiac dysrhythmia

High blood pressure

Sleep Disorders and Obesity: Obstructive Sleep Apnea

Reference/s: [33] [34]

Slide51

DiagnosisQuestionnaires:

Berlin Sleep Questionnaire

Epworth Sleepiness Scale

STOP-Bang QuestionnaireSTOP = Snoring, Tiredness, Observed apnea and high blood Pressure)Bang: BMI, age, neck circumference,

ender

Testing

In-lab overnight sleep studies

Apnea hypopnea index (AHI)

5-15/hour = mild sleep apnea

15-30/hour = moderate sleep apnea

> 30/hour = severe sleep apnea

Home sleep test

Multiple sleep latency test

Adverse Consequences of Untreated Obstructive Sleep Apnea

Worsening obesity

Congestive heart failure

Atrial fibrillation

Nocturnal dysrhythmias

Stroke

High blood pressure

Type 2 diabetes mellitus

Pulmonary hypertension

Sleep Disorders and Obesity: Obstructive Sleep Apnea

Reference/s: [33] [34] [35]

Slide52

TreatmentReduction of fat massBehavior therapy to improve sleep patterns

Oral appliances

Mandibular reposition devices

Tongue retaining devices Nasal expiratory positive airwayContinuous positive airway pressureAdaptive servo-ventilationSurgeryLaser-assisted uvulopalatoplastyRadiofrequency ablationPalatal implantsElectrical stimulation of upper airway muscles

Sleep Disorders and Obesity: Obstructive Sleep Apnea

Reference/s: [36]

Slide53

Adiposopathy (Sick Fat Disease):Abnormal Endocrine and Immune Responses

Slide54

Anatomic ChangesPositive caloric balance may lead to adipocyte hypertrophy with variable increases in adipocyte number, as regulated by intracellular:

Sterol regulatory element binding protein-1 (SREBP1),

Peroxisome proliferator-activated receptor (PPAR) gamma

Slide55

Anatomic ChangesWhen adipogenesis (proliferation and differentiation) is impaired in peripheral subcutaneous adipose tissue (SAT), then inadequate storage of excess energy in SAT may result in energy overflow and increased circulating free fatty acids

Worsening adipocyte hypertrophy and adipocyte dysfunction

Increasing (“ectopic”) fat deposition in other depots

Visceral fatSubcutaneous SATPericardiac fat Perivascular fatIncreasing (“ectopic”) fat deposition in other body organsLiverMusclePancreas

Heart

Kidney

Reference/s: [37] [38]

Slide56

Functional ChangesIncreased adipocyte hypertrophy and adipose tissue accumulation may contribute to:

Adipocyte and adipose tissue hypoxia

Increased adipose tissue immune cell infiltration

Increased adipocyte apoptosisIncreased reactive oxygen species and oxidative stressExtracellular matrix abnormalitiesIntraorganelle dysfunction (e.g., mitochondrial and endoplasmic reticulum stress)Changes in adipose tissue neural network and innervationsObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [37] [38]

Slide57

Adiposopathic EndocrinopathiesAngiogenesisAdipogenesisExtracellular matrix dissolution and reformation

Lipogenesis

Growth factor production

Hormone production

Steroid metabolism

Immune response

Hemostasis

Element binding (e.g., sterol regulatory element-binding proteins, and calcium)

Multiple receptors:

Traditional peptides and glycoprotein hormones

Nuclear hormones

Cytokines or adipokines with cytokine-like activity

Growth factors

Catecholamine receptors

Reference/s: [38] [39] [40] [41] [42]

Slide58

Adiposopathic ImmunopathiesProinflammatory adipose tissue factorsFactors with cytokine activity (e.g., leptin)Acute-phase response proteins (e.g., C-reactive protein)

Proteins of the alternative complement system

Chemotactic or chemo-attractants for immune cells

Slide59

Obesity, Health, and Harmony of Function of Body OrgansAdiposopathy most often results in metabolic disease when accompanied by:Dysfunction other body organs

Limitations of the metabolic “flexibility” of other body organs to mitigate the pathogenic metabolic, endocrine, and immune responses promoted by obesity

Metabolic health is dependent upon the interactions or crosstalk with adipose tissue and other body organs:

Liver Muscle Pancreas Immune system Heart and vasculature Brain Endocrine glands Intestine Other body organs

Reference/s: [38]

Slide60

Metabolic Manifestations of AdiposopathyHigh blood glucose (prediabetes mellitus, type 2 diabetes mellitus)

High blood pressure

Metabolic syndrome

Adiposopathic dyslipidemiaIncreased triglyceride levelsDecreased high-density lipoprotein cholesterol levelsIncreased atherogenic particle number (increased apolipoprotein B)Increased proportion of small, dense, low-density lipoprotein particlesIncreased triglyceride-rich lipoproteinsIncreased lipoprotein-remnants

Insulin resistance

Hepatosteatosis (fatty liver)

Hyperuricemia and gout

Cholelithiasis

Acanthosis Nigricans

Nephrolithiasis

Glomerulopathy

Pro-thrombotic predisposition

Neuropsychiatric diseases (such as worsening depression due to adiposopathic immune and endocrine responses)

Asthma (due to adiposopathic immune and endocrine responses)

Worsening of other inflammatory diseases (osteoarthritis, atherosclerosis, etc.)

Reference/s: [38] [39] [40] [42]

Slide61

Gender-specific Manifestations of AdiposopathyWomenHyperandrogenemiaHirsutism

Acne

Polycystic ovarian syndrome

Menstrual disordersInfertilityGestational diabetes mellitusPreeclampsiaThrombosisMenHypoandrogenemiaHyperestrogenemiaErectile dysfunctionLow sperm countInfertilityObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [43] [44] [45]

Slide62

Obesity and Adiposopathy Increases the Risk of Cancers Bladder cancer Brain cancerBreast cancer (postmenopausal)

Cervical cancer

Colon cancer

Endometrial/uterine cancerEsophageal cancerGallbladder cancerHead and neck cancerKidney/renal cancerLeukemiaLiver cancerMultiple myelomaNon-Hodgkin lymphomaOvarian cancerPancreatic cancer Prostate cancer (prognosis is worse, not necessarily increased risk)Stomach cancerThyroid cancer

Reference/s: [46] [47] [48] [49] [50] [51]

Slide63

Adiposopathic and/or Fat Mass Pathologies: Genitourinary and Reproductive Manifestations

Genitourinary

Urinary stress incontinence

Pelvic prolapse (e.g. cystocele, rectocele, uterine prolapse, vault prolapse)Reproductive Pre-pregnancyMenBuried or hidden penisErectile dysfunction

Psychological barriers to sexual behavior

Infertility

Women

Psychological barriers to sexual behavior

Infertility, anovulation, polycystic ovary syndrome

Reproductive Pregnancy

Gestational diabetes mellitus

Preeclampsia

Increased risk of miscarriage and stillbirth

Overdue pregnancy

Increased need for induction

Increased need and complications of cesarean section in women (delayed healing and wound infection)

Large for gestational age offspring

Thrombosis

Obstructive sleep apnea

Reference/s: [52] [53] [54]

Slide64

Obesity Paradox

Slide65

ANATOMIC OBESITY PARADOXAre some fat depots protective while others are “paradoxically” pathogenic?

PHYSIOLOGIC OBESITY PARADOX

Are some individuals who are overweight or with obesity “paradoxically” healthy?

Do some individuals who are normal weight, or only mildly overweight, “paradoxically” have metabolic disease?DEMOGRAPHIC (GENDER AND RACE) PARADOXAre women at a “paradoxically” lower age-adjusted cardiovascular disease risk than men?Are some races “paradoxically” at increased risk for metabolic diseases for the same amount of body weight?THERAPEUTIC OBESITY PARADOX

Can adding body fat “paradoxically” treat metabolic diseases typically associated with too much body fat?

Does an increase in fat mass always predispose to metabolic disease?

Does a decrease in fat mass always improve metabolic disease?

Obesity Paradox

Reference/s: [14] [38] [57]

Slide66

CARDIOVASCULAR OUTCOMES OBESITY PARADOXWhy are individuals who are modestly overweight often report to have a better prognosis after cardiovascular disease (CVD) events and cardiovascular procedures?

ATHEROSCLEROSIS “OUTSIDE-TO-IN” OBESITY PARADOX

What is the role of pericardial and perivascular adipose tissue in promoting atherosclerosis?

STROKE OBESITY PARADOXWhy do individuals with obesity seem to have a better outcome with stroke?ACUTE RESPIRATORY DISTRESS OBESITY PARADOXWhy do individuals with obesity seem to have better outcome with acute respiratory distress? KIDNEY DISEASE OBESITY PARADOXWhy do patients with chronic kidney disease and increased body mass index have lower risk of end-stage renal disease and death?THERAPEUTIC APPROACH OBESITY PARADOX

How do clinicians best navigate the apparent paradox of “blame” versus “accountability” in obesity management?

Obesity Paradox

Reference/s: [14] [38] [57]

Slide67

Obesity increases mortality, especially when maximum body mass index (BMI) is assessed rather than a single baseline BMI

Obesity increases morbidity, including increased risk of cardiovascular disease even without major metabolic cardiovascular risk factors

More than one “obesity paradox” exists

Obesity paradoxes are less paradoxical when viewed from the perspective of both fat mass

and

fat function

Obesity Paradox: General Concepts

Reference/s: [58] [59] [60] [61] [62]

Slide68

Are some fat depots protective while others are “paradoxically” pathogenic?

Peripheral Subcutaneous Adipose Tissue (SAT) Can Be Protective

Provides storage of energy

Physical padding

Thermal insulation

During positive caloric balance, if adipocyte proliferation and differentiation are sufficient to mitigate adiposopathic adipocyte hypertrophy, endocrinopathies, inflammation, and lipotoxic energy overflow to other fat depots and other body organs, then an increase in body fat may not be as pathogenic in promoting metabolic disease

Anatomic Obesity Paradox

Reference/s: [14] [38] [57]

Slide69

Are some fat depots protective while others are “paradoxically” pathogenic?

Peripheral Subcutaneous Adipose Tissue (SAT) Can Be Pathogenic

Fat mass diseases

During positive caloric balance, if adipocyte proliferation and differentiation are

not

sufficient to mitigate adiposopathic adipocyte hypertrophy, endocrinopathies, inflammation, and lipotoxic energy overflow to other fat depots and other body organs, then this may increase the risk of metabolic diseases such as diabetes mellitus, high blood pressure, and dyslipidemia.

SAT is ~80% of total fat mass

Majority of adipose tissue-derived systemic free fatty acids originate from SAT, with extrahepatic lipotoxicity potentially contributing to insulin resistance in muscle

Majority of adipose tissue-derived free fatty acids in the portal system originate in SAT (not VAT), with lipotoxicity potentially contributing to insulin resistance in the liver

An increase in abdominal SAT is associated with adiposopathic predisposition to metabolic disease, not unlike VAT

Anatomic Obesity Paradox

Reference/s: [14] [38] [57]

Slide70

Are some fat depots protective while others are “paradoxically” pathogenic?

Visceral Adipose Tissue (VAT) Can Be Protective

Provides storage of energy

Physical padding to protect against mechanical damage to abdominal organs

May protect against peritoneal catastrophes (perforated visceral organs)

Thermal insulation

Anatomic Obesity Paradox

Reference/s: [14] [38] [57]

Slide71

Are some fat depots protective while others are “paradoxically” pathogenic?

Visceral Adipose Tissue (VAT) Can Be Pathogenic

VAT adipocytes have higher basal lipolysis than SAT adipocytes

Increased sensitivity to catecholamines

Decreased sensitivity to insulin

Direct portal access to the liver

More active expression of adiposopathic endocrinopathies than SAT

More active expression of adiposopathic immunopathies than SAT

More associated with increased risk of metabolic disease, possibly because increased visceral adiposity reflects dysfunctions of all fat depots

Anatomic Obesity Paradox

Reference/s: [14] [38] [57]

Slide72

Both subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) are potentially protective and pathogenic

SAT and VAT mass and function are interdependent

Both SAT and VAT express adiposopathic endocrinopathies and immunopathies when promoting metabolic diseasesAn increase in visceral adiposity is a surrogate marker for the dysfunction of SAT and other fat depots

An increase in visceral adiposity is a surrogate marker for global fat dysfunction, helping to account for its association with metabolic diseases

Central obesity is a clinical measure that reflects both an increase in visceral fat and an increase in subcutaneous abdominal fat

Are some fat depots protective while others are “paradoxically” pathogenic?

Anatomic Obesity Paradox

Reference/s: [14] [38] [57]

Slide73

Benign Multiple Symmetrical Lipomatosis

Increased fat accumulation in the subcutaneous adipose tissue regions of the arms, legs, shoulders, and neck.

Increased proliferation of small adipocytes in subcutaneous adipose tissueIncreased secretion of anti-inflammatory adipokines (e.g. adiponectin)

Typically, glucose or lipid disorders do not develop

Inherited Lipodystrophy

Variable lack of body fat and impaired adipose tissue function (e.g., low adiponectin levels and inability to adequately store fat)

High circulating free fatty acids (lipotoxicity)

Hyperglycemia and dyslipidemia

Are some fat depots protective while others are “paradoxically” pathogenic?

Anatomic Obesity Paradox

Reference/s: [14] [38] [57]

Slide74

Are some individuals who are overweight or with obesity “paradoxically” healthy?

Do some individuals who are normal weight, or only mildly overweight “paradoxically” have metabolic disease?

“Metabolically Healthy But Obese” (MHO) Phenotype

Some individuals are reported to have increased body fat, but without metabolic disease

No standard definition exists for MHO

The more detailed the evaluation for metabolic disease, the less the prevalence of MHO

Prevalence of MHO has considerable variation, depending on the criteria (6 – 75%)

MHO have higher rate of heart disease and heart failure

MHO experience fat mass diseases, such as sleep apnea, stress / damage to joints, and increased risk of cancers

With aging, MHO are at greater risk of future development of metabolic disease, with 30 – 40% developing metabolic disease within 6 years

Physiologic Obesity Paradox

Reference/s: [14] [38] [57] [63]

Slide75

Are some individuals who are overweight or with obesity “paradoxically” healthy?

Do some individuals who are normal weight, or only mildly overweight “paradoxically” have metabolic disease?

“Metabolically Obese Normal Weight” (

MONW

) Phenotype

Defined as normal-weight individuals who express metabolic diseases typically associated with an increased in body fat

Some individuals may express adiposopathy with increased body fat not outside the upper range of normal

Some individuals may have genetic or acquired dysfunction of other body organs that result in disharmonious physiologic interactions with adipose tissue (“metabolic inflexibility”)

Physiologic Obesity Paradox

Reference/s: [14] [38] [57]

Slide76

Are women at a “paradoxically” lower age-adjusted cardiovascular disease risk than men?

Are some races “paradoxically” at increased risk for metabolic diseases for the same amount of body weight?

For the Same Age and Weight, Men Have a Higher Rate of CVD Compared to Women

Cardiovascular disease (CVD) is the most common cause of death in women and men

During positive caloric balance:

Men often expand fat deposition via the more pathogenic adipocyte hypertrophy and android or “apple” fat distribution.

Women often expand fat deposition via the less pathogenic adipocyte proliferation and gynoid or “pear” fat distribution

Demographic (Gender and Race) Obesity Paradox

Reference/s: [14] [38] [57]

Slide77

For the Same Increase in Body Fat, Individuals of Asian Descent Have an Increased Risk for Type 2 Diabetes Mellitus, Metabolic Syndrome, and Cardiovascular Disease Compared to Other Races

Greater adipocyte size; reduced number of adipocytes

Increased visceral adiposityIncreased free fatty acid and leptin levels

Increased pro-inflammatory factors (e.g., C-reactive protein), and decreased anti-inflammatory factors (e.g., adiponectin)

Increased insulin resistance

Asians require a lower cut-off point for the clinical determination of overweight and obesity

Are women at a “paradoxically” lower age-adjusted cardiovascular disease risk than men?

Are some races “paradoxically” at increased risk for metabolic diseases for the same amount of body weight?

Demographic (Gender and Race) Obesity Paradox

Reference/s: [14] [38] [57]

Slide78

Peroxisome proliferator-activated receptor agonists (thiazolidinediones)

increase the proliferation and differentiation of adipocytes, increasing fat mass, providing increased adipocyte functionality, and are approved as glucose-lowering agents

Weight loss with human immune virus antiretroviral (HIV) therapy

may result in HIV lipodystrophy, with impairment in adipocyte differentiation, reduction in mean fat cell size, possible decrease in adipocyte proliferation, decrease in subcutaneous adipose tissue accumulation, relative increase in visceral adipose tissue accumulation, and increased risk of hyperglycemia and dyslipidemia.

Can adding body fat “paradoxically” treat metabolic diseases typically associated with too much body fat?

Does an increase in fat mass always predispose to metabolic disease?

Does a decrease in fat mass always improve metabolic disease?

Therapeutic Obesity Paradox

Reference/s: [14] [38] [57]

Slide79

Transplantation of Fat in Lipoatrophic Mice

Lipoatrophic mice have virtually no white adipose tissue

Severe hyperglycemia. Fat transplant improves hyperglycemia, hyperinsulinemia, and muscle insulin sensitivity

Liposuction of Subcutaneous Adipose Tissue (SAT)

Removal of SAT does not improve hyperglycemia, high blood pressure, and dyslipidemia

Can adding body fat “paradoxically” treat metabolic diseases typically associated with too much body fat?

Does an increase in fat mass always predispose to metabolic disease?

Does a decrease in fat mass always improve metabolic disease?

Therapeutic Obesity Paradox

Reference/s: [14] [38] [57]

Slide80

The Obesity CVD Paradox May Be Risk-factor Dependent

Individuals who are modestly overweight may have improved CVD prognosis only if they are physically fit

Cigarette smoking decreases body weight (especially with chronic lung disease), but increases CVD risk

Why are individuals who are modestly overweight often reported to have a better prognosis after cardiovascular disease (CVD) events and cardiovascular procedures?

Cardiovascular Disease Outcomes Obesity Paradox

Reference/s: [14] [38] [57]

Slide81

The Obesity CVD Paradox May Reflect Different Cardiovascular Pathologies

The pathophysiology applicable to obesity and adiposopathy may differ from other pathophysiologies leading to CVD events; the prognosis may differ as well

Inherent vasculopathies predisposing to CVD events may be independent of body weight, be of greater severity, and have poorer outcomes compared with CVD events that occur due to obesityFamilial hypercholesterolemia (FH) is an inherited disorder that is independent of body weight, results in severe elevations in cholesterol, and which has a disproportionally high rate of (premature) CVD morbidity and mortality

A patient with FH who is a heavy smoker and not overweight may be at greater risk for an ST segment elevated myocardial infarction (STEMI) than a nonsmoker without FH who is overweight or with obesity

Why are individuals who are modestly overweight often reported to have a better prognosis after cardiovascular disease (CVD) events and cardiovascular procedures?

Cardiovascular Disease Outcomes Obesity Paradox

Reference/s: [14] [38] [57] [64] [65]

Slide82

The Obesity CVD Paradox Might Be Partially Explained by Enhanced Cardiovascular Autorepair Potential

Adipocytes, blood vessels, and cardiomyocytes share a similar lineage of mesenchymal stem cells

Individuals who are overweight often have a greater reservoir of adipose tissue mesenchymal cellsAfter an acute CVD event, increased circulating reparative mesenchymal cells might conceivably migrate to the injured myocardial site, and assist with cardiovascular tissue repair

Why are individuals who are modestly overweight often reported to have a better prognosis after cardiovascular disease (CVD) events and cardiovascular procedures?

Cardiovascular Disease Outcomes Obesity Paradox

Reference/s: [14] [38] [57]

Slide83

The Obesity CVD Paradox Might Be Partially Explained by a Disproportional Attention Directed towards CVD Prevention among Patients with Obesity

Patients with obesity often have medical conditions that prompt earlier access and more frequent access to medical care

In the global management of patients with obesity, preventative interventions may be disproportionately implemented, perhaps involving earlier and more frequent CVD diagnostic procedures, and initiation of therapeutic agents proven to reduce CVDObesity increases the risk of type 2 diabetes mellitus (T2DM); while it remains unclear the degree by which glucose-lowering reduces CVD risk, patients with T2DM are often treated with antihypertensive, lipid-altering, and perhaps antithrombotic agents that reduce CVD morbidity and mortality

Why are individuals who are modestly overweight often reported to have a better prognosis after cardiovascular disease (CVD) events and cardiovascular procedures?

Cardiovascular Disease Outcomes Obesity Paradox

Reference/s: [14] [38] [57]

Slide84

Atherosclerosis is most often described as an

“inside-to-in”

pathogenic process wherein atherogenic apoB containing lipoproteins enter the subendothelia, become oxidized, and then help promote inflammation, plaque formation, and ultimately, plaque rupture leading to CVD events

What is the role of pericardiac and perivascular adipose tissue in promoting atherosclerosis?

Atherosclerosis “Outside-to-In” Obesity Paradox

Reference/s: [14] [38] [57]

Slide85

An “Outside-to-in” Atherogenic Model Suggests That Adiposopathic Adipose Tissue Surrounding the Heart and Arteries Also Contributes to Atherosclerosis

Coronary calcium correlates to epicardial fat

Coronary calcium scoring is used to assess atherosclerosisAdipose tissue surrounding the heart and arteries may serve as a local supplier of toxic, free fatty acids to the myocardium, and thus contribute to “fatty heart”

Pericoronary adipose tissue may serve as a supply site for oxidized low density lipoproteins in coronary plaques, possibly via transport through the interstitial space

What is the role of pericardiac and perivascular adipose tissue in promoting atherosclerosis?

Atherosclerosis “Outside-to-In” Obesity Paradox

Reference/s: [14] [38] [57]

Slide86

An “Outside-to-in” Atherogenic Model Suggests That Adiposopathic Adipose Tissue Surrounding the Heart And Arteries Also Contributes to Atherosclerosis

Adipose tissue surrounding the heart and arteries may secrete factors that alter endothelial cells and function

“Sick” epicardial adipose tissue may have reduced anti-inflammatory secretions (e.g., reduced adiponectin) and increased pro-inflammatory adipokine secretion that can be transported into vessel walls via transcellular passing or diffusion (vasocrine regulation)Adipose tissue surrounding the heart and arteries may help supply macrophages to an expanded adventitial vas vasorum, resulting in even greater pro-atherogenic inflammatory signaling

What is the role of pericardiac and perivascular adipose tissue in promoting atherosclerosis?

Atherosclerosis “Outside-to-In” Obesity Paradox

Reference/s: [14] [38] [57]

Slide87

Why do individuals with obesity seem to have a better outcome with stroke?

Stroke Obesity Paradox

Reference/s: [66]

Obesity increases the risk of stroke

Poorer nutritional state and affiliated diseases may contribute to underweight, which may worsen stroke outcomes

Improved nutritional state and energy reserve may improve stroke outcomes

No obesity stroke paradox occurs with intravenous thrombolysis

Slide88

Why do individuals with obesity seem to have better outcomes with acute respiratory distress?

Acute Respiratory Distress Obesity Paradox

Reference/s: [67]

Obesity increases the risk of diseases leading to acute respiratory distress

Poorer nutritional state and affiliated diseases may contribute to underweight, which may worsen acute respiratory distress

Improved nutritional state and energy reserve may improve acute respiratory distress outcomes

Slide89

Why do patients with chronic kidney disease and increased body mass index have lower risk of end-stage renal disease and death?

Kidney Disease Obesity Paradox

Reference/s: [68] [69]

Patients with renal disease and increased body mass index (BMI) may have reduced progression to end-stage renal disease (

ESRD

), and better survival compared to patients with lower BMI

Progression to

ESRD

may be independent of BMI in patients with metabolic syndrome

Explanations of the kidney disease obesity paradox may include:

Patients at lower BMI may be undernourished with protein-muscle-energy wasting

Worsened hemodynamic stability at lower BMI

Increased sequestration of uremic toxins in adipose tissue among those with higher BMI

Alterations in circulatory cytokines and endotoxin-lipoprotein interactions

Slide90

Individual responsibility can encompass both “blame” and “accountability”

“Blame” often goes beyond assigning responsibility and often leads to condemnation and accusations, with the intent to elicit guilt

Promoting guilt is often counterproductive in changing behavior“Accountability” most often refers to record keeping and shared decision-making

Promoting accountability is a critical component towards modifying behavior

A lack of acknowledging individual responsibility may invite counterarguments and reduce feelings of empathy by others

A reluctance to recommend accountability via record keeping and shared decision-making may deprive the patient of an important behavior modification technique

How do clinicians best navigate the apparent paradox of “blame” versus “accountability” in obesity management?

Therapeutic Approach Obesity Paradox

Reference/s: [3] [70]

Slide91

Stress and Obesity:Cause and Effect

Slide92

Psychological or Medical StressStress ResponsesCognitive changes

Increased (e.g., some cases of emergent stress)

Decreased (e.g., some cases prolonged stress)

Physiological changesBehavioral changesPainPotential analgesia with emergent stressPotential worsening of pain with chronic stress

Reference/s: [71] [72] [73] [74]

Slide93

Psychological or Medical Stress: Endocrine ResponseEmergent “Fight or Flight” Response

(Increased Sympathomimetic Activity)

Increase in short-term sympathetic nervous system activation

Increased catecholamines (e.g., norepinephrine and epinephrine)Cardiovasculopulmonary responses Increased blood pressureVasoconstrictionIncreased heart rate and contractilityImpaired blood flow to kidneyBronchial dilationMetabolic responses

Potential increase in glucose levels (increased insulin resistance, increased hepatic glycogenolysis, and increased hepatic gluconeogenesis)

Increased adipose tissue lipolysis

Reference/s: [71] [72] [73] [74]

Slide94

Psychological or Medical Stress: Endocrine ResponseChronic “Submit and Stay” Response

(Increased hypothalamic pituitary axis activity)

Increased Longer-term Stress Hormone Release

Increased corticotropin-releasing hormoneIncreased adrenocorticotropinIncreased arginine, vasopressin, and oxytocin

Increased blood cortisol

Metabolic Responses to

Increased Cortisol

Potential increase in glucose levels (increased insulin resistance and increased hepatic gluconeogenesis)

Increased blood pressure

Increased adipose tissue lipolysis (cortisol is a catabolic hormone)

Reference/s: [71] [72] [73] [74] [75]

Slide95

Medical or Psychological Stress: Immune Response

Acute Response

(Catecholamine-mediated)

Immune effects can be mixed, but in general, may enhance immune response:Demargination of leukocytes from vascular endothelia increases leukocyte blood concentrationIncreased:Innate immune response

Adaptive immune response

T-lymphocyte cytokine response

Prolonged Response

(Glucocorticoid-mediated)

Immune effects can be mixed, but in general, may dysregulate immune response:

Decreased leukocyte mobilization with decrease in leukocyte blood concentration

Decreased:

Innate immune response

Adaptive immune response

T-lymphocyte cytokine response

Reference/s: [71] [72] [73] [74] [76]

Slide96

Enhanced desire for hyperpalatable foods

Chronic Psychological Stress and Eating Behavior

Limbic System

(Thalamus, hypothalamus, amygdala, hippocampus)

Chronic stress-induced endocrinopathies and immunopathies may adversely affect the limbic system

Hypothalamic dysfunction (such as with trauma) is an important cause of obesity

Cerebrum

(Frontal, parietal, occipital, and temporal lobes)

Priority replacement: personal, work, or emotional priorities may overtake priorities relative to nutrition, physical activity, and/or health

Chronic stress-induced endocrinopathies and immunopathies may adversely affect the cerebrum

Gourmand Syndrome

While not necessarily a stress disorder, Gourmand Syndrome is illustrative of how cerebral disorders may affect eating behaviors

Occurs with damage to right frontal lobe (trauma/stroke)

Post-injury passion for gourmet foods

Reference/s: [71] [72] [73] [74]

Slide97

Adiposopathy Stress Cycle

Reference/s: [1]

Slide98

Patient Evaluation: History

Slide99

HistoryMedical History and Review of SystemsAge, gender, race, ethnicity

Fat mass disease (i.e., osteoarthritis, sleep apnea)

Adiposopathy (i.e., type 2 diabetes mellitus, high blood pressure)

Eating disordersMental stressSleep patternOther medical and surgical conditionsMedication and food allergies Medications that may affect body weightCigarette smokingAlcohol intake

Recreational drug use (e.g., marijuana, cocaine)

Family History

Family members affected by obesity

Applicable familial medical diseases

Support Systems

Person who selects and purchases food

Availability and involvement of family and friends

Educational access to healthy nutrition and physical activity (e.g., current knowledgebase, availability of Internet, knowledge centers, etc.)

Socioeconomic and Cultural History

Economic status

Social status

Cultural background

Occupation

Family structure

Parenting behavior

Marital status

Living situation

Abuse (physical, mental, sexual)

Geographic location (e.g., urban food desert)

Reference/s: [77]

Slide100

Nutrition History

Meals and Snacks

Timing

Frequency (via questionnaire)Nutritional contentPreparer of foodAccess to foodsLocation of home food consumption (i.e., eating area, television, computer, etc.)

Location of away food consumption (i.e., workplace restaurants, fast food, etc.)

Behavior

Previous nutritional attempts to lose weight and/or change body composition

If unsuccessful or un-sustained, what were short- and long-term barriers to achieving or maintaining fat weight loss

Triggers (hunger, cravings, anxiety, boredom, reward, etc.)

Nighttime eating

Binge eating

Emotional eating

Family/cultural influences

Community influences

Readiness for change

Records

Food and beverage diary, including type of food or beverage consumed and amount consumed

72-hour recall

Keep food and beverage record for a week and return for evaluation

Electronic application tools

Reference/s: [78] [79] [80]

Slide101

Physical Activity HistorySuccess and/or failure of previous physical activity/exercise effortsIf no longer engaged in a routine physical activity/exercise regimen:

When? (Date of change)

What? (Cause of change)

Why? (Identify barriers to re-engagement)Current physical activity (FITTE)FrequencyIntensityTime or DurationTypeEnjoyment (physical activity/exercise preferences) Current fitness level, endurance capacity, mobility, and equipment needsAccess to locations amenable to increased physical activity/exercise (e.g., gym, workplace, exercise facilities, bicycle paths and walk ways, urban or rural home setting) Perceived barriers to increased physical activity

Reference/s: [81] [82] [83]

Slide102

Physical Activity HistoryExamples of common medical conditions that should be evaluated before prescribing an exercise program:Diseases of the heart, lung, musculoskeletal, and other body systems

Metabolic diseases having potential risks with increased physical activity:

Atherosclerotic coronary heart disease (worsening ischemia)

Reference/s: [81] [82] [83]

Slide103

Routine Preventive Medical CareEnsure individuals with overweight or obesity receive standard preventive medical care, which, depending upon gender and age, may include:

Breast cancer screening

Pelvic exam & pap smear screening

Reference/s: [5]

Slide104

Patient Evaluation: Physical Exam

Slide105

Physical ExamVital SignsHeight with bare or stocking feet measured with a stadiometer

Weight using calibrated scale and method consistent from visit to visit (i.e., light indoor clothing or gown)

Body mass index

Waist circumferenceStanding using superior iliac crestMay not provide additional diagnostic information among patients with BMI > 35 kg/m2Blood pressure using appropriately sized cuff Pulse Neck circumference General Physical Exam

Comprehensive physical exam

Special emphasis on physical exam of the nose, throat, neck, lung, heart, abdomen, musculoskeletal system, and integument

Reference/s: [84]

Slide106

Patient Evaluation: Laboratory and Diagnostic Testing

Slide107

Laboratory: Routine Adiposity-relevant Blood TestingFasting blood glucose

Hemoglobin A1c

Fasting lipid levels

TriglyceridesLow-density lipoprotein (LDL) cholesterolHigh-density lipoprotein (HDL) cholesterolNon-HDL cholesterolLiver enzymes and other liver blood testsAspartate aminotransferase (AST)Alanine aminotransferase (ALT)

Alkaline phosphatase

Total bilirubin

Electrolytes (i.e., potassium, sodium, calcium, phosphorous, etc.)

Renal blood testing (i.e., creatinine, blood urea nitrogen, etc.)

Uric acid

Thyroid stimulating hormone (TSH)

Vitamin D levels

General Laboratory Testing

Complete blood count

Urinalysis

Urine for microalbumin

Reference/s: [84] [85]

Slide108

Glucose tolerance testingFasting insulin testing Fasting proinsulin, C-peptide, and insulin if hyperinsulinemia is suspected as a secondary cause of obesity (e.g. insulinoma, nesidioblastosis, etc.)

One milligram (mg) overnight dexamethasone cortisol suppression test, 24-hour urine collection for (free) cortisol, or repeated measures salivary cortisol collection at 11:00 PM if endogenous hypercortisolism is suspected as a secondary cause of obesity

Prolactin, estradiol, follicle-stimulating hormone, luteinizing hormone, and pregnancy test in women with unexplained oligomenorrhea or amenorrhea

Testosterone and other androgen levels (i.e., dehydroepiandrosterone sulfate/DHEAS) for women with hirsutism or polycystic ovarian syndromeTestosterone (and if low to a clinically significant degree: possibly prolactin, follicle-stimulating hormone, and luteinizing hormone) for men with impotence or physical findings of hypogonadismApolipoprotein B and/or lipoprotein particle number, especially if triglyceride levels are elevatedIron studies (iron, total iron binding capacity, ferritin)High-sensitive C-reactive protein (hs-CRP)Obesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Laboratory: Individualized Blood Testing

Reference/s: [86] [87]

Slide109

Magnetic-resonance imaging or computed tomography of the brain if a structural lesion of the pituitary/hypothalamus is suspected (i.e., craniopharyngioma, pituitary tumor)Resting electrocardiogramCardiac stress testing

Echocardiogram

Coronary calcium scores

Cardiac positron emission tomography imaging (computed tomography)Ankle-brachial index Sleep studiesImaging studies of the liver (i.e., ultrasound)Anaerobic threshold/VO2 testingResting metabolic rate (RMR)Obesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Diagnostic Testing: Individualized

Reference/s: [88] [89] [90]

Slide110

Body Composition

Dual-energy X-ray absorptiometry (

DXA

), ideally with visceral fat assessmentBioelectric impedanceNear-infrared interactanceWhole-body air displacement plethysmography (BOD POD)

Myotape measurements (to assess muscle mass as well as wrist and neck size for use in percent body fat equations)

Caliper percent body fat measurements (e.g., three-site skinfold calculations)

Underwater weighing

Quantitative magnetic resonance (QMR)

Computerized tomography (single slice or volume method)

Deuterium dilution

Emerging Science Testing

Leptin

Adiponectin

Leptin-to-adiponectin ratio

Free fatty acids

Immune markers

Tumor necrosis factor

Interleukin 1 and 6

Infectious testing

Gut microbiota

Adenovirus assays

Evaluation for other microbes

Diagnostic Testing: Individualized

Reference/s: [91] [92] [93] [94] [95]

Slide111

Slide112

Fat free mass

is total body mass less any body fat. It includes:WaterMineralProtein and glycogen

*Usually what is directly measured by two compartment techniques, such as

DXA

Lean body mass

is total body mass less adipose tissue. It includes:

Water

Mineral

Protein and glycogen

Essential fat in organs, central nervous system, and bone marrow

*Usually differs from fat-free mass by only ~5%, slightly less in men, slightly more in women)

Body Compartments: Fat-free Mass versus Lean Body Mass

Reference/s: [93] [96] [97] [98]

Slide113

Three Compartment:

Fat mass

Total body waterFat-free dry mass (bone and protein)

(Although

DXA

measures two compartments at a time, it can assess the “three compartments” of fat mass, lean soft tissue mass, and bone mineral mass. Similarly, assuming total body water is a constant proportion of fat free mass may allow BIA to estimate more compartments (e.g., fat free mass, fat mass, and total body water)

Two Compartment:

Fat mass

Fat-free mass

Can be assessed by:

Dual-energy x-ray absorptiometry (

DXA

)

Underwater, or hydrostatic weighing

Air displacement plethysmography (BOD POD)

Bioelectrical impedance (BIA)

Skin fold thickness-derived calculations

Deuterium dilution

Four Compartment:

Fat mass

Total body water

Bone mineral

Protein

Can be assessed by combination of two compartment assessments, such as hydrostatic weighing, plus dual-energy x-ray absorptiometry (

DXA

), plus deuterium dilution or hydrostatic weighing, plus

DXA, plus bioimpedance spectroscopySix Compartment:Fat massTotal body waterBone mineralNon-Bone mineralProteinGlycogenFat mass = stored and essential lipidsWater = usually largest single component of body mass~55% intracellular~45% extracellularMinerals = calcium, phosphorous, magnesium, etc.Protein & glycogen = “residual”Body CompartmentsReference/s: [99] [100]

Slide114

Method

Accuracy*

ExpenseLimitations

Calipers

User dependent

Inexpensive

Not

optimal measuring technique for patients with very high body mass index

Dual-energy X-ray absorptiometry (

DXA

)

Accurate

Relatively expensive

Not

all

DXA

(1)

distinguish visceral versus subcutaneous fat, or (2) accommodate patients with very high

body mass index

Air displacement (BOD POD)

Accurate with some potential variability

Inexpensive

Clothing and hydration dependent

Bioelectrical impedance

Accurate

with some potential

variabilityInexpensiveHydration dependentUnder water weighing densitometryAccurateRelatively inexpensiveTime consuming, requires water submersion, and depends upon adequate lung exhalationComputerized Tomography / Magnetic Resonance ImagingAccurate ExpensiveNot all CT & MRI can accommodate individuals with very high body mass indexDeuterium dilution hydrometryAccurateRelatively inexpensiveNot readily available for commercial use*The accuracy of all methods depends on the degree of training, and quality of equipment. Body Compartments: Measurement SummaryReference/s: [101]

Slide115

Cadaver analysis

is the only true “gold standard” for body composition assessment

Body weight or body mass index are not direct measures of body compositionSkinfold calipers can be used to estimate proportion of body fat

Hydrodensitometry (underwater weighing)

estimates proportion of body fat based upon the Archimedes principle that the buoyant force of a body immersed in fluid is equal to the weight of the displaced fluid.

Lean tissues (bone and muscle) are more dense than water, and a person with more muscle will weigh more underwater

Fat is less dense than water, and a person with more body fat will weigh less underwater

Two-compartment model

Body Compartments: Measurements

Reference/s: [102] [103]

Slide116

Depending on software,

DXA

can measure both body fat and bone-mineral densityLow risk of radiation exposure, ~5% of standard chest X-rayGreatest accuracy and consistency achieved with appropriate user training, same machine, standard operating procedures, and routine calibration

Waist circumference and metabolic risk best correlates to total abdominal fat (intraperitoneal / visceral adipose tissue + abdominal subcutaneous adipose tissue)

DXA

can measure abdominal visceral fat (intraabdominal fat around body organs) and android fat (total abdominal fat = visceral adipose tissue + abdominal subcutaneous adipose tissue)

Android fat may often be ~ 7 pounds, with >= 3 pounds often associated with being overweight

Visceral fat may often be ~ 3 pounds in men and ~ 2 pounds in women

Best to have minimal visceral fat, such as <= 1 pound in men, and <= 0.5 pounds in women. Values above these are often associated with being overweight

Body Compartments: Dual Energy X-Ray Absorptiometry (

DXA

)

Reference/s: [96] [104]

Slide117

Monoenergetic X-Ray measures an homogenous absorber component

Dual-energy X-Ray quantitates densities of two absorber components

In body areas with no bone, DXA can measure the “two compartments” of fat mass and lean soft tissue mass

In body areas with bone,

DXA

can measure the “two compartments” of soft tissue mass and bone mineral mass

By combining these two analyses,

DXA

can provide data regarding three compartments (fat, lean tissue, and bone)

Body Compartments: Dual Energy X-Ray Absorptiometry (

DXA

)

Reference/s: [96] [104]

Slide118

DXA

assessment of bone provides results having established ranges applicable to osteoporosis risk (e.g., T and Z scores)

About 60% of body weight is water; approximately:75% of muscle and body organs are water30% of bone is water & 70% mineral salts and collagen

Regarding dry skeletal weight, 65% is hydroxyapatite (mainly calcium/phosphorous) and 35% organic protein matrix (mostly type 1 collagen)

DXA

Bone Mineral Content (BMC) is mineral content of bone (e.g., mainly calcium and phosphorous), and is typically about 5 pounds

Ash body weight is mainly bone mineral calcium and phosphate residual (approximately 5 – 10 pounds)

Body Compartments: Dual Energy X-Ray Absorptiometry (

DXA

)

Reference/s: [105] [106]

Slide119

Many

DXA

assessments of muscle have values without “normal ranges”Lean body mass and fat composition are widely variable between individuals based upon genetics, gender, race, age, nutrition and physical activityIn general, lean body mass is 75% of total body mass (40% muscle, 10% bone, and 25% organs)

Fat may be around 25% of total body mass, although percent body fat may be as high as > 70%

While variable among individuals and not intended to represent absolute values:

Mean fat-free lean mass of men athletes can be approximately 130 pounds

Mean fat-free lean mass of women athletes can be approximately 110 pounds

Men athletes often have approximately 10% body fat (7 kg or 15 pounds of fat for a man weighing 70 kg or 154 pounds) - some have less

Women athletes often have approximately

% body fat (6 kg or 26 pounds of fat for a woman weighing 60 kg or 132 pounds) – some have less

Body Compartments: Dual Energy X-Ray Absorptiometry (

DXA

)

Reference/s: [107]

Slide120

Plethusmos = Greek for enlargement

Measures body volume by air displacement

Displacement principles similar to water displacement by hydrodensitometry weighingNo strenuous exercise two hours before procedureNo eating or drinking one hour before procedure

Light clothing (tight swimsuit is preferred)

Two-compartment model

Body Compartments: Whole Body Plethysmography (BOD POD)

Reference/s: [91] [108] [109]

Slide121

BIA measures impedance by body tissues to flow of electrical current (electrical resistance = impedance)

Electrical current passes more easily through water and muscle and less easily through fat

Many BIA analyses assume fat-free mass has a constant proportion of water (~70%)Preparation: remove all metal, eliminate body waste prior to procedure, and avoid exercise causing sweat eight hours before, avoid large amounts of caffeine or alcohol 12 hours before

While often considered a two-compartment model (fat versus fat-free mass), the assumption that total body water is a constant proportion of fat-free mass may allow estimation of more compartments (e.g., fat-free mass, fat mass, and total body water)

Body Compartments: Bioelectrical Impedance Analysis (BIA)

Reference/s: [110] [111]

Slide122

In adults, intra and extracellular water constitutes ~70% of Fat Free Mass (FFM)

With an estimate of total body water (TBW), the amount of Fat Mass can, in turn, be estimated via Body Mass minus FFM

Deuterium is a stable (non-radioactive) isotope of hydrogen (2H), administered as deuterium oxide (2

After mixing with body water, deuterium is eliminated from the body in urine, saliva, sweat and human milk

One technique is to collect post-dose saliva samples 3 and 4 hours after the deuterium oxide is administered

While correction is required for some deuterium that distributes to non aqueous tissues, TBW (kg) can be calculated by the dose of

O (mg) /

H in saliva (mg/kg) less baseline (pre-dose)

Two-compartment model

Body Compartments: Deuterium Dilution

Reference/s: [112]

Slide123

Both computerized tomography (CT) and magnetic resonance imaging (MRI) accurately measure adipose tissue and skeletal muscle

CT increases exposure to ionizing radiation, a potential clinical concern with repeat CT testing

MRI = No radiation exposureBoth CT and MRI accurately assess visceral and hepatic fatBody Compartments: CT and MRI

Reference/s: [113] [114] [115]

Slide124

Slide125

Energy Expenditure: Components Overall

In moderately sedentary individuals, components of total energy expenditure:

70% resting metabolic rate20% physical activity 10% dietary thermogenesis

Reference/s: [116]

Slide126

Energy Expenditure: Component Variability

With the exception of individuals engaged in physical exercise outside typical study populations, the coefficient of variation in humans regarding energy expenditure:

Resting metabolic rate = 5 – 10%Physical exercise = 1 – 2%Diet-induced thermogenesis = 20%

Reference/s: [117]

Slide127

Energy Expenditure: Component of NEAT

Often the widest variance in energy expenditure among individuals is non-exercise activity thermogenesis (NEAT)

Working, fidgeting, and other activities of daily living, not including physical exerciseCan range between 150-500 kcal/day, which is often greater than bouts of physical exerciseNEAT can help explain perception that some individuals:Are “naturally skinny”

Can maintain body weight compared to others, even with the same caloric intake and same exercise activity

Reference/s: [118]

Slide128

Energy Expenditure: Component of NEAT

Increasing the number of steps taken per day can be achieved by altering daily activity, or by increasing walking/running.

Compared to being seated for hours (such as in the workplace), it is better to walk around at least 10 minutes per hour.Take stairs instead of elevators; park further from your destination, etc.Monitor number of steps per day via a pedometer:

The number of steps recorded by different pedometers can vary

< 5000 steps per day is average number of steps for US adults

< 5000 steps per day is sedentary

5000-7500 steps per day is low active

7500-10,000 steps per day is somewhat active

~10,000 steps per day is active

Although variable due to a number of factors, in general, one calorie is “burned” for every 20 steps (i.e., 3000 steps / 20 = 150 calories)

10,000 steps per day per week = 3500 calories “burned” = one pound of fat

Reference/s: [119]

Slide129

Basal Metabolic Rate

Energy expended while fasting, rested, and supine in a thermoneutral environment

Increased with increased body weight

Resting Metabolic Rate (

RMR

)

Energy expended at rest, does not require overnight supine measurement

Increased with increased body weight

For most individuals:

Muscle accounts for < 25% of

RMR

Liver and brain accounts for ~ 50% of

RMR

Energy Expenditure: Metabolic Rate

Reference/s: [120] [121] [122] [123]

Slide130

Direct Calorimetry

Measures heat generated by an organism

Measures differences in temperature of water entering and leaving the chamber via a heat exchanger

Value of generated heat can estimate total energy expenditureEnclosed chamber/calorimeter

Indirect Calorimetry

Estimates basal energy expenditure and resting energy expenditure via measuring oxygen consumption and carbon dioxide production

A metabolic cart is an electronic device, typically on a mobile push “cart, ”that measures O

consumption (VO

) and CO

production (VCO

)

Computer system

Monitor

Breathing tubes

Energy Expenditure: Measurement via Direct and Indirect Calorimetry

Reference/s: [111]

Slide131

Total energy expenditure = ~60% from heat + ~40% from ATP production

Utilized by direct calorimetry

Requires knowledge of generated heat, such as through the differences in water temperature entering and leaving a chamberEnergy Expenditure: Direct Calorimetry Formula

Reference/s: [124]

Slide132

Abbreviated Weir equation: Energy expenditure = VO

+ VCO

Energy Expenditure: Indirect Calorimetry Formulas

Utilized by indirect calorimetry

Requires knowledge of:

Oxygen consumption (VO

in - VO

out)

production (expired CO

)

(Nitrogen level for full Weir equation)

Assumes FIO

+ FIN

= 1

Inhaled ambient air = 21% O

+ 79% N

+ less than 1% CO2Reference/s: [125] [126]

Slide133

Respiratory quotient (RQ) = CO

production / O

Utilized by indirect calorimetry to assess proportion of metabolized fuels

RQ for carbohydrates = 1.0

RQ for fats = 0.7

RQ for proteins = variable

Overfeeding = increase in RQ to as high as 1.3 due to lipogenesis

Underfeeding and ketosis = decrease in RQ due to lipolysis

In treating severe chronic obstructive lung disease, increasing the proportion of dietary fats (relative to carbohydrates) decreases CO

production and decreases amount of energy spent on respirations

Higher RQ may be predictive of future increase in fat mass

Reference/s: [125] [126] [127]

Slide134

Measurements

Doubly labeled water is administered orally using traceable hydrogen isotope (deuterium or

2H) and oxygen isotope (18O)The difference found in body fluids (sampling urine, saliva, or blood) is used to calculate the body’s production of CO

over time

Background

Estimates carbon dioxide production, which is reflective of energy expenditure via tissue respiration (carbon dioxide from body cells is exchanged for oxygen in blood)

Oxygen component will decay quicker because oxygen is lost as both CO

(in expired air) + H

O (urine and sweat)

Hydrogen component will decay slower because hydrogen is lost only as H

Energy Expenditure: Measurement by Doubly Labeled Water

Reference/s: [128]

Slide135

Resting metabolic rate energy expenditure

can be estimated by calculations

AgeGenderWeightHeight

Harris-Benedict and Mifflin St. Jeor Equation = age, gender, weight, height

Maintenance of Hemodialysis Energy (MHDE) Equation for dialysis patients

Physical activity energy expenditure

can be estimated by:

Physical activity records as input data to validated energy-expenditure tables

Calculations based on heart rate

Motion sensors (e.g., pedometers)

Accelerometers (uniaxial, bi-axial, tri-axial)

Wearable technologies such as watches or attachment to belt around waist or ankle

Energy Expenditure: Measurement by Non-calorimetric Methods

Reference/s: [125] [129] [130]

Slide136

Slide137

Nutrition

Physical Activity

Behavior Therapy

Pharmacotherapy

Bariatric Surgery

Medical Management and Coordination

Treatment of Adult Patients with Overweight or Obesity

Reference/s: [1]

Slide138

Treat adipocyte and adipose tissue dysfunction, which treats sick fat disease (SFD or adiposopathy)Treat excessive body fat, which treats fat mass disease (FMD)Treating diseases due to increased body fat and its adverse metabolic and biomechanical consequences may improve patient health, quality of life, body weight, and body composition

Treatment of Adult Patients with Overweight or Obesity

Reference/s: [1]

Slide139

Identify and Manage Secondary/Contributing Causes of SFD and FMD

Conditions that may promote fat mass gain:

Genetic Syndromes

Isolated (i.e., Prader Willi)

Familial (melanocortin 4 receptor deficiency)

Medical Conditions

Hypothalamic damage

Immobility

Insulinoma

Some cases of untreated hypothyroidism

Hypercortisolism (Cushing’s disease)

Sleep disorders

Psychological and Behavioral Conditions

Mental stress

Depression

Anxiety

Post-traumatic stress syndrome

Binge-eating disorder

Night-eating syndrome

Eating disorders not otherwise specified

Reference/s: [88] [131] [132]

Slide140

Slide141

Identify and Manage Concomitant Pharmacotherapy That Might Alter Body Weight

Cardiovascular Medications

May increase body weight:

Some beta-blockersPropranololAtenolol

Metoprolol

Older and/or less lipophilic dihydropyridine (“dipine”) calcium channel blockers may increase body weight gain due to edema, compared to non-dihydropyridines and lipophilic dihydropyridines, and the increased edema may exacerbate obesity-related edema (and sleep apnea related peripheral edema), and also confound body weight as a measure of body fat

Nifedipine

Amlodipine

Felodipine

Diabetes Mellitus Medications

May increase body weight:

Most insulins

Sulfonylureas

Thiazolidinediones

Meglitinides

May decrease body weight:

Metformin

Glucagon-like peptide-1 agonists

Sodium glucose co-transporter 2 inhibitors

Alpha glucosidase inhibitors

Reference/s: [15] [31] [133] [134]

Slide142

MetforminMay help improve adiposopathic disorders: Insulin resistance

Polycystic ovarian syndrome

Fatty liver

Cardiovascular disease (especially when compared to sulfonylurea)May help treat complications of other concurrent drug treatments:Antipsychotic-related weight gain Human immunodeficiency virus (HIV) protease inhibitor-associated abnormalities (i.e., HIV lipodystrophy)May help reduce the overall cancer rate and help improve the treatment of multiple cancers:ColonOvaryLung

Breast

Prostate

May reduce appetite with via multifactorial effects, such as enhancing the effects of gastrointestinal hormones applicable to weight loss (e.g., glucagon-like peptide-1, Peptide

)

In addition to improving insulin sensitivity, metformin may also improve leptin sensitivity, reduce neuropeptide Y levels, and increase glucagon like peptide-1 (GLP-1) activity (i.e., increased GLP-1 levels and receptors).

Reference/s: [135] [136] [137] [138] [139]

Slide143

Identify and Manage Concomitant Pharmacotherapy That Might Alter Body Weight

Hormones

May increase body weight:

GlucocorticoidsEstrogensVariable effects on body weight:

Progestins

Injectable or implantable progestins may have greatest risk for weight gain

May be dependent upon the individual

Testosterone

May reduce percent body fat and increase lean body mass, especially if used to replace testosterone deficiency in men

Anti-seizure Medications

May increase body weight:

Carbamazepine

Gabapentin

Valproate

May decrease body weight:

Lamotrigine

Topiramate

Zonisamide

Reference/s: [133] [140]

Slide144

May increase body weight:Some tricyclic antidepressants (tertiary amines)

Amitriptyline

Doxepin

ImipramineSome selective serotonin reuptake inhibitors (e.g. paroxetine)Some irreversible monoamine oxidase inhibitorsIsocarboxazid PhenelzineMirtazapine May decrease body weight:Bupropion

Variable effects on body weight:

Some tricyclic antidepressants (secondary amines)

Desipramine

Nortriptyline

Protriptyline

Some selective serotonin reuptake inhibitors

Citalopram

Escitalopram

Fluoxetine

Sertraline

Some serotonin and norepinephrine re-uptake inhibitors

Desvenlafaxine

Duloxetine

Venlafaxine

Some irreversible monoamine oxidase inhibitors (i.e., tranylcypromine)

Identify and Manage Concomitant Pharmacotherapy That Might Alter Body Weight

Reference/s: [133] [141] [142] [143]

Slide145

Identify and Manage Concomitant Pharmacotherapy That Might Alter Body Weight

Mood Stabilizers

May increase body weight:

GabapentinLithiumValproateVigabatrin

Variable/neutral effects on body weight:

Carbamazepine (sometimes reported to increase body weight)

Lamotrigine (sometimes reported to decrease body weight)

Oxcarbazepine

Migraine Medications

May increase body weight:

Amitriptyline

Gabapentin

Paroxetine

Valproic acid

Some beta-blockers

May decrease body weight:

Topiramate

Reference/s: [133] [141] [142] [143]

Slide146

Identify and Manage Concomitant Pharmacotherapy That Might Alter Body Weight

Antipsychotics

May somewhat increase body weight:

Asenapine

Chlorpromazine

Iloperidone

Paliperidone

Quetiapine

Risperidone

Sertindole

Lithium

May substantially increase body weight:

Clozapine

Olanzapine

Zotepine

Variable/neutral effects on body weight:

Amisulpride

Aripiprazole

Haloperidol

Lurasidone

Ziprasidone

Hypnotics

May have limited effects on body weight:

Benzodiazepines

Melatonergic hypnotics

Trazodone

May increase body weight:DiphenhydramineReference/s: [133] [141] [142] [143]

Slide147

Identify and Manage Concomitant Pharmacotherapy That Might Alter Body Weight

Human Immunodeficiency

Virus (HIV) Medications

May increase body weight:Some highly active antiretroviral therapies (HAART) protease inhibitors without HIV lipodystrophyMay decrease body weight:

Some highly active antiretroviral therapies (HAART) protease inhibitors with HIV lipodystrophy

Chemotherapies

May increase body weight:

Tamoxifen

Cyclophosphamide

Methotrexate

5-fluorouracil

Aromatase inhibitors

Corticosteroids

Reference/s: [133] [144] [145]

Slide148

Slide149

General NutritionThe principles outlined here pertain to general nutrition and may not apply to the individual patient.

Slide150

CarbohydratesCarbohydrates contain 4 kcal/gramCarbohydrates can serve as a source of energy and as well cellular structural elements such as hyaluronic acid and proteoglycans

Carbohydrates may contain sugars, starch and/or fiber

The digestion and absorption of carbohydrates results in monosaccharide (glucose, fructose, galactose) molecules

Carbohydrates are not an essential macronutrient, as the liver and kidney can synthesize glucoseCalorie deficiency can lead to marasmus (insufficient calories), but there is no known carbohydrate deficiencyUSDA DRI for carbohydrate is 130 grams/dayObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [146]

Slide151

Fat contains 9 kcal/gramFats or lipids are a diverse group of compounds used as an energy source and for many metabolic processes: Immune response (omega-3 fatty acids)

Cell membrane structure (phospholipids)

Brain tissue (cerebrosides)

Synthesis of bile acid, cholesterol, vitamin D, steroid hormonesInsulationSeveral fatty acids cannot be made by the body and these “essential” fatty acids must be consumed in the dietFatty acid deficiency can lead to a disease stateUSDA DRI for fat is at least 30 grams/dayReplacing saturated fats with polyunsaturated or monounsaturated fats may reduce cardiovascular disease riskReplacing saturated fats with refined carbohydrates and sugar is not associated with reduced cardiovascular disease riskObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Fat

Reference/s: [146] [147]

Slide152

ProteinProtein contains 4 kcal/gram

Protein contains amino acids and serves as the major structural building blocks of the human body: bone, muscle, skin, brain, nucleic acids

Essential amino acids are those which cannot be made by the human body and must be consumed in the diet

Some amino acids can be used as an energy source (converted to glucose or ketones when needed)Protein deficiency can lead to a disease state (Kwashiorkor is sufficient calories but insufficient protein)USDA DRI (Dietary Reference Intake) for protein is 0.8 to 2.0 grams/kg/day depending upon age, gender, physical activity

Reference/s: [146]

Slide153

Insulin Controls Fat MetabolismInsulin promotes fatty acid and triglyceride synthesis (lipogenesis) and storage, and it inhibits fat breakdown (lipolysis)

Foods that cause a rise in blood glucose, such as sugars, starches, or amino acids will stimulate the secretion of insulin from the pancreas

A diet that lowers the amount of insulin secreted is beneficial for weight loss

Slide154

Slide155

Principles of Healthy NutritionLimit:Highly processed foods of minimum nutritional value: sweets, “junk foods,” cakes, cookies, candy, pies, chips

Energy-dense beverages: sugar-sweetened beverages, juice, cream

Encourage:

Consumption of healthy proteins and fats, vegetables, leafy greens, fruits, berries, nuts, legumes, whole grainsComplex carbohydrates over simple sugars: Low glycemic index over high glycemic index foodsHigh-fiber foods over low-fiber foodsReading labels rather than marketing claimsManaging the quality of calories is important when reducing the quantity of calories, such as during weight loss.

Reference/s: [1] [148]

Slide156

Nutritional Therapy for Obesity

Evidence-based

Quantitative

QualitativePatient preference

Patient adherence

Factors related to improved outcomes:

Reference/s: [1]

Slide157

Choosing Nutritional Therapy for ObesityEncourage foods that result in a negative caloric balance to achieve and maintain a healthy weight

Consider the following:

Individual food preferences, eating behaviors, and meal patterns

Cultural background, traditions, and food availabilityTime constraints and financial issuesNutritional knowledge and cooking skillsThe most appropriate nutritional therapy for weight loss should be safe, effective, and one to which the patient can adhere.

Reference/s: [1]

Slide158

Choosing Nutritional Therapy for ObesityNutritional approaches for weight loss typically focus on the caloric manipulation of the three macronutrients: carbohydrate, fat, or protein

Very low-calorie diets contain less than 800 kcal/day and require close medical supervision for safety reasons

Low calorie diets range from 1200-1800 kcal/day (1200-1500 for women, 1500-1800 for men)

Restricting dietary fat leads to a greater reduction in total and LDL cholesterol, whereas restricting dietary carbohydrate leads to a greater reduction in serum triglycerides and an increase in HDL-cholesterolReduction of carbohydrates can lead to a greater reduction in serum glucose and hemoglobin A1CObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [1]

Slide159

Nutritional Therapy for Obesity

Reference/s: [149] [150] [151] [152]

Slide160

Low-calorie Diets: Restricted-carbohydrate DietWeight LossMay produce modestly greater weight loss compared to fat-restricted dietary intake for the first 6 months, wherein afterwards, the net weight loss may be similar to other calorie restricted nutritional interventions

May assist with reducing food cravings

Metabolic Effects

Reduces fasting glucose, insulin and triglycerides Modestly increases high-density lipoprotein cholesterol levelsMay increase low-density lipoprotein cholesterol levelsMay modestly reduce blood pressureThe metabolic effects noted above may occur with or without weight lossIn patients with epilepsy, a very low carbohydrate ketogenic diet (VLCKD) may reduce seizuresLCKD may possibly improve diabetes mellitus complications (i.e., nephropathy)

Risks

May produce carbohydrate cravings within the first few days of implementation, which may be mitigated by adding low-glycemic-index carbohydrate foods

May induce gout flare if history of gout

May present challenges in patients undergoing dietary protein restriction (severe kidney disease)

Low-carbohydrate diet defined as 50-150 grams of carbohydrates per day.

Very low-carbohydrate diet defined as <50 grams of carbohydrates per day.

Reference/s: [153] [154] [155] [156] [157] [158]

Slide161

Low-calorie Diets: Restricted-fat DietWeight LossAfter six months, fat-restrictive, low-calorie nutritional intervention generally produces the same amount of weight loss compared to the “low-carb diet”

Metabolic Effects

May reduce fasting glucose and insulin levels

Modestly decreases low-density and high-density lipoprotein cholesterol levelsMay modestly reduce blood pressureRisksHunger control may present challenges, which may be mitigated with weight-management pharmacotherapy If fat restriction results in a substantial increase in carbohydrate consumption, and if weight loss is not achieved, an increase in carbohydrate dietary intake may potentially contribute to hyperglycemia, hyperinsulinemia, hypertriglyceridemia, and reduced levels of high-density lipoprotein cholesterol

Defined as 10-30% of total calories from fat.

Reference/s: [159] [160]

Slide162

Very Low-calorie DietsWeight LossProduces more rapid weight loss than low calorie (low-fat or carbohydrate restricted) diets due to the lower energy intake

Metabolic Effects

Reduces fasting glucose, insulin and triglycerides May modestly increase high-density lipoprotein cholesterol levelsMay modestly decrease low-density lipoprotein cholesterolReduces blood pressureRisksFatigue, nausea, constipation, diarrhea, hair loss, and brittle nailsCold intolerance, dysmenorrheaSmall increase in gallstones, kidney stones, gout flare

If insufficient mineral intake, then may predispose to palpitations and cardiac dysrhythmias, muscle cramps

Weight regain

will

occur if patients are not taught how to maintain healthy eating when transitioning

to non-meal replacement

Defined as less than 800 kcal/day, typically implemented utilizing specifically formulated meal-replacement products

supervised by a trained clinician.

Reference/s: [161] [162]

Slide163

Dietary PatternsMediterranean diet

Therapeutic lifestyle diet

DASH (Dietary Approaches to Stop Hypertension)

Atkins dietOrnish dietPaleo dietVegetarian dietCommercial diet programs

Includes many dietary patterns but must be calorically restricted to effectively treat obesity.

Weight loss and metabolic effects vary.

Slide164

Partially hydrogenated vegetable oils were developed because they favorably affected taste in applicable foods and were less expensive than saturated fats from animals (lard)Some early shortenings (fats) were made from partially hydrogenated vegetable oil (cottonseed and soybean oil), originally contained 50% trans fats, and were marketed as being a healthier alternative to animal fat, because they were derived from “vegetables”

Although it contains partially hydrogenated palm and soybean oils, common shortenings now contain minimal trans fats, soybean oil, fully hydrogenated palm oil (i.e., 3 grams saturated fats, 6 grams polyunsaturated fats, 2.5 monounsaturated fats)

Trans fats may increase low-density lipoprotein cholesterol, reduce high-density lipoprotein cholesterol, and increase the risk of cardiovascular disease (myocardial infarction and stroke), type 2 diabetes mellitus, and certain cancers

While the FDA has banned partially hydrogenated oil by 2018, trans fats can still be found in some cakes, pies, cookies (especially with frosting), biscuits, microwavable breakfasts, stick margarine, crackers, microwave popcorn, cream-filled candies, doughnuts, fried fast foods, and frozen pizzaConjugated linoleic acid (CLA) is a naturally occurring trans fat derived from ruminants (fermentation of plant-based foods via microbes in the stomach prior to digestion) which is not proven to be detrimental to health; conjugated trans linkages are not included as trans fats for nutritional regulations and food labeling

Trans fats are created through a process of artificially hydrogenating polyunsaturated fats (vegetable oils) into more saturated fats, allowing for higher melting temperatures more desirable for processed foods, cooking and frying.

Trans Fats

Reference/s: [163] [164] [165]

Slide165

The Mediterranean Diet is not a defined “diet,” but rather a generalized term to described several meal pattern variants often found in Greece, Italy, and Spain. The Mediterranean Diet has the most consistent and robust scientific support in reducing atherosclerotic cardiovascular disease risk.

Encouraged

Olive oil as main source of fat

Vegetables, fruit, legumes, whole grains, nuts, and seeds

Moderate intake of red wine

Moderate consumption of seafood, fermented dairy products (cheese and yogurt), poultry, and eggs

Discouraged

Limit consumption of high amounts of red meat, meat products, and sweets*

*Olive oil is a staple of most definitions of the Mediterranean diet; however, some Mediterranean cuisine includes lard and butter for cooking, and olive oil for dressing salads and vegetables

Mediterranean

Diet

Reference/s: [166] [167] [168] [169]

Slide166

The TLC Diet is a low-fat meal-plan variant that was recommended by the National Cholesterol Education Program, Adult Treatment Panel. It is the “diet” most often utilized in the conduct of lipid clinical trials.

Encouraged

Total fat: 25–35% of daily calories

Polyunsaturated fat: Up to 10% of total daily calories

Monounsaturated fat: Up to 20% of total daily calories

Carbohydrate: 50% to 60% of total calories

Soluble fiber: At least 5-10 grams a day, preferably 10-25 grams a day

2 grams per day of plant stanols or sterols through foods or dietary supplements

Discouraged

Limit saturated fat: < 7% of total calories

Limit cholesterol: < 200 mg a day

Avoid foods with

trans

fatty acids.

Therapeutic Lifestyle Change Diet (TLC)

Reference/s: [170] [171] [172]

Slide167

The Atkins Diet is illustrative of a carbohydrate-restricted nutritional intervention which promotes utilization of fat for energy and generates ketosis, which may reduce appetite.

Encouraged

The induction phase allows no more than 20 grams of carbohydrate per day from non-starchy vegetables and leafy greens; encourages adequate proteins from foods such as beef, pork, bacon, fish, chicken, eggs, and cheese, to reduce insulin levels and generate ketosis.

The ongoing weight loss phase

allows a wider variety of vegetables, seeds and nuts, and low-glycemic fruits (i.e., strawberries and blueberries).

The pre-maintenance phase

, after the goal weight is achieved, allows carbohydrate intake to be slowly increased as long as weight gain does not occur.

In the maintenance phase,

60 to 90 grams of carbohydrates per day is allowed, which may allow legumes, whole grains, and fruits.

All phases encourage a balance of saturated, monounsaturated, and polyunsaturated fatty acids.

Discouraged

Avoid:

Processed and refined foods

Foods with a high glycemic index

Foods rich in

trans

fatty acids

In all but the maintenance phase, limit:

Cereals, breads, and grains

Dairy products, except cheese

Starchy vegetables

Most fruits

Atkins Diet

Reference/s: [173] [174] [175]

Slide168

The Ornish Diet is illustrative of a fat-restricted nutritional intervention.

Encouraged

Foods are best eaten in their natural form

Vegetables, fruits, whole grains, and legumes

One serving of a soy product each day

Limited amounts of green tea

Fish oil 3-4 grams each day

Small meals eaten frequently throughout the day

Discouraged

Limit dietary fat: < 10% of total daily calories

Limit dietary cholesterol:

10 mg per day

Limit sugar, sodium, and alcohol

Avoid animal products (red meat, poultry, and fish) and caffeine (except green tea)

Avoid foods with

trans

fatty acids, including vegetable shortening, stick margarines, and commercially prepared foods, such as frostings; cake, cookie, and biscuit mixes; crackers and microwave popcorn; and deep-fried foods

Avoid refined carbohydrates and oils

Ornish

Diet

Reference/s: [176] [177] [178]

Slide169

The “Dietary Approaches to Stop Hypertension” (DASH) is a diet pattern promoted by the U.S. National Heart Lung and Blood Institute, primarily to treat high blood pressure.

Encouraged

Vegetables, fruits, and whole grains

Fat-free or low-fat dairy products

Fish, poultry, and lean meats

Nuts, seeds, and legumes

Fiber and the minerals calcium, potassium, and magnesium

Discouraged

Limit sodium: 1,500-2,300 mg per day

Limit total fat: ~27% of total daily calories

Limit saturated fat: <6% of total daily calories

Limit cholesterol:

150 mg per day for a 2,100-calorie eating plan

Avoid red and processed meats

Avoid sugar-sweetened beverages

Avoid foods with added sugars

DASH

Diet

Reference/s: [179] [180]

Slide170

Paleolithic nutritional intervention is based upon a diet pattern presumed to exist during the Paleolithic period (lasting 3.4 million years, and ending 6000-2000 BC). It differs from some other diets in that it excludes grains, dairy, and processed foods.

Encouraged

Fresh vegetables, fruits, and root vegetables

Grass-fed lean red meats

Fish/seafood

Eggs

Nuts and seeds

Healthful oils (olive, walnut, flaxseed, macadamia, avocado, and coconut)

Discouraged

Avoid:

Cereal grains

Legumes, including peanuts

Dairy products

Potatoes

Processed foods

Refined sugar, refined vegetable oils, and salt

Paleolithic Diet

Reference/s: [181] [182] [183]

Slide171

A vegetarian nutritional intervention includes a meal plan consisting of foods that come mostly from plants.

Encouraged

Vegetables

Fruits

Whole grains

Legumes

Seeds

Nuts

May include eggs and milk

Discouraged

Fowl

Fish

Beef

Pork

Lamb

Vegetarian Diet

Reference/s: [184] [185]

Slide172

Vegan (“Total Vegetarian”)

: Only plant-based foods (e.g., fruits, vegetables, legumes, grains, seeds, and nuts) with no animal proteins or animal by-products, such as eggs, milk, or honey

Lacto-vegetarian

: Plant foods plus some or all dairy products (e.g., cheese)Lacto-ovo Vegetarian (or Ovo-lactovegetarian): Plant foods, dairy products, and eggsSemi or Partial Vegetarian: Plant foods and may include chicken or fish, dairy products, and eggs, but not red meat

Pescatarian

: Plant foods and seafood

Vegetarian Diet Variants

Reference/s: [184] [185]

Slide173

Slide174

Physical Activity to Improve HealthAdiposopathy (Sick Fat Disease)Assist with weight maintenance

Assist with weight loss

Improve body composition

Improve adiposopathic psychological disturbances Possibly improve adipocyte function (“train” fat cells)Improve insulin sensitivityIncrease mitochondrial biogenesisIncrease browning (“beiging”) of fat cellsNon-adipose ParametersImprove metabolic healthImprove musculoskeletal healthImprove cardiovascular healthImprove pulmonary health

Improve mental health (e.g., mood, happiness, sense of well-being)

Improve sexual health

Reference/s: [186] [187] [188] [189]

Slide175

Medical Evaluation to Ensure Safety before Beginning New Exercise ProgramAssess current physical activity levelAssess readinessAgree upon patient expectations and goals with written “contract”

Assess potential need for medical testing/evaluation (i.e., cardiac stress testing, pulmonary function tests, musculoskeletal assessment, etc.)

Assess mobility, fitness, and potential equipment needs or modifications

Potential adjustment of medicationsBefore start of physical activity planDuring implementation of physical activity planOptimal defaultBack-up planObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [190]

Slide176

Unable to Walk

Seated exercise program

Arm exercises (i.e., arm cycling)

Swimming/aquatic exercises (e.g., shallow or deep water exercises) Gravity-mediated physical activity Consider physical therapy evaluation

Recommend rehabilitation & physical therapy guided activity program

Set physical activity goals

Assess special equipment needs

Limited Mobility,

Able to Walk

Walking

Swimming/aquatic exercises (e.g., shallow or deep water exercises)

Gravity-mediated physical activity

Assess for special equipment needs

No Substantial Limitations to Mobility

Exercise/physical activity prescription plan driven by patient and guided by clinician

Assess for special equipment needs

Assess Mobility

Reference/s: [191] [192]

Slide177

Priority: Increase Energy ExpenditureDynamic (Aerobic) Training

Some physical activity is better than none

At least 150 minutes (2.5 hours) per week of moderate physical activity or at least 75 minutes (1.25 hours) per week of vigorous intensity aerobic exercise = most health benefits, promote modest weight loss, and prevent weight gain

> 300 minutes (5 hours) per week of moderate physical activity or 150 minutes (2.5 hours) per week of vigorous intensity aerobic exercise = promote more robust weight loss and prevent weight regain after weight lossResistive (Anaerobic) Strength TrainingPercent body fat better assessment of body composition than BMIUtilize appropriate weight-lifting techniqueEmphasize “core” muscle exercisesUsing a variety of free weights, machines, and resistance bands may elicit less boredom and provide greater flexibility regarding scheduling and locationShort-term sore muscles may be expected

Sore joints suggests poor technique, with possible need for medical evaluation and physical activity modification

Prioritize muscle mass metrics (e.g., myotape measurements) versus amount of weight lifted

Reference/s: [193] [194]

Slide178

Leisure Time Physical Activity Engage in competitive sport activities involving substantial physical activity, best if on a routine basisEngage in non-competitive sports such as running, hiking, cycling, cross-fit training, etc.

Outdoor warm-weather physical activity in sunlight may facilitate negative caloric balance and have other health benefits, but need to avoid excessive sun exposure

Engage in physical activity sport-alternatives, such as dancing

Transportational/Occupational Non-exercise Activity Thermogenesis (NEAT)Walk short distances instead of automated transportationTake stairs instead of elevatorCarry overnight travel bags instead of using rollersActive work environment (i.e., standing desks, walking desks)Avoid prolonged inactivityTake breaks from inactivityWalk, stand, incidental movements

Priority: Increase Energy Expenditure and Decrease Sedentary Time

Reference/s: [195] [196]

Slide179

Exercise PrescriptionExercise prescription (FITTE) Frequency

ntensity

Time spentTypeEnjoyment levelExercise prescription (FITT-VP)FrequencyIntensityTime or durationType or mode

olume or total energy expenditure of the exercise

rogression of the exercise

Reference/s: [190] [197]

Slide180

METS are used to assess the intensity of physical exercise: Kcal = METS x weight x timeEqual to the amount of energy expended during one minute while lying down at restEqual to ~3.5 milliliters of oxygen consumption per kilogram of bodyweight per minute (3.5 ml/kg/min)Oxygen consumption may be decreased with increased age

Standing = 2 METS

Walking 4 miles per hour = 4 METS

Slide181

Tracking ProgressDaily activity logs (written or electronic)Pedometer/accelerometer logs

Dynamic training metrics (i.e., miles run, laps swam, etc.)

Resistance training metrics (i.e., muscle-circumference measurements, reps, sets, etc.)

Slide182

Slide183

Motivational Interviewing: Stages of Change

Progress

Reference/s: [204] [205]

Slide184

Motivational Interviewing: FocusCollaborationWorking together to find and implement pragmatic solutions

Not focusing on who is right and who is wrong

Evocation

Drawing out the patient’s thoughts and ideas regarding solutionsNot telling the patient what to do AutonomyEmpowering the patient to own the solutionNot the authoritarian power of the clinician Obesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [206] [207] [208]

Slide185

Motivational Interviewing: Principles

Express empathy

Avoid argumentation

Develop discrepancyResolve ambivalence

Support self-efficacy

Reference/s: [209] [210] [211]

Slide186

CommunicateUnderstand

Collaborate

Support

Reference/s: [209] [212]

Slide187

Types of ResistanceResistance in changing behavior may arise when the patient:

Views the problem or solution differently than the clinician

Feels the clinician is being too judgmental and/or authoritative

Types of resistanceArguingDenyingIgnoringInterruptingRoll with ResistanceRolling with resistance avoids arguments and confrontations by choosing not to challenge patient actions and statements that suggest resistance to changeMay be especially useful during initial interactions with the patientTherapeutic Paradox

Therapeutic paradox is analogous to “reverse psychology,” wherein the clinician makes a statement seemingly in support of no change in hopes the patient will make an argument for change

“It sounds like now is not the best time for you to make changes.”

“You seem to be saying you have a lot going on right now that keeps you from making changes, so what do you think is the best way for us to move forward at this time?”

Avoid Arguments: Resistance

Reference/s: [211] [213]

Slide188

Avoid Arguments: Roll with Resistance ExamplesReflection

Simple reflection:

“You don’t think you can lose weight right now.”

Amplified reflection: “People worry too much about your weight; your current body weight is not really a problem.”Double-sided reflection: “You had previously suggested you were committed to weight loss, but now you no longer feel commitment is necessary.”Shifting Focus“Your conflict with your contractor is obviously stressful to you, but you are a bit ahead of me; I would like for us to go back and talk about what led to your entries in your diet diary.”Reframing “I get the sense that when your family expresses concern about your body weight, they do so in a way that makes you angry. Maybe their intent is not to frustrate you but rather meant to reflect how much they care for you.”

Siding with the Negative

“You previously gave us permission to discuss your body weight. But now you seem resistant to talk about it, much less talk about change. At this point, I am not sure you would be able to change even if you wanted to change.”

Reference/s: [211] [214] [215] [216]

Slide189

Discrepancy and Ambivalence

Identify Discrepancy

Discrepancy explores the mismatch between where patients are today and where they want to be in the future

Contrasts current behavior and life goalsCan involve acknowledging positive and negative aspects of current behavior Can promote motivation for change

Amplify Discrepancy

Amplifying discrepancy can help resolve ambivalence

May facilitate thoughts of change

Resolve Ambivalence

(defined as uncertainty in the desire for change)

Resolution of ambivalence helps facilitate change

Can involve discussing:

Benefits for change

Risks of change

Benefits and risk of no change

Reference/s: [211] [217] [218]

Slide190

Motivational Questioning: Evoking Change-talk ExamplesElicit Talk of Change“Why do you want to change?”

“How important is it that you change?”

“What values are most important to you?”

“How do your actions fit your values?”“How do you plan to change?”“How confident are you that you can change?”Exploring Past and Future“How were things better in the past?”“What may happen if things stay the same?”“How would you like for things to change within the next year?”“What are the best ways for you to change in the next year?”Query Extremes“How accurate is this statement: ‘Some might think your current actions are so important to you that you won’t give them up, no matter what the cost’?”

“What is the worst case scenario if you do not change?”

“What is the best case scenario if you do change?”

Reference/s: [211] [216] [219]

Slide191

Importance of Change“On a scale of 1-10, where one is not important and 10 is most important, how important is it for you to change?”

“Why are you not at a lower/higher number?”

Readiness to Change

“On a scale of 1-10, where one is not ready to change and 10 is absolutely ready to change, how ready are you to change?”“Why are you not at a lower/higher number?”Confidence in Ability to Change“On a scale of 1-10, where one is not at all confident and 10 is absolutely confident, how confident are you in your ability to change?”“Why are you not at a lower/higher number?”

Change Metric Examples

Reference/s: [211] [216]

Slide192

Decision-balancing Examples“Write down some of the good things and bad things about your current eating and physical activity levels.”“It sounds like you enjoy many aspects about what has led to your current body weight, but now you have reasons why this needs to change.”

Reference/s: [211] [216]

Slide193

Supporting Self-efficacyMotivational interviewing assumes the patient is capable of making changeChange is promoted by focusing on past patient successes and highlighting existing patient skills and strengths

“You have lost weight. What do you think were the main things you did to achieve this?”

“How do you feel about your success?”

Affirmation“Your weight loss shows a real commitment toward improving your health.”“It is clear you have made some real changes.”“It seems that despite a lot of things happening, you have managed to stay on course, and that is really impressive.”“Although you have not lost weight, the fact you have returned reflects how serious you are about losing weight.”

Self-efficacy: Affirmation

Reference/s: [211] [220] [221]

Slide194

Self Efficacy: Advice/Feedback and Summary ExamplesAdvice/Feedback“What do you know about how body fat can affect your…?”

Blood sugar/pressure/cholesterol

Heart

BreathingBones and jointsPossible pregnancyQuality of life[Other clinical consequences experienced by the patient]Summary“From what you’ve said, you want to lose weight mainly because you are concerned about your health and because your family is concerned.”“It seems that with your commitment to the weight-management plan, and with support from your family, most everyone agrees that overall you are making great progress.”“Although you had made progress in the past, your weight went up a bit this time. But it is good you did not get so discouraged as to cancel your appointment.”

Reference/s: [221] [222]

Slide195

Motivational Interviewing Techniques: Micro-Counseling (OARS)Open-ended Questions

Avoids binary answers such as “yes” or “no”

Invites expression of elaborative thoughts

May help patient explore reasons for and possibility of changeAffirmationAn expressed recognition of the patient’s strengths and how these strengths can be applied to implement favorable change Affirmations to the patient by the clinician should be: RelevantGenuineReflectionsCareful listening can often be the most effective form of empathy

After careful listening, the clinician is better able to:

Facilitate evocation

Develop discrepancy

Amplify and resolve ambivalence

Offer collaboration

Support self-efficacy

ummaries

Each counseling session should conclude with a summary of:

What was discussed

Shift attention from negative past failures and toward positive but realistic future goals

Establish metrics to measure success of future goals

Outline follow-up plans

Reference/s: [223]

Slide196

Motivational Questioning: General Approach ExamplesOpen-ended Questions

“If you don’t mind, can you tell me why are you here today?”

(Incorporates permission.)

“What do you hope we can accomplish today?”“What do you realistically think we can accomplish today?”Reflective Listening“From what you are telling me, it sounds like you (or your family/friends) want you to lose weight, but you…”“ . . . have concerns.”“ . . . are unsure how.”“ . . . are unsure if you need to.”“ . . . are unsure if you want to.”“ . . . are unsure if you can.”“ . . . are unsure if you are committed to change.”

Normalizing

“While no situation is the same, in general, many people often have problems losing weight.”

“Many people feel like you: they want to lose weight but find it difficult.”

“Many people have repeatedly tried to lose weight in the past before they were finally successful.”

Reference/s: [224] [225]

Slide197

Motivational Interviewing Techniques: 5A’s of Obesity Management

Reference/s: [226] [227]

Slide198

Motivational Interviewing Techniques: FRAMES

eedback about Personal Risk

Responsibility of PatientAdvice to Change

enu of Strategies

mpathetic Style

elf-efficacy

Reference/s: [228] [229]

Slide199

Slide200

Why Do People Eat Like They Do?

Strong biologic forces that resist weight loss

Weak biologic forces that resist weight gain

Hypothalamic dysfunctionTraumaInflammationHunger before mealsLack of satiety after meals

Eating to facilitate sleep

Physiologic

Five senses central nervous system signaling:

Sight of food

Smell of food

Hear talk of food, sounds of food (cooking, wrapper opening)

Taste of food

Feel of lack of food (i.e., vibration of “empty stomach,” borborygmi, texture, size)

Reference/s: [230] [231] [232] [233] [234] [235] [236]

Slide201

Why Do People Eat Like They Do?

Mental Stress

Chronic stress-induced limbic (e.g., hypothalamic) endocrinopathies and immunopathies

Chronic stress-induced cerebral endocrinopathies and immunopathiesChronic stress-induced priority replacement of personal, work, or emotional priorities that overtake nutritional and physical activity priorities

Timing and Emotions

Timing

It’s mealtime

Special occasions

Holidays

Emotions

Surrogate for love and/or affection

For self

For others (children and friends)

Celebrate happiness

Soothe sadness

Avoidance: Cooking or eating can be a successful accomplishment, preferable to more challenging activities or situations

Treat:

Boredom

Fatigue

Stress

Reference/s: [230] [231] [232] [233] [234] [235] [236]

Slide202

Why Do People Eat Like They Do?

Environment

Others are eating

Food is availableOffers of free foodHighly researched and effective advertisements for energy dense foodsPerceived obligationsFamily gatherings

Business meetings

Clean-plate syndrome

Information Gap

Lack of education about proper nutrition

Challenges regarding access to nutritional information, especially when eating out

Caloric content

Nutritional content

Marketing messages

“low fat”

“whole grain”

“no added sugar”

“natural sugar”

“cholesterol free”

Reference/s: [230] [231] [232] [233] [234] [235] [236]

Slide203

Why Do People Eat Like They Do?

Reward

Eating as a remuneration for an accomplishment or “good day”

Eating as compensation for a “bad day”Eating for pleasure, not because of hungerOver-consumption of palatable food may affect the brain’s reward systemStimulates opioid releaseDecreases biologic stress response

May ultimately simulate addiction-like reward deficits, which promotes compulsive eating

Reference/s: [230] [231] [232] [233] [234] [235] [236]

Slide204

Why Do People Eat Like They Do?

Eating Disorders

Binge-eating disorder

Reference/s: [230] [231] [232] [233] [234] [235] [236]

Slide205

Eating Disorders and Obesity: Binge-eating Disorder

Diagnosis:

Frequent episodes of consuming large amounts of food more than once per week for at least three monthsNo self-induced vomiting (purging)No extra exercisingFeelings of lack of self control, shame, and guiltOccurs in 2-3 percent of U.S. adultsOften considered the most common eating disorderMay occur in up to 50 percent of patients with severe obesityEating Attitudes Test may assist with diagnosisTreatment:Often requires treatment by a qualified clinicianCognitive behavior therapyLisdexamfetamine dimesylate is the only pharmacotherapy with an FDA indication to treat binge-eating disorderAlthough not FDA indicated for this use, clinical trials suggest other pharmacotherapies may be efficacious

Some selective serotonin reuptake inhibitors

Topiramate

Reference/s: [237] [238] [239] [240] [241] [242]

Slide206

Lisdexamfetamine dimesylate is a central nervous system stimulant indicated for the treatment of:

Moderate to severe binge-eating disorder (BED)

Attention Deficit Hyperactivity Disorder (ADHD)Limitations: Not indicated for weight loss; safety and effectiveness for the treatment of obesity have not been establishedDrug Enforcement Agency Schedule II drug

Dosing for BED: Once in the morning with or without food. Avoid afternoon doses. Capsule may be opened and mixed with yogurt, water, or orange juice (see drug interactions).

Starting dose = 30 mg every morning for one week

Titration dose = 50 mg every morning for one week

Top dose = 70 mg every morning

Recommended dose = 50-70 mg every morning

Severe renal impairment: Maximum dose is 50 mg per day

End-stage renal disease: Maximum dose is 30 mg per day

Lisdexamfetamine Dimesylate: Indications and Use

Reference/s: [243]

Slide207

Potential Drug Interactions

Agents that alter urinary pH can alter blood levels of amphetamine

Acidifying agents decrease amphetamine blood levels (e.g., ascorbic acid)Alkalinizing agents increase amphetamine blood levels (e.g., sodium bicarbonate)Concurrent administration with monoamine oxidase (MAO) inhibition may contribute to hypertensive crisis PharmacokineticsLisdexamfetamine is rapidly absorbed from the gastrointestinal tract, converted to dextroamphetamine and l-lysine primarily in the blood due to the hydrolytic activity of red blood cellsLisdexamfetamine is not metabolized by cytochrome P450 enzymes

Approximately 96 percent of oral dose radioactivity is recovered in the urine (42 percent related to amphetamine, 25 percent to hippuric acid, and 2 percent to intact lisdexamfetamine)

Plasma elimination half-life is less than one hour

Lisdexamfetamine Dimesylate

Reference/s: [243]

Slide208

Lisdexamfetamine Dimesylate: Potential Adverse ExperiencesMost Common Adverse Reactions:AnorexiaAnxiety

Decreased appetite

Decreased weight

Reference/s: [243]

Slide209

Lisdexamfetamine Dimesylate: Contra-indicationsCentral nervous system stimulants (amphetamines and methylphenidate-containing products), including lisdexamfetamine dimesylate, have high potential for abuse and dependenceRisk of abuse should be assessed prior to prescribing

Patients should be monitored for signs of abuse and dependence while on therapy

Known hypersensitivity (e.g., anaphylactic reactions, Stevens-Johnson Syndrome, angioedema, and urticarial) to amphetamine products or other ingredients in lisdexamfetamine dimesylate

Slide210

Lisdexamfetamine Dimesylate: WarningsSerious cardiovascular reactionsDue to reports of sudden death in children and adolescents with serious heart problems, as well as sudden death, stroke, and myocardial infarction in adults, avoid use in patients with known structural cardiac abnormalities, cardiomyopathy, serious health arrhythmia, or coronary artery disease.

Blood pressure or heart rate increases

Blood pressure and pulse should be monitored. Benefits and risks should be considered before use in patients for whom blood pressure increases may be problematic.

Psychiatric adverse reactionsMay cause psychotic or manic symptoms in patients with no prior history or exacerbation of symptoms in patients with pre-existing psychosis. Evaluate for bipolar disorder prior to stimulant use.Suppression of growthHeight and weight should be monitored in pediatric patients during treatment.Peripheral vasculopathy, including Raynaud’s phenomenonStimulants are associated with peripheral vasculopathy, including Raynaud’s phenomenon. Careful observations for digital changes is necessary during treatment with stimulants.Obesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [243]

Slide211

Eating Disorders and Obesity: Bulimia NervosaDiagnosis:Cycle of recurrent binge eating and compensatory purging, laxative abuse, diuretic abuse, extra exercising, fasting, or strict dieting

Occurs in approximately 1% of adults (mostly women)

Russell sign: Calluses and abrasions on dorsum of the hands caused by repeated contact with the teeth during self-induced vomiting

Laboratory: Hypokalemia due to hypomagnesemiaTreatment: Often requires treatment by a qualified clinicianFluoxetine is an FDA-approved pharmacotherapy for bulimia nervosaAlthough not FDA-indicated for this use, topiramate and naltrexone may be efficaciousObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [238] [239] [240] [241] [242]

Slide212

Diagnosis:

At least 25% of daily food consumption (often greater than 50%) consumed after evening meal

Recurrent awakenings from sleep that require eating to go back to sleep, often involving carbohydrate-rich snacks Little interest in breakfast (morning anorexia)Night-eating syndrome may occur in as much as 5% of the U.S. populationTreatment: Behavioral therapy regarding nutritional timing and content Eating Disorders and Obesity: Night-eating SyndromeReference/s: [244] [245] [246] [247]

Slide213

Why Don’t People Engage in Routine Physical Activity?

Physiologic

Musculoskeletal, neurologic, pulmonary, cardiac, and other health disorders

Pain or sorenessFatigueConveniences which limit the physiologic need for physical activityAutomated transportation (i.e., cars, buses, etc.)Elevators and escalators

Online shopping

Automated equipment that lessens manual labor

Lack of Time

Work commitments

Family responsibilities

Time preferentially allotted for other entertainments with minimal energy expenditure

Television

Movies

Video games

Internet

Watching sports

Reference/s: [248] [249]

Slide214

Why Don’t People Engage in Routine Physical Activity?

Disinterest

“Exercise is boring”

Past failures to achieve exercise goalsPast failures in observing body changesConcerns of being seen: In workout clothes In gyms surrounded by others more fit

Desire to avoid perspiration

General appearance

Hair

Odor

Environment

Lack of:

Others (family, friends, etc.) engaged in physical activity

Safe environment

Parks or other areas for leisure activity

Accessible gym

Workplace exercise equipment

Inadequate maintenance of increased physical activity, once started

Insufficient education on physical activity

Benefits

Risks

Techniques

Recommendations

Reference/s: [248] [249]

Slide215

Why Do People Regain Body Weight?

Physiologic Priority Imbalance

Neuro-biologic processes strongly resist starvation

Neuro-biologic processes weakly resist over-nutritionAnalogous example:Hypoglycemia can be profoundly symptomatic and may promote physiologic and behavioral priority for immediate caloric intakeHyperglycemia is often asymptomatic and rarely promotes physiologic and behavioral priority for immediate reduced caloric intake

Neurobiology

Weight loss may decrease neuroendocrine factors, which in turn may increase appetite

Leptin

Insulin

Cholecystokinin

Peptide YY

Weight loss may increase ghrelin, which in turn may increase appetite

To the extent that within the central nervous system, insulin and leptin “resistance” limits appetite reduction and negative caloric balance, an increase in physical activity may increase the brain’s sensitivity to insulin and leptin.

A lack of maintaining routine physical activity after weight loss may contribute to body fat regain

Reference/s: [250] [251] [252] [253]

Slide216

Why Do People Regain Body Weight?

Energy Expenditure

Decrease in resting energy expenditure with weight loss

Greater muscle efficiency with weight loss, resulting in less energy expenditure with physical activity BehaviorCommitment amnesia

Forgetfulness of the degree of change and effort required to achieve initial weight loss success

Lack of maintaining accountability logs

Altered priorities:

Intervening stress

Changing life circumstances

Changing health status

Priority fatigue

Lack of maintaining healthy body weight priorities

Resorting to previous nutritional and/or physical activity habits after achieving initial weight-loss success

Setpoint fallacy

The mistaken belief that once achieved, maintenance of weight loss will persist, irrespective of behavior, nutrition, and physical activity

“I know if I could just get the weight off, I could keep it off”

Reference/s: [250] [251] [252] [253]

Slide217

Behavior Therapy Techniques: Elements for Optimal SuccessDoablePractical

Accessible

Frequency

ConsistencyEfficaciousEvidence-based Measurable

Feedback

Trackable

Verifiable

Self-ownership

Autonomous stakeholder

Personal stakeholder

Positive reinforcement

Negative reinforcement

Reference/s: [1]

Slide218

Behavior Therapy: Encounters and EducationFrequent Encounters with Medical Professional or Other Resources Free from Provider Bias

Physician

Dietitian

Nurse educatorAdvanced practitioners Physical activity professional trainer (i.e., trainer, physiologist, etc.)Mental-health professional Certified health coachWeb-based programs Mobile access (i.e., text messages, applications, etc.)Multidisciplinary approach Clinicians with professional expertise

Patient with self expertise

Education

Medical health

Mental health

Nutrition

Physical activity

Establish healthy sleep habits

Establish healthy eating habits (i.e., reduce speed of eating, drink water between meals, choose and

have available healthy snacks, etc.)

Recognize and anticipate inevitable weight-loss plateaus

Reference/s: [254] [255] [256]

Slide219

Behavior Therapy: Stimulus Control and Cognitive RestructuringStimulus ControlAvoid eating for reasons other than hunger

Avoid frequent snacking

Avoid binge eating

Utilize portion controlEnvironmental removal of foods identified as especially tempting for the individual patientBeing habitually mindful of eating stimuli may allow best chance for stimulus controlCognitive Restructuring Address matters of body imageIdentify and establish a plan to counteract unhelpful or dysfunctional thinking leading to unhealthy behaviors and actions Emphasize rationale of aggressive yet realistic weight-loss expectations through an emphasis on weight loss as a matter of medical and mental healthEncourage patient to:

Acknowledge he/she is capable of positive thoughts and behaviors

Replace unhelpful thoughts and behaviors with more productive ones

Practice behavior therapy skills between clinician encounters

Reference/s: [255] [257]

Slide220

Behavior Therapy: Goal Setting and Self-MonitoringGoal SettingPatients are given step-by-step instructions to accomplish goals (i.e., nutrition and physical activity prescriptions)

SMART

pecificMeasurableAssignableRealisticTime-relatedGoals beyond body weight alone may include overall improvement in physical and mental healthSelf Monitoring

Daily or weekly body weights

Other routine self-anthropometric measurements (i.e., calipers for percent body fat, tape measure for waist circumference, myotape for muscle mass, etc.)

Food diaries (including online services or mobile applications)

Physical activity logs

Pedometer/accelerometer measures

Changes in clothing size

Photo journaling

Reference/s: [255] [258]

Slide221

Behavior Therapy: Behavioral Contracting and Problem SolvingBehavioral ContractingTokens of reward

Financial incentives

Problem Solving, Social Support, and Other Reinforcement Contingencies

Stress management Establish alternative back-up procedures to engage during times that challenge adherence to agreed upon plans (e.g., stressful periods, life changes, etc.)Health care team supportMental-health professionalOther group or social supportCommercial weight loss/maintenance programsEncourage interactions with others that may provide positive recognitions for successes

Reference/s: [255] [259] [260]

Slide222

Technologies for Weight Management

Slide223

Technologies and Social MediaApplicationsRecord and assess nutritional and physical activity metrics

May be assessed and reviewed by clinicians between face-to-face evaluations

Interactive Technology

Body-weight scales that provide interactive feedback via email or text messaging Wearable technologies Tracks active minutes, steps, floors climbed, distance, and caloric consumption Monitors heart rate and sleep patternsProvides daily exercise statisticsWirelessly syncs with smartphones and computers, providing interactive information to userWebsitesWebsites can provide educational information regarding:

Nutrition

Caloric content of foods

Physical activity

Expected energy expenditure with certain physical activities

Meal plans

Recipes

Social Media

Post daily meals and snacks to followers to enhance accountability (Twitter, Facebook, etc.)

Obtain nutritional and physical activity advice from others (Twitter, Facebook, blogs, forums, etc.)

Reference/s: [130] [202] [203] [261] [262]

Slide224

Slide225

Anti-obesity MedicationsObjectives:Treat disease

Adiposopathy or sick fat disease (SFD)

Fat mass disease (FMD)

Facilitate management of eating behavior Slow progression of weight gain/regainImprove the health, quality of life, and body weight of the patient with overweight or obesity Adjunct to nutritional, physical activity, and behavioral therapies.

5-10 percent weight loss may improve both metabolic and fat mass disease.

Reference/s: [263]

Slide226

Food and Drug Administration (FDA) PrinciplesFDA-approved Anti-obesity Medication Indications:Patients with obesity (e.g., BMI

30kg/m

2)*Patients who are overweight (e.g., BMI > 27kg/m2) with presence of increased adiposity complications (e.g., type 2 diabetes mellitus, hypertension, dyslipidemia)*Anti-obesity medications are contraindicated in patients hypersensitive to the drugsOther PrinciplesAnti-obesity medications promote variable weight loss over variable duration in patients with overweight or obesity.Some patients having an average of around 5 – 10% weight loss, with greater weight loss in hyper-responders, and less than 5% weight loss (or even weight gain) in hypo-responders.If no clinical improvement (e.g., at least 4 - 5% loss of baseline body weight) after 12-16 weeks with one anti-obesity medication, then consider alternative anti-obesity medication or increasing anti-obesity medication dose (if applicable).*While body mass index (BMI) is the only measure listed in the prescribing information for anti-obesity medications, BMI has limitations. Especially in muscular individuals or those with sarcopenia, overweight and obesity are more accurately assessed by other measures.

Reference/s: [264]

Slide227

Pregnancy and Lactation CategorizationUpdate to FDA Pregnancy and Lactation Labeling

In December 2014, the FDA issued its “Pregnancy and Lactation Labeling Final Rule” (PLLR), which went into effect on June 30, 2015.

The PLLR removed letter pregnancy categories - A, B, C, D, and X.

Due to the fact that the prescribing information materials for most anti-obesity medications have yet to be updated to reflect the new rules, the Obesity Algorithm continues to include pregnancy and lactation categories.In general, anti-obesity drugs are contraindicated in pregnancy, and should not be administered to, nor taken by women who are pregnant or trying to become pregnantObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s:

[272]

Slide228

Reference/s: [

265]

[266] [267] [268]

Drug

Description

Main Side Effects

Illustrative Drug Interactions

Phentermine

Phentermine was approved in 1959, and is the oldest available approved anti-obesity drug. It is a DEA Schedule IV stimulant agent approved for short-term use (12 weeks). Some patients may lose about 5% of body weight.

Side effects include headache, high blood pressure, rapid or irregular heart rate, overstimulation, tremor, and insomnia. Should not use with overactive thyroid or uncontrolled high blood pressure or seizure disorder. Contraindicated in patients with history of cardiovascular disease, within 14 days of monoamine oxidase inhibitors, glaucoma, agitated states, drug abuse

Monoamine oxidase inhibitors, sympathomimetics, antidepressants, alcohol, adrenergic neuron blocking drugs, and some anesthetic agents

Orlistat

Orlistat impairs digestion of dietary fat. Lower doses are approved over-the-counter. Some patients may lose about 5% of body weight.

Side effects include oily discharge with flatus from the rectum, especially after fatty foods. (May help with constipation.) May promote gallstones and kidney stones. Will need to take a multivitamin daily. Contraindicated in chronic malabsorption syndrome and cholestasis.

Cyclosporine, hormone contraceptives, seizure medications, thyroid hormones, warfarin

Lorcaserin

is a DEA Schedule IV agent that improves the sense of fullness. Some patients may lose 5 – 10% of body weight.

Lorcaserin

is a generally well-tolerated drug, with headache, dizziness, fatigue, nausea, dry mouth, and constipation occurring more frequently compared to placebo. Warnings and Precautions include serotonin syndrome, heart failure, psychiatric disorders, and priapism.

Serotonergic (SSRI’s,

SNRI’s

, MAO inhibitors) or anti-dopaminergic medications, St John’s wort, triptans, bupropion, dextromethorphan,

CYP

2D6 substrates

Anti-Obesity Drug Summary (All have contraindications for hypersensitivity and pregnancy)

Slide229

Reference/s:

[269]

[270] [271]

Drug

Description

Main Side Effects

Some Drug Interactions

Liraglutide

Liraglutide is an injectable drug, that in lower doses (1.8 mg per day), is also used to lower blood sugar. Some patients may lose 5 – 10% of body weight with the higher dose of the liraglutide 3.0 mg per day, which is the dose approved for treatment of obesity.

Adverse reactions include nausea, hypoglycemia, diarrhea, constipation, vomiting, headache, decreased appetite, dyspepsia, fatigue dizziness, abdominal pain, increase lipase, and renal insufficiency. Contraindicated with personal of family history of medullary thyroid cancer or Type 2 Multiple Endocrine Neoplasia syndrome. Discontinue with suspected pancreatitis, gall bladder disease, or suicidal behavior and ideation.

May slow gastric emptying, which may impact absorption of concomitantly administered oral medication.

Naltrexone /

bupropion

This is a combination of naltrexone (opioid antagonist used for addictions) and bupropion (used for depression and smoking cessation). Some patients may lose 5 - 10% of body weight.

Naltrexone / bupropion can cause nausea, constipation, diarrhea, and headache. The bupropion component is an antidepressant, and antidepressants can increase the risk of suicide thinking in children, adolescents, and young adults; monitor for suicidal thoughts and behaviors. Should not be used in patients with uncontrolled high blood pressure, seizure disorders, or drug/alcohol withdrawal.

Opioid pain medications, anti-seizure medications, MAO inhibitors, and possible drug interactions with other drugs.

Phentermine

/ topiramate

This is a combination of phentermine (anti-obesity drug) and topiramate (used to treat seizures and migraine headaches). This DEA Schedule IV drug is approved as a weight management pharmacotherapy. Some patients may lose 5 – 10% of body weight.

Phentermine / topiramate can cause tingling or numb feelings to extremities, abnormal taste, insomnia, constipation, and dry mouth. Should not be used in patients with glaucoma, uncontrolled high blood pressure, heart disease, or hyperthyroidism. Topiramate can cause birth defects. Therefore, phentermine / topiramate should not be started until a pregnancy test is negative, unless the woman is using acceptable contraception, and pregnancy tests should be done monthly during use.

Monoamine oxidase inhibitors. May alter oral contraceptive blood levels.

Anti-Obesity Drug Summary

(All have contraindications for

hypesensitivity

and pregnancy)

Slide230

Pharmacotherapy

Examples of Anti-obesity Medications Approved in

1999 or Before

PhentermineDiethylpropionPhendimetrazineBenzphetamineOrlistat

Examples of Anti-obesity Medications Approved in

2012 and Beyond

Lorcaserin

Phentermine HCL/topiramate extended release

Naltrexone HCL/bupropion HCL extended release

Liraglutide

Reference/s: [274]

Slide231

Sympathomimetic AminesExamples: Phentermine, diethylpropion, phendimetrazine, benzphetamineIncreases satiety

Drug Enforcement Agency (DEA) Schedule weight-management agents

DEA IV for phentermine and diethylpropion

DEA III for phendimetrazine and benzphetaminePotential adverse experiences include:PalpitationTachycardia Increased blood pressureOverstimulationTremorDizzinessInsomniaDysphoria Headache Dryness of mouth Dysgeusia Diarrhea

Constipation

Pregnancy category X

Reference/s: [31] [265] [275] [276] [277]

Slide232

Gastrointestinal Lipase InhibitorsExample: OrlistatImpairs gastrointestinal energy absorptionPotential adverse experiences include:

Oily discharge from the rectum

Flatus with discharge

Increased defecationFecal incontinence May increase risk of cholelithiasis May increase risk of urinary oxalate Rare post-marketing reports of severe liver injury May decrease fast-soluble vitamin absorption (e.g., vitamins A, D, E, K, and beta carotene)Pregnancy category X Obesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [266] [275] [278]

Slide233

LorcaserinIndications and UseSerotonin (5-hydroxytryptamine) 2c receptor agonist anti-obesity medication

Drug Enforcement Agency Schedule IV drug

Dose = 10 milligrams (mg) twice per day for immediate release formulation;

20 mg once per day for extended release formulationPotential Drug InteractionsThe safety of lorcaserin co-administration with other serotonergic or anti-dopaminergic agents is not yet established, which includes selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, monoamine oxidase inhibitors, triptans, bupropion, dextromethorphan, St. John’s Wort: use with extreme caution due to the risk of serotonin syndrome or neuroleptic malignant syndrome. Similarly, other listed potential drug interaction include tricyclic antidepressants, lithium, tramadol, dopamine antagonists, and CYP 2D6 substrates.PharmacokineticsLorcaserin is metabolized in the liver with metabolites excreted in the urineLorcaserin can be administered with and without food

Reference/s: [264] [266] [267] [268] [274] [278]

Slide234

Lorcaserin

Contra-indications

Hypersensitivity & Pregnancy

Warnings and Precautions

The safety of coadministration with other serotonergic or antidopaminergic agents has not been established. If Serotonin Syndrome or Neuroleptic Malignant Syndrome (NMS) – like Reactions occur,

lorcaserin

should be immediately discontinued and the patient provided supportive treatment.

If signs or symptoms of valvular heart disease develop, then consider lorcaserin discontinuation and evaluate the patient for possible valvulopathy.

May cause disturbances in attention or memory; use with caution in patients working with hazardous machinery when starting lorcaserin treatment

Due to potential euphoria and dissociation, do not exceed recommended dose of lorcaserin 10 mg twice daily, or 20 mg extended-release formulation once a day.

Discontinue lorcaserin if depression or suicidal thoughts develop.

Among patients treated with diabetes mellitus medications, weight loss may cause hypoglycemia.

Patients experiencing priapism should seek emergency treatment if an erection lasts

>4 hours, and lorcaserin should be used with caution in patients predisposed to priapism.

Due to the potential for lower heart rate,

lorcaserin

should be used with caution in patients with bradycardia or history of heart block greater than first degree.

Should consider periodic monitoring of complete blood count due to reported decreases in white blood cell count and red blood cell count

Lorcaserin

may moderately increase prolactin levels

Clinical trial experience is inadequate to determine if

lorcaserin

increases the risk of pulmonary hypertension

Reference/s: [264] [266] [267] [268] [274] [278]

Most Common Adverse Reaction:

Headache, dizziness, fatigue, nausea, constipation, cough, dry mouth, and hypoglycemia (mainly in patients with diabetes mellitus treated with anti-diabetes drugs).

Slide235

Phentermine HCl/Topiramate Extended ReleaseCompletion of Risk Evaluation and Mitigation Strategy (REMS) program to inform prescribers and female patients about the increased risk of congenital malformations (especially orofacial clefts) in infants exposed to phentermine HCL/topiramate extended release during the first trimester of pregnancy*

Indications and Use

Drug Enforcement Agency Schedule IV drug

Phentermine is a shorter-acting sympathomimetic amine approved as monotherapy as a weight-management drug Topiramate is a longer-acting neurostabilizer approved as monotherapy for seizure disorders and migraine headache preventionDoses = Once daily in the morning with or without foodStarting dose = 3.75 mg/23 mg (phentermine/topiramate extended release)After 14-day intervals, and as clinically indicated, escalate doses to: Recommended dose = 7.5 mg/46 mgTitration dose = 11.25 mg/69 mgTop dose = 15 mg/92 mg

*Completion of the FDA-mandated REMS program is optional and not required prior to prescribing phentermine HCL/topiramate extended release. Implementation of a REMS program by clinicians and pharmacies is intended to provide appropriate safety information to females of reproductive potential.

Reference/s: [266] [271] [274] [278] [279] [280]

Slide236

Phentermine HCl/Topiramate Extended ReleasePotential Drug InteractionsMay alter the exposure to oral contraceptives, causing irregular menstrual bleeding but not an increased risk of pregnancy

Oral contraceptives should not be discontinued if spotting occurs

May potentiate central nervous system depressants such as alcohol

Patients should avoid concomitant alcohol May potentiate hypokalemia of non-potassium-sparing diuretics Pharmacokinetics Phentermine is metabolized by the liver, with most excreted by the kidneyTopiramate is excreted mainly by the kidney

Reference/s: [266] [271] [274] [278] [279] [280]

Slide237

Phentermine HCl/Topiramate Extended ReleaseMost Common Adverse Reactions

In clinical trials, adverse reactions occurring more than or equal to 5 percent of the time include:

Paresthesia

DizzinessDysgeusia (taste distortion/perversion)Insomnia ConstipationDry mouthLaboratory Abnormalities May IncludeMetabolic acidosisElevated creatinineLowering of glucose levels

Reference/s: [266] [271] [274] [278] [279] [280]

Slide238

Phentermine HCl/Topiramate Extended ReleaseContra-indications

Contra-indicated:

Glaucoma

HyperthyroidismDuring or within 14 days of taking monoamine oxidase inhibitors Women of reproductive potential should have a negative pregnancy test before treatment and monthly thereafter and should use effective contraception while on phentermine HCL/topiramate extended release Pregnancy or nursing (Pregnancy category X)Should be discontinued in patients with:Unacceptable increases in adrenergic responses, such as increase in heart rate, especially in those with cardiac and/or cerebrovascular diseaseSuicidal behavior and ideationAcute myopia and secondary angle-closure glaucomaUnacceptable mood and sleep disorders

Cognitive impairment

Pregnancy or nursing

Reference/s: [266] [271] [274] [278] [279] [280]

Slide239

Naltrexone HCl/Bupropion HCL Extended ReleaseIndications and UseNaltrexone is an opioid antagonist

Bupropion is an aminoketone antidepressant with relatively weak inhibition of neuronal reuptake of norepinephrine and dopamine

Drug Enforcement Agency Schedule: Not a scheduled drug

Tablets = 8 mg/90 mg (naltrexone HCL/bupropion HCL extended release)Dosing:Week 1 = 1 tablet in AM, no tablets in PMWeek 2 = 1 tablet in AM, 1 tablet in PMWeek 3 = 2 tablets in AM, 1 tablet in PMWeek 4 and beyond = 2 tablets in AM, 2 tablets in PMObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [266] [270] [274] [278]

Slide240

Naltrexone HCl/Bupropion HCL Extended ReleasePotential Drug Interactions

Should not be administered with opioids due to naltrexone component, which is an opioid receptor antagonist

Monoamine oxidase inhibitors: Increased risk of hypertensive reactions

Drugs Metabolized by CYP2D6: Bupropion inhibits CYP2D6 and can increase concentrations of: Antidepressants (e.g., selective serotonin reuptake inhibitors and many tricyclics) Antipsychotics (e.g., haloperidol, risperidone, and thioridazine) Beta-blockers (e.g., metoprolol) Type 1C antiarrhythmics (e.g., propafenone and flecainide)CYP2B6 inhibitors (e.g., ticlopidine or clopidogrel) can increase bupropion exposure. Do not exceed one tablet twice daily when taken with CYP2B6 inhibitors.CYP2B6 inducers (e.g., ritonavir, lopinavir, efavirenz, carbamazepine, phenobarbital, and phenytoin) may reduce efficacy by reducing bupropion exposure. Avoid concomitant use.Should be dosed with caution with drugs that lower seizure threshold

CNS toxicity can occur when used concomitantly with dopaminergic drugs (e.g., levodopa and amantadine)

Drug laboratory test interactions:

Can cause false positive urine test results for amphetamines

Reference/s: [266] [270] [274] [278]

Slide241

Naltrexone HCl/Bupropion HCL Extended ReleasePharmacokineticsBoth parent and the 6-beta-naltrexol metabolite are active

Naltrexone and 6-beta-naltrexol are not metabolized by cytochrome P450 enzymes

Naltrexone and its metabolites are excreted primarily by the kidney

Bupropion is extensively metabolized CYP2B6 is the principal isozyme involved in the formation of hydroxybupropion, whereas cytochrome P450 isozymes are not involved in the formation of the other active metabolites Bupropion and its metabolites inhibit CYP2D6Following oral administration of 200 mg of 14C-bupropion in humans, 87 percent and 10 percent of the radioactive dose were recovered in the urine and feces, respectively Obesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [266] [270] [274] [278]

Slide242

Naltrexone HCl/Bupropion HCL Extended ReleaseMost common adverse reactions

Nausea

Constipation

Contra-indications

Uncontrolled hypertension

Seizure disorders, anorexia nervosa or bulimia, or undergoing abrupt discontinuation of alcohol, benzodiazepines, barbiturates, and antiepileptic drugs

Use of other products containing bupropion

Chronic opioid use

During or within 14 days of taking monoamine oxidase inhibitors

Known allergy to any of its ingredients

Contra-indicated during pregnancy or nursing mothers (pregnancy category X)

Reference/s: [266] [270] [274] [278]

Slide243

Naltrexone HCl/Bupropion HCL Extended ReleaseWarningsMonitor for depression or suicidal thoughts and discontinue if these symptoms develop

Risk of seizure may be minimized by adhering to the recommended dosing schedule and avoiding co-administration with high-fat meals

Monitor blood pressure and heart rate in all patients, especially those with cardiac or cerebrovascular disease

Hepatotoxicity: Cases of hepatitis and clinically significant liver dysfunction observed with naltrexone exposureAngle-closure glaucoma has occurred in patients with untreated anatomically narrow angles treated with antidepressantsWeight loss may cause hypoglycemia in patients treated with anti-diabetes mellitus medications. Glucose levels should be monitored.Obesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [266] [270] [274] [278]

Slide244

Liraglutide*Indications and UseLiraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist

Drug Enforcement Agency Schedule: Not a scheduled drug

Solution for subcutaneous injection, pre-filled, multi-dose pen that delivers doses of 0.6 mg, 1.2 mg, 1.8 mg, 2.4 mg, or 3 mg

Inject subcutaneously in the abdomen, thigh, or upper arm; the injection site and timing can be changed without dose adjustmentThe lower dose of liraglutide 1.8 mg per day is approved for the treatment of type 2 diabetes mellitus. The recommended dose of liraglutide for treatment of obesity is 3 mg daily, any time of day, without regard to the timing of mealsDosing:Week 1 = 0.6 mg per dayWeek 2 = 1.2 mg per dayWeek 3 = 1.8 mg per dayWeek 4 = 2.4 mg per dayWeek 5 and onward = 3.0 mg per day

*Liraglutide for obesity was approved by the Food and Drug Administration (FDA) with a Risk Evaluation and Mitigation Strategy (REMS) program. While optional and not required prior to prescribing Liraglutide for obesity, the manufacturer provides a communication plan, implemented towards healthcare providers likely to prescribe Liraglutide for obesity. The goal is to inform healthcare providers about the potential risk of medullary thyroid carcinoma and the risk of acute pancreatitis (including necrotizing pancreatitis) associated with Liraglutide for obesity.

Evaluate the change in body weight after 16 weeks and discontinue Liraglutide for obesity if the patient has not lost at least 4% of baseline body weight since it is unlikely that the patient will achieve and sustain clinically meaningful weight loss with continued treatment.

Reference/s: [266] [269] [274] [278]

Slide245

LiraglutidePotential Drug InteractionsLiraglutide delays gastric emptying. This may impact absorption of concomitantly administered oral medications.

Liraglutide has low potential for pharmacokinetic drug-to-drug interactions related to cytochrome P450 and plasma-protein binding

Pharmacokinetics

Unlike native GLP-1, liraglutide is stable against metabolic degradation by both neutral endopeptidase and dipeptidyl peptidase IV and has a plasma half-life of 13 hours after subcutaneous administrationLiraglutide exposures are similar among three subcutaneous injection sites (upper arm, abdomen, and thigh); absolute bioavailability of liraglutide following subcutaneous administration is approximately 55 percent Liraglutide is endogenously metabolized similar to large proteins without a specific organ as a major route of eliminationFollowing a [3H]-liraglutide dose, intact liraglutide is not detected in urine or feces, with only a minor part excreted as liraglutide-related metabolites in urine or feces (6 percent and 5 percent, respectively)

Reference/s: [266] [269] [274] [278]

Slide246

LiraglutideMost common adverse reactionsNausea

Hypoglycemia

Diarrhea

ConstipationVomitingHeadacheDecreased appetiteDyspepsiaFatigueDizzinessAbdominal painIncreased lipase

Contra-indications

Personal or family history of medullary thyroid carcinoma or Multiple Endocrine Neoplasia syndrome type 2

Hypersensitivity to liraglutide or any product components

Pregnancy

Reference/s: [266] [269] [274] [278]

Slide247

LiraglutideWarnings Prescribing information boxed warning:

Liraglutide causes dose-dependent and treatment-duration-dependent thyroid C-cell tumors at clinically relevant exposures in both genders of rats and mice. It is unknown whether liraglutide causes thyroid C-cell tumors, including medullary thyroid carcinoma (

MTC

), in humans, as the human relevance of liraglutide-induced rodent thyroid C-cell tumors has not been determined. Liraglutide is contraindicated in patients with a personal or family history of MTC and in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk of MTC with use of liraglutide and inform them of symptoms of thyroid tumors (eg, a mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound is of uncertain value for early detection of MTC in patients treated with liraglutide.Discontinue promptly if pancreatitis is suspected; do not restart if pancreatitis is confirmed If cholelithiasis or cholecystitis are suspected, gallbladder studies are indicatedSerious hypoglycemia can occur when liraglutide is used with an insulin secretagogue (i.e., a sulfonylurea)

Consider lowering the dose of anti-diabetes drugs to reduce the risk of hypoglycemia

Monitor heart rate at regular intervals to evaluate for possible heart rate increase

Renal impairment has been reported post-marketing, usually in association with nausea, vomiting, diarrhea, or dehydration, which may sometimes require hemodialysis

Use caution when initiating or escalating doses of liraglutide in patients with renal impairment

Post-marketing reports exist regarding serious hypersensitivity reactions (e.g., anaphylactic reactions and angioedema)

If these occur, then liraglutide and other suspect medications should be discontinued, and the

patient instructed to promptly seek medical advice

Monitor for depression or suicidal thoughts and discontinue liraglutide if symptoms develop

Reference/s: [266] [269] [274] [278]

Slide248

*The Obesity Medicine Association has not endorsed any supplements. This section is

intended to provide information the authors believe may be relevant to the clinical management

of patients with obesity.

Slide249

Potential for Publication BiasPotential publication biasClinicians should be cautious of the published literature regarding supplements or other therapies (including drugs), when the only available evidence is via infrequent, and/or small studies.

The disproportionate publication of positive or significant results compared to negative or non-significant results potentially compromises the objectivity of literature review and meta-analyses.

Negative or non-significant study results may not be submitted for publication, are often less likely to be accepted by journals for publication, and potentially less likely to be cited by other journals and the media compared to studies with positive results

Drugs are regulated differently than supplementsSupplements (do not require a clinical trial development program acceptable to the FDA):Can be marketed without FDA approvalAre generally considered safe until proven unsafeDrugs (requires a development program acceptable to the FDA):Cannot be marketed until FDA approvedNot considered safe until proven safe

Reference/s: [281] [282]

Slide250

Definitions

Prescription Drugs

Over-The-Counter

Medications (OTC)

Definition

A therapeutic medicine intended for the diagnosis, cure, mitigation, treatment, or prevention of disease

Drugs the FDA considers to be safe and effective, but that do not require a prescription by a health professional (e.g., orlistat)

Approval process

Requires FDA approval before administered and/or prescribed to patients

Requires FDA approval for OTC use via the regulatory process of an OTC drug monograph

Marketing

Regulated by FDA*

Regulated by Federal Trade Commission*

* The FDA Office of Prescription Drug Promotion / OPDP (formerly DDMAC or Division of Drug Marketing, Advertising and Communications). Prescription Drug Advertising: Questions and Answers

https://www.fda.gov/Drugs/ResourcesForYou/Consumers/PrescriptionDrugAdvertising/ucm076768.htm

(accessed April 23, 2018)

Slide251

Definitions

Supplements*

Functional Foods

Definition

Substances taken in addition to dietary intake, such as concentrated form of a nutrient (e.g., vitamins), isolated formulations of a nutrient (e.g., herbs or botanicals), minerals, and amino acids.

Nutrients with potentially favorable effects beyond basic nutrition, such as oatmeal or foods high in substances that may have health benefits (e.g., many phytochemicals)

Approval process

Not applicable. The FDA considers supplements more of a food than drug.

Not applicable

Marketing

Supplements are not permitted to be marketed for the purpose of treating, diagnosing, preventing, or curing diseases. Supplement manufacturers are responsible for ensuring the supplement is safe, claims of benefit are not false or misleading. **

Not applicable

*US Food & Drug Administration. Dietary Supplements.

https://www.fda.gov/Food/DietarySupplements/

(accessed April 23, 2018)

**USDA Nutrition.gov.

https://www.nutrition.gov/subject/dietary-supplements

(accessed April 23, 2018)

Slide252

Supplements – HepatotoxicityIncreased herbal and dietary supplement (HDS) use is directly proportional to increased HDS-induced liver injuryHDS-induced liver injury accounts for 20% of cases of hepatotoxicity in the US

Major implicated agents include anabolic steroids and green tea extract

Majority of cases of HDS-induced liver injury are from multi-ingredient nutritional supplements

Slide253

Reference/s: [284] [285] [286]

Intervention

Mechanism of Action

Effects

Side Effects

Dietary fiber

May increase sense of fullness with meals, delay carbohydrate absorption, reduce fatty liver, and increase insulin sensitivity

While increased fiber may increase satiety and marginally decrease percent body fat, reported weight loss is inconsistent

Some patients may experience abdominal bloating or flatulence

Prebiotics

Indigestible oligosaccharides (e.g.,

fructo

-oligosaccharides) that may stimulate intestinal growth (colonic lactobacilli and

bifidobacteria

), which may promote microbiome conducive to weight loss

Some human studies support weight loss; weight loss most consistently reported in rodents

Bloating, flatulence

Probiotics

Bacteria such as lactobacilli (found in yogurt, dairy products, and sauerkraut) may provide protection against unfavorable yeast overgrowth and pathogenic bacteria

Some human studies support weight loss; weight loss most consistently reported in rodents

Bloating, flatulence

Common Functional Foods

Slide254

Reference/s: [287] [288] [289] [290]

Intervention

Mechanism of Action

Effects

Side Effects

Caffeine with or without plant extracts

May reduce appetite, increase fat oxidation, and improve alertness

Some studies suggest minor weight loss with caffeine containing foods and products

High doses can cause anxiety, tremors, cardiac dysrhythmias

Green tea (not extract)

Contains caffeine, as well as epicatechin, epicatechin gallate, and

epigallocatchin

gallate (EGCG). While they may have antioxidant effects, it is unclear that the catechin component of green tea contributes to weight loss beyond the caffeine

Meta-analyses suggest minor weight reduction

Caffeine side effects include anxiety, tremors, cardiac dysrhythmias; catechins may cause indigestion and constipation. Green tea extract is an important cause of liver injury.

Green coffee and extract

Green coffee contains less caffeine than black coffee; but also contains chlorogenic acid which may have peroxisome proliferator activated receptor alpha activity

Isolated studies suggest minor weight reduction with green coffee extract

Caffeine side effects include anxiety, tremors, cardiac dysrhythmias; catechins may cause indigestion and constipation

Common Functional Foods

Slide255

Reference/s: [291] [292] [293] [294] [295]

Intervention

Mechanism of Action

Effects

Side Effects

Phytoestrogens

Plant-derived substances with potential estrogenic effects (isoflavones, flavones, and

coumestans

) often found in soy products.

If soy-based foods are substituted for higher fat, higher calorie foods, then this may promote minor weight reduction

Mild nausea, bloating, constipation. In women, phytoestrogens may disrupt endogenous hormone levels and ovulatory cycle. In men, typical doses are unlikely to cause feminization. Should be used with caution in women who are pregnant, nursing, or attempting to become pregnant.

Conjugated linoleic acid (

CLA

)

Natural trans-fat (meats, milk, cheeses, butter, white mushrooms) may act upon lipogenesis, lipolysis, thermogenesis, and browning of white and brown adipose tissue.

May promote short-term, minimal weight reduction, with inconsistent data supporting sustained weight loss or clinically relevant long-term effects on body composition.

Supplements may cause nausea, indigestion, diarrhea, fatigue, fatty liver, insulin resistance, increased triglycerides, reduced high density lipoprotein cholesterol, and increase in inflammatory markers and white blood cell count.

Common Functional Foods

Slide256

Reference/s: [296]

Intervention

Mechanism of Action

Effects

Side Effects

Orlistat

Intestinal lipase inhibitor that impairs intestinal fat absorption

Mild weight reduction

Loose, oily stools. Possible deficiency in fat soluble vitamins, liver toxicity, and kidney stones

Over-the-counter Anti-obesity Therapy

Slide257

Position Statement: Recommendations for Dietary Supplements Sold as Medicinal or Curative for Obesity*

Healthcare providers should:

Be aware of the lack of credible evidence for efficacy and safety of many supplements promoted for the purpose of weight loss.Query patients who desire to accomplish weight loss regarding their use of dietary supplements for this purpose.Advise patients who desire to accomplish weight loss of the limited evidence supporting the efficacy and safety of many supplements and the lack of oversight by government agencies regarding the claims made about such supplements

Be educated on the

Dietary Supplement Health and Education Act (DSHEA)

and the

roles of FDA and FTC

in safety and claims monitoring of supplements promoted for the purpose of weight loss.

Healthcare providers are strongly discouraged from engaging in entrepreneurial activities in which they directly profit from the prescribing of non-FDA approved weight-loss remedies where both safety and efficacy have not been proven.

The Obesity Society with co-signatories = Obesity Action Coalition, Obesity Medicine Association, Academy of Nutrition and Dietetics.

www.obesity.org/publications/position-and-policies/medicinal-or-curative

(accessed April 23, 2018)

Slide258

Reference/s: [288] [300] [301] [302] [303] [304] [305]

Intervention

Side Effects

Description

Glucomannan

Bloating, flatulence and soft stools

Hemicellulose polysaccharide soluble fiber from roots of the elephant yam

Irvingia

gabonensis

Flatulence, headache, sleep disturbances

Seeds from African mango / soluble fiber

Chitosan

Indigestion, bloating, constipation

Derived from chitin, a component of crustacean/arthropod exoskeletons (starch similar to cellulose), has both insoluble and soluble properties

Raspberry ketones

Raspberry eructation (burps)

Extracted from raspberries.

Garcinia

Cambogia

Nausea, possible rare cases of liver toxicity

Small green fruit extract containing

hydroxycitric

acid

Glucosinolates

High doses may cause goiter and hypothyroidismThioesters containing sulfur (mustard family)ForskolinIndigestion, hypotension with lightheadedness, syncope, blurred vision, nausea, pale skin, and fatigueExtract from mint family / Coleus forskohliiHoodia gordonii (p57)Increased blood pressure and pulseSucculent plant consumed by Bushmen in South Africa to reduce appetiteSide Effects of Supplements with Insufficient Human Data to Confirm Consistent, Clinically Meaningful, Long-term Weight Loss

Slide259

Reference/s: [306]

Intervention

Side Effects

Mechanism of Action

1,3-dimethylamylamine methylhexanamine-

DMAA

(geranium or pelargonium

graveolens

extract)

Adverse adrenergic side effects (e.g., high blood pressure, myocardial infarction, psychiatric disorders, nervous system disorders, and sudden death)

Stimulant, often illegally combined with caffeine

Ephedra (ma

huang

)

Adverse adrenergic side effects (e.g., high blood pressure, palpitations, myocardial infarction, stroke, seizure, and sudden death)

Ephedrine and pseudoephedrine may reduce appetite

Bitter orange/ synephrine

Adverse adrenergic side effects

Synephrine may reduce appetite

Dangers of Weight Loss Supplements Banned by the FDA

Many banned weight loss supplements are illegally available via the Internet. Clinicians and patients should be aware of these products and their associated risks.

Slide260

Reference/s: [306]

Intervention

Side Effects

Mechanism of action

2,4 Dinitrophenol (2,4 DNP or DNP)

Hyperthermia, tachycardia, diaphoresis, tachypnea, cardiac arrest, and death

Uncoupling of mitochondrial oxidative phosphorylation and increased fat metabolism

Phenylpropanolamine (PPA)

Headache, tremor, insomnia, agitation, palpitations, high blood pressure, cerebral vasculitis, myocardial infarction, and hemorrhagic strokes

Synthetic sympathomimetic amine, functionally similar to amphetamine and ephedrine, with appetite suppressant effects

Dangers of Weight Loss Supplements Banned by the FDA

Many banned weight loss supplements are illegally available via the Internet. Clinicians and patients should be aware of these products and their associated risks.

Slide261

Reference/s: [288] [307] [308] [309]

Intervention

Proposed mechanism of action

Effects

Warnings

Human chorionic gonadotropin (HCG)

Marketed as reducing appetite and preserving muscle mass during administration of very low-fat diets

Meta-analyses do not support clinically significant weight loss. Since 1976, the FDA has mandated a disclaimer for those who administer HCG*

In 2016, the American Medical Association passed policy that

“The use of HCG for weight loss is inappropriate.”

*1976 FDA disclaimer for HCG:

“There is no substantial evidence that HCG increases weight loss beyond that resulting from caloric restriction, that it causes a more attractive or normal distribution of fat, or that it decreases the hunger and discomfort associated with calorie restrictive diets.”

Weight Loss Therapies with Mandated Disclaimer by the FDA

Slide262

Investigational Anti-obesity Pharmacotherapy

Slide263

Investigational Anti-Obesity TherapiesSGLT 1 & 2 antagonistsOxyntomodulin analogues

Activates glucagon-like peptide-1 receptors (GLP1R)

Activates glucagon receptor (

GCGR)Glucose raising effects of glucagon activation is counteracted by GLP-1 receptor activation and weight loss, with a net reduction in glucose levelsReduces food intakeMay increase energy expenditureReduces body weightObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [134] [310]

Slide264

Investigational Anti-Obesity TherapiesLorcaserin and phentermine (?)*

Canagliflozin

and phentermine (?)*

*Combination metabolic drug therapies are commonly used in clinical practice to treat diabetes mellitus, hypertension, and dyslipidemia. Phentermine combined with some other anti-obesity agents have now been investigated within the context of controlled clinical trials. According to the prescribing information of phentermine preparations, phentermine does not have an FDA indication and is not yet recommended for combined use with other anti-obesity agents due to lack of established safety and efficacy. Phentermine HCl/Topiramate Extended Release in a fixed-dose combination is an FDA-approved treatment for obesity (see prior section).Obesity Algorithm®. ©2017-2018 Obesity Medicine Association.

Reference/s: [311] [312]

Slide265

Early versus Late Weight-Management Intervention: Illustrative Consequences

Slide266

Early Treatment/Prevention44-year-old woman with overweight/obesityPre-diabetes mellitus

Pre-hypertension

Mild dyslipidemia

Discomfort to weight-bearing jointsMild snoringLow self-esteem due to increased body weightOptimal Treatment Strategy

Decide to engage in early, proactive interventions intended to

prevent

onset of adverse health consequences from sick fat disease (diabetes mellitus, dyslipidemia, and hypertension) and fat mass disease (osteoarthritis):

Optimize nutritional therapy and physical activity

Initiate behavioral therapy

Consider anti-obesity medications

Consider bariatric surgery

Prevent onset of metabolic disease:

Diabetes mellitus

Dyslipidemia

Hypertension

Prevent fat mass diseases:

Osteoarthritis

Sleep apnea

Depression

Reference/s: [38] [313]

Slide267

Delayed Treatment44-year-old woman with overweight/obesity

Pre-diabetes mellitus

Pre-hypertension

Mild dyslipidemiaDiscomfort to weight-bearing jointsMild snoringLow self-esteem due to increased body weightSub-optimal Treatment Strategy

Simply tell the patient to diet and exercise and otherwise wait for the onset of diabetes mellitus, dyslipidemia, hypertension, osteoarthritis, sleep apnea, and depression. Once adverse health consequences are blatantly apparent:

Optimize nutritional therapy and physical activity

Initiate behavioral therapy

Consider anti-obesity medications

Consider bariatric surgery

Continued…

Reference/s: [23] [85] [274] [314] [315] [316] [317] [318]

Slide268

Delayed Treatment

If optimal intervention for obesity treatment and prevention is delayed, and the patient develops adverse consequences:

Follow diabetes mellitus evaluation and treatment guidelines

American Diabetes Association Clinical Practice RecommendationsAmerican Association of Clinical Endocrinology Comprehensive Diabetes Management Algorithm Follow lipid evaluation and treatment recommendations and guidelines National Lipid Association Dyslipidemia Summary and Recommendations

American College of Cardiology/American Heart Association Cholesterol Guidelines

Follow blood pressure guidelines

Report of the Joint National Committee for Management of High Blood Pressure in Adults

Follow other disease-specific guidelines

Utilize diabetes mellitus therapies most likely to improve adipose tissue function

In patients with fat mass disease, utilize diabetes mellitus therapies having neutral or body weight loss effects, such as metformin, glucagon-like peptide-1 (GLP-1) agonists, sodium glucose contransporter-2 (SGLT2) inhibitors, etc.

Utilize lipid therapies most likely to reduce atherosclerotic coronary heart disease risk and least likely to increase body weight

Utilize blood pressure therapy most likely to reduce cardiovascular disease risk, which may also provide other health benefits (e.g. diuretics, angiotensin converting enzyme inhibitors, etc.)

Utilize non-steroidal anti-inflammatory agents to treat osteoarthritis

Treat sleep apnea

Utilize anti-depressant medications least likely to promote further weight gain

Administer additional pharmaceuticals and/or treatment modalities as indicated

Reference/s: [23] [85] [274] [314] [315] [316] [317] [318] [319]

Slide269

Bariatric Surgery

Slide270

Before eating (during fasting): GI hormones may increase hunger

Ghrelin

Neuropeptide Y

GI Hormone Regulation of Caloric Balance, Food Digestion, and Nutrient Utilization

Reference/s: [37] [320]

Slide271

After eating: GI hormones may decrease hunger/promote satiety

Somatostatin

CholecystokininMotilin

Insulin

Glucagon

Pancreatic polypeptide

Amylin

Fibroblast growth factor19

Glucagon like peptide-1

Oxyntomodulin

Peptide YY

GI Hormone Regulation of Caloric Balance, Food Digestion, and Nutrient Utilization

Reference/s: [37] [320]

Slide272

After eating: GI hormones may help manage digestion through slowed gastric motility/emptying

Cholecystokinin

AmylinGlucagon like peptide-1

Oxyntomodulin

Peptide YY

GI Hormone Regulation of Caloric Balance, Food Digestion, and Nutrient Utilization

Reference/s: [37] [320]

Slide273

After eating: GI hormones may stimulate the release of digestive enzymes

Gastrin

CholecystokininSecretin

GI Hormone Regulation of Caloric Balance, Food Digestion, and Nutrient Utilization

Reference/s: [37] [320]

Slide274

After eating: GI hormones may have counter-regulatory functions impairing digestive enzyme release

Somatostatin

SecretinPancreatic polypeptide

Glucagon like peptide-2

Oxyntomodulin

Peptide YY

GI Hormone Regulation of Caloric Balance, Food Digestion, and Nutrient Utilization

Reference/s: [37] [320]

Slide275

After eating: GI hormones may assist with post-absorptive nutrient management

Somatostatin

InsulinGlucagon

Fibroblast growth factor19

GI Hormone Regulation of Caloric Balance, Food Digestion, and Nutrient Utilization

Reference/s: [37] [320]

Slide276

Large Intestine

Stomach

Duodenum

Jejunum

Ileum

Water

Sodium chloride

Potassium

Intestinally derived vitamin K

Water

Alcohol

Fatty acids

Amino acids

Minerals (e.g., calcium during calcium deficiency, iron)

Some vitamins

Due to length and location, the jejunum absorbs the greatest amount of:

Simple sugars

Fatty acids

Proteins

Minerals

Vitamins

Bile salts

Bile acids

Vitamin B12

Some vitamins

Some minerals

Nutrient AbsorptionReference/s: [37] [320]

Slide277

Potential Bariatric Surgery Patient

Reference/s: [321] [322] [323]

Slide278

Bariatric SurgeryRegardless of the bariatric surgical procedure chosen, the surgery is best performed by an appropriately trained surgeon at an accredited surgery center.The accreditation of a bariatric surgery center is determined by the Metabolic and Bariatric Surgery Accreditation and Quality Improvement Program (MBSAQIP).

Reference/s: [324]

Slide279

Potential Bariatric Surgery Candidate

*BMI 30-34.9 with one or more AHC: Mounting evidence supports surgical intervention as a treatment option in this group

Reference/s: [16] [321] [322] [323] [325] [326] [327] [328] [329] [330]

Slide280

Bariatric Surgery Pre-operative EvaluationMedical evaluation by physician specializing in the care of patients with overweight or obesity Surgical consultation by bariatric surgery specialist

Cardiology, pulmonary, gastroenterology, and/or other specialty consultation as indicated

Mental health assessment: underlying eating disorders; mood disorders; substance abuse; history of physical or emotional trauma; education regarding potential for increased suicide risk and transfer addictions post op; evaluation of existing coping mechanisms

Reference/s: [323]

Slide281

Excess Weight Loss

“Excess weight loss” is a term, mainly used in the surgical literature, to describe the percent amount of weight lost in excess of ideal body weight

May have variances based upon how ideal body weight is determinedIt is challenging to directly compare “excess weight loss” often described in the surgical literature to the “weight loss” described in the medical literature, which is simply the percent of weight loss from baseline

For the same amount of actual weight loss, the percent “excess weight loss” is often a higher reported value compared to “weight loss”

Reference/s: [331]

Slide282

Bariatric Surgical Procedures

Pros

Cons

Expected

loss in percent excess body weight* at two years

Optimally

suited for patients with:

Other comments

Roux-en-Y Gastric Bypass

Greater

mprovement

metabolic disease

Increased risk of malabsorptive complications over sleeve

60-75%

Higher BMI,

GERD, Type 2 DM

Largest

data set, more technically challenging than LAGB, VSG

Vertical Sleeve Gastrectomy

Improves metabolic disease; maintains small intestinal

anatomy;

micronutrient deficiencies infrequent

No long term

data

50-70% (*3- year data)Metabolic diseaseCan be used as the first step of staged approach; most common based on 2014 dataLaparoscopic Adjustable Gastric Banding

Least invasive; removable

25-40%

5 year removal rate internationally

30-50%

Lower

BMI

; no

metabolic disease

Any metabolic benefits achieved are

dependent

eight loss

Biliopancreatic Diversion

with

Duodenal

Switch

Greatest amount of weight loss and resolution of metabolic disease

Increased risk macro- and micronutrient deficiencies over bypass

70-80%

Higher BMI, Type 2 DM

Most technically challenging

*Excess body weight (EBW) = (total body weight) - (lean body weight)

Reference/s: [332] [333]

Slide283

Roux-en-Y Gastric Bypass (RNY)A surgical procedure wherein the stomach is completely divided into a small proximal gastric pouch leaving a large “bypassed” gastric remnant in situ. The proximal gastric pouch is attached to a “roux” limb of small bowel, bypassing the large gastric remnant, all of the duodenum, and a portion of the proximal small intestine.

General

Hospital stay = 1-4 days

Recovery = 1-2 weeksContra-indications: Poor surgical candidate

Severe psychiatric disorder

Intolerance to general anesthesia

Pregnancy

Drug or alcohol addiction

Untreated gastric ulcer

Crohn’s disease

Patient demonstrates an unwillingness or an inability to follow long term recommendations which can lead to life threatening micronutrient deficiencies

Most Common Acute Complications

Nausea/Vomiting

Dehydration

Gastrointestinal obstruction

Gastrointestinal bleeding

Acute gout exacerbation

Anastomotic leaks

Infection

Cardiac dysrhythmias

Atelectasis and pneumonia

Deep vein thrombosis

Pulmonary emboli

Death

Reference/s: [323] [334] [335] [336]

Slide284

Roux-en-Y Gastric Bypass (RNY)

Weight regain

Pouch/Anastomotic dilation

Anastomotic/Marginal ulcersEsophageal dilationDumping syndrome with reactive hypoglycemia

Small bowel obstruction caused by internal hernias or adhesions

Anastomotic stenosis/stricture

Gallstones

Calcium deficiency

Secondary hyperparathyroidism

Bacterial overgrowth

Kidney stones (oxalosis)

Metabolic acidosis

Iron deficiency

Protein malnutrition

Other nutritional and mineral deficiencies (i.e., deficiencies of vitamins A, C, D, E, B, and K, folate, zinc, magnesium, thiamine)

Anemia (often related to mineral and nutrition deficiencies)

Neuropathies (resulting from nutritional deficiencies)

Gout exacerbation

Osteoporosis (often caused by calcium deficiency and chronically elevated parathyroid hormone levels)

Depression

Potential need for revision or conversion to another procedure

Common Chronic Complications

Reference/s: [323] [334] [335] [336]

Slide285

Vertical Sleeve Gastrectomy (VSG)A surgical procedure wherein the stomach is reduced to about 25 percent of its original size by the surgical removal of a large portion of the stomach along the greater curvature, resulting in a narrower sleeve or tube-like structure.

General

Hospital stay = 1-2 days

Recovery = 1-2 weeksContra-indications: Poor surgical candidate

Severe psychiatric disorder

Intolerance to general anesthesia

Pregnancy

Drug or alcohol addiction

Untreated gastric ulcer

Barrett’s esophagus

Achalasia

Previous gastrectomy

Previous gastric bypass

Sometimes used as a staged approach to gastric bypass or doudenal switch

Most Common Acute Complications

Nausea/Vomiting

Dehydration

Gastrointestinal obstruction

Gastrointestinal bleeding

Staple line leaks

Infection

GERD

Cardiac dysrhythmias

Atelectasis and pneumonia

Deep vein thrombosis

Pulmonary emboli

Death

Slide286

Vertical Sleeve Gastrectomy (VSG)

Weight regain or lack of long-term weight loss

Sleeve dilation

Worsening GERD or de novo GERDLuminal stenosis/stricturesAlkaline reflux gastritis

Staple line ulcers and leaks

Fistula formation

Gallstones

Calcium deficiency

Secondary hyperparathyroidism

Iron deficiency

Anemia (related to mineral and nutrition deficiencies)

B12 & B1 deficiency(IF)

Protein malnutrition uncommon

Vitamin deficiencies uncommon

Kidney stones (oxalosis)

Depression

Potential need for revision or conversion to another procedure

Most Common Chronic Complications

Reference/s: [332] [337]

Slide287

Laparoscopic Adjustable Gastric Banding (LAGB)A surgical procedure where an adjustable band is placed around the upper stomach creating a small pouch. The band diameter is adjustable through the percutaneous introduction of saline via a subcutaneous port which is accessed in the upper abdomen.

*Performance of LAGB has declined due to limited long-term efficacy and international removal rate of at least 25 percent at five years.

General

Outpatient procedure

Recovery usually one week

Food bolus obstruction (dry meat; starches)

Contra-indications:

Poor surgical candidate

Severe psychiatric disorder

Intolerance to general anesthesia

Pregnancy

Drug or alcohol addiction

Untreated gastric ulcer, severe GERD, Barrett’s disease

Autoimmune disease

Reference/s: [338] [339]

Slide288

Laparoscopic Adjustable Gastric Banding (LAGB)

Most Common Acute

Complications

Nausea/vomitingDehydrationBand too tight with gastrointestinal obstructive symptoms (i.e., dysphagia)HemorrhageGastrointestinal bleeding

Infection

Cardiac dysrhythmias

Atelectasis and pneumonia

Deep vein thrombosis

Most Common Chronic Complications

No weight loss or weight regain

Band slippage, erosion, ulceration, port infection, disconnection, and displacement

Esophageal dilation

Rare nutrient deficiencies if persistent vomiting or marked and sustained decrease in nutritional intake

Depression

Potential need for removal, revision or conversion to another procedure

Reference/s: [338] [339]

Slide289

Biliopancreatic Diversion with Duodenal Switch (BPD/DS) Procedure in which a partial gastrectomy (much like a sleeve) is performed, removing 70-80% greater curvature of the stomach sparing the pylorus and a small portion of the duodenum and the creation of a Roux-en-Y duodenoenterostomy

bypassing a large portion of the intestine.

General

Hospital stay = 2-4 daysRecovery = 2-4 weeksContra-indications:

Poor surgical candidate

Severe psychiatric disorder

Intolerance to general anesthesia

Pregnancy

Drug or alcohol addiction

Untreated gastric ulcer

Crohn’s disease

Irritable bowel syndrome

Patient demonstrates an unwillingness or an inability to follow / afford long-term recommendations (e.g., blood testing and post-operative vitamins) which can lead to life threatening micronutrient deficiencies

Most Common Acute Complications

Nausea/Vomiting

Dehydration

Gastrointestinal obstruction

Gastrointestinal bleeding

Acute gout exacerbation

Anastomotic leaks

Infection

Cardiac dysrhythmias

Atelectasis and pneumonia

Deep vein thrombosis

Pulmonary emboli

Death

Reference/s: [340] [341]

Slide290

Biliopancreatic Diversion with Duodenal Switch (BPD/DS)

*The BPD/DS has a much higher incidence of both macro- and micronutrient deficiencies compared to other bariatric surgeries.

Weight regain

Pouch dilationAnastomotic/Marginal ulcers

Small bowel obstruction caused by internal hernias or adhesions

Anastomotic stenosis/stricture

Gallstones

Calcium deficiency

Secondary hyperparathyroidism

Bacterial overgrowth

Kidney stones (oxalosis)

Metabolic acidosis

Iron deficiency

Protein malnutrition*

Other nutritional and mineral deficiencies (i.e., deficiencies of vitamins A, C, D, E, B, and K, folate, zinc, magnesium, thiamine)*

Anemia (often related to mineral and nutrition deficiencies)

Neuropathies* (resulting from nutritional deficiencies)

Gout exacerbation

Osteoporosis (often caused by calcium deficiency and chronically elevated parathyroid hormone levels)

Depression

Potential need for revision

Most Common Chronic Complications

Reference/s: [340] [341]

Slide291

Other FDA-approved Bariatric TechnologiesAspiration Therapy via Modified Percutaneous Endoscopic Gastrostomy (PEG)

Mechanism: Drains 30% of ingested meal

Indication: Body mass index 35-55 kg/m

2Efficacy: 12% excess weight loss at one yearSafety: Potential tube site inflammation/infectionElectrical Vagal Blocking SystemMechanism: Pacemaker-like implantable device surgically placed under skin, with lead wires placed around the vagus nerve just above the stomach; blocks vagal impulses to brain resulting in decreased hunger and increased satiety

Indication: Body mass index > 40 kg/m

or > 35 kg/m

among those with adverse consequences of obesity

Efficacy: 8.5% excess weight loss

Safety: Potential gastroparesis (vagal trunk injury or entrapment)

Reference/s: [342] [343]

Slide292

Other FDA-approved Bariatric TechnologiesIntragastric Balloons

Mechanism: Balloon is inserted into stomach and filled

Indication: Body mass index

> 30 and < 40 kg/m2; approved for up to 6 monthsTypes: Intragastric

fluid-filled and

swallowable

gas filled balloons

Efficacy: 12-31% excess weight loss over 6 months

Safety: Stomach blockage with uncomfortable fullness, vomiting, stomach ulcer, gastric hypertrophy

Endoscopic Plication Devices

Mechanism: Endoscopic suturing of the stomach reduces gastric volume

Indication: Investigational

Efficacy: 30-50% excess weight loss for up to 1-2 years

Safety: Stitch failure with weight regain

Reference/s: [309] [344] [345] [346] [347] [348] [349] [350]

Slide293

Bariatric Surgery: Early Complications (First 30 Days)Leak or Perforation (Typically after RNY, BPD/DS, VSG):

Can lead to acute peritonitis

Technical failure within the first 72 hours (with ischemia can occur up to 14 days post-op)

Can also occur at any time due to ulcer perforation (avoid NSAIDS, steroids, nicotine, caffeine, alcohol)Often with acute and severe abdominal pain (may NOT have peritonitis symptoms if on steroids)Fever, tachycardia, abdominal or back pain, and leukocytosisUrgent surgical exploration may be required but can sometimes be managed with endoscopic stent and drain (in selected cases)Imaging not always diagnostic but when performed, water soluble contrast preferred (abdominal CT or Upper GI)Immediate surgical consultation is critical for suspected leak or perforation EVEN if imaging is negative

The complications listed here are unique to bariatric surgery and not inclusive of more general

post-operative complications that can occur (e.g., pneumonia, PE).

Reference/s: [351] [352]

Slide294

Bariatric Surgery: Early Complications (First 30 Days)Bleeding at the Surgical Site or Rarely Intraluminal/Gastrointestinal (More Likely with RNY, BPD/DS, and VSG):

Usually within 72 hours post-op, may require early intervention or reoperation

Symptoms: tachycardia, hypotension, drop in hemoglobin/hematocrit, oliguria

From three to seven days out, cause is more likely due to erosions and ulcerations at the anastomoses or along staple linesWound Infection (Possible after All Procedures):Abdominal pain, excessive drainage, fever/chills, decreased appetite, leukocytosis, change in bowel patternPresence of intra-abdominal infection/abscess may require drainage percutaneously or by re-operation

The complications listed here are unique to bariatric surgery and not inclusive of more general

post-operative complications that can occur (e.g., pneumonia, PE).

Reference/s: [353]

Slide295

Bariatric Surgery: Late Complications (Beyond 30 Days)Gastro-gastric Fistula (RNY):

Results in increased capacity to ingest food, and/or increased passing of food into the gastric remnant (where it is more completely digested and absorbed)

Possible contributing factor to suboptimal weight loss/weight regain and recurrence of metabolic disease

A non-healing ulcer should raise concern for a gastro-gastric fistulaBand Erosion through Gastric Wall into the Lumen (LAGB):Suspect if band is full but patient perceives no restriction or obstructive symptoms with empty or minimally filled bandCan also present as infection with pain, fevers, leukocytosisPain/infection may or may not be presentDiagnose with EGD, surgical consult for removal is required for eroded band

The complications listed here are unique to bariatric surgery and not inclusive of more general

post-operative complications that can occur (e.g., pneumonia, PE).

Reference/s: [354] [355] [356]

Slide296

Bariatric Surgery: Late Complications (Beyond 30 Days)Incisional Hernias (More Common with Open Procedures):

Pain at one of the incisional sites

Maybe be palpable defect but due to body habitus this may be difficult to ascertain on exam and CT or US is needed to confirm

Repair usually postponed until significant weight loss unless signs of bowel incarceration/strangulation (bowel obstruction)Internal Hernias (RNY/BPD-DS):Usually accompanied by intermittent, post prandial pain and emesis, sometimes only painHerniation through defect in the mesentery created during the surgical procedureChallenging to diagnose both clinically and radiographically- if suspected, diagnostic laparoscopy often neededSurgical emergency if sudden/acute onset

The complications listed here are unique to bariatric surgery and not inclusive of more general

post-operative complications that can occur (e.g., pneumonia, PE).

Reference/s: [357] [358]

Slide297

Bariatric Surgery: Early or Late ComplicationsIntestinal (Small Bowel) Obstruction (RNY, BPD-DS, or Open Procedure):

Abdominal pain, nausea/vomiting, (constipation/obstipation not present if partial)

Usually six months or longer out from surgery but can be anytime

May be associated with an internal hernia, narrowing of the roux limb due to scarring, intussusception, and/or adhesionsEvaluation: CT scan abdomen most common but can also be seen on plain flat/upright abdominal x-rays Stricture (Stomal Stenosis) (RNY or BPD-DS):Post-prandial, epigastric abdominal pain and vomiting (often with frothy emesis)Usually 4-6 weeks following RNYMay result from narrowing of the anastomosis or angulation of the intestinal limbsMay be associated with anastomotic ulcer (RNY and BPD-DS)EGD +/- balloon dilation. Surgery only after multiple failed dilations

Band Obstruction: Band Too Tight, Band Slip/Prolapse (LAGB):

Abdominal pain, reflux, and regurgitation of undigested food which occurs post-prandially

Weight gain can occur due to dependence on liquid calories

Diagnostic testing: Can be clinical diagnosis, or upper GI imaging/EGD

Surgery indicated for a slip which is not relieved after the complete removal of all band fluid

The complications listed here are unique to bariatric surgery and not inclusive of more general

post-operative complications that can occur (e.g., pneumonia, PE).

Reference/s: [356] [359] [360] [361] [362]

Slide298

Dumping Syndrome (RNY):Unique complication of RNY (due to bypass of the pyloric emptying mechanism), which is common in the first 18 months postoperatively

Occurs in approximately 70-85 percent of patients with RNY

Symptoms: facial flushing, lightheadedness, fatigue, reactive hypoglycemia, and postprandial diarrhea

Treatment: often includes avoidance of foods with high glycemic index/load, avoidance of drinking fluid with mealsGallbladder or Gallstone Disease:Right upper quadrant or epigastric post-prandial or nocturnal pain (classically radiating to back or right shoulder)Diagnostic testing includes labs (if elevated white blood cell count, alkaline phosphatase, bilirubin, liver transaminases, or amylase lipase send to Emergency Room for urgent surgical consult)

Imaging: Abdominal ultrasound (abdominal CT if abdominal wall thickness impairs ultrasound), consider HIDA scan if ultrasound is negative

Marginal Ulcer (at an anastomotic site-most common with RNY)

Abdominal pain +/- vomiting

Must stop NSAIDS, steroids, nicotine, caffeine, alcohol, and/or illicit drugs to heal

Proton pump inhibitor 3 times/day plus Carafate 4 times/day; optimize protein intake; surgery for failed refractory ulcer

Diagnose with upper endoscopy, consider surgery for refractory disease

The complications listed here are unique to bariatric surgery and not inclusive of more general

post-operative complications that can occur (e.g., pneumonia, PE).

Bariatric Surgery: Early

Late Complications

Reference/s: [335] [363] [364]

Slide299

Bariatric Surgery: Common Micronutrient Deficiencies

Vitamins

Minerals

B12

Zn/Cu

RNY

Sleeve

LAGB

BPD

*Vitamin D deficiency is seen in a significant number of patients with obesity at baseline. However, due to malabsorption, the risk is further increased post-op.

For a complete explanation of micronutrient deficiencies, refer to “Clinical Practice Guidelines for the Perioperative Nutritional, Metabolic, and Nonsurgical Support of the Bariatric Surgery Patient” at www.asmbs.org.

Reference/s: [320] [366]

Slide300

Derived from plant and animal foods, and necessary for metabolic processes, such as serving as a non-protein facilitator (coenzyme) for protein enzymes.

Micronutrients: Vitamins

Reference/s: [320]

Slide301

Bariatric Surgery

Vitamin A deficiency is rarely reported after laparoscopic adjustable gastric banding, gastric sleeve, or Roux-en-Y gastric bypass

Vitamin A deficiency is reasonably common with biliopancreatic diversion/duodenal switch Retinol levels are often routinely monitored after biliopancreatic diversion/duodenal switch

Background

Vitamin A is an essential fat-soluble nutrient important for vision

Vitamin A deficiency may lead to night blindness

Vitamin A is also involved with adipocyte function, as well as lipid and possibly glucose metabolism

Vitamin A Deficiency

Reference/s: [320]

Slide302

Bariatric Surgery

Preoperative thiamine deficiency is more common in African-American and Hispanic patients

Vitamin B1 deficiency is sometimes reported after laparoscopic adjustable gastric banding, gastric sleeve, Roux-en-Y gastric bypass, or biliopancreatic diversion/duodenal switch The risk of thiamine deficiency is increased with post-operative vomiting, which sometimes requires monitoring post-operative thiamine levels Thiamine deficiency may itself contribute to anorexia, indigestion, constipation and even nausea and vomiting – potentially worsening vitamin deficiency

Background

Vitamin B1/thiamine is an essential water- soluble nutrient involved in cellular processes such as mitochondrial function (fatty acid oxidation)

Vitamin B1 deficiency is known as beriberi, which may present as weakness

“Dry” beriberi includes Wernicke-Korsakoff encephalopathy (e.g., ophthalmoplegia, dementia, ataxia, amnesia)

“Wet” beriberi includes congestive heart failure

Patients with alcoholism are at risk for Vitamin B1 deficiency

Vitamin B1 (Thiamine) Deficiency

Reference/s: [320]

Slide303

Background

Vitamin B2/riboflavin is an essential water- soluble nutrient involved with many cellular processes

Its deficiency may cause a distinctive bright pink tongue, cracked lips, throat swelling, scleral erythema, lowered blood cell count, coma, and death Vitamin B2 (Riboflavin) Deficiency

Bariatric Surgery

Vitamin B2 deficiency is rarely reported after laparoscopic adjustable gastric banding, sleeve gastrectomy, Roux-en-Y gastric bypass, or biliopancreatic diversion / duodenal switch

Vitamin B2 deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplement

Post-operative riboflavin levels are usually monitored only with signs and symptoms of deficiency

Reference/s: [320]

Slide304

Background

Vitamin B3/niacin is an essential water- soluble nutrient highly expressed in adipose tissue

Niacin deficiency is known as pellagraPresentation includes the “4 Ds” of diarrhea, dermatitis, dementia, and death

Mainly located in sun-exposed areas, the dermatologic manifestations include erythema, desquamation, scaling, and keratosis

Vitamin B3 (Niacin) Deficiency

Bariatric Surgery

Vitamin B3 deficiency is rarely reported with laparoscopic adjustable gastric banding, sleeve gastrectomy, Roux-en-Y gastric bypass, or biliopancreatic diversion/duodenal switch

Vitamin B3 deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplement

Post-operative niacin levels are usually monitored only if signs and symptoms of deficiency

Reference/s: [320]

Slide305

Background

Vitamin B5/pantothenic acid is an essential water-soluble nutrient used to synthesize coenzyme-A, as well as proteins, carbohydrates, and fats

Pantothenic acid is derived from a Greek word meaning “from everywhere,” is found in most foods, and its deficiency may cause numerous, wide-ranging adverse effects, such as paresthesias and other signs and symptomsVitamin B5 (Pantothenic Acid) Deficiency

Bariatric Surgery

Vitamin B5 deficiency is rarely reported with laparoscopic adjustable gastric banding, sleeve gastrectomy, Roux-en-Y gastric bypass, or biliopancreatic diversion / duodenal switch

Vitamin B5 deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplement

Post-operative pantothenic acid levels are usually monitored only if signs and symptoms of deficiency

Reference/s: [320]

Slide306

Background

Vitamin B6/pyridoxine is an essential water- soluble nutrient important for nutrient metabolism and neurologic function

Pyridoxine deficiency can cause skin eruptions resembling seborrheic dermatitis, intertrigo, atrophic glossitis, angular cheilitis, conjunctivitis, sideroblastic anemia, and neurologic symptoms (e.g., somnolence, confusion, and peripheral neuropathy)Vitamin B6 (Pyridoxine) Deficiency

Bariatric Surgery

Vitamin B6 deficiency is rarely reported with either laparoscopic adjustable gastric banding, sleeve gastrectomy, Roux-en-Y gastric bypass, or biliopancreatic diversion / duodenal switch

Vitamin B6 deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplement

Post-operative pyridoxine levels are usually monitored only if signs and symptoms of deficiency

Reference/s: [320]

Slide307

Background

Vitamin B7/biotin is an essential water- soluble nutrient important in fatty acid synthesis, amino acid catabolism, and gluconeogenesis

Biotin is usually produced in more than adequate amounts by intestinal bacteria Biotin deficiency causes hair loss, conjunctivitis, scaly/erythematous rash (around eyes, nose, mouth, and genital area), anemia, and central/peripheral nervous system disorders

Biotin deficiency can be exacerbated by consumption of raw eggs, which bind vitamin B7, making it relatively inactive

Vitamin B7 (Biotin) Deficiency

Bariatric Surgery

Vitamin B7 deficiency is rarely reported with laparoscopic adjustable gastric banding, sleeve gastrectomy, Roux-en-Y gastric bypass, or biliopancreatic diversion / duodenal switch

Vitamin B7 deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplement

Post-operative pyridoxine levels are usually monitored only if signs and symptoms of deficiency

Reference/s: [320]

Slide308

Bariatric Surgery

Vitamin B9 deficiency is sometimes reported with laparoscopic adjustable gastric banding, sleeve gastrectomy, Roux- en-Y gastric bypass, or biliopancreatic diversion / duodenal switch

Vitamin B9 deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplementPost-operative folic acid levels (red blood cell folate) are often routinely monitored

Folic acid supplements are often administered after bariatric surgeries, especially in premenopausal, menstruating women of childbearing potential

Background

Vitamin B9/folic acid is an essential water- soluble nutrient absorbed in the duodenum and proximal jejunum

Folic acid deficiency may cause megaloblastic anemia, as well as loss of appetite and weight loss

Preconception folate deficiency is associated with fetal neural tube defects

Vitamin B9 (Folate) Deficiency

Reference/s: [320] [367]

Slide309

Bariatric Surgery

Vitamin B12 deficiency is commonly reported with laparoscopic adjustable gastric banding, sleeve gastrectomy, Roux- en-Y gastric bypass, or biliopancreatic diversion / duodenal switch

Vitamin B12 deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplement Post-operative vitamin B12 levels are often routinely monitored

Vitamin B12 supplements are often administered after bariatric surgeries

Background

Vitamin B12/cyanocobalamin is an essential water-soluble nutrient cleaved from its protein by the hydrochloric acid in the stomach, then combined with a protein called intrinsic factor, and then absorbed in the terminal ileum

Vitamin B12 deficiency may induce sterol regulatory element binding, protein-mediated cholesterol biosynthesis, and impaired metabolism of odd-chain fatty acids

Vitamin B12 deficiency may also cause megaloblastic anemia and contribute to central nervous system disorders

Vitamin B12 (Cyanocobalamin) Deficiency

Reference/s: [320]

Slide310

Bariatric Surgery

Vitamin C deficiency is rarely reported with laparoscopic adjustable gastric banding, sleeve gastrectomy, Roux-en-Y gastric bypass, or biliopancreatic diversion / duodenal switch

Vitamin C deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplementPost-operative vitamin C levels are usually monitored only if signs and symptoms of deficiency

Background

Vitamin C is an essential water-soluble nutrient and cofactor for many enzymatic processes

Vitamin deficiency is known as scurvy

Signs and symptoms include lethargy, weight loss, dry hair and skin, bruising, bleeding gums, loss of teeth, fever, and death

Vitamin C Deficiency

Reference/s: [320]

Slide311

Bariatric Surgery

Vitamin D deficiency is common among pre-operative patients with overweight or obesity

Among African Americans with and without obesity, vitamin D levels may be lower than whitesVitamin D deficiency should be treated in African AmericansLow normal vitamin D levels may not adversely affect bone mineral density in African Americans; vitamin D excess may have adverse health consequences

Vitamin D deficiency is rarely reported to worsen with laparoscopic adjustable gastric banding

Vitamin D deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplement

Vitamin D deficiency sometimes occurs with sleeve gastrectomy and Roux-en-Y gastric bypass and commonly occurs with biliopancreatic diversion/duodenal switch

After bariatric procedures, 25-hydroxy- (OH)-vitamin D, calcium, phosphorous, and parathyroid hormone are often monitored post-operatively

Calcium and vitamin supplements are commonly administered after bariatric surgeries

Background

Vitamin D is an essential fat-soluble nutrient important for calcium metabolism (and other minerals), bone health, and adipocyte function

Vitamin D deficiency may result in decreased bone mineralization, osteopenia, secondary hyperparathyroidism, and hypocalcemia

Vitamin D Deficiency

Reference/s: [320] [368]

Slide312

Bariatric Surgery

Vitamin E deficiency is rarely reported with laparoscopic adjustable gastric banding, sleeve gastrectomy, or Roux-en-Y gastric bypass.

Vitamin E deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplementVitamin E deficiency may more often occur in patients undergoing biliopancreatic diversion/duodenal switch

Alpha-tocopherol levels are often routinely monitored after biliopancreatic diversion/duodenal switch.

Background

Vitamin E is an essential fat-soluble nutrient important for antioxidant and enzymatic activities, and gene expressions, as well as neurologic function and adipocyte function

Vitamin E deficiency may cause neuropathy and ataxia

Vitamin E Deficiency

Reference/s: [320]

Slide313

Bariatric Surgery

Vitamin K deficiency is rarely reported with laparoscopic adjustable gastric banding, sleeve gastrectomy, or Roux-en-Y gastric bypass

Vitamin K deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplement Vitamin K deficiency is reasonably common with biliopancreatic diversion/duodenal switch

Prothrombin time is often routinely measured after biliopancreatic diversion/duodenal switch

Background

Vitamin K is an essential fat-soluble nutrient important for blood coagulation

Vitamin K deficiency may cause bruising and increased risk for bleeding

Vitamin K Deficiency

Reference/s: [320]

Slide314

Micronutrients

Chemical substances from foods which are required in small amounts for the normal growth and development of an organism

Deficiency of micronutrients can contribute to body organ/tissue dysfunction

Phytochemicals

Bioactive compounds found in plants

Deficiency of phytochemicals may contribute to organ/tissue dysfunction, deprive the body of metabolic benefits, and may potentially worsen metabolic diseases - including obesity

Phytochemicals derived from plant sources may protect against oxysterol-induced cellular damage, and thus have potential anti-cancer and anti-aging effects, as well as favorable activity regarding cardiovascular diseases, diabetes mellitus, obesity, and neurogenerative disorders

Thousands of plant derived micronutrients exist (e.g., terpenoids, phenolic compounds,

glucosinolates

betalains

, chlorophylls, organic acids, amines, carbohydrates, protease inhibitors) with commercial testing not available for many (if not most) of these phytochemicals likely important for human health

Micronutrients: Phytochemicals

Reference/s: [369] [370] [371]

Slide315

Minerals

Non-organic substances necessary for important biological processes (e.g., vital part of an enzyme)

Calcium, phosphorous, magnesium, potassium, and sodium

Trace Elements

Non-organic substances required by the body for biological functions (e.g., vital part of an enzyme), but only in minute amounts

Iron, cobalt, zinc, selenium, molybdenum, and iodine

Micronutrients: Minerals and Trace Elements

Reference/s: [320]

Slide316

Bariatric Surgery

Calcium deficiency is rarely reported with laparoscopic adjustable gastric banding

Relative calcium deficiency is sometimes reported with gastric sleeve or Roux-en-Y gastric bypass, when assessed by elevated parathyroid levels (even if calcium levels are within normal limits) Calcium deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplement

Calcium deficiency commonly occurs with biliopancreatic diversion/duodenal switch

Although calcium levels may not be decreased in all patients with overweight or obesity, vitamin D deficiency may be present

25-hydroxy-(OH)-vitamin D, calcium, phosphorous, and parathyroid hormone are often monitored post-operatively

Calcium and vitamin D supplements are commonly administered after bariatric surgeries

Background

Calcium is an essential mineral necessary for proper nerve transmission, muscle contraction, bone structure, and cellular function

Concurrent magnesium deficiency may worsen hypocalcemia by impairing parathyroid hormone secretion (hypomagnesemia may also promote hypokalemia)

Calcium deficiency may result in decreased bone mineralization, osteopenia, and secondary hyperparathyroidism

Severe hypocalcemia can lead to tetany (e.g., muscle contractions, spasms, paresthesias)

Calcium Deficiency

Reference/s: [320]

Slide317

Bariatric Surgery

Copper deficiency is rarely reported with laparoscopic adjustable gastric banding, gastric sleeve, Roux-en-Y gastric bypass, or biliopancreatic diversion/duodenal switch

Copper deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplement Post-operative copper levels are usually monitored only if signs and symptoms of deficiency

Background

Copper is a trace element absorbed from the small intestine

Copper deficiency (which may accompany iron deficiency) may clinically manifest by anemia, neuropathies, difficulty walking, increased muscle tone or spasticity, and cardiomegaly

Copper Deficiency

Reference/s: [320]

Slide318

Bariatric Surgery

Iron deficiency is rarely reported with laparoscopic adjustable gastric banding

Iron deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplementIron deficiency commonly occurs with gastric sleeve, Roux-en-Y gastric bypass and biliopancreatic diversion/duodenal switch

After bariatric procedures, iron, ferritin, transferrin, and total iron binding capacity are often monitored

Iron supplements are often administered after bariatric surgeries, especially among premenopausal, menstruating women of childbearing potential

Iron and calcium compete for intestinal absorption, and supplements should be scheduled several hours apart

Background

Iron is a trace element and is normally absorbed in the duodenum and jejunum of the intestine

Iron deficiency can result in microcytic anemia (possibly manifested clinically by pica), with low iron levels, low ferritin levels, and increased transferrin or total iron-binding capacity

Iron Deficiency

Reference/s: [320]

Slide319

Bariatric Surgery

Selenium deficiency is rarely reported after laparoscopic adjustable gastric banding, gastric sleeve, Roux-en-Y gastric bypass, or biliopancreatic diversion/duodenal switch

Selenium deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplement Post-operative selenium levels are usually monitored only if signs and symptoms of deficiency

Background

Selenium is a trace element that helps protect cells from free radical damage

Selenium deficiency may cause cardiomyopathy (Keshan disease)

Selenium Deficiency

Reference/s: [320]

Slide320

Bariatric Surgery

Zinc deficiency is rarely reported after laparoscopic adjustable gastric banding

Zinc deficiency can be mitigated with appropriate nutrition and a high-quality multivitamin supplement Zinc deficiency sometimes occurs with sleeve gastrectomy, Roux-en-Y gastric bypass and is common with biliopancreatic diversion/duodenal switch

Post-operative zinc levels are usually monitored only if signs and symptoms of deficiency

Background

Zinc is a trace element and is important for intestinal mucosal function

Zinc deficiency can cause poor wound healing, hair loss, acrodermatitis enteropathica-like rash, taste alterations, glossitis, and impaired folate absorption (potentially contributing to folic acid deficiency)

Zinc Deficiency

Reference/s: [320]

Slide321

Nutritional advice will depend upon type of bariatric procedureThree to five small meals a day

Chew small bites of food thoroughly

Avoid consuming liquids during meals, delay for at least 30 minutes after meals

Protein: At least 60 grams/day, optimally 1.2 to 1.5 grams/kg/dayAvoid concentrated sweets to minimize dumping and to reduce caloric intakeHigh-quality multivitamins are routinely recommended after bariatric procedures, irrespective of deficiencies, which are often recommended to be chewable or liquidOther routine supplements often include:Vitamin B12 500 μg/d tablet or sublingual, or 1000 μg/mo IMIron at least 27 mg of elemental iron daily, given with at least 500 mg vitamin CCalcium citrate 1200 mg/d, preferably with vitamin D3

Nutritional Principles Following Bariatric Surgery

Reference/s: [320]

Slide322

Vitamin/

Mineral

AssessmentReplacement of DeficiencyVitamin A

Retinol

corneal keratinization, ulceration or necrosis: 50-100,000 IU IM for 3 days, followed by IU IM for 2 weeks

If no corneal changes: 10,000 - 25,000 IU orally for 1-2 weeks

Further treatment depends on persistent malabsorptive effects, as may most be a concern with biliopancreatic diversion/duodenal switch

Vitamin B1 (Thiamine)

Thiamine

If hyperemesis, then 100mg IV

for 7 days, then 50 mg/d until thiamine in normal range

Vitamin B9

(Folate)

Red blood

cell (RBC) folate

If daily multivitamin has

400ug of folic acid, then replacement dose for deficiency is an additional 800 ug/d orally (total of 1200 ug/d of folic acid until RBC folate in normal range), and then a multivitamin with at least 400 ug/d of folic acid

B12

(Cobalamin)

Vitamin B12

A typical dose to treat B12 deficiency 10

00 ug/mo IM, 1000 ug/wk sublingually, or 350-500 ug/d orally until B12 in normal range

Calcium

In addition to ensuring adequate vitamin D, calcium deficiency is typically treated with calcium citrate 1200-1800 mg/d. Calcium citrate may be better absorbed than calcium carbonate Calcium should be taken at least 1 hour apart from other supplements, especially iron (which competes for absorption)IronFerritin, iron, total iron binding capacityFor moderate deficiency, menstruating women, or patients at risk for iron deficiency anemia, total elemental iron intake (including in a multivitamin) should be 50-100 mg/dMinimum iron supplementation should be 18 mg/d, which may be more effective with vitamin C supplementation 500 mg/dFor severe deficiency, IV iron is sometimes required, which is provided in multiple different formulations, some of which require test doses. Micronutrient Deficiency Replacement after Bariatric Surgery: Vitamins/MineralsReference/s: [320]

Slide323

Vitamin/Mineral

Assessment

Replacement of DeficiencyVitamin D

25-hydroxyl-(OH)-vitamin D

A typical oral dose for mild deficiency of vit. D3 is 3000 IU/d, followed by at least 1000 IU/d after gastric bypass and 2000 IU/d after biliopancreatic

diversion/duodenal switch once normal range vitamin D levels are achieved

For severe deficiency, a single dose of vit. D2 50,000 IU/wk orally until vit. D levels in normal range, then D3 3000 IU if still with substantial malabsorptive signs and symptoms, or if stable with vitamin D values in the normal range, then at least D3 1000 IU/d after gastric bypass and D3 2000 IU/d after biliopancreatic diversion/duodenal switch

Regarding

formulation, vit. D2 (ergocalciferol) is a form of dietary vit. D found in plants. Vit.D3 (cholecalciferol) is found in foods of animal origin and is similar to the vit. D3 generated when 7-dehydrocholesterol in the skin is converted by ultraviolet radiation from sunlight. Both D2 and D3 are reported as 25-hydroxyvitamin D, which is then converted by the kidneys into the more active 1,25 dihydroxyvitamin D (calcitriol). Vit. D3 may be preferred (longer half-life and potentially more potent) than vit. D2. Although the most potent, calcitriol is more rarely used (.25 or .50 mcg/d orally)

Vitamin E

-Tocopherol

A typical dose to treat vitamin E deficiency is 400 to 800 IU/d orally.

Vitamin K

Prothrombin time

If vitamin K deficiency occurs during substantial gastrointestinal

malabsorption, then vitamin K can be replaced 10 mg by slow IV. Otherwise, typical oral replacement dose is 300 ug/d. Continued treatment depends on persistent malabsorptive effects, as may most be a concern with biliopancreatic diversion/duodenal switch.

Zinc

A typical replacement dose for

zinc deficiency is 60 mg of elemental zinc twice daily. Zinc consumption may impair copper absorption, thus 1 mg of copper should be given per each 10 mg of zinc administered. Once zinc is in normal range, if malabsorption remains a risk, a typical supplemental dose is zinc 30 mg/d.

Micronutrient Deficiency Replacement after Bariatric Surgery: Vitamins/Minerals

Reference/s: [320] [372] [373] [374]

Slide324

Microbiome: Gut Flora Basics

Microbiome = Collection of micro-organisms

Microbiota = Organisms themselvesReference/s: [37]

Slide325

Microbiome: Gut Flora Basics

Humans organism has ~10 trillion human cells

Human gut is colonized by 100 trillion cells (bacteria, fungi and viruses)Unless due to a pathogenic infection, the gut microbiome is usually neither healthy or unhealthy; the clinical implications are dependent upon the individualIndividuals who are underweight may benefit from microbiota that promote more efficient absorption of nutrients

Individuals who are overweight or with obesity may not benefit from microbiota that promote more efficient absorption of nutrients

Reference/s: [37]

Slide326

Microbiome: Gut Flora Bacteria

Over 1,000 bacterial species, with over 90% anaerobic

Substrates: Sloughed intestinal cells, plant polysaccharides, starch cellulose, and bile componentsFunctions include:Metabolizing essential nutrients

Synthesizing vitamin K

Fermentation of sugars to acids, gasses, or alcohol

Digesting cellulose

Promoting angiogenesis

Enhancing enteric nerve function

Reference/s: [37]

Slide327

Microbiome: Gut Flora Bacteria

Stomach and proximal small intestine = limited amounts of bacteria (e.g., acid-tolerant lactobacilli and streptococci bacteria)

Ileum and colon = trillions of bacteriaMajor phyla of intestinal microbiomeGram Negative Bacteroidetes: May assist with epithelial cell maturation and function

Gram Positive Firmicutes: May more efficiently extract calories from carbohydrates through fermentation of indigestible foods into short-chain fatty acids

Obesity = Firmicutes proportionally increases compared to Bacteroidetes

Reference/s: [37]

Slide328

Microbiome: Gut Microbiota Promotion of Increased Body Fat

Increased Nutrient Absorption

Enhanced monosaccharide intestinal uptake through enriched carbohydrate enzymes in the gut (e.g., microbial glycoside hydrolases, polysaccharide lyases, and carbohydrate esterases)Increased fermentation of nutrients to short-chain fatty acids, which are absorbed and utilized for gluconeogenesis, lipogenesis, and which may increase the permeability of the intestinal epithelium, increasing absorption of macromolecules from the intestine

Increased density of small intestinal villi capillaries allowing for greater nutrient absorption

Reference/s: [37]

Slide329

Microbiome: Gut Microbiota Promotion of Increased Body Fat

Increased Lipogenesis

Increased Sterol Regulatory Element Binding Protein-1 (SREBP-1) activity, promoting lipogenesisReduced hepatic and muscle fatty acid oxidation

Reference/s: [37]

Slide330

Microbiome: Gut Microbiota Promotion of Increased Body Fat

Increased Inflammation

Pro-inflammatory signaling, such as that generated in response to lipopolysaccharide component of bacterial outer membranes, may affect neurobehavioral brain centers, and adversely affect adipocyte function leading to adiposopathy and increased risk for metabolic diseaseReference/s: [37]

Slide331

Microbiome: Gut Microbiota Promotion of Increased Body Fat

Alterations in Bile Acid Metabolism

Relationship between microbiota and bile acids are interdependent, with the types of bile acids delivered by the liver affecting the microbiome, and the microbiome affecting bile acid structure once in the gut, and thus affecting the types of bile acids composing the bile-acid poolGut microbiota promotes bile acid deconjugation, dehydrogenation, and dehydroxylation, increasing the chemical diversity of intestinal and systemic bile acids

Bile acids affect glucose and lipid metabolism via interactions with bile acid receptors such as farnesoid X receptor (FXR), takeda G protein coupled receptor 5 (TGR5), and fibroblast growth factor 19 (FGF19)

Reference/s: [37]

Slide332

Microbiome: Gut Microbiota Promotion of Increased Body Fat

Alterations in Gut Hormones

Suppressed secretion of fasting-induced adipose factor (angiopoietin-like protein), which may reduce adipose tissue fatty-acid oxidation, reduce uncoupling of the process of mitochondrial adipose tissue adenosine triphosphate generation, and reduce thermogenesisDecreased glucagon-like peptide 1, which may impair increased satiety after meals

Reference/s: [37]

Slide333

Bariatric Surgery May:

Reduce availability of nutrients delivered to the gut

Reduce lipogenic signaling (gut and systemic)Reduce inflammation (gut and systemic)Alter bile-acid metabolism and increase bile-acid pool favoring metabolic processes involving glucose and lipids

Alter gut hormones favoring metabolic processes involving glucose and lipids

Decrease the Firmicutes:Bacteroidetes ratio, potentially reducing the efficiency of extracting calories from gut carbohydrates

Microbiome: “Favorable” Weight and Metabolic Effects of Bariatric Surgery

Reference/s: [37]

Slide334

Slide335

Assess for the Presence of Obesity, Adiposopathy, Fat Mass Disease

Obesity may be assessed using several criteria (thresholds vary based on gender and ethnic differences):

Body Mass Index (BMI)

18.5-24.9

kg/m

25.0-29.9

kg/m

30 kg/m

Percent Body Fat

Male: <25%

Female:

<32%

Male: >25%

Female:

>32%

Waist Circumference

Male: <40 in.

Female: <35 in.

Male: >40 in.

Female: >35 in.

Edmonton Obesity Staging System

Stage 0,

1, 2, 3, 4

No ObesityOverweightObesityClass I: BMI 30.0-34.9Class II: BMI 35-39.9Class III: BMI > 40.0Prevention

Primary care provider or dietitian

If treatment is ineffective, refer to an obesity medicine specialist.

Consider referring to an obesity medicine specialist.

Reference/s: [1]

Slide336

Assess for the Presence of Obesity, Adiposopathy, Fat Mass Disease

Body Mass Index

BMI = (weight in kg)/(height in m)

2 OR703 x (weight in pounds)/(height in inches)

Percent Body Fat

Can

be calculated using bio-impedance, near infrared reactance,

DXA

scan or whole

body air-displacement plethysmography.

Waist Circumference

Can be measured by tape measure around the abdomen at the level of the anterior superior iliac crests, parallel to the floor. Tape should be snug against skin without compressing.

Edmonton

Obesity

Staging System

STAGE 0: No apparent risk factors, no physical symptoms, functional limitations, and/or impairment of well-being

STAGE 1: Presence of obesity-related subclinical risk factors, mild physical symptoms, mild psychopathology, mild functional limitations, and/or mild impairment of well-being

STAGE 2: Presence of established obesity-related chronic disease, moderate psychopathology, moderate functional limitations, and/or impairment of well-being

STAGE 3: Established end-organ damage, significant psychopathology, significant functional limitations, and/or impairment of well-being

STAGE 4: Severe (potentially end-stage) disabilities from obesity-related chronic diseases, severe disabling psychopathology, severe functional limitations, and/or severe impairment of well-being

Obesity medicine specialists, certified by the American Board of Obesity Medicine, dedicate a portion or all of their practice to the treatment of obesity. They perform a medical evaluation (history, physical, laboratory, body composition) and provide medical supervision for lifestyle change (nutrition, activity, behavior change), medications, or very low-calorie diets. Obesity is a chronic medical disease and often requires lifelong treatment.

Reference/s: [1] [375]

Slide337

Comprehensive Evaluation

of the Patient with Overweight/Obesity

History

Weight history, past medical history, family history, social history, screening for weight-promoting medications, food intake, activity, review of systems

Physical Examination

Height, weight, blood pressure, body composition analysis, waist measurement, complete physical examination

Laboratory Tests*

Complete blood count, electrolytes, liver function, kidney function, fasting lipid profile, thyroid tests, hemoglobin A1c, uric acid, vitamin D

Diagnostic Testing*

EKG, echocardiogram, exercise stress test, sleep study, barium swallow or esophagoduodenoscopy

*lab

and diagnostic testing should be individualized

Individualized Treatment Plans*

Diet

Use calorie restriction, carbohydrate restriction, food journaling, very

low-calorie diet programs

Activity

Give exercise prescription, use pedometers, limit TV and computer time, decrease sedentary time, initial goal of 150 minutes

per

week of moderate-intensity physical activity

Counseling

Eliminate provider bias

and

stigma, identify self-sabotage, develop strong support, address stress management, sleep optimization, other psychological support as needed

Pharmacotherapy

Use pharmacotherapy as part of a comprehensive program

Referral

Consider referral to an obesity medicine specialist

*If ineffective, consider referral to a metabolic and bariatric surgeon. Optimal pre- and post-operative care includes an obesity medicine specialist.

Evaluation and Treatment Summary

Reference/s: [1]

Slide338

*Potency includes many factors, such as the amount, rate, and sustainability of weight loss, and the long-term resolution of adiposopathy and fat mass disease. Potency varies greatly for each individual (i.e., long-term adherence to a lifestyle program can be as potent as gastric bypass surgery).

Potency*

Risk/Cost

Lifestyle

Includes nutrition, physical activity, and behavioral programs

Lifestyle + Medication

Includes lifestyle, and anti-obesity medications

Surgery

(In order of lowest risk/cost and potency): LAGB<VSG<RNY

Very Low Calorie Diet

Current Treatment Options for Obesity

Reference/s: [1]

Slide339

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DisclosuresHarold E. Bays, MD, FOMA,

FTOS

FACC, FACE, FNLA, FOMA: Neither Dr. Harold Bays or his affiliated research center / weight management center own pharmaceutical stocks or patents. In the past 12 months, Dr. Harold Bays’ research site has received research grants from Amarin, Amgen, Alere, Allergan, Arisaph, AstraZeneca, Boehringer Ingelheim, Bristol Meyers Squibb, Catabasis, Dr. Reddy, Eisai, Elcelyx, Eli Lilly, Esperion, Ferrer/Chiltern, Gemphire

, Gilead, GSK,

iSpecimen

, Janssen, Johnson and Johnson, Kowa, Merck,

Necktar

Nichi-Iko, Novartis, NovoNordisk, Pfizer, Regeneron, Sanofi, Selecta, Takeda, and

TIMI

. In the past 12 months, Dr. Harold Bays has served as a consultant/advisor for

Alnylam

Akcea

, Amgen, AstraZeneca, Eisai, Eli Lilly, Esperion,

Ionis

(ISIS), Janssen, Johnson & Johnson, Kowa, Merck, Novartis,

Prosciento

, Regeneron, and Sanofi. In the past 12 months, Dr. Harold Bays has served as a speaker for

Amarin

, Amgen, Eisai, Kowa,

Orexigen

, Regeneron, and Sanofi.

Jennifer Seger, MD, FOMA: Nothing to discloseCraig Primack, MD, FACP, FAAP, FOMA: Orexigen Therapeutics, Inc. (Speakers bureau); Novo Nordisk, Inc. (Speakers bureau); Nestle Nutrition (Advisory activities); Your Better Self

Joshua Long, MD,

FACS

, FASMBS: Titan Medical Inc. (Company holdings); Lexington Medical (Advisory activities)Nihar Shah, MD, FACP: Nothing to discloseThomas W. Clark, MS, MD, FACS, FASMBS: Nothing to discloseWilliam McCarthy, MD, FOMA: Nothing to discloseObesity Algorithm®. ©2017-2018 Obesity Medicine Association.

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Historic Citation and Authorship2017-2018Bays HE, Seger

, J, Primack C, Long J, Shah NN, Clark TW, McCarthy W. Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2017-2018. www.obesityalgorithm.org (Accessed = Insert date)

2016-2017

Bays HE, Seger JC, Primack C, McCarthy W, Long J, Schmidt SL, Daniel S, Horn DB, Westman EC: Obesity Algorithm, presented by the Obesity Medicine Association. www.obesityalgorithm.org. 2016-2017. www.obesityalgorithm.org (Accessed = Insert date)2015-2016Seger JC, Horn DB, Westman EC, Primack C, Long J, Clark T, McCarthy W, Bays HE. Obesity Algorithm, presented by the Obesity Medicine Association, 2015-2016. 2014-2015Seger JC, Horn DB, Westman EC, Primack C, Schmidt SL, Ravasia D, McCarthy W, Ferguson U, Sabowitz BN,

Scinta

W, Bays HE. Obesity Algorithm, presented by the American Society of Bariatric Physicians, 2014-2015.

2013-2014

Seger JC, Horn DB, Westman EC, Lindquist R,

Scinta

W, Richardson LA, Primack C, Bryman DA, McCarthy W, Hendricks E,

Sabowitz

BN, Schmidt SL, Bays HE. Obesity Algorithm, presented by the American Society of Bariatric Physicians, 2013-2014.