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Weight In The Workplace: What’s Working & Where

Change Is Needed Julie Friedman, Ph.D.

Director of Binge Eating and Weight Management Programs

Insight Behavioral Health Centers

Assistant Professor, Northwestern University Medical School

What is Obesity & Why Has It Been Targeted In The

Workplace?

What do “Overweight” & “Obese” Mean?

• Ranges of weight that are greater than what is generally considered healthy for a given height.

• Ranges of weight shown to increase likelihood of certain diseases and other health problems.

• Determined by Body Mass Index- a number calculated from weight and height, waist circumference, and other anthropometric measures (CT, MRI, US.)

Obesity is a Chronic Medical Condition

• 2004 - Medicare removes language from its coverage manual saying obesity was not a disease.

• 2013 -The American Medical Association officially recognizes obesity as a chronic disease.

• February 2015- The Endocrine Society released new, more aggressive guidelines for the treatment of obesity.

BMI Chart

BMI by Category

• BMI <18.5 Underweight

• BMI 18.5 – 24.9 Healthy Weight

• BMI 25 – 29.9 Overweight

• BMI 30 – 34.9 Class I Obesity

• BMI 35 – 39.9 Class II Obesity

• BMI > / = 40 Class III Obesity

BMI Classification- Example

Height Weight BMI Category

5’9” < / = 124# < 18.5 Underweight

5’9” 125 - 168 18.5 – 24.9 Healthy Weight

5’9” 169 – 202 25 – 29.9 Overweight

5’9” >203 > / = 30 Obese

BMI – What Works and What Doesn’t

What Works

• Observational studies consistently report an association between elevated BMI & mortality

• Each five-unit increment in BMI above 25 kg/m2 is associated with increases of 29% for overall mortality, 41% for cardiovascular mortality and 210% for diabetes-related mortality

What Doesn’t

• Underestimates fat in elderly who have lost lean muscle

• Overestimates fat in “body builders”

• Does not necessarily reflect the presence of underlying obesity-related comorbidity, reduced quality of life or diminished functional status

• Implications may vary by age, race

Waist Circumference

• Associated with higher risk of CVD & T2DM

• Male central obesity: 102 cm or 40”

• Female central obesity: 88 cm or 35”

Medical Complications of Obesity

Phlebitis

venous stasis

Coronary heart disease

Pulmonary disease

abnormal function

obstructive sleep apnea

hypoventilation syndrome

Gall bladder disease

Gout

Diabetes

Osteoarthritis

Nonalcoholic fatty liver disease

steatosis

steatohepatitis

cirrhosis Hypertension

Dyslipidemia

Skin

Idiopathic intracranial hypertension

Cancer

breast, uterus, cervix, prostate, kidney

colon, esophagus, pancreas, liver

Gynecologic abnormalities

abnormal menses

infertility

polycystic ovarian syndrome

Stroke

Did You Say Cancer??? • Colon and Rectal, Post-menopausal Breast,

Kidney, Endometrial – 40% of cases attributed to obesity, Esophagus, Pancreas, Thyroid, & Gallbladder.

• (National Cancer Institute report 1-3-2012) In 2007, 34,000 new cases of cancer were attributed to obesity. With existing trends in obesity staying stable, 500,000 new cases of cancer will be attributable to obesity in 2030. If every adult reduced their BMI by one point (2.2 pounds) we could stave off 100,000 new cases.

• Mechanisms of Action – fat tissue produces excess estrogen (breast and endometrial,) obesity is associated with increased insulin which promotes development of certain tumors, fat cells produce hormones that stimulate cell and thus tumor growth.

Treatment Guidelines Based on BMI

What is the impact of obesity in the workplace?

Costs of Obesity - Direct • Health care costs are increasingly costly for

employers – ranging from $36-$73.1 billion per year depending on the study.

• Well designed study puts total cost of obesity to private employers at approximately $45 billion per year (Finkelstein EA, Fiebelkorn IC, Wang G. American Journal

of Health Promotion. 2005; 20(1):45-51.)

• Health spending is approximately 36% higher in obese vs. normal weight adults. (Sturm R. Health Affairs

2004; 23(2): 199-205.)

Costs of Obesity - Direct

• Pharmaceutical expenses are 87% higher for obese than non-obese individuals. (Gazmararian, JA,

Frisvold, D., Zhang, K., & Koplan, J. Journal of Obesity 2015; 2015:298698.)

• Rise in obesity prevalence rates have also increased spending for 3 weight related medical comorbidities – diabetes, hyperlipidemia, and heart disease. (Thorpe, KE, Florence, CS, Howard, DH, & Joski, P.

Health Affairs. 2004;W4:480-86.)


• The estimated annual medical cost of obesity in the U.S. was $147 billion in 2008.

• The medical costs for people who have obesity were $1,429 higher than healthy weight peers (2008).

• Compared with normal-weight individuals, patients w/ obesity incur 46% higher inpatient costs & 27% more outpatient costs.


• Clear linear relationship/positive correlation between BMI and frequency of workers’ compensation claims, lost workdays, & medical claims costs. (Ostbye T, Dement JM, & Krause KM. Archives of

Internal Medicine 2007 Apr 23; 167(8):766-773.)

• Obesity associated with higher likelihood of worker illness absenteeism – effect is doubled for workers with BMI > 40 & DM. (Howard JT & Potter, LB.

Obes Res Clin Prac 2014 Jan-Feb; 8(1) e1-15.)

Costs of Obesity - Indirect

• HRQOL decreases as BMI increases – worsens significantly with weight gain, decreases moderately with weight loss. (Van Nunen AMA, et. al.,

Obesity Surgery 17.10 (2007) 1357-1366.)

- UCSD Study – Pediatric Obesity

• As BMI increases, early mortality increases & work productivity decreases. (Dee, Anne et. al., BMC

Research Notes 7(2014): 242.)


• Higher premiums for higher weight employees & those who do not participate in employee wellness programs can increase weight stigma and weight discrimination at work. – CVS - $50/month surcharge for those not disclosing weight each

month.

– ACA – allows upcharge for employees who do not participate in wellness programs.

Costs of Obesity – Indirect (Puhl R. & Brownell, K. (2001). Obesity Research, 9:788-805)

• Weight discrimination increased 66% from the mid ‘90s to mid ‘00s.

• Fewer obese employees are being hired for high level positions.

• Obese employees are less likely to get hired in general & less likely to be promoted at all levels.

• Obese employees earn between 3-6% less than lean counterparts.


• Employee Wellness programs- if executed poorly - can reinforce reported (in repeated laboratory settings) work-related stereotypes. (Roehling, M.V.

(1999). Personnel Psychology 52: 969-1017.)

– lack self-discipline, less conscientious, lazier, sloppier, emotionally unstable, disagreeable.

What Are Employers Doing to Address Weight in the

Workplace?

Corporate Wellness – Obesity Specific Interventions

(Lemon SC, et. al., American Journal of Preventive Medicine 2010 38(1), 27.; Kerr, MA, et. Al., American Journal of Health Promotion 2004 Mar-

Apr 18(4):312-5.; Linde JA, et. al., International Journal of Behavioral Nutrition & Physical Activity 9 (2012): 14.)

• “Stair WELL”, pedometer, “walk with upper management” & other campaigns to increase participant steps per day.

• Nutrition Intervention with Food Services Sites/Staff: healthy entrees in workplace cafeterias, signs noting “healthy options.”




• Decreased pricing & targeted promotion of “healthy” options in workplace vending machines.

• Distribution of media detailing healthy weight behaviors (i.e. frequent self monitoring of food and weight.)




• Increased opportunities to weigh at work – scales and BMI charts scattered throughout site.

• “Weight Watchers at Work” across sites.

Are workplace wellness interventions working??

…evidence is MIXED at best

Efficacy of Weight Control Interventions in the Workplace

• RAND analysis – 170 page analysis of workplace wellness programs – 2013. (Rand Corp Research Report,

2013.)

– One year participation in a weight control program significantly associated with a reduction in BMI – 1 pound lost vs 2 pounds gained per year.

– Effect persists 2 years.

– Participating employees only saved the company $2.00/month – not statistically significant.

Efficacy of Weight Control in the Workplace

• (Anderson LM et. al. American Journal of Preventive Medicine 2010 July; 39(1): 104.)

• Reviewed 9 Randomized Controlled Trials

• Pooled effect estimate of -2.8 pounds; decrease in BMI of -0.5.

• Better than gaining weight but limited utility in decreasing health care costs.


• (Almeida FA et. al., Obesity (Silver Spring) 2015 April 23(4):737-745.)

• No significant impact of financial incentives to lose weight.

• 28 worksites, 1790 employees.

• Delivered daily vs. quarterly emails.

• Participants lost an average of 2 pounds across both conditions.


(Horwitz, JR et. al. Health Affairs March 2013 32(3) 468-476.);

•Review of the research raised doubts that obese employees spend more on medical care than others- mediators (Gender & Disease State)

•Concluded – “Although there may be other valid reasons, beyond

lowering costs, to institute workplace wellness programs, we found little evidence that such programs can easily save costs through health improvement without being discriminatory. Our evidence suggests that savings to employers may come from cost shifting, with the most vulnerable employees… bearing greater costs that in effect subsidize their healthier colleagues.”

“Weight Watchers” at Work (Tsai AG & Wadden TA, Annals of Internal Medicine 2005; 142:56-66.)

• Reviewed 3 RCT’s with total n=551.

• Only 1 showed that participants had a mean loss of 3% of IBW after 2nd year.

• New research (Gudzune et. Al., Annals of Internal Medicine

2015; 162(7):501-512.) suggests that participants who enroll in commercial weight loss programs lose 2-4% more weight than controls with WW participants at 2.6%.

How Can We Improve “Weight Control” Interventions at Work

Without Adding to Weight Stigma?

Reclaiming a Missed Opportunity…

First, Address Obesity With Evidence Based Theory &

Practice

Abandoning the Eat Less, Move More Rhetoric

“Eat Less, Move More?”

• An outdated obesity paradigm—

• Calories In, Calories Out – High availability of highly processed, highly

palatable food -- increased calories in + technological advances/less lifestyle activity—decreased calories out creating ENERGY IMBALANCE.

(JAMA: 311,21 – 2167-8)

Meal-related

(Short-term)

Adiposity-related

(long-term) Meal-related

(Short-term)

Leptin

PYY

Insulin

GLP-1

PYY

Oxyntomodulin

Gastric distension

Hypo-

thalamus

Hindbrain

CCK

Adiposity-related

(Long-term)

Vagus

Nerve

Spinal

Nerves

Ghrelin

Ghrelin

Adapted from

Marx J,

Science

299:846, 2003

Adapted from

Marx J,

Science

299:846, 2003

DECREASED GHRELIN

+ INCREASED GLP-1

& PYY=BETTER

APPETITE CONTROL=

BETTER CONTROL OF

FOOD INTAKE. Suzuki et. Al., (2014.)Endocrine Journal

Advance Publication; doi:10.1507/

endocrij.K10E-077

A complex set of

hormones dictates

how someone thinks

and feels about food.

Physiological Model of Overeating

• “Chronic overeating is a MANIFESTATION of increasing adiposity vs. a primary CAUSE of increasing adiposity.” (JAMA, 311: 21; June 4, 2014.)

Increasing Adiposity Hormonal & Nervous System Disruption Increased Hyperphagia + Palatable Food Intake

How Can Interventions Look Different and Work Better in

Accordance with This Model?

• New Models of Obesity:

– Educate employees regarding:

• Role of high glycemic foods

• Role of stress – brain detects threat – triggers

release of cortisol (long term) and adrenaline (short term)

– cortisol binds to receptors in the brain and increases appetite and cravings for fat and sugar

Delivery of Effective Interventions


• New Models of Obesity:

– Role of sleep

• disrupts functioning of ghrelin (+) and leptin (-)

• weakens “willpower” and resistance to highly palatable foods in the environment.


• Shift work, long working hours, and increased commute times add to sleep debt which promotes obesity. (Bayon V et.

al. Annals of Medicine 2014 August; 46(5):264-272.; St-Onge MP Journal of Clinical Sleep Medicine 2013 Jan 15;9(1)73-80.)

– Short sleep duration associated with elevated BMI through several pathways: • Increased food intake, decreased energy expenditure;

Dysregulation of appetite and satiety hormones – reduced leptin, elevated ghrelin; Impairment of cognitive control in response to food cues.


– Incorporate interventions that help with quality vs. quantity of available food. • Reduce but not eliminate refined sugars/high GI foods at

work.

– Improve sleep quality and quantity/

reduce sleep deprivation. • Sleep Hygiene, Stimulus Control,

Sleep Restriction, Work Hours

Adjusted

– Onsite stress management classes

Second, Identify & Treat Eating Pathology in Employees

Binge Eating, Night Eating, Emotional/Stress Eating, Compulsive

Overeating

Binge Eating Disorder

• Binge = eating, in a discrete period of time, an amount of food that is definitely larger than what most people would eat in a similar time period under similar circumstances accompanied by a sense of lack of control over eating during the episode.

Binge Eating Disorder - Definition

• DSM-V Criteria:

• A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following: – 1) Eating, in a discrete period of time (e.g. within any 2 hour

period), an amount of food that is definitely larger than what most people would eat in a similar period of time under similar circumstances.

– 2) A sense of lack of control over eating during the episode (e.g. a feeling that one can not stop eating or control what or how much one is eating.)

Binge Eating Disorder • B. The binge eating

episodes are associated with 3 or more of the following:

1) Eating much more rapidly than normal.

2) Eating until uncomfortably full.

3) Eating large amounts of food when not feeling physically hungry.

4) Eating alone because of feeling embarrassed by how much one is eating.

5) Feeling disgusted with oneself, depressed, or very guilty afterward.

Binge Eating Disorder

• C. Marked distress regarding binge eating is present.

• D. The binge eating occurs, on average, at least once a week for three months.

• E. The binge eating is not associated with the use of inappropriate compensatory behavior as in bulimia nervosa and does not occur exclusively during the course of bulimia nervosa or anorexia nervosa.

Binge Eating Disorder • Prevalence rates ---

– General population – 2.0% males; 3.5% females – most prevalent ED.

– Obese treatment seeking adults - 32-35%

– ***Associated with work productivity impairment: “Binge eating remained a significant correlate of productivity impairment. Estimated annual productivity loss due to binge eating in a company of 1000 employees was $107,965.”(Bedrosian RC et.al., Journal of

Occupational and Environmental Medicine 2012 April; 54(4):385-393.)

Other Specified Feeding and Eating Disorder (OSFED)

• Includes:

• Binge Eating Disorder of low frequency and/or limited duration.

• Bulimia Nervosa of low frequency and/or limited duration.

• Purging Disorder


Night Eating Syndrome

– Evening Hyperphagia (25% or more of

total daily calories consumed after the evening meal and before bedtime.)

AND/OR

– Nocturnal awakening and ingestion of food two or more times per week.


Night Eating Syndrome 3 of 5 must also be present:

1) Morning anorexia

2) Urges to eat in the evening and at night

3) Belief that one must eat in order to return to sleep

4) Depressed mood- frequently worsens in evening

5) Sleep disturbance

Night Eating Syndrome • Prevalence rates of NES:

(Problematic as criteria vary between studies:)

• Prevalence rates tend to increase with degree of obesity. (Cleator J et.al., Nutrition & Diabetes 2012 Sept. 2(9).)

• Prevalence rates in severe obesity estimated to be between 15 and 51% (Stunkard et. al., Int Jour of Obesity Rela

Metab Disorder 1996; 20(1):1-6; Aronoff et. al., Journal of Amer Diet Assoc 2001 Jan; 101(1): 102-4.)

“Food Addiction”

• Assessed by the Yale Food Addiction Scale

• Prevalence Rates – about 25% in obese population; 57% in obese population with Binge Eating Disorder (Flint AJ et. al., American Journal of Clinical Nutrition

2014 March; 99(3):578-586; Pursey et. al., 2014. Nutrients, 6, 4552-4590.)

• BED- when coupled with obesity- represents a form of eating and weight dysregulation driven and maintained by physiological abnormalities associated with addictions. (Volkow et. al., 2012 Current Topics

in Behavioral Neuroscience 11, 1-24.)


“Food addiction” = disruption in neurobiological processes sensitive to reward & those that underlie inhibitory control (Volkow et. al., 2013.)

• Reward Deficiency Hypothesis – – Greater anticipated reward (anticipatory food reward) increases

DESIRE to overeat.

– BUT-less activation of the meso-limbic reward system in response to food=reward deficiency.

– Thus, patients are vulnerable to overeating to make up for this “gap” in the same way that alcohol and drug users use substances to stimulate reward circuitry.

– FMRI study –looked at brain activity before and after chocolate milkshake consumption- higher weight adolescent girls showed higher ANTICIPATORY reward and lower CONSUMMATORY reward than lower weight counterparts.

Stice, E. & Spoor, S. (2008.) Journal of Abnormal Psychology; 117(4):924-935.



FOOD vs. “EATING” addiction craving, preoccupation, compulsive use despite negative consequences, denial of problem, use of substance to relieve negative affect with distress following use, genetic links, high recidivism, overeating and weight gain in early stages of recovery from drug addiction. (Gold et. al, 2003.)

How can interventions work better given prevalence rates of

eating pathology in higher weight employees?

Improving Employee Wellness Programs

• Eating pathology is common but highly treatable.

• Screening for Binge Eating Disorder particularly needs to be part of any health screening or weight management program offered by employers. This screening can be done easily & quickly with self-report measures.

Improving Employee Wellness Programs

• Treatment referrals for appropriate services.

• Treatment referrals for appropriate levels of care/service intensity.

– Intensive Outpatient Program, Partial Hospitalization Programs, Residential Programs

– Shameless Plug

If you have to start somewhere…

• Self-monitoring – apps – Recovery Record; Rise Up and away from My Fitness Pal

• Prescribed Pattern of Regular Eating

Prescribed Pattern of Regular Eating

Sample:

Breakfast - 9:00

Lunch - 12:00

Snack 1 – 3:00

Dinner – 7:00

Snack 2 - 10:00

Prescribed Pattern of Regular Eating

• Eliminates “intuitive eating.”

• Prescribed Pattern of Regular Eating

– Eliminates emotional decision making.

– Regulates appetite and satiety hormones.

– 3 meals, 2 snacks – 3/5 “sweet spot.”

Why Start with PPRE? • Consistent research show that food cues activate lateral

hypothalamus orexin neurons in the absence of food or physiological hunger & chronic low levels of hunger hormones in obese patients. (Marzullo, P et. Al., 2004 J Clin

Endocrinol Metab 2004 Feb; 89(2):936-9.)

• Food cues stimulate persistent feeding even in sated rats – thus even animals feel stimulated by food cues independent of hunger. (Reppucci, CJ & Petrovich, GD (2012)

Appetite 59(2):437-447.)

• Biological mechanisms (survival) encourage opportunistic eating. (Petrovich (2013.) Physiology & Behavior 121: 10-18.)

Why Start with PPRE? (Cornier et. al., 2013 Feb 17; 110-11:122-8 Physiology & Behavior)

FMRI studies:

Overfed lean individuals – hunger decreases in subsequent 2 days and less responsive to food cues.

Overfed obese subjects – lack of sensitivity to excess feeding; hunger stayed the same and food became MORE rewarding with persistent activity in attention and motivation related brain centers.

Why Start with PPRE?

--Consistent with research that shows dysregulation of appetite and fullness hormones is part of pathophysiology of excess weight and overeating.

--Research unconditionally supports a tendency for external vs. internal cues to promote food intake.

--Hypersensitivity to food related cues occurs BEFORE the onset of excess weight and is exacerbated by excess weight – CHICKEN-EGG

Stimulus Control

Binge Eating & Enhanced Reinforcement –

– Positively AND Negatively Reinforcing behavior

– More reinforcement = more habit strength – even rats eat more where they have always eaten!!

Stimulus Control Examples

• Only eating while eating – only bingeing while bingeing.

• Decrease restaurant and fast food eating to no more than 3 times per week.

– Stimulus Control Rationale

Third, Treat Excess Weight as the Chronic, Treatment Resistant

Medical Issue That It Is

Treating Obesity as a Disease vs. A Character Flaw

Why is Obesity Pathological?

Release of adipokines (lipotoxicity)

Increased mechanical burden

Increased respiratory burden

Fluid and hemodynamic changes/CV burden

Increased abdominal pressure

Dietary and physical activity changes associated with obesity

Obesity as Medical Disease

• Disease – “ a condition of the living animal … that impairs normal functioning and is typically manifested by distinguishing signs and symptoms” (Miriam Webster)

• Weight begets weight in a series of physiological changes that start at the level of increasing adiposity.

PAI-1 = plasminogen activator inhibitor-1. Kershaw EE, et al. J Clin Endocrinol Metab. 2004;89:2548-2556.

Traditional View Fat is an inert storage depot

Modern View Fat is a secretory endocrine organ

Adipose Tissue as an Endocrine Organ

Wildman RP et al. Arch Intern Med 2008;168:1617-24.

BMI & Metabolic Health

Metabolically healthy (0 or 1)

Metabolically abnormal (≥ 2)

Cardiometabolic abnormalities: • Elevated blood pressure • Elevated triglycerides • Decreased HDL-C • Elevated blood glucose • Insulin resistance (HOMA-IR) • Systemic inflammation (hsCRP)

100

80

60

40

20

0

Pre

vale

nce

, %

Men

Normal Weight Overweight Obese

70.8

29.2

51.2 48.8

30.1

69.9

100 Women

80

60

40

20

0

Pre

vale

nce

, %

35.4

64.6 78.9

21.1

57.0 43.0

Normal Weight Overweight Obese

Despres J-P et al. BMJ 2001;322:716

Edmonton Obesity Staging System (EOSS)

Stage 0

Sharma AM & Kushner RF, Int J Obes 2009

Stage 1

Stage 2

Stage 3

Stage 4

co-morbidity

moderate

moderate

Obesity

Stage Cardiometabolic Mechanical/Functional

0 No Risk Factors No functional impairments or impairments in well-being

1 “Sub-clinical Risk Factors”: Prediabetes, Metabolic Syndrome, NAFLD

Mild limitations and impairment of well-being: reduced QOL, arthalgias

2 End-Stage Metabolic Disease: T2DM, Hypertension, Sleep Apnea;

Moderate limitations and impairment of well-being: uncomfortable around others, arthritis

3 End-Stage CVD Disease: MI, heart failure, stroke; Significant limitations and impairment of well-being: poor

QOL

4 End-Stage Disabilities Severe limitations and impairment of well-being

Sharma AM & Kushner RF, Int J Obes 33:289, 2009; Padwal RS et al CMAJ 183:E1059, 2011

Edmonton Obesity Staging System

(EOSS)

EOSS Predicts Mortality in NHANES III

Padwal RS, et al. CMAJ. 2011;183(14):E1059-66

0.4

0

.5

0.6

0

.7

0.8

0

.9

1.0

0 50 100 150 200

NHANES III (1988-1994)

Pro

po

rtio

n s

urv

ivin

g

EOSS Stage Zero

One

Two

Three

Months Since MEC

Examination

0.4

0

.5

0.6

0

.7

0.8

0

.9

1.0

0 50 100 150 200

NHANES III (1988-1994)

BMI Classification Overweight

Class I Obese

Class II Obese

Class III Obese

Months Since MEC

Examination

Validation Of EOSS

• Thus, the Edmonton Obesity Staging System is a better predictor of obesity risk & increasing mortality independent of BMI, metabolic syndrome & waist circumference which addresses limitations of BMI alone.

BMI + Waist Circumference + EOSS

• EOSS is intended to complement anthropometric indices & provide clinically relevant prognostic information in a manner analogous to the “tumor, node, metastasis” system used in oncology to define the size and extent of the spread of cancer.

And this is a disease with a strong hold on its sufferers:

• Over 150 alleles discovered that genetically predispose one to obesity.

• Gut hormone, neural circuitry, and gut microbiota are dysfunctional with obesity and become more dysfunctional as weight increases.

Ex: LEPTIN (Lin S, Thomas TC, Storlien LH, Huang XF International Journal of Obesity and Related Metabolic Disorders: Journal of the International Association for the Study of Obesity

[2000, 24(5):639-646; Y. Zhang, P.J Scarpace Physiology & Behavior, 88 (2006) 249-256.)

• Leptin = satiety hormone. Made by adipose cells. Helps regulate energy balance by inhibiting hunger and regulating fat storage.

– Acts on receptors in hypothalamus

• Obese animals and humans have decreased leptin receptors and impaired leptin signaling resulting in chronically elevated leptin levels AND leptin resistance.

LEPTIN

• What does this mean????

• Higher weight employees are unable to detect satiety despite high levels of energy stores and thus high levels of leptin.

• “Portion control” will backfire!!!

Ex: Peptide YY (P. Sumithran, L. Prendergast, E. Delbridge, K. Purcell, A. Shulkes, A. Kriketos, & J. Proietto.

New England Journal of Medicine 2011; 365: 1597-1604.)

•PYY - gut hormone peptide.

•PYY replacement reverses obesity ; PYY deficiency makes rodents hyperphagic and obese.

•As humans become overweight, PYY decreases.

•“Dieting” caused further decrease in PYY in overweight/obese patients.

Once weight is gained, body works hard to defend it-

• Biological adaptations occur with the development of excess weight that serve to protect- or even increase- an individual’s highest weight.

– Body interprets even 10% weight loss as a “stress”-

• Reacts by:

- Decreasing resting energy expenditure

- Decreasing thyroid hormone production

- Increasing appetite hormones

- Increasing cortisol which increases desire for hyperpalatable foods.

- Increasing fat storage capacity with preadipocyte proliferation.

What does this mean for higher weight employees?

• Popular diets alone are doomed to fail –

– 1/3-2/3 of participants regain more weight than they lost on diets. (Mann et.al., American Psychologist 2007 April

62(3):220-33.)

– Weight Watchers at Work –

Weight Watchers effective – (-6 pounds OR about 3% OF BODY MASS) in 12 months – but much of weight was regained at 24 months (Atallah et.al., Circulation:

Cardiovascular Quality & Outcomes 2014;7:815-827.)

New (Proposed) Guidelines for Obesity Treatment

(Ochner CN et. al., Lancet Diabetes Endocrinology April 2015 3(4), pgs. 232-234. )

• Address obesity prevention with ALL overweight patients (BMI 25-30) prior to the development of obesity.

• Focus on overall lifestyle choices- lifestyle activity, deliberate activity, and quality of diet. Monitor aggressively over time.

New (Proposed) Guidelines for Obesity Treatment

(Ochner CN et. al., Lancet Diabetes Endocrinology April 2015 3(4), pgs. 232-234. )

• Encourage patients with BMI 30 + to consider treatment even if weight is not their primary complaint.

• Encourage aggressive lifestyle modification & pharmacotherapy.

• If lifestyle modification & pharmacotherapy are ineffective, consider bariatric surgery.

What does this mean for weight in the workplace?

• Lifestyle modification needs to be really aggressive – and encompass movement and nutrition- in order to work.

• Employees should be referred out for bariatrician consults if they meet criteria for pharmacotherapy and/or bariatric surgery. – Weight loss – about 10% behaviorally; 25% bariatric surgery.

– Shameless plug.

What does this mean for weight in the workplace?

• “Workplace wellness” should focus on individualizing care and treatment plans OR refer out for this and help implement in the work environment.

• Examples: office candy dishes, lunch & dinner breaks at prescribed times, time off for disease management appointments.

• Example: breaks from “sitting” vs. formal exercise at work.

Conclusions

• Current methods of addressing weight in the workplace are only mildly effective and yet have great potential to increase weight discrimination and weight stigma.

• Understanding obesity as a medical disease is crucial even for behavioral treatment paradigms.

Conclusions

• Identifying and treating weight-related eating pathology is crucial for generating improvements in productivity, quality of life, and health status.

• Lifestyle modification must be aggressive and multidisciplinary and will often require off site service seeking.

Acknowledgements • Insight Behavioral Health Centers/Eating Recovery

Center

• Susan McClanahan, CEO of Insight.

• Laura Adams, Suzanne Smith, and the rest of our fabulous Professional Relations team.

• My wonderful CORE team – Dr. Lynn Chehab, Dr. Lisa Oldson, Dr. Shana Small, Dr. Kat Karasina, Dr. Peter Zemenides, Samantha Weinstein, Laura Lange, Michelle Abruzzo, Tara Javidan, Christine Sinak Sweeney, & Matt Lawson.

weight in the workplace - nieapa · gallbladder. • (national cancer institute report 1-3-2012) in...

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