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A. abdominoplasty

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permanent weight reduction from abdominoplasty see http://www.plasticsurgery.org/news-and-resources/many-women-have-long-term-weight-loss-after-tummy-tuck-reports-plastic-and-reconstructive-surgery.html
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Permanent Weight Reduction after Abdominoplasty: Neurocrine Factors, A Pilot Study Rex Moulton-Barrett, MD & Jennifer Fuller, B.A. Plastic & Reconstructive Surgery Alameda and Brentwood, Ca
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Page 1: A. abdominoplasty

Permanent Weight Reduction after Abdominoplasty: Neurocrine Factors, A Pilot Study

Rex Moulton-Barrett, MD & Jennifer Fuller, B.A. Plastic & Reconstructive Surgery Alameda and Brentwood, Ca

Page 2: A. abdominoplasty

The Role for Abdominoplasty ?

Just because you can, does not mean you should ?

Page 3: A. abdominoplasty

After Abdominoplasty Some Patients: Lost weight & Lost no weight

Page 4: A. abdominoplasty

Questions

• Does abdominoplasty lead to long-term weight loss ?

• Which group of patient’s benefit most ?

• What are the cause(s) of weight loss after surgery ?

Page 5: A. abdominoplasty

Obesity Epidemic

• BMI: Body Mass Index: weight kg/(height m)2

• <1/3 of U.S. Normal BMI 19-25

• 1/3 of U.S. Overweight BMI 25-30

• 1/3 of U.S. Obese BMI 30-40

• The prevalence of obesity has more than doubled since 1980

• 3% of U.S. Morbid-Super Obese BMI> 40

Page 6: A. abdominoplasty

Treatment of Obesity

3 main methods of treatment:

• Life Style Modification – Moderately effective but difficult to monitor and sustain

• Pharmacological Therapy– Few effective treatments exist

• Surgical Treatment– Significant and permanent weight loss

– Insurance criteria morbid obesity (BMI ≥40)

Page 7: A. abdominoplasty

Life Style Modification

• Convert to ‘ negative energy gap ’

• Increased energy expenditure:reduce non-active time: car, chair, sofaincreased exercise time

increased energy lost during exercise

• Diet: high protein low carbohydrate low sugar ‘+ ketogenic diets’ reduce appetite ( Am J of Clin Nutrition, 2008: 87(1), 44-55 )

avoid exercise before meals: 20 minute run = 20oz ie avoid post exercise ‘calorie rewards’

Page 8: A. abdominoplasty

Current Weight Reduction Drugs( 1% of 59 billion dollars spent to loose fat in USA / yr )

% body weight lost % pts lost at least

minus placebo 5% body weight

a.c.t. placebo ‘/x’

• FDA Approved– Meridia: Sibutramine 4.3 55/27– Xenical: Orllstat 2.9 54/33

• New drugs pending approval– Qnexa 9.0 67/19– Contrave 4.6 53/21– Lorcaserin 3.4 47/23

1997:fen-phen (fenfluramine-phentermine) & Redux (dexfenfluramine) removed from market

Page 9: A. abdominoplasty

Mechanism of Action

• Meredia: Monoamine RI (serotonin & noradrenaline)

(Abbott) may BP, HR: not to use if hypertensive

unlike fenfluramine does not elevate serum serotonin

controls binge eating

• Qnexa: Phentermine & Topiramate

(Vivus) 56 week course: 37 lb loss: BP, glucose, cholesterol

may be useful in type 2 DM

Phentermine: hypothalamic norepinephrine release

high dose: potential for dependence

Topiramate: ( Topamax ), anti-epileptic,

anti-migraine,

bipolar/binge eating

Page 10: A. abdominoplasty

Surgical TreatmentGastric Bands

Partial Gastric & Intestinal Bypass

( Roux en Y )

Abdominoplasty ?

Page 11: A. abdominoplasty

Abdominoplasty Work-Up

• Obese versus abdominal laxity or symptomatic pannus ?

• First consultation: attempt weight reduction if >200lbs

• Charge about 25% more if over 200lbs

• ‘3 S plan’: South Beach Diet, Sugarless house, Stationary bike with 45 minute 3x week TV contract after meals

• + Meridia if unsuccessful > 4 weeks & binge eating ?

Page 12: A. abdominoplasty

Abdominoplasty Technique

• Low incision 4 cm above the anterior labial commissure

• Aggressive midline Rectus Abdominus plication

• Jack knife sitting / Trendelenburg position closure

• Closure: interrupted Scarpa’s fascia

running dermal barbed 3.0 V -Lock Suture

skin glue and 1 inch Steri-Strips

• Lateral flank liposuction for contour

• 5 day pain pump & overnight in surgery center

• Rented surgical bed at home for 2-4 weeks

• Prolonged paper taping for 6 months when clothed

• 3 S’s starting 6 weeks post-op

Page 13: A. abdominoplasty
Page 14: A. abdominoplasty

Methods

• Retrospective case review: chart & structured interview

• same surgeon and one post-graduate student

• n= 21 patients post-abdominoplasty

• Follow up to > 1 year: 2007-2009

Page 15: A. abdominoplasty

Methods

Data collected included:

• Age, sex, and height

• Weight prior to abdominoplasty

• Minimum weight and time attained

• Time when weight regained

• Weight at 1 year post-surgery

• Current Weight

• Complications of surgery

• Previous bariatric surgery ?

• Changes in satiety

• Patient’s beliefs about cause of wt loss

• Patient satisfaction with surgical results

• Changes in diet & exercise after surgery

• Weight of pannus resected

Page 16: A. abdominoplasty

Results: Patient Population

Range Mean

Age 21-61 years 45 years

Height 5’0” – 6’0” 5’5”

Pre-op Weight 105-245 lbs 167.5 lbs

Pannus Weight 1.8 – 12.5 lbs 5.74 lbs

5/21 patients previously underwent bariatric surgery

Page 17: A. abdominoplasty

Results: BMI’s

My patients BMI US population

• 21 % Normal 33 %

• 50 % Overweight 33 %

• 29 % Obese 33 %

• None Morbid Obesity 3 %

My patients BMI mean: 27.66, lowest 18, highest 33.5

Page 18: A. abdominoplasty

Results: Patient Weight loss

• 90.5 % reported weight loss

• 47.6% maintained weight loss > 1 yr after surgery

Page 19: A. abdominoplasty

Results: Patient Weight Loss

Percent of Patients

Mean Pre-op Weight(lbs)

Mean Maximum Weight loss (lbs)

Mean Time of Max Weight Loss (months)

Mean Time of Weight Regain (months)

Short term weight loss only (<1 year)n=9

42.9 161.8 8.7 2.3 7.1

Long term weight loss (> 1 year)n=10

47.6 170.4 16.4 3.7 ___

No Weight lossn=2

9.5 175.5 ___ ___ ___

Page 20: A. abdominoplasty

Results: Patient Weight loss Weight loss as a function of Pannus Weight:

Weight of Pannus

No. of Patients

Pre-op Weight

Maximum weight loss

% with long-term weight loss(> 1 year)

≤ 4 lbs 7 144.9 5.3 33 %

> 4 lbs 14 178.7 14.7 54 %

Page 21: A. abdominoplasty

Results: Patient Weight Loss

• The greatest predictor of weight loss: pre-operative weight

Pre-op Weight (lbs)

No. of Patients

Mean Weight of Pannus (lbs)

Mean Maximum Weight Loss (lbs)

Mean Time Max Weight Loss reached (months)

No. Patients with long term weight loss (>1year)

< 140 lbs 4 2.5 1.8 1.4 0

140 ≥ to < 210 14 5.6 15 3.5 9 (64.3%)

≥ 210 3 9.2 8.6 2.2 1 (33.3%)

Page 22: A. abdominoplasty

Pre-operative weight associated with long term weight loss

WEIGHT

(LBS)

LONG TERM

WEIGHT LOSS

( >/= 4lbs & >1 YR )

NO LONG TERM

WEIGHT LOSS

( < 4lbs & > 1 YR )

< 140 & ≥ 210 1 6

≥ 140 to 210 9 5

p<0.0005

Page 23: A. abdominoplasty

Pre-operative BMI associated With long term weight loss

BMI

LONG TERM

WEIGHT LOSS

( >/= 4lbs & >1 YR )

NO LONG TERM

WEIGHT LOSS

( < 4lbs & > 1 YR )

<24.5 & ≥ 33.5 1 8

≥ 24.5 to <33.5 9 3

p<0.0023

Page 24: A. abdominoplasty

Results: Weight Loss & Satiety

No change

in appetite

(%)

Sense of satiety only after eating (%)

Lack of appetite at

all times (%)

Unpleasant abdominal sensation

Short-term weight loss only (<1year) n=9

2 (22.2) 4 (44.4) 3 (33.3) 2 (22.2)

Long-term weight loss (>1 year) n=10

1 (10) 4 (40) 5 (50) 1 (10)

No weight lossn=2

2 (100) 0 (0) 0 (0) 0 (0)

All Patientsn=21

5 (23.8) 8 (38.1) 8 (38.1) 3 (14.3)

Page 25: A. abdominoplasty

Reason(s) for Weight Loss

• Most frequent reason sited for weight loss: increased sense of satiety

• 84.2 % experienced an increase in satiety– 1/2 report satiety throughout the day, 1/2 report satiety only after eating

• 90% of long-term weight loss patients: reported increased satiety

• Mean duration of sense of satiety 7.3 months

Page 26: A. abdominoplasty

Conclusions

• The greatest predictor of long-term weight

loss was pre-operative weight then BMI

• 64.3% of patients weighing between 140

and 210 lbs had long term weight loss

• Only 14.3 % of patients outside this range

had long-term weight loss

Page 27: A. abdominoplasty

Conclusions

• The key factor in patient weight loss is

an increase in satiety

• Short-term weight loss patients began

to regain their weight at 7.1 months,

about the same time when their

satiety dissipated

Page 28: A. abdominoplasty

CNS Regulation of CNS Regulation of Appetite / SatietyAppetite / Satiety

2 Areas :2 Areas :

Page 29: A. abdominoplasty

The HypothalamusThe Hypothalamus

• One of the Hypothalamic Nuclei is called One of the Hypothalamic Nuclei is called the the Arcuate Nucleus (ARC)Arcuate Nucleus (ARC)

• ARC incomplete blood-brain barrier ARC incomplete blood-brain barrier

• Allows CNS entry of peripheral peptidesAllows CNS entry of peripheral peptides

and proteinsand proteins

Page 30: A. abdominoplasty

The ARCThe ARC• ARC contains two major populations of ARC contains two major populations of

neurotransmitter releasng neurons :neurotransmitter releasng neurons :

• stimulatestimulate feeding: feeding:– agouti-related peptide (agouti-related peptide (AgRPAgRP) & neuropeptide Y () & neuropeptide Y (NPYNPY))

• inhibit inhibit feeding:feeding:– Cocaine & amphetamine regulated transcript (Cocaine & amphetamine regulated transcript (CARTCART) & ) &

proopiomelanocortin (proopiomelanocortin (POMCPOMC), ),

– POMCPOMC cleaves into cleaves into -MSH-MSH. . Feeding

Feeding

ARC

Hypothalamus

2nd order neurons

Neural/ endocrine signals

-MSH

Page 31: A. abdominoplasty

The ARCThe ARC

-MSH-MSH acts as a ligand at the melanocortin - 4 acts as a ligand at the melanocortin - 4 receptor ( receptor ( MC4 MC4 ))

• Defects of this receptor: implicated in up to 4-6% Defects of this receptor: implicated in up to 4-6% of all of all

monogenetic childhood onset obesity in humansmonogenetic childhood onset obesity in humans

-MSH-MSH inhibits the receptor to inhibits the receptor to AgRPAgRP: inhibiting : inhibiting appeptiteappeptite

• AgRPAgRP inhibits the inhibits the MC4MC4 receptor: stimulating receptor: stimulating appetiteappetite

Page 32: A. abdominoplasty

The BrainstemThe Brainstem

Appetite signals: Appetite signals:

A.A. from circulating hormones via the area from circulating hormones via the area postremapostrema: incomplete blood-brain barrier: incomplete blood-brain barrier

B.B. neural signals from the vagus nerve neural signals from the vagus nerve

C.C. Bidirectional connections with Bidirectional connections with hypothalamushypothalamus

Page 33: A. abdominoplasty

The Vagus NerveThe Vagus Nerve

• Afferent signalsAfferent signals: mechanical & chemical: mechanical & chemical

• Cell bodies of afferent neurons in the Cell bodies of afferent neurons in the Nodose GangliaNodose Ganglia

• Projects into brainstem to interface with hypothalamusProjects into brainstem to interface with hypothalamus

Page 34: A. abdominoplasty

The Vagus Nerve ContinuedThe Vagus Nerve Continued

• The stretch receptor stimulation The stretch receptor stimulation

dependent on gastric volumedependent on gastric volume

• May suppress meal size independent of contentMay suppress meal size independent of content

• Effect is abolished by subdiaphragmatic vagotomyEffect is abolished by subdiaphragmatic vagotomy

• Gastric distension Gastric distension is insufficient to account for all is insufficient to account for all

aspects of satietyaspects of satiety

Page 35: A. abdominoplasty

The Vagus NerveThe Vagus Nerve

• Contains receptors for a number of gut Contains receptors for a number of gut hormoneshormones

• Vagotomy abolishes appetite-modifying Vagotomy abolishes appetite-modifying action ofaction of

many gut hormones: many gut hormones: CCK, PYY, GLP-1

• Vagus nerve is thought to be a major Vagus nerve is thought to be a major sight of gut hormone signalingsight of gut hormone signaling

Page 36: A. abdominoplasty

A Very Quick Overview of Appetite Regulating Hormones

Page 37: A. abdominoplasty

Appetite-regulating hormones:

• Ghrelin, released from the stomach, is the only known appetite stimulant, acting via hypothalamic expression of NPY and AgRP.

– Ghrelin levels rise preprandially in humans

– Administration of exogenous ghrelin leads to increased food intake and weight gain

Page 38: A. abdominoplasty

Appetite-regulating Hormones:

• In contrast, a growing number of peptide hormones have been found to produce satiety and decrease food intake.

Adiponectin

Insulin

Amylin

Cholecystokinin (CCK)

Apolipoprotein A-IV (apo A-IV)

Peptide YY (PYY)Pancreatic

Polypeptide (PP)Leptin

Oxyntomodulin (OXM)

Vasoactive Intestinal Polypeptide (VIP)

Glucagon-like peptide-1 (GLP-1)

Vagus

Nerve

Bombesin

Page 39: A. abdominoplasty

Intestines

Vagus

Summary: Gut HormonesSummary: Gut Hormones

Ghrelin

OXM

CCK

GLP-1

PYY

VIP

Apo A-IV

PP

PP

Bombesin

Pancreas

Stomach

Energy Regulatio

n

+

-

-

-

-

Page 40: A. abdominoplasty

Another Important Satiety Another Important Satiety Regulator: LeptinRegulator: Leptin

• Leptin, is released from adipose tissue, Leptin, is released from adipose tissue, mammary glands, ovarian follicles, placenta, mammary glands, ovarian follicles, placenta, skeletal muscle, and the P cell and chief cells of skeletal muscle, and the P cell and chief cells of the stomachthe stomach

• 25% of circulating leptin is derived from the 25% of circulating leptin is derived from the stomachstomach

• Leptin levels positively correlate with body fat: Leptin levels positively correlate with body fat: higher circulating leptins with greater BMI higher circulating leptins with greater BMI

• Leptin mediates central regulation of energy Leptin mediates central regulation of energy homeostasis via receptors in the ARC and homeostasis via receptors in the ARC and peripherally via the vagus nerveperipherally via the vagus nerve

Page 41: A. abdominoplasty

Leptin StudiesLeptin Studies• after binding in the hypothalamus receptor:

• leptin inhibits NPY and AgRP and

stimulates POMC and CART

• decreasing appetite & increasing energy expenditure (Cowley M, et al; Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus. 2001)

• mice with mutation of the Leptin receptor are profoundly obese. (Farooqi I, et al; Clinical and molecular genetic spectrum of congenital deficiency of the leptin receptor. 2007)

Ob /Ob mouse

Page 42: A. abdominoplasty

Appetite-regulating hormones:

• Starvation: : ghrelin, : PYY-3-36, insulin, leptin

• Post-prandial satiety: : ghrelin, : PYY-3-36, insulin, leptin

• Receptor mutations: CCK, OXM, insulin, PYY, leptin & bombesin : food intake and obesity

• Receptor antagonist or antisera for CCK, OXM, apo A-IV, PYY, and GLP-1 : food intake

• Jejuno-ileal bypass surgery or vertical-banded gastroplasty : GLP-1, PYY & PP levels

• Roux-en-Y : : 77% reduction in serum ghrelin

• 2 clinical studies from U London: a. s/cut injections CCK: Med students ate 25% less curry b. s/cut Modulin: 17 % less food intake & 26 % increased energy expenditure : 1 pound / wk. weight loss

Page 43: A. abdominoplasty

Future Study

• Patients are tested before abdominoplasty and incrementally after for levels of specific gut hormones

• Is there an association between hormone expression levels, reported satiety, and patient weight loss?

Page 44: A. abdominoplasty

Methods

• 15 patients to participate in our study

• Prior to surgery: age, weight, height, gynecological history, previous bariatric surgeries, and exercise regimens

• Fasting blood draw: Prior to & 1, 3, 6, and 12 months after surgery • At surgery weight of the pannus will be recorded

Page 45: A. abdominoplasty

Methods

• Blood plasma specimens will be shipped to Inter Science Institute on dry ice then assayed for PYY, GLP-1, PP, CCK, leptin, bombesin, and ghrelin

• At 0, 1, 3, 6, and 12 months post-abdominoplasty, document:

– Ranking on a 0-3 scale of:

» Appetite at rest

» Postprandial satiety

» Unpleasant abdominal feeling associated with poor appetite

» Amount of food consumed during a meal

Page 46: A. abdominoplasty

Budget

Page 47: A. abdominoplasty

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