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
1. 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
2. The Role for Abdominoplasty ?
Just because you can, does not mean you should ?
4. 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 ?
5. 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
6. 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)
7. Life Style Modification
• Convert to ‘ negative energy gap ’
• Increased energy expenditure:
reduce non-active time: car, chair, sofa
increased 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’
8. Current Weight Reduction Drugs
( 1% of 59 billion dollars spent to loose fat in USA / yr )
1997:fen-phen (fenfluramine-phentermine) &
Redux (dexfenfluramine) removed from market
% 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
9. 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
11. 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 ?
12. 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
13.
14. 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
15. Methods
Data collected included:
• Age, sex, and height • Previous bariatric surgery ?
• Weight prior to abdominoplasty • Changes in satiety
• Minimum weight and time attained • Patient’s beliefs about cause of wt
loss
• Time when weight regained
• Patient satisfaction with surgical
• Weight at 1 year post-surgery results
• Current Weight • Changes in diet & exercise after
surgery
• Complications of surgery
• Weight of pannus resected
16. Results: Patient Population
5/21 patients previously underwent bariatric
surgery
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
17. Results: BMI’s
My patients BMI mean: 27.66, lowest 18, highest 33.5
My patients BMI US population
• 21 % Normal 33 %
• 50 % Overweight 33 %
• 29 % Obese 33 %
• None Morbid Obesity 3%
18. Results: Patient Weight loss
• 90.5 % reported weight loss
• 47.6% maintained weight loss > 1 yr after surgery
19. Results: Patient Weight Loss
Percent of Mean Mean Mean Time Mean Time of
Patients Pre-op Maximum of Max Weight Regain
Weight Weight Weight Loss (months)
(lbs) loss (lbs) (months)
Short term 42.9 161.8 8.7 2.3 7.1
weight loss
only (<1 year)
n=9
Long term 47.6 170.4 16.4 3.7 ___
weight loss
(> 1 year)
n=10
No Weight loss 9.5 175.5 ___ ___ ___
n=2
20. Results: Patient Weight loss
Weight loss as a function of Pannus Weight:
Weight of No. of Pre-op Maximum % with long-term
Pannus Patients Weight weight loss weight loss
(> 1 year)
≤ 4 lbs 7 144.9 5.3 33 %
> 4 lbs 14 178.7 14.7 54 %
21. Results: Patient Weight Loss
• The greatest predictor of weight loss: pre-operative weight
Pre-op Weight No. of Mean Mean Mean Time No. Patients
(lbs) Patients Weight of Maximum Max Weight with long
Pannus Weight Loss reached term weight
(lbs) Loss (lbs) (months) 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%)
22. Pre-operative weight associated with
long term weight loss
LONG TERM NO LONG TERM
WEIGHT WEIGHT LOSS WEIGHT LOSS
(LBS) ( >/= 4lbs & >1 YR ) ( < 4lbs & > 1 YR )
< 140 & ≥ 210 1 6
≥ 140 to 210 9 5
p<0.0005
23. Pre-operative BMI associated With
long term weight loss
LONG TERM NO LONG TERM
BMI WEIGHT LOSS WEIGHT LOSS
( >/= 4lbs & >1 YR ) ( < 4lbs & > 1 YR )
<24.5 & ≥ 33.5 1 8
≥ 24.5 to <33.5 9 3
p<0.0023
24. Results: Weight Loss & Satiety
No Sense of satiety Lack of Unpleasant
change only after appetite at abdominal
in eating (%) all times (%) sensation
appetite
(%)
Short-term 2 (22.2) 4 (44.4) 3 (33.3) 2 (22.2)
weight loss
only (<1year)
n=9
Long-term 1 (10) 4 (40) 5 (50) 1 (10)
weight loss
(>1 year)
n=10
No weight 2 (100) 0 (0) 0 (0) 0 (0)
loss
n=2
All Patients 5 (23.8) 8 (38.1) 8 (38.1) 3 (14.3)
n=21
25. 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
26. 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
27. 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
29. The Hypothalamus
• One of the Hypothalamic Nuclei is called
the Arcuate Nucleus (ARC)
• ARC incomplete blood-brain barrier
• Allows CNS entry of peripheral peptides
and proteins
30. The ARC
• ARC contains two major populations of
neurotransmitter releasng neurons :
• stimulate feeding:
– agouti-related peptide (AgRP) & neuropeptide Y (NPY)
• inhibit feeding:
– Cocaine & amphetamine regulated transcript (CART) &
proopiomelanocortin (POMC),
– POMC cleaves into α -MSH.
↑ Feeding
Neural/ endocrine
signals
2 nd order
neurons
ARC
Hypothalamus
α-MSH ↓ Feeding
31. The ARC
∀ α -MSH acts as a ligand at the melanocortin - 4
receptor ( MC4 )
• Defects of this receptor: implicated in up to 4-
6% of all
monogenetic childhood onset obesity in
humans
∀ α -MSH inhibits the receptor to AgRP: inhibiting
appeptite
• AgRP inhibits the MC4 receptor: stimulating
appetite
32. The Brainstem
Appetite signals:
A. from circulating hormones via the area
postrema: incomplete blood-brain
barrier
B. neural signals from the vagus nerve
C. Bidirectional connections with
hypothalamus
33. The Vagus Nerve
• Afferent signals: mechanical & chemical
• Cell bodies of afferent neurons in the Nodose Ganglia
• Projects into brainstem to interface with hypothalamus
34. The Vagus Nerve Continued
• The stretch receptor stimulation
dependent on gastric volume
• May suppress meal size independent of content
• Effect is abolished by subdiaphragmatic vagotomy
• Gastric distension is insufficient to account for all
aspects of satiety
35. The Vagus Nerve
• Contains receptors for a number of gut
hormones
• Vagotomy abolishes appetite-modifying
action of
many gut hormones: CCK, PYY, GLP-1
• Vagus nerve is thought to be a major
sight of gut hormone signaling
36. A Very Quick Overview of Appetite
Regulating Hormones
37. 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
38. Appetite-regulating Hormones:
• In contrast, a growing number of peptide hormones have been found to
produce satiety and decrease food intake.
Vagus
Nerve
Peptide YY (PYY) Adiponectin
Pancreatic
Cholecystokinin (CCK) Leptin
Polypeptide (PP) Bombesin
Oxyntomodulin (OXM)
Amylin
Apolipoprotein A-IV (apo A-IV)
Insulin Vasoactive Intestinal
Polypeptide (VIP)
Glucagon-like peptide-1
(GLP-1)
39. Energy
Summary: Gut Hormones
Regulation
PP
-
Pancreas
+ -
- Vagu
s
PP
Ghrelin -
Bombesi CC
n K
PYY
Stomac GLP-
h 1
OX
M
VIP
Apo A-IV Intestines
40. Another Important Satiety
Regulator: Leptin
• Leptin, is released from adipose tissue,
mammary glands, ovarian follicles, placenta,
skeletal muscle, and the P cell and chief cells of
the stomach
• 25% of circulating leptin is derived from the
stomach
• Leptin levels positively correlate with body fat:
higher circulating leptins with greater BMI
• Leptin mediates central regulation of energy
homeostasis via receptors in the ARC and
peripherally via the vagus nerve
41. Leptin 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
42. 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
43. 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?
44. 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
45. 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