Long Term Weight Loss Following Abdominoplasty: Neurocrine Factors

1,122 views

Published on

Long term weight loss was associated with abdominoplasty in a group of 22 patients providing that the BMI was 25 or greater at the time of teh procedure, p< 0.001. Neuropcrine factors are discussed in this pilot study, whish is the first of it's kind.

0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total views
1,122
On SlideShare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
8
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide

Long Term Weight Loss Following Abdominoplasty: Neurocrine Factors

  1. 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. 2. The Role for Abdominoplasty ? Just because you can, does not mean you should ?
  3. 3. After Abdominoplasty Some Patients: Lost weight & Lost no weight •
  4. 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. 5. Obesity Epidemic • BMI: Body Mass Index: weight kg/(height m) 2 • <1/3 of U.S. 19-25 Normal • 1/3 of U.S. 25-30 Overweight • 1/3 of U.S. BMI 30-40 BMI Obese BMI • The prevalence of obesity has more than doubled since 1980 • 3% of U.S. BMI> 40 Morbid-Super Obese
  6. 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. 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. 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 – Xenical: Orllstat 4.3 2.9 55/27 54/33 9.0 4.6 3.4 67/19 53/21 47/23 • New drugs pending approval – Qnexa – Contrave – Lorcaserin
  9. 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: (Vivus) Phentermine & Topiramate 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
  10. 10. Surgical Treatment Gastric Bands Partial Gastric & Intestinal Bypass ( Roux en Y ) Abdominoplasty ?
  11. 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. 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. 13. 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
  14. 14. 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 • Weight at 1 year post-surgery • Current Weight • Complications of surgery • Patient satisfaction with surgical results • Changes in diet & exercise after surgery • Weight of pannus resected
  15. 15. 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
  16. 16. 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%
  17. 17. Results: Patient Weight loss • 90.5 % reported weight loss • 47.6% maintained weight loss > 1 yr after surgery
  18. 18. Results: Patient Weight Loss Percent of Mean Patients 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 ___ 9.5 175.5 ___ ___ ___ No Weight loss n=2
  19. 19. 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 %
  20. 20. 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%)
  21. 21. Pre-operative weight associated with long term weight loss WEIGHT (LBS) LONG TERM WEIGHT LOSS ( >/= 4lbs & >1 YR ) < 140 & ≥ 210 1 6 ≥ 140 to 210 9 5 p<0.0005 NO LONG TERM WEIGHT LOSS ( < 4lbs & > 1 YR )
  22. 22. Pre-operative BMI associated With long term weight loss BMI LONG TERM WEIGHT LOSS ( >/= 4lbs & >1 YR ) <24.5 & ≥ 33.5 1 8 ≥ 24.5 to <33.5 9 3 p<0.0023 NO LONG TERM WEIGHT LOSS ( < 4lbs & > 1 YR )
  23. 23. Results: Weight Loss & Satiety No change in appetite (%) Sense of satiety only after eating (%) Lack of appetite at all times (%) Unpleasant abdominal sensation 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 loss n=2 2 (100) 0 (0) 0 (0) 0 (0) All Patients n=21 5 (23.8) 8 (38.1) 8 (38.1) 3 (14.3) Short-term weight loss only (<1year) n=9
  24. 24. 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
  25. 25. 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
  26. 26. 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
  27. 27. CNS Regulation of Appetite / Satiety 2 Areas :
  28. 28. 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
  29. 29. 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. Neural/ endocrine signals ↑ Feeding 2 nd order neurons ARC Hypothalamus α-MSH ↓ Feeding
  30. 30. The ARC ∀ α -MSH acts as a ligand at the melanocortin - 4 receptor ( MC4 ) • Defects of this receptor: implicated in up to 46% of all monogenetic childhood onset obesity in humans ∀ α -MSH inhibits the receptor to AgRP: inhibiting appeptite • AgRP inhibits the MC4 receptor: stimulating appetite
  31. 31. 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
  32. 32. The Vagus Nerve • Afferent signals: mechanical & chemical • Cell bodies of afferent neurons in the Nodose Ganglia • Projects into brainstem to interface with hypothalamus
  33. 33. 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
  34. 34. 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
  35. 35. A Very Quick Overview of Appetite Regulating Hormones
  36. 36. 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
  37. 37. Appetite-regulating Hormones: • In contrast, a growing number of peptide hormones have been found to produce satiety and decrease food intake. Vagus Nerve Pancreatic Polypeptide (PP) Amylin Insulin Peptide YY (PYY) Cholecystokinin (CCK) Adiponectin Leptin Oxyntomodulin (OXM) Apolipoprotein A-IV (apo A-IV) Vasoactive Intestinal Polypeptide (VIP) Glucagon-like peptide-1 (GLP-1) Bombesin
  38. 38. Energy Regulation Summary: Gut Hormones PP Pancreas - + Vagu s Ghrelin Stomac h - PP Bombesi n CC K PYY GLP1 OX M VIP Apo A-IV Intestines
  39. 39. 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
  40. 40. 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
  41. 41. 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
  42. 42. 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?
  43. 43. 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
  44. 44. 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
  45. 45. Budget

×