Birth Place / Date : Medan, March 14th 1964

Home Address : Jl. Tanimbar Blok H No. 228 Cinere Megapolitan, Depok. Phone number : 087885176141

Office Address : Medical Rehabilitation Department

RSUPN.Dr Cipto Mangunkusumo

Phone number / Fax number : 021. 3150358 / 3907561 / 3915593

Dr.dr. Tirza Z. Tamin, SpKFR-K

Curriculum Vitae

Educational Background : 2006 – 2009 : Doctoral Program, Faculty of Medicine Universitas

Indonesia, Jakarta 1994 – 1998 : Physical Medicine and Rehabilitation Specialist,

Faculty of Medicine Universitas Indonesia, Jakarta

1983 – 1989 : General Practitioner, North Sumatera University, Medan

Position : Januari 2002 – Now : Head Division of Sport Injury and Obesity Clinic,

Physical Medicine and Rehabilitation Department, RSUPN Cipto Mangunkusumo, Jakarta

November 2007 – 2013 : Secretary of Specialist Program Physical Medicine and Rehabilitation RSUPN Cipto

Mangunkusumo, Jakarta / Faculty of Medicine Universitas Indonesia, Jakarta

Organization : IDI PERDOSRI

Curriculum Vitae

Dr.dr. Tirza Z Tamin, SpKFR (K)Department of Physical Medicine and Rehabilitation

Dr. Cipto Mangunkusumo General Hospital /Faculty of Medicine Universitas Indonesia

COMPREHENSIVE MANAGEMENT OF OBESITYA PHYSIATRIST PERSPECTIVES

In Elderly Patients

Sarcopenic Obesity (SO)A combination of excess

weight, reduced muscle mass and / or strength and endurance

Maximize their effects on physical disability, morbidity and mortality

Possible Consequence of SO in the Elderly

Figure 3

Physiatrist Role in Obesity with Complication

Goals :Quality of LifePhysical Function ImprovementMuscle Mass MaintenanceImproved Risk Factors (Blood Pressure, DM,

Dislipidemic)Reduced Body Weight

Physiatrist ManagementGuide to selecting treatment in obesity

Treatment BMI Category (kg/m2)

25-26.9(OW)

27- 29.9(OW)

30 – 34.9( OB1)

35 – 39.9(OB2)

>40(OB3)

Diet, PA and behavior therapy

With co-morbidities

With co-morbidities

+ + +

Pharmacotherapy

With co-morbidities

+ + +

Surgery With co-morbidities

• Bessesen DH, Medical evaluation of the overwight & obese patients In: Bessesen DH, Kussner R, evaluation & management of obesity. Philadelphia, Hanley and Belfus Inc, 2002, p85

Medical Rehabilitation for

Obstructive Sleep Apnea

Epidemiology of OSA

Approximately 25% of adults with a BMI 25 kg/m2 - 28 kg/m2 have at least mild OSA ( [AHI] > 5)

The prevalence varies according to gender (~30% in men and ~15% in women), age, and body weight.

Men’s risk for OSA is 2x -higher than women. Postmenopausal women >>risk than premenopausal OSA prevalence increases until age 65 years

Obesity may worsen OSA fat deposition in the tissues surrounding the upper airway smaller lumen and increased collapsibility of the upper airway, predisposing to apnea.

Fat deposits around the thorax ↓ chest compliance and functional residual capacity, and may ↑ O2 demand.

Visceral obesity is common in subjects with OSA.

Obesity and OSA

OSA, Sleep Deprivation, and Metabolic Dysregulation

OSA patients have been shown to have increased triglycerides, total cholesterol HDL ratio and LDL and lower HDL values.

Intermittent hypoxia, a key feature of OSA, causes an increase in the liver content of triglycerides in mice.

OSA patients may also have reduced HDL-mediated inhibition of low density lipoprotein oxidation ex vivo .

The independent roles of OSA and obesity in these abnormalities remain unclear

OSA, Sleep Deprivation, and Metabolic Dysregulation

Leptin is a hormone produced by adipose tissue and binds to the ventral medial nucleus of hypothalamus

Binding of leptin to this nucleus sensation of satiety. Sleep deprivation inhibits leptin production, suggesting a

potential mechanism for the early development of obesity. Paradoxically, subjects with obesity have higher levels of

leptin, likely due to increase fat mass

OSA, Sleep Deprivation, and Metabolic Dysregulation

This hyperleptinemia is believed to be accompanied by desensitized cellular responses to leptin so that the effect of leptin is not achieved.

Leptin also modulates ventilatory control, and may therefore be implicated in abnormal breathing patterns in obesity.

adipokines, TNF-a and IL-6, are also elevated in obesity and may be linked to depression of CNS activity and airway neuromuscular control,perhaps increasing OSA severity

OSA, Sleep Deprivation, and Metabolic Dysregulation

Leptin in OSA is higher than would be expected because of the obesity alone, and leptin ↓after as little as days of CPAP

Serum adiponectin have been shown to improve glucose and lipid metabolism and prevent inflammation and atherosclerosis.

Adiponectin is low in obesity and also in OSA. Adiponectin levels have been shown to increase with CPAP Ghrelin, a hormone produced by cells lining the stomach, stimulates

appetite a counter-regulator to leptin. Ghrelin is increased during the night in obese subjects, and reduced sleep

has been shown to increase of ghrelin, stimulates appetite, and obesity and worsening of OSA.

Interaction OSA, Sleep Deprivation, and Metabolic Dysregulation

Weight Loss as a Treatment of OSAKajaste and colleagues Assess changes in the severity of OSAusing a cognitive-

behavioral program and an initial low-calorie diet with or without additional CPAP therapy, followed for 2 years

The O2 desaturation index was ↓ from 51 + 31 to 23 + 18 This trial suggests that weight loss in obese patients with

OSA might be an important therapeutic intervention

Lam et al

67 randomized patients (79% men) with mild-to-moderate OSA to one of three treatment groups:

(1) conservative measure (sleep hygiene) alone or

(2) with the addition of CPAP

(3) with the addition of oral appliances.

Only CPAP therapy was associated with improvements in OSA severity, daytime sleepiness, and QOL.

Weight Loss as a Treatment of OSA

Tuomilehto and colleagues 68 randomized a small group of subjects (70% men, mean

BMI 32 kgm 2 ) with mild, mostly supine-position predominant OSA (mean AHI 10) to either a 600 to 800 kcal/day diet plus supervised lifestyle counseling or routine lifestyle counseling over 1 year

the treatment group lost 10 kg of weight, associated with a reduction in AHI of 4,

Weight Loss as a Treatment of OSA

A longitudinal cohort study

followed 2,968 men and women for 5 years

assess the effects of weight loss/gain on OSA severity.

Men were more likely to develop worsening OSA severity with a given increase in weight than were women (risk increased 2.5 x)

Weight Loss as a Treatment of OSA

CPAP Treatment of OSA

CPAP is considered the mainstay of treatment of OSA

These benefits include: ↓ daytime sleepiness improving quality of life lowering blood pressure attenuate some of the cardiometabolic alteratioon ↓in visceral fat and total cholesterol and ↑ HDL better glycemic control and improved insulin sensitivity attenuation in inflammatory biomarker fewer cardiovascular events

Thank You

THANK YOU