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    Metabolic Syndrome

    Uploaded by

    Shreya Agarwal

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
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    of 34

    Metabolic syndrome and

    Obesity

    Piyusha Atapattu
    MBBS, MD, MSc, FRCP
    What is metabolic syndrome?

    • A true ‘syndrome’
    • Constellation of interrelated risk factors of metabolic origin

    Dyslipidaemia Elevated BP

    Abdominal Elevated
    obesity glucose
    Metabolic
    syndrome
    Associated with..
    • Proinflammatory/ prothrombotic state
    – Elevated CRP
    – Endothelial dysfunction
    – Hyperfibrinogenaemia
    – Increased platelet aggregation and PAI-1
    – Microalbuminuria
    What is the global situation?
    • 1/4th of adults worldwide have
    metabolic syndrome (similar in SL)

    • People with metabolic syndrome


    – x 2 as likely to die from, x 3 as likely to
    have a MI or stroke
    – x 5 greater risk of developing type 2
    DM

    • Up to 80% of the 200 million people


    with DM globally will die of CVD

    • Metabolic syndrome and DM are


    way ahead of HIV/AIDS in morbidity
    and mortality
    Associated clinical conditions

    • Insulin resistance and type 2 DM


    • CVD
    • Fatty liver
    • PCOD
    • Sleep apnoea
    • Cholesterol gallstones
    • Others…….
    What contributes to atherosclerosis in
    metabolic syndrome?

    • Atherogenic Dyslipidemia
    – High TG
    – High apoB
    – Low HDL-C
    – High LDL-C
    • HT
    • Elevated plasma glucose
    • Proinflammatory state
    • Prothrombotic state

    • Risk increased even when only marginally abnormal!!


    Diagnosis of metabolic syndrome
    Component ATP III (3 of the following)

    • WHO/ ATP III


    Abdominal obesity Men >102 cm (40’’)
    (Waist circumference) Women > 88 cm (35’’)

    Hypertriglyceridaemia >150mg/dL (1.7mmol/L)

    Low HDL - C Men -<40mg/dL (1.036mmol/L)


    Women-<50mg/dL (1.295mmol/L)

    Elevated BP >130/85 or use of anti HT Rx

    Elevated fasting glucose >110mg/dL (6.1 mmol/L)


    What causes metabolic syndrome?

    – Abdominal obesity
    – Physical inactivity
    – Ageing
    – Hormonal imbalance
    (eg. cortisol in chronic stress)
    • It’s the fat – in wrong places!!!
    • Causes insulin resistance –and many
    other metabolic derangements

    • Seen in
    – Any obese –’fat in the middle’
    – With ageing
    – South Asians

    • Abdominal obesity (even in otherwise


    thin people) is associated with insulin
    resistance!!! (Redinger, 2007)
    Obesity
    • A disease due to exaggeration of normal adiposity

    • 50% obese in UK and USA by 2015

    • Sri Lanka (Katulanda et al. 2010)


    – overweight -25.2%
    – obese - 9.2%
    – centrally obese - 26.2%,

    • Clinical measurement by
    – BMI - >23 and 25Kg/m2
    – WC - 90cm (Men) and 80 cm (Women)
    What causes obesity?
    Poor diet Sedentary
    lifestyle
    Social Medical
    determinants disorders

    Attitudes
    Obesity Genetics

    Drugs
    Ageing
    Lack of
    Hormones sleep
    Obesogenic environment
    • Abundant access to energy dense food
    (supermarkets, vending machines,
    roadside food venders)
    • Food habits –holiday eating, eating out,
    fast foods as snacks
    • Mechanization – machines have taken
    over
    • Sedentary lifestyle –transport,
    movement within work and home,
    leisure activities
    • Children –less play and more work,
    more comp and more TV
    Map of dietary energy availability
    per person per day
    1961

    2001–2003
    How does obesity cause metabolic
    syndrome?
    • Adipose tissue is not only a store of fat!

    – Immune function (Tchkonia et al, 2006)


    • Cytotoxic fatty acids sequestered
    • Production of cytokines, complement proteins
    Usually no infections and no metastases in fat tissue!!

    – Largest endocrine organ (Tchkonia et al, 2010)


    • Secrete hormones (Eg. leptin, adiponectin, visfatin,
    angiotensin II, IGF1)
    • Activates hormones (Eg. glucocorticoids, sex steroids)
    • Visceral fat depots release inflammatory
    adipokines (Eg. TNF-a, IL-1, IL-6)

    • Inflammatory adipokines and FFA form the


    pathophysiological basis for co-morbid
    conditions in obesity

    • Antiinflammatory and anti-atherogenic


    substances are also secreted
    (eg. adiponectin, visfatin) (Tchkonia et al, 2006)

    • Buttock fat and subcutanous fat–mostly


    storage function (Redinger, 2007)
    Adipokine promotors Inhibitory/ atheroprotective

    Inflammatory Anti-inflammatory

    IL-1, IL-6, TNF-a, IFN-a, IFN-b, IL-8. IP-10, IL_4, IL-10, TGF-b
    TGF-b, MCP-1, leptin, resistin
    Hypertensive Antihypertensive

    Renin, angiotensinogen, angiotensin II Angiotensin II receptor blockers

    Insulin resistance Insulin sensitivity

    TNF-a, IL-6, resistin Adiponectin, leptin, AgRP, MMIF,


    Acylation-stimulating protein
    Procoagulant Anticoagulant

    PAI-I, tissue factor, TNF-a, IL-6, TGF-b Adiponectin

    Angiogenetic Atheroprotective

    Leptin, IL-8, VEGF, FGF-2, MCP-1, IP-10, Adiponectin


    VCAM, ICAM, monobutyrin
    Lipogenetic (adipogenesis) Lipolytic

    IGF-1, angiotensinogen, angiotensin II, TNF-a, IL-6,


    visfatin, acylation-stimulating protein
    Obesity –fat tissue distribution
    What happens with ageing?
    • Fat tissue mass increases through middle age and
    declines in old age
    • Fat redistribution occurs especially during and
    after middle age
    Waist circumference
    • Most important
    • Standard
    – Men >102 cm (40’’)
    – Women > 88 cm (35’’)

    • But South Asians – lower cutoffs


    – Men > 90 cm
    – Women > 80 cm

    • Measured at the top of iliac crest


    Management

    • Primary goal – reduce risk for CVD

    • Individualized management

    • Each aspect contributing to metabolic syndrome and


    other risk factors for CVD should be managed

    • Should be continued for long - ? Lifelong

    • Mostly lifestyle modifications with attitudinal changes


    +/- drugs
    Weight
    10% of basal weight
    in 6-12 months

    Exercise 30-40mt/d
    on
    BP
    3-5 d/week
    <130/85 mmHg

    Goals

    Correct blood lipids according to CVD risk


    LDL <100/130 mg/dL (2.6/3.35 mmol/L)
    TG <130/160/190 mg/dL (3.35/4.19/4.5mml/L)
    HDL maximum achievable!!
    Exercise
    • Skeletal muscle
    – most insulin-sensitive tissue
    – primary target for improving insulin
    resistance

    • The impact of exercise on insulin


    sensitivity is evident for 24-48 hrs, but
    disappears in 3-5 days

    • Regular physical activity necessary to


    improve insulin resistance
    Regular Exercise
    • Walking or light jogging for 1 hr daily will produce significant
    loss of visceral fat (even without caloric restriction)!!

    • Any Exercise –better than No Exercise!!!

    • Break up the exercise

    • Gradual increase in intensity and frequency

    • 30-40 min/d on 3-5 days of the week


    Diet
    • Individualized, affordable, practical, sustainable

    Reduce Increase

    • Portion size to limit calorie • Whole grain


    intake • Fruit and vegetables
    • refined sugar/ carbohydrates (5 servings/ day)
    • Full fat dairy products/ red • Fish – especially in
    meat/ polyunsturated fat hypertriglyceridaemia
    • Alcohol
    • Salt if blood pressure elevated

    • Diet very low (< 25%) in fat may increase TG and decrease HDL-C
    Dos and Don’ts
    Weight reduction
    • Improves all aspects of metabolic syndrome
    • Decreases all-cause and CVD mortality
    • By exercise and dietary changes
    • Aim for BMI 20-23kg/m2

    • Even though NO weight loss, exercise and dietary changes


    – Lower BP
    – Improve lipids
    – Improve insulin resistance
    Why is it so difficult to lose
    weight?
    Calorie content of some foods
    Food item Quantity Calories
    (Approx)
    Butter / oil I table spoon 100 -120
    Banana 1 100
    Bread 1 slice 65
    Chocolate cake 1 piece 340
    Rice 1 cup 200
    Roasted peanuts 1 cup 840
    Hot dog 1 250
    Samosa 1 150
    Vade/ Chocolate piece 1 70
    Ice cream 1 cup 350
    Carbonated soft drinks 1 bottle (300 ml) 150
    Calorie expenditure during
    activities
    Exercise Calories burned
    per hour (App)
    Walking 4.0 mph, very brisk 300
    Cycling, 12-13.9mph, moderate 475
    Running, 5 mph (12 minute mile) 475
    Swimming laps, freestyle, slow 400
    Cricket (batting, bowling) 300
    Aerobics, general 400
    Stretching, yoga 250
    Housework, moderate 200
    Gardening, general 250
    Typing, computer data entry 90
    Music, playing guitar 180
    Pharmacotherapy
    • Needed when lifestyle changes have not improved
    risk factors
    • Anti HT
    • OHG (especially metformin)
    • LDL – statin
    • TG – statin/ fibrate/ nicotinic acid
    • HDL - nicotinic acid/ fibrate
    • ??
    Summary
    Metabolic syndrome is the collection of high blood pressure,
    blood glucose, abdominal obesity and abnormal blood lipids

    It would soon be the No 1 risk factor for DM and CVD

    Most important cause is abdominal obesity causing a chronic


    inflammatory and prothrombotic state
    Lifestyle changes (weight reduction by diet and physical
    activity) are the most important management strategies

    Pharmacotherapy is added when lifestyle changes are


    inadequate
    Thank you
    References
    • AHA/NHLBI Scientific Statement. Diagnosis and Management of the Metabolic Syndrome. An American
    Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. 2005.
    • Carr DB, Utzschneider KM, Hull RL, Kodama K, Retzlaff BM, Brunzell JD, Shofer JB, Fish BE, Knopp RH,
    Kahn SE. Intra-abdominal fat is a major determinant of the National Cholesterol Education Program
    Adult Treatment Panel III criteria for the metabolic syndrome. Diabetes. 2004; 53: 2087–2094
    • Katulanda P, Jayawardena MAR, Sheriff MHR, Constantine GR, Matthews DR. Prevalence of overweight
    and obesity in Sri Lankan adults. Obesity Reviews . 2010;.11:751–756
    • M Deen. Metabolic syndrome: Time for action. Am Fam Physician. 2004; 69:2875-2882.
    • National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of
    High Blood Cholesterol in Adults (Adult Treatment Panel III). Third Report of the National Cholesterol
    Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood
    Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002; 106: 3143–3421
    • Nied RJ and Franklin B. Promoting and Prescribing Exercise for the Elderly. Am Fam
    Physician. 2002;65(3):419-427.
    • Afridi A K and Khan A. Prevalence and Etiology of Obesity - An Overview. Pakistan Journal of Nutrition 3
    (1): 14-25, 2004
    • Redinger R N. The Pathophysiology of Obesity and Its Clinical Manifestations. Gastroenterology &
    Hepatology. 2007;3(11): 856-863.
    • Weinsier RL, Hunter GR, Heini AF, Goran MI and Sell SM. The etiology of obesity: relative contribution of
    metabolic factors, diet, and physical activity. Am J Med. 1998;105(2):145-50.
    • WHO Regional Office for the Western Pacific/ International Association for the Study of Obesity/
    International Obesity Task Force, 2002. The Asia-Pacific Perspective: Redefining Obesity and Its
    Treatment. Western Pacific Region: WHO, IASO, IOTF.

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