12.05.03 sosialisasi sun-ugm

7/31/2019 12.05.03 Sosialisasi SUN-UGM

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Penyakit Tidak Menular

Sebagai Akibat

Beban Ganda Masalah Gizi

Abdul Razak Thaha

Kuliah Umum

Dalam Rangka Sosialisasi SUN Movemnet

Fakultas Kedokteran UGM, Jogyakarta, 3 Mei 2012


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Total deaths around the world:58 million

WHO, 2009


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Deaths from noncommunicablediseases around the world:35 million

WHO, 2009


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Deaths from noncommunicable

diseases in developingcountries:28 million

WHO, 2009


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Deaths from noncommunicable

diseases in developingcountries:28 million

Deaths from noncommunicablediseases in developing

countries which could havebeen prevented: an estimated14 million

WHO, 2009


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Noncommunicable Diseases

Mortality among men and women aged 15-59 years (2004)

WHO, 2009


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0

5

10

15

20

25

30

2004 2015 2030 2004 2015 2030 2004 2015 2030

Deaths(m

illions)

High income Middle income Low income

HIV, TB, malaria

Other infectious

Mat//peri/nutritional

CVD

Cancers

Other NCD

Road traffic accidents

Other unintentional

Intentional injuries

Noncommunicable Diseases

Projected Deaths in 2015 and 2030

WHO, 2009


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Indonesia negara kelima stunted terbanyak(UNICEF 2003-2008)

8


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KECENDERUNGAN PREVALENSI GIZI KURANG DAN PENDEKANAK BALITA INDONESIA 1986 - 2007

0

01

20

30

40

50

60

1986 1989 1992 1995 1998 1999 2000 2001 2002 2003 2005 2007

year

% UnderweightStunting


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Kematian Semua Umum menurut Kelompok umurSKRT (HHS) 1995-2001 and Riskesdas 2007

10.1

44.241.7

5.96.0

31.2

49.9

7.36.0

28.1

59.5

6.5

0.0

10.0

20.0

30.0

40.0

50.0

60.0

70.0

Maternal/Pre-natal Communicable Disease Non-CommunicableDisease

Injury

HHS '95 HHS '01 Riskesdas '07


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Penyebab Kematian(Riskesdas 2007)

NoCommunicable

Disease%

Non-CommunicableDisease

%

1 TB 27.8 Stroke 26.9

2 Liver Disease 19.1 Hypertension 12.3

3 Pneumonia 14.4 Diabetes mellitus 10.24 Diarrhea 13.2 Severe Tumor 10.2

5 Typhoid 6.0 Ischemic heart disease 9.3

6 Malaria 4.6Chronic ObstructionaryPulmanary Disease

9.2

7 Meningitis/encephalitis 3.2 Other hearth diseases 7.5

8 Dengue 2.1Ulcus ventriculli and ulcusduodeni

3.4

9 Tetanus 1.9 Congenital malformations 1.0

10 Septicemia 1.2 Malnutrition 0.4


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fromPreventing Chronic Diseases: a vital investment. Geneva, World Health Organization, 2005.

Aetiology of chronic non-communicable diseases


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PNEYAKIT TIDAK MENULAR4 Penyakit , 4 Faktor Risiko Utama yang Dapatt Dimodifikasi

MerokokDietsTidakSehat KurangAktvitas

Fisik

PneggunaanAlkoholBerlebihan

Kardio-vascular

Diabetes

Kanker

PenyakitRespirasiKronik


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IUGR-Stunting

sebagai pintu masuk ke

PTM


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Seri Lancet 2008


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Seri Lancet 2008


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Seri Lancet 2008


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D.J.P. Barker (2012). Developmental origins of chronic disease. Public Health 126 (2012 ) 18 5-189


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SUMMARYCoronary heart disease, type 2 diabetes, breast cancerand many other chronic diseases are unnecessary. Theiroccurrence is not mandated by genes passed down to usthrough thousands of years of evolution. Chronicdiseases are not the inevitable lot of humankind. Theyare the result of the changing pattern of humandevelopment. We could readily prevent them, had we thewill to do so. Prevention of chronic disease, and an

increase in healthy ageing require improvement in thenutrition of girls and young women.

D.J.P. Barker (2012). Developmental origins of chronicdisease. Public Health 126 (2012 ) 18 5-189


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SUMMARY

Many babies in the womb in the Western worldtoday are receiving unbalanced and inadequatediets. Many babies in the developing world aremalnourished because their mothers are chronically

malnourished. Protecting the nutrition and health ofgirls and young women should be the cornerstoneof public health. Not only will this prevent chronicdisease, but it will produce new generations who have

better health and well-being through their lives..

D.J.P. Barker (2012). Developmental origins of chronicdisease. Public Health 126 (2012 ) 18 5-189


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Sumber: WHO, 2005


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Patomekanisme Gizi-IUGR

P k i H b Gi i d IUGR


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Placental and fetal

arginine

Placental and fetal

ornithin

Placental arginine and

ornithine transport

Maternal undernutirition

and overnutrition

mTOR signaling

Embryogenesis

Placental angiogenesis and growth

Placental-fetal blood flows

Nutrient and O2 supplies from mother to fetus

Fetal growth and development

NO Polyamines

NOS

BH4

ODC

SAM

Patomekanisme Hubungan Gizi dan IUGR

Wu G et al. 2004. J. Nutr. p 2169-72

Mean standard deviation scores for height weight and body mass index


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Barker et al. 2010. Eur J Haert Failure. 12.819-825

Mean standard deviation scores for height, weight,and body mass index(BMI) in the first 11 years after birth among children who had chronic heart

failure as adults.


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Post-natal growthFigure shows the growth of children who as adults hadchronic heart failure. At birth their mean height, weight,

and body mass index was below the average. Thereafter,

it fell further below the average. After around 2 years of

age, however, their mean weight and body mass indexincreased rapidly so that by 11 years both measures were

above the average. At no age from birth to 11 years did

weight or body mass index predict chronic heart failure in

later life. Rather it was the change between 2 and 11

years that predicted the disease.



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Post-natal growthIn a simultaneous regression, chronic heart failure wasassociated with a low body mass index at 2 years and a

high body mass index at 11 years (P 0.008 and 0.001,

respectively). These trends were similar for people with

and without type 2 diabetes. Low body mass index atage 2 was strongly correlated with a small lesser

placental diameter and area (P , 0.001 for both). We

examined the combined effects of the lesser placental

diameter and body mass index at 2 and 11 years. In a

simultaneous regression, each was statistically

significant (P 0.02, 0.01, and 0.001).



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Sindroma Metabolik

Pintu Masuknya ke

PTM


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Defenisi Metabolic Syndrom

Miranda et al. (2005). Am Heart J. Vol 49, No 1:35


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PATOMEKANISME

METABOLIC SYNDROM


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Patofisiologi Sindroma Metabolik

Logo et al. 2012. Harrisons Principles of Internal Medicine. 18

th

Ed.

M t b li S d ( di t b li Ri k)


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Metabolic Syndrome (cardimetabolic Risk)


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Hubungan Resistensi Insulin

dengan Dislipidemia

Phillippa et al (2010). Am Heart J, Vol 149, No 1: 33-45


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Pathway of Insulin Signaling

Miranda et al. (2005)Am Heart J. Vol 49,

No 1:37


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Isyu mengenai Fructosa

Adalah suatu simple sugar yang terdapat

di dalam:

Madu

Berbagai buah

Gula meja (sucroda)

High fructose corn syrup (HFCS)


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Sifat Fruktosa

Struktur sama dengan glukosa (C6H12O6)

Metobolisme berbeda dengan glukosa

tidak menekan pusat lapar

Hampir semuanya diekskresikan olehhati

Dikoneversi dengan cepat oleh hati menjadi

glukosa, glikogen, laktat dan fat

Berpotensi besar menginduksi terjadinya

resistensi insulin

Potensi induksi fruktosa terhadap resistensi insulin


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Fructose

Lipogenesis

Dislipidemia

Body fat

Visceral fat

ROS Hyperuricemia

Ectopic fat

LipogenesisDislipidemia

ER Stress IamparedVasodilation

Impared Insulin signaling

Insulin resistance

Potensi induksi fruktosa terhadap resistensi insulin


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