12.05.03 sosialisasi sun-ugm
TRANSCRIPT
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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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Total deaths around the world:58 million
Deaths from noncommunicablediseases around the world:35 million
WHO, 2009
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Total deaths around the world:58 million
Deaths from noncommunicablediseases around the world:35 million
Deaths from noncommunicable
diseases in developingcountries:28 million
WHO, 2009
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Total deaths around the world:58 million
Deaths from noncommunicablediseases around the world:35 million
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.
Barker et al. 2010. Eur J Haert Failure. 12.819-825
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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).
Barker et al. 2010. Eur J Haert Failure. 12.819-825
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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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Terima kasih