QGK3013Tugasan2.pdf

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TUGASAN QGK 3013 KESIHATAN DAN KESEJAHTERAAN

QGK 3013

KESIHATAN DAN KESEJAHTERAAN

TUGASAN 2 (ULASAN ARTIKEL)

Group UPSI - 102 ( A 142PJJ )

DISEDIAKAN OLEH

NAMA NO MATRIKS /

NO.IC

NO.

TELEFON

LEE POH

KUEN

D20112052475

711031105392 016-7282388

PENSYARAH

E-PEMBELAJARAN: THARIQ KHAN BIN AZISUDDIN KHAN

TARIKH SERAHAN: 24 / 4 / 2015

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PERKARA MUKA

SURAT

1.0 pENGENALAN 3

2.0 ULASAN JURNAL 1

HINGGA 5

3 -9

3.0 RUMUSAN

KESELURUHAN

10

4.0 LAMAN WEB 5

buah JURNAL

10-11

5.0 RUJUKAN 11

4.0 LAMPIRAN

JURNAL

1 HINGGA 5

12-36

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1.0 Pengenalan

Secara umumnya, obesiti merupakan pengumpulan lemak yang berlebihan yang

menimbun di dalam badan seseorang. Obesiti kini dianggap sebagai satu penyakit dan

terjadi apabila tisu-tisu lemak menjadi keterlaluan. Lebih teruk lagi, obesiti boleh

mengganggu dan mencederakan organ-organ badan dan seterusnya akan menyebabkan

masalah kesihatan yang serius.

Salah satu isu kesihatan kanak-kanak dan remaja kini adalah obesiti di kalangan

kedua-dua golongan ini. Kajian menunjukkan bahawa obesiti yang berlaku pada usia

muda maka akan berterusan masalah ini sepanjang hayat mereka. Masalah obesiti di

kalangan kanak-kanak dan remaja perlu diberi perhatian serius memandangkan terdapat

pelbagai risiko kesihatan sampingan yang timbul disebabkan oleh gejala tersebut.

Masalah obesiti atau berat berlebihan adalah masalah kian meningkat di

kalangan masyarakat. Golongan kanak-kanak obesiti lazimnya mengalami masalah

berat badan apabila dewasa kelak. Obesiti selalunya dikaitkan dengan penyakit

kardiovaskular, pernafasan dan juga diabetes.

Oleh itu, kanak-kanak yang obesiti mempunyai risiko lebih tinggi mengalami

masalah berkenaan. Mereka yang tergolong dalam obesiti biasanya mempunyai berat

badan sekurang-kurangnya dua kali lebih berat berbanding ukuran ideal. Mereka ini

juga mempunyai berat badan sekurang-kurangnya 45 kilogram melebihi berat badan

yang sepatutnya. Selain itu, Indeks Jisim Badan(BMI) melebihi 40 atau 35 dan

mengalami beberapa penyakit seperti tekanan darah tinggi atau diabetis serta mereka

yang gagal mengekalkan berat badan yang sihat dalam jangka panjang sekalipun

mengikut diet yang disarankan oleh pakar-pakar pemakanan.

2.0 ULASAN 5 BUAH ARTIKEL ILMIAH

Lemak yang terlalu tebal boleh menyebabkan saluran darah tersumbat dalam

organ tubuh kita dan menyebabkan tubuh badan kita tidak mendapat oksigen yang

mencukupi. Mereka yang mengalami obesiti iaitu pada ukuran BMI dalam lingkungan

25 ke atas terdedah dan menyebabkan penyakit seperti serangan jantung, mati mengejut,

sakit dada dan denyutan jantung yang tidak normal.

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Mereka yang mempunyai berat badan berlebihan berekemungkinan mendapat

tekanan darah tinggi. Puncanya kandungan lemak darah (triglycerides) tinggi dan HDL

kolestrol baik yang rendah di dalam darah pengidap obesiti.Trigliseride yang tinggi

boleh menyebabkan saluran darah tersumbat dengan cepat. Apabila ruang salur darah

telah menyempit tekanan di dalamnya akan meningkat.

Golongan obesiti mempunyai risiko lebih tinggi terhadap pelbagai jenis kanser

seperti kanser endometrical iaitu kanser lining uterus, kolon, gall bladder , prostat,

buah pinggang dan post menopausal, breast kanser. Perubahan fizikal seseorang akan

membahayakan kesihatan badan sendiri. Perubahan fizikal dari aspek berat badan,

lilitan pinggang dan kolesterol dalam darah selama 13 tahun terhadap serangan penyakit

kardiovaskular boleh menyebabkan kematian.

Menurut jurnal pertama yang bertajuk Abdominal Adipose Distribution,

Obesity, and Risk of Cardiavacular Disease and Death : 13 Year Follow Up of

Participants in the Study of Men Born in 1913 yang dituliskan oleh B Larsson, K

Svardsudd, L Wilhelmsen, P Bjorntorp dan G Tibblin. dari sumber British Medical

Journal Volumm 288 ( Clinical Research) menyatakan bahawa obesity boleh

menyebabkan serangan penyakit kardiovaskular disebabkan jantung hati disumbat oleh

lemak yang tebal. Jurnal ini menulis tentang risiko penyakit jantung yang menyerang

lelaki obesiti pertengahan usia setelah kajian dijalankan selama 13 tahun. Peredaran

masa menyebabkan perubahan fizikal mula berlaku seperti pertambahan berat badan,

lilitan pinggang, serta tahap kolesterol dalam darah. Penggunaan subjek atau kumpulan

sasaran yang sama menjadikan kajian ini amat konkrit dan boleh dijadikan rujukan.

Jurnal ini menyatakn adakah perubahan fizikal atau obesiti merangsang

penyakit kardiovaskular? Adakah penyakit kardiovaskular tidak menyerang lelaki

bukan obesity? Dengan menggunakan temu bual, analisis dokumen serta ujian pra ke

atas 855 orang lelaki yang lahir pada tahun 1913 selama 13 tahun. Kumpulan sasaran

ini sama-sama memberikan maklumat untuk penyimpanan rekod dan juga melakukan

3 kali ujian post bagi mendapatkan hasil yang boleh dipercayai. Dalam pengumpulan

maklumat berkaitan latar belakang, gaya kehidupan, sejarah merokok dan juga rekod

kesihatan direkodkan. Ujian post dijalankan sebanyak 3 kali sepanjang 13 tahun bagi

mendapatkan hasil yang tepat. Daripada hasil skor ujian post, seramai 33 orang lelaki

yang menginjak pertengahan usia dan menghadapi obesiti merangsang penyakit

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kardiovaskular. Selain itu, hasil kajian juga menunjukkan bahawa 622 orang daripada

855 orang lagi tidak menghidap obesity dan juga tidak mengalami penyakit

kardiovaskular. Jurnal ini menyatakan bahawa kajian pada masa hadapan perlu

mengkaji langkah mengurangkan berat badan atau obesiti.

Menurut Elwes & Simnett, 1986, menyampaikan ilmu pengetahuan

merupakan salah satu cara untuk mengatasi masalah ataupun isu-isu. Walaupun sesuatu

isu kesihatan telah wujud di masyarakat ataupun pada seseorang individu maka mereka

tidak memahami dengan bahaya dan akibat akan terjadi. Oleh kerana kekurangan

pengetahuan yang berkaitan maka mereka tidak akan memahami dan hanya

membiarkan masalah sehingga apabila timbul hal ataupun perkara yang tidak dingini.

Masalah obesiti bukan satu isu ataupun masalah kesihatan yang baru.

Sebenarnya kebanyakan masyarakat kita tahu akan bahaya dan kesan terhadap

kesihatan tetapi tidak mengatasinya. Salah satu sebab ialah mereka tidak tahu

bagaimana hendak mengatasi masalah obesiti.

Dalam jurnal kedua yang bertajuk Obesity : Effects on Cardiovascular

Disease yang ditulis oleh Boban Matthew, Lisa Francis, Attila Kayalar dan jesse Cone

dari sumber Journal American Board of Family Medicine (JABFM) menguji sejauh

mana obesiti mempengaruhi kewujudan penyakit kardiovaskular dalam kalangan

penduduk di Amerika Syarikat.

Jurnal ini menulis tentang peranan utama obesiti terhadap kewujudan penyakit

kardiovaskular. Kajian menunjukkan lebih daripada 30% penduduk Amerika Syarikat

mengalami obesiti. Faktor genetik, keluarga, persekitaran, gaya pemakanan dan amalan

gaya hidup sihat turut dikupas sebelum kesimpulan berkaitan perkaitan obesiti dan

penyakit kardiovaskular dibuat. Jurnal ini menimbulkan persoalan tentang peratus

kematian akibat serangan penyakit kardiovaskular oleh pesakit obesiti lebih tinggi

berbanding orang normal dan kadar degupan jantung menurun seiring penurunan berat

badan.

Jurnal ini menggunakan pemerhatian dan analisis dokumen. Kajian melibatkan

5881 orang pesakit lelaki dan perempuan di Framigham selama 14 tahun. Pengumpulan

data dilakukan dengan menggunakan pemerhatian di mana dapat dilihat peningkatan

jumlah penduduk di Amerika Syarikat yang mengalami obesiti kian meningkat. Selain

itu, pengkaji turut menggunakan kaedah analisis data yang melibatkan 5881 pesakit

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lelaki dan wanita yang terdiri daripada dua kumpulan iaitu penghidap obesiti dan juga

kumpulan bukan penghidap obesiti. Penganalisisan maklumat akan dibuat dengan

melihat peratusan penghidap penyakit kardiovaskular dalam kalangan pesakit obesiti

dan juga kadar degupan jantung setelah penurunan berat badan.

Daripada hasil penemuan skor analisis dokumen, 11% pesakit obesiti lelaki

dan 14% wanita mengalami penyakit kardiovaskular. Mengikut data Framigham juga,

peratus kematian kerana sakit jantung oleh pesakit obesity adalah 40 kali ganda lebih

tinggi daripada orang normal dan degupan jantung juga berkuranagn seiring dengan

penurunan berat badan. Jurnal ini mencadangkan bahawa kajian pada masa hadapan

perlu menyiasat secara khusus aspek utama penyebab obesiti yang membawa kepada

penyakit kardiovaskular.

Obesiti yang teruk juga boleh menyebabkan Penyakit jantung. Penyakit jantung

yang jenis Hyperthropic Cardiomyopathy (HCM), ketebalan otot-otot pada dinding

ventrikel yang mengganggu aliran darah keluar dari jantung. Jantung gagal untuk

berehat semasa proses penerimaan darah, seterusnya mengganggu perjalanan keluar

darah dari jantung ke organ-organ lain termasuk ke saluran darah koronari. Denyutan

jantung yang tidak seragam pula akan menjadikan pengaliran darah di dalam jantung

tidak teratur dan kurang berkesan. KEJADIAN mati secara mengejut akibat serangan

jantung dan angin ahmar (strok) semakin meningkat setiap tahun. Malah, ia menjadi

ancaman yang perlu diberi perhatian serius oleh Malaysia.

Menurut Pakar Perunding Perubatan, Hospital Kuala Terengganu, penyakit

jantung merupakan penyebab paling biasa SADS dalam kesemua peringkat umur. Di

kalangan individu berusia 30 tahun ke atas, penyakit jantung lazimnya berpunca

daripada pembuluh yang membekalkan darah ke jantung telah tersumbat menyebabkan

penyakit jantung koronari.

Dalam jurnal ketiga yang bertajuk Obesity : Impact of Cardiovascular Disease

yang ditulis oleh Ronald M Krauss, Mary Winston, Barbara J Fletcher dan Scott M

Grundy dari sumber American Heart Association menerangkan tentang obesiti sebagai

antara penyebab utama kepada masalah jantung. Kajian menunjukkan bahawa risiko

serangan jantung kini mula menular dalam kalangan golongan muda. Penambahan

berat badan yang ketara dari zaman kanak-kanak hingga dewasa juga memainkan

peranan yang penting. Begitu juga dengan faktor genetik terutamanya bagi ibu bapa

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penghidap obesiti dan juga persekitaran yang tidak mengamalkan pemakanan dan cara

hidup sihat.

Tujuan kajian jurnal ini ialah menguji faktor-faktor penyebab obesiti dan juga

kesan terhadap kesihatan jantung. Persoalan kajian jurnal ini menyatakan bahawa

pertambahan berat badan atau obesity merupakan faktor utama penyakit

kardiovaskular. Jurnal ini juga menyatakan penyakit kardiovaskular dapat dirawat jika

pesakit obesiti berjaya mengurangkan berat badan. Jurnal ini menggunakan

pemerhatian dan juga analisis dokumen dijalankan bagi mengkaji punca obesiti serta

kesan terhadap kesihatan jantung. Subjek dipilih dalam kalangan tanpa dinyatakan

bilangannya. Pengumpulan dan penganalisisan data dilakukan dengan menggunakan

temu bual. Kemudian, ujian pra dan post pula digunakan untuk menganalisis maklumat.

Pesakit yang menjadi subjek menjalani ujian kesihatan bagi mengenalpasti masalah

kesihatan yang dihadapi seterusnya dilihat jika mempunyai perkaitan dengan penyakit

kardiovaskular. Hasil analisis data menjelaskan bahawa obesiti adalah penyebab utama

penyakit kardiovaskular dan tekanan darah meningkat seiring pertumbuhan berat,

manakala ia menurun seiring penurunan berat badan. Cadangan jurnal ini menujukkan

bahawa kajian pada masa hadapan perlu mengkaji kesan hipertensi terhadap obesity.

Dalam jurnal keempat yang bertajuk Obesity and Cardiovascular Disease yang

ditulis oleh Caroline M. Apovian dan Noyan Gokee bertujuan mengkaji tentang kesan

obesiti terhadap penyakit kardiovaskular dan langkah untuk mengatasinya. Obesiti

menyebabkan pelbagai penyakit seperti hypertensi, masalah tidur, gastrik, gout dan

juga penyakit diabetes. Subjek yang dikaji mengalami masalah obesiti sejak awal lagi

dan keadaanya semakin buruk apabila terlantar dan hilang upaya setelah mengalami

kemalangan jalan raya lima tahun lalu. Namun begitu, subjek yang berusia 43 tahun ini

berjaya menjalani rawatan yang bersesuaian untuk kembali normal.

Jurnal ini menguji kesan obesiti terhadap penyakit kardiovaskular dan kesesuaian

langkah atau rawatan yang diambil untuk mengatasinya. Persoalan kajian jurnal ini

menyatakan bahawa obesiti menjadi beban kepada kardiovaskular pesakit dan rawatan

yang dijalani sesuai dan boleh merawat obesiti. Jurnal ini menggunakan analisis

dokumen serta ujian pra dan post. Kajian ini melibatkan peskit obesiti, lelaki yang

berusia 43 tahun dan keadaannya selepas hilang upaya apabila terlibat dalam

kemalangan lima tahun yang lalu.

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Dari pengumpulan dan pengalisasi data menunujukkan maklumat awal pesakit

dikumpul dengan melakukan ujian pra. Pesakit diketahui sebagai penghidap obesiti

tahap 1 dan keadaan menjadi semakin teruk setelah kemalangan sehingga tahap obesiti

pesakit meningkat mejadi obesiti tahap 2. Pesakit juga menghidap penyakit lain iaitu

hypertensi, masalah tidur, gastrik gout. Ujian post pula dijalankan apabila pesakit mula

mendapatkan rawatan untuk mengurangkan obesiti dengan langkah mengawal

pemakanan, senaman, dan diakhiri dengan pembedahan Gastrik Bypass. Daripada hasil

skor ujian pra, keadaan kardiovaskular pesakit menjadi lebih teruk setelah terlantar

kerana lemak mula meliputi organ dalaman terutamanya bahagian jantung. Kajian juga

menunjukkan bahawa rawatan yang dijalani oleh pesakit berjaya mengurangkan tahap

obesiti iaitu daripada 296 kg kepada 177 kg. Kajian pada masa hadapan perlu menyiasat

waktu yang sesuai untuk mendapatkan rawatan awal bagi mencegah penyakit obesiti

menjadi lebih teruk.

Jurnal yang kelima bertajuk Obesiti Faktor, Kesan dan Rawatan yang ditulis

oleh Wan Mohd Syafnan bin dari sumber Academia. Edu menulis tentang faktor

penyebab kepada obesiti dan juga kesan atau penyakit yang dibawa bersama serta

rawatan yang boleh diberikan untuk mengubatinya. Obesiti berlaku kerana

ketidakkawalan terhadap pemakanan, genetik dan juga amalan gaya hidup yang tidak

aktif. Ini mengakibatkan wujudnya pelbagai penyakit sampingan seperti strok, kanser,

diabetes dan yang paling utama iaitu penyakit kardiovaskular. Obesiti membawa

banyak keburukan dan langsung tidak membawa kebaikan dan kajian ini membawa

kepada langkah rawatan yang bersesuaian.

Tujuan kajian jurnal ini ialah menguji sejauh mana obesiti menarik bersama

pelbagai penyakit lain dan juga melihat kesan rawatan yang sesuai. Persoalan kajian

jurnal ini ialah menyatakan obesiti menarik bersama pelbagai penyakit lain terutamanya

penyakit kardiovaskular dan perlu mempunyai rawatan yang diberikan untuk merawat

pesakit obesiti. Metodologi jurnal ini ialah menggunakan pemerhatian dan analisis

dokumen. Kajian dijalankan pada kanak-kanak Amerika Syarikat berusia 6 hingga 11

tahun di mana hampir 20% daripa danya menghidapi obesiti. Pengumpulan data

menggunakan pemerhatian tidak berstruktur untuk mengetahui peratus obesiti dalam

kalangan kanak-kanak Amerika Syarikat berusia 6 hingga 11 tahun. Penganalisisan

data pula menggunakan analisis dokumen. Jenis penyakit yang dihidapi oleh kumpulan

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sasaran setelkah disahkan sebagai obesiti dikaji. Setelah itu, pengkaji mula

menggalakkan pesakit untuk mendapatkan rawatan seperti kawalan pemakanan,

bersenam, berpuasa dan lain-lain lagi untuk mengurangkan kadar obesiti ke tahap yang

lebih rendah.

Hasil penemuan menunjukkan skor analisi data, 20% daripada kanak-kanak

Amerika Syarikat mengalami masalah obesiti dan kebanyakannya berisiko

menghidapi penyakit jantung, darah tinggi, kencing manis dan kanser. Hasil kajian

juga menunjukkan bahawa rawatan yang diberikan mampu mengubah tahap obesiti

menjadi lebih rendah. Cadangan jurnal ini ialah membuat kajian pada masa hadapan

perlu mengkaji menu yang seusia untuk kawalan makanan bagi pesakit obesiti

3.0 RUMUSAN KESELURUHAN

Berdasarkan jurnal Abdominal Adipose Tissue Distribution, Obesity, and Risk

of Cardiovascular Disease and Death : 13 Year Follow Up of Participants in the Study

of Men Born in 1913, Obesity : Effects on Cardiovascular Disease, Obesity : Impact

of Cardiovascular Disease, Obesity and Cardiovascular Disease dan Obesiti Faktor,

Kesan dan Rawatan, dapat disimpulkan bahawa kelima-lima jurnal ini

membincangkan permasalahan obesiti.

Obesiti diterangkan sebagai punca utama pesakit-pesakit menghidapi penyakit

serius yang lain seperti hypertensi, gout, kanser, darah tinggi, kencing manis dan juga

penyakit paling utama iaitu penyakit kardiovaskular.

Kepadatan lemak yang menyeliputi organ dalaman memberikan tekanan

kepada kardiovaskular untuk menjalankan aktiviti mengepam darah dan pernafasan

dengan baik. Semakin tinggi tahap obesiti, semakin besar risiko untuk mengalami

kegagalan fungsi kardiovaskular sekaligus membawa kepada kematian.

Kelima-lima jurnal ini turut memberikan petanda awal bagi mengesan obesiti

iaitu pertambahan berat badan dua kali ganda daripada berat normal, lilitan pinggang

yang besar dan juga tahap BMI yang melepasi 30. Apabila mula mendapat tanda-

tanda ini, pesakit juga akan mula merasai tanda-tanda awal untuk penyakit

kardiovaskular pula seperti hypertensi, kesukaran untuk tidur, strok sakit pada ulu hati

dan lain-lain lagi.

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Obesiti bagaimanapun boleh dirawat dengan menjaga pemakanan, bersenam,

minum air yang banyak, dan terdapat juga sesetengah pesakit mengambil jalan yang

lebih mudah iaitu dengan menjalani pembedahan Gastrik Bypass. Kesemua langkah

ini tidak salah untuk diikuti asalalkan pesakit mampu mengawalnya untuk tempoh

yang seterusnya.

Hasil daripada rawatan yang dijalankan, pesakit dapat mengurangkan berat

badan sekaligus mengurangkan risiko penyakit kardiovaskular yang lebih teruk. Dapat

juga disimpulkan bahawa kurangnya berat seseorang individu mempengaruhi

kurangnya tekanan darah dan risiko penyakit kardiovaskular. (2255 perkataan)

4.0 LAMAN WEB 5 BUAH ARTIKEL ILMIAH :

B Larsson, K Svardsudd, L Welin, L Wilhelmsen, P Bjorntorp dan G Tibblin.

Abdominal Adipose Tissue Distribution, Obesity, and Risk of Cardiovascular

Disease and Death : 13 Year Follow Up of Participants in the Study of Men

Born in 1913.

From http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1441047/

Boban Matthew, Lisa Francis, Attila Kayalar dan jesse Cone.

Obesity : Effects on Cardiovascular Disease.

From http://www.jabfm.org/content/21/6/562.full.pdf

Ronald M Krauss, Mary Winston, Barbara J Fletcher dan Scott M Grundy

Obesity : Impact of Cardiovascular Disease

From http://circ.ahajournals.org/content/98/14/1472.full

Caroline M. Apovian dan Noyan Gokee

Obesity and Cardiovascular Disease.

From http://circ.ahajournals.org/content/125/9/1178.extract

Wan Mohd Syafnan bin Wan Mohd Zain

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Obesiti Faktor, Kesan dan Rawatan.

From http://www.academia.edu/4122301/Obesiti-Faktor_Kesan_dan_Rawatan

5.0 BAHAN RUJUKAN

1. American Gastroenterological Association (2002, reapproved 2008). AGA technical

review on obesity. Gastroenterology, 123(3): 882-932. [Erratum in Gastroenterology,

123(5): 1752.]

2.. U.S. Department of Health and Human Services (2008). 2008 Physical Activity

Guidelines for Americans (ODPHP Publication No. U0036). Washington, DC: U.S.

Government Printing Office. Available online:

3. Azizi Yahaya, Shahrin Hashim, Jamaludin Ramli, Yusuf Boon dan Abdul Rahim

Hamdan(2007). Menguasai Penyelidikan Dalam Pendidikan

4. Cara BE, Dorota BP, David SL. Childhood Obesity:Public Health Crisis, Common

Sense Cure.

5. The Lancet (2002), 360: ms 473-82Deckelbaun RJ, Williams CL. Childhood

Obesity: The Health Issue.

6 .Obes Res (2001) ; 9 :ms.239-243.Darus, N. 1996. Exercise - The way to stay trim

and healthy. Malaysian Society For The StudyOf Obesity.

7. Rahsia kesihatan. Shah Alam, Fajar BaktiJones K.L, Shain berg L.W, and Byer C.O

(19972) dlm Amri B. Yahya (2007). Nutrien for helth, fitness and sport

8..McGraw Hill. New York Mo-suwan, L. Junjana, C. and Puetpoiboon, A. 1993.

Increasing obesity in school children in atransitional society and the effect of the weight

control Program

9. Prevalence and Metabolic Susceptibility to Obesity in Malaysia

10.Total Fitness Exercise: Nutrient and wellness need ham height , M.A: Ally and

BeconPollock, M.L. & Wilmore, J.H. 1984. Exercise in health and disease: Evaluation

and prescription for prevention and rehabilitation

11.http://nota-notapismppj.blogspot.com/2012/06/pengenalan-kepada-pendidikan-

jasmani.html

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Lampiran :

ARTIKEL 1

Abdominal adipose tissue distribution, obesity, and risk of cardiovascular disease and death: 13 year follow up of participants

in the study of men born in 1913.

B Larsson, K Svrdsudd, L Welin, L Wilhelmsen, P Bjrntorp, and G Tibblin

Copyright and License information

This article has been cited by other articles in PMC.

Abstract

In a prospective study of risk factors for ischaemic heart disease 792 54 year old

men selected by year of birth (1913) and residence in Gothenburg agreed to

attend for questioning and a battery of anthropometric and other measurements

in 1967. Thirteen years later these baseline findings were reviewed in relation to

the numbers of men who had subsequently suffered a stroke, ischaemic heart

disease, or death from all causes. Neither quintiles nor deciles of initial indices

of obesity (body mass index, sum of three skinfold thickness measurements,

waist or hip circumference) showed a significant correlation with any of the three

end points studied. Statistically significant associations were, however, found

between the waist to hip circumference ratio and the occurrence of stroke (p =

0.002) and ischaemic heart disease (p = 0.04). When the confounding effect of

body mass index or the sum of three skinfold thicknesses was accounted for the

waist to hip circumference ratio was significantly associated with all three end

points. This ratio, however, was not an independent long term predictor of these

end points when smoking, systolic blood pressure, and serum cholesterol

concentration were taken into account. These results indicate that in middle aged

men the distribution of fat deposits may be a better predictor of cardiovascular

disease and death than the degree of adiposity.

13 | P a g e


ARTIKEL 2 CLINICAL REVIEW

Obesity: Effects on Cardiovascular Disease and its Diagnosis

Boban Mathew, MD, MRCP, DM, Lisa Francis, MD, MRCP, Attila Kayalar, MD,

and

Jesse Cone, MD

The higher prevalence of cardiovascular disease in obese individuals is indirectly

mediated, to a large extent, by the increased frequency of various well known risk

factors like hypertension, diabetes, and dyslipidemia, either individually or as part of

the metabolic syndrome. However, there are several ways in which obesity directly

affects the cardiovascular system; these will be discussed in detail. We also focus on

various challenges posed by obesity in the performance and interpretation of cardiac

investigations and how they can be addressed. (J Am Board Fam Med 2008;21:562 8.)

The incidence of obesity started growing to epidemic proportions in the 1980s.

Currently more than 30% of the US population is obese (body mass index [BMI] _30)

and nearly two thirds are overweight (BMI between 25 and 29.9). These figures are

expected to rise further if the current trend continues13 (see Table 14). There are 2 distinct genetic mechanisms involved in obesity. One is caused by the infrequent

presence of certain genes, which produce rare syndromes associated with significant

obesity. However, obesity is much more commonly mediated by the presence of other

susceptibility genes. More than 41 such genetic sites have been identified and in their presence obesity will develop only if there is a favorable environment. 5,6 These

genes control different processes, such as regulation of fat distribution, metabolic rate,

response to exercise and diet, control of feeding, and food preferences, etc. But the

striking rise in the incidence of obesity, which has happened in the last few decades,

is not because of changes in the genetic background of the human race, since these

changes take thousands of years to evolve.

This epidemic is mainly caused by rapid lifestyle changes involving eating habits and exercise.5,7 Obesity increases adverse cardiac events in many ways. These may be

indirectly mediated through risk factors associated with metabolic syndrome like

dyslipidemia, hypertension, and glucose intolerance, or effects from sleep disorders

associated with obesity.8,9 Metabolic syndrome is associated with central or

abdominal obesity, with the distribution of fat predominantly in the abdominal viscera

rather than the extremities. Waist circumference or waist hip ratio are useful ways of assessing this type of fat distribution and increased values confer additional

cardiovascular risk. In abdominal obesity, there is an increase in the level of various

inflammatory markers as well as the occurrence of a prothrombotic state.10,11 Many

adipokines and other chemical mediators like tumor necrosis factor- alpha, interleukin-

6, plasminogen activator inhibitor- 1, resistin, lipoprotein lipase, acylation stimulating

protein, cholesteryl ester transport protein, retinal binding protein, estrogens, leptin,

angiotensinogen, and insulin-like growth factor-1 are present in increased

concentrations in obese patients. These have various adverse effects on the

cardiovascular system by creating a pro-inflammatory and prothrombotic state as well

14 | P a g e


as causing endothelial damage and vascular hypertrophy.12,13 There is also a higher

incidence of sleep apnea/ hypoventilation syndromes in obesity, which can affect the

heart in different ways. There are, however, also many direct effects of obesity on

the heart and the cardiovascular system, which are not mediated through components

of the metabolic syndrome or through the associated effects of sleep disorders. These

will be the main focus of this article. Obesity also poses considerable challenges to

making a precise cardiovascular diagnosis because of limitations in physical

examination as well as with various investigations like electrocardiograms (EKGs),

imaging studies, and cardiac catheterization. We will discuss these limitations and

make recommendations as to how these may be addressed.

Pathophysiology of the Circulatory System in Obese Patients

The adipose tissue has a resting blood flow of 2 to 3 mL/100 g/min, but can increase

up to 10-fold; this occurs usually after food intake.14 However, with increasing

obesity the perfusion per unit mass decreases. It falls from 2.36 mL/min to 1.53 mL/

min when the percentage of fat increases from 20% to 36% of the body weight, and so

the increase in cardiac output is not directly proportional to the total fat.15 The

increased cardiac output in obese patients is to meet the metabolic demand of the

adipose tissue and is achieved mainly through an increase in stroke volume. The left

ventricular chamber dilates to accommodate the increased venous return and, in turn,

develops an eccentric type of hypertrophy to keep the wall stress normal. The left

atrium also enlarges in obese individuals and is initially caused by the increased blood

volume and venous return. Later, other factors like left ventricular hypertrophy and

diastolic dysfunction may also be responsible for increased left atrial size. However,

in the Strong Heart Study cohort, it was observed that increases in stroke volume,

cardiac output, and left ventricular mass were more closely related to the associated

increase in lean body mass than to the amount of fat in obese patients. Left ventricular

filling pressure increases with exercise, often to more than 20 mm Hg, even if it is

normal at rest. The left ventricle undergoes

hypertrophy of the eccentric type but, less commonly, can be concentric. Initially there

is left ventricular diastolic dysfunction with hyperkinetic systole but with longer

duration of obesity diastolic dysfunction progressively worsens and gradually systolic

dysfunction also sets in. Cardiomyopathy of obese individuals (adipositas cordis) is

caused by a direct effect of obesity on the heart. Initially, the increase in the fat content

of the heart is because of a metaplastic phenomenon and is not an infiltrative process.

Various tissues of heart, like the sinus node, atrioventricular node, right bundle branch,

and the myocardium near the atrioventricular ring, are replaced by fat cells. These can

occasionally cause conduction defects like sinoatrial block, bundle branch block, and,

rarely, atrioventricular block.20 Subsequently, irregular bands of adipose tissue may

separate and cause pressure-induced atrophy of the myocardial cells. These adipose

cells may also secrete locally active molecules like adipokines, which indirectly cause

injurious effects on the adjacent myocardial cells. Accumulation of triglycerides in

nonfat cells like myocytes can also directly cause cell dysfunction because of

lipotoxicity.

Congestive Heart Failure

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Several factors primarily caused by obesity, like increased blood volume, elevated

cardiac output, left ventricular hypertrophy, and left ventricular diastolic dysfunction,

in addition to adipositas cordis, play a role in causing heart failure. This is in addition

to indirect effects mediated through other frequently coexisting conditions like

diabetes, hypertension, and coronary artery disease. Clinical assessment for heart

failure is often difficult in obese patients for several reasons. Dyspnea during exertion

and leg edema can occur even without congestive heart failure. They can have

orthopnea caused by the protuberant abdominal contents pressing on the diaphragm

when they are recumbent.

Physical examination is complicated because neck veins are difficult to see, heart

and breath sounds are distant, and the liver, even if enlarged because of right heart

failure, is difficult to feel. In the Framingham heart study, after 14 years of follow-up

for 5881 patients (mean age, 55 years; 54% women) heart failure developed in 496.

After adjustment for established risk factors there was a calculated increase in the risk

of developing heart failure by 5% in men and 7% in women for each increment of 1

above 30 on the BMI. The hazard ratio was 2.12 in women (95% CI, 1.512.97) and 1.9 in men (95% CI, 1.3.79) who were obese.23 Ejection fraction of _40% was seen in 42% of obese compared with 54% of normal-weight patients with heart failure.

Thus, there are more patients with diastolic heart failure among the obese.

Approximately 11% of heart failure in men and 14% in women in the community are

because of obesity alone.

Arrhythmias

There is an increase in the incidence of sudden cardiac death and arrhythmias in

obesity.24 Fatal arrhythmias may be the most frequent cause of death among obese

patients. According to the Framingham data, sudden cardiac death was 40 times higher

in obese men and women.24 In another study of severely obese individuals, this was

6-fold and 12-fold higher in those aged 25 to 34 years and 35 to 44 years,

respectively.25 In the NHANES III study, 30% of obese patients with glucose

intolerance had a prolonged corrected QT (QTc) interval. Schouten et al26 found that

8% of obese individuals had a QTc interval of more than 0.44 seconds and, in 2%, it

was more than 0.46 seconds. A QTc interval of more than 0.42 seconds was associated

with increased mortality in healthy obese patients followed for 15 years. QT dispersion, which measures the difference in duration between the maximum and the

minimum QT interval in different leads in the EKG is a good noninvasive measurement

for quantifying the degree of myocardial repolarization inhomogeneity, which was also

increased in the obese. Both QTc interval and QT dispersion are mediated by changes

in sympatheticvagal balance. Catecholamine levels are increased in the obese. In

addition, increased free fatty acid levels in the obese may also affect repolarization. In

patients with myocardial infarction, there is a relation between ventricular arrhythmias

and long chain saturated fatty acid level. Various changes occur in the autonomic

system with weight gain. A 10% increase in body weight causes a decrease in

parasympathetic tone and increase in heart rate. On the other hand, heart rate decreases

with weight reduction. There is a significant improvement in heart rate variability with

10% weight loss. Both increased resting heart rate and decreased heart rate variability

are predictors of mortality, independent of the ejection fraction. In a study of obese

16 | P a g e


patients without clinical heart disease, the prevalence of late potentials (high-

frequency, low-amplitude signals at the terminal part of the QRS complex

demonstrated using high-resolution signal averaged recording) are seen to be increased

proportionately with BMI. The presence of late potentials has been documented to be

associated with increased risk of ventricular arrhythmias in several cardiac conditions

and is present in less than 3% of normal controls. In those with a BMI score between

31 to 40, 41 to 50, and _50, the incidence of late potentials were 35%, 86% and 100%,

respectively. This increased frequency may be related to fat and mononuclear

infiltration, fibrosis, focal myocardial disarray, or myocyte hypertrophy.

Coronary Artery Disease

Obesity is an independent predictor of coronary artery disease, as observed in the

Framingham heart study,30 Manitoba study,31 and Harvard public health nurses

study.32 In the Framingham cohort, patients aged 28 to 62 years were followed for a

mean of 26 years. Among men younger than 50 years, the heaviest group experienced

twice the risk of coronary disease compared with the leanest group. The risk was

increased 2.4-fold among obese women of similar age, and this was after adjusting for

the influence of other major cardiovascular risk factors.30 Autopsy among 15 to 34

year olds who died from accidental causes revealed plaques and ulceration in the

coronary arteries and abdominal aorta, the extent of which correlated with the amount

of abdominal fat and BMI (PDAY study).33 Obesity accelerates atherosclerosis

decades before clinical manifestations appear and this remained significant even after

adjustment of other risk factors like high cholesterol, hypertension, smoking, and

increased HbA1c.30 The density of macrophages per mm2 of plaques also correlated

with visceral obesity.

After coronary artery bypass surgery also there are more adverse outcomes in obese

patients. They have increased incidence of postoperative thromboembolism, infections

of the sternum, and saphenous vein harvest sites. There is also a higher incidence of

atrial arrhythmias. However mortality or postoperative cerebrovascular events were

not significantly higher. Even pulmonary complications were comparable, except in

the severely obese (BMI _35) and when complicated by diabetes, renal dysfunction or

age _60.35 .

Hypertension

Among men, the prevalence of hypertension is 15% in those with BMI _25 and 42%

if BMI is _30; in women, these are 15% and 38%, respectively. 36 Blood pressure is

the product of cardiac output and systemic vascular resistance, and cardiac output is

increased in obese patients because of increased blood flow to the adipose tissue. We

should expect the systemic vascular resistance to be low in obese individuals because

of the increased cross-sectional area of the vascular bed. However, it is often

inappropriately normal or even high, and this increases the likelihood of hypertension.

Various factors like low-grade inflammation mediated through adipokines,

hyperinsulinemia, and insulin resistance, over-activity of the sympathetic nervous

system and a disordered sleep pattern increase the systemic vascular resistance in

obese patients. With increasing severity of obesity, hypertension becomes more

prevalent. It may initially be diurnal, especially if there is coexisting sleep apnea. On

the right side also there is an increase in the filling pressures, systolic pressure, and

17 | P a g e


pulmonary vascular resistance. Increased pulmonary vascular resistance may be

because of a combination of intrinsic pulmonary disease, sleep apnea/hypoventilation,

recurrent pulmonary thromboembolism, or left ventricular dysfunction, all of which

are more common in obese individuals. Pulmonary artery pressure is elevated in more

than 50% of obese patients but usually only to a mild degree. Fifteen percent to 20%

of patients with obstructive sleep apnea have pulmonary hypertension. This is often

mild and ranges from 30 to 35 mm Hg and is rare in the absence of daytime hypoxia.

EKG signs of right ventricular overload are very late manifestations. Nocturnal

dysrhythmias, right and left heart failure, myocardial infarction, stroke, and mortality

are more common in those with obstructive sleep apnea.

Stroke

Increased BMI and waist hip ratio are independent risk factors for stroke, even after adjusting for hypertension, hypercholesterolemia, and diabetes. In the prospective

Physicians Health study cohort of 21,414 men, those patients with BMI between 25 and 30 (8,105 men) and _30 (1,184 men) had a multiple adjusted relative risk of total

stroke of 1.32 (95% CI, 1.14 1.54) and 1.91 (95% CI, 1.452.52), respectively, compared with men with BMI _25. In these groups the relative risk of ischemic stroke

was 1.35 (95% CI, 1.151.59) and 1.87 (95% CI, 1.38 2.54) and hemorrhagic stroke was 1.25 (95% CI, 0.84 1.88) and 1.92 (95% CI, 0.94 3.93), respectively. 39 With each 1-unit increase in BMI score, the multiple adjusted rate of ischemic stroke

increased by 4% and 6% for hemorrhagic stroke. The underlying mechanisms by

which increased BMI score affects stroke risk, independent of established risk factors

such as hypertension and diabetes, is not fully understood. This could be mediated by

the prothrombotic (higher levels of plasminogen activator inhibitor-1 antigen and

activity, fibrinogen, von Willebrand factor, and factor VII) and proinflammatory state

(increased levels of C-reactive protein and lymphokines) in obesity.

Echocardiography

Large accumulation of subepicardial fat can mimic pericardial effusion

pseudopericardial effusion). Lipomatous hypertrophy caused by fat deposition in the

interatrial septum can cause it to be up to more than 20 mm thick and can even suggest

a tumor. Left ventricular diastolic dysfunction is very common. When compared with

normal people, subclinical changes in the structure and function of the left ventricle,

such as differences in the regional or global strain, were identified in asymptomatic

obese patients many years before they developed signs and symptoms of heart failure.

Poor images are commonly a problem in obese individuals and techniques like tissue

Doppler and pulmonary venous Doppler may be useful.

Electrocardiogram

Interplay between several factors, such as horizontal displacement of the heart by the

elevated diadoi phragm, cardiac hypertrophy, increase in the distance between the heart

and the electrodes, and coexisting sleep apnea/obesity/hypoventilation syndrome, tend

to modify the EKG in obese patients. The EKG may show low voltage, leftward axis,

flat inferolateral T waves, left atrial enlargement, increased false positive criteria for

inferior wall myocardial infarction, and less prevalence of left ventricular hypertrophy

than that based on echo criteria (only around two thirds).44 The left ventricular forces

are more posteriorly and laterally oriented with deep S waves in V3 and tall R waves

18 | P a g e


in aVL. The sum of R wave in aVL and S wave in V3, if more than 35 mm in men and

25 mm in women, has a sensitivity of 49% and a specificity 93% when compared with

echo in diagnosing left ventricular hypertrophy and is more helpful than many of the

more commonly used voltage criteria. 20 With weight loss, the QRS amplitude may

increase, decrease, or have no change.

Stress Tests and Cardiac Catheterization

The diagnosis of coronary artery disease also poses many challenges in the obese.

Stress EKG is difficult because of resting EKG abnormalities caused by obesity and

difficulty in performing adequate exercise. Nuclear imaging is plagued by attenuation

artifacts and higher incidence of false positives. Cardiac catheterization and nuclear

imaging is often not possible because of weight limitations of the table;

transesophageal dobutamine stress echo may be a good safe alternative even though it

is not widely used. For cardiac catheterization, radial approach is preferable. With

femoral access, the increased volume of adipose tissue to be passed through by the

needle to enter the femoral artery causes difficulty in hemostasis even though various

closure devices currently available makes this less challenging than in the past. Duke

university catheterization lab data from1986 to 1997 in 9405 patients show that obesity

increased from 20% to 33% during this period.46 Even though obese patients were

younger and had a higher percentage of single vessel disease, they had more

comorbidity, which resulted in increased clinical events in the 30 days after the test.

Inpatient medical cost was also increased.

Conclusions

Obesity affects the cardiovascular system directly in many ways, in addition to its

indirect effects, and it increases morbidity and mortality. Technical difficulties make

cardiac investigations difficult to perform and interpret in obese patients. Halting this

obesity epidemic is an important hurdle we must overcome in our effort to reduce the

burden of cardiovascular diseases in the population.

ARTIKEL 3

AHA Conference Proceedings

Obesity

Impact on Cardiovascular Disease

1. Ronald M. Krauss, MD; 2. Mary Winston, EdD; 3. Barbara J. Fletcher, RN, MN, FAAN, (conference codirectors); 4. Scott M. Grundy, MD, PhD (conference codirectors)

Key Words:

obesity

cardiovascular diseases

AHA Conference Proceedings

morbidity

The American Heart Association conference entitled Obesity: Impact on Cardiovascular Disease was held May 2224, 1998, in Amelia Island, Fla. It was cosponsored by Futura Media Services and the American Heart Association Councils

on Cardiovascular Nursing; Arteriosclerosis, Thrombosis, and Vascular Biology;

Cardiovascular Disease in the Young; Clinical Cardiology; Epidemiology and

19 | P a g e


Prevention; and High Blood Pressure Research; the AHA Nutrition Committee; and the

AHA Prevention Coordinating Committee. The proceedings are summarized briefly in

this report. A monograph of the conference will be published by Futura

Publishing Company, Inc.

Obesity is an important determinant of cardiovascular disease (CVD). Previous

epidemiological studies of obesity have documented a modest association of obesity

and risk of CVD, especially in younger age groups. The study of obesity and CVD

should now focus on weight change over time, especially differences between

childhood versus younger and older adult weight gains, and the distribution of body fat,

especially visceral or intra-abdominal fat. Weight gain during young adult life may be

one of the most important determinants of cardiovascular risk factors. Increased intra-

abdominal fat, or waist circumference, is probably related to a constellation of risk

factors, the so-called insulin resistance syndrome. It is also associated with higher levels

of inflammatory markers such as C-reactive protein and fibrinogen.

Age and Sex as Determinants of Obesity

The increasing prevalence of obesity in children is cause for great concern. There is no

definition of obesity in children that relates body mass index (BMI) to health outcomes.

However, >20% of children aged 6 to 17 years are >20% overweight at the 85th

percentile of BMI, and 10% of children aged 6 to 17 are overweight at the 95th

percentile. It appears that 50% of children who are overweight are also overweight as

adults, but it is not possible to identify any individual child who will become an

overweight adult. CVD risk factors, such as elevated blood pressure, elevated total

cholesterol and LDL cholesterol (LDL-C), and low levels of HDL cholesterol (HDL-

C) track from childhood, although less strongly than BMI. Overweight children also

tend to have a cluster of risk factors. Risk factors tend to occur in families and are

especially evident in children when an adult relative is obese. Children with a family

history of CVD are heavier than those without family history of disease. All of this

suggests that the obese child has an elevated risk of developing CVD in adulthood. A

few studies have linked childhood obesity with adult morbidity and mortality. One

study showed a trend toward an increase in all-cause mortality; in another, very obese

children (before and after puberty) were at greater risk for adult mortality from CVD.

A BMI greater than the 70th percentile versus the 25th to 50th percentiles in childhood

resulted in a greater relative risk of coronary heart disease (CHD) mortality in men but

not in women. Increased relative risk for all-cause mortality was present in both men

and women in this study population

Weight gain occurs differently in men and women. The greatest weight gain in men

occurs in those with the highest BMI and those in the older age groups. Compared with

women, men live longer and are obese later in life. In women, the greatest weight gain

is in the younger age groups. Recent epidemiological studies have shown that in

women, weight loss is also accompanied by bone loss. Another difference in weight

gain between men and women is that as womens educational level rises, obesity decreases, for both white and black women, whereas in men, educational level appears

not to be related to obesity.

Genetics

The causes of obesity are many, but there is little doubt that genetic factors play an

important role in its etiology. Humans carry probably dozens of genes that are directly

20 | P a g e


related to body size. One of the specific roles for genes is the determination of set points.

Identification of such genes is important, and several types of studies must be

performed to address this. Linkage analysis can be used to find physical locations of

genes that are relevant to a phenotype. If a specific gene plays a role in the

determination of a given phenotype, the gene and the phenotype will be transmitted

together (cosegregate) across generations. The fact that the etiology of obesity is so

complex underscores the need for better understanding of genetic determinants as a

basis for more rational interventions to treat obesity.

Several approaches have been used to search for specific genes involved in obesity:

identification of mutations responsible for obesity in rodent models, association or

linkage of obesity measures with candidate genes in humans, and chromosomal

localization of genes by linkage of polymorphic markers to obesity and related

phenotypes in humans and mice. To date, causative genes have been found for 5 obese

mouse models. Two, leptin and leptin receptor, have been linked with variation in body

fat in some human studies, but, for leptin, causation has been shown only in 2 obese

children with homozygous missense mutations in the leptin gene. Linkages or

associations with body fat measures have been reported for >20 other candidate genes

in humans, but relationships involving these genes were generally not strong and in

some cases were inconsistent among studies. Chromosomal sites of genes responsible

for several rare familial human obesity syndromes have been identified, but none to

date have been linked to obesity in the general population. On the other hand, with

genome-wide searches, quantitative trait linkages of body fat indexes have been

reported for several genetic markers in both humans and mouse models. Although

multiple genetic influences on obesity phenotypes are suggested by these studies, in

most cases the responsible gene variants, their pathophysiological effects, and their

interactions with other genes and environmental factors remain to be determined.

Environmental Factors

Environmental as well as genetic factors greatly affect the expression of obesity across

the lifespan. The relative contribution of each of these factors to the phenotypic

variance of obesity is not fully understood. Knowledge of the nongenetic determinants

of obesity-CVD risk factor clustering is essential for planning effective

multidisciplinary interventions focused on primary prevention of CVD. Data from a

longitudinal twin-family study and co-twin control studies combined with population-

based data on patterns of dietary intake and physical activity provide persuasive

evidence for an environmental hypothesis. Collectively, these data point to the

importance of primary prevention beginning early in life, emphasize the role of health

behaviors including physical activity and dietary intake, and suggest the need for

modification of health-related practices and policies focused on consumers, providers,

schools, and communities.

Obesity and Cardiovascular Health

The effects of obesity on cardiovascular health and disease are many, one of the most

profound of which is hypertension. Risk estimates from population studies suggest that

75% of hypertension can be directly attributed to obesity. However, the precise mechanisms of hypertension related to obesity are not fully understood. Contemporary

thinking concerning the link between obesity and subsequent renal failure has evolved

21 | P a g e


from repeated observations of the relationship between body weight and blood pressure.

It is well documented that blood pressure increases with weight gain and decreases with

weight loss. In addition, there is increasing evidence that obesity may provide the

impetus for sympathetic nervous system activation as well as for changes in renal

structure and function. There is considerable evidence that renal dysfunction,

characterized by increased tubular sodium reabsorption and resetting of pressure

natriuresis, plays a key role in increasing blood pressure in obese subjects. The

increased tubular pressure reabsorption is closely related to the sympathetic nervous

and renin-angiotensin systems, as are structural changes that cause compression of the

renal medulla. Renal vasodilation, glomerular hyperfiltration, and increased arterial

pressure are compensations that help overcome increased renal tubular reabsorption and

maintain sodium balance in obesity. This also leads to increased glomerular capillary

wall stress, which, along with activation of the neurohumoral systems, increased lipids,

and glucose intolerance, eventually causes glomerulosclerosis and loss of nephron

function in obese subjects. Further research is needed to identify the mechanisms

involved in sympathetic nervous system activation and changes in enal structure and

function that accompany obesity.

Obesity has a strong effect on lipoprotein metabolism, regardless of ethnic group.

Increased weight is a determinant of higher levels of triglycerides, elevated LDL-C,

and low HDL-C. Conversely, weight loss is associated with a healthier lipoprotein

profile in both men and women: triglycerides decrease, HDL-C increases, and LDL-C

decreases. Changes in HDL-C levels are more pronounced in women than in men. The

association between obesity and LDL-C is more complex. LDL-C concentrations

increase with BMI in men, but such increases are not as pronounced in women, the

elderly, and some ethnic groups. Increasing BMI is associated with small, atherogenic

LDL. Furthermore, central obesity in women is associated with elevated LDL-C

concentrations. Research should be directed toward understanding the relative

importance of obesity-related changes in lipoproteins in predicting actual and potential

CVD.

There is a strong link between obesity and a generalized metabolic disorder of which

insulin resistance is an indicator. It is difficult to define the precise contribution of

obesity to insulin resistance, but most analyses suggest that it can account for 50% of the variance in insulin sensitivity in the general population. Insulin resistance is

associated with a constellation of metabolic abnormalities, including obesity, diabetes,

dyslipoproteinemia, hypertension, and atherosclerosis. It is also linked to a

prothrombotic state. Because of the complex nature of insulin resistance, it is not known

whether it is independently related to atherogenesis by an unknown mechanism. Future

research should explore whether insulin resistance can promote atherosclerosis

independently of other risk factors.

The response of various ethnic groups to insulin resistance is variable; eg, Asian Indians

are more susceptible to insulin resistance than are other ethnic groups and are at very

high risk of coronary disease. The role of body fat distribution in insulin resistance is

important; the key may be abdominal fat, which is highly correlated with insulin

resistance. It is also necessary to consider the role of aging, exercise, diet, and genetics

in insulin resistance.

Biological Factors in Obesity

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Currently, little is known about the basic causes of obesity, but a great deal is happening

in the area of translational research that will lead to the therapeutics of tomorrow. An

important focus of research is the biology of weight reduction. The role of proteins and

receptors in the regulation of obesity is not yet fully understood. A good example is

orphan receptors, the recent screening of which revealed orexin A and B. These

receptors are found in the lateral hypothalamus of the brain, the area known to be

associated with regulation of body weight. Orexin peptides A and B are

neurotransmitters responsible for regulation of fasting and feeding. It is possible that

other peptides and amines that regulate energy are present, but this remains to be

demonstrated. The function of such peptides and amines and their relationship to

obesity remains to be shown and is an area for future research.

The uncoupling proteins UCP-2 and -3 may be important in regulating metabolic rate

and therefore in obesity. The relationships between these proteins, which act in the

mitochondria, and obesity are not completely understood. Because UCP-3 is thought to

regulate energy balance, research in this area would be valuable.

Sleep apnea is a major factor to consider in obesity. This dysfunction may be associated

with the release of the cytokines tumor necrosis factor and interleukin-6. Sequelae

associated with sleep apnea appear to play a role in mortality of severely obese patients.

Circulating estrogens increase with body weight. However, an association of weight

gain with hormone replacement therapy (HRT) has not been supported by findings from

scientific studies. The relation between HRT and incidence of CVD is similar at all

levels of BMI. Breast cancer increases only in the group with the lowest BMI. HRT

appears to protect against initial myocardial infarction and hip fractu re in both obese

and lean women.

Assessing the Obese Patient

In assessing the obese patient, it is critical to determine the relative contributions made

by fat and fat-free mass to total body mass. Body composition assessment has improved

over the century. Various measures are used to grossly estimate the degree of obesity

in large-scale epidemiological settings, including body weight, BMI, waist

circumference, and the waist-to-hip ratio. In smaller-scale studies and clinical settings,

measurements of triceps and subscapular skinfolds are more practical and accurate

methods. Bioelectrical impedance, total body electrical conductivity methods, and dual-

energy x-ray absorptiometry are also used in clinical settings. Indirect methods such as

hydrostatic weighing and measurement of total body potassium and deuterated

and 18O2-labeled water are used in research settings.

It is essential that valid and reliable measures of dietary intake be used in studies aimed

at determining the links between dietary intake and obesity. Various instruments are

available, but a valid assessment requires clear identification of the primary objective

of the assessment and the intended uses of the derived information. Other

considerations include defining what components of the diet will be assessed,

participant burden, and reporting bias. Understanding the strengths and weakness of

food records, dietary recalls, and food frequency questionnaires is important for the

selection of methods, the development of strategies to minimize problems, and the

appropriate interpretation of the data.

A better understanding of why modest weight reduction benefits many of the

comorbidities and why the elderly may be relatively protected from obesity-related

consequences may better delineate who should be treated and how aggressively. For

23 | P a g e


example, in hypertensives, nonpharmacological treatment combined with

pharmacological treatment is the most effective, and the development of diabetes can

be prevented by weight loss and exercise.

Another factor to consider is diet composition. The recommendations for dietary intake

for the prevention of CVD may require modification. The following areas are being

considered: increasing monounsaturated fatty acids to replace saturated fatty acids; the

role of water in obesity; the role of high energy density in obesity; and the role of meal

replacements, diet supplements, vitamin and mineral supplements, and macronutrients.

Altering the diet composition for short-term weight loss (12 to 20 weeks) adds little to

the amount of weight loss achieved. However, diet composition is important for weight

maintenance. Small changes, such as eating 50 fewer calories a day, exercising for 15

to 20 minutes a day, or expending 100 additional calories per day, can result in a 10-lb

weight loss per year or can help maintain weight. Small changes are additive.

Obesity is the normal physiological response to an environment in which energy intake

exceeds energy output. It is an adaptive mechanism. Major environmental changes that

support this adaptive mechanism are the greater availability of foods and the increase

in sedentary lifestyle. The social environment has moved from being obesity retardant

to being obesity conducive. This has important implications for patients with certain

genotypes. Metabolic rates differ between patients and may be important in determining

who becomes obese.

Obesity can develop when an imbalance exists between energy intake and energy

expenditure. Despite this seemingly simple statement, the relative contributions of

energy intake and energy expenditure in obesity development are poorly understood.

Total energy expenditure can be divided into the following components:

Resting metabolic rate, the largest single component of energy expenditure.

Approximately 60% to 80% of the variation in resting metabolic rate can be explained

by fat-free body mass; The thermic effect of food, or the increase in energy expenditure

that occurs after eating; and Energy expended in physical activity. This varies due to

differences in body mass. The energy expended in physical activity is an important

component in understanding both why obesity occurs and how it can be treated.

In the context of a 3000-calorie diet, typical energy expenditure can be anywhere from

450 to 1500 calories. There is little evidence that defective energy expenditure exists. Efforts to increase energy expenditure by increasing physical activity are considered an

important treatment for obesity. Physical activity is beneficial to cardiovascular health

in many ways. For example, HDL-C levels increase and triglyceride, glucose, and blood

pressure levels decrease. These changes occur in connection with small changes in

weight. Diet and exercise strategies provide relatively equal amounts of weight loss in

premenopausal and postmenopausal women. In men, this combination is also a very

effective means of achieving weight loss. Further research is needed to determine a

prescription of exercise; that is, its intensity, frequency, duration, and total amount as well as the length of the training period. The most important factor in successful weight

loss is likely to be adherence to whatever exercise regimen a person adopts.

Medical Treatment of Obesity

One group of medications currently available for treatment of obesity works primarily

by reducing food intake. The central regulation of food intake involves both monoamine

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and peptide neurotransmitters. Sibutramine, a newly approved sympathomimetic drug,

reduces food intake and increases thermogenesis in experimental animals. There is a

dose-related reduction in body weight. Sibutramine is associated with a 1 to 3 mm Hg

increase in blood pressure and a 4 to 5 bpm increase in heart rate. Another group of

drugs works by altering metabolism; orlistat, a lipase inhibitor, is in this group. Five

long-term trials lasting 1 to 2 years have been reported in which drug-treated patients

lost significantly more weight than control subjects. Gastrointestinal symptoms were

rather severe the first year but subsided the second year. Yet another way to increase

energy expenditure is through thermogenic mechanisms; however, no drugs are

currently available that work in this manner. The impact of drug treatment on cardiac

mechanics was discussed at the conference. The most striking example, of course, was

the recent withdrawal of the combination of fenfluramine and phentermine (fen/phen)

from the market by the Food and Drug Administration (FDA). This was prompted by a

report from the Mayo Clinic of 24 cases of valvular heart disease in women who were

treated with fen/phen. In addition, unpublished data on the World Wide Web provided

the basis for the withdrawal of the combination drug. The percentage of patients

meeting the FDA criteria for valvulopathy was 31.7%; 68.3% f patients taking these

drugs did not exhibit valvular changes. It will be necessary to determine whether

obesity without pharmacological intervention is associated with valvular changes

before cause can be attributed to any drug used to treat human obesity. There is clearly

a need to first identify which heart valve changes occur as a direct result of obesity

before deciding that pharmacological therapy is the cause of valvular disease. At

present, little is known about the incidence of new, significant valvular disorders

associated with fen/phen. Information will come from case-control studies and smaller

retrospective studies with patients serving as their own control subjects. The risk factors

for valvulopathy must be identified, as well as whether the valve abnormalities are

reversible if the obesity drugs are discontinued.

Nondrug Treatment of Obesity

Lifestyle and psychosocial treatments have their roots in behavior modification and

include techniques and approaches that focus on changing behaviors that are thought to

contribute to or maintain obesity. Most of the various lifestyle approaches have several

factors in common, including the following: the use of self-monitoring and goal setting;

stimulus control; modification of eating style and habits; the use of reinforcement for

healthy behaviors; nutrition education; moderate physical activity; and cognitive

restructuring, including stress management, relaxation skills, meditation, and relapse-

prevention training. These approaches produce moderate weight loss and have minimal

side effects. They are most useful for individuals with mild obesity (BMI of 27 to 30).

Individuals who follow such an approach to weight loss maintain on average about two

thirds of their initial weight loss 12 months after treatment termination. In studies with

extended follow-up, patients return gradually to baseline within a few years after

treatment termination. Thus far, only a continuous-care model of lifestyle intervention

that views obesity as a chronic disease requiring support or contact after the conclusion

of formal treatment produces significant results in terms of long-term maintenance.

Future research needs to address the barriers to this approach, such as insurance

reimbursement for obesity-related treatments and the lack of data to support the cost-

effectiveness and feasibility of continuous care. Research should also focus on methods

of implementing lifestyle interventions at the lowest cost possible and evaluating which

elements of multicomponent treatments are most effective for which individuals.

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Despite the lack of substantive evidence to support specific strategies to achieve weight

maintenance, empirical evidence has provided some insight into this problem. Factors

related to weight maintenance are different from those involved in initial weight loss.

Regular exercise is crucial, as is social support. Effective strategies for maintaining

weight loss include ongoing contact with a physician or counselor, provision of problem

solving, and enhancement of interactions. These can be accomplished by telephone

and/or mail contacts. Multicomponent and home-based strategies appear to be the most

effective. Social support can be enhanced by looking beyond the usual sources. For

example, program participants can be asked to bring in 3 friends. Intragroup activities

and intergroup competition have been shown to be effective. In summary, weight

maintenance requires ongoing contact with a physician or other weight-loss counselor,

exercise, social support, and extended treatment. In the long term, the most effective

approach to controlling obesity may be to view it as a chronic disease. Maintenance of

quality of life (QOL) has recently emerged as a standard for the successful treatment of

obesity. Investigators agree that QOL consists of the following domains: physical

functioning, psychological functioning, social functioning, overall life satisfaction, and

perceptions of health status. In one focus group of moderately obese individuals, an

attempt to gain insight into patients perceptions of why obesity is problematic revealed that in the area of physical functioning, such things as lack of energy, esophageal reflux,

and pain emerged. In the psychological arena, patients felt out of control and were

entangled in a cycle of depression and weight gain. Socially, they were withdrawn, they

avoided certain situations such as air travel because of the seating difficulties, and they

felt embarrassed to take part in their childrens activities. Finally, the economic costs were significant with regard to food and clothing. The economic cost of obesity is

enormous. The monetary burden on society of illness and premature death is measured

in terms of direct and indirect costs. Direct costs represent the value of resources

(personal health care, other professional services, and drugs) that could be allocated to

other uses in the absence of disease. Indirect costs are the value of lost output because

of the cessation or reduction of productive activity due to morbidity and mortality. The

direct costs of CHD, noninsulin-dependent diabetes mellitus, and hypertension attributed to obesity have been shown in 1 study to amount to $42.62 billion. The

indirect costs of noninsulin-dependent diabetes attributed to obesity were $30.74 billion. A 1998 article showed that 17% of the costs of CHD were related to obesity.

The economic costs of weight-related disease become significant at a BMI >25. In

1995, 5.7% ($99.2 billion) of the US health expenditure was related to individuals with

a BMI of 29. Using a BMI of 25, this cost would be even greater. It is important to

recognize that obesity is not confined to the United States; it is an international problem.

With regard to personal costs, >$16 million is spent on diet sodas, $9 million in health

clubs, $600 million in medically supervised programs, $5 million on diet meals, $4

million on exercise equipment, and $2 million on commercial weight reduction

programs. The cost and benefits of obesity to society represent a very important issue

that needs to be thoroughly examined. The challenge is how to reduce the increasing

prevalence of obesity and its sequelae in both children and adults. It is difficult to lose

weight and maintain the loss; there are side effects; people tend to regain weight once

pharmacological agents are withdrawn; and surgery is not without problems. These

concepts clearly support a preventive approach to obesity beginning in early childhood,

with a focus on eating and activity patterns and on health as opposed to cosmetics. A

family approach should be adopted. Two strategies should be used, ie, the population

approach and the individual approach. The population-based effort should focus on

such areas as the media, community, and schools. The individual strategy will probably

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require a multidisciplinary approach consisting of physicians, dietitians, nurses, and

physical therapists. To date, health professionals have focused most of their efforts on

an individual approach, but serious consideration should be given to a population

approach. The scientific community has not yet reached consensus on viable ways to

approach the problems associated with obesity. However, several lines of attack are

being investigated. Because of the complexity of the obesity problem, a multifactorial

approach will undoubtedly be required. The pharmacological approach has yielded

disappointing results, but promise is on the horizon regarding possible drugs to modify

appetite and others that reduce absorption of foods or enhance energy expenditure. The

public health approach requires a systematic education of the public about the dangers

of obesity. Various health agencies could work together to promulgate such a message

that would reach all population groups. There is a great need to address the social factors

that contribute to obesity and to initiate efforts on a broad scale to modify these factors.

Much skepticism exists regarding the possibility of achieving success in the treatment

of obesity. It is important to note that many of the cardiovascular complications of

obesity arise as a result of mild to moderate degrees of overweight. The availability of

ancillary personnel, eg, dietitians and exercise therapists, will be required to assist

physicians in the treatment of obesity in the clinical setting. Finally, management of

associated risk factors (atherogenic dyslipidemia, hypertension, prothrombic state, and

insulin resistance) will help prevent the cardiovascular complications of obesity.

ARTIKEL 4 Clinician Update

Obesity and Cardiovascular Disease

Caroline M. Apovian, MD;

Noyan Gokce, MD

+Author Affiliations

From the Department of Medicine, Section of Endocrinology, Diabetes and Nutrition

(C.M.A.) and Department of Medicine and Whitaker Cardiovascular Institute (N.G.),

Boston University School of Medicine, Boston, MA.

Correspondence to Caroline M. Apovian, MD, Professor of Medicine, Boston

Medical Center, 88 E Newton St, Robinson Bldg, Suite 4400, Boston, MA 02118. E-

[email protected]

Case study: A 43-year-old man with a long history of obesity presented to our Weight

Management Center 5 years after being disabled in a motor vehicle accident and gaining

weight to a lifetime high of 269 kg and body mass index (BMI) of 85 kg/m2. His

comorbidities were hypertension, obstructive sleep apnea, gastroesophageal reflux

disease, gout, and osteoarthritis, and he had recently developed type 2 diabetes mellitus.

Medications used included metformin, glyburide, losartan, hydrochlorothiazide, and

diltiazem. He was motivated and met criteria for weight loss via a surgical intervention.

Preoperatively, he was placed on a high-protein diet plus an appetite suppressant

(phentermine) to achieve 10% weight loss. His weight declined, but he developed new-

onset atrial fibrillation 3 weeks later, which was thought to be related to phentermine

use and was cardioverted back to sinus rhythm.

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Several months later, the patient underwent gastric bypass bariatric surgery with a

preoperative weight of 252 kg. His type 2 diabetes mellitus resolved immediately after

surgery, as did his gastroesophageal reflux and hypertension. Ten months after surgery,

his weight was down to 177 kg (BMI=56 kg/m2) with hemoglobin A1c of 5.9%, fasting

blood glucose of 82 mg/dL, and blood pressure of 137/82 mm Hg, and he was no longer

taking any medication.

Obesity: Relationship to Cardiovascular Disease

Although there are multiple long-term deleterious health effects of excess weight,

obesity as defined by BMI 30 kg/m2 is associated with premature atherosclerosis, increased risk of myocardial infarction and heart failure, and decreased survival, largely

because of cardiovascular deaths,

[Full Text of this Article]

ARTIKEL 5

PENGENALAN

Secara umumnya, obesiti merupakan pengumpulan lemak yang berlebihan yang

menimbun didalam badan seseorang. Obesiti kini dianggap sebagai satu penyakit dan

terjadi apabila tisu-tisulemak menjadi keterlaluan. Lebih teruk lagi, obesiti boleh

mengganggu dan mencederakanorgan-organ badan dan seterusnya akan menyebabkan

masalah kesihatan yang serius. Selaindaripada menghadkan aktiviti fizikal dan sosial,

jangka hayat penghidapnya juga semakin pendek. Masalah obesity/ berat berlebihan

adalah masalah kian meningkat di kalangan kanak-kanak. Kanak-kanak obes lazimnya

mengalami masalah berat badan apabila dewasa kelak.Obesiti selalunya dikaitkan

dengan penyakit kardiovaskular, pernafasan dan juga diabetes. Olehitu kanak-kanak

yang obes mempunyai risiko lebih tinggi mengalami masalah berkenaan.Mereka yang

tergolong dalam obesiti biasanya mempunyai berat badan sekurang-kurangnya duakali

lebih berat berbanding ukuran ideal. Mereka ini juga mempunyai berat badan sekurang-

kurangnya 45 kilogram melebihi berat badan yang sepatutnya. Selain itu, Indeks Jisim

Badan(BMI) melebihi 40 atau 35 dan mengalami beberapa penyakit seperti tekanan

darah tinggi ataudiabetis serta mereka yang gagal mengekalkan berat badan yang sihat

dalam jangka panjangsekalipun mengikut diet yang disarankan oleh pakar-pakar

pemakanan. Menurut kamus DBP,Kuala Lumpur, obesiti bermakna kegemukan yang

disebabkan terdapatnya lemak yang berlebihan Obesiti menimbulkan pelbagai masalah

kesihatan seperti penyakit jantung, dantekanan darah tinggi. Orang yang mengalami

masalah obesiti juga tidak dapat menikmatikehidupan mereka sepenuhnya kerana

badan yang terlalu gemuk sudah pasti membataskan pergerakan mereka. Mereka juga

akan mengalami tekanan akibat perasaan malu dan rendah diri.

Obesiti menimbulkan pelbagai masalah kesihatan seperti penyakit jantung, dantekana

n darah tinggi. Orang yang mengalami masalah obesiti juga tidak dapat

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menikmatikehidupan mereka sepenuhnya kerana badan yang terlalu gemuk sudah pasti

membataskan pergerakan mereka. Mereka juga akan mengalami tekanan akibat

perasaan malu dan rendah diri.

FAKTOR OBESITI

Perubahan lemak badan bergantung kepada ketidakseimbangan antara tenaga yang

diambil dan yang digunakan. Lebihan berat badan dan obesiti terjadi apabila

pengambilan tenaga melebihi pengeluaran untuk jangkamasa yang tertentu. Terdapat

banyak penyebab yang dikaitkan dengan lebihan berat badan dan obesiti tetapi faktor

sosial dan persekitaran sama ada peningkatan pengambilan tenaga atau berkurangan

aktiviti fizikal memainkan peranan penting terjadi keadaan ini. Ini berkaitan dengan

peningkatan taraf ekonomi masyarakat dan penurunan aktiviti fizikal generasi muda

dan yang telah berusia. Aspek keturunan terhadap kejadian lebihan berat badan dan

obesiti sukar untuk ditentukan. Kajian yang telah dibuat telah mencadangkan

lebihan berat badan dan obesiti di kalangan kanak-kanak lebih kepada kurangnya

aktiviti fizikal dan bukannya lebihan makanan dan pada remaja ia lebih dipengaruhi

oleh kurangnya aktiviti fizikal dan lebihan makanan (WHO, 1990).

Kajian lain menunjukkan lebihan berat badan dan obesiti adalah faktor risiko

pada penyakit kardiovaskular. Lebihan berat badan dan obesiti merupakan faktor

primer bagi penyakit koronari jantung dan bersama faktor risiko lain yang telah

dibuktikan seperti diabetes, hiperkolesterolemia atau kekurangan tahap lipoprotein

kepadatan tinggi (HDL)(Pollock & Wilmore, 1984). Hipertensi yang di alami oleh

mereka yang obes adalah signifikan lebih tinggi jika di banding dengan yang tidak

obes. Peningkatan tekanan darah adalah dicatat pada kedua-dua bacaan sistolik dan

diastolik (Wan Mohamad et al., 1996). Lebihan berat badan dan obesiti juga

mempunyai hubungan dengan penyakit diabetes. Kajian telah menunjukkan bahawa

walaupun terdapat peningkatan pengeluaran insulin oleh pankreas antara 100-200%

dalam keadaan obes tetapi masih wujud tanda-tanda klinikal kekurangan hormon

tersebut. Ini menjelaskan terdapat kekurangan tapak reseptor, penurunan kadar

sensitiviti reseptor atau kedua-duanya. Penurunan berat badan mengakibatkan tapak

reseptor kembali kepada asal dari segi jumlah serta sensitiviti dan ini akan mengawal

paras glukosa darah (Pollock & Wilmore, 1984). Kajian ini dijalankan bagi mengukur

magnitud lebihan berat badan dan obesiti di kalangan pelajar sekolah menengah

(tingkatan IV & V) di Kelantan dan faktor-faktor yang menyumbang kepada masalah

tersebut.

Masalah berat badan ini sebenarnya berpunca dari kesalahan dan kelalaian diri kita

kerana kemudahan dan kemewahan hidup yang diperolehi oleh kita. Menurut

Norkumala (2007), masyarakat negara kita sering terdedah dengan pelbagai masalah

kesihatan yang kronik dan akhirnya mengundang kepada kematian. Ia adalah kesan

daripada amalan gaya hidup yang tidak sihat dan ketidakseimbangan kesihatan rohani

dan jasmani dalam kitaran hidup seharian.

Ini sejajar dengan kenyataan oleh Menteri Kesihatan, Chua Soi Lek iaitu jika kita tidak

membetulkan tabiat makan akan mengakibatkan kita mengalami masalah berat badan

pada masa akan datang ( Berita harian, 2007). Ini menunjukkan bahawa tabiat amalan

pemakanan yang tidak sihat dan betul akan mengakibatkan masalah berat badan kepada

seseorang individu. Aspek pemakanan ini perlu diberikan penekanan dari kecil lagi

sebagai langkah untuk mengelakkan tabiat pemakanan dan berat badan bertambah

seiring dengan peningkatan usia seseorang individu.

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Namun begitu menurut Hanee (2006), berat badan seseorang dapat

menunjukkan bahawa jumlah nutrien dan pemakanan yang mesti diambil. Jika tidak ia

mungkin akan mengakibat seseorang itu mengalami masalah berat badan. Pendapat ini

dapat disokong oleh Zainab (2001), ia menyatakan bahawa orang dewasa perlu

menentukan pengambilan makanan dan penggunaan tenaga seimbang untuk menetap

dan mengawal berat badan. Jika ini dijadikan sebagai panduan kepada pelajar ia boleh

mengelakkan pelajar mengalami masalah berat badan. Ia bermakna pelajar itu sendiri

yang menentukan jumlah pemakanan berat yang perlu diambil pada setiap hari, tidak

semestinya tiga kali sehari jika ia merasakan memadai untuk hanya mengambil dua kali

menu hidangan berat sehari.

Jika masa makan yang tidak menentukan diamalkan ia pastinya memberikan

kesan bukan sahaja kepada berat badan tetapi kesihatan juga. Ia sejajar dengan apa

yang diperkatakan oleh Azmi (2005), kesibukkan bekerja, menonton televisyen dan

banyak menghabiskan masa didepan komputer menjadi punca masalah berat badan.

Jika perkara ini tidak diberikan penekanan pastinya akan mengakibat masalah berat

badan akan terus meningkat.

Kegemukan boleh diturunkan daripada generasi sebelumnya kepada

generasi berikutnya. Itulah sebabnya kita seringkali menemui ibu bapa yang gemuk

cenderung memiliki anak-anak yang gemuk juga. Hal ini demikian kerana pada ketika

ibu obesiti sedang hamil, maka unsur sel lemak yang berjumlah besar dan melebihi

ukuran normal, secara automatik akan diturunkan kepada bayi dalam kandungan.

Sistem pengawal yang mengatur perilaku makan terletak pada satu bahagian otak yang

disebut hipotalamus, iaitu kumpulan inti sel otak yang berhubung dengan

bahagian- bahagian lain daripada otak dan kalenjar di bawah otak. Dua bahagian

hipotalamus yang mempengaruhi penyerapan makanan, iaitu hipotalamus lateral(HL) yang mengger

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