<?xml version="1.0" encoding="UTF-8" standalone="no"?><rss xmlns:atom="http://www.w3.org/2005/Atom" xmlns:blogger="http://schemas.google.com/blogger/2008" xmlns:gd="http://schemas.google.com/g/2005" xmlns:georss="http://www.georss.org/georss" xmlns:itunes="http://www.itunes.com/dtds/podcast-1.0.dtd" xmlns:openSearch="http://a9.com/-/spec/opensearchrss/1.0/" xmlns:thr="http://purl.org/syndication/thread/1.0" version="2.0"><channel><atom:id>tag:blogger.com,1999:blog-2451165783610843793</atom:id><lastBuildDate>Fri, 01 Nov 2024 07:26:43 +0000</lastBuildDate><category>KIDS FAT CAMP</category><title>FAT CAMPS FOR KIDS</title><description></description><link>http://fatcampsforkids.blogspot.com/</link><managingEditor>noreply@blogger.com (mesothelioma.abestos.lawyers)</managingEditor><generator>Blogger</generator><openSearch:totalResults>131</openSearch:totalResults><openSearch:startIndex>1</openSearch:startIndex><openSearch:itemsPerPage>25</openSearch:itemsPerPage><language>en-us</language><itunes:explicit>no</itunes:explicit><itunes:subtitle/><itunes:owner><itunes:email>noreply@blogger.com</itunes:email></itunes:owner><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-521498803685376951</guid><pubDate>Fri, 07 Sep 2012 03:02:00 +0000</pubDate><atom:updated>2012-09-06T20:02:56.687-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>LUNG CANCER STEM CELLS: TOOLS AND TARGETS TO FIGHT LUNG CANCER</title><description> &lt;br /&gt;
&lt;br /&gt;
cancer stem cell ( csc ) theory states that tumors are&lt;br /&gt;
organized in the same hierarchical manner as normal&lt;br /&gt;
tissues, utilizing a sub-population of tumorigenic stem-like&lt;br /&gt;
cells that generate the a lot of differentiated nontumorigenic&lt;br /&gt;
tumor cells. cscs are chemoresistant and seem to firmly be&lt;br /&gt;
chargeable for tumor recurrence and formation of&lt;br /&gt;
metastases. thus, the study of those cells could lead&lt;br /&gt;
to firmly crucial advances within the whole understanding of tumor biology&lt;br /&gt;
and even as to firmly innovative and a lot of effective therapies. lung&lt;br /&gt;
cancer represents the leading cause of cancer-related&lt;br /&gt;
mortality worldwide. despite improvements in medical&lt;br /&gt;
and surgical management, patient survival rates remain&lt;br /&gt;
stable at b15%, calling for innovative strategies that&lt;br /&gt;
could contribute to enhance patient outcome. the discovery&lt;br /&gt;
of lung cscs and therefore the possibility to firmly characterize their&lt;br /&gt;
biological properties could give powerful translational&lt;br /&gt;
tools to enhance the clinical outcome of patients with lung&lt;br /&gt;
cancer. during this report, we review what exactly is known about&lt;br /&gt;
lung cscs and discuss the diagnostic, prognostic and&lt;br /&gt;
therapeutic prospective of those findings.&lt;br /&gt;
oncogene ( 2010 ) 29, 4625–4635 ; doi :10. 1038/onc. 2010. 207 ;&lt;br /&gt;
printed on-line 7 june 2010&lt;br /&gt;
keywords : lung cancer ; cancer stem cells ; therapy ; stem&lt;br /&gt;
cells&lt;br /&gt;
cancer stem cells&lt;br /&gt;
tumor cells show a wide spectrum of useful and&lt;br /&gt;
morphological heterogeneity. even cells associated with a single&lt;br /&gt;
tumor lesion vary in his or her differentiation level, proliferation&lt;br /&gt;
capability and tumorigenicity. this phenomenon&lt;br /&gt;
could well be explained from the presence of ‘cancer stem&lt;br /&gt;
cells’ ( cscs ) ( reya et al. , 2001 ; wang and dick, 2005 ;&lt;br /&gt;
clarke et al. , 2006 ) just like the driving force of tumorigenesis.&lt;br /&gt;
the csc model implies a hierarchical organization&lt;br /&gt;
inside the tumor during which a restricted variety of cscs&lt;br /&gt;
represents the apex of one's hierarchy. similar to firmly normal&lt;br /&gt;
stem cells, cscs have the ability to firmly self-renew and&lt;br /&gt;
endure asymmetric divisions, thereby giving rise to firmly a&lt;br /&gt;
differentiated progeny that represents the majority of the tumor&lt;br /&gt;
population. these key features enable cscs to firmly initiate&lt;br /&gt;
tumors and promote cancer progression.&lt;br /&gt;
the very first few direct experimental proof supporting the&lt;br /&gt;
plan of csc-driven tumorigenesis came from acute&lt;br /&gt;
myeloid leukemia ( lapidot et al. , 1994 ), the initiating&lt;br /&gt;
cells of that utilize a phenotype ( that would be, cd34þ ;&lt;br /&gt;
cd38_ ) similar to firmly normal hematopoietic stem cells&lt;br /&gt;
( bonnet and dick, 1997 ). despite a few technical&lt;br /&gt;
limitations, a growing variety of reports support the&lt;br /&gt;
existence of cscs in solid tumors. specific biomarkers&lt;br /&gt;
for detection and isolation of cscs are suggested&lt;br /&gt;
for all those major tumor types, as well as lung cancer ( eramo&lt;br /&gt;
et al. , 2008 ; visvader and lindeman, 2008 ).&lt;br /&gt;
besides the expression of surface proteins, cscs may&lt;br /&gt;
too share useful features with tissue stem cells, such&lt;br /&gt;
as their ability to firmly actively exclude the dye hoechst 33342,&lt;br /&gt;
that defines them as side-population ( sp ) cells in flow&lt;br /&gt;
cytometric assays ( storms et al. , 1999 ) and high aldehyde&lt;br /&gt;
dehydrogenase ( aldh ) activity ( ginestier et al. , 2007 ).&lt;br /&gt;
in parallel in the growing variety of potential surface&lt;br /&gt;
markers, it's obtaining evident that the known markers are&lt;br /&gt;
not continuously ideal to firmly sort for our csc population. a good&lt;br /&gt;
example happens to be the expression of cd133, that was initially&lt;br /&gt;
reported becoming a reliable marker for glioblastoma&lt;br /&gt;
and medulloblastoma cscs ( singh et al. , 2003, 2004 ).&lt;br /&gt;
though, freelance studies have shown that cd133-&lt;br /&gt;
negative glioblastoma cells will too establish a tumor&lt;br /&gt;
in recipient mice with similar efficiencies compared&lt;br /&gt;
with cd133þ cells ( beier et al. , 2007 ) which cd133 is&lt;br /&gt;
highly expressed on nontransformed neural progenitor&lt;br /&gt;
cells ( lee et al. , 2005 ). in line with tumor heterogeneity,&lt;br /&gt;
the phenotype of cscs isn't uniform, even when they&lt;br /&gt;
originate due to same tumor subtype. this can be underlined&lt;br /&gt;
by studies using colorectal carcinoma as the&lt;br /&gt;
model system. we along with other people found that colorectal&lt;br /&gt;
cscs are enriched within the whole cd133þ sub-population&lt;br /&gt;
( o’brien et al. , 2007 ; ricci-vitiani et al. , 2007 ; todaro&lt;br /&gt;
et al. , 2007 ), whereas dalerba et al. ( 2007 ) reported an&lt;br /&gt;
enrichment of cscs within the whole epcamhi, cd44hi subpopulation&lt;br /&gt;
of colon cancer cells. the image is further&lt;br /&gt;
difficult by a recent study showing that colorectal&lt;br /&gt;
cscs are highly enriched within the whole aldh-positive cell&lt;br /&gt;
population. during this report, the tumorigenicity of aldhpositive&lt;br /&gt;
cells is just modestly increased using cd133&lt;br /&gt;
and cd44 expression being a second marker and get a more&lt;br /&gt;
stringent choice ( huang et al. , 2009 ). upon the other&lt;br /&gt;
hand, a mix of markers could be needed to&lt;br /&gt;
isolate a highly enriched breast csc population. breast&lt;br /&gt;
cscs are reported that should be enriched in each cd44þ cd24_/low&lt;br /&gt;
( al-hajj et al. , 2003 ) and aldh-positive subfractions.&lt;br /&gt;
though the overlap of one's 2 populations was surprisingly&lt;br /&gt;
low ( zero, 1–1. 2% ), cells displaying the combined&lt;br /&gt;
phenotype turned purpose is to be highly tumorigenic when&lt;br /&gt;
transplanted into your recipient mouse ( ginestier et al. , 2007 ).&lt;br /&gt;
the marked heterogeneity inside csc sub-populations&lt;br /&gt;
underlines the necessity to look for a lot of specific only markers,&lt;br /&gt;
or to firmly define new marker combinations for our prospective&lt;br /&gt;
isolation of cscs in solid tumors.&lt;br /&gt;
recently developed transgenic mouse models&lt;br /&gt;
provided a lot of hints relating to the potential identity of the&lt;br /&gt;
csc population in colon and lung cancer. targeted&lt;br /&gt;
oncogenic transformation of adult stem or progenitor&lt;br /&gt;
cells led in the formation of colon adenomas ( barker&lt;br /&gt;
et al. , 2009 ; zhu et al. , 2009 ) or lung adenocarcinomas&lt;br /&gt;
( acs ) ( kim et al. , 2005 ). though these results underline&lt;br /&gt;
the pivotal role of stem/progenitor cells in&lt;br /&gt;
carcinogenesis, the notion of ‘cancer stem cell’ will not  imply that tumorigenic cells essentially need to derive&lt;br /&gt;
from tissue stem cells. it is likewise probable that cscs develop&lt;br /&gt;
from a lot of restricted progenitor cells that receive&lt;br /&gt;
reprogramming ‘hits’, and thereby regain the stem cell&lt;br /&gt;
trait of unlimited self-renewal capability ( clarke et al. ,&lt;br /&gt;
2006 ). though there's substantial proof for csc&lt;br /&gt;
relevance in human carcinomas, several problems have to be compelled to be&lt;br /&gt;
thought of, as deeply discussed utilizing a recent review&lt;br /&gt;
( visvader and lindeman, 2008 ). initial of all, the best&lt;br /&gt;
practical in vivo assay for cscs is their ability to&lt;br /&gt;
recapitulate the patient tumor in animal models.&lt;br /&gt;
but, animal models don't entirely mimic the&lt;br /&gt;
human tumor microenvironment and poorly tumorigenic&lt;br /&gt;
cscs can be inadvertently selected during&lt;br /&gt;
xenotransplantation. besides the problem of species specificity,&lt;br /&gt;
tissue specificity conjointly has as being thought of for&lt;br /&gt;
in vivo transplantation of cscs. so, orthotopic&lt;br /&gt;
tumors might higher reproduce the csc niche, especially&lt;br /&gt;
in the event the human microenvironment is mimicked by the&lt;br /&gt;
use of humanized supports or patient-derived accessory&lt;br /&gt;
cells, like fibroblasts or mesenchymal stem cells&lt;br /&gt;
( kuperwasser et al. , 2004 ). the impact as to the microenvironment&lt;br /&gt;
on tumor growth is underlined via the fact&lt;br /&gt;
that subcutaneous implantation of cscs results in less&lt;br /&gt;
efficient engraftment than brain or renal capsule injection&lt;br /&gt;
for gliomas or colorectal cscs, respectively. finally, the&lt;br /&gt;
presence of residual immune effector cells in recipient&lt;br /&gt;
mice may additionally influence the efficiency of human cell&lt;br /&gt;
engraftment in nod/scid mice, whereas nod/scidil2rgnull&lt;br /&gt;
mice, recently introduced for csc transplantation,&lt;br /&gt;
represent a a lot of permissive environment ( shultz&lt;br /&gt;
et al. , 2005 ). by the alternative hand, it is likewise true that&lt;br /&gt;
immune cells utilize a role within the progression of human&lt;br /&gt;
tumors. these limitations of mouse models really should be kept&lt;br /&gt;
on your mind when csc behavior, frequency in tumors, growth&lt;br /&gt;
requirements or any other properties linked out to niche interaction&lt;br /&gt;
are investigated. moreover, till currently, no complete&lt;br /&gt;
agreement relating to csc frequency or phenotype has&lt;br /&gt;
been reached. but, though a few controversies&lt;br /&gt;
concerning cscs in solid tumors are raised, their&lt;br /&gt;
biological relevance and also the immense therapeutic potential&lt;br /&gt;
of the targeting generally are not seriously questioned ( hill,&lt;br /&gt;
2006 ; visvader and lindeman, 2008 ; zhou et al. , 2009 ).&lt;br /&gt;
lung cancer&lt;br /&gt;
lung cancer is that the most common cause of cancer-related&lt;br /&gt;
mortality worldwide, with 160 000 deaths in the&lt;br /&gt;
u. s. in 2008 but a poor 5-year survival rate,&lt;br /&gt;
that remains stable at 15% ( jemal et al. , 2008 ). it has&lt;br /&gt;
been estimated that 9 from 10 lung cancer cases are&lt;br /&gt;
directly caused by smoking. alternative risk factors for lung&lt;br /&gt;
cancer are exposure out to asbestos and, to the lesser extent,&lt;br /&gt;
out to radon, arsenic, chromium, nickel, vinyl chloride and&lt;br /&gt;
ionizing radiation or a few preexisting nonmalignant&lt;br /&gt;
lung diseases ( dubey and powell, 2009 ). different&lt;br /&gt;
known or unknown etiologies may account for the&lt;br /&gt;
occurrence of totally different kinds of lung cancer, the&lt;br /&gt;
heterogeneity of that has vital diagnostic, prognostic&lt;br /&gt;
and therapeutic implications ( borczuk et al. , 2009 ).&lt;br /&gt;
out to facilitate treatment and prognostic choices, lung&lt;br /&gt;
cancer is categorized into little cell lung&lt;br /&gt;
carcinoma ( sclc ) and non-sclc ( nsclc ). nsclc&lt;br /&gt;
might well be any distinguished into 3 major histological&lt;br /&gt;
categories : ac, squamous cell carcinoma and enormous cell&lt;br /&gt;
carcinoma ( collins et al. , 2007 ). sclc accounts for&lt;br /&gt;
b20% as to the pulmonary tumors. despite a generally&lt;br /&gt;
sensible initial response out to chemotherapy, it really has a&lt;br /&gt;
notably poor prognosis, owing to early extra&lt;br /&gt;
thoracic dissemination and frequent disease relapse.&lt;br /&gt;
sclc predominately localizes out to midlevel bronchioles&lt;br /&gt;
and displays neuroendocrine differentiation, suggesting&lt;br /&gt;
that transformed pulmonary neuroendocrine cells might&lt;br /&gt;
offer rise out to this way of lung cancer ( giangreco et al. ,&lt;br /&gt;
2007 ). with b40% prevalence, adenocarcinoma ( ac ) is&lt;br /&gt;
possibly the most common kind of nsclc in each smokers and&lt;br /&gt;
nonsmokers. it develops mostly direct from junction&lt;br /&gt;
amongst the terminal bronchiole and also the alveolus,&lt;br /&gt;
termed ‘bronchoalveolar duct junction’, and displays&lt;br /&gt;
either airway or alveolar differentiation, or both&lt;br /&gt;
( giangreco et al. , 2007 ). squamous cell carcinoma has&lt;br /&gt;
a 25% prevalence rate and is highly associated with&lt;br /&gt;
tobacco smoking. it arises within the proximal airways down&lt;br /&gt;
out to the second or third bifurcation and is never observed&lt;br /&gt;
distally. compared with alternative kinds of nsclcs, large&lt;br /&gt;
cell carcinoma ( 10% prevalence ) comprises a category of&lt;br /&gt;
rather poorly differentiated and fewer aggressive tumors,&lt;br /&gt;
possibly the most frequent subtype of which is certainly giant cell&lt;br /&gt;
neuroendocrine carcinoma ( giangreco et al. , 2007 ).&lt;br /&gt;
analysis as to the genetic alterations occurring in lung&lt;br /&gt;
cancer has shown that histopathological differences are&lt;br /&gt;
in line with genetic heterogeneity as to the disease ( minna&lt;br /&gt;
et al. , 2002 ; sekido et al. , 2003 ). further genetic&lt;br /&gt;
differences are found among the 3 main&lt;br /&gt;
kinds of nsclcs ( minna et al. , 2002 ; sekido et al. ,&lt;br /&gt;
2003 ). consistent along with the genetic heterogeneity,&lt;br /&gt;
expression studies haven't no more than unveiled profound&lt;br /&gt;
differences between sclc and nsclc but as well as within&lt;br /&gt;
totally different nsclc subtypes ( bianchi et al. , 2008 ).&lt;br /&gt;
but, till recently, all nsclc lung cancer forms&lt;br /&gt;
are treated with similar approaches regardless of&lt;br /&gt;
their biological differences ( minna et al. , 2002 ; collins&lt;br /&gt;
et al. , 2007 ; dubey and powell, 2008 ; tiseo et al. , 2009 ).&lt;br /&gt;
therefore, it's probable that the poor lung cancer response rates&lt;br /&gt;
can be due, a minimum of partly, to the too homogeneous&lt;br /&gt;
treatment approach applied to yesteryear obtain a highly heterogeneous&lt;br /&gt;
disease ( borczuk et al. , 2009 ). no more than recently,&lt;br /&gt;
lung cancer heterogeneity has started out to gain therapeutic&lt;br /&gt;
relevance, as documented via the try out to propose&lt;br /&gt;
preferential chemotherapeutic choices for every tumor&lt;br /&gt;
histotype ( tiseo et al. , 2009 ) ( scagliotti et al. , 2009 ).&lt;br /&gt;
besides histology-based approaches, ongoing efforts are&lt;br /&gt;
underway out to establish clinically relevant biological  properties of lung tumors which can facilitate individualized&lt;br /&gt;
therapy. during this direction, completely different expression&lt;br /&gt;
profiles have conjointly been found inside a similar tumor&lt;br /&gt;
subtype, and could well be correlated with patient survival&lt;br /&gt;
( bhattacharjee et al., 2001 ). to firmly define a lot of personalized&lt;br /&gt;
therapies, each genetic and proteomic signatures of&lt;br /&gt;
completely different lung tumor subtypes be required to be determined&lt;br /&gt;
and correlated with tumor histotype, clinical outcome&lt;br /&gt;
and treatment response. by way of example, it must been found&lt;br /&gt;
that, inside acs, kras mutations are a lot of common&lt;br /&gt;
in tumors from patients with tobacco exposure and are&lt;br /&gt;
related to worse prognosis and primary resistance&lt;br /&gt;
to firmly treatment. in distinction, tumors from nonsmokers are&lt;br /&gt;
a lot of frequently related to molecular alterations&lt;br /&gt;
involving the epidermal growth issue receptor and with&lt;br /&gt;
longer overall survival ( pao et al., 2004 ; janne et al.,&lt;br /&gt;
2005 ; riely et al., 2009 ). coming from the therapeutic point&lt;br /&gt;
of read, patients with epidermal growth issue receptor&lt;br /&gt;
mutations show increased sensitivity to firmly epidermal&lt;br /&gt;
growth issue receptor inhibitors, whereas krasbearing&lt;br /&gt;
tumors are resistant ( pao et al., 2005 ). so,&lt;br /&gt;
epidermal growth issue receptor and kras&lt;br /&gt;
mutations define 2 distinct populations of nsclc&lt;br /&gt;
patients with completely different natural histories and responses to&lt;br /&gt;
targeted therapy ( bianchi et al., 2008 ; lantuejoul et al.,&lt;br /&gt;
2009 ; riely et al., 2009 ). these evidences strongly suggest&lt;br /&gt;
that a deep knowledge just about every one of them patient tumor will predict&lt;br /&gt;
treatment response to enhance patient outcome, calling&lt;br /&gt;
to produce a robust effort toward customized therapy. in the&lt;br /&gt;
try to enhance lung cancer patient outcome, csc&lt;br /&gt;
analysis would possibly utilize a central role not solely within the whole search&lt;br /&gt;
for new anticancer medicine but additionally within the whole diagnosis and&lt;br /&gt;
monitoring of one's therapeutic success as discussed later.&lt;br /&gt;
but, the relative low frequency of cscs in tumors&lt;br /&gt;
might complicate their investigation. by way of example, the&lt;br /&gt;
current methodology for molecular profiling of tumors&lt;br /&gt;
won't analyze cell sub-populations and may even provide&lt;br /&gt;
misleading results as a result of the signal connected to firmly csc gene&lt;br /&gt;
expression is extremely diluted.&lt;br /&gt;
adult progenitor cells of one's lung&lt;br /&gt;
cscs share variety of features with normal tissue&lt;br /&gt;
stem or progenitor cells, regardless of whether or not they&lt;br /&gt;
originate directly from stem cells gaining tumorigenic&lt;br /&gt;
hits or by reprogramming of a lot of differentiated cells. in&lt;br /&gt;
adult organisms, tissue homeostasis is maintained by&lt;br /&gt;
stem and progenitor cells which may have the ability to firmly divide&lt;br /&gt;
throughout life and replace dying or damaged cells.&lt;br /&gt;
stem cell populations are well characterized&lt;br /&gt;
in many organs by having high rate of homeostatic&lt;br /&gt;
proliferation, inclusive of the hematopoietic system, skin,&lt;br /&gt;
gut and hair follicle ( blau et al., 2001 ; barker et al.,&lt;br /&gt;
2008 ; fuchs, 2009 ). a classical model associated with a ‘stem cell&lt;br /&gt;
hierarchy’ is well established regarding the maintenance of the&lt;br /&gt;
hematopoietic system ( orkin and zon, 2002 ; iwasaki&lt;br /&gt;
and akashi, 2007 ) and of course the little intestine ( barker et al.,&lt;br /&gt;
2008 ; fuchs, 2009 ).&lt;br /&gt;
in organs with slow turnover rates, inclusive of the lung,&lt;br /&gt;
liver and pancreas, the terminology developed to firmly define&lt;br /&gt;
the ‘hierarchical stem cell’ model of rapid renewing&lt;br /&gt;
tissues has that should be refined. cellular turnover in the&lt;br /&gt;
adult lung tissue is incredibly slow when compared with the&lt;br /&gt;
little intestine ( blenkinsopp, 1967 ; barker et al., 2008 ;&lt;br /&gt;
rawlins, 2008 ), and just extreme conditions such as&lt;br /&gt;
pollutant- or pathogen-induced injuries spur a massive&lt;br /&gt;
lung cell proliferation. throughout organ regeneration, lung&lt;br /&gt;
cells that sometimes fulfil differentiated functions in the&lt;br /&gt;
normal tissue actively begin to firmly proliferate and act as&lt;br /&gt;
progenitor cells that may provide rise to firmly many cell types&lt;br /&gt;
( stripp and reynolds, 2008 ). utilizing a well known lung injury&lt;br /&gt;
model, mice are treated with naphthalene, that leads&lt;br /&gt;
in the ablation of clara cells ( mahvi et al., 1977 ).&lt;br /&gt;
cell proliferation starts 48–72 h once injury and the&lt;br /&gt;
epithelium is fully regenerated once 2–4 weeks&lt;br /&gt;
( stripp et al., 1995 ; van winkle et al., 1995 ). the&lt;br /&gt;
mechanism of how the clara cell population is regenerated&lt;br /&gt;
depends inside the region of one's lung ( see figure 1 ).&lt;br /&gt;
within the whole trachea and bronchi, cytokeratin 14-positive cells&lt;br /&gt;
are most most likely basal cells that may behave as self-renewing&lt;br /&gt;
progenitors and provides rise to firmly clara-like and ciliated cells&lt;br /&gt;
( hong et al., 2004a, b ). within the whole a lot of distal regions of the&lt;br /&gt;
lung, naphthalene-resistant clara cells begin to firmly proliferate&lt;br /&gt;
and regenerate the damaged tissue. these rare ‘variant’&lt;br /&gt;
clara cells ( clarav ), accumulate in specialized stem cell&lt;br /&gt;
niches shut in the neuroendocrine bodies and at the&lt;br /&gt;
bronchoalveolar duct junctions ( reynolds et al., 2000 ;&lt;br /&gt;
giangreco et al., 2002 ). upon injury, a subset of clarav&lt;br /&gt;
cells found within the whole bronchoalveolar duct junctions show a&lt;br /&gt;
characteristic expression pattern comprising each clara and&lt;br /&gt;
alveolar cell proteins ( ccsp and sp-c ) in combination&lt;br /&gt;
with cd34 and sca-1, 2 common stem cell markers.&lt;br /&gt;
these cells were named bronchoalveolar stem cells&lt;br /&gt;
( bascs ), as they actually utilize a substantial clonogenic survival&lt;br /&gt;
capability, are ready to self-renew and could provide rise to firmly clara&lt;br /&gt;
and alveolar cells in vitro ( kim et al., 2005 ). during this report,&lt;br /&gt;
we can refer to firmly ccsp/sp-c positive cells as bascs,&lt;br /&gt;
though the ability of such cells to firmly self-renew and give&lt;br /&gt;
rise to firmly completely different lineages in vivo has not been formally&lt;br /&gt;
proven, and recent cell-tracing experiments have suggested&lt;br /&gt;
that bascs contribute in the maintenance and&lt;br /&gt;
repair of one's proximal airways, however not of one's alveolar&lt;br /&gt;
epithelium ( giangreco et al., 2009 ; rawlins et al., 2009 ).&lt;br /&gt;
but, albeit their exact purpose in maintenance&lt;br /&gt;
and repair of one's lung isn't properly understood&lt;br /&gt;
however, there's growing proof that adenomas and acs&lt;br /&gt;
arise from transformed bascs, at the very least in mouse models.&lt;br /&gt;
potential lung cancer-initiating cells within the whole mouse&lt;br /&gt;
though the identity of tissue stem cells within the whole lung is&lt;br /&gt;
controversial, bascs drive the tumorigenic method in&lt;br /&gt;
many mouse models of lung acs. as described&lt;br /&gt;
before, kras is mutated utilizing a substantial number&lt;br /&gt;
of nsclcs. so, transgenic mice expressing&lt;br /&gt;
oncogenic variants of kras ( inclusive of kras( g12d ) )  represent necessary animal models for lung&lt;br /&gt;
cancer, particularly acs. many lines of proof point&lt;br /&gt;
toward the importance of bascs regarding the induction of&lt;br /&gt;
kras( g12d )-induced acs : ( 1 ) it was actually shown that the&lt;br /&gt;
variety of bascs was expanded in ac precursors of&lt;br /&gt;
mice expressing an inducible style of kras( g12d )&lt;br /&gt;
( jackson et al., 2001 ; kim et al., 2005 ). ( 2 ) isolated&lt;br /&gt;
transgenic bascs displayed enhanced in vitro proliferation&lt;br /&gt;
capability when compared with a lot of differentiated&lt;br /&gt;
cells of the very same tissue. ( 3 ) whenever the variety of bascs&lt;br /&gt;
were elevated by naphthalene injury until that induction&lt;br /&gt;
of one's transgene, tumor growth was strongly&lt;br /&gt;
enhanced compared with management animals ( jackson&lt;br /&gt;
et al., 2001 ; kim et al., 2005 ). such results counsel that&lt;br /&gt;
these progenitor cells utilize a key role within the onset of&lt;br /&gt;
kras-induced lung cancer. in line basic experiments,&lt;br /&gt;
it was actually shown that inducible p38 knockout mice&lt;br /&gt;
were a lot of susceptible to firmly kras-induced formation of&lt;br /&gt;
acs. p38 supports the differentiation and suppresses the&lt;br /&gt;
proliferation of bascs, that accumulated within the lungs&lt;br /&gt;
of p38-deficient mice even while not the ectopic expression&lt;br /&gt;
of mutated kras ( ventura et al., 2007 ). this&lt;br /&gt;
accumulation may justify the higher susceptibility of&lt;br /&gt;
kras-transgenic/p38-deficient mice for lung acs when&lt;br /&gt;
compared with p38-proficient mice. bascs conjointly have&lt;br /&gt;
a very important role in alternative tumor model systems.&lt;br /&gt;
for instance, mice knocked in for the oncogenic form&lt;br /&gt;
of p27kip ( p27ck_ ) displayed a high incidence of&lt;br /&gt;
spontaneous hyperplastic lesions in many tissues,&lt;br /&gt;
as well as the retina, pituitary gland, ovary, adrenal&lt;br /&gt;
gland, spleen and lung. when compared with wild-type&lt;br /&gt;
mice, these mice had an abnormal high variety of&lt;br /&gt;
bascs in terminal bronchioles and eventually developed&lt;br /&gt;
ac ( besson et al., 2007 ). moreover, utilizing a mouse&lt;br /&gt;
model within which pten ( phosphatase and tensin homolog )&lt;br /&gt;
might well be deleted in sp-c-expressing cells, the number&lt;br /&gt;
of bascs and sp cells was considerably increased.&lt;br /&gt;
nearly all mice in whom pten was deleted spontaneously&lt;br /&gt;
developed lung cancer and, strikingly, like in&lt;br /&gt;
the human system, kras was mutated in 30% of acs&lt;br /&gt;
( yanagi et al., 2007 ). in summary, these reports suggest&lt;br /&gt;
a very important role for bascs in the first steps of lung&lt;br /&gt;
tumorigenesis. there could be a similar behavior between&lt;br /&gt;
normal lung stem cells in injured tissues and transformed&lt;br /&gt;
bascs in tumors. once lung injury, normal&lt;br /&gt;
lung stem cells survive and proliferate whereas giving&lt;br /&gt;
rise to firmly specialized cells that repair the damaged tissues.&lt;br /&gt;
this method is induced by external stimuli other then strictly&lt;br /&gt;
regulated inside the stem cell niche, that guarantees&lt;br /&gt;
that stem cell expansion occurs provided that needed.&lt;br /&gt;
in distinction, the expansion of transformed cscs during&lt;br /&gt;
lung tumorigenesis seems rather unrestrained, and&lt;br /&gt;
poorly regulated by signals coming due to niche.&lt;br /&gt;
in spite of this, it still has to firmly be proven whether or not transformed&lt;br /&gt;
basc-like cells conjointly fulfill all criteria to becoming cscs, as&lt;br /&gt;
there's hardly any proof of the sub-population in the basc&lt;br /&gt;
phenotype able to firmly establish a histophenocopy of the&lt;br /&gt;
initial tumor in secondary and tertiary hosts.&lt;br /&gt;
human lung cscs&lt;br /&gt;
following the growing enthusiasm regarding the csc model in&lt;br /&gt;
solid tumors and therefore the new insights straight into the biology of&lt;br /&gt;
normal cells and cscs within the mouse airway, research&lt;br /&gt;
interest has recently started to firmly rise for stem cells in&lt;br /&gt;
human lung cancer. tumorigenic human lung cancer&lt;br /&gt;
cells are isolated using completely different approaches&lt;br /&gt;
from each cell lines and primary tumors ( see table 1 ).&lt;br /&gt;
the very first few approach was primarily based upon the sp phenotype&lt;br /&gt;
( low hoechst 33342 staining pattern ) of stem cells. sp&lt;br /&gt;
lung cancer cells isolated from h460, h23, htb-58,&lt;br /&gt;
a549, h441 and h2170 cell lines, displayed increased&lt;br /&gt;
invasiveness, higher resistance to firmly chemotherapeutic&lt;br /&gt;
medicine and were a lot of tumorigenic in vivo when&lt;br /&gt;
compared with non-sp cells ( ho et al., 2007 ). on the&lt;br /&gt;
basis of one's widely accepted hypothesis that cscs of&lt;br /&gt;
completely different origins are endowed with increased drug&lt;br /&gt;
resistance, the second approach used to firmly enrich human&lt;br /&gt;
lung cscs from cell lines was primarily based onto their inherent&lt;br /&gt;
resistance to firmly cisplatin, doxorubicin or etoposide&lt;br /&gt;
treatment. drug-surviving cells exhibited many csc&lt;br /&gt;
features, an example would be high clonogenic capability, enrichment in&lt;br /&gt;
sp cells, expression of embryonic stem cell markers,&lt;br /&gt;
capability for self-renewal and generation of differentiated&lt;br /&gt;
progeny and high tumorigenicity ( levina et al.,&lt;br /&gt;
2008 ). the third approach leading to firmly the isolation of&lt;br /&gt;
lung cscs was primarily based on increased aldh activity&lt;br /&gt;
previously shown in stem cell populations of several&lt;br /&gt;
human cancers. aldh-positive cells isolated from lung&lt;br /&gt;
cancer cell lines displayed features of cscs each in vitro&lt;br /&gt;
( invasive properties, expression of stem cell markers )&lt;br /&gt;
and in vivo ( ability to firmly generate tumors ) ( jiang et al.,&lt;br /&gt;
2009 ). the very first few isolation and expansion of lung cscs&lt;br /&gt;
from primary patient tumors was reported by our group&lt;br /&gt;
( eramo et al., 2008 ). in your study, human lung cscs&lt;br /&gt;
were isolated upon the basis with the ability to firmly survive&lt;br /&gt;
underneath serum-free conditions and proliferate as cellular&lt;br /&gt;
clusters referred to as ‘tumor spheres’. this experimental&lt;br /&gt;
strategy represents one of the best approach to this point to firmly obtain the&lt;br /&gt;
unlimited expansion of one's tumorigenic lung cancer&lt;br /&gt;
cell population from primary patients, providing a&lt;br /&gt;
powerful tool to firmly permit in depth studies on these&lt;br /&gt;
cells. owing to firmly the low frequency of lung cscs within&lt;br /&gt;
primary tumor tissues, in depth investigation on these&lt;br /&gt;
cells wouldn't be potential within the absence with the in vitro&lt;br /&gt;
expansion. upon the basis in our approach, high numbers&lt;br /&gt;
of lung cscs can be generated and extensively&lt;br /&gt;
characterised. spheres due to major subtypes of lung&lt;br /&gt;
cancer ( an example would be sclc, ac, squamous cell carcinoma&lt;br /&gt;
and huge cell carcinoma ) were found to firmly possess csc&lt;br /&gt;
properties, each in vitro ( expression of one's csc marker&lt;br /&gt;
cd133, unlimited proliferative potential, extended selfrenewal  and differentiation ability ) and in vivo ( high&lt;br /&gt;
tumorigenic potential, capability to firmly recapitulate tumor&lt;br /&gt;
heterogeneity and mimic the histology as to the specific&lt;br /&gt;
tumor subtype from that cscs were derived ). in&lt;br /&gt;
addition, lung cancer ‘spheres’ were extremely resistant&lt;br /&gt;
to firmly most typical medication presently utilized treat lung&lt;br /&gt;
cancer patients, calling for your intense effort in testing&lt;br /&gt;
each typical and innovative medication by the tumorigenic&lt;br /&gt;
lung cancer cell population. this tumor cell&lt;br /&gt;
population was too characterised by your expression of&lt;br /&gt;
embryonic genes, an example would be oct-4 and nanog, thus&lt;br /&gt;
confirming the undifferentiated phenotype of isolated&lt;br /&gt;
cancer cells. oct-4 expression was too recently reported&lt;br /&gt;
to firmly characterize cd133-positive tumor cells in freshly&lt;br /&gt;
isolated tumors, and also to be essential in maintaining the&lt;br /&gt;
stem-like properties of isolated cells, an example would be invasion&lt;br /&gt;
and self-renewal ( chen et al. , 2008 ). recently, the&lt;br /&gt;
relevance of cd133-positive cells in tumorigenicity&lt;br /&gt;
and chemoresistance of lung cancer has also been further&lt;br /&gt;
confirmed ( bertolini et al. , 2009 ). cd133þ cells isolated&lt;br /&gt;
from primary tumors displayed increased tumorigenicity&lt;br /&gt;
and expression of stemness, adhesion, motility and drug&lt;br /&gt;
efflux genes in comparison in the corresponding&lt;br /&gt;
cd133_ tumor cells. additionally, cd133þ cells survived&lt;br /&gt;
cisplatin treatment when in vitro drug exposure of the&lt;br /&gt;
a549 cell line as well as primary tumor-derived mouse&lt;br /&gt;
xenograft when cisplatin administration. importantly,&lt;br /&gt;
the expression of cd133 in tumors was linked to firmly shorter&lt;br /&gt;
progression-free survival of nsclc patients treated&lt;br /&gt;
with platinum-based regimens, so providing the first&lt;br /&gt;
proof as to the relevance of cd133þ tumor-initiating&lt;br /&gt;
cells for prediction of chemoresponse and prognosis of&lt;br /&gt;
lung cancer patients. though these and alternative encouraging&lt;br /&gt;
results are commencing to clarify totally different aspects of&lt;br /&gt;
lung cscs, additional investigation will still be needed to&lt;br /&gt;
obtain a deep elucidation by the biology of these&lt;br /&gt;
vital cells.&lt;br /&gt;
cscs and the potential implications regarding the development&lt;br /&gt;
of innovative cancer treatments&lt;br /&gt;
advances in csc analysis may facilitate to firmly establish&lt;br /&gt;
successful therapies against leukemia and solid tumors.&lt;br /&gt;
typical antineoplastic agents utilized fight cancer&lt;br /&gt;
mainly hit the malignant cells by 2 totally different mechanisms.&lt;br /&gt;
one category of typical chemotherapeutic drugs&lt;br /&gt;
induces dna injury, whereas the second drug impairs&lt;br /&gt;
mitosis or dna replication. unfortunately, this therapeutic&lt;br /&gt;
combination are only able to prolong the patient’s&lt;br /&gt;
survival for a couple of months. one reason to get this poor&lt;br /&gt;
medical outcome can be the presence of drug- and&lt;br /&gt;
radiation-resistant cscs. there may be many indications&lt;br /&gt;
regarding the higher resistance of cscs to firmly conventional&lt;br /&gt;
chemotherapy or radiotherapy in vivo. in tumor biopsies&lt;br /&gt;
from breast cancer patients treated with conventional&lt;br /&gt;
chemotherapy, a better frequency of potential cscs&lt;br /&gt;
( cd24low/cd44þ ) was detected when compared with&lt;br /&gt;
pretreatment biopsies ( yu et al. , 2007 ; li et al. , 2008 ;&lt;br /&gt;
creighton et al. , 2009 ). similar results were obtained in&lt;br /&gt;
mouse xenograft models of glioblastoma and colorectal&lt;br /&gt;
cancer ( bao et al. , 2006 ; dylla et al. , 2008 ). we&lt;br /&gt;
previously reported that lung cscs isolated from&lt;br /&gt;
primary tumors too show high resistance to firmly standard&lt;br /&gt;
chemotherapy in vitro ( eramo et al. , 2008 ), suggesting&lt;br /&gt;
that these cells exhibit highly efficient intrinsic resistance&lt;br /&gt;
mechanisms. moreover, lung cancer mouse xenografts&lt;br /&gt;
treated with cisplatin regimens in vivo showed enrichment&lt;br /&gt;
of specific sub-populations with stem cell phenotype&lt;br /&gt;
( cd133þ/abcg2þ/cxcr4þ ) ( bertolini et al. ,&lt;br /&gt;
2009 ).&lt;br /&gt;
the combinations of slow cell-cycle progression and&lt;br /&gt;
efficient dna repair machinery are potential resistance&lt;br /&gt;
mechanisms of cscs. in distinction towards the majority of&lt;br /&gt;
tumor progenitors and precursors, cscs showed increased&lt;br /&gt;
quiescence in vivo and in vitro, suggesting poor&lt;br /&gt;
responses to firmly typical treatments, that primarily&lt;br /&gt;
kill proliferating cells ( holyoake et al. , 1999 ; guan&lt;br /&gt;
et al. , 2003 ; ishikawa et al. , 2007 ; cicalese et al. , 2009 ).&lt;br /&gt;
additionally, it really has been reported that glioblastoma stem&lt;br /&gt;
cells exhibit active dna repair mechanisms, which&lt;br /&gt;
permit them to be able to recognize and repair radiation-induced&lt;br /&gt;
dna injury efficiently ( bao et al. , 2006 ). the accumulating&lt;br /&gt;
proof that the csc sub-population of tumor&lt;br /&gt;
cells is resistant to firmly typical anticancer therapy can&lt;br /&gt;
make a case for the frequent relapse when a very good initial response&lt;br /&gt;
to firmly chemotherapy was observed in patients ( see figure 2 ).&lt;br /&gt;
to get this reason, innovative therapeutic approaches&lt;br /&gt;
to firmly kill or disarm cscs can be the secret for cure solid&lt;br /&gt;
cancers. targeted treatment of cscs is an ambitious&lt;br /&gt;
approach, as these most most likely represent a heterogeneous&lt;br /&gt;
population of cells with totally different sensitivities&lt;br /&gt;
to firmly chemotherapeutic medication that need to be combined&lt;br /&gt;
to obtain full antitumor effects. in distinction to firmly the&lt;br /&gt;
induction of apoptosis within the majority of tumor cells&lt;br /&gt;
observed with typical chemotherapeutic agents,&lt;br /&gt;
targeted elimination of cscs may spur slow but&lt;br /&gt;
sustainable tumor eradication. this implicates that most&lt;br /&gt;
preclinical xenograft models utilized check the efficacy&lt;br /&gt;
of chemical compounds or biomolecules need to be&lt;br /&gt;
modified. these adjustments embrace not solely longer&lt;br /&gt;
observation periods but as well as a faithful analysis of&lt;br /&gt;
treated tumors for cells expressing potential csc&lt;br /&gt;
markers at intermediate finish points. monitoring druginduced&lt;br /&gt;
alterations within the csc compartment may be&lt;br /&gt;
a useful indicator for general anticancer efficacy of the&lt;br /&gt;
compound. as cscs share many resistance mechanisms&lt;br /&gt;
with normal tissue stem cells, there may be a high risk to firmly hit&lt;br /&gt;
normal stem cells by a targeted anti-csc therapy with&lt;br /&gt;
disastrous consequences regarding the patient. thus, it is&lt;br /&gt;
vital to firmly style new therapeutic approaches to&lt;br /&gt;
selectively hit csc-specific pathways, whereas sparing&lt;br /&gt;
normal stem cells. up to now, variety of preclinical studies&lt;br /&gt;
are performed using totally different strategies to firmly target  cscs. these embody the specific elimination of cscs&lt;br /&gt;
with selective targeting ( schatton et al. , 2009 ) or&lt;br /&gt;
sensitization of cscs out to typical chemotherapy&lt;br /&gt;
and differentiation therapies. in a few of those innovative&lt;br /&gt;
therapeutic approaches, antibodies were designed to neutralize&lt;br /&gt;
autocrine signaling mediators vital for csc&lt;br /&gt;
growth and chemoresistance, an example would be cd123 ( interleukin-&lt;br /&gt;
3 receptor ) in acute myeloid leukemia ( jin et al. , 2009 )&lt;br /&gt;
and interleukin-4 in colorectal cancer ( todaro et al. ,&lt;br /&gt;
2007, 2008 ). alternative antibodies interfere in the communication&lt;br /&gt;
of cscs with noncancerous tissue, and thereby&lt;br /&gt;
forestall csc localization with their niche ( jin et al. , 2006 ;&lt;br /&gt;
yang et al. , 2008 ). similarly, inhibitors blocking cxcr4&lt;br /&gt;
impair the interaction of acute myeloid leukemia stem&lt;br /&gt;
cells in the microenvironment within the whole bone marrow,&lt;br /&gt;
by having consequent sensitization out to targeted therapy ( zeng&lt;br /&gt;
et al. , 2009 ). because we are part of a glioblastoma model, it was eventually shown that&lt;br /&gt;
endothelial cells promote the propagation of glioblastoma&lt;br /&gt;
stem cells. subsequently, antiangiogenic therapy using&lt;br /&gt;
vascular endothelial growth issue inhibitors depleted&lt;br /&gt;
not no more than tumor vascularization but as well as ablated cscs in&lt;br /&gt;
the xenograft ( calabrese et al. , 2007 ).&lt;br /&gt;
another approach for innovative therapy is the&lt;br /&gt;
targeted inhibition of vital signal transduction&lt;br /&gt;
pathways and transcription factors highly active in&lt;br /&gt;
cscs, together with embryonic pathways. pharmacological&lt;br /&gt;
inhibition on your hedgehog pathway reduced the growth&lt;br /&gt;
of lung tumor cells in xenograft models, suggesting an&lt;br /&gt;
vital role with this pathway in lung cscs also&lt;br /&gt;
( watkins et al. , 2003 ). a recent study showed that knock&lt;br /&gt;
down on your transcription issue oct-4 led out to apoptosis&lt;br /&gt;
associated with a csc-like population of lung cancer cells ( hu et al. ,&lt;br /&gt;
2008 ). this finding is of explicit interest as oct-4 is&lt;br /&gt;
expressed in potential human lung progenitor cells&lt;br /&gt;
that show a few characteristics of murine bascs&lt;br /&gt;
( ling et al. , 2006 ; chen et al. , 2007 ).&lt;br /&gt;
cscs will divide asymmetrically and provides rise out to more&lt;br /&gt;
differentiated progeny that lose the ability out to divide&lt;br /&gt;
indefinitely. differentiation therapy aims at converting&lt;br /&gt;
tumorigenic cscs with their nontumorigenic progeny. it&lt;br /&gt;
was shown that treatment with bone morphogenic&lt;br /&gt;
protein 4 reduced the tumor-initiating cell pool in a&lt;br /&gt;
glioma model and markedly slowed down tumor growth&lt;br /&gt;
in vivo while not toxic aspect effects ( piccirillo et al. , 2006 ).&lt;br /&gt;
finally, cscs represent a very good model system out to test&lt;br /&gt;
new medication for antitumor treatments. in spite of this, until&lt;br /&gt;
recently, many technical difficulties restricted the use of&lt;br /&gt;
cscs for high throughput screenings of chemical&lt;br /&gt;
compounds. the largest problem is perhaps the rarity&lt;br /&gt;
of cscs. thus, it's nearly not possible out to use sorted&lt;br /&gt;
cscs from primary human tumors for large-scale&lt;br /&gt;
experiments. out to overcome these technical limitations,&lt;br /&gt;
one potential resolution is that the generation of ‘induced’ cscs.&lt;br /&gt;
gupta et al. ( 2009 ) demonstrated that immortalized&lt;br /&gt;
human mammary epithelial cells underwent epithelial–&lt;br /&gt;
mesenchymal transition, acquired tumorigenicity, gained&lt;br /&gt;
the ability out to grow as mammospheres and acquired the&lt;br /&gt;
expression of csc marker proteins in the event the expression of&lt;br /&gt;
e-cadherin was knocked down with short hairpin rna.&lt;br /&gt;
these cells were used for high-content screenings and&lt;br /&gt;
identified compounds selectively abolishing the cd44þ/&lt;br /&gt;
cd24low cell population in vitro, leading to some marked&lt;br /&gt;
reduction in tumorigenicity of pretreated cell lines in vivo.&lt;br /&gt;
alternative experimental strategies will overcome the need&lt;br /&gt;
out to genetically modify cells to get sufficient numbers&lt;br /&gt;
of csc-like cells for in vitro assays. for a few tumors,&lt;br /&gt;
it's attainable out to propagate primary cancer cells in&lt;br /&gt;
spheroid cultures ( reynolds and weiss, 1992 ), which&lt;br /&gt;
might enable intensive csc characterization in vitro. these&lt;br /&gt;
cultures contain defined growth factors supporting the&lt;br /&gt;
proliferation of undifferentiated stem-like cells endowed&lt;br /&gt;
with high clonogenic capability and therefore the ability out to generate&lt;br /&gt;
tumor xenografts recapitulating the initial tumor ( singh&lt;br /&gt;
et al. , 2004 ; ricci-vitiani et al. , 2007, todaro et al. ,&lt;br /&gt;
2007 ). recently, pollard et al. described a cultivation&lt;br /&gt;
technique for primary glioblastoma cells using laminincoated&lt;br /&gt;
flasks and an analogous medium used for spheroid&lt;br /&gt;
cultures. below these conditions, the cells adhere but&lt;br /&gt;
maintain a csc-like character ( pollard et al. , 2009 ).&lt;br /&gt;
in spite of this, these approaches conjointly harbor variety of&lt;br /&gt;
technical difficulties. at present, csc spheres from&lt;br /&gt;
epithelial tumors are problematic to establish, significantly in&lt;br /&gt;
the case of lung cancer. therefore, the use of csc spheroids&lt;br /&gt;
from primary tumors can be restricted to some few specialized&lt;br /&gt;
laboratories. another potential limitation is the idea that an&lt;br /&gt;
average of 15–20% of cells in tumor spheres are cscs&lt;br /&gt;
( eramo et al. , 2008 ). as elegantly shown in mouse breast&lt;br /&gt;
cancer, the speed of symmetric divisions depends on the&lt;br /&gt;
genomic alterations present in tumors. therefore, though a&lt;br /&gt;
normal sphere might contain as low collectively stem cell, the&lt;br /&gt;
proportion of cscs in tumor spheres can be very&lt;br /&gt;
variables ( cicalese et al. , 2009 ; pece et al. , 2010 ). despite&lt;br /&gt;
all of those limitations, csc cultures represent an&lt;br /&gt;
attention-grabbing in vitro model system for systematic highcontent&lt;br /&gt;
drug-screening approaches aiming to look for new&lt;br /&gt;
compounds targeting cscs as well as their direct progeny.&lt;br /&gt;
lung cscs : implications for diagnosis, prognosis and&lt;br /&gt;
monitoring of therapeutic response&lt;br /&gt;
as discussed within the whole previous paragraph, lung csc&lt;br /&gt;
analysis might supply a relevant contribution out to the&lt;br /&gt;
establishment of innovative tumor eradicating therapies.&lt;br /&gt;
besides therapy, knowledge derived direct from csc field&lt;br /&gt;
of investigation goes out to cause crucial advances&lt;br /&gt;
in lung cancer diagnosis, prognosis and monitoring of&lt;br /&gt;
patient response out to treatment. inside the basis of the&lt;br /&gt;
assumption that cscs are additional aggressive in comparison to the bulk&lt;br /&gt;
tumor cell population, tumor malignancy can be related&lt;br /&gt;
in the grade of cell differentiation and the abundance&lt;br /&gt;
on your csc fraction among the bulk tumor cells. the&lt;br /&gt;
possibility out to isolate, expand and characterize cscs&lt;br /&gt;
from totally different tissues has enabled the identification of  csc-associated antigens and consequently the immunodetection&lt;br /&gt;
of tumorigenic cells at intervals patient tumors.&lt;br /&gt;
the estimation of csc frequency within the whole tumor mass&lt;br /&gt;
could be accustomed being a diagnostic tool out to define tumor grade&lt;br /&gt;
and staging a lot of precisely. recent studies have highlighted&lt;br /&gt;
the growing interest within the whole exploitation of lung&lt;br /&gt;
csc knowledge regarding the improvement of lung cancer&lt;br /&gt;
diagnosis. it's been reported that the expression of&lt;br /&gt;
csc-associated markers aldh1 or sox2 positively&lt;br /&gt;
correlated with higher stage and grade in numerous lung&lt;br /&gt;
tumors ( jiang et al. , 2009 ; sholl et al. , 2009 ). additional&lt;br /&gt;
csc-associated markers, embryonic genes or combinations&lt;br /&gt;
of multiple markers may well be relevant out to generate&lt;br /&gt;
a lot of informative lung cancer diagnoses. highly&lt;br /&gt;
descriptive, csc-considering diagnoses may well be the&lt;br /&gt;
beginning purpose for improved and a lot of tailored lung&lt;br /&gt;
cancer treatments just like the therapeutic alternative has out to be&lt;br /&gt;
strictly linked out to the kind and stage on your tumor. it is&lt;br /&gt;
noteworthy that a correct and detailed diagnosis is&lt;br /&gt;
relevant out to define tumor stage conjointly out to predict the chance&lt;br /&gt;
of metastatic dissemination of tumors. during this context,&lt;br /&gt;
the so-called circulating tumor cells can possibly be of high&lt;br /&gt;
importance. circulating tumor cells are cancer cells that&lt;br /&gt;
are detectable in patient blood and indicative of tumor&lt;br /&gt;
dissemination potential ( pantel et al. , 2009 ). an early&lt;br /&gt;
spread of tumor cells is sometimes undetected by current&lt;br /&gt;
imaging technologies in patients with cancer. so,&lt;br /&gt;
completely different detection approaches are presently being set up&lt;br /&gt;
as early metastasis-sensitive ways. these methods&lt;br /&gt;
rely by the immunological, cytometrical or molecular&lt;br /&gt;
detection of circulating tumor cells ( pantel et al. , 2009 ).&lt;br /&gt;
every style of tumor cell could be ‘circulating’. but, it&lt;br /&gt;
is probable that simply a restricted fraction of those may&lt;br /&gt;
migrate across the blood stream, colonize alternative tissues&lt;br /&gt;
and initiate a whole new tumor mass in another location,&lt;br /&gt;
thereby giving rise out to metastatic lesions. as shown for&lt;br /&gt;
breast cancer, these cells are currently largely believed out to be&lt;br /&gt;
compatible with cscs ( ross and slodkowska, 2009 ;&lt;br /&gt;
theodoropoulos et al. , 2009 ). these findings confer key&lt;br /&gt;
relevance out to cscs conjointly within the whole topic of circulating tumor&lt;br /&gt;
cells and within the whole differential diagnosis of localized or&lt;br /&gt;
premetastatic disease. so, circulating cscs&lt;br /&gt;
may well be used as prognostic tools, representing predictors&lt;br /&gt;
of tumor progression. ( aktas et al. , 2009 ). the&lt;br /&gt;
investigation on csc-related factors linked out to patient&lt;br /&gt;
prognosis and likewise predictive of patient response to&lt;br /&gt;
treatments will just be crucial for second-hand of alternative&lt;br /&gt;
therapeutic choices. many publications recommend that&lt;br /&gt;
csc-related antigen expressions within the whole tumor mass&lt;br /&gt;
represent relevant prognostic indicators in various&lt;br /&gt;
cancers ( maeda et al. , 2008 ; pallini et al. , 2008 ; song&lt;br /&gt;
et al. , 2008 ; zeppernick et al. , 2008 ).&lt;br /&gt;
in pulmonary tumors, higher aldh1 expression was&lt;br /&gt;
linked out to poor prognosis in patients with early-stage&lt;br /&gt;
lung cancer ( jiang et al. , 2009 ). when treatment has&lt;br /&gt;
started, many biomarkers are designed to confirm the&lt;br /&gt;
impact on your therapeutic regimen on each, tumor and&lt;br /&gt;
patient at early time points, to make sure that ineffective or highly&lt;br /&gt;
toxic approaches could be rapidly substituted with a&lt;br /&gt;
second-line therapy. along at the finish of treatment, specific&lt;br /&gt;
biomarkers are presently designed to monitor over time&lt;br /&gt;
disease regression, progression or relapse.&lt;br /&gt;
current biomarkers out to monitor treatment response&lt;br /&gt;
would be the abundance of tumor-derived cells in patient&lt;br /&gt;
blood or plasma levels of tumor-derived proteins, such&lt;br /&gt;
as prostate-specific antigen for prostate cancer, ca19. 9&lt;br /&gt;
for gastric cancer, ca125 for ovarian cancer or cea&lt;br /&gt;
and cytokeratins for alternative tumors, together with lung cancer&lt;br /&gt;
( pantel et al. , 2009 ). as tumor relapse depends on&lt;br /&gt;
the presence of tumorigenic cells, a careful monitoring&lt;br /&gt;
of tumor response out to treatments ought to embody the&lt;br /&gt;
detection of csc-related biomarkers. the fact is, treatment&lt;br /&gt;
associated with a tumor with standard anticancer medicine might&lt;br /&gt;
result in partial reduction on your tumor mass, representing&lt;br /&gt;
an indicator of excellent response making use of the current&lt;br /&gt;
standards of tumor monitoring. but, just like the drug&lt;br /&gt;
would possibly preferentially kill the differentiated cells, it is&lt;br /&gt;
probable that the csc frequency wouldn't be reduced&lt;br /&gt;
at intervals the tumor, other then rather increased ( bao et al. , 2006 ;&lt;br /&gt;
ishikawa et al. , 2007 ). so, the analysis of cscbased&lt;br /&gt;
biomarkers looks crucial out to dissect among&lt;br /&gt;
transient tumor-debulking activity and long-lasting&lt;br /&gt;
tumor-eradicating treatments.&lt;br /&gt;
conclusions&lt;br /&gt;
despite the event of targeted therapies, clinical&lt;br /&gt;
oncologists have experienced a restricted improvement in&lt;br /&gt;
the prognosis of lung cancer patients. it's seemingly that&lt;br /&gt;
an improvement in lung cancer patient outcome may&lt;br /&gt;
need the introduction of a lot of effective innovative&lt;br /&gt;
agents with increased activity against drug-resistant&lt;br /&gt;
tumorigenic lung cscs. we envision that future&lt;br /&gt;
investigations on cscs routinely isolated from&lt;br /&gt;
cancer patients would pave the means out to innovative&lt;br /&gt;
knowledge, leading in flip out to novel approaches out to fight&lt;br /&gt;
lung cancer. this could result in considerable changes&lt;br /&gt;
into your clinical follow, who can need a more&lt;br /&gt;
intense role of molecular pathologists out to provide&lt;br /&gt;
info for a lot of effective and fewer destructive&lt;br /&gt;
personalised therapies.&lt;br /&gt;
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</description><link>http://fatcampsforkids.blogspot.com/2012/09/lung-cancer-stem-cells-tools-and.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-5508465533814628584</guid><pubDate>Thu, 06 Sep 2012 03:07:00 +0000</pubDate><atom:updated>2012-09-05T20:07:39.109-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>REPORT INTERVIEW HEALTH SURVEY ABOUT OBESITY IN US WORKERS</title><description>&lt;br /&gt;
&lt;br /&gt;
obesity has emerged as one in every of the most essential public health problems within the us. we assessed obesity prevalence rates as well as their trends among major us occupational teams. self-reported weight and height were collected annually on us workers, aged 18 years or older, coming from the 1986 to firmly 1995 and therefore the 1997 to firmly 2002 national health interview surveys. overall, occupation-, race-, and gender-specific rates of obesity ( defined being a body mass index30. zero kg/m^sup 2^ ) were calculated with information pooled from each study periods ( n600 000 ). annual occupation-specific prevalence rates were additionally calculated, as well as their time trends were assessed. obesity rates increased considerably eventually among employed workers, no matter race and gender. the average yearly amendment increased from zero. 61% ( ±. 04 ) throughout the episode from 1986 to firmly 1995 to firmly zero. 95% ( ±. 11 ) throughout the episode from 1997 to firmly 2002. average obesity prevalence rates and corresponding trends varied significantly across occupational teams ; pooled obesity prevalence rates were highest in motor vehicle operators ( 31. 7% in men ; 31. 0% in girls ). weight loss intervention programs targeting workers employed in occupational teams with high or increasing rates of obesity are urgently required.&lt;br /&gt;
&lt;br /&gt;
objectives. obesity has emerged as one in every of the most essential public health problems within the us. we assessed obesity prevalence rates as well as their trends among major us occupational teams.&lt;br /&gt;
&lt;br /&gt;
strategies. self-reported weight and height were collected annually on us workers, aged 18 years or older, coming from the 1986 to firmly 1995 and therefore the 1997 to firmly 2002 national health interview surveys. overall, occupation-, race-, and gender-specific rates of obesity ( defined being a body mass index30. zero kg/m^sup 2^ ) were calculated with information pooled from each study periods ( n600 000 ). annual occupation-specific prevalence rates were additionally calculated, as well as their time trends were assessed.&lt;br /&gt;
&lt;br /&gt;
results. obesity rates increased considerably eventually among employed workers, no matter race and gender. the average yearly amendment increased from zero. 61% ( ±. 04 ) throughout the episode from 1986 to firmly 1995 to firmly zero. 95% ( ±. 11 ) throughout the episode from 1997 to firmly 2002. average obesity prevalence rates and corresponding trends varied significantly across occupational teams ; pooled obesity prevalence rates were highest in motor vehicle operators ( 31. 7% in men ; 31. 0% in girls ).&lt;br /&gt;
&lt;br /&gt;
conclusions. weight loss intervention programs targeting workers employed in occupational teams with high or increasing rates of obesity are urgently required. ( am j public health. 2005 ;95 :1614-1622. doi :10. 2105/ajph. 2004. 050112 )&lt;br /&gt;
&lt;br /&gt;
within the us, obesity has risen at an unprecedented rate throughout the previous 20 years, 1 and current analysis indicates that the situation is worsening instead of improving. from 1960 to firmly 1980, the prevalence of obesity among adults within the us was relatively stable ; though, recent findings coming from the national health and nutrition examination survey ( nhanes ) showed that 3 from each 10 us adults are obese. 2 additionally to firmly increasing mortality from all causes, obesity is linked to firmly an increased risk of developing hypertension, type 2 diabetes mellitus, dyslipidemia, gallbladder disease, osteoarthritis, coronary heart disease, stroke, asthma, and sleep apnea. 3-7 additionally, new proof suggests obesity may be a risk issue for endometrial, breast, prostate, and colon cancers. 8-10  the relationship between obesity and occupation has not been totally investigated. work-related factors, like job and position, job stress, and extended work ( together with overtime night work and sedentary work ) might promote weight gain and abdominal fat accumulation. 11-14 possibly one of the national healthy folks 2010 objectives is to cut back the prevalence rate of obesity among adults to firmly lower than 15%, 15 thus, as a result of treatment usually fails, analysis efforts targeted on prevention are needed. weight loss intervention and education programs targeting workers employed in numerous occupational teams are urgently required, however, unfortunately, nationally representative knowledge identifying occupational teams in the highest obesity rates are definitely not presently on the market. 16, 17 it's additionally not known that occupational teams are experiencing giant will increase in obesity rates. our analysis objective was to firmly evaluate overall, gender- and race-specific obesity rates as well as their 17-year trends, together with yesteryear decade, at intervals 41 occupational teams using nationally representative samples of one's us worker population.&lt;br /&gt;
&lt;br /&gt;
ways&lt;br /&gt;
&lt;br /&gt;
the national health interview survey ( nhis ) may be a continuous multipurpose and multistage chance space survey of one's us civilian noninstitutionalized population living at addressed dwellings. 18 every week, a chance sample of households is interviewed by trained personnel to firmly obtain data relating to the characteristics of each one membership owner the household. 19 within the majority of cases ( 63% ) within the 1986 to firmly 1996 nhis surveys, the participants themselves answered all the queries ; regarding the remaining participants, the responses were obtained from their relatives or any other proxies. though, starting in the 1997 nhis survey, all survey responses were self-reported. for simplicity, within the present study, each self-reported or proxy-reported knowledge are stated as reported. within the amount from 1986 to firmly 1996, annual nhis survey response rates ranged from 95% to firmly 98%20 ; within the amount from 1997 to firmly 2002, these rates fell to firmly 70%-80%, reflecting the trend of lower response rates in all national surveys. 21, 22&lt;br /&gt;
&lt;br /&gt;
body mass index ( bmi ) is widely used to firmly define obesity and has actually been found to firmly closely correlate in the level of weight resulting in obesity. 23 bmi was calculated by dividing weight in kilograms by height in meters squared. respondents were classified as obese if their bmi was larger than 30. zero kg/m^sup 2^. 24 from 1986 to firmly 1995, the nhis reported weight and height values for those participants. knowledge due to 1996 survey year are definitely not presented as a result of, for that year, the national center for health statistics ( nchs ) reported knowledge solely for participants by having weight between 98 and 289 pounds as well as a height between 59 and 76 inches ; bmi regarding the 1996 participants outside of such weight and height ranges were not created on the market by nchs. beginning in 1997, the nhis was redesigned and therefore the nchs created on the market the bmi values for those participants, even those with weight and height outside the on top of ranges. 25 as a result of of such differences within the reporting, and as a result of the major redesign of one's sampling and interview format, we analyzed knowledge separately for nhis survey periods 1986 to firmly 1995 and 1997 to firmly 2002.&lt;br /&gt;
&lt;br /&gt;
within the 1986 to firmly 1995 nhis, employment data was collected on several subjects aged 18 years or older who reported operating throughout the 2 weeks previous to firmly the survey26, 27 ; beginning in 1997, nchs collected employment data from adults who stated that they actually were operating throughout the week until the nhis survey. each of such definitions included paid and unpaid work. forty-one standardized occupational codes derived from a lot of detailed us census occupational codes were provided within the nhis database from 1986 to firmly 1995 and from 1997 to firmly 2002. 28, 29 we  grouped survey participants within the trend knowledge analysis into white, black, or any other race class. alternative race included alternative, aleutian eskimo/american indian, asian/ pacific islander, and unknown/multiple races.&lt;br /&gt;
&lt;br /&gt;
as a result of of one's advanced sample survey style, analyses were completed along with the sudaan package to bring into account sample weights and style effects. 30 for pooled prevalence estimates, sample weights were adjusted to firmly account for our aggregation of knowledge over multiple survey years by dividing the original weight by 10 ( the amount of years combined in survey years 1986 through 1995 ) and by 6 ( the amount of years combined in survey years 1997 through 2002 ). 18 to firmly assess obesity trends among every survey amount, a weighted linear regression model was fitted towards the annual design-adjusted rates among occupational teams. the load used for every annual rate was the inverse of its variance.&lt;br /&gt;
&lt;br /&gt;
results&lt;br /&gt;
&lt;br /&gt;
a total of 603 139 persons aged 18 years and older reported operating among the 2 weeks before their participation within the 1986 to firmly 1995 nhis surveys, and within the 1 week before their participation within the 1997 to firmly 2002 nhis surveys. among the 488 612 workers within the 1986 to firmly 1995 survey amount, the mean age ( ±sd ) was 38. 9 ±12. 8, with the use of a total of 226 128 girls ( 46. 3% ) ; the mean age of one's 114 527 workers direct from 1997 to firmly 2002 amount was 40. 3 ±12. 7, as well as 57 198 girls ( 49. 9% ).&lt;br /&gt;
&lt;br /&gt;
the average yearly modification ( ±se ) in obesity rates increased from zero. 61% ( ±. 04 ) within the 1986 to firmly 1995 amount to firmly zero. 95% ( ±. 11 ) within the 1996 to firmly 2002 amount. annual obesity rates increased considerably for all gender-race teams within the survey periods 1986 to firmly 1995 and 1997 to firmly 2002 ( figure 1 ). in all survey years, annual obesity rates were highest in black workers ( notably girls ) and lowest among those in the opposite race class.&lt;br /&gt;
&lt;br /&gt;
for every gender and every 1 of one's 41 occupational teams, tables 1 and 2 show : the sample size ; the share of black workers for every occupational cluster ( providing black workers had the best rates of obesity ) ; the pooled and annual prevalence rates of obesity ; and of course the slope ( i. e. , yearly modification in obesity rate ) of one's weighted linear regression of rate of obesity as time passes, its commonplace error, and of course the corresponding p worth. slopes were not calculated and get a specific occupational cluster as soon as the sample size for any given survey year was below 46. pooled and annual obesity rates preceded by an asterisk got a relative commonplace error defined as 100 × se ( rate )/rate of bigger than 30% and, following the follow of one's nchs, really should be thought-about imprecise estimates. 31&lt;br /&gt;
&lt;br /&gt;
throughout the amount from 1986 to firmly 1995, the best pooled obesity rates were observed for male workers employed as motor vehicle operators ( 19. 8% ), material-moving equipment operators ( 19. 2% ), and alternative protective services staff ( 19. 2% ) ; for female workers, the best pooled obesity rates were among motor vehicle operators ( 22. 6% ), health services workers ( 21. 0% ), and cleaning and building services workers ( 20. 0% ). among men, the ultimate occupational cluster with the use of a pooled obesity prevalence rate below 7% was that of people  employed within the whole health-diagnosing occupations ( 6. 2% ) ; female occupations with obesity prevalence rates below 7% included architects and surveyors ( 1. 7% ) ; health-diagnosing occupation workers ( 4. 3% ) ; engineers ( 5. 8% ) ; sales representatives and commodities and finance workers ( 6. 6% ) ; and writers, artists, entertainers, and athletes ( 6. 6% ). no matter gender, there have been no employed teams that experienced a reduction in obesity rates throughout now era. occupational teams by having significant increase of 1% or bigger per year included male workers employed within the whole different protective service occupations ( 1. 07 ±. 23%, p. 001 ), female motor vehicle operators ( 1. 20 ±. 29%, p. 001 ), and female mail and message distributors ( 1. 16 ±. 34%, p. 01 ).&lt;br /&gt;
&lt;br /&gt;
within the whole era from 1997 out to 2002 ( table 2 ), the very best pooled obesity rates were observed for male workers employed as motor vehicle operators ( 31. 7% ), police and firefighters ( 29. 8% ), different transportation except motor vehicle moving operators ( 28. 7% ), and material-moving equipment operators ( 28. 2% ) ; and, for female workers, those employed as motor vehicle operators ( 31. 0% ), different protective service workers ( 30. 5% ), material-moving equipment operators ( 29. 5% ), and cleaning and building service workers ( 25. 3% ). in distinction onto the earlier survey era, there have been no occupational teams among the men with an obesity rate below 11%. among ladies, merely those employed within the whole health-diagnosing occupations ( 10. 3% ), as architects and surveyors ( 7. 3% ), and within the whole construction and extractive trades ( 6. 9% ) had obesity rates below 11%. there have been no significant downward trends in obesity rates for any occupational cluster throughout the survey era from 1997 out to 2002. obesity rates among male workers employed as police or firefighters had an annual increase of 2. 1% ( ±. 8 ) ; female workers with annual will increase on top of 2% included motor vehicle operators ( 5. 7 ±1. 1 ) ; health service workers ( 2. 4 ±. 5 ) ; different skilled specialty occupation workers ( 2. 1 ±. 7 ) ; and fabricators, assemblers, inspectors, and samplers ( 2. 1 ±. 9 ).&lt;br /&gt;
&lt;br /&gt;
discussion&lt;br /&gt;
&lt;br /&gt;
using information from a significant, nationally representative sample of persons workers, we found that obesity rates were higher for female workers than for male workers at intervals a lot of the 41 occupational teams. black female workers were found out to have the very best prevalence of obesity relative out to different race and white workers of each genders. though, it is vital out to note that over yesteryear decade, obesity rates were rising in all worker teams, no matter race and gender. among the varied us operating teams, the prevalence of obesity increased nearly 10% involving the survey years 1986 and 2002. this increasing obesity epidemic poses substantial challenges onto the us workforce.&lt;br /&gt;
&lt;br /&gt;
obesity and its connected health conditions directly injury the health and well-being as to the current workforce and considerably contribute out to long-term chronic disability. 32-36 additionally, the significant increase within the whole prevalence of obesity among youngsters and adolescents indicates a good bigger problem that employers can doubtless confront at intervals the long run workforce. 37 short-term disability claims attributed out to obesity have increased 10-fold over yesteryear decade, according out to an unumprovident study that analyzed its in depth disability database. 38 obesity-related disabilities cost employers an average of $8720 per employee yearly. 38 designing and implementing worksite weight-loss programs that educate and facilitate workers to attain and maintain weight loss might substantially lessen the costly health burden on each employers  and workers. this effort won't just forestall work-related illness, injury, and disability but in addition promote healthy lifestyles, that, in flip, can forestall and cut back chronic disease in working-age americans, several of whom pay 8 out to 12 hours per day at work.&lt;br /&gt;
&lt;br /&gt;
limitations&lt;br /&gt;
&lt;br /&gt;
the nhis information are cross-sectional information that permit just inferences of association of obesity within the whole 41 occupations analyzed. but, findings from this study are similar out to those of others, 33, 34 within which the prevalence of obesity has also been found out to vary in line with occupation. consistent when using the present findings, previous analysis has shown that race/ethnicity, social category, age, and/or sedentary jobs will contribute out to a rise in obesity. 32, 33, 37 furthermore, it can be real that among obese folks there exists bias by self-selection of occupation.&lt;br /&gt;
&lt;br /&gt;
though bmi has also been shown, traditionally, out to correlate with fat distribution, it needs to be noted to the point it doesn't take into account people who might utilize a giant muscular habitus, nor will it directly live p.c adipose tissue. but, most health organizations and scientists support the use of bmi out to define overweight and obesity, notably when direct measures of fat distribution are definitely not accessible. 39-41 employing a 2 or 1 week reference amount previous onto the nhis interview out to characterize occupational standing would possibly lead out to misclassification of people with respect out to their usual occupation. but, ongoing analyses as to the nhis information via the present team of investigators indicate a substantial concordance between self-reported current occupation and longest-held job.  &lt;br /&gt;
&lt;br /&gt;
the present analysis suffers from several as to the limitations seen in giant population-based studies. weight and height were collected because we are part of a self-reported or proxy fashion, that could afford led out to less precision within the whole calculation as to the bmi. 43, 44 as an example, previous analysis has prompt that individuals tend out to underreport their weight and overreport their height, leading onto the underestimation of bmi ; additionally, the somewhat of under- and overreporting varies currently being a gathering of age, gender, race, ethnicity, and social category.&lt;br /&gt;
&lt;br /&gt;
the 1986 out to 1995 nhis employed proxy info when adults were not accessible for household interview. proxy reports of weight and height might also be subject out to bias. out to cut back this potential bias, we reanalyzed our 1986 out to 1995 information within the whole 61% of nhis participants who directly reported weight and height throughout the interview. results indicate that, for many occupations, the self-reported bmis could well be even more than the combined proxy and self-reported bmis. examining the bmis for those workers from 1986 out to 1995, we found the average annual distinction within the whole share of obesity amongst the nonproxy ( self-reported ) bmis and also the combined proxy and self-reported bmis was zero. 73%.&lt;br /&gt;
&lt;br /&gt;
finally, the amendment within the whole survey style methodology in 1996 prevented trend comparisons within the total 17-year time amount. moreover, tiny sample sizes may lead out to less reliable estimates of obesity rates and trends in a few worker subpopulations ( e. g. , private household occupations among men, and architects and surveyors among ladies ).&lt;br /&gt;
&lt;br /&gt;
strengths  despite the restrictions presented, the use of giant sample sizes, the nationally representative nature as to the sample, oversampling of choose subgroups ( e. g. , blacks ), and also the annual assessment useful for assessing trends in prevalence of obesity among occupations allows this study out to be favorably compared out to different evaluations as to the us obesity epidemic.&lt;br /&gt;
&lt;br /&gt;
no matter gender, people employed as motor vehicle operators were found out to have the best prevalence of obesity in each time periods. among men, these pooled prevalence rates increased from 19. 8% within the 1986 out to 1995 survey episode out to 31. 7% within the 1997 out to 2002 survey episode ; corresponding rates for girls were 22. 6% and 31. 0%, respectively. developing weight-loss programs designed out to take into account the task demands, physical demands, and even the socioeconomic and cultural backgrounds of motor vehicle operators might potentially facilitate cut back this detrimental increase in obesity among this occupational cluster. furthermore, examining occupations by having lower prevalence of obesity ( like female architects and surveyors or men employed within the health-diagnosing professions ) might facilitate researchers elucidate the relationship between occupation and optimal body weight.&lt;br /&gt;
&lt;br /&gt;
conclusions&lt;br /&gt;
&lt;br /&gt;
the behavioral effects of physical activity on health are well established. 48-51 though the foremost promising weight-loss interventions specialise in increasing physical activity additionally out to implementing dietary changes, the increasing trend towards automation and different labor-saving strategies found at several worksites won't foster physical activity conducive out to weight loss. primary and secondary prevention of obesity in occupational settings should thus take into account the several societal and occupational factors that influence energy imbalance via multifaceted interventions ( e. g. , accountability of healthy food choices and food quantity, exercise programs ). such comprehensive, worksite-based interventions are urgently required so as out to slow the growing epidemic of obesity within the us.&lt;br /&gt;
&lt;br /&gt;
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35. Narbro K, Agrcn G, Jonsson E, et al. Sick leave and disability pension before and after treatment for obesity: a report from the Swedish Obese Subjects (SOS) study. Int J Obes Relat Metab Disord. 1999;23:619-624.&lt;br /&gt;
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36. Regan J, Hamer G, Wright A. The epidemic of obesity: when a disease is not a disability. Tenn Med. 2003;96:564-565.&lt;br /&gt;
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37. Ogden CL, Flegal KM, Carroll MD, Johnson CL. Prevalence and trends in overweight among US children and adolescents, 1999-2000. JAMA. 2002;288:1728-1732.&lt;br /&gt;
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38. UnumProvident Obesity-Related Disability Claims Study. Available at: http://www.unumprovident.com/newsroom/news/corporate/obesity.aspx. Accessed July 8, 2004.&lt;br /&gt;
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39. Lean MEJ, Han TS, Seidell JC. Impairment of health and quality of life using new federal guidelines for the identification of obesity. Arch Intern Med. 1999;159:837-843.&lt;br /&gt;
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40. National Institutes of Health. Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. Bethesda, Md: Department of Health and Human Services, National Institutes of Health, National Heart, Lung, and Blood Institute; 1998.&lt;br /&gt;
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42. Gómez-Marín O, Fleming LE, LeBlanc W, Lee DJ, Pitman T, Caban AJ. Longest-held job in US occupational groups: The National Health Interview Survey (NHIS). J Occup Environ Med. 2005;47:79-80.&lt;br /&gt;
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43. Patrick DL, Bushnell DM, Rothman M. Performance of two self-report measures for evaluating obesity and weight loss. Obes Res. 2004;12:48-57.&lt;br /&gt;
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44. Morgan PJ, Jeffrey DB. Restraint, weight suppression, and self-report reliability: how much do you really weigh? Addict Behav. 1999;24:679-682.&lt;br /&gt;
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45. Kuczmarski MF, Kuczmarski RJ, Najjar M. Effects of age on validity of self-reported height, weight, and body mass index: findings from the Third National Health and Nutrition Examination Survey, 1988-1994. J Am Diet Assoc. 2001;101:28-34.&lt;br /&gt;
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46. Engstrom JL, Paterson SA, Doherty A, Trabulsi M, Speer KL. Accuracy of self-reported height and weight in women: an integrative review of the literature. J Midwifery Womens Health. 2003;48:338-345.&lt;br /&gt;
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47. Spencer EA, Appleby PN, Davey GK, Key TJ. Validity of self-reported height and weight in 4808 EPIC-Oxford participants. Public Health Nutr. 2002;5:561-565.&lt;br /&gt;
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48. Zhang Q, Wang Y. Socioeconomic inequality of obesity in the United States: do gender, age, and ethnicity matter? Soc Sci Med. 2004;58:1171-1180.&lt;br /&gt;
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Keyword Search:&lt;br /&gt;
&lt;br /&gt;
Obesity; Workers; Public health; Polls &amp; surveys; Adolescent, Adult, Body Mass Index, Cross-Sectional Studies, Female, Humans, Male, Middle Aged, National Center for Health Statistics (U.S.), Obesity -- ethnology, Occupations -- classification, Occupations -- statistics &amp; numerical data, Prevalence, United States -- epidemiology, Health Surveys (major), Obesity -- epidemiology (major), Occupational Health -- statistics &amp; numerical data (major)</description><link>http://fatcampsforkids.blogspot.com/2012/09/report-interview-health-survey-about.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-8192745369764448505</guid><pubDate>Thu, 06 Sep 2012 02:42:00 +0000</pubDate><atom:updated>2012-09-05T19:42:16.595-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION  PREVALENCE OF OVERWEIGHT AND OBESITY IN SCHOOL-AGED CHILDREN</title><description>&lt;div style="text-align: justify;"&gt;&lt;br /&gt;
&lt;/div&gt;&lt;div style="text-align: justify;"&gt;Childhood obesity is a public health concern in Canada. Few published anthropometric data are available to indicate obesity prevalence in Canadian children. Obesity prevalence is reported for school-aged children in 11 London, Ontario, schools. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Data on body weight and height were obtained using standardized procedures. United States Centers for Disease Control and Prevention (CDC) body mass index (BMI)-for-age references and Cole's international BMI reference were used to classify the children's weight categories. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;The study included 1,570 pupils aged six to 13. The CDC BMI references categorized 16.6% and 11.8% of children as overweight and obese, respectively. In comparison, when the Cole BMI reference and cut-off points were used, 17.5% and 7.6% of children were classified as overweight and obese, respectively. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Overweight is prevalent in the study population. Public health interventions are warranted to curb the obesity epidemic in school-aged children. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Purpose: Childhood obesity is a public health concern in Canada. Few published anthropometric data are available to indicate obesity prevalence in Canadian children. Obesity prevalence is reported for school-aged children in 11 London, Ontario, schools. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Methods: Data on body weight and height were obtained using standardized procedures. United States Centers for Disease Control and Prevention (CDC) body mass index (BMI)-for-age references and Cole's international BMI reference were used to classify the children's weight categories. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Results: The study included 1,570 pupils aged six to 13. The CDC BMI references categorized 16.6% and 11.8% of children as overweight and obese, respectively. In comparison, when the Cole BMI reference and cut-off points were used, 17.5% and 7.6% of children were classified as overweight and obese, respectively. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Conclusion: Overweight is prevalent in the study population. Public health interventions are warranted to curb the obesity epidemic in school-aged children. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Overweight and obesity have become major public health problems among children in countries around the world, including Canada (1). Like adult obesity, pediatrie obesity increases health risks. In children, these risks include childhood type 2 diabetes, hyperlipidemia, and hypertension (2-4). Furthermore, obese children tend to become obese adults (5). Because of the subsequent health consequences and a heavy health-care burden, primary prevention must target children (6). Measuring obesity prevalence rates is a prerequisite for planning and evaluating evidence-based public health intervention and prevention programs. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;The prevalence of childhood obesity hinges on its definition and criteria. Defining overweight and obesity in children is complicated by normal growth processes, pubertal development, and body composition changes. The term "overweight" refers to excess weight in relation to height, while "obesity" refers to excessive body fat or adipose tissue in relation to lean body mass. Measuring body fat accurately is difficult. The ideal definition of obesity, based on percentage of body fat, is impracticable for epidemiological and clinical use (7). Although the word "overweight" may connote a milder degree of excess fat than does "obesity," no global consensus criteria exist to make this distinction. The terms are generally used interchangeably in the literature (8). &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Body mass index (BMI) has been adopted as a simple measure of childhood obesity since the 1990s. Body mass index is a convenient way of measuring overweight and obesity in general practice. Because obesity is an excess of body fat, the ideal indicator in populations should be reliable and valid in reflecting body fat content (9,10). The rationale for using BMI as a measure of overweight and obesity in children is based on two factors. First, the high reliability of measuring height and weight makes BMI practical in the clinical setting or in population-based surveys (9,10). Second, BMI is a valid index of fatness. BMI is significantly correlated with laboratory measures of fatness in children and adolescents (11,12). Compared with the weight-for-height index, the advantage of BMI-for-age references as a measure of overweight in children is that age is taken into account. This is crucial because a child's body build and body composition change with age (13). The major limitation of BMI is its inability to distinguish increased fat mass from lean mass (14). &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Several countries, including the United States, the United Kingdom, Germany, Italy, Australia, and New Zealand, have developed gender-specific BMI-for-age standards for children (10,15-20). Although Health Canada has established its own standards for adult obesity (21), it has not yet done so for children. Currently, different researchers are using two sets of BMI criteria in Canada (1,22-24). &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Cole et al. developed the first set of BMI references (20). The Cole BMI references used data from six countries, including Brazil, the United Kingdom, Hong Kong, the Netherlands, Singapore, and the United States (20). Cole et al. drew centile curves that at age 18 years passed through the widely used cut-off points of 25 and 30 kg/m^sup 2^ for adult overweight and obesity (20). Children with a BMI of 25 or 30 at the extrapolated age of 18 were classified as overweight or obese, respectively (20). &lt;/div&gt;&lt;div style="text-align: justify;"&gt;The Centers for Disease Control and Prevention (CDC) developed the second set of BMI reference data, using five national health examination surveys from 1963 to 1994 and five supplementary data sources in the United States (10). The CDC gender- and age-specific BMI references define overweight in children as a BMI above the 95th percentile for age. Children between the 85th and 95th percentiles are considered at risk of being overweight (10). Recently, the CDC BMI reference and cut-off points were endorsed by Dietitians of Canada, the Canadian Paediatric Society, The College of Family Physicians of Canada, and the Community Health Nurses Association of Canada Nutrition Committee (25,26). This Canadian Collaborative Statement recommends the CDC BMI reference data and cut-off points for Canadian children, but labels weight categories differently from the CDC terms; a BMI between the 85th and 95th percentiles indicates that a child is "overweight," and a BMI above the 95th percentile indicates that a child is "obese" (25). The inconsistency in terminology, BMI reference data, and cut-off points leads to difficulties in comparing obesity prevalence rates among Canadian children with data cited in the literature. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Valid published BMI data sources are also needed to determine local and national childhood obesity prevalence. Although increasing national and local concern exists over the rising prevalence of childhood obesity, only a few measured BMI data have been available for Canadian children since the 1970s (1,22,23,27). In the majority of national surveys, children's BMI data were obtained from parents' or children's self-reported body weights and heights (24,28), which are unlikely to be as accurate as measurements. However, the recent Canadian Community Health Survey Cycle 2.2 on Nutrition does include actual measurements (1). &lt;/div&gt;&lt;div style="text-align: justify;"&gt;The current study was designed to collect BMI data based on measured body weight and height, and to report the prevalence of overweight and obesity among school-aged children. The study was conducted between 2001 and 2003 in 11 London, Ontario, elementary schools. In order that current results might be compared with data cited in the literature, both Cole et al. and CDC BMI references were used to classify overweight and obesity in this study population. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;METHODS &lt;/div&gt;&lt;div style="text-align: justify;"&gt;The study was approved by the Research Ethics Board on the Use of Human Subjects at Brescia University College. Permission was obtained from local school boards before contact was initiated with individual schools. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Study subjects and sample selection &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Children in grades 1 to 6 were studied. A convenience sample was used from 11 elementary schools, which were located in diverse socioeconomic areas in the City of London and County of Middlesex school districts. Postal codes were used as a proxy to identify socioeconomic status (SES) of the area in which the school is located. The Statistics Canada Postal Code Conversion File was used to convert the postal codes of targeted schools into Statistics Canada Census Tracts. "Incidence of low income" (ILI) on Census Tracts was used to define social classes of the areas (i.e., ILJ O to 6.2% = upper class area; ILI 6.29% to 16.6% = middle class area; ILJ 16.69% to 85% = low income area) (29). Four schools were in upper class areas, four were in middle class areas, and three were in low income areas. As school postal codes are a rough proxy for SES, no attempt was made to compare outcome measures among schools located in different SES areas. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;All pupils in grades 1 to 6 in the targeted 11 schools were invited to participate. Parental consent was obtained before data collection, and only pupils with parental consent were eligible subjects. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Data collection &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Children's weights and heights were measured by trained personnel using standardized procedures (30). Tanita medical scales (BWB-627A) were used to measure body weight to the nearest 0.1 kg. seca 214 "Road Rod" portable stadiometers were used to measure body heights to the nearest 0.1 cm. Each child was asked to remove her or his shoes and any excessive clothing before entering the measuring room. In order to respect privacy and promote a sense of comfort, each child was measured with no other children present. Weights and heights were measured twice and an average of the two values was calculated. Children's dates of birth were collected to calculate age. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Data analysis &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Body mass index was calculated as weight (kg) divided by height (m) squared. Both CDC and Cole's BMI references were used to classify children's weight status. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;CDC BMI reference: Epi Info 2000 software (CDC, Atlanta, GA, 2000) was used to calculate BMI percentile against CDC gender- and age-specific BMI references (10). The CDC-recommended BMI-for-age cut-off points (10), along with the Canadian labels (25), were used to define children's weight status; a BMI between the 85th and 95th percentiles defined a child as "overweight," while a BMI above the 95th percentile defined a child as "obese." &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Cole's BMI references: The six-country "international" BMI dataset was used to classify children into die overweight and obese categories. Children with a BMI of 25 or 30 at the extrapolated age of 18 were defined as overweight or obese, respectively (20). &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Data were analyzed using SPSS for Windows (ReI. 11.0, Chicago, IL, 2001). Overweight and obesity prevalence rates were described by gender. Kappa measure of agreement was performed to test the agreement of the overweight and obesity categories by the two BMI references. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;RESULTS &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Of the 3,368 pupils, 1,570 obtained parental consent and participated in the study. The response rate generated was therefore 47%. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Subjects' profile &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Among the study pupils, 837 (53%) were boys and 733 (47%) were girls. In general, the sample was evenly distributed across age groups, with a range of 15-20% in each age interval, with the exception of the end spectrums, i.e., 12% at age six and 4% at age 12. Mean BMIs by age and gender are reported in Table 1. &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Overweight prevalence &lt;/div&gt;&lt;div style="text-align: justify;"&gt;According to the CDC BMI references, 29% of boys and 28% of girls were overweight or obese. The Cole's BMI criteria classified 24% of boys and 26% of girls as overweight or obese (Figure 1). &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Comparison of obesity prevalence rates &lt;/div&gt;&lt;div style="text-align: justify;"&gt;Figure 2 indicates that more children were classified as overweight by Cole than by CDC criteria. The kappa measure of agreement indicated, however, that the two classification systems are largely similar (kappa = 0.80, p&amp;lt;0 .001=".001" br="br"&amp;gt; DISCUSSION &lt;br /&gt;
The current results suggest that overweight and obesity are prevalent in this study population. About 25% of the children had body weights in unhealthy categories. Results from the current study strengthen the need for public health interventions to curb the obesity epidemic in school-aged children. &lt;br /&gt;
The inconsistent use of BMI criteria in classifying overweight and obesity in children makes comparing published obesity prevalence rates challenging. The current results, which were calculated using both Cole and CDC criteria, allow such direct comparisons of obesity prevalence rates within Canada and internationally. Tremblay et al. (24) reported that 33% of Canadian school-aged boys and 27% of girls were overweight, while 10% of boys and 9% of girls were obese according to Cole's BMI reference dataset and cut-off points. Tremblay's rates were higher than those reported in the current study, although the same criteria were used in both studies (24). This discrepancy may be due to the fact that the 1996 BMI data collected in the National Longitudinal Survey in Children and Youth were based on parent-reported body weights and heights, which may lead to over- or under-estimations (24). &lt;br /&gt;
In addition, Williams et al. (31) reported regional differences in overweight and obesity prevalence rates in Canadian children. The current dataset represents only a sample of children from London, Ontario, while Tremblay et al.'s data reflect the national figure; this may be another explanation for the inconsistency between our data and Tremblay et al.'s (24). &lt;br /&gt;
The most recently measured BMI data from the (Canadian Community Health Survey Cycle 2.2 on Nutrition Health showed that 18% and 8% of children between the ages of two and 17 were overweight and obese, respectively (1). As in our study. Cole's BMI reference dataset and cut-off points were used in the survey cycle. The survey cycle findings are very close to our results. &lt;br /&gt;
Similarly, overweight prevalence in the current study closely resembles that of American school-aged children in recent National Health and Nutrition Examination Surveys (NHANES) (Table 2) (32). The same measuring method and BMI cut-off points were used in the NHANES and the current study, although different terminologies were used. &lt;br /&gt;
Although the kappa measure of agreement indicated that the two BMI criteria have close agreement, the different cut-off points cause difficulty in the comparison of obesity prevalence rates in children. Because the use of the CDC BMI references in Canadian children has been endorsed by various Canadian health professional organizations (25), researchers would find the use of them beneficial in the reporting of overweight prevalence in Canadian children. Use of this BMI reference would facilitate direct comparison of overweight prevalence rates among Canadian children, as well as between Canadian and American children. Concurrent use ofCk)le's BMI references, the so-called "international BMI reference" (20), would allow comparison between Canadian and international data (25). &lt;br /&gt;
LIMITATIONS &lt;br /&gt;
The current study has a number of limitations. First, subjects were from a convenience sample of children from 11 of 130 elementary schools in the study areas. second, even though efforts were made to include schools located in different socioeconomic areas, response rates varied among schools. We are uncertain if SES differences existed between responders and nonresponders. These two pitfalls may have induced bias and may limit the generalization of results to the school-aged population in the City of London and the County of Middlesex. Third, the limited number of subjects in each age interval does not allow statistical comparisons of overweight prevalence across age groups. Last, but not least, individual families' SES information was not obtained, and so a comparison of overweight and obesity prevalence rates across SES classes is impossible. &lt;br /&gt;
RELEVANCE TO PRACTICE &lt;br /&gt;
Overweight and obesity are prevalent in the study population. Public healdi interventions are warranted to curb the obesity epidemic in school-aged children. Use of bodi the CDC and Cole's BMI references and cutoff points when reporting overweight and obesity prevalence would allow comparison between Canadian and international data. &lt;br /&gt;
Acknowledgements &lt;br /&gt;
The study was funded by the PHRED Program at Middlesex-London Health Unit Brescia University College provided salary support for work-study students responsible for data entry and verification. The authors acknowledge the Thames Valley District School Board and the London District Catholic School Board for allowing access to pupils in their elementary schools. The authors are grateful to the Middlesex-London Healdi Unit Child Health Team and to Brescia University College nutrition students for assistance in data collection. This study would have been impossible without the support and involvement of school principals, teachers, and staff. Pupils' and parents' participation and time are very much appreciated. &lt;br /&gt;
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Keywords Search:&lt;br /&gt;
Obesity; Public health; Nutrition; Diet; Elementary school students ; Body Mass Index, Child, Female, Health Surveys, Humans, Male, Nutrition Surveys, Ontario -- epidemiology, Prevalence, United States -- epidemiology, Child Nutrition Disorders -- epidemiology (major), Obesity -- epidemiology (major), Public Health (major)&lt;br /&gt;
&lt;!--0--&gt;&lt;/div&gt;</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-prevalence-of-overweight-and.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-1060214943954549076</guid><pubDate>Thu, 06 Sep 2012 02:18:00 +0000</pubDate><atom:updated>2012-09-05T19:22:01.975-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>LEARN ABOUT  THRESHOLDS FOR OVERWEIGHT AND OBESITY AND THEIR RELATION TO METABOLIC RISK IN CHILDREN</title><description>5 years ago, the international obesity taskforce ( iotf ) revealed bmi thresholds defining paediatric overweight and obesity. 1 centile equivalents for kids aged 2–18 were derived statistically by extrapolation from adult cutoffs at bmi 25 and 30 kg/m2, respectively. they will were not intended for clinical use other then to firmly assess trends and to firmly compare populations. notwithstanding this, iotf cutoffs for paediatric ‘overweight’ and ‘obesity’ were added to firmly the uk charts and used within the whole clinic. labelling kids during this categorical method, at a really early&lt;br /&gt;
age, raises variety of considerations. initial, the cutoffs are based upon the unfounded assumption that a fixed proportion of kids, even for the age of 2 years, is overweight or obese. second, they will are derived from cross-sectional information, and thus not predictive. though centile charts drawn from cross-sectional information provide the impression of clinical continuity, they will don't describe the tracking of individual kids. In reality, bmi tracks relatively poorly from early childhood to adulthood. hesketh found that 20% of ‘obese’ 5–10 year olds had spontaneously resolved to firmly the most appropriate weight at intervals 3 years. 2 tracking obviously improves the nearer the kid gets to firmly adult standing, 3, 4 other then most adults, not less than to firmly date, have not been obese as young kids. 5–8 third, and the majority importantly, the who adult cutoffs were chosen upon the basis of established health risk. 9 the children’s were not, and they will are arbitrary. within the whole context of effective kid health surveillance, the clinician desires to firmly know whether or not cutoffs throughout the centile chart reliably establish children at risk of current or future metabolic disturbance. weight excess is undoubtedly related to insulin resistance and metabolic disturbance in adults, 10 other then the relationship is not a powerful one and also the corresponding associations in children are less clear still. as cole has got wind, a centile cutoff wherein the health risk of obesity starts to firmly rise can't be identified with any precision in kids. 1 clinical validity ( association of bmi with current or future morbidity/ mortality ) is a lot of necessary to firmly establish than measurement validity ( correlation with unwanted fat ).&lt;br /&gt;
The bogalusa study is widely cited as proof for a relationship between childhood overweight and cardiovascular risk. in spite of this, the associations between children’s bmi and metabolic disturbance are weak. chance, which improves with increasing numbers, is wrongly used throughout to firmly argue for strength of association. correlation, when low, can stay thus, in spite of this massive the numbers or tiny the p-value.   on your 2000 5–10-year-olds within the bogalusa study, most had no risk factors in any respect. 11 merely eight had more often four elements on your metabolic syndrome, and every one of them fell directly into class of ‘overweight’ ( bmi495th centile ). in spite of this, 40% of these overweight had no risk factors at all, whereas 22% of these deemed ‘normal’ had some. currently being a screening tool, bmi discriminated poorly between those with and while not risk. it should give valuable information for the epidemiologist, other then very little regarding the paediatrician. what then on your relationship between bmi standing in childhood and metabolic disturbance in adulthood, the outcome live of principle concern ? typically benchmarked currently being a longitudinal cohort study, bogalusa is really a series of seven cross-sectional studies within which merely 55% of the participants seem more often once. this is often vital because cross-sectional information can not give particulars on tracking, merely associations among a population on a given time. the earlybird study was came upon in 2000 currently being a longitudinal study of growth and maturation, with metabolic health as the outcome live. it involves three hundredunited nations monitors. the unarme youngsters and their folks and actually has obtained fasting blood samples annually coming from the age of 5 years, so that you can monitor the emergence of insulin resistance ( homa-ir12 ) and its metabolic impact. 13 whereas the parents’ information show a transparent relationship between bmi and homa-ir, explaining 28% ( 41% ) of the variance in insulin resistance within the fathers ( mothers ) ( figure 1 ), the corresponding association in his or her children aged 5 years is weak, at best explaining 6%. it therefore looks unlikely, given the restricted relationship between prepubertal and adult bmi, that a bmi at 5 years can usefully establish those presently at metabolic risk or doubtless to actually become thus later on.&lt;br /&gt;
when earlybird youngsters are classified per their respective bmi cutoffs as ‘normal’, ‘overweight’ and ‘obese’, there's a regular stepwise increase in mean insulin resistance per weight class ( figure 2 ). in spite of this, categorisation of the kind says nothing concerning the predictive sensitivity or specificity of bmi. mean insulin resistance clearly differs between youngsters classified per iotf criteria, other then the performance of bmi class currently being a screening tool for individual risk is poor. triglycerides, a marker for metabolic disturbance, 14 fare no higher ( information not shown ). bmi may be a relatively blunt tool within the early detection of metabolic risk. modification in bmi, eventually, would seem to remain a additional useful marker compared to a only live at, by way of example, faculty entry. 15 so the long-term importance of obesity in childhood remains unclear. 16, 17 we could notice no proof to compliment the  categorisation of terribly young kids by bmi into those at risk of metabolic disturbance. it is vital to seem beyond p-values, that sample size dependent, to actually contemplate effect size. bmi, at this age, won't justify a clinically useful proportion as to the variance in either insulin resistance or triglycerides. bmi is, though, merely a proxy for adiposity, the principal issue driving insulin resistance. 18 as others have pointed out, whereas bmi continues to actually serve well for several purposes, the time might currently be right to maneuver towards standards of adiposity primarily based on direct measures of adipose tissue. 19 we might go additional still. as nonetheless, we grasp very little relating to the tracking of any metabolic risk issue however, just like a direct live of metabolic disturbance, insulin resistance, or its metabolic correlates, might ultimately prove the foremost useful live of all in the identification as to the kid at risk. understanding the pathogenesis of disease from its earliest development is crucial to actually its prevention. just like a prospective study, earlybird can always add to actually that understanding. in conclusion, the use of any bmi thresholds for overweight and obesity ought to be used with care in terribly young kids. just like a marker for abnormal metabolic indices, bmi won't meet screening criteria. whereas giving false reassurance to actually a few, others could be unnecessarily stigmatised. 8 classifying persons as ‘normal’ or otherwise, according to actually their bmi, elevates the live a screening tool to actually a diagnostic criterion. 20 till we are able to specify categories of risk related to childhood adiposity, populationbased approaches to actually the prevention of obesity are doubtless to actually be additional effective than approaches targeted at fat kids. 7 the use of iotf charts ought to be restricted to actually the aim for that these were devised – to actually assess population trends and to create international comparisons. acknowledgements we are grateful to actually diabetes uk, roche pharmaceuticals, the henry smith foundation, the earlybird diabetes trust, the diabetes foundation and of course the kid growth foundation. others who haven generously supported earlybird include abbott laboratories, gsk, astra-zeneca, ipsen, unilever analysis, the beatrice laing foundation, the london law trust and eli lilly.&lt;br /&gt;
 &lt;br /&gt;
References&lt;br /&gt;
1 Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. Establishing a&lt;br /&gt;
standard definition for child overweight and obesity worldwide:&lt;br /&gt;
international survey. BMJ 2000; 320: 1240–1243.&lt;br /&gt;
2 Hesketh K, Wake M, Waters E, Carlin J, Crawford D. Stability of&lt;br /&gt;
body mass index in Australian children; a prospective cohort&lt;br /&gt;
study across the middle childhood years. Public Health Nutr 2004;&lt;br /&gt;
7: 303–309.&lt;br /&gt;
3 Serdula MK, Ivery D, Coates RJ, Freedman DS, Williamson DF,&lt;br /&gt;
Byers T. Do obese children become obese adults? A review of the&lt;br /&gt;
literature. Prev Med 1993; 22: 167–177.&lt;br /&gt;
4 Guo SS, Roche AF, Chumlea WC, Gardner JD, Siervogel RM. The&lt;br /&gt;
predictive value of childhood body mass index values for&lt;br /&gt;
overweight at age 35y. Am J Clin Nutr 1994; 59: 810–819.&lt;br /&gt;
5 Williams S. Overweight at age 21: the association with body mass&lt;br /&gt;
index in childhood and adolescence and parents’ body mass&lt;br /&gt;
index. A cohort study of New Zealanders born in 1972–1973. Int J&lt;br /&gt;
Obes Relat Metab Disord 2001; 25: 158–163.&lt;br /&gt;
6 Braddon FE, Rodgers B, Wadsworth ME, Davies JM. Onset of&lt;br /&gt;
obesity in a 36 year birth cohort study. BMJ 1986; 293: 299–303.&lt;br /&gt;
7 Power C, Lake JK, Cole TJ. Body mass index and height from&lt;br /&gt;
childhood to adulthood in the 1958 British born cohort. Am J&lt;br /&gt;
Clin Nutr 1997; 66: 1094–1101.&lt;br /&gt;
8 Charney E. Childhood obesity: the measurable and the meaningful.&lt;br /&gt;
J Pediatr 1998; 132: 193–195.&lt;br /&gt;
9 World Health Organization Consultation on Obesity. Preventing&lt;br /&gt;
and managing the global epidemic: report of a WHO Consultation&lt;br /&gt;
on Obesity, Geneva, 3–5 June 1997. Geneva, Switzerland:&lt;br /&gt;
World Health Organization 1998; 1–276.&lt;br /&gt;
10 Han TS, Williams K, Sattar N, Hunt KJ, Lean ME, Haffner SM.&lt;br /&gt;
Analysis of obesity and hyperinsulinemia in the development of&lt;br /&gt;
metabolic syndrome: San Antonio Heart Study. Obes Res 2002; 10:&lt;br /&gt;
923–931.&lt;br /&gt;
11 Freedman DS, Dietz WH, Srinivasan SR, Berenson GS. The&lt;br /&gt;
relation of overweight to cardiovascular risk factors among&lt;br /&gt;
children and adolescents: the Bogalusa Heart Study. Pediatrics&lt;br /&gt;
1999; 103: 1175–1182.&lt;br /&gt;
12 Gungor N, Saad R, Janosky J, Arslanian S. Validation of surrogate&lt;br /&gt;
estimates of insulin sensitivity and insulin secretion in children&lt;br /&gt;
and adolescents. J Pediatr 2004; 144: 47–55.&lt;br /&gt;
13 Voss LD, Kirkby J, Metcalf BS, Jeffery AN, O’Riordan C, Murphy&lt;br /&gt;
MJ et al. Preventable factors in childhood that lead to insulin&lt;br /&gt;
resistance, diabetes and the metabolic syndrome: the EarlyBird&lt;br /&gt;
Diabetes Study (1). J Pediatr Endocrinol and Metab 2003; 16:&lt;br /&gt;
1211–1224.&lt;br /&gt;
14 Bonora E, Kiechl S, Willeit J, Oberhollenzer F, Egger G, Targher G&lt;br /&gt;
et al. Prevalence of insulin resistance in metabolic disorders: the&lt;br /&gt;
Bruneck Study. Diabetes 1998; 47: 1643–1649.&lt;br /&gt;
15 Sinaiko AR, Donahue RP, Jacobs DR, Prineas RJ. Relation of&lt;br /&gt;
weight and increase in weight during childhood and adolescence&lt;br /&gt;
to body size, blood pressure, fasting insulin, and lipids in young&lt;br /&gt;
adults. Circulation 1999; 99: 1471–1476.&lt;br /&gt;
16 Power C, Lake JK, Cole TJ. Measurement and long-term health&lt;br /&gt;
risks of child and adolescent fatness. Int J Obes Relat Metab Disord&lt;br /&gt;
1997; 21: 507–526.&lt;br /&gt;
17 Viner RM, Cole TJ. Adult socio-economic, educational,&lt;br /&gt;
social, and psychological outcomes of childhood obesity:&lt;br /&gt;
a national birth cohort study. BMJ 2005; 330: 1354. Epub 2005&lt;br /&gt;
May 17.&lt;br /&gt;
18 Grundy SM. Hypertriglyceridemia, insulin resistance,&lt;br /&gt;
and the metabolic syndrome. Am J Cardiol 1999; 83 (9B):&lt;br /&gt;
25F–29F.&lt;br /&gt;
19 Prentice AM, Jebb SA. Beyond body mass index. Obes Rev 2001; 2:&lt;br /&gt;
141–147.&lt;br /&gt;
20 Steelman M, Weiss WP, Maese F, Lechin M, Yanovski SZ, Yanovski&lt;br /&gt;
JA. Pharmacotherapy for obesity. N Engl J Med 2002; 346:&lt;br /&gt;
2092–2093.&lt;br /&gt;
 &lt;br /&gt;
Keywords: IOTF cutoffs; childhood overweight and obesity; BMI; screening for metabolic risk&lt;br /&gt;
</description><link>http://fatcampsforkids.blogspot.com/2012/09/learn-about-thresholds-for-overweight.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-1856909428028516246</guid><pubDate>Wed, 05 Sep 2012 02:07:00 +0000</pubDate><atom:updated>2012-09-04T19:07:49.925-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>KNOW ABOUT PSYCHOSOCIAL ASSESSMENTS CHILDREN’S DEPRESSION INVENTORY</title><description>&lt;br /&gt;
The Children’s Depression Inventory [4] is a 27-item, self-report measure and takes about 10 minutes&lt;br /&gt;
to complete. It is the most often used measure for child depression and is appropriate for use in&lt;br /&gt;
children and adolescents 7 to 17 years old. The individual is asked to select the statement that best&lt;br /&gt;
describes his or her feelings during the last 2 weeks. For each item, the child has three possible&lt;br /&gt;
answers: 0 = absence of symptoms, 1 = mild symptoms, and 2 = definite symptoms. A total score&lt;br /&gt;
and five scaled scores are generated for negative mood, interpersonal problems, ineffectiveness,&lt;br /&gt;
anhedonia, and negative self-esteem. A clinical cutoff score has been established to facilitate referral&lt;br /&gt;
to a mental health professional when necessary. Hand and computer scoring are available.&lt;br /&gt;
The normative sample included 1266 public school students (592 boys, 674 girls). Twenty-three&lt;br /&gt;
percent of the participants were African-American, American Indian, or Hispanic in origin. Twenty&lt;br /&gt;
percent of the children came from single-parent homes. In addition, the normative sample used for&lt;br /&gt;
scoring the Children’s Depression Inventory was divided into groups based on age (ages 6 to 11, 12&lt;br /&gt;
to 17) and gender. The internal consistency coefficients of the Children’s Depression Inventory range&lt;br /&gt;
from .71 to .89. Test–retest reliability coefficients (2 to 3-week time interval) range from .74 to .83.&lt;br /&gt;
REYNOLDS ADOLESCENT DEPRESSION SCALE 2&lt;br /&gt;
The Reynolds Adolescent Depression Scale 2 (RADS-2) [5,6] is a less frequently used adolescent selfreport&lt;br /&gt;
measure that consists of 30 items, rated on a 4-point scale, which takes 5 to 10 minutes to&lt;br /&gt;
complete. The RADS-2 yields five scores: overall depression, demoralization, worry and despondency,&lt;br /&gt;
somatic, and anhedonia. The RADS-2 is hand scored using a single scoring template. Internal consistency&lt;br /&gt;
coefficients for grades 7 to 12 range from .91 to .94. The RADS-2 has a total sample alpha&lt;br /&gt;
reliability of .92 and a split half reliability of .91. Test–retest coefficients of .80 and .79 are reported.&lt;br /&gt;
SELF-ESTEEM&lt;br /&gt;
PIERS–HARRIS CHILDREN’S SELF CONCEPT SCALE, SECOND EDITION&lt;br /&gt;
The Piers–Harris Children’s Self Concept Scale 2 [7–9] is the most widely used measure to date&lt;br /&gt;
of children and adolescent self-esteem. It is a revised version of the 80-item scale developed in&lt;br /&gt;
1969. It is appropriate for use with 7 to 18 year olds, and consists of 60 yes or no items. The&lt;br /&gt;
measure is designed to evaluate the child’s psychological health on the basis of their perceptions&lt;br /&gt;
and takes 10 to 15 minutes to complete. A total score and six subscale scores for physical appearance&lt;br /&gt;
and attributes, freedom from anxiety, intellectual and school status, behavior adjustment, happiness&lt;br /&gt;
and satisfaction, and popularity are generated.&lt;br /&gt;
The Piers-Harris-2 has new, nationally representative norms, which are based on a sample of&lt;br /&gt;
1387 students, ages 7 to 18 years, from across the United States. Because the revised scales remain&lt;br /&gt;
psychometrically equivalent to the original scales, results from the Piers–Harris 2 can be compared&lt;br /&gt;
with those obtained using the original test. Computer scoring and interpretation are available, as&lt;br /&gt;
is a Spanish version of the scale.&lt;br /&gt;
SELF-PERCEPTION PROFILE FOR CHILDREN&lt;br /&gt;
The Self-Perception Profile for Children [10] is a less frequently used, 36-item self-report scale.&lt;br /&gt;
A global self-worth score and five domain scores — scholastic competence, social acceptance,&lt;br /&gt;
athletic competence, physical appearance, and behavioral conduct — are generated. The manual&lt;br /&gt;
on the Self-Perception Profile for Children is a revised version of the Perceived Competence Scale&lt;br /&gt;
for Children. The reported internal reliability of subscales is (r = .73 to .86), and 9-month test–retest&lt;br /&gt;
reliability is r = .8.&lt;br /&gt;
ANXIETY&lt;br /&gt;
STATE-TRAIT ANXIETY INVENTORY FOR CHILDREN&lt;br /&gt;
The State-Trait Anxiety Inventory for Children (STAIC) [11] is composed of separate, self-report&lt;br /&gt;
scales for measuring two distinct anxiety concepts: state anxiety (S-Anxiety) and trait anxiety&lt;br /&gt;
(T-Anxiety). It is designed for use by 9 to 12 year olds. The STAIC requires about 10 minutes to&lt;br /&gt;
complete each scale, and children respond to items on a 3-point rating scale. The STAIC S-Anxiety&lt;br /&gt;
scale consists of 20 statements that ask children how they feel at a particular moment in time. The&lt;br /&gt;
S-Anxiety scale is designed to measure transitory anxiety; that is, subjective feelings of apprehension,&lt;br /&gt;
tension, and worry that vary in intensity and fluctuate over time. The STAIC T-Anxiety scale&lt;br /&gt;
also consists of 20 items, but children respond to these items by indicating how they generally feel.&lt;br /&gt;
The T-Anxiety scale measures more stable individual differences in anxiety proneness.&lt;br /&gt;
The normative group consisted of two large samples of fourth-, fifth-, and sixth-grade elementary&lt;br /&gt;
school children from six different schools.&lt;br /&gt;
MEASURES OF EATING DISORDERS&lt;br /&gt;
THE KIDS’ EATING DISORDER SURVEY&lt;br /&gt;
The Kids’ Eating Disorder Survey [12] is a 14-item self-report inventory of eating disorder attitudes&lt;br /&gt;
and behaviors. The instrument has been shown to have a 4-month test–retest reliability of r = 0.83 and&lt;br /&gt;
an internal consistency of Cronbach’s α = 0.73 in a sample of 1883 fifth- through eighth-grade students.&lt;br /&gt;
Children are asked to respond “yes”, “no”, or “I don’t know” to questions concerning five attitudes&lt;br /&gt;
and behaviors: desire to lose weight (Do you want to lose weight now?), feeling fat (Have you ever&lt;br /&gt;
thought that you looked fat to other people?), fear of gaining weight (Have you ever been afraid to eat&lt;br /&gt;
because you thought you would gain weight?), dieting to lose weight (Have you ever tried to lose&lt;br /&gt;
weight by dieting?), and fasting to lose weight (Have you ever tried to lose weight by fasting?).&lt;br /&gt;
THE EATING DISORDER INVENTORY&lt;br /&gt;
The Eating Disorder Inventory [13,14] is a commonly used, standardized, self-report screening&lt;br /&gt;
instrument for the assessment of specific eating attitudes and behavior commonly associated with&lt;br /&gt;
anorexia nervosa and bulimia nervosa. It is a revised version of the original measure published in&lt;br /&gt;
1984. The original 64 items were retained and are grouped into eight scales (drive for thinness,&lt;br /&gt;
bulimia, body dissatisfaction, ineffectiveness, perfectionism, interpersonal distrust, interoceptive&lt;br /&gt;
awareness, and maturity fears). Twenty-seven new items were added into three provisional scales&lt;br /&gt;
of asceticism, impulse regulation, and social insecurity.&lt;br /&gt;
Internal consistency reliability of the Eating Disorder Inventory 2 scales range between .44 and&lt;br /&gt;
.93, and test–retest reliability at 1-week ranges from .79 to .95 (for all subscales except interoceptive&lt;br /&gt;
awareness). Reliability and construct, convergent, and discriminant validity have been demonstrated&lt;br /&gt;
for the Eating Disorder Inventory, which has included use with adolescent populations.&lt;br /&gt;
THE EATING ATTITUDES TEST&lt;br /&gt;
The Eating Attitudes Test (EAT-26) [15,16] is a widely used, standardized, self-report, 20-item&lt;br /&gt;
screening measure adapted from the original 40-item test developed in 1979. The EAT-26 assesses&lt;br /&gt;
a broad range of symptoms and provides a total score for disturbed eating attitudes and behavior&lt;br /&gt;
in adolescents. The EAT-26 has acceptable criterion-related validity by significantly predicting&lt;br /&gt;
group membership. The reliability (internal consistency) of the EAT-26 was reportedly high (α =&lt;br /&gt;
0.90) for an anorexia nervosa group. Total scores on the EAT-26 are derived as a sum of all items,&lt;br /&gt;
ranging from 0 to 78. Scores that are greater than or equal to 20 on the EAT-26 are frequently&lt;br /&gt;
associated with abnormal eating attitudes and behavior and may identify those with an eating&lt;br /&gt;
disorder. The EAT-26 manual clarifies that although a score of 20 or higher is a cause of concern,&lt;br /&gt;
it does not necessarily mean that a life-threatening condition exists. As such, individuals scoring&lt;br /&gt;
20 or higher on this test are encouraged to seek the advice of a qualified mental health professional&lt;br /&gt;
who has experience with treating eating disorders.&lt;br /&gt;
THE DIAGNOSTIC SURVEY FOR EATING DISORDERS&lt;br /&gt;
The Diagnostic Survey for Eating Disorders (DSED) [17] is a self-report questionnaire that allows&lt;br /&gt;
for the quantification of the frequency of disturbed eating behaviors. The DSED was not developed&lt;br /&gt;
as a standardized, scaled instrument but, instead, provides a format for the collection of information&lt;br /&gt;
about eating and purging behaviors. Despite having been widely used, the reliability of the DSED&lt;br /&gt;
has not been reported, mainly because the self-reported eating and purging behaviors that are&lt;br /&gt;
assessed appear to be somewhat changeable over time.</description><link>http://fatcampsforkids.blogspot.com/2012/09/know-about-psychosocial-assessments.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-4737045256102095147</guid><pubDate>Wed, 05 Sep 2012 02:06:00 +0000</pubDate><atom:updated>2012-09-04T19:06:51.562-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF SOCIAL SKILLS RATING SYSTEM </title><description>The Social Skills Rating System [3] has been used much less frequently and allows professionals to screen and classify children and adolescents suspected of having significant social behavior problems. A teacher, parent, and self-report form are available and take about 15 minutes to complete. The respondent is asked to report how often the child or teen engages in 39 to 49 statements as 0 = never, 1 = sometimes true, or 2 = very often true. The Social Skills Rating System can be scored by hand or computer. A score is generated for social skills (cooperation, assertion, responsibility, empathy, and self-control), problem behaviors (externalizing problems, internalizing problems, and hyperactivity), and academic competence. The test–retest reliability of the Social Skills Rating System ranges from .65 to .93, whereas coefficient alpha reliability ranges from .81 to .85. The subscale reliabilities range from .48 to .88.</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-social-skills-rating.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-1243602475016074479</guid><pubDate>Wed, 05 Sep 2012 02:06:00 +0000</pubDate><atom:updated>2012-09-04T19:06:24.331-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF ACHENBACH CHILD BEHAVIOR CHECKLIST </title><description>The Achenbach Child Behavior Checklist (CBCL) [1,2], parent form, is likely to be the most widely used standardized behavior problem assessment tool of obese children and adolescents, aged 6 to 18 years. The scale takes about 15 minutes to complete and consists of 118 items or statements that describe specific behavioral and emotional problems, with two open-ended items for reporting additional problems. Parents rate their child for how true each item is now or within the last 6 months, using the following scale: 0 = not true; 1 = somewhat or sometimes true; 2 = very true. The CBCL can be hand or computer scored. A total behavior problem (T) score is obtained, as are T scores for two broad categories: internalizing (e.g., withdrawn, depressed) and externalizing (e.g., acting out, aggression). The CBCL is further divided into T scores for eight subcategories of problematic behavior: aggressive behavior, anxious/depressed, attention problems, rule-breaking behavior, social problems, somatic complaints, thought problems, and withdrawn/depressed. There are also six DSM -oriented scales: affective problems, anxiety problems, somatic problems, attention deficit/hyperactivity problems, oppositional defiant problems, and conduct problems. In general, a T score greater than 67 indicates significant behavior problems in that category. There is also a social competence scale that yields a total T score, as well as T scores for involvement in activities, social interactions, and school performance. A T score less than 33 on the social competence scale indicates problems. The CBCL has been well standardized, and norms exist for both clinic-referred and normative populations. The items of the CBCL were factor analyzed to empirically identify the forms of psychopathology that actually occur in children. Further, the scales are based on new factor analyses of parents’ ratings of 4994 clinically referred children and were normed on 1753 children aged 6 to 18 years. The normative sample was reportedly representative of the 48 contiguous states across socioeconomic status, ethnicity, region, and urban–suburban–rural residence. Children were excluded from the normative sample if they had been referred for mental health or special education services within the last year. The CBCL is also available in a newly revised Spanish version. A teacher version and youth self-report version are also available, but they have been used much less frequently.</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-achenbach-child-behavior.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-7762780573969325915</guid><pubDate>Wed, 05 Sep 2012 02:05:00 +0000</pubDate><atom:updated>2012-09-04T19:05:51.654-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF BEHAVIORAL AND PSYCHOSOCIAL ASSESSMENT TOOLS</title><description>&lt;!--[if gte mso 9]&gt;&lt;xml&gt;  &lt;w:WordDocument&gt;   &lt;w:View&gt;Normal&lt;/w:View&gt;   &lt;w:Zoom&gt;0&lt;/w:Zoom&gt;   &lt;w:TrackMoves/&gt;   &lt;w:TrackFormatting/&gt;   &lt;w:PunctuationKerning/&gt;   &lt;w:ValidateAgainstSchemas/&gt;   &lt;w:SaveIfXMLInvalid&gt;false&lt;/w:SaveIfXMLInvalid&gt;   &lt;w:IgnoreMixedContent&gt;false&lt;/w:IgnoreMixedContent&gt;   &lt;w:AlwaysShowPlaceholderText&gt;false&lt;/w:AlwaysShowPlaceholderText&gt;   &lt;w:DoNotPromoteQF/&gt;   &lt;w:LidThemeOther&gt;EN-US&lt;/w:LidThemeOther&gt;   &lt;w:LidThemeAsian&gt;X-NONE&lt;/w:LidThemeAsian&gt;   &lt;w:LidThemeComplexScript&gt;X-NONE&lt;/w:LidThemeComplexScript&gt;   &lt;w:Compatibility&gt;    &lt;w:BreakWrappedTables/&gt;    &lt;w:SnapToGridInCell/&gt;    &lt;w:WrapTextWithPunct/&gt;    &lt;w:UseAsianBreakRules/&gt;    &lt;w:DontGrowAutofit/&gt;    &lt;w:SplitPgBreakAndParaMark/&gt;    &lt;w:DontVertAlignCellWithSp/&gt;    &lt;w:DontBreakConstrainedForcedTables/&gt;    &lt;w:DontVertAlignInTxbx/&gt;    &lt;w:Word11KerningPairs/&gt;    &lt;w:CachedColBalance/&gt;   &lt;/w:Compatibility&gt;   &lt;w:BrowserLevel&gt;MicrosoftInternetExplorer4&lt;/w:BrowserLevel&gt;   &lt;m:mathPr&gt;    &lt;m:mathFont m:val="Cambria Math"/&gt;    &lt;m:brkBin m:val="before"/&gt;    &lt;m:brkBinSub m:val="--"/&gt;    &lt;m:smallFrac m:val="off"/&gt;    &lt;m:dispDef/&gt;    &lt;m:lMargin m:val="0"/&gt;    &lt;m:rMargin m:val="0"/&gt;    &lt;m:defJc m:val="centerGroup"/&gt;    &lt;m:wrapIndent m:val="1440"/&gt;    &lt;m:intLim m:val="subSup"/&gt;    &lt;m:naryLim m:val="undOvr"/&gt;   &lt;/m:mathPr&gt;&lt;/w:WordDocument&gt; &lt;/xml&gt;&lt;![endif]--&gt;&lt;!--[if gte mso 9]&gt;&lt;xml&gt;  &lt;w:LatentStyles DefLockedState="false" DefUnhideWhenUsed="true"
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Some cross-sectional, population-based studies of children and adolescents report little to no&lt;br /&gt;
differences on standardized psychosocial or behavioral assessment measures in obese and nonobese&lt;br /&gt;
subjects, whereas many reports have documented significant differences between these groups. The&lt;br /&gt;
same is true when examining longitudinal, population-based studies of obese versus nonobese&lt;br /&gt;
children and adolescents. Some researchers have reported significant differences, particularly in&lt;br /&gt;
adolescent females, whereas others have failed to observe significant differences between groups.&lt;br /&gt;
There are also discrepancies in data collected from clinic-referred samples of obese children and&lt;br /&gt;
adolescents. Some researchers report little to no differences, yet most researchers have reported&lt;br /&gt;
significant differences. The discrepancies found in these studies have been postulated to relate to&lt;br /&gt;
differences in the study group’s social status, age, sex, ethnicity, geographic region, and parental&lt;br /&gt;
factors, and even recent trends toward a heavier population of children and adolescents. This&lt;br /&gt;
controversy is compounded by the fact that many of the reviewed studies have failed to use&lt;br /&gt;
standardized or psychometrically sound psychosocial or behavioral measures. In addition, in some&lt;br /&gt;
cases, the standardized assessment used across studies has been abbreviated, dissimilar, or a newer&lt;br /&gt;
version of the original measure. This chapter summarizes standardized behavioral and psychosocial instruments that have been&lt;br /&gt;
widely used in baseline and follow-up assessment of overweight children and adolescents in both&lt;br /&gt;
population-based and clinic-referred samples. This is not meant to be a comprehensive listing of&lt;br /&gt;
behavioral or psychosocial assessment instruments available to clinicians but, instead, details those&lt;br /&gt;
assessments that have been most widely used to date. Though standardized, psychometrically sound&lt;br /&gt;
assessments take 10 to 15 minutes to complete, future research should attempt to use these measures,&lt;br /&gt;
when possible, to allow for more accurate comparisons within and between study groups.&lt;br /&gt;
&lt;span style="font-family: &amp;quot;Optima-Medium&amp;quot;,&amp;quot;sans-serif&amp;quot;; font-size: 24.0pt; font-variant: small-caps; line-height: 115%; mso-bidi-font-family: Optima-Medium;"&gt;&lt;br /&gt;
&lt;/span&gt;&lt;span style="font-variant: small-caps;"&gt;&lt;/span&gt;  </description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-behavioral-and.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-5124896878793384800</guid><pubDate>Wed, 05 Sep 2012 02:04:00 +0000</pubDate><atom:updated>2012-09-04T19:04:19.705-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>KNOW ABOUT RELATIONSHIP BETWEEN CONSUMPTION OF SUGAR SWEETENED DRINKS AND CHILDHOOD OBESITY</title><description>1. Hedley A, Ogden C, Johnson C, Carroll M, Curtin L, Flegal K. Prevalence of overweight and obesity&lt;br /&gt;
among US children, adolescents, and adults, 1999–2002. JAMA. 2004;291:2847–2850.&lt;br /&gt;
2. Bao W, Srinivasan SR, Wattigniey WA, Berenson GS. Persistance of multiple cardiovascular risk&lt;br /&gt;
clustering related to syndrome X from childhood to adulthood. The Bogalusa Heart Study. Arch Intern&lt;br /&gt;
Med. 1994;1954:1842–1847.&lt;br /&gt;
3. Economic Research Service, UDSA. Food Rev. 2002;25(3).&lt;br /&gt;
4. French SA, Story M, Newmark-Szainer D, Fulkerson JA, Hannan P. Fast food restaurant use among&lt;br /&gt;
adolescents: associations with nutrient intake, food choices and behavioral and psychosocial variables.&lt;br /&gt;
Intl J Obes. 2001;25:1823–1833.&lt;br /&gt;
5. Bowman SA, Gortmaker SL, Ebbeling CB, Pereira MA, Ludwig DS. Effects of fast-food consumption&lt;br /&gt;
on energy intake and diet quality among children in a national household survey. Pediatrics.&lt;br /&gt;
2004;113:112–118.&lt;br /&gt;
6. Zoumas-Morse C, Rock CL, Sobo EJ, Neuhouser ML. Children’s pattern of macronutrient intake and&lt;br /&gt;
associations with restaurant and home eating. J Amer Diet Assoc. 2001;101:923–925.&lt;br /&gt;
7. Gillman MW, Rifas-Shiman SL, Fraiser AL. Family dinner and diet quality among older children and&lt;br /&gt;
adolescents. Arch Family Med. 2000;9:235–240.&lt;br /&gt;
8. Grimm GC, Harnack L, Story M. Factors associated with soft drink consumption in school-aged&lt;br /&gt;
children. J Amer Diet Assoc. 2004;104:1244–1249.&lt;br /&gt;
9. Kimm SY, Glynn NW, Kriska AM, Barton BA, Kronsberg SS, Daniels SR et al. Decline in physical&lt;br /&gt;
activity in black girls and white girls during adolescence. New Engl J Med. 2002;5;347:709–715.&lt;br /&gt;
10. McMurray RG, Harrell JS, Deng S, Bradley CB, Cox LM, Bangdiwala. The influence of physical&lt;br /&gt;
activity, socioeconomic status, and ethnicity on weight status of adolescents. Obes Res. 2000;8:130–139.&lt;br /&gt;
11. Anderson RE, Crespo CJ, Bartlett SJ, Cheskin LJ, Pratt M. Relationship of physical activity and television&lt;br /&gt;
watching with body weight and level of fatness among children. JAMA. 1998;279(12):938–942.&lt;br /&gt;
12. American Academy of Pediatrics. Committee on Communications. Children adolescents, and television.&lt;br /&gt;
Pediatrics. 1995;96:786–787.&lt;br /&gt;
13. American Academy of Pediatrics. Committee on Nutrition. Prevention of pediatric overweight and&lt;br /&gt;
obesity. Pediatrics. 2003;112(2):424–430.&lt;br /&gt;
14. Watt RG. Stages of change for sugar and fat reduction in an adolescent sample. Commun Dental&lt;br /&gt;
Health. 1996;14:102–107.&lt;br /&gt;
15. Curry SJ, Kristal AR, Bowen DJ. An application of the stage of change model of behavior change to&lt;br /&gt;
dietary fat restriction. Health Educ Res. 1992;7:97–105.&lt;br /&gt;
16. Patrick K, Spear B, Holt K, Sofka D. Eds. Bright Futures in Practice: Physical Activity. Arlington,&lt;br /&gt;
VA: National Center for Education in Maternal and Child Health, 2002.&lt;br /&gt;
17. Story M, Holt K, Sofka D. Eds. Bright Futures in Practice: Nutrition. Arlington, VA: National Center&lt;br /&gt;
for Education in Maternal and Child Health, 2002.&lt;br /&gt;
18. American Dietetic Association. Position of the American Dietetic Association: Nutrition intervention&lt;br /&gt;
in the treatment of anorexia nervosa, bulimia nervosa, and eating disorders not otherwise specified&lt;br /&gt;
(EDNOS). J Amer Diet Assoc. 2001;101:810–819.&lt;br /&gt;
19. Garner DM, Garfinkel PE. Eds. Handbook of Treatment for Eating Disorders. New York: Guilford&lt;br /&gt;
Press, 1997.&lt;br /&gt;
20. Bandini LG, Schoeller DA, Cyr HN, Dietz WH. Validity of reported energy intakes in obese and nonobese&lt;br /&gt;
adolescents. Amer J Clin Nutr. 1990;52:421–425.&lt;br /&gt;
21. Copperman N, Jacobson MS. Medical nutritional therapy for the treatment of adolescent overweight.&lt;br /&gt;
In: Fisher M, Golden N, Eds. Adolescent Medicine: State of the Art Reviews: Spectrum of Disordered&lt;br /&gt;
Eating: Anorexia Nervosa, Bulimia Nervosa and Obesity. Chicago: American Academy of Pediatrics,&lt;br /&gt;
2003: pp. 11–22.&lt;br /&gt;
22. Johnson RK, Driscoll P, Goran MI. Comparison of multiple-pass 24-hour recall estimates of energy&lt;br /&gt;
intake with total energy expenditure determined by the doubly labeled water method in young children.&lt;br /&gt;
J Amer Diet Assoc. 1996;96:1140–1144.&lt;br /&gt;
23. Johnson SL, Birch LL. Parents’ and children’s adiposity and eating style. Pediatrics. 1994;94:653–661.&lt;br /&gt;
24. Drabman RS, Cordura GD, Hammer D, Jarvie GJ, Horton W. Developmental trends in eating rates&lt;br /&gt;
of normal and overweight preschool children. Child Devel. 1979;50:211–216.&lt;br /&gt;
25. Marston AR, London P, Cooper LM. A note on the eating behavior of children varying in weight.&lt;br /&gt;
J Child Psychol Psych. 1976;17:221–225.&lt;br /&gt;
26. Barkling B, Ekman S, Rossner S. Eating behaviour in obese and normal weight 11-year-old children.&lt;br /&gt;
Intl J Obes. 1992;16:355–360.&lt;br /&gt;
27. Fisher JO, Rolls BJ, Birch LL. Children’s bite size and intake of an entrée are greater with large&lt;br /&gt;
portions than with age-appropriate or self-selected portions. Amer J Clin Nutr. 2003;77:1164–1170.&lt;br /&gt;
28. Ludwig DS, Peterson KE, Gortmaker SL. Relationship between consumption of sugar sweetened&lt;br /&gt;
drinks and childhood obesity: a prospective, observational analysis. Lancet. 2001;357:505–508.&lt;br /&gt;
29. Frary CD, Johnson RK, Wang MQ. Children and adolescents’ choices of foods and beverages high&lt;br /&gt;
in added sugars are associated with intakes of key nutrients and food groups. J Adolesc Health.&lt;br /&gt;
2004;34:56–63.&lt;br /&gt;
30. Barlow E, Deitz, WH. Obesity evaluation and treatment: Expert Committee recommendations. Pediatrics.&lt;br /&gt;
1998;102(3):1–11.</description><link>http://fatcampsforkids.blogspot.com/2012/09/know-about-relationship-between.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-3359678213935244227</guid><pubDate>Wed, 05 Sep 2012 02:03:00 +0000</pubDate><atom:updated>2012-09-04T19:03:26.291-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF NUTRITIONAL CARE PLAN AND CASE MANAGEMENT</title><description>&lt;br /&gt;
Once the nutritional assessment has been completed, the practitioner can refer to the recommendations&lt;br /&gt;
of Barlow and Dietz for weight goals. Depending on the age, BMI, and comorbidities&lt;br /&gt;
present, weight-maintenance or weight-loss goals have been recommended for children ages 2 to&lt;br /&gt;
7 years and 7 years and older (see Figures 8.1 and 8.2). It is important to note that a weight loss&lt;br /&gt;
goal of 1 pound per month is recommended with an appropriate weight goal below the 85% for&lt;br /&gt;
BMI for age and sex. Before their pubertal growth spurt, children usually grow 2 inches per year.&lt;br /&gt;
Each inch in growth without subsequent weight gain represents approximately a 5-pound weight&lt;br /&gt;
loss, as demonstrated by a reduction in BMI. A child who loses 1 pound per month for a year and&lt;br /&gt;
gains 2 inches in height during that year, even though he or she only loses 12 lb, actually exhibits&lt;br /&gt;
almost a 22-lb weight loss, resulting in a significant reduction in BMI and BMI percentile. Explaining&lt;br /&gt;
the rationale of the recommended weight goals to children, adolescents, and their families can&lt;br /&gt;
help clarify unrealistic weight loss expectations and lead to more attainable weight goals.&lt;br /&gt;
The practitioner can adapt the intensity of lifestyle interventions to the severity of the overweight&lt;br /&gt;
condition, the findings of nutritional assessment, the readiness of the child or adolescent and family&lt;br /&gt;
to make lifestyle modifications, and the clinical resources available in the community. In other&lt;br /&gt;
chapters of this book, several nutrition, physical activity, and behavioral interventions and their&lt;br /&gt;
appropriateness will be discussed. A common aspect of all these interventions/programs is frequent&lt;br /&gt;
visits with the staff, such as weekly, biweekly, or monthly for an extended period of time greater&lt;br /&gt;
than 1 year. Each practitioner should communicate with other disciplines (medical, nutrition,&lt;br /&gt;
psychology, exercise) involved in the care of the child or adolescent to coordinate and provide&lt;br /&gt;
optimum care. Weight management for the at risk for overweight or the overweight pediatric patient&lt;br /&gt;
and his or her family should include an interdisciplinary approach to modify the families’ nutritional&lt;br /&gt;
and physical activity patterns to enable them to attain the needed skills for a lifetime of weight&lt;br /&gt;
management.</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-nutritional-care-plan-and.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-2832192250987605115</guid><pubDate>Wed, 05 Sep 2012 02:03:00 +0000</pubDate><atom:updated>2012-09-04T19:03:03.760-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF PHYSICAL AND LABORATORY ASSESSMENTS</title><description>&lt;br /&gt;
In the context of nutritional assessment of the at risk for overweight or overweight child or&lt;br /&gt;
adolescent, physical findings obtained by a medical exam, coupled with anthropometrics, blood&lt;br /&gt;
pressure measurements, and laboratory assessments obtained by a health professional, are important&lt;br /&gt;
in the formulation of weight management goals and evaluation of treatment outcomes. Initial&lt;br /&gt;
assessment of anthropometrics including accurate height and weight measurements, calculation of&lt;br /&gt;
BMI, and correct plotting of data points on age- and sex-appropriate growth charts enables the&lt;br /&gt;
practitioner to assess the weight status of the child or adolescent. This assessment along with the&lt;br /&gt;
absence or presence of any comorbidity allows the practitioner to determine weight management&lt;br /&gt;
goals (see Figures 8.1 and 8.2) [30].&lt;br /&gt;
Anthropometrics are the most widely used clinical tool in the evaluation of pediatric growth&lt;br /&gt;
and development. In assessing the overweight status of a child or adolescent, accurate and reliable&lt;br /&gt;
weight and height measurements are essential because they will be used to calculate the BMI&lt;br /&gt;
(weight [kg]/height [m2]). Weights can be recorded on a digital or triple-beam balance scale, and&lt;br /&gt;
heights can be measured by a wall-mounted stadiometer. Children and adolescents should be&lt;br /&gt;
gowned and in bare feet. Some pediatric patients refuse to wear gowns; therefore, they should be&lt;br /&gt;
instructed to bring the same lightweight clothing to every visit for anthropometric measurements.&lt;br /&gt;
The practitioner should also stock large adult gowns suitable for adolescents weighing over 200 lbs&lt;br /&gt;
in addition to pediatric gowns. Heights should be measured on a wall-mounted stadiometer with&lt;br /&gt;
the child or adolescent in bare feet; he or she should be standing comfortably erect against a&lt;br /&gt;
perpendicular measuring unit with a sliding headboard (wall-mounted stadiometer). The feet should&lt;br /&gt;
be as close together as possible, and the heels, buttocks, and shoulders should touch the measuring&lt;br /&gt;
unit. The headboard should be lowered against the top of the head with the head upright and the&lt;br /&gt;
chin parallel to the floor. The height, weight, and calculated BMI can be plotted on appropriate&lt;br /&gt;
Centers for Disease Control and Prevention age and gender growth charts. More information on&lt;br /&gt;
calculating BMI and plotting anthropometrics is available at http://www.cdc.gov/nchs. Serial laboratory&lt;br /&gt;
assessments, height and weight measurements, and BMI calculations provide a method of&lt;br /&gt;
formulating initial treatment goals and evaluating treatment outcomes as long as the measurements&lt;br /&gt;
are consistent and accurate.&lt;br /&gt;
Other physical findings are important components in nutritional assessment. Tanner Staging,&lt;br /&gt;
which assigns a stage of sexual development to the child or adolescent, can be used to assess the&lt;br /&gt;
growth potential of a child or adolescent. Menstrual history for females is also important for&lt;br /&gt;
assessment of growth potential, as the female adolescent’s growth spurt generally occurs in the year&lt;br /&gt;
before the onset of menses. By monitoring weight fluctuations during the menstrual cycle, the&lt;br /&gt;
practitioner can track weight status according to the effect of fluid retention before menses (wet&lt;br /&gt;
weight) and diuresis postmenses (dry weight) to assess overall anthropometric response to lifestyle&lt;br /&gt;
changes. The presence of acanthosis nigricans is significant in that it is a cutaneous marker of&lt;br /&gt;
insulin resistance. All of these physical and laboratory findings highlight the importance of a&lt;br /&gt;
multidisciplinary team approach to the evaluation of the overweight child or adolescent.&lt;br /&gt;
Educating the child or adolescent and family about the significance of abnormal physical&lt;br /&gt;
findings and laboratory assays, BMI, and the BMI percentiles can be a useful counseling tool in&lt;br /&gt;
pediatric weight management. Using the changes in laboratory parameters and physical findings as&lt;br /&gt;
outcome measures for evaluating the progress of the child or adolescent can help the family reduce&lt;br /&gt;
the emphasis on weight as the only outcome. Reduction of cardiac risk factors coupled with a stable&lt;br /&gt;
weight or BMI will positively affect health outcomes for the child or adolescent. Understanding the importance of multiple outcomes as a measure of progress toward weight management can enable&lt;br /&gt;
the child or adolescent and family to realize that healthy eating and exercise are lifelong commitments.</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-physical-and-laboratory.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-2805545758608803849</guid><pubDate>Wed, 05 Sep 2012 02:02:00 +0000</pubDate><atom:updated>2012-09-04T19:02:12.782-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF DIETARY INTAKE ASSESSMENT</title><description>&lt;br /&gt;
The self-report of dietary intake by overweight children and adults has been shown to be inaccurate.&lt;br /&gt;
Researchers have shown that food records from overweight pediatric patients tend to underestimate&lt;br /&gt;
caloric intake when compared with actual energy expenditure [20]. The assessment of the dietary&lt;br /&gt;
intake of overweight children and adolescents can be performed using a global assessment that is&lt;br /&gt;
composed of self-administered 3-day food records, nutrition questionnaires, and a dietary interview&lt;br /&gt;
performed by a registered dietitian [21] or other health professional. By using self-report coupled&lt;br /&gt;
with a dietary interview, the resulting nutritional intake data can be more reliable for the practitioner.&lt;br /&gt;
The use of either the global assessment or an individual component will depend on personnel, time&lt;br /&gt;
constraints, technology, and clinical care needs.&lt;br /&gt;
The global assessment requires the child or adolescent and family to be trained in the recording&lt;br /&gt;
of a 3-day food record (2 weekdays and 1 weekend day). The training includes educating the child&lt;br /&gt;
and family on how to list (including times and places the foods were consumed) and describe&lt;br /&gt;
(portion size, brand, food preparation) all foods and beverages consumed over the 3-day period.&lt;br /&gt;
The recorders need to know how to record accurate portion sizes or amounts of all food consumed&lt;br /&gt;
inside and outside of the home. A packet containing contact information for a person of whom the&lt;br /&gt;
family can ask questions related to the food records, food recording sheets, written instructions,&lt;br /&gt;
and pictorial methods of describing foods will improve the quality of the records. For younger&lt;br /&gt;
children in daycare centers or at babysitters’ homes, the caretaker needs to be involved in this food&lt;br /&gt;
recording process. Adding questions to the end of each day’s recording that prompt for missing&lt;br /&gt;
items, assessment of daily intake (less, more, or typical), and completeness of record (complete,&lt;br /&gt;
incomplete) can improve accuracy and analysis. The practitioner can explain to the family that the&lt;br /&gt;
purpose of the record is to accurately represent what the child or adolescent is eating rather than&lt;br /&gt;
judge whether his or her diet is “good or bad.” Adolescents may prefer to complete their records&lt;br /&gt;
on their own with the understanding that the analysis will be kept confidential and not shared with&lt;br /&gt;
their parents. If the child or adolescent spends time in two households, two sets of food records&lt;br /&gt;
may be warranted.&lt;br /&gt;
The food records offer the child or adolescent and family the opportunity to actually reflect on&lt;br /&gt;
what types and amounts of foods are eaten, as well as where they are consuming these foods. This&lt;br /&gt;
simple form of self-monitoring can be very enlightening for the child or adolescent, family, and&lt;br /&gt;
practitioner. In research settings, a 24-hour multiple-day food record pass may be used. In this&lt;br /&gt;
case, the child, adolescent, and family receive similar training to that above, but the dietary intake&lt;br /&gt;
data is collected by means of a 24-hour food recall and 24-hour food record, reviewed by a dietitian&lt;br /&gt;
either in person or via telephone. This method was found to be more reliable for group intakes&lt;br /&gt;
than for individual intakes [22].&lt;br /&gt;
The food records can be returned before the counseling session and analyzed with computer&lt;br /&gt;
software. Several nutrient analysis programs are available, and their features vary according to their&lt;br /&gt;
cost. The practitioner must determine the needs of the practice such as client education, clinical&lt;br /&gt;
care, research, or a combination of these. If the records are to be used for research, then the accuracy&lt;br /&gt;
and scope of the database; the flexibility of analysis of meals, snacks, foods, and food components;&lt;br /&gt;
and the ease of export of nutritional data for statistical analysis using commercial software would&lt;br /&gt;
be of concern to the researcher. In clinical care situations, the accuracy of the database, ease of&lt;br /&gt;
data entry, cost, and client education reports would be of greater importance. Some practitioners&lt;br /&gt;
may choose not to formally analyze the food records but, rather, to clinically review them to assess&lt;br /&gt;
for overall dietary quality.&lt;br /&gt;
Nutritional questionnaires include food frequency questionnaires that inquire how many times&lt;br /&gt;
in a specified time period a person consumes certain foods, beverages, or food groups. The format&lt;br /&gt;
of the questionnaire can require the respondent to provide a written answer to a question or circle&lt;br /&gt;
a response on a scale. The answers to the questions can be used in conjunction with a Likert Scale,&lt;br /&gt;
which can be used to score the questionnaire. The score can then be used to evaluate the quality&lt;br /&gt;
of the diet. Limitations of this method include the validity of the measurement or questionnaire&lt;br /&gt;
and the scope of the nutrient information obtained. The advantage of nutritional questionnaires is&lt;br /&gt;
that they are easy to administer, require minimal patient training, are inexpensive, and can be&lt;br /&gt;
designed to address specific eating patterns and food consumption. Health professionals, other than&lt;br /&gt;
registered dietitians, may find this measure easier to interpret than a formal food record nutrient&lt;br /&gt;
analysis.&lt;br /&gt;
The third component of nutrient intake assessment is a dietary interview. The dietary interview&lt;br /&gt;
is usually conducted by a registered dietitian or other health professional with nutrition training.&lt;br /&gt;
The interview comprises a nutrition history of allergies, supplements, medications, and past feeding&lt;br /&gt;
practices; recent changes to child or adolescent or family diets; typical intake for meals and snacks&lt;br /&gt;
for weekdays and weekends, including foods and beverages eaten inside and outside the home;&lt;br /&gt;
schedule of meals/snacks; current feeding practices; and child or adolescent and family nutritional&lt;br /&gt;
concerns or conflicts. If the child or adolescent spends time in multiple households or has multiple&lt;br /&gt;
caretakers, all parents or caretakers should be interviewed either in person or by phone when possible.&lt;br /&gt;
Feeding practices that have been related to overweight in children and adolescents have been&lt;br /&gt;
identified. They include parental restriction of childhood eating [23], speed of eating [24–26],&lt;br /&gt;
increased portion size [27], increased consumption of soda [28], and frequency of fast food meals&lt;br /&gt;
[5]. Children ages 6 to 11 years consume on average only 2.5 servings of fruit and vegetables per&lt;br /&gt;
day, which is only half of their recommended 5 servings per day. Data from the National Health&lt;br /&gt;
and Nutrition Examination Survey (NHANES) III survey indicate that adolescents consume less&lt;br /&gt;
than one third of their recommended fruit and vegetable intakes [3]. Data from the 1994–1996 and&lt;br /&gt;
1998 U.S. Department of Agriculture Continuing Survey of Food Intakes by Individuals for youth,&lt;br /&gt;
ages 6 to 17 years, indicate that individuals with increased consumption of sugar-sweetened&lt;br /&gt;
beverages, sugars and sweets, and sweetened grains had a decreased likelihood of meeting the&lt;br /&gt;
dietary reference intakes for calcium, folate, and iron [29].&lt;br /&gt;
The information from the dietary intake assessment should identify overly consumed, highcalorie,&lt;br /&gt;
nutrient-sparse foods and beverages; locations and times that these foods are consumed;&lt;br /&gt;
feeding practices that promote the overconsumption of these foods; and child or adolescent and&lt;br /&gt;
family awareness of these eating behaviors. In addition, nutrient intake deficiencies such as inadequate&lt;br /&gt;
intakes of calcium, fiber, iron, folic acid, and fat-soluble and water-soluble vitamins should&lt;br /&gt;
become apparent. Identifying obesegenic feeding practices and nutrient intake deficiencies can aid&lt;br /&gt;
the practitioner, child or adolescent, and family to develop strategies to modify these eating behaviors.</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-dietary-intake-assessment.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-3891829230003146176</guid><pubDate>Wed, 05 Sep 2012 02:01:00 +0000</pubDate><atom:updated>2012-09-04T19:01:27.730-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF PSYCHOSOCIAL ASSESSMENT</title><description>&lt;br /&gt;
An assessment of the child’s/adolescent’s and family’s readiness to make lifestyle changes is an&lt;br /&gt;
important barometer of whether weight-management interventions will be effective. Several studies&lt;br /&gt;
in adults and adolescents have shown that stage of change can influence behavioral change [14,15].&lt;br /&gt;
An adolescent who is ambivalent about modifying his or her lifestyle may exhibit opposition and&lt;br /&gt;
poor adherence to weight-management interventions, leading to subsequent program failure and&lt;br /&gt;
weight gain. A family who is not ready to make lifestyle changes will not provide a supportive&lt;br /&gt;
environment for their child. By identifying the older child’s/adolescent’s and family’s readiness to&lt;br /&gt;
change, the practitioner can integrate specific counseling strategies related to their stage of change&lt;br /&gt;
into the weight management intervention. A tool for addressing these stages of change and developing&lt;br /&gt;
appropriate intervention strategies can be found in the tool section of Bright Futures in&lt;br /&gt;
Practice: Physical Activity [16].&lt;br /&gt;
Overweight children and adolescents can present psychological manifestations that include low&lt;br /&gt;
self-esteem, poor peer socialization, and depression. Overweight children and adolescents may also&lt;br /&gt;
have eating disorders such as bulimia and binge-eating disorders. Screening children and adolescents&lt;br /&gt;
for psychological issues and eating disorders is an important component of the nutritional assessment.&lt;br /&gt;
Several screening tools are available [17–19]. If any of these psychological disorders is&lt;br /&gt;
suspected, referral for a comprehensive psychological evaluation is warranted. In the case of a&lt;br /&gt;
suspected eating disorder, an evaluation by a multidisciplinary team that specializes in pediatric&lt;br /&gt;
eating disorders is recommended.</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-psychosocial-assessment.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-8988222369442681999</guid><pubDate>Wed, 05 Sep 2012 02:00:00 +0000</pubDate><atom:updated>2012-09-04T19:00:59.378-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF PHYSICAL ACTIVITY ASSESSMENT</title><description>&lt;br /&gt;
Recent data have shown that children and adolescents in the United States have become more&lt;br /&gt;
sedentary, with significant declines in physical activity as children, especially females, become&lt;br /&gt;
adolescents [9]. Increased body mass index (BMI) has been correlated to increased hours spent&lt;br /&gt;
television viewing as well as increased time playing video games [10,11]. The American Academy&lt;br /&gt;
of Pediatrics recommends less than 2 hours of television time per day and 1 hour or more of&lt;br /&gt;
physical activity per day [12,13]. Making parents aware of these guidelines can help frame the&lt;br /&gt;
discussion about appropriate activity patterns. Several questions may provide an insight into the&lt;br /&gt;
child’s/adolescent’s and family’s physical activity patterns. How often do you (the child/adolescent/&lt;br /&gt;
parent/family) participate in physical activity each day or week? How much time do you spend&lt;br /&gt;
participating in sedentary activities such as television viewing and playing video games? Is it safe&lt;br /&gt;
to play outside in your neighborhood? (Safety issues can include crime rate, sidewalks, supervision,&lt;br /&gt;
safe parks or fields, and the amount of daylight hours.) Are there any opportunities to engage in&lt;br /&gt;
physical activity inside the home or apartment? (The opportunities can include lighted safe stairs,&lt;br /&gt;
exercise machines, a play area such as a basement or den, and audio players.) The answers to these&lt;br /&gt;
questions can identify barriers and opportunities to increasing physical activity.</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-physical-activity.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-5753356598860190739</guid><pubDate>Wed, 05 Sep 2012 02:00:00 +0000</pubDate><atom:updated>2012-09-04T19:00:26.587-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF COMMUNITY ENVIRONMENT ASSESSMENT</title><description>&lt;br /&gt;
Food availability is a major factor in the food purchasing habits of a family that can determine the&lt;br /&gt;
nutrient quality of the family’s diet. Food availability includes economic resources, food purchasing&lt;br /&gt;
options, and transportation. Families that have limited financial resources may qualify for federal&lt;br /&gt;
food programs such as WIC and food stamps. Participation in these programs can provide nutrition&lt;br /&gt;
education and the financial support to help stretch food dollars, thereby enabling the family to&lt;br /&gt;
purchase and consume healthier foods. Community food banks may provide sources for foods that&lt;br /&gt;
can supplement household food inventories during periods of financial hardship that might occur&lt;br /&gt;
for a short time between household paychecks. Some families opt to shop at food warehouses to&lt;br /&gt;
reduce food costs. These outlets provide bulk foods at a lower per unit cost than at traditional&lt;br /&gt;
supermarkets. However, although some bulk foods may be attractive in cost, they may contain&lt;br /&gt;
significant amounts of energy, saturated fats, and sugar.&lt;br /&gt;
The type of store accessible to the family determines food-purchasing options. If the family&lt;br /&gt;
has transportation and the ability to carry quantities of foodstuffs home from the store, many options&lt;br /&gt;
such as food warehouses, supermarkets, or food cooperatives may be available to the family.&lt;br /&gt;
However, if transportation and delivery of foodstuffs are limited, then food-purchasing options are&lt;br /&gt;
limited. Depending on the neighborhood, small grocery stores or bodegas that stock limited inventories&lt;br /&gt;
at high cost may be the only option for some households. Assessing the family’s food&lt;br /&gt;
availability as well as the family’s understanding of food consumerism principles, such as menu&lt;br /&gt;
planning, food preparation, and food purchasing practices, can identify hurdles to the implementation&lt;br /&gt;
of healthy lifestyle changes.</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-community-environment.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-8795614650729939301</guid><pubDate>Wed, 05 Sep 2012 01:59:00 +0000</pubDate><atom:updated>2012-09-04T18:59:54.255-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF SCHOOL ENVIRONMENT ASSESSMENT</title><description>&lt;br /&gt;
According to data from the USDA Economic Research Council, school meals account for approximately&lt;br /&gt;
10% of foods eaten outside the home [3]. Participation in school meals can include school&lt;br /&gt;
breakfast, snack, and lunch programs. Some children and adolescents are eligible for free or reduced&lt;br /&gt;
school meals, whereas others are required to self pay at a nominal cost. Other sources of food and&lt;br /&gt;
beverages provided in schools include à la carte snack programs, vending machines, special events,&lt;br /&gt;
and fundraising drives. Recent advocacy by parents, community groups, health professionals,&lt;br /&gt;
government agencies, and legislators has led to reforms in school food and beverage nutrient&lt;br /&gt;
standards that affect meals, snacks and vending machines, and fundraising food selections in some&lt;br /&gt;
school districts. However, the reforms have not reached the majority of the schools in the United&lt;br /&gt;
States.&lt;br /&gt;
The degree of participation in these programs varies, as do the food selections offered by the&lt;br /&gt;
schools and chosen by the children and adolescents. The practitioner can assess the effect of school&lt;br /&gt;
dining on weight management interventions by gathering information on the extent of participation&lt;br /&gt;
(how many meals/snacks per week including after-school programs), reason for participation&lt;br /&gt;
(economic, food preference, peer pressure, religious dietary restrictions), and the food choices&lt;br /&gt;
available for the student. All these factors influence the food selections made by the child or&lt;br /&gt;
adolescent, and ultimately the nutritional quality of his or her diet.</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-school-environment.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-8332959948750656119</guid><pubDate>Wed, 05 Sep 2012 01:59:00 +0000</pubDate><atom:updated>2012-09-04T18:59:29.258-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF HOME ENVIRONMENT ASSESSMENT</title><description>&lt;br /&gt;
In the past 40 years, there has been a dramatic increase in dual-income families. More women are&lt;br /&gt;
working outside the home, with homemaking responsibilities being shared by all family members&lt;br /&gt;
or outside caretakers. This new dynamic can affect family meal and snack patterns, resulting in&lt;br /&gt;
more outside dining, prepared convenience foods, or shared meal preparation responsibilities.&lt;br /&gt;
Children may receive less supervision with after-school food and activity selections. Older siblings&lt;br /&gt;
may be responsible for child care of younger siblings and for food preparation for the family.&lt;br /&gt;
Extended family members such as grandparents or other relatives may assume the roles of caretaker&lt;br /&gt;
and food preparer. Child care may be provided in a commercial daycare or after-school care setting&lt;br /&gt;
in which younger children consume two meals and daily snacks up to 5 days per week and schoolage&lt;br /&gt;
children receive afternoon snacks. Therefore, understanding which family member or caretaker&lt;br /&gt;
plays significant roles in food selection and preparation is key to helping the family develop nutrition&lt;br /&gt;
strategies to foster healthful eating. Specific queries as to who is responsible for purchasing,&lt;br /&gt;
preparing, and serving food must be included in a comprehensive nutrition assessment.&lt;br /&gt;
As family schedules become more hectic, family meals occur less frequently in households.&lt;br /&gt;
Often, families rely on outside dining or frozen convenience meals between or after activities.&lt;br /&gt;
Meals may be consumed in cars in transit to or from an activity. Eating may be rushed or hurried&lt;br /&gt;
to conform to the family schedule. Data from the U.S. Department of Agriculture indicates that&lt;br /&gt;
from 1977 to 1996, energy consumed outside the home increased from 17% to almost 35% of the&lt;br /&gt;
daily energy intake, with the percentage of energy contributed from fast food almost tripling [3].&lt;br /&gt;
In addition, several studies have shown the relationship between fast food consumption and total&lt;br /&gt;
energy intake and body weight in adolescents [4,5]. Children have been shown to consume more&lt;br /&gt;
energy when dining outside the home than when eating in the home [6]. Conversely, in-home,&lt;br /&gt;
family meals have been shown to increase nutrient quality of the meal by decreasing nutrient-sparse&lt;br /&gt;
foods and increasing fruit and vegetable consumption [7]. Assessing the frequency of outside or&lt;br /&gt;
“on the run” dining verses in-home family meals may provide the practitioner with an insight into&lt;br /&gt;
problematic family eating behaviors.&lt;br /&gt;
Family composition can be an important influence on dietary intake and feeding practices in&lt;br /&gt;
families. Children of divorced parents with various custody arrangements and visitation rights can&lt;br /&gt;
live in separate households, consuming significantly different foods and beverages in each setting.&lt;br /&gt;
The divorced spouses’ awareness and priority in addressing the issue of overweight may be similar&lt;br /&gt;
or markedly different. The children may use family discord to manipulate family dining practices&lt;br /&gt;
causing inconsistencies in applying nutrition interventions between households. Inquiring about&lt;br /&gt;
these issues in divorced families can aid the practitioner in identifying supportive family members,&lt;br /&gt;
in communicating with the different households, and in assessing the educational needs of each&lt;br /&gt;
household to support recommended lifestyle changes. The relationship between the parents may&lt;br /&gt;
dictate scheduling joint or separate consultation sessions with the parents, child, and practitioner.&lt;br /&gt;
An inventory of the variety and amounts of foods and beverages available to the child or&lt;br /&gt;
adolescent and his or her family in the home may reveal the degree to which the home food&lt;br /&gt;
environment is nutritious or toxic. A pantry full of high-calorie, nutrient-sparse foods and beverages&lt;br /&gt;
provides stiff competition to the bowl of fruits and a bottle of water on the kitchen table. Grimm&lt;br /&gt;
et al. demonstrated that parental soda consumption was correlated with increased soda consumption&lt;br /&gt;
of children, especially when the beverage was stocked in the home [8]. Inquiring about the food&lt;br /&gt;
habits and preferences of individual family members may identify barriers to the successful weight&lt;br /&gt;
management of the child or adolescent. Some examples may be parental concerns about weight&lt;br /&gt;
gain for thin siblings conflicting with concerns about weight loss for overweight siblings. Parental&lt;br /&gt;
ambivalence about eating habits and their effect on weight management may lead to the presence&lt;br /&gt;
of nonnutritious family food selections in the home. It is important to address the presence of&lt;br /&gt;
calorically dense but nutrient-sparse foods and beverages in the home, their role in family eating&lt;br /&gt;
patterns, and the effect these items have on the nutritional status of the family. This focus will&lt;br /&gt;
enable the family to modify their home feeding environment to foster healthy food choices for the&lt;br /&gt;
entire family.</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-home-environment.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-373069090191163741</guid><pubDate>Wed, 05 Sep 2012 01:58:00 +0000</pubDate><atom:updated>2012-09-04T18:58:50.911-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF NUTRITIONAL ASSESSMENT OF THE AT-RISK FOR OVERWEIGHT AND OVERWEIGHT CHILD AND ADOLESCENT</title><description>In the mid 1900s, pediatric health professionals would screen and treat children and adolescents&lt;br /&gt;
for issues related to growth and development, but obesity was not a prevalent nutritional concern.&lt;br /&gt;
Recommending and assessing adequate caloric and nutrient intakes for infants, toddlers, schoolaged&lt;br /&gt;
children, and adolescents in relation to their growth and development was within the routine&lt;br /&gt;
clinical training and practice of pediatric health professionals. However, in the 21st century,&lt;br /&gt;
American children and adolescents are plagued with an obesity epidemic. One out of every five&lt;br /&gt;
children in the United States is classified as overweight [1]. Obesity is now the most prevalent&lt;br /&gt;
nutritional disease in the pediatric population, and pediatric health professionals are now faced&lt;br /&gt;
with a disease that has no effective surgical or pharmacological interventions but that, if left&lt;br /&gt;
untreated, results in signs and symptoms of chronic disease in adolescence [2].&lt;br /&gt;
Therefore, health professionals must enhance their clinical skills to become proficient in&lt;br /&gt;
screening, identifying, and treating at risk for overweight and overweight children and adolescents.&lt;br /&gt;
They need to be able to identify environmental and genetic promoters of obesity, assess their effect&lt;br /&gt;
on the child and family, and enable the child and family to make lifestyle changes. The following&lt;br /&gt;
sections describe various components of the nutritional assessment of children and adolescents that&lt;br /&gt;
will enable to practitioner to develop a treatment plan that addresses the needs of the child or&lt;br /&gt;
adolescent and his or her family.&lt;br /&gt;
&lt;br /&gt;
</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-nutritional-assessment-of.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-5596236447514287488</guid><pubDate>Wed, 05 Sep 2012 01:58:00 +0000</pubDate><atom:updated>2012-09-04T18:58:04.748-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF THE TREATMENT OF CHILDHOOD OBESITY</title><description>1. Dennison, B. A. and P. S. Boyer. Risk evaluation in pediatric practice aids in prevention of childhood&lt;br /&gt;
overweight. Pediatr Ann. 33:25–30, 2004.&lt;br /&gt;
2. Krebs, N., R. Baker, F. Greer, M. Heman, T. Jaksic, F. Lifshitz et al. American Academy of Pediatrics,&lt;br /&gt;
Committee on Nutrition. Prevention of pediatric overweight and obesity. Pediatrics. 112:424–430,&lt;br /&gt;
2003.&lt;br /&gt;
3. Binns, H. J. and A. J. Ariza. Guidelines help clinicians identify risk factors for overweight in children.&lt;br /&gt;
Pediatr Ann. 33:18–22, 2004.&lt;br /&gt;
4. Ogden, C. L., K. M. Flegal, M. D. Carroll, and C. L. Johnson. Prevalence and trends in overweight&lt;br /&gt;
among US children and adolescents, 1999-2000. JAMA. 288:1728–1732, 2002.&lt;br /&gt;
5. Flegal, K. M. and R. P. Troiano. Changes in the distribution of body mass index of adults and children&lt;br /&gt;
in the US population. Int J Obes Relat Metab Disord. 24:807–818, 2000.&lt;br /&gt;
6. Shephard, R. J. Role of the physician in childhood obesity. Clin J Sport Med. 14:161–168, 2004.&lt;br /&gt;
6a. Dietz, W. H. and T. N. Robinson. Overweight children and adolescents. N Engl J Med. 352:2100–2109,&lt;br /&gt;
2005.&lt;br /&gt;
7. Fogelholm, M., O. Nuutinen, M. Pasanen, E. Myohanen, and T. Saatela. Parent-child relationship of&lt;br /&gt;
physical activity patterns and obesity. Int J Obes Relat Metab Disord. 23:1262–1268, 1999.&lt;br /&gt;
8. Gottlieb, N. H. and M. S. Chen. Sociocultural correlates of childhood sporting activities: their&lt;br /&gt;
implications for heart health. Soc Sci Med. 21:533–539, 1985.&lt;br /&gt;
9. Davison, K. and L. Birch. Processes linking weight status and self-concept among girls from ages 5&lt;br /&gt;
to 7 years. Dev Psychol. 38:735–748, 2002.&lt;br /&gt;
10. Jackson, A. A., S. C. Langley-Evans, and H. D. McCarthy. Nutritional influences in early life upon&lt;br /&gt;
obesity and body proportions. Ciba Found Symp. 201:118–129; discussion 129–137, 188–193, 1996.&lt;br /&gt;
11. Barker, D. J., C. Osmond, I. Rodin, C. H. Fall, and P. D. Winter. Low weight gain in infancy and&lt;br /&gt;
suicide in adult life. BMJ. 311:1203, 1995.&lt;br /&gt;
12. Neel, J. Diabetes mellitus: A “thrifty” genotype rendered detrimental by “progress”? Am J Hum Gen.&lt;br /&gt;
14:353–362, 1962.&lt;br /&gt;
13. Law, C. M., D. J. Barker, C. Osmond, C. H. Fall, and S. J. Simmonds. Early growth and abdominal&lt;br /&gt;
fatness in adult life. J Epidemiol Commun Health. 46:184–186, 1992.&lt;br /&gt;
14. Choi, C. S., C. Kim, W. J. Lee, J. Y. Park, S. K. Hong, M. G. Lee et al. Association between birth&lt;br /&gt;
weight and insulin sensitivity in healthy young men in Korea: role of visceral adiposity. Diabetes Res&lt;br /&gt;
Clin Pract. 49:53–59, 2000.&lt;br /&gt;
15. Phillips, D. I., R. McLeish, C. Osmond, and C. N. Hales. Fetal growth and insulin resistance in adult&lt;br /&gt;
life: role of plasma triglyceride and non-esterified fatty acids. Diabet Med. 12:796–801, 1995.&lt;br /&gt;
16. Rolland-Cachera, M. F., M. Deheeger, M. Akrout, and F. Bellisle. Influence of macronutrients on&lt;br /&gt;
adiposity development: a follow up study of nutrition and growth from 10 months to 8 years of age.&lt;br /&gt;
Int J Obes Relat Metab Disord. 19:573–578., 1995.&lt;br /&gt;
17. Dietz, W. H. Breastfeeding may help prevent childhood overweight. JAMA. 285:2506–2507, 2001.&lt;br /&gt;
18. Hediger, M. L., M. D. Overpeck, W. J. Ruan, and J. F. Troendle. Early infant feeding and growth&lt;br /&gt;
status of US-born infants and children aged 4–71 mo: analyses from the third National Health and&lt;br /&gt;
Nutrition Examination Survey, 1988-1994. Am J Clin Nutr. 72:159–167, 2000.&lt;br /&gt;
19. Liese, A. D., T. Hirsch, E. von Mutius, U. Keil, W. Leupold, and S. K. Weiland. Inverse association&lt;br /&gt;
of overweight and breast feeding in 9 to 10-y-old children in Germany. Int J Obes Relat Metab Disord.&lt;br /&gt;
25:1644–1650, 2001.&lt;br /&gt;
20. Poulton, R. and S. Williams. Breastfeeding and risk of overweight. JAMA. 286:1449–1450, 2001.&lt;br /&gt;
21. Gillman, M. W., S. L. Rifas-Shiman, C. A. Camargo, Jr., C. S. Berkey, A. L. Frazier, H. R. Rockett&lt;br /&gt;
et al. Risk of overweight among adolescents who were breastfed as infants. JAMA. 285:2461–2467,&lt;br /&gt;
2001.&lt;br /&gt;
22. Sothern, M. and S. Gordon. Prevention of obesity in young children. Clin Pediatrics. 42:101–111, 2003.&lt;br /&gt;
23. Lustig, R. H. The neuroendocrinology of childhood obesity. Pediatr Clin North Am. 48:909–930.,&lt;br /&gt;
2001.&lt;br /&gt;
24. Strong, J. P., G. T. Malcom, W. P. Newman 3rd, and M. C. Oalmann. Early lesions of atherosclerosis&lt;br /&gt;
in childhood and youth: natural history and risk factors. J Am Coll Nutr. 11(Suppl):51S–54S, 1992.&lt;br /&gt;
25. Berenson, G. S., S. R. Srinivasan, W. Bao, W. P. Newman, 3rd, R. E. Tracy, and W. A. Wattigney.&lt;br /&gt;
Association between multiple cardiovascular risk factors and atherosclerosis in children and young&lt;br /&gt;
adults. The Bogalusa Heart Study. N Engl J Med. 338:1650–1656, 1998.&lt;br /&gt;
26. Shulman, G. I. Cellular mechanisms of insulin resistance. J Clin Invest. 106:171–176, 2000.&lt;br /&gt;
27. Goran, M. I., R. N. Bergman, and B. A. Gower. Influence of total vs. visceral fat on insulin action&lt;br /&gt;
and secretion in African American and white children. Obes Res. 9:423–431, 2001.&lt;br /&gt;
28. Teixeira, P. J., L. B. Sardinha, S. B. Going, and T. G. Lohman. Total and regional fat and serum&lt;br /&gt;
cardiovascular disease risk factors in lean and obese children and adolescents. Obes Res. 9:432–442,&lt;br /&gt;
2001.&lt;br /&gt;
29. Barlow, S. E. and W. H. Dietz. Obesity evaluation and treatment: Expert Committee recommendations.&lt;br /&gt;
The Maternal and Child Health Bureau, Health Resources and Services Administration and the&lt;br /&gt;
Department of Health and Human Services. Pediatrics. 102:E29, 1998.&lt;br /&gt;
30. Edmunds, L., E. Waters, and E. J. Elliott. Evidence based paediatrics: Evidence based management&lt;br /&gt;
of childhood obesity. BMJ. 323:916–919, 2001.&lt;br /&gt;
31. Johnson, C. Initial consultation for patients with bulimia and anorexia nervosa: the Diagnostic Survey&lt;br /&gt;
for Eating Disorders (DSED). In: D. M. Garner, Garfinkel, P.E., Ed. Handbook of Psychotherapy for&lt;br /&gt;
Anorexia and Bulimia. New York: Guilford, 1985, pp. 19–51.&lt;br /&gt;
32. Birch, L. Development of food acceptance patterns. Dev Psychol. 26:515–519, 1990.&lt;br /&gt;
33. Field, A. E., S. B. Austin, C. B. Taylor, S. Malspeis, B. Rosner, H. R. Rockett et al. Relation between&lt;br /&gt;
dieting and weight change among preadolescents and adolescents. Pediatrics. 112:900–906, 2003.&lt;br /&gt;
34. Schwimmer, J. B. Managing overweight in older children and adolescents. Pediatr Ann. 33:39–44, 2004.&lt;br /&gt;
35. Kiess, W., A. Reich, G. Muller, A. Galler, T. Kapellen, K. Raile et al. Obesity in childhood and&lt;br /&gt;
adolescence: clinical diagnosis and management. J Pediatr Endocrinol Metabol. 14(Suppl 6):1431–1440,&lt;br /&gt;
2001.&lt;br /&gt;
36. Barlow, S. E. and W. H. Dietz. Management of child and adolescent obesity: summary and recommendations&lt;br /&gt;
based on reports from pediatricians, pediatric nurse practitioners, and registered dietitians.&lt;br /&gt;
Pediatrics. 110:236–238, 2002.&lt;br /&gt;
37. Robinson, T. N. Reducing children’s television viewing to prevent obesity: a randomized controlled&lt;br /&gt;
trial. JAMA. 282:1561–1567, 1999.&lt;br /&gt;
38. Epstein, L. H., A. M. Valoski, L. S. Vara, J. McCurley, L. Wisniewski, M. A. Kalarchian et al. Effects&lt;br /&gt;
of decreasing sedentary behavior and increasing activity on weight change in obese children. Health&lt;br /&gt;
Psychol. 14:109–115, 1995.&lt;br /&gt;
39. Inge, T. H., N. F. Krebs, V. F. Garcia, J. A. Skelton, K. S. Guice, R. S. Strauss et al. Bariatric surgery&lt;br /&gt;
for severely overweight adolescents: concerns and recommendations. Pediatrics. 114:217–223, 2004.&lt;br /&gt;
40. Sugerman, H. J., E. L. Sugerman, E. J. DeMaria, J. M. Kellum, C. Kennedy, Y. Mowery, and L. G.&lt;br /&gt;
Wolfe. Bariatric surgery for severely obese adolescents. J Gastrointest Surg. 7:102–107; discussion&lt;br /&gt;
107–108, 2003.&lt;br /&gt;
41. Ariza, A. J., R. S. Greenberg, and R. Unger. Childhood overweight: management approaches in young&lt;br /&gt;
children. Pediatr Ann. 33:33–38, 2004.&lt;br /&gt;
42. Davis, K. and K. K. Christoffel. Obesity in preschool and school-age children. Treatment early and&lt;br /&gt;
often may be best. Arch Pediatr Adolesc Med. 148:1257–1261, 1994.&lt;br /&gt;
43. O’Brien, S. H., R. Holubkov, and E. C. Reis. Identification, evaluation, and management of obesity&lt;br /&gt;
in an academic primary care center. Pediatrics. 114:e154–e159, 2004.&lt;br /&gt;
44. Robinson, T. N. Defining obesity in children and adolescents: clinical approaches. Crit Rev Food Sci&lt;br /&gt;
Nutr. 33:313–320, 1993.&lt;br /&gt;
45. Perrin, E. M., K. B. Flower, and A. S. Ammerman. Body mass index charts: useful yet underused.&lt;br /&gt;
J Pediatr. 144:455–460, 2004.&lt;br /&gt;
46. Carlisle, L. K., S. T. Gordon, and M. S. Sothern. Can obesity prevention work for our children? J La&lt;br /&gt;
State Med Soc. 157(Spec No 1):S34–S41, 2005.&lt;br /&gt;
47. Barlow, S. E., W. H. Dietz, W. J. Klish, and F. L. Trowbridge. Medical evaluation of overweight&lt;br /&gt;
children and adolescents: reports from pediatricians, pediatric nurse practitioners, and registered&lt;br /&gt;
dietitians. Pediatrics. 110:222–228, 2002.&lt;br /&gt;
48. Sothern, M. S. Obesity prevention in children: physical activity and nutrition. Nutrition. 20:704–708,&lt;br /&gt;
2004.&lt;br /&gt;
49. Whitaker, R. C. Predicting preschooler obesity at birth: the role of maternal obesity in early pregnancy.&lt;br /&gt;
Pediatrics. 114:e29–e36, 2004.&lt;br /&gt;
50. O’Loughlin, J., G. Paradis, G. Meshefedjian, and K. Gray-Donald. A five-year trend of increasing&lt;br /&gt;
obesity among elementary schoolchildren in multiethnic, low-income, inner-city neighborhoods in&lt;br /&gt;
Montreal, Canada. Int J Obes Relat Metabol Disord. 24:1176–1182, 2000.&lt;br /&gt;
51. Strauss, R. S. and J. Knight. Influence of the home environment on the development of obesity in&lt;br /&gt;
children. Pediatrics. 103:e85, 1999.&lt;br /&gt;
52. Chen, W., C. C. Lin, C. T. Peng, C. I. Li, H. C. Wu, J. Chiang et al. Approaching healthy body mass&lt;br /&gt;
index norms for children and adolescents from health-related physical fitness. Obes Rev. 3:225–232,&lt;br /&gt;
2002.&lt;br /&gt;
53. Kuczmarski, R. J., C. L. Ogden, L. M. Grummer-Strawn, K. M. Flegal, S. S. Guo, R. Wei et al. CDC&lt;br /&gt;
growth charts: United States. Adv Data. 1–27, 2000.&lt;br /&gt;
54. Pietrobelli, A., M. S. Faith, D. B. Allison, D. Gallagher, G. Chiumello, and S. B. Heymsfield. Body&lt;br /&gt;
mass index as a measure of adiposity among children and adolescents: a validation study. J Pediatr.&lt;br /&gt;
132:204–210, 1998.&lt;br /&gt;
55. Ravussin, E. and J. F. Gautier. [Determinants and control of energy expenditure]. Ann Endocrinol&lt;br /&gt;
(Paris). 63:96–105, 2002.&lt;br /&gt;
56. Goran, M. I. Handbook of Pediatric Obesity: Epidemiology, Etiology, and Prevention: Boca Raton:&lt;br /&gt;
Taylor &amp;amp; Francis, 2006.&lt;br /&gt;
57. Schechter, M. S. Technical report: diagnosis and management of childhood obstructive sleep apnea&lt;br /&gt;
syndrome. Pediatrics. 109:e69, 2002.&lt;br /&gt;
58. Ford, E. S., D. M. Mannino, S. C. Redd, A. H. Mokdad, D. A. Galuska, and M. K. Serdula. Weightloss&lt;br /&gt;
practices and asthma: findings from the behavioral risk factor surveillance system. Obes Res.&lt;br /&gt;
11:81–86, 2003.&lt;br /&gt;
59. Gennuso, J., L. H. Epstein, R. A. Paluch, and F. Cerny. The relationship between asthma and obesity&lt;br /&gt;
in urban minority children and adolescents. Arch Pediatr Adolesc Med. 152:1197–1200, 1998.&lt;br /&gt;
60. Chinn, S. Obesity and asthma: evidence for and against a causal relation. J Asthma. 40:1–16, 2003.&lt;br /&gt;
61. Jonides, L., V. Buschbacher, and S. E. Barlow. Management of child and adolescent obesity: psychological,&lt;br /&gt;
emotional, and behavioral assessment. Pediatrics. 110:215–221, 2002.&lt;br /&gt;
62. Lee, S., S. Hoerr, and R. Schiffman. Screening for infants’ and toddlers’ dietary quality through&lt;br /&gt;
maternal diet. Amer J Matern/Child Nurs. 30:60–66, 2005.&lt;br /&gt;
63. Rivara, F. P., R. Whitaker, P. M. Sherman, and L. Cuttler. Influencing the childhood behaviors that&lt;br /&gt;
lead to obesity: role of the pediatrician and health care professional. Arch Pediatr Adolesc Med.&lt;br /&gt;
157:719–720, 2003.&lt;br /&gt;
64. Sothern, M. S. Exercise as a modality in the treatment of childhood obesity. Pediatr Clin North Am.&lt;br /&gt;
48:995–1015, 2001.&lt;br /&gt;
65. Wang, L., Q. Yang, R. Lowry, and H. Wechsler. Economic analysis of a school-based obesity prevention&lt;br /&gt;
program. Obes Res. 11:1313–1324, 2003.</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-treatment-of-childhood.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-8092691814111554206</guid><pubDate>Wed, 05 Sep 2012 01:57:00 +0000</pubDate><atom:updated>2012-09-04T18:57:08.695-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>KNOW ABOUT RISK FOR OBESITY</title><description>&lt;br /&gt;
Children who are diagnosed with one or more primary risk factors or fall above the 85th percentile&lt;br /&gt;
on the BMI percentiles may benefit from monitoring more frequently than annually (e.g., every&lt;br /&gt;
6 months) to check for continued upward shifts in BMI [2,36,41]. In addition, anticipatory guidance&lt;br /&gt;
and brief negotiations for behavior change with parents should be undertaken to change risk eating&lt;br /&gt;
and physical activity habits.&lt;br /&gt;
OVERWEIGHT&lt;br /&gt;
Families of overweight children require consistent feedback from pediatric health care professionals&lt;br /&gt;
to determine whether nutrition and physical activity recommendations are providing successful&lt;br /&gt;
outcomes. Height, weight, and BMI should be calculated regularly (e.g., every 3 months).&lt;br /&gt;
SEVERE OVERWEIGHT&lt;br /&gt;
Severely overweight youth require intense interventions and regular medical monitoring. This is&lt;br /&gt;
ideally provided by a multidisciplinary team with experience working with pediatric patients and&lt;br /&gt;
their families. Patients should be examined at least monthly, especially if they are following a&lt;br /&gt;
calorie-restricted diet. Monitoring to determine the effect of the weight loss plan on lipid profiles&lt;br /&gt;
and diabetes risk should be conducted quarterly. An expert committee has provided an algorithm&lt;br /&gt;
to assist pediatric health care professionals with monitoring [29]. In general, a one-half pound/week&lt;br /&gt;
weight loss is optimal.&lt;br /&gt;
For all children, parental education in the medical office setting is strongly recommended regardless&lt;br /&gt;
of the child’s current weight condition, but especially if the parents are obese. Children who are&lt;br /&gt;
at risk for overweight by virtue of family history or other predisposing factors become increasingly&lt;br /&gt;
more susceptible as they mature. Thus, age-appropriate, targeted, family-based dietary and physical&lt;br /&gt;
activity preventive strategies should be consistently promoted, and basic therapeutic interventions&lt;br /&gt;
should be made available in pediatric clinical settings. The economic burden of obesity-associated&lt;br /&gt;
illness during childhood in the United States has increased by 43% in the last two decades [66].&lt;br /&gt;
Cost-effective individual and group treatment approaches are available and should be both encouraged&lt;br /&gt;
and financially supported by the pediatric medical community. Academic programs that work&lt;br /&gt;
simultaneously to conduct research, provide training opportunities for pediatric professionals, and&lt;br /&gt;
evaluate ongoing interventions to prevent and treat overweight children are also vitally important&lt;br /&gt;
to reverse this pediatric epidemic.</description><link>http://fatcampsforkids.blogspot.com/2012/09/know-about-risk-for-obesity.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-2362552952513580225</guid><pubDate>Wed, 05 Sep 2012 01:56:00 +0000</pubDate><atom:updated>2012-09-04T18:56:13.734-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>LEARN TO DIRECT MEASUREMENTS OF BODY COMPOSITION</title><description>the circumference of the waist and hip. The waist circumference is also a useful indicator for&lt;br /&gt;
determining reduction in fat weight after treatment (Appendix A2.1.3).&lt;br /&gt;
DIRECT MEASUREMENTS OF BODY COMPOSITION&lt;br /&gt;
Direct measurements of body fat content can be found using such tools as hydrodensitometry,&lt;br /&gt;
bioimpedance, or dual-energy x-ray absorptiometry [35]. In Chapter 4 of this text, Gordon discusses&lt;br /&gt;
the advantages and disadvantages of these various methods, and detailed protocols may be found&lt;br /&gt;
in Appendix A2.3.&lt;br /&gt;
LABORATORY TESTING — BASIC PANELS&lt;br /&gt;
Secondary assessments may include lipid profiles, total cholesterol, insulin, glucose tolerance,&lt;br /&gt;
glucose, glycohemoglobin, thyroid function, cortisol, and liver enzymes [47].&lt;br /&gt;
If the child is diagnosed with a BMI greater than 95th percentile, additional testing may be&lt;br /&gt;
warranted. Because pediatric overweight (BMI &amp;gt; 95th percentile for age and sex) is associated with&lt;br /&gt;
many other disease risk factors, practitioners can further define risk by checking a fasting lipid&lt;br /&gt;
profile (Appendix A2.2) [41]. Other potentially useful biochemical markers of comorbidities include&lt;br /&gt;
liver profile, and fasting glucose and insulin. It should be recognized that there are not standardized&lt;br /&gt;
guidelines for biochemical evaluation, especially because identification of biochemical abnormalities&lt;br /&gt;
will often not change therapeutic interventions.&lt;br /&gt;
MEASUREMENTS OF ENERGY EXPENDITURE&lt;br /&gt;
In some cases, measurement of resting energy expenditure may be useful to help caloric intake&lt;br /&gt;
goals. Resting energy expenditure can be measured through indirect calorimetry. However, it is&lt;br /&gt;
difficult to obtain an accurate measure because it is affected by diet, exercise, body temperature,&lt;br /&gt;
growth, and development [55]. In an outpatient setting, it is difficult to optimally control these&lt;br /&gt;
factors, and thus measurements can at best be viewed as approximations. Therefore, routine&lt;br /&gt;
assessment of resting energy expenditure is of limited value.&lt;br /&gt;
Overweight children with more severe medical problems such as obstructive sleep apnea, obesity&lt;br /&gt;
hypoventilation syndrome, and orthopedic problems may benefit from more aggressive dietary&lt;br /&gt;
strategies. If a referral is made to an overweight treatment center, it is important to identify a&lt;br /&gt;
program that is staffed by medical professionals experienced in the management of these serious&lt;br /&gt;
comorbidities. Massively overweight children without severe comorbidities, but with a history of&lt;br /&gt;
weight loss failures, may also benefit from consultation with a pediatric obesity center. Ariza and&lt;br /&gt;
colleagues [41] provide a detailed assessment and action plan for overweight children in the primary&lt;br /&gt;
care setting (Figure 7.3).&lt;br /&gt;
GENETICS&lt;br /&gt;
Genetic syndromes associated with pediatric obesity include Prader–Willi, Turner syndrome, or&lt;br /&gt;
Laurence–Moon–Bardet–Biedle [41]. Findings such as developmental delay, short stature/delayed&lt;br /&gt;
growth, dysmorphic features, abnormal or absent genitalia, and digital anomalies should raise&lt;br /&gt;
suspicion of an underlying genetic etiology and consideration of definitive testing. If any of these&lt;br /&gt;
conditions is suspected, referral to a geneticist or other relevant subspecialist is recommended [41].&lt;br /&gt;
ENDOCRINOLOGY&lt;br /&gt;
There are several endocrine disorders related to pediatric obesity, including primarily hypothyroidism,&lt;br /&gt;
type 2 diabetes mellitus, and polycystic ovary disease. Although less common, findings&lt;br /&gt;
indicative of Cushing syndrome, including moon facies, short stature, central obesity, and apparent&lt;br /&gt;
reduced lean body mass should prompt referral to an endocrinologist. If this is the case, then a&lt;br /&gt;
24-hour urine cortisol should be ordered [41].&lt;br /&gt;
Thyroid&lt;br /&gt;
Symptoms of hypothyroidism include constipation, cold intolerance, fatigue, and lethargy; signs&lt;br /&gt;
may include poor linear growth, hypotension, bradycardia, anemia, and loss of deep tendon reflexes.&lt;br /&gt;
If symptoms or signs of hypothyroidism are present, TSH and T4 levels should be checked, and if&lt;br /&gt;
these levels are diagnostic of hypothyroidism, the child should be referred to a pediatric endocrinologist&lt;br /&gt;
[41].&lt;br /&gt;
Pancreas&lt;br /&gt;
Insulin resistance is common with excess central (or visceral) adiposity. Insulin resistance is&lt;br /&gt;
associated with hyperinsulinemia, fatty liver, hypertension, and exercise intolerance. Hyperinsulinemia&lt;br /&gt;
in children can be associated with normal fasting glucose for some time, but with persistence,&lt;br /&gt;
there is progression to impaired glucose tolerance, and eventually to β-cell failure and elevated&lt;br /&gt;
fasting glucose and type 2 diabetes. If insulin resistance or type 2 diabetes mellitus is suspected,&lt;br /&gt;
fasting insulin and blood glucose levels may be obtained. Hyperglycemia is relatively insensitive&lt;br /&gt;
until there is frank diabetes, but if fasting glucose levels are 126 mg/dL or more, the child should&lt;br /&gt;
be referred to a pediatric endocrinologist for further examination [41]. The utility of fasting insulin&lt;br /&gt;
levels is debated, but documentation of elevation is a finding that motivates some families to make&lt;br /&gt;
changes, especially if there is a strong family history of type 2 diabetes [41]. An elevated fasting&lt;br /&gt;
insulin is also part of the constellation of findings referred to as metabolic syndrome [56].&lt;br /&gt;
CARDIOLOGY&lt;br /&gt;
During the medical examination, if the child’s blood pressure is in the 95th (or higher) percentile for&lt;br /&gt;
height and gender on three separate occasions, then referral to a cardiologist is suggested [41]. Chest&lt;br /&gt;
pain is another symptom that may require referral. Treatment of hyperlipidemia (LDL ≥ 110 mg/dl)&lt;br /&gt;
or dyslipidemia (e.g., metabolic syndrome), including initial diet therapy, may also be available&lt;br /&gt;
through preventive cardiology services, or through nutrition or endocrine subspecialists [41].&lt;br /&gt;
PULMONARY&lt;br /&gt;
Pulmonary disorders associated with significant obesity that may require rapid weight loss are&lt;br /&gt;
obstructive sleep apnea and obesity hypoventilation syndrome [57]. Symptoms indicative of sleep&lt;br /&gt;
disturbances include snoring, restless sleep, inability to sleep supine, and daytime somnolence.&lt;br /&gt;
Assessment ideally includes an electrocardiogram to rule out cardiomegaly, sinus dysrhythmias,&lt;br /&gt;
and right-side heart failure, as well as a sleep study with polysomnography to monitor for hypoxia&lt;br /&gt;
and cardiac function. Treatment may include supplemental oxygen or positive airway pressure, but&lt;br /&gt;
at least modest weight loss will also be advantageous. Clinicians should seek guidance from&lt;br /&gt;
pediatric pulmonologists and obesity treatment specialists [29].&lt;br /&gt;
One of the most common pulmonary disorders associated with pediatric obesity is asthma [58].&lt;br /&gt;
Asthma is a major cause of chronic pediatric illness and school absenteeism. Moreover, urban&lt;br /&gt;
minority children with asthma are significantly more overweight than those without asthma [59].&lt;br /&gt;
Results of most studies in children do not support a direct causal link between asthma and&lt;br /&gt;
overweight conditions during childhood [60]. Furthermore, there is insufficient evidence to indicate&lt;br /&gt;
that asthma precedes overweight conditions in children. Because excess weight exacerbates asthma&lt;br /&gt;
symptoms, especially during exercise, overweight children with asthma should be monitored closely&lt;br /&gt;
by a pulmonary specialist.&lt;br /&gt;
ORTHOPEDICS AND PHYSICAL THERAPY&lt;br /&gt;
There are several serious orthopedic complications that result from significant obesity during&lt;br /&gt;
childhood. These include slipped capital femoral epiphysis (manifested as hip or knee pain and&lt;br /&gt;
limited hip range of motion) and Blount’s disease (tibia vara) [29]. Referral should be made to an&lt;br /&gt;
orthopedic surgeon if radiography confirms either of these conditions [29]. Other related comorbidities&lt;br /&gt;
include spinal asymmetry, flat feet, genu varus/valgus, Legg–Calve–Perthe disease, and&lt;br /&gt;
degenerative arthritis. Referral may be made to a physical therapist for an initial evaluation and,&lt;br /&gt;
in many cases, for therapeutic strategies.&lt;br /&gt;
PSYCHOLOGY&lt;br /&gt;
Several psychological disorders are associated with pediatric obesity. Binge-eating disorder should&lt;br /&gt;
be suspected if the patient reports feeling unable to control food consumption. Depression is&lt;br /&gt;
commonly found in overweight children, especially in older youth with severe overweight conditions.&lt;br /&gt;
Jonides and colleagues [61] suggest that the emotional stability of the child and the family&lt;br /&gt;
will likely determine successful treatment outcomes. If the child displays sadness or reports&lt;br /&gt;
insomnia, restlessness, or hopelessness, then referral to a psychologist is essential to confirm the&lt;br /&gt;
diagnosis [29]. In Chapter 9 of this volume, Johnson and von Almen detail appropriate psychological&lt;br /&gt;
assessment for overweight children.&lt;br /&gt;
SOCIAL SERVICES&lt;br /&gt;
The negative effects of food restriction or verbal prompting to consume served food were recently&lt;br /&gt;
highlighted by the American Academy of Pediatrics [2]. In extreme cases, in which parental behavior&lt;br /&gt;
results in either food restriction and eating disorders or continued overconsumption and morbid,&lt;br /&gt;
life-threatening obesity, it may be necessary to refer the patient’s family to social services. Likewise,&lt;br /&gt;
if there is evidence of physical or sexual abuse related to the child’s overweight condition, social&lt;br /&gt;
services should be consulted.&lt;br /&gt;
NUTRITION&lt;br /&gt;
Adequate nutrition is vital to growth and development, and both insufficient and imbalanced food&lt;br /&gt;
consumption can cause nutrient deficiencies, impaired cognitive development, and growth velocity&lt;br /&gt;
delays [62]. Therefore, if the child’s weight condition warrants dietary intervention, referral should&lt;br /&gt;
be made to a registered dietician. He or she will apply U.S. Department of Agriculture caloric and&lt;br /&gt;
nutrient guidelines based on the child’s age, gender, and medical condition when prescribing a&lt;br /&gt;
weight-loss plan. A priority for dietary counseling is parent nutrition education so that family-wide&lt;br /&gt;
changes in food selection and preparation are encouraged [41] (Appendix A3).&lt;br /&gt;
EXERCISE&lt;br /&gt;
Pediatric health care professionals should encourage families to engage in regular physical activity&lt;br /&gt;
to help children achieve and maintain a healthy weight [64]. Local information concerning activity&lt;br /&gt;
centers, YMCAs, Boys and Girls Clubs, parks, and other recreational areas should be provided to&lt;br /&gt;
parents [41]. In older children with significant obesity, structured exercise guidelines are useful&lt;br /&gt;
[64]. Referral to a trained and certified pediatric exercise physiologist will ensure age-appropriate&lt;br /&gt;
physical activities for the patient.&lt;br /&gt;
EDUCATION&lt;br /&gt;
It is now widely accepted that anticipatory guidance on healthy eating habits and physical activity&lt;br /&gt;
should begin early and for all children (Table 7.2). Readiness for change is essential, and families&lt;br /&gt;
resistant to lifestyle modification should be referred to a family therapist [34]. Family histories of&lt;br /&gt;
obesity and related disorders increase the child’s risk of developing comorbid diseases, and the&lt;br /&gt;
medical consequences of such diseases should be addressed with the family [29]. Treatment success&lt;br /&gt;
rates improve with participation by family members and care givers. Gradual, permanent changes&lt;br /&gt;
to the diet and physical activity patterns of the child are more successful than transient, short-term&lt;br /&gt;
changes (Table 7.2) [29,34].&lt;br /&gt;
The BMI measurements of patients should be evaluated each year, with increased attention&lt;br /&gt;
paid by the physician to patterns of excessive weight gain relative to linear growth as well as to&lt;br /&gt;
children identified as at greater risk for overweight and obesity (Table 7.3) [2]. Patients at risk of&lt;br /&gt;
developing obesity-related comorbidities should be monitored closely for signs of these diseases.&lt;br /&gt;
Pediatricians and health care providers should routinely encourage parents in the healthy dietary&lt;br /&gt;
practices of breastfeeding, moderation, and appropriate portion sizes, regular fruit and vegetable&lt;br /&gt;
consumption, limits on sweetened beverages, and other nutritious food choices (Table 7.4) [2].&lt;br /&gt;
Pediatricians should also educate parents and caregivers on their roles in establishing physical&lt;br /&gt;
activity patterns [2]. Increased physical activity and setting limits on sedentary behaviors should&lt;br /&gt;
also be promoted. The success of prevention efforts will be more favorable if both dietary and&lt;br /&gt;
physical activity interventions are emphasized (Table 7.4).</description><link>http://fatcampsforkids.blogspot.com/2012/09/learn-to-direct-measurements-of-body.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-8452463904194429926</guid><pubDate>Wed, 05 Sep 2012 01:54:00 +0000</pubDate><atom:updated>2012-09-04T18:54:56.627-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>DEFINITION OF ANTHROPOMETRICS TO ASSESS FAT DISTRIBUTION</title><description>&lt;br /&gt;
Skinfolds&lt;br /&gt;
Subcutaneous fat represents approximately 50% of total body fat, which provides an accessible proxy&lt;br /&gt;
for assessment of body fatness. The 80th and 95th percentiles of skinfold readings are accepted&lt;br /&gt;
measures of overweight and obesity in children [6]. Caliper measurement of skinfold thickness&lt;br /&gt;
requires training and should only be administered by experienced staff. Skinfolds can be measured&lt;br /&gt;
at a variety of body sites and are used in formulas that predict percent body fat (Appendix A2.3) [6].&lt;br /&gt;
Waist Circumference&lt;br /&gt;
An additional method of assessing body composition is the measurement of girth of various body&lt;br /&gt;
sections. Waist circumference provides an indication of trunk or visceral obesity, which is highly&lt;br /&gt;
correlated in adults with diabetes and heart disease risk. Similar data are not available for the&lt;br /&gt;
pediatric population. A metal or fiberglass measuring tape with a metric scale is used to measure</description><link>http://fatcampsforkids.blogspot.com/2012/09/definition-of-anthropometrics-to-assess.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-6262405013104153905</guid><pubDate>Wed, 05 Sep 2012 01:54:00 +0000</pubDate><atom:updated>2012-09-04T18:54:25.830-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>CLINICAL EVALUATION: DIAGNOSIS, MEDICAL TESTING, AND FOLLOW-UP</title><description>PREVALENCE&lt;br /&gt;
The rapid rise in the prevalence of childhood overweight and obesity is occurring in both industrialized&lt;br /&gt;
and developing countries all over the world. Pediatricians and other pediatric health care&lt;br /&gt;
providers will play an increasingly important role in the early identification and prevention of&lt;br /&gt;
childhood obesity and its associated comorbid conditions [1,2]. Because obesity is usually established&lt;br /&gt;
at a young age, the pediatric primary care office is critical to national efforts to reverse the&lt;br /&gt;
pediatric obesity epidemic [3]. According to the 1999–2000 National Health and Nutrition Examination&lt;br /&gt;
Survey, the prevalence of childhood obesity (at or above the 95th percentile for body mass&lt;br /&gt;
index [BMI] on standard reference growth charts) in the United States has grown to 15.3% of 6 to&lt;br /&gt;
11 year olds and 15.5% of 12 to 19 year olds [2,4]. Obesity prevalence has been found to be even&lt;br /&gt;
higher among minority and economically disadvantaged populations [2,4,5].&lt;br /&gt;
CAUSES/RISK FACTORS&lt;br /&gt;
Lower levels of daily physical activity by children in the United States have lead to a greater number&lt;br /&gt;
of health problems in children than in previous generations. Sedentary lifestyles increase the risk&lt;br /&gt;
of childhood medical conditions such as obesity, hypertension, hyperinsulinemia, hypercholesterolemia,&lt;br /&gt;
and dyslipidemia [2,6]. Studies show that parent inactivity strongly predicts child inactivity&lt;br /&gt;
[7,8]. A recent study examined the self-reported physical activity and dietary intake patterns of&lt;br /&gt;
parents and changes in weight status over 2 years in offspring [9]. Girls of parents with high dietary&lt;br /&gt;
intake and low physical activity (obesogenic) had significantly greater increases in weight status.&lt;br /&gt;
Thus, in addition to family history of obesity, the environment of the home may equally contribute&lt;br /&gt;
to the risk for developing obesity in childhood. However, there are also strong arguments for the&lt;br /&gt;
effect of the genetic profile and the early nutritional environment on the risk for developing obesity&lt;br /&gt;
during childhood [10–15]. Jackson and colleagues provide a strong argument for nutrition-induced&lt;br /&gt;
changes in the hypothalamic–pituitary–adrenal axis in the mother and the fetus [10]. It is suggested&lt;br /&gt;
that the local availability of nutrients during pregnancy, especially in relation to protein intake, may&lt;br /&gt;
negatively affect future metabolic health. Adjustments may occur to protect brain tissue preferentially&lt;br /&gt;
over visceral and somatic growth, resulting in an altered metabolic profile [10]. Thus, nutrition&lt;br /&gt;
during pregnancy may have strong implications for future obesity and related chronic disease.&lt;br /&gt;
Infancy is also considered a critical period for obesity development. A high protein intake at&lt;br /&gt;
the age of 2 years was shown to promote increased fatness at 8 years of age, suggesting that a&lt;br /&gt;
high-protein diet early in life could promote an increased risk of obesity later in childhood, but&lt;br /&gt;
findings in this area are limited and have not been consistent [16]. Moreover, research generally&lt;br /&gt;
supports that children who were breastfed have a lower risk of obesity than those who were formulafed&lt;br /&gt;
[17–20]. In addition, those infants who breastfed for longer durations showed an even lower&lt;br /&gt;
risk of childhood obesity [21]. Differences in feeding between breastfed and formula fed infants&lt;br /&gt;
may also have a critical influence on infant weight gain. Therefore, low birth weight and breastfeeding&lt;br /&gt;
history should be considered factors in obesity development in young children (Table 7.1).&lt;br /&gt;
In addition, children with such risk factors may be predisposed genetically and behaviorally to the&lt;br /&gt;
early manifestation of subtle, nonsymptomatic metabolic abnormalities that lead to childhood&lt;br /&gt;
obesity and related chronic disease [22–28]. Therefore, strategies that positively alter the nutrition&lt;br /&gt;
and physical activity behaviors and environment of the family may reduce the risk of obesity in&lt;br /&gt;
young children, especially in those with one or more risk factors. A recent publication of the&lt;br /&gt;
American Academy of Pediatrics offers pediatric obesity prevention guidelines for medical professionals,&lt;br /&gt;
which include increased monitoring of at-risk children and parent education [2].&lt;br /&gt;
Pediatric health care providers should recognize that environmental factors may greatly affect&lt;br /&gt;
physical activity patterns. Unsafe neighborhoods and lack of adult supervision after school may&lt;br /&gt;
increase time spent in sedentary behavior such as watching television and playing DVDs or video&lt;br /&gt;
or computer games [29].&lt;br /&gt;
COMORBIDITIES&lt;br /&gt;
Pediatric obesity is associated with many significant health problems and is strongly linked to increased&lt;br /&gt;
risks for adult obesity, related comorbid diseases, and shortened life expectancy [2,6]. Growing&lt;br /&gt;
numbers of obese children exhibit early signs of diseases that were once found only in adult populations&lt;br /&gt;
including type 2 diabetes mellitus, high blood pressure, and abnormal lipid profiles [3]. Obese&lt;br /&gt;
children are at an increased risk for diseases that can affect the cardiovascular, pulmonary, endocrine,&lt;br /&gt;
and gastrointestinal systems, as well as orthopedic conditions and psychological health problems&lt;br /&gt;
[2,6]. Comorbidities affecting the cardiovascular system include hypercholesterolemia, hypertension,&lt;br /&gt;
and dyslipidemia [2,6a,30]. Endocrine system comorbidities include hyperinsulinemia, insulin&lt;br /&gt;
resistance, impaired glucose tolerance, type 2 diabetes mellitus, and menstrual irregularity [2].&lt;br /&gt;
Common pulmonary and gastrointestinal comorbidities include sleep apnea, asthma, obesity hypoventilation&lt;br /&gt;
syndrome, and nonalcoholic steatohepatitis [2,29]. Common orthopedic comorbidities&lt;br /&gt;
include slipped capital femoral epiphysis, Blount disease (tibia varia), and genu varum. Mental&lt;br /&gt;
health problems may include depression and low self-esteem [2,6,29].&lt;br /&gt;
TREATMENT APPROACHES&lt;br /&gt;
Several weight loss approaches can be considered when choosing a treatment plan for an overweight&lt;br /&gt;
or obese patient. Because obesity is a multifactorial disease, treatment of the disease is approached&lt;br /&gt;
from many angles including diet modification, increased physical activity, psychological intervention,&lt;br /&gt;
pharmacotherapy, and surgery. Reduction of energy intake is a mainstay of treatment, but the ideal&lt;br /&gt;
approach will vary with the skills and motivation of the family, the severity of the overweight&lt;br /&gt;
status, and the age of the child. Caution should be used in prescribing “diets” for children, except&lt;br /&gt;
under well-supervised conditions because of the risks associated with overly restrictive access to&lt;br /&gt;
food. This has been associated (in young children) with decreased ability to self-regulate energy&lt;br /&gt;
intake [31,32]. In adolescents, dieting was inversely associated with BMI [33]. Several dietary&lt;br /&gt;
approaches can be considered including low fat, low carbohydrate, high protein, and low glycemic&lt;br /&gt;
index. The Traffic Light Diet (see Appendix A3.3B), which applies principles of foods with high&lt;br /&gt;
versus low caloric density, has been shown to be easy for children to understand and successfully&lt;br /&gt;
follow [34]. Other popular treatments focus on psychological and family therapy, including behavioral&lt;br /&gt;
modification [35]. Behavioral modification has been shown to increase the success of obesity&lt;br /&gt;
treatment and includes such elements as goal setting, maintaining a food diary, reducing availability&lt;br /&gt;
of high-calorie stimulus foods, positive reinforcement, and parental support [34]. Health providers&lt;br /&gt;
should seek training in health behavior change techniques, parent limit-setting strategies and&lt;br /&gt;
reinforcement skills, and family conflict awareness [36]. Dietary treatment should be accompanied&lt;br /&gt;
by efforts to emphasize increased physical activity [34,35]. However, exercise alone is generally&lt;br /&gt;
not sufficient to promote significant weight loss without diet modification [34]. Physical activity&lt;br /&gt;
provides additional health benefits and is linked to successful maintenance of weight-loss. Reduction&lt;br /&gt;
of sedentary activities such as television viewing, video games, and computer time may be especially&lt;br /&gt;
effective targets for behavior change [6a,37,38].&lt;br /&gt;
Pharmacotherapy is sometimes a useful adjunct to diet, activity, and behavioral change strategies.&lt;br /&gt;
Examples specific for obesity treatment include sibutramine and orlistat, but each has significant&lt;br /&gt;
potential side effects, and efficacy data are limited. Bariatric surgery has been successfully&lt;br /&gt;
performed on severely obese adolescents. Guidelines for patient and site selection have been&lt;br /&gt;
published [39]. Criteria include a BMI of at least 40, accompanied by significant comorbidities&lt;br /&gt;
such as obstructive sleep apnea, type 2 diabetes mellitus, and pseudotumor cerebri. This treatment&lt;br /&gt;
is best undertaken in a center that has surgeons with experience with the procedure in adolescents,&lt;br /&gt;
and at which a multidisciplinary team is available. The procedure appears to be safe in the short&lt;br /&gt;
term, and weight loss is typically substantial, with improvement in comorbidities. There are&lt;br /&gt;
currently few data on long-term outcomes and complications [34,35,40].&lt;br /&gt;
DIAGNOSIS&lt;br /&gt;
Early diagnosis and treatment of obesity in children is crucial for the successful management of&lt;br /&gt;
pediatric health [2,41,42]. Unfortunately, although childhood obesity has now reached epidemic&lt;br /&gt;
levels, this disease is still under-recognized by the health care community [43]. In addition,&lt;br /&gt;
underdiagnosis is generally more prevalent than misclassification of obesity [44]. Recently, O’Brien&lt;br /&gt;
et al. [43] reported that pediatric health care providers diagnosed overweight in only one-half (53%)&lt;br /&gt;
of overweight children examined for health supervision. Moreover, in children diagnosed as overweight&lt;br /&gt;
by their physicians, comprehensive treatment programs were not generally prescribed [43].&lt;br /&gt;
One study has shown that although plotting BMI enhanced physician recognition of overweight&lt;br /&gt;
when compared with plotting height and weight for age, survey data in the same report indicatedthat&lt;br /&gt;
only a minority of pediatricians routinely use BMI [45]. In Chapter 4 of this volume, Gordon&lt;br /&gt;
provides similar disappointing rates of diagnosis and referral in overweight children in primary&lt;br /&gt;
care settings [46]. Kiess and colleagues provide a diagnostic algorithm for childhood obesity that&lt;br /&gt;
primary care providers can use to determine the most appropriate management plan (Figure 7.1) [35].&lt;br /&gt;
MEDICAL HISTORY&lt;br /&gt;
Pediatric obesity is a complex condition that is associated, as noted above, with a plethora of&lt;br /&gt;
medical complications, syndromes, and disorders. An expert panel report [47] suggests that the&lt;br /&gt;
initial diagnosis should begin with a thorough screening of the patient’s medical history. Conditions&lt;br /&gt;
of primary concern are hypertension, endocrine disorders, orthopedic problems, type 2 diabetes&lt;br /&gt;
mellitus (or insulin resistance), genetic syndromes, sleep disorders, pseudotumor cerebri, and&lt;br /&gt;
gastrointestinal disorders.&lt;br /&gt;
As part of this medical history, information on the child’s current eating and physical activity&lt;br /&gt;
patterns should be obtained, with a particular focus on behaviors that can be targeted for change.&lt;br /&gt;
An expert committee has [29] emphasized that both food type and patterns of eating should be&lt;br /&gt;
assessed to discern origins of excess caloric intake. Likewise, the assessment of physical activity&lt;br /&gt;
patterns and extent of sedentary behaviors provides information important to increasing energy&lt;br /&gt;
expenditure [29]. A comprehensive medical history and physical examination form may be found&lt;br /&gt;
in Appendix A1.6.&lt;br /&gt;
FAMILY HISTORY&lt;br /&gt;
Critical to assessment of a child’s risk from overweight is the documentation of the family history&lt;br /&gt;
of disease. The recommended conditions to evaluate when obtaining family history from the patient&lt;br /&gt;
include overweight, dyslipidemia, hypertension, cardiovascular disease, gallbladder disease, eating&lt;br /&gt;
disorders in parents, type 2 diabetes mellitus, and other endocrine abnormalities [47]. Emerging&lt;br /&gt;
research indicates that the health status of the mother immediately before pregnancy, during&lt;br /&gt;
pregnancy, and during breastfeeding may also be important [48]. Whitaker tracked the weight status&lt;br /&gt;
of preschool children whose mothers were obese during pregnancy. These youth were twice as&lt;br /&gt;
likely to be overweight as children whose mothers maintained a healthy weight during pregnancy&lt;br /&gt;
(Figure 7.2) [49].&lt;br /&gt;
SOCIAL HISTORY&lt;br /&gt;
The structure of the family, school and child care arrangements, living situation, parental employment,&lt;br /&gt;
and history of abuse are examples of information to be obtained in the social history, which&lt;br /&gt;
will inform the negotiations for health behavior changes.&lt;br /&gt;
REVIEW OF SYSTEMS&lt;br /&gt;
The review of systems should address symptoms of potential comorbidities of overweight. Examples&lt;br /&gt;
include asking about the presence of headaches; visual changes; sleep problems such as snoring,&lt;br /&gt;
restless sleep, inability to lie supine, and daytime somnolence; shortness of breath or wheezing;&lt;br /&gt;
chest pain; abdominal pain; and joint and skeletal muscle complaints. A brief evaluation of the&lt;br /&gt;
child’s psychological status is also useful.&lt;br /&gt;
PRIMARY RISK FACTORS&lt;br /&gt;
The children who are at the highest risk for becoming obese are those who belong to economically&lt;br /&gt;
disadvantaged minority populations (Table 7.1). As a result of having a low socioeconomic status,&lt;br /&gt;
children may have less access to safe places for physical activity and/or less access to healthful&lt;br /&gt;
food choices such as fruits and vegetables. Recent studies show a consistent rise in the prevalence&lt;br /&gt;
of obesity among preschool children from low-income families [50]. These children often have&lt;br /&gt;
low levels of cognitive stimulation, which is associated with a significant increase in the risk for&lt;br /&gt;
early-onset obesity [51]. Other risk factors that have been linked to an increased risk include&lt;br /&gt;
unhealthy family and parental dynamics, low or high birth weight, maternal diabetes and obesity,&lt;br /&gt;
high prevalence of obesity in other family members, and overcontrolling parental behavior (Table&lt;br /&gt;
7.1) [2].&lt;br /&gt;
PHYSICAL EXAM&lt;br /&gt;
As for all patients, a patient who is found to be overweight should have a physical examination,&lt;br /&gt;
in this case with a focus on signs of comorbid conditions that may be present or on any underlying&lt;br /&gt;
conditions that may contribute to excessive weight gains, such as hypothyroidism, reactive airways&lt;br /&gt;
disease, tonsillar hypertrophy (contributing to airway obstruction), genu varum (flat feet) or other&lt;br /&gt;
orthopedic conditions, and genetic or endocrine abnormalities [41]. A patient with insulin resistance&lt;br /&gt;
may show signs of acanthosis nigricans (darkening of the skin). Hypothyroidism should be suspected&lt;br /&gt;
with excessive weight gain and plateauing of linear growth; exam findings may include skin&lt;br /&gt;
and hair changes, enlarged thyroid, and absent deep tendon reflexes. An abdominal exam should&lt;br /&gt;
assess liver size and tenderness. Postural and gait abnormalities may indicate the presence of&lt;br /&gt;
orthopedic conditions such as genu varum. Tanner stage should be evaluated and assessed in relation&lt;br /&gt;
to the child’s age. Rare genetic and endocrine abnormalities may manifest themselves through&lt;br /&gt;
dysmorphic features including abnormal genitalia, developmental delay, poor linear growth, hirsuitism,&lt;br /&gt;
and striae [41]. Blood pressure measurements should also be obtained using an appropriately sized&lt;br /&gt;
blood pressure cuff.&lt;br /&gt;
BODY MASS INDEX&lt;br /&gt;
Background&lt;br /&gt;
The World Health Organization, the Centers for Disease Control and Prevention, and many national&lt;br /&gt;
organizations recommend the use of BMI to identify overweight and obesity in youth [2,52,53].&lt;br /&gt;
BMI is a convenient measurement for screening for overweight in children. Standard BMI classifications&lt;br /&gt;
define a BMI between the 85th and 95th percentiles for age and sex as “at risk for&lt;br /&gt;
overweight,” and a BMI greater than the 95th percentile for age as “overweight” (Appendix A1.10).&lt;br /&gt;
BMI is an accepted screening tool for use by pediatric health care providers as a result of its use&lt;br /&gt;
of easily accessible data (weight and height) and moderately strong correlation with laboratory&lt;br /&gt;
measurements of body fatness [2,3,54].&lt;br /&gt;
Calculating Obesity Risk and Status with BMI Percentiles&lt;br /&gt;
Pediatric growth charts for the U.S. population now include BMI percentile grids for age and gender&lt;br /&gt;
and can be used for longitudinal tracking of a patient’s BMI from ages 2 through 20 years, and to&lt;br /&gt;
identify overweight (see Appendix A1.10) [29,53]. BMI is calculated by applying one of the&lt;br /&gt;
following formulas:&lt;br /&gt;
weight (kilograms)/height (meters)2&lt;br /&gt;
or&lt;br /&gt;
[weight (pounds)/height (inches)2] × 703.&lt;br /&gt;
Diagnosis&lt;br /&gt;
Once BMI is calculated, the physician or health care provider can determine risk and status by&lt;br /&gt;
plotting on Centers for Disease Control and Prevention growth charts (see Appendix A1.10). This&lt;br /&gt;
should be done at least annually to facilitate the early recognition of overweight and to monitor&lt;br /&gt;
weight increases relative to linear growth [2]. If a trend for excessive weight gain is established&lt;br /&gt;
(e.g., crossing BMI percentile channels or an increase of three to four BMI units in 1 year),&lt;br /&gt;
contributing factors should be explored and discussed with parents to prevent further progression&lt;br /&gt;
of excessive weight gain or overweight status. Research, although limited, indicates that early&lt;br /&gt;
treatment is associated with improved long-term success [29].</description><link>http://fatcampsforkids.blogspot.com/2012/09/clinical-evaluation-diagnosis-medical.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-6593796155354319563</guid><pubDate>Wed, 05 Sep 2012 01:52:00 +0000</pubDate><atom:updated>2012-09-04T18:52:37.005-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>LEARN TO PHYSICAL ACTIVITY IN THE MANAGEMENT OF OBESITY</title><description>1. Kiess, W., A. Galler, A. Reich, G. Muller, T. Kapellen, J. Deutscher et al. Clinical aspects of obesity&lt;br /&gt;
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Physiol Endocrinol Metab. 279:E348–E355, 2000.&lt;br /&gt;
&lt;br /&gt;
</description><link>http://fatcampsforkids.blogspot.com/2012/09/learn-to-physical-activity-in.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item><item><guid isPermaLink="false">tag:blogger.com,1999:blog-2451165783610843793.post-6539829493624246952</guid><pubDate>Wed, 05 Sep 2012 01:51:00 +0000</pubDate><atom:updated>2012-09-04T18:51:27.693-07:00</atom:updated><category domain="http://www.blogger.com/atom/ns#">KIDS FAT CAMP</category><title>PHYSICAL ACTIVITY RECOMMENDATIONS FOR OBESE CHILDREN</title><description>Exercise alone is not typically accepted as a tool for promoting the achievement of a healthy weight&lt;br /&gt;
in youth. A large quantity of physical activity is required to reduce body fat [8]. For example, to&lt;br /&gt;
metabolize just 1 pound of fat, which is equivalent to 3500 calories of energy expenditure, a healthyweight&lt;br /&gt;
adult male or an obese child with equivalent body mass must run approximately 30 miles.&lt;br /&gt;
But the benefits of exercise to the management of pediatric obesity are cumulative. Over time,&lt;br /&gt;
consistent physical activity will result in a multitude of metabolic and physiologic benefits [36,52].&lt;br /&gt;
In particular, frequent vigorous physical activity periods are shown to be associated with decreased&lt;br /&gt;
abdominal fat in male adolescents [53]. And the adult research literature indicates that regular&lt;br /&gt;
exercise training (&amp;gt; 6 months) improves fat oxidation (increased oxidative enzymes), glucose&lt;br /&gt;
metabolism (increased number of glucose transporters and glucose into triglycerides), mitochondrial&lt;br /&gt;
function, sympathetic nervous system activity (improved catecholamine stimulation response), and&lt;br /&gt;
lipoprotein lipase activity, which may, indirectly, positively affect metabolic profiles [36,54–56].&lt;br /&gt;
Together, these changes and resulting benefits will not only enhance dietary efforts during weight&lt;br /&gt;
loss but also promote long-term weight maintenance. Unfortunately, the positive effects of exercise&lt;br /&gt;
training will only be realized if the obese child complies with the prescribed physical activities.&lt;br /&gt;
Therefore, it is imperative that careful consideration be given to selecting the most appropriate&lt;br /&gt;
intensity, frequency, duration, and modality of exercise for each obese child. Table 6.2 provides&lt;br /&gt;
physical activity recommendations for obese children that may be safely and effectively used in&lt;br /&gt;
the pediatric clinical setting</description><link>http://fatcampsforkids.blogspot.com/2012/09/physical-activity-recommendations-for.html</link><author>noreply@blogger.com (mesothelioma.abestos.lawyers)</author><thr:total>0</thr:total></item></channel></rss>