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العنوان
Metabolic syndrome as a predictor of cancer /
المؤلف
Alhag Mudather, Manahil Abdelmaged.
هيئة الاعداد
باحث / مناهل الحاج
مشرف / ناديه مبروك
مشرف / محمد هانى
مشرف / محمد كامل
الموضوع
Family Medicine. Cancer.
تاريخ النشر
2014.
عدد الصفحات
165 P. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
ممارسة طب الأسرة
تاريخ الإجازة
1/1/2014
مكان الإجازة
جامعة قناة السويس - كلية الطب - طب الاسره
الفهرس
Only 14 pages are availabe for public view

from 165

from 165

Abstract

The symptoms of the metabolic syndrome arenot immediate and direct ones (of the cause –effect type), but they are shifted in time and morefinely interconnected, so that, although thedeteriorations are obvious, it is quite hard toestablish with absolute certainty how they were gotto, the decisive factors having still to be properlyelucidated.
Metabolic syndrome necessitates more thoroughgoingstudies, before its definition as a “syndrome”would be fully justified and before its clinical
usability would be adequately defined.
the central features of the metabolic syndrome areinsulin resistance, visceral adiposity, atherogenic dyslipidemia andendothelial dysfunction. These conditions are interrelated and sharecommon mediators, pathways and pathophysiological mechanisms.
A comprehensive definition of the metabolic syndrome, expressed
as simply as possible, would contain only these features. Therequirement of multiple criteria would ensure the exclusion ofpeople with individual components (e.g. isolated hypertension orisolated hyperlipidemia), as opposed to the compositepathophysiology discussed above. Inclusion of both TG and HDLcriteria increases the specificity for atherogenic dyslipidemia, andinclusion of the blood pressure criterion ensures that thephysiologic derangements are severe enough to have resulted in
endothelial dysfunction.
Of the various definitions for the metabolic syndrome, theNCEP ATP III definition is the easiest to apply clinically andepidemiologically, because it uses straightforward criteria thatare measured readily. Despite the ongoing controversy aboutwhether the concept of metabolic syndrome is useful, it clearlydefines specific pathophysiological mechanisms that link thecentral features. Consideration of metabolic syndrome as aspecific entity allows for research on the genetic basis forsusceptibility to this syndrome, a better understanding of itsunderlying pathophysiology and thedevelopment of treatmentapproaches.
from an anthropological point of view, themetabolic syndrome can only be defined byanthropometry, as the populational/racial anthropologicalstudies are, for the time being, at an incipientstage.
The clustering of risk factors that constitute the MetS is foundto be common in most countries of the world. In theAmericas, in Europe, and in India, at least one-fourth of theadults carry the syndrome. Because the MetS at least doublesthe risk for ASCVD, compared with the population withoutthe syndrome, the MetS likely accounts for up to half of all
ASCVD. But because it also is associated with a very risk fortype 2 diabetes, or with diabetes itself, the cardiovascular riskimparted by the MetS may be even greater than currentestimates indicate.
For this reason, there is urgency for development of betters approaches to the prevention andmanagement of the syndrome. It is not enough to say “justtreat the established risk factors.” More importantly, an effort
must be made to strike at the underlying causes of thesyndrome. Certainly reversal of the worldwide epidemic ofobesity and physical inactivity must be a high priority. But inaddition, better means to treat underlying susceptibility to thesyndrome also are needed. Both approaches represent a greatchallenge to research in the cardiovascular and diabetesfields.
Prevalence of obesity and the metabolic syndrome has shown a
rapid rise in developing countries in the past few decades and has
led to increased risk ofCVDand consequent morbidity and mortality.
Because both undernutrition and overnutrition are seensimultaneously in developing countries, the double burden ofdiseases makes the situation more difficult. The various factorsresponsible for increasing non communicable diseases NCDs are rapid nutrition transition,rural-to-urban migration, increasingly sedentary occupationsand lifestyle, and maternal-fetal factors. Both genetic and environmentalfactors seem to contribute to it; however, the role ofenvironment seems to be predominant. Health interventions requiredto prevent or reduce the morbidity/mortality need to beaddressed in both children and adults. Interventions should beaimed at increasing the physical activity along with healthierfood patterns and health education. Successful communitybasedintervention programs have been reported in developedcountries, and a similar approach is required in developing countries.
Reports of interventional programs in China and India,especially directed toward children, have shown encouragingresults, but large-scale programs involving adults/children arerequired. Various other health strategies consisting of individualand community initiatives, backed up by governmental and legislativeefforts, would also help in minimizing the increasingprevalence of obesity and the metabolic syndrome in developingcountries.
The present review has highlighted the high prevalence of MetS in adults and children across the Middle East. This epidemic has great negative public health potential, which is not limited to any single country, age group or gender. National health authorities in the Middle East, as well as across the globe, need to take immediate and urgent action to arrest the MetS epidemic. Raising awareness about this lurking disease is but the first step in ensuring affirmative and aggressive action in tackling MetS in the Middle East.
Most studiesshow that the MetS is associated with an approximate doublingof CVD risk and that the risk for incident T2D is morethan five times higher in individuals with the MetS comparedwith those without the syndrome. In addition, the MetS isassociated with a number of other comorbidities such asNAFLD, sleep disorders, reproductive tract disorders, andmicrovascular disease.
It is unclear whether there is a unifying pathophysiologicalmechanism resulting in the MetS, so it is unclearwhether the MetS can be treated in and of itself. It is ouropinion that lifestyle modification and weight loss should beat the core of treating or preventing the MetS and itscomponents.It is well established that weight loss with diet andphysical activity is beneficial for treating all of the componentsof the MetS, including excessive adiposity, dyslipidemia,hypertension, insulin resistance, and hyperglycemia. Inaddition, there is someconsensus on treating the individualcomponents of the MetS with the overall goals of reducingthe risk for or preventing CVD and T2D.
Metabolic syndrome is recognized as a multiplex riskfactor for cardiovascular disease and type 2 DM. Althoughthe predictive usefulness of metabolic syndrome willcontinue to be debated, it does have practical utility in theclinical setting.
Available evidence from epidemiological, clinical, translational, and experimental studies supports the hypothesis that metabolic syndrome or components of metabolic syndrome may be important etiologic factors for certain cancers, progression of some cancers as well as altering the outcome of some cancers such as colorectal cancer, prostate cancer , breast cancer , liver cancer and so on . we describe the effects of the metabolic syndrome (obesity and Type 2 diabetes) on cancer development and progression. We stress that the insulin and IGF systems are important causal factors in this connection. However, there are a number of other factors that may play important roles as well. Clearly the tumor promoting potential of the insulin resistant IR and IGF-1R might be a promising answer to identify major cancer promoting mechanisms, with therapeutic possibilities, in such a high-prevalent disease like the metabolic syndrome.While research continues to work toward preventing cancers, nutritional and lifestyle modifications may alleviate metabolic syndrome and reduce the risk.