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The syndrome X or metabolic syndrome may be defined as a
constellation of several interrelated risk factors of metabolic
origin which includes centrally distributed obesity, decreased high
density lipoprotein cholesterol, elevated triglycerides, elevated
blood pressure and hyperglycemia. Persons with syndrome X are at
twice the risk of developing cardiovascular disease, and are at
about five-fold the risk of type 2 diabetes mellitus as compare to
persons with this syndrome. There are considerable evidences of
important ethnic differences in the prevalence of syndrome X, its
components and sequelae. The prevalence varied between ethnic
groups even within the same geographical location. Apart from
multifactorial (genetic vs. environmental) nature, there are
intriguing metabolic and anthropometric differences found across
different ethnic groups. The estimates vary by ethnicity, for
instance, high prevalence in nonaEuropean groups such as Black
AfricanaCaribbeans, Hispanics, indigenous populations of North
America, South Asians, and the Western Pacific Region and lower
prevalence in Chinese populations, and EuropeanaWhite. Public
health strategies that are well known to be important for chronic
disease prevention in general can substantially reduce the
prevalence of syndrome X. Population-specific studies will be
important in identifying subgroups for which syndrome X is a health
issue and for which disease management strategies are needed.
Simultaneously, studies to identify different biomarkers associated
with syndrome X that are linked with the development of specific
chronic diseases, such as CVD and diabetes, will significantly
enhance the early detection of these diseases. Existing preventions
strategies, if implemented in population subgroups at highest risk,
may have a substantial effect on reducing these trends. The
prevalence of syndrome X increases with advancing age suggests that
the efforts to increase awareness of prevention strategies must
begin early. Intensive treatment and effective targeting efforts
would help in avoiding future sequelae of syndrome X across
different ethnicity. This book will be an assemblage of
similarities and differences in the risk of syndrome X and related
disorders among different ethnic groups worldwide, and reviews
potential mechanisms for ethnic differences. It would certain help
in translational research for early intervention and better
prevention of syndrome X and its associated public health burden
worldwide.
Obesity is a major risk for both cardiovascular disease (CVD) and
type 2 diabetes mellitus (T2DM). Obesity has reached epidemic
proportions globally, and evidence suggests that the situation is
likely to get worse in both developed and developing countries. It
is considered to be a predisposing factor for several chronic
diseases which include CVD, ischemic stroke, hypertension, T2DM,
vascular dysfunction, and proinflammatory and prothrombotic state.
This is where Syndrome X intersects with obesity and plays the role
of a common denominator for CVD and T2DM. Persons with Syndrome X
are more susceptible to CVD & T2DM.It is particularly relevant
to recognize that variation in disease susceptibility among
individuals in the population at large is a consequence of the
intersection of the distribution of genotypes with the distribution
of past environmental exposures and future environmental
trajectories. For instance, many individuals who have a genotype
that is found in those with disease will remain healthy because of
the compensatory effects of a different environmental history on
the same initial conditions. Similarly, individuals who do not have
a high risk genotype may develop a disease of an adverse
environmental history. That is, interaction between a particular
genotype and particular environmental exposures.In the thrifty
genotype hypothesis as proposed by Neel (1962), entire populations
have an increased predisposition to T2DM due to genetic selection.
They are better adapted to different nutritional circumstances than
those they experience today. In the thrifty phenotype hypothesis
(also known as Barkers Hypothesis), maladaptive responses occur as
a result of environmentally induced alteration of physiology in the
early life of the individual. Both hypotheses offer explanations of
why the frequency of diabetes and obesity may differ in different
populations and why predisposition to diabetes is common, albeit by
very different mechanisms. A third hypothesis called the common
soil hypothesis as mentioned by Lebovitz (2006) that diabetes and
CVD might share an underlying cause(s) is also described. Insulin
resistance is central both to the progression from normal glucose
tolerance to T2DM and to a constellation of CVD risk factors known
as Syndrome X or Metabolic Syndrome. Then there is the epigenome
that directly impacts gene expression and can be modified by both
genetic and environmental factors. It is the potentially heritable
changes in gene expression that does not involve changes to the
underlying DNA sequences a change in phenotype without a change in
genotype. The epigenoytpe is dynamic and varies over time and
tissues as a result of environmental exposure, aging, and diseases
and other factors.The present book is an assembly of the vast
knowledge that has been generated over the last decade worldwide in
the field of obesity and metabolic syndrome related disorders, and
an attempt to translate research findings into a clinically useful
tool for better diagnosis, intervention, and prevention of this
global public health burden. We hope this book will not only expand
the practice in the coming years, but that it will create new
avenues for future research as well.
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