Unlock Phase 1:-The question we can we unlock those genes
of PCO?? : The unlock phase -1: Can we unlock
the candidate genes resulting in to PCO and killing hundreds of women in India
a daily due to DM, CVS (MI in particular), hemorrhagic stroke , Thrombotic
stroke , endometrial Ca ?? PCOS is a multifactorial polygenic disease
(interaction between several genetic and environmental factors), with a
heritability of ~70 %. It is intrinsically difficult to study by a genetic
point of view, and most of the current literature (>70 studies based on the
candidate gene approach) is inconclusive, with many studies resulting
inconsistent, controversial, and without a clear consensus. Recently, the inheritance
was confirmed by some authors who found that PCOS was present in 35 % of the
mothers and 40% of the sisters of PCOS patients. Moreover, increased incidence
of insulin resistance in the fathers and brothers of PCOS women has been
considered as the “male phenotype” in PCOS families.
Ethnic
variations of genetic expression for hyperandrogenism: à phenotypic
variability of hyperandrogenic disorders. -The genes involved in the
pathogenesis of hyperandrogenism are expressed in a variable way depending on
the factors predominating in every different ethnic population. This explains
the phenotypic variability of hyperandrogenic disorders.
What is nongenetic inheritance?? Environmental cause of PCO??
.Some insults during pregnancy may induce to intrauterine growth retardation,
which probably induces a “thrifty phenotype” in small for gestational age
babies potentiated by in adult life by environmental factors such as a sedentary lifestyle
and a diet rich in saturated fat. . To summarize there is
one nongenetic theory of PCO
which is of no less importance than genetic cause of PCO.:-theory is
that the features of PCOS families result from nongenetic inheritance,and they
are related to environmental factors that are present only in the affected
families. Researchers have hypothesized that some insults during pregnancy may
induce to intrauterine growth retardation, which probably induces a “thrifty
phenotype” in small for gestational age babies.These have a high risk of
suffering from insulin resistance, which may result in hypertension, glucose intolerance,
adrenal axis hyperactivity with relative cortisol excess, functional
hyperandrogenism, and PCOS later in life, especially if they are exposed to
environmental factors such as a sedentary lifestyle and a diet rich in
saturated fat. These environmental factors may cluster in certain families
because exercising and dieting are greatly influenced by parental lifestyle.
The metabolic abnormalities of the “thrifty phenotype” can induce additional
insult to the pregnancies of these SGA (small for gestational age) and PCOS
women, and these defects might be transmitted to another generation without the
participation of any genetic abnormality.
Q. Can we prevent nongenetic inheritance of PCO?? If small for
gestational age babies , after birth and during upbringing have healthy habits,
insulin resistance and its consequences might be improved, and theoretically,
the third generation -à their fetuses will not be exposed to a hostile
metabolic environment during pregnancy(as mother has god lifestyle during her
childhood and puberty, adolescent and such good health habits continue to be
practiced in childbearing age too then her siblings will not have PCO. This
dedication of adhering to strict good eating and exercising habit will ,
prevent nongenetic inheritance of these conditions, PCO, DM, MI in particular .
However, intrauterine growth restriction might be influenced by genetic
variants as well, and the most likely scenario is represented by an interaction
between predisposing genetic abnormalities and unfavorable environmental
conditions.
Thus, even if several studies conducted in families of women
with PCOS have demonstrated the genetic basis of the syndrome, nowadays a
genetic pattern certainly involved in PCOS predisposition has not been
identified.
Most studies have included different kinds of genes: those
related to androgen biosynthesis and action and their regulation, genes
involved in insulin resistance and associated disorders, and also genes
involved in chronic inflammation and atherosclerosis
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