Biomedical Therapy - International Academy of Homotoxicology

) 16
) Refresh Your Homotoxicology
Which Came First:
Insulin Resistance or Inflammation?
It is well established that persistently
elevated levels of inflammatory
cytokines play a significant role
in the development of chronic disease.
For example, persistently high
levels of 1 or more of the proinflammatory
cytokines (ie, interleukins 1
and 6 and tumor necrosis factor α)
are common to the pathogenesis of
diseases such as cardiovascular disease,
cancers, inflammatory bowel
disease, chronic fatigue syndrome,
and neurological disorders (eg, depression,
Parkinson disease, and
Alz heimer disease). 1
The elevation of these cytokines has
become such a common thread for
the development of these diseases
that the term sickness behavior2,3 has
recently been proposed to describe
the associated signs and symptoms
of fever, anorexia, fatigue, sleepiness,
and social withdrawal. Additional
support for the paramount
importance of inflammation in disease
development has recently come
from the Justification for the Use of
Statins in Primary Prevention: An
Intervention Trial Evaluating Rosuvastatin
(JUPITER). The results of
this trial suggest that the proposed
benefit of statin drugs in the prevention
of cardiovascular disease was
more likely because of their ability
to reduce levels of high-sensitivity
C-reactive protein (a nonspecific inflammatory
marker) than their effects
on lowering cholesterol. 4
By David W. Lescheid, PhD, ND
Although there are some similarities,
the inflammatory component of
chronic diseases is different from the
inflammatory response associated
with tissue repair and recovery that
follows acute injury or infection.
This subclass of inflammation may
be termed metainflammation (metabolic
inflammation), because of its
initiation by nutrients and metabolic
surplus 5 ; or parainflammation, because
it shares intermediate characteristics
between the basal and acute
inflammatory state. 6
Chronic inflammation does play an
important role in disease processes.
An important question to ask is as
follows: Why has the inflammation
occurred in the first place (ie, what is
the nature of the inflammatory inducer
or trigger)? There are several
different theories and proposed
mechanisms; however, one of the
most promising current models suggests
that dysregulated cell metabolism,
particularly from nutrient excess
and the associated altered
insulin signaling, 7 is one of the most
important initiating events. This article
will discuss the roles of hyperinsulinemia
and of a few potential
triggers of excess insulin in the development
of disease, with some examples
of the effect on women’s
health issues.
Men and women have substantial
differences in body composition,
such as distribution of visceral and
hepatic adipose tissue and lean body
Journal of Biomedical Therapy 2011 ) Vol. 5, No. 1
mass, and in sex hormone and adipokine
levels. These differences tend
to improve insulin sensitivity in
women compared with men 8 and
suggest that sex differences must be
considered when preventing and
treating diseases associated with insulin
resistance.
There is no question that obesity has
reached epidemic proportions in
many parts of the world. In many
countries, particularly those of industrialized
and developed nations,
there is a regular excess intake of
calories from increasingly caloriedense
but nutrient-poor foods and
drinks. The excess of calories, combined
with an increasingly less
physically active society, creates a
daily energy surplus that eventually
leads to a dysregulation of the
body’s key storage hormone, insulin
(Figure). 9 With cells no longer sensitive
to insulin and a surplus of blood
glucose triggering the continued release
of insulin from the pancreas,
hyperinsulinemia develops.
Adipose tissue is an endocrine organ
releasing many different signaling
molecules, some of which have direct
localized and systemic inflammatory
effects. 10 The development
of adipose tissue is preceded by an
impairment of energy balance that is
primarily associated with the inability
of the cells to respond to insulin,
either through inadequacy of insulin
receptor signaling or some other
defect in the biochemical pathway.