Inflammaging
Taka
Inflammaging is a term coined to describe one way in which the immune
system runs awry with age. Like a malfunctioning thermostat, the level
of inflammatory response is consistantly too high, leading to damage
to aged tissue:
Inflammation is necessary to cope with damaging agents and is crucial
for survival, particularly to cope with acute inflammation during our
reproductive years. But chronic exposure to a variety of antigens,
especially to some viruses such as cytomegalovirus, for a period much
longer than that predicted by evolution, induces a chronic low-grade
inflammatory status that contributes to age-associated morbidity and
mortality. This condition carries the proposed name "inflammaging".
I noticed a paper today which contains an interesting take on how
inflammation leads to damage. It's not just the inflammatory response,
per this theory, but also the anti-inflammatory systems evolved to
shut off an inflammatory response after it has served its purpose. If
inflammation is constantly jammed on, then so is the anti-inflammatory
system - based on the hormone cortisol - that is trying to shut it
down. So you have at once all the downsides of both a constantly
active immune system, and an immune system that is constantly damped
down: damage from constant activity yet poor immune response when you
do need it to fight off disease:
"Inflamm-aging" denotes the up-regulation of certain pro-inflammatory
cytokines at older ages, and associated chronic diseases. It is well
known that blood levels of cortisol also increase with age, an
increase commonly considered to be due to activation of the
Hypothalamus-Pituitary-Adrenal (HPA) axis by many non-specific
stressors.
On the contrary, herein I describe how the activation of Hypothalamus-
Pituitary-Adrenal (HPA), far from being unspecific, constitutes: a)
the main specific response and counterbalance to "Inflammaging" ('anti-
inflammaging'), b) an explanation for the well known paradox of immune-
senescence: i.e. the coexistence of inflammation and immunodeficiency,
as well as c) a complex mechanism of remodelling elicited by
inflammaging, explaining the long and winding pathophysiological road
that goes from robustness to frailty.
Indeed, the phenomenon of anti-inflammaging, mainly exerted by
cortisol, with the passage of time becomes the cause of a marked
decline of immunological functions, and its coexistence with the
increased levels of pro-inflammatory cytokines of inflammaging,
ultimately have negative impacts on metabolism, bone density,
strength, exercise tolerance, the vascular system, cognitive function,
and mood. Thus inflammaging and anti-inflammaging together determine
many of the progressive pathophysiological changes that characterize
the "aged-phenotype", and the struggle to maintain robustness finally
results in frailty.
The author points to cortisol, and if you look at the Wikipedia entry
you will see touches upon a wide range of vital systems in the body.
If inflammation is always on, then excess cortisol is constantly
trying to turn it off, causing harm along the way.
Fortunately solutions to prevent the immune system from getting into
this state in the first place are within sight. If the medical
research community makes a sane shift from a philosophy of futile
attempts to patch up the end results of aging to preventing and
reversing specific degenerations earlier in life, then I imagine we'll
see a range of ways to restore a damaged immune system in the clinic
by 2030.
SOURCE: http://www.fightaging.org/archives/001642.php
----------------------------
How about the Mead acid-charged inflammatory responses, wouldn't they
be fast and promptly turned off, i.e. non-chronic ? The "experts"
just keep blaming everything on the viruses while they are missing the
role of arachidonic acid and lipid peroxidation in the chronic
inflammatory states ...
Taka
Taka
Inflamm Res. 2008 Dec;57(12):558-563.
Exploring the complex relations between inflammation and aging
(inflamm-aging): anti-inflamm-aging remodelling of inflamm- aging,
from robustness to frailty.
Sergio G.
Clinical Laboratory & Molecular Diagnostics, Geriatric Hospital INRCA-
IRCCS-, 60100, Ancona, Italy.
"Inflamm-aging" denotes the up-regulation of certain pro-inflammatory
cytokines at older ages, and associated chronic diseases. It is well
known that blood levels of cortisol also increase with age, an
increase commonly considered to be due to activation of the
Hypothalamus- Pituitary- Adrenal (HPA) axis by many non-specific
stressors. On the contrary, herein I describe how the activation of
Hypothalamus- Pituitary-Adrenal (HPA), far from being unspecific,
constitutes: a) the main specific response and counterbalance to
"Inflammaging" ('anti-inflammaging'), b) an explanation for the well
known paradox of immune-senescence: i.e. the coexistence of
inflammation and immunodeficiency, as well as c) a complex mechanism
of remodelling elicited by inflammaging, explaining the long and
winding pathophysiological road that goes from robustness to
frailty.Indeed, the phenomenon of anti-inflammaging, mainly exerted by
cortisol, with the passage of time becomes the cause of a marked
decline of immunological functions, and its coexistence with the
increased levels of pro-inflammatory cytokines of inflammaging,
ultimately have negative impacts on metabolism, bone density,
strength, exercise tolerance, the vascular system, cognitive function,
and mood. Thus inflammaging and anti-inflammaging together determine
many of the progressive pathophysiological changes that characterize
the "aged-phenotype", and the struggle to maintain robustness finally
results in frailty.The same consequences also result the age-dependent
decline of dehydroepiandrosterone (DHEA).
PMID: 19109735