ISIS Press Release 10/11/09
Overstimulation of the immune system may trigger acute heart
disease and sudden deaths in the increasing number of people
with atherosclerosis; this hidden risk of mass vaccination
programmes against swine flu could far outweigh the benefits
Dr. Mae-Wan Ho
This report has been submitted to the US FDA and Sir Liam
Donaldson, UK Chief Medical Officer. Please circulate
widely. You have permission to repost this article provided
you leave it unchanged and with all links intact.
Mass vaccinations amid mounting safety concerns
***********************************************
Mass vaccinations for the pandemic H1N1 'swine flu' have
begun in Britain, the United States, Sweden and elsewhere,
targeting hundreds of millions around the world as concerns
mount over the safety of the fast-tracked vaccines [1-3] (
Fast-tracked Swine Flu Vaccine under Fire , SiS 43; Swine
Flu Pandemic - To Vaccinate or Not to Vaccinate? , Flu
Vaccines and the Risk of Cancer , SiS 44). The risks
identified so far include neurological damage, developmental
defects, and autoimmune diseases from vaccine adjuvants; the
potential for generating more virulent disease agents from
live attenuated viral vaccines, and cancer from contaminants
of cultured cells used to grow the vaccine viruses, or from
chemical agents employed in killing the vaccine viruses.
Now, researchers at Mainz University Medical Center in
Germany led by Sucharit Bhakdi have added cardiovascular
risks that are not generally appreciated. Animal experiments
and epidemiological data suggest that over-stimulation of
the immune system may accelerate atherogenesis (the build-up
of fatty deposits or plaques on the inner wall of arteries)
[4]. They are especially concerned about vaccines containing
adjuvants to boost immune response, which could aggravate
the formation of plagues and atherosclerosis disease. The
risks of other widespread diseases due to deregulated immune
systems are also possible. Safety trials of vaccines
conducted so far have not specifically taken those possible
side-effects into account, and 'unexpected serious adverse
effects' may follow in the wake of mass vaccination
programmes. This proved prophetic.
Four deaths in less than two weeks
**********************************
Less than two weeks into its mass vaccination, Sweden
reported four deaths [5], among which were at least two with
underlying heart condition. According to the Swenska
Dagladet newspaper, there were also 350 side effects
recorded [6]. The Swedish Institute for Infectious Disease
Control denies that the deaths are connected with the
vaccine.
But this possibility was predicted in the paper published by
Bhakdi and colleagues [4].
Two vaccines with adjuvants
***************************
There are two main vaccines with adjuvants. One, modeled
after Fluad and widely used in European countries including
Germany contains the adjuvant MF59 made by Novartis, and is
also deployed worldwide mainly for people over 65 years of
age. MF59 is a squalene oil-in-water emulsion; but its
mechanism of action is still poorly understood. It appears
to induce recruitment of macrophages (white blood cells that
ingests foreign material and dead cells) to the injection
site and promote uptake of antigen by macrophage and
dendritic cells that process antigens to promote production
of specific antibodies. Injection of flu vaccines with the
adjuvant frequently causes local pain and occasionally
fever, indicating that pro-inflammatory cytokines (signaling
molecules produced by immune cells) are generated [7]. There
is further evidence that injection of squalene can provoke
autoimmune responses [1, 2].
Flu vaccines with MF59 adjuvant have been given to children,
but there is little experience with their use in pregnant
women who are currently in the priority group for
vaccination [1, 2].
Another H1N1 vaccine with adjuvant is developed by
GlaxoSmithKline (GSK). The adjuvant is AS03 [1], similar to
MF59 in that it contains squalene, and in addition, the non-
ionic detergent polysorbate 80 (Tween 80)., which is yet
uncharacterized in terms of pharmacokinetic and
immunological properties [4]. Studies with vaccines
containing AS03 in infants, young children or pregnant women
have not been published. And current clinical studies are
being conducted with children aged 3-17 years.
Hidden dangers of H1N1 vaccines with adjuvants
**********************************************
Immune mechanisms are now implicated in such a diversity of
chronic diseases that no common denominator would have come
to mind before the advent of modern immunology [4]. That is
why the potential dangers of vaccine adjuvants such as those
used with the current H1N1 swine flu vaccines are still not
adequately addressed.
A major hurdle to addressing the dangers is the lack of
specificity in the self-destructive processes perpetrated by
an over-stimulated immune system. It is now recognized that
the innate, relatively non-specific immune mechanisms are
just as culpable as the specific, adaptive immune mechanisms
in the pathology of some of the most widespread human
diseases including atherosclerosis, inflammatory bowel
disease, demyelinating disease and non-infectious arthritis;
and the list is ever growing.
More baffling still is that such pathological processes
sometimes have their roots in normal physiological events
that serve useful biological functions.
For example, macrophages are involved in clearing tissues of
cholesterol, which is poorly soluble. Atherosclerosis
disease becomes manifest only when this cholesterol clearing
role breaks down through overload, and lesions develop in
the artery wall. The macrophages then cease to perform their
physiological function and become the perpetrator of disease
(see box).
Macrophages and atheroclerosis
******************************
Macrophages are large white blood cells that have the
ability to phagocytose (engulf) foreign materials such as
bacteria and viruses and debris from dead cells. They are a
very important component of innate immunity, not only in
protecting the body against pathogens, but also in
scavenging and tissue repair. However, macrophages are also
involved in the development of atherosclerosis 'hardening
of the arteries due to fatty deposits (plaques) in the
arterial wall' and especially in the acute clinical disease
resulting from the rupture of the plaques [8].
Atherosclerosis is an inflammatory disease triggered by the
over-stimulation of the immune system. It accounts for 39
percent of deaths in the UK, while 12 million in the USA
have atherosclerosis-associated disease. Atherosclerosis
results in narrowing the arteries, producing stable angina
(chest pains due to blockage of arterial blood flow) or else
dramatic rupture, producing acute syndromes such as unstable
angina, myocardial infarction (heart attack, when the blood
supply to part of the heart is interrupted causing some
heart muscle cells to die), or sudden death . Macrophages
are abundant in ruptured atherosclerotic plaques and are
suspected of causing the rupture. As they belong to the
innate immunity branch that does not require specific
recognition, macrophages may damage tissues
indiscriminately. Macrophages are recruited and activated by
many signals and they have an impressive arsenal of
molecules to promote tissue damage.
Macrophage recruitment to the developing atherosclerotic
plaques is aided by the expression of special inflammatory
adhesion molecules in the abnormal lining of the arterial
wall over the plaques, which are up-regulated by multiple
atherosclerosis risk factors including oxidized low density
lipoprotein (oxLDL, bad cholesterol), smoking, hypertension
and diabetes. The activated macrophages express effector
molecules that kill cells and degrade the extracellular
matrix. These include Fas-L and nitric oxide (NO).
Macrophage NO up-regulates vascular smooth muscle cell
(VSMC) surface Fas (the binding partner for Fas-L) priming
the VSMC for apoptosis (programmed cell death). As VSMCs
promote plaque stability, their apoptosis may contribute to
plaque rupture. Macrophages also express multiple
metalloproteinases ( e.g. stromelysin) and serine proteases
( e.g. urokinase) that degrade the extracellular matrix,
weakening the plaque and making it prone to rupture. In
addition, macrophages secrete numerous other effectors
including reactive oxygen species that kill bacteria under
normal conditions [9] (see The Body Does Burn Water , SiS
43) , but will cause oxidative damage to cells when
overproduced as the result of environmental stress.
Read the rest of this article here:
http://www.i-sis.org.uk/CRSFV.php
========================================================
This article can be found on the I-SIS website at
http://www.i-sis.org.uk/
If you like this original article from the Institute of
Science in Society, and would like to continue receiving
articles of this calibre, please consider making a donation
or purchase on our website
http://www.i-sis.org.uk/donations.
ISIS is an independent, not-for-profit organisation
dedicated to providing critical public information on
cutting edge science, and to promoting social accountability
and ecological sustainability in science.
========================================================
CONTACT DETAILS
The Institute of Science in Society, PO Box 51885, London
NW2 9DH
telephone: [44 20 8452 2729] [44 20 7272 5636]
Foe email details, see http://www.i-sis.org.uk/contact.php
| . |
|
. |