Newsgroup: it.salute
Titolo: CRONIC FATIGUE SINDROME_1

Salve sono Roberto, ho 29 anni e da 11 ammalato di una firma grave di CFS
dopo una forte varicella ed un morbillo a circa 18 anni. Come spesso accade
per chi è ammalato di CFS mi è stata diagnosticata prima una malattia
autoimmunitaria "morbo di crohn"; conosco persone a cui era stata
diagnostica una sclerosi multipla o una artrite reumatoide. Questo accade
perchè la sindrome dafatica cronica produce un complesso di sintomi ed
anomalie biologighe che se non ben differenziate portano a simulazioni vere
e proprie di malattie autoimmunitarie o malattie allergiche.
Ho voluto postare questo messaggio per informare i medici ed le persone che
seguono questo post delle ultime ricerche in merito sulle cause e sulle
terapie che si stanno attuando nel mondo.
Anche a me come leggerete nella documentazione in seguito riportata la
terapia a base di cicli di antibiotici per mesi da buoni risultati fino a
far sparire del tutto alcune dei vari sintomi che caratterizzano questa
sindrome e quindi anche la mia malattia.
Date un'occhiata a questo sito
www.immed.org
è il sito del centro americano che più si sta occupando delle implicazioni
batteriche nella cfs e nella sindrome della guerra del Golfo. Oltre
naturalmente ai CDC (Center for Diseas Control) di Atlanta dove la CFS è
considerata una delle priorità; è dove sono stati predisposti i criteri per
poter fare diagnosi di CFS.
P.S. Vanoli per favore fuori dalle balle, perchè tu non dici niente di cui
una persona sana di mente possa giovarsi.
Clinical Practice of Alternative Medicine 2000; 1(2): 42 - 102
Diagnosis and Integrative Treatment of Intracellular Bacterial Infections in
Chronic Fatigue and Fibromyalgia Syndromes, Gulf War Illness, Rheumatoid
Arthritis and other Chronic Illnesses
Garth L. Nicolson,* PhD, Marwan Y. Nasralla,*+ PhD, A. Robert Franco, MD,
Nancy L. Nicolson,* PhD,  Robert Erwin,* MD, Richard Ngwenya, MD, and Paul
A. Berns,* MD
*The Institute for Molecular Medicine, Huntington Beach, CA 92649 USA,
+International Molecular Diagnostics, Inc., Huntington Beach, CA 92649 USA
 Arthritis Center of Riverside, Riverside, CA 92501  USA,
James Mobb Immune Enhancement, Harare, Zimbabwe
Address correspondence to: Prof. Garth L. Nicolson, The Institute for
Molecular Medicine, 15162 Triton Lane, Huntington Beach, CA 92649.  Tel:
714-903-2901
; Fax: 
714-379-2082
;  Website: 
http://www.immed.org
;/ Email:
gnic...@immed.org
.
ABSTRACT
Bacterial and viral infections are associated with many chronic illnesses as
causative agents, cofactors or more likely as opportunistic infections in
immune suppressed individuals.  The prevalence of invasive pathogenic
Mycoplasma species infections (and possibly other bacterial infections, such
as Chlamydia, Borrelia, etc.) in patients with Chronic Fatigue Syndrome,
Fibromyalgia Syndrome, Gulf War Illness, Rheumatoid Arthritis and other
chronic illnesses was significantly higher than in healthy controls.  When
we examined chronic illness patients for multiple Mycoplasma species
infections, we found that almost all patients had multiple intracellular
infections, suggesting that multiple bacterial infections commonly occur in
certain chronic illness patients.  These patients generally respond to
particular antibiotics if administered long-term, but an important part of
their recovery involves nutritional supplementation with appropriate
vitamins, minerals, immune enhancement and other supplements.
Nutraceuticals appear to be necessary for recovery and maintenance of a
strong immune system.  In addition, patients should be removed from
potentially immune-depressing drugs, such as some antidepressants, to allow
recovery of their immune systems. Other chronic infections (viral), may also
be involved in various chronic fatigue illnesses with or without mycoplasmal
and other bacterial infections, and these multiple infections could be
important in causing patient morbidity and resulting difficulties in
treating these illnesses.
INTRODUCTION
        Most if not all debilitating chronic illnesses are characterized by
the presence of chronic fatigue (1), the most commonly reported medical
complaint of all patients seeking medical care (2).  The fatigue syndromes,
such as Chronic Fatigue Syndrome (CFS or Myalgic Encephalomyelitis [ME]),
Fibromyalgia Syndrome (FMS) and Gulf War Illnesses (GWI), share many
complex, multi-organ signs and symptoms (3-6), including immune system
abnormalities (7), but are distinguishable as separate syndromes that have
muscle and overall fatigue as major signs.  These syndromes usually have
overlapping signs and symptoms, including muscle pain, chronic fatigue,
headaches, memory loss, nausea, gastrointestinal problems, joint pain,
vision problems, breathing problems, depression, low grade fevers, skin
disorders, tissue swelling, chemical sensitivities, among others (5, 6, 8).
Because of the complex nature of these illnesses, many patients are often
diagnosed with multiple syndromes, and their potential to recover from their
chronic illness is usually poor at best.
Chronic illness patients usually have cognitive problems, such as short-term
memory loss, depression, difficulty concentrating and psychological problems
that can result in practitioners diagnosing chronic illness patients with
somatoform disorders rather than organic problems (6, 8). Thus due to the
lack of definitive laboratory or clinical tests that could identify the
cause(s) of chronic illnesses, such disorders are thought to be caused for
the most part by psychological stressors.  In fact, emotional stress is
often an important factor in somatoform disorders, and stress itself can
have many effects on the hormonal and immune systems that could be
detrimental in virtually any chronic illness (9).  But we feel strongly that
stress alone is unlikely to cause most of the chronic illnesses discussed
here, the most classic being GWI (6, 8), where battlefield stress was
promoted as the cause of the illness (10). GWI patients are often diagnosed
with Post Traumatic Stress Disorder (PTSD), but the evidence that stress or
PTSD is the source of GWI is based on the assumption that veterans must have
suffered from stress by virtue of the stressful environment in which they
found themselves during the Gulf War (10).  The notion that stress is the
major factor in GWI or indeed in other chronic illnesses, we feel, is not
supported by most evidence that suggests that these illnesses were caused by
toxic exposures (10, 11).
There is growing awareness that the chronic fatigue illnesses, such as
CFS/ME, FMS, GWI and certain autoimmune illnesses, such as Rheumatoid
Arthritis (RA), among others, can have an infectious nature that is either
responsible (causative) for the illness, a cofactor for the illness
(required but not the only causative factor) or more likely appears as an
opportunistic infection(s) responsible for aggravating or causing patient
morbidity (8, 11, 12).  There are several reasons for this notion, including
the nonrandom or clustered appearance of the illnesses, often in immediate
family members, the course and signs/symptoms of the illnesses and their
responses to therapies based on treatments directed at infectious agents and
enhancement of immune responses.  Most chronic fatigue illnesses are
difficult to treat and do not have effective therapies, and these patients
rarely recover from their illnesses (11), causing in some cases catastrophic
economic problems.  Here we will discuss methods for diagnosing chronic
infections in patients with CFS/ME, FMS, GWI, RA and other chronic illnesses
and offer some suggestions for appropriate treatments directed at some of
the chronic infections that play important roles in these illnesses.
SIMILAR SIGNS AND SYMPTOMS OF CHRONIC ILLNESSES
        Most chronic illnesses have complex but relatively nonspecific signs
and symptoms that are not characteristic for a particular disease.  However,
other chronic illnesses, such as RA, are well established in their
diagnostic profiles (13, 14).  One difference between some of the most
common chronic illnesses appears to be in the severity of particular signs
and symptoms.  For example, in CFS/ME essentially all patients complain of
chronic fatigue and joint pain, stiffness and soreness, whereas in FMS
essentially all patients complain of muscle and overall pain, soreness and
weakness.  But when secondary signs and symptoms of these chronic illnesses
are compared, they look very similar (6, 8).  For the most part, the
signs/symptom profiles of CFS/ME, FMS, GWI illnesses are similar (Fig. 1).
Thus the chronic illnesses under discussion here have overlapping signs and
symptoms, suggesting that these illnesses may be related (8).  In addition,
CFS/ME, FMS and GWI patients often show increased sensitivities to various
environmental irritants and chemicals and enhanced allergic responses,
suggesting that their immune systems are, at least in part, dysfunctional.
This is supported by laboratory studies on the natural immune and other
immunological abnormalities in chronic illness patients (7).
The overlapping signs and symptoms of many chronic illness patients are
easily documented.  For example, the patient signs/symptoms data presented
in Figure 1 were obtained using patient Illness Survey Forms to determine
common signs and symptoms at the time when blood was drawn from patients for
analysis.  In this figure the intensity of approximately 120 patient signs
and symptoms prior to and after onset of illness were recorded on a 10-point
rank scale (0-10, extreme).  The data were then arranged into 29 different
signs and symptoms groups and were considered positive if the average value
after onset of illness was two or more points higher than prior to the onset
of illness.  The CFS/ME and FMS patients had complex signs and symptoms that
were similar to those reported for GWI, and the presence of rheumatic signs
and symptoms in each of these disorders indicates that there are also some
similarities to RA (13-15) (Fig. 1). Some differences were noted, however,
when patients with chronic illnesses without evidence of intracellular
bacterial infections were compared to the above groups (Fig. 1).  The data
suggest that patients with intracellular bacterial infections have more
complex clinical signs/symptoms.
In our signs/symptom analyses it was not unusual to find immediate family
members who displayed similar chronic signs and symptoms.  For example, we
found that the spouses and children of GWI patients often slowly developed
chronic illnesses with signs and symptoms similar to GWI, but only some time
after the return home of veterans who developed GWI (8, 10, 11).  That these
civilian patients contracted their illnesses from chronically ill family
members with GWI was a likely explanation (8) that was supported by the
finding of similar chronic infections in these families (8, 11).
CHRONIC INFECTIONS AND MORBIDITY IN CFS/ME, FMS AND GWI
Although chronic illnesses have been known in the medical literature for
years, most patients with CFS/ME, FMS, GWI and in some cases RA have had few
treatment options.  This is probably due to the fact that the underlying
causes of most chronic illnesses are unknown and treatments have been mainly
palliative or supportive.  Even if the causes or triggering events in
chronic illnesses are not understood, these illnesses may show similarities
in their progression; that is, they could have different initial causes or
triggers but similar secondary events that result in progression (8, 11).
We have proposed that the secondary event(s) could be opportunistic viral
and/or bacterial infections that cause significant morbidity and illness
progression (10-12).  With time these secondary events may evolve or
progress to be important or even dominant factor(s) in determining overall
signs/symptoms and treatment strategies.
Since indirect evidence suggests the infectious nature in at least certain
subsets of chronic illness patients (8, 11, 12), we have been examining
chronic illness patients for pathogens that could explain, at least in part,
their complex signs and symptoms.  One type of infection that could fulfill
the criteria of association with a wide range of chronic illness signs and
symptoms are certain microorganisms of the class Mollicutes (8, 11, 12).
This is a class of small bacteria, lacking cell walls and genetics for lipid
and other macromolecule synthesis pathways.  It is primarily composed of
Mycoplasmas, and although most species are nonpathogenic, some pathogenic
Mycoplasma species are capable of invading several types of human cells and
tissues and are associated with a wide variety of human diseases (11,
15-19).
Are pathogenic Mycoplasma species and other intracellular bacteria
(Chlamydia, Borrelia, etc.) associated with chronic illnesses such as
CFS/ME, FMS, GWI and RA?  We (6, 8, 11, 15, 17-19, 24) and others (20-23)
have examined chronic illness patients for the presence of mycoplasmal blood
infections and have found a strong association with the presence of chronic
illnesses.  In our studies the clinical diagnosis of these disorders was
obtained from referring physicians according to the patients' major signs
and symptoms.  Blood was collected, shipped over night at 4°C and processed
immediately for Nucleoprotein Gene Tracking (NPGT) after isolation of blood
leukocyte nuclei (17, 18) or Polymerase Chain Reaction (PCR) after
purification of blood leukocyte DNA using a Chelex procedure (6, 8, 15, 19).
These procedures are very sensitive and specific and can detect down to a
few copies of intracellular bacteria in a blood sample.  The sensitivity and
specificity of the methods were determined by examining serial dilutions of
purified DNA of M. fermentans, M. pneumoniae, M. penetrans and M. hominis in
blood samples.  Amounts as low as 1-10 fg of purified microorganism DNA were
routinely detectable.  Using PCR the amplification with the appropriate
primers produced the expected fragment size in all tested species, which was
confirmed by hybridization with an inner probe or DNA sequencing to confirm
the sequence of the PCR product.
We used the NPGT and the PCR procedures to examine chronic illness patients
for Mycoplasma species and Chlamydia species infections.  For example, using
NPGT to analyze the blood leukocytes of GWI patients we found that 91/200
(~45%) were positive for mycoplasmal infections.  In contrast, in
nondeployed, healthy adults the incidence of mycoplasmal infections was 4/62
(~6%) (17, 18).  Similarly, others have more recently used PCR to examine
GWI patients and found that 55% were positive for Mycoplasma species and 36%
were found to have M. fermentans infections (23).  The slight difference in
percentage of positive patients is probably due to the differences in
sensitivities of these two methods.  Using PCR procedures 52-63% of CFS/ME
and FMS patients (n~1,000) had mycoplasmal infections (6, 19-24), whereas
only 6-15% of controls (n~450) tested positive.
An important observation was that patients with chronic illnesses that test
positive for mycoplasmal infections usually have multiple infections.  When
we examined mycoplasma-positive CFS/ME and FMS patients (~60% of such
patients are usually mycoplasma-positive) for the presence of M. fermentans,
M. pneumoniae, M. penetrans, M. hominis infections, multiple infections were
found in the majority of approximately 100 patients (19).  CFS/ME/FMS
patients had two (>30%) or three (>20%) species of mycoplasmal infections,
but only when one of the species was M. fermentans or M. pneumoniae (19).
We also found higher score values for increases in the severity of signs and
symptoms after onset of illness in CFS/ME/FMS patients with multiple
infections.  Also, CFS/FMS patients with multiple mycoplasmal infections
generally had a longer history of illness, suggesting that patients may have
contracted additional infections during their illness (19).  Most of these
patients also show evidence of various viral and Chlamydia species
infections.  Thus it is likely that most CFS/ME and FMS patients have
multiple bacterial and viral infections.
DIAGNOSIS OF CHRONIC INFECTIONS IN ARTHRITIS PATIENTS
The causes of rheumatic diseases are for the most part unknown, but RA and
other autoimmune diseases could be triggered or more likely exacerbated by
infectious agents (25).  In some animal species infection by certain
Mycoplasma species can result in remarkable clinical and pathological
similarities to RA and other rheumatic diseases.  Aerobic and anaerobic
intestinal bacteria, viruses and mycoplasmas have all been proposed as
possible agents in the etiology of RA (25-30), and there has been increasing
evidence that mycoplasmas may play a role in the initiation or more likely
progression of RA (13, 15, 30-32).  Mycoplasmas have been proposed to
interact nonspecifically with B-lymphocytes, resulting in modulation of
immunity, autoimmune reactions and promotion of rheumatic diseases (31), and
mycoplasmas have been found in the joint tissues of patients with rheumatic
diseases, suggesting their pathogenic involvement in these and other chronic
illnesses (29).
Using PCR Mycoplasma species are commonly found in RA patients' blood.  For
example, when Haier et al. (15) and Vojdani and Franco (23) examined RA
patients' blood leukocytes for the presence of mycoplasmas, they found that
approximately one-half were infected with various species of mycoplasmas.
The most common species found was M. fermentans, followed by M. hominis, M.
pneumoniae and finally M. penetrans (15, 23). Similar to what we reported in
CFS/FMS patients (19), there was a high percentage of multiple mycoplasmal
infections in RA patients when one of the species was M. fermentans (15).
Mycoplasma species and other intracellular pathaogenic bacteria could be
important factors or cofactors in the development of inflammatory responses
in rheumatic diseases and for progression of RA.  As an example of the
possible role of Mycoplasma species in rheumatic diseases, M. arthritidis
infections in animals can trigger and exacerbate autoimmune arthritis in
animal models of RA (32, 33). M. arthritidis can also suppress immune cells
and release substances that act on polymorphonuclear granulocytes, such as
oxygen radicals, chemotactic factors and other substances (33). Mycoplasmal
infections can increase pro-inflammatory cytokines, such as
Interleukin-1, -2 and -6 (34), suggesting that they are involved in the
development and possibly progression of rheumatic diseases such as RA.  In
addition, mycoplasmas have been detected in the synovial fluid of RA
patients' joints (29).
A variety of microorganisms have been under investigation as cofactors or
causative agents in rheumatic diseases (8, 15, 25, 26).  The discovery of EB
virus (27) and cytomegalovirus (28) in the cells of the synovial lining in
RA patients suggested their involvement in RA, possibly as cofactors.  There
are a number of bacteria and viruses that are candidates in the induction or
progression of RA (15, 25, 26).  In support of a bacterial involvement in
RA, antibiotics like minocycline can alleviate the clinical signs and
symptoms of RA (Table 1) (35).  This and similar drugs are likely
suppressing infections of sensitive microorganisms like mycoplasmas,
although certain antibiotics could also cause other effects in susceptible
patients.
MYCOPLASMAL INFECTIONS IN OTHER CHRONIC ILLNESSES
Mycoplasmas have been associated with the progression of immunosuppressive
diseases, such as HIV-AIDS (36).  These infections have also been associated
with certain lethal human diseases, such as an acute fatal illness found
with M. fermentans infections in non-AIDS patients (37).  Importantly,
mycoplasmal infections are now thought to be a major source of morbidity in
HIV-AIDS (38). Expanding further on this, Blanchard and Montagnier (38) have
proposed that certain mycoplasmas like M. fermentans are important cofactors
in the progression of HIV-AIDS, accelerating disease progression and
accounting, in part, for the increased susceptibility of AIDS patients to
increased viral replication and additional opportunistic infections.   Since
most studies on the incidence of mycoplasmal infections in HIV-AIDS patients
have employed relatively insensitive tests, it is likely that the actual
prevalence of mycoplasmal infections in HIV-AIDS patients is much greater
than previously thought and may be associated with a rapid fatal course of
the disease.  For example, in HIV-AIDS mycoplasmas like M. fermentans can
cause renal and CNS complications (39), and mycoplasmas have been found in
various tissues, such as the respiratory epithelial cells of AIDS patients
(40).  Other species of mycoplasmas have been found in AIDS patients where
they have also been associated with disease progression (41), and it is
likely that several viral and bacterial infections are involved in the
progression of this disease. In addition to immune suppression, some of this
increased pathogenecity may be the result of mycoplasma-induced host cell
membrane damage from toxic oxygenated products released from intracellular
bacteria  (42). Also, mycoplasmas may regulate HIV-1 virus replication.
Interestingly, HIV-LTR-dependent gene expression can be regulated by the
presence of certain pathogenic mycoplasmas (43).
There is some preliminary evidence that mycoplasmal and other infections are
associated with various autoimmune diseases.  For example, in some
mycoplasma-positive GWI cases some of the signs and symptoms of Multiple
Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS), Lupus, Graves' Disease
and other complex autoimmune diseases have been seen.  Such usually rare
autoimmune responses are consistent with certain chronic infections, such as
mycoplasmal infections, that penetrate into nerve cells, synovial cells and
other cell types and probably stimulate autoimmune responses by their own or
host antigens.  Thus the autoimmune signs and symptoms in these patients
could be the result of intracellular pathogens, such as mycoplasmas,
escaping from cellular compartments and incorporating into their own
structures pieces of host cell membranes that contain important host
antigens that can trigger autoimmune responses.  Alternatively, mycoplasma
surface components, sometimes called 'superantigens,' may directly stimulate
autoimmune responses (44).  Perhaps the most important event, the molecular
mimicry of host antigens by mycoplasma surface components, may explain, in
part, their ability to stimulate autoimmune responses (45).
Pulmonary infections are often seen in chronic illness patients.  For
example, asthma, airway inflammation, chronic pneumonia and other
respiratory diseases are known to be associated with mycoplasmal infections
(46).  It has been noted that M. pneumoniae is a common cause of upper
respiratory infections (47), and severe asthma is frequently associated with
mycoplasmal and other infections (48).  Chronic illness patients with
respiratory signs and symptoms usually have bacterial infections.
An emerging area of interest is the possible involvement of chronic
infections in a variety of coronary conditions.  Cardiopathies can be caused
by chronic Mycoplasma species (49) and Chlamydia species (50) infections,
resulting in myocarditis, endocarditis, pericarditis and other types of
infections.  These cardiac infections are often due to Mycoplasma  species,
Chlamydia  species and possibly other intracellular bacteria and other
infectious agents, and they are emerging agents in coronary diseases.
Mycoplasmal infections are also associated with a variety of miscellaneous
illnesses, such as M. hominis infections in patients with
hypogamma-globulinemia (30), and M. genitalium infections in nongonococcal
urethritis patients (51).  Mycoplasmas can exist in the oral cavity and gut
as normal flora, but when they penetrate into the blood and tissues, they
may be able to cause or promote a variety of acute or chronic illnesses.
These cell-penetrating  species, such as M. penetrans, M. fermentans, M.
hominis and M. pirum, among others, can cause infections that result in
complex systemic signs and symptoms  Mycoplasmal infections can also cause
synergism with other infectious agents. Similar types of chronic infections
caused by cell-invasive Chlamydia, Brucella, Coxiella or Borriela species
may also be present either as single agents or as complex, multiple
infections in many chronic illnesses (8, 11).
CONVENTIONAL TREATMENT OF CHRONIC BACTERIAL INFECTIONS
Once chronic intracellular bacterial infections, such as Mycoplasma species
infections, have been identified in the blood of subsets of CFS/ME, FMS,
GWI, RA and other chronic illness patients, they can be treated using
conventional and alternative approaches.  Appropriate treatment with
antibiotics should result in patient improvement and even recovery, and this
has been found in most but not all chronic illness patients (8, 11, 17, 18,
52-54) (Table 1).  The recovery is usually slow and gradual after an initial
period of Herxheimer and other adverse reactions that make patients
temporarily more symptomatic.  This period can last for several weeks.  The
recommended treatments for mycoplasmal blood infections are usually
long-term antibiotic therapy, usually multiple 6-week cycles of doxycycline
(200-300 mg/day), ciprofloxacin (1,500 mg/day), azithromycin (250-500
mg/day) or clarithromycin (750-1,000 mg/day), among others (53).  Multiple
6-week cycles are required, because few patients recover after only a few
cycles of antibiotics.  This is probably due to the intracellular locations
of mycoplasmas like M. fermentans and M. penetrans or other bacteria, such
as Chlamydia species, the slow-growing nature of these infections, their
inherent insensitivity to most antibiotics and the persistence of the
infections in metabolically inactive forms.  For most patients, treatment
must be continuous for at least 6 months, followed by additional 6-week
cycles of antibiotics, if necessary.  Some treat these infections by
administration of antibiotics every other day, and some recommend daily
dosing.  Due to poor gastrointestinal absorption in certain patients or the
acuteness of signs and symptoms, intravenous therapy has been used for a few
weeks, followed by oral antibiotics.  Most patients cannot tolerate
intravenous antibiotics for more than a few weeks or complications can then
occur, so follow-on therapy with oral antibiotics is necessary.
Can antibiotic therapy be successful in treating intracellular bacterial
infections often found in chronic illness patients?  Yes, but antibiotics
should not be used solely or exclusively to treat intracellular bacterial
infections.  They have proven successful for many if not most patients;
however, many patients eventually fail on antibiotic therapy alone.  For
example, of 87 GWI patients that tested positive for mycoplasmal infections,
all patients relapsed after the first 6-week cycle of antibiotic therapy,
but after up to 6 cycles of therapy 69/87 previously mycoplasma-positive
patients recovered and returned to active duty (17, 18).  Since few patients
recovered within 6 months of antibiotic therapy, as discussed above, this is
now the minimal recommendation of antibiotic treatment (54).  These were
relatively young patients (most <25 years of age) that were healthy before
their illness, and this could have played a role in their higher response
rates compared to civilians with chronic illnesses which tend to be on the
average older and not as healthy.  The clinical responses that were seen in
patients were not due to placebo effects, because administration of some
antibiotics, such as penicillins, resulted in patients becoming more not
less symptomatic, and they were not due to immunosuppressive effects that
can occur with some of the recommended antibiotics.  Interestingly, CFS/ME,
FMS and GWI patients that slowly recovered after several cycles of
antibiotics were generally less environmentally sensitive, suggesting that
their immune systems were slowly returning to pre-illness states.  If such
patients had illnesses that were caused by psychological or psychiatric
problems or solely by chemical or viral exposures, they should not have
responded to the recommended antibiotics and slowly recovered.  In addition,
if such treatments were just reducing autoimmune responses, then patients
should have immediately relapsed after the treatments were discontinued and
they should not have responded to antibiotics that do not suppress immune
systems.
Although the majority of GWI patients in these unblinded, initial studies
responded to antibiotic therapy, the studies have been justifiably
criticized for not being controlled, blinded clinical trials.  In the case
of GWI, large double-blinded, placebo-controlled studies have recently been
initiated using doxycycline.  In the case of RA, however, double-blinded,
placebo-controlled antibiotic trials using minocycline have been
successfully conducted.  These trials show that the treatment of RA patients
with minocycline is clinically effective and results in recovery of
approximately one-half of an unselected group (not tested for chronic
infections) of patients (Table 1) (35, 55).  The reason for the incomplete
responses among RA patients was probably due to the fact that only a portion
of the patients under study probably had intracellular bacterial pathogens
as their main clinical problem.  Viruses and other pathogens may also play
an important role in these patients, and minocycline would not be expected
to have any effect on this type of infection.
Another less conventional approach to the treatment of chronic illness
patients with intracellular bacterial infections is oxygen therapy.
Hyperbaric oxygen, intravenous ozone and hydrogen peroxide have been used to
treat anaerobic infections similar to the infections discussed here.  Most
patients with anaerobic infections respond to such therapy with at least
temporary alleviation of signs and symptoms, but additional evidence is
needed before one can conclude that such therapy results in sustained
suppression of anaerobic infections, such as those caused by Mycoplasma and
Chlamydia species.  Since these therapies are mainly cytostatic not
cytotoxic, they must be sustained for some period of time.  However, the use
of long-term protocols that include oxygen therapy is likely to prove
useful, and it is certainly beneficial in patients who cannot tolerate
antibiotics due to chemical sensitivities or other reasons.  In some
patients, alternating antibiotic and oxygen therapies may be useful, but
this has not been done in a controlled study.
NUTRITIONAL SUPPLEMENTS FOR CHRONIC ILLNESS PATIENTS
For the therapy of chronic illness patients to be successful we believe that
a comprehensive approach involving conventional and alternative therapies
must be undertaken with each patient.  An important part of chronic illness
treatment programs should be the use of certain dietary supplements,
particularly to boost and maintain immune systems (Table 2).  In addition to
treatments like antibiotics and antivirals, oxygen therapy and removal of
toxic agents from the patients' systems, nutritional supplementation should
also be undertaken, especially in those patients with environmental toxic
exposures (56).  Although for the most part these alternative medical
approaches have not been carefully evaluated in blinded trials,
practitioners that have used them strongly support their usefulness.
Since chronic illness patients often have nutritional and other
deficiencies, these should be corrected with the use of various supplements
(Table 2) (53).  For example, chronic illness patients are often depleted in
vitamins B, C and E, among others, and certain minerals.  Unfortunately,
patients with chronic illnesses often have poor gastrointestinal absorption
capacities.  Therefore, relatively high doses of some vitamins must be used
(vitamins C and E).  Others, such as vitamin B complex, cannot be easily
absorbed by the gastrointestinal systems of chronic illness patients, so
sublingual or parentral natural B-complex vitamins (riboflavin, niacin,
vitamin B-6, B-12 and pantothenic acid) should be substituted for oral
preparations.  General vitamins plus extra C, E, CoQ-10, beta-carotene,
folic acid, bioflavoids and biotin are necessary.  L- cysteine, L-tyrosine,
L-glutamine, L-carnitine, malic acid and flaxseed or fish oils are reported
by some to be useful.  Certain minerals are also often depleted in these
patients, such as zinc, magnesium, chromium and selenium, and these should
be supplemented as well (Table 2) (56).  One problem with providing
supplements in a program that also uses antibiotics is that they cannot be
taken at the same time of day as the antibiotics because they may inhibit
antibiotic uptake or interfere with antibiotic transport.  Another problem
is the consumption of foods that can naturally suppress immune systems, such
as processed sugar.  We generally suggest that chronic illness patients
undergoing therapy should make an effort to eliminate if possible sugar,
alcohol, caffeine or other foods that may interfere with a patient's immune
system.
There are also other important considerations in patients undergoing
antibiotic or antiviral therapy (53).  Antibiotics deplete normal gut
bacteria, which can result in over-growth of less desirable bacteria.  To
supplement bacteria in the gastrointestinal system live cultures of
Lactobacillus acidophillus in tablets, capsules or powder are recommended.
One product is a mixture of Lactobacillus acidophillus, Lactobacillus
bifidus and other bacteria with FOS (fructoologosaccharides) to promote
growth in the gastrointestinal system.  Various commercial formulations of
probiotics are available to replenish gastrointestinal bacteria that have
been killed or suppressed by antibiotic therapy.
A number of natural remedies that boost the immune system can be useful in
the therapy of chronic illnesses.  Among these are whole lemon/olive extract
drink or an extract of olive leaves with antioxidants, plant extracts or
purified plant products or milk proteins, such as whey.  These products are
useful during or after antibiotic therapy has been completed.   Although
these products appear to help some patients, their clinical effectiveness in
various chronic illness patients for the most part has not been carefully
evaluated.  An exception is a Chinese herbal formulation (Calm Colon; Samra)
that has been tested for benefit in Irritable Bowel Syndrome.  In a
randomized, double-blinded, placebo-controlled clinical trial this
formulation was found to be effective in reducing the symptoms of Irritable
Bowel Syndrome (57).  In some cases natural products are known to stimulate
immune systems, as shown in various in vitro assays (58).  They should be
used by patients during therapy to boost immune systems and especially after
antibiotic therapy in a maintenance program to prevent relapse of illness
(53).
Traditional herbal supplements have proven useful in the treatment of
chronic illness patients (57, 58), especially in a maintenance program to
prevent relapse of illness.  African and Chinese natural immune enhancers
and cleansers can help to restore natural immunity and aid absorption.  This
is an often overlooked but nonetheless important recommendation (Table 2).
Unfortunately, it is difficult to recommend specific supplements as useful
in all patients, but many patients that have undergone more traditional
antibiotic and/or antiviral therapies often relapse after the therapy is
completed without continued support with dietary supplements.  Some of the
recommended products in Table 2 have mild natural antibiotic, antiviral and
antifungal properties, so they can be useful in certain patients.  Although
these natural products are known to help many chronic illness patients,
their clinical effectiveness in GWI/CFS/FMS/RA patients has not been
carefully evaluated.
Another consideration is the elimination of drugs that might suppress
immunity.  We have recommended that patients be taken off antidepressants
and other potentially immune-suppressing drugs.  Some of these drugs are
used to help alleviate certain signs and symptoms, but in our opinion they
can interfere with therapy, and they should be gradually reduced or
eliminated.
CONCLUSIONS
We have proposed that chronic infections, especially multiple chronic
bacterial and viral infections, are an appropriate explanation for much of
the morbidity seen in rather large subsets of CFS/ME, FMS, GWI and RA
patients, and in a variety of other chronic illnesses.  Not every patient,
however, will have this as a diagnostic explanation or have the same types
of chronic infections.  These infections need not be the triggering factor
or cause of chronic illnesses and are probably more important in causing
progression of disease.  Nonetheless, chronic infections may cause most of
the morbidity seen in these patients, and selective therapy of chronic
infections supports this view.  Additional research will be necessary to
clarify the role of multiple infections in chronic diseases, but these
patients should benefit from appropriate antibiotic, antiviral and
nutraceutical therapies that alleviate morbidity.  Additional controlled
studies should be performed to determine the clinical effectiveness of
alternative therapies and nutritional supplements in treating chronic
illnesses.
References
1.        Morrison JD.  Fatigue as a presenting complaint in family
practice.  J Family Pract  1980; 10: 795-801.
2.        Kroenke K, Wood DR, Mangelsdorff AD, et al. Chronic fatigue in
primary care.  Prevalence, patient characteristics and outcome.  JAMA  1988;
260: 929-934.
3.        Fukuda K, Straus S, Hickie I, et al. The Chronic Fatigue Syndrome:
a comprehensive approach to its definition and study. Ann Internal Med
1994; 121: 953-959.
4.        Buchwald D,  Garrity D.  Chronic fatigue, fibromyalgia and
chemical sensitivity: overlapping disorders. Arch Internal Med  1994; 154:
2049-2053.
5.        Nicolson GL, Nicolson NL.  Chronic Fatigue illness and Operation
Desert Storm.  J Occup Environ Med  1995; 38: 14-17.
6.        Nicolson GL, Nasralla M, Haier J, et al.  Diagnosis and treatment
of mycoplasmal infections in Fibromyalgia and Chronic Fatigue Syndromes:
relationship to Gulf War Illness.  Biomed Therapy  1998; 16:266-271.
7.        Klimas N, Salvato F, Morgan R, et al.  Immunologic abnormalities
in chronic fatigue syndrome.  J Clin Microbiol  1990; 28:1403-1410.
8.        Nicolson GL, Nasralla MY, Franco AR, et al., Role of Mycoplasmal
Infections in Fatigue Illnesses: Chronic Fatigue and Fibromyalgia Syndromes,
Gulf War Illness and Rheumatoid Arthritis.  J Chronic Fatigue Syndr 2000; 6:
in press.
9.        Dunn AJ, Wang J, Ando T.  Effects of cytokines on cerebral
neurotransmission.  Comparison with the effects of stress.  Adv Exp Med Biol
1999;  461:117-127.
10.     Nicolson GL, Nicolson NL.  Gulf War Illnesses: complex medical,
scientific and political paradox.  Med Confl Surv. 1998; 14:156-165.
11.     Nicolson GL, Nasralla MY, Haier J, et al. Mycoplasmal infections in
chronic illnesses: Fibromyalgia and Chronic Fatigue Syndromes, Gulf War
Illness, HIV-AIDS and Rheumatoid Arthritis.  Med Sentinel  1999: 5:172-176.
12.     Nicolson GL. Chronic infections as a common etiology for many
patients with Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Gulf War
Illnesses. Intern J Med. 1998; 1:42-46.
13.     Hoffman C, Rice D, Sung H-Y. JAMA  1996; 276:1473-1479.
14.     Arnet FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF, Cooper NS et
al. The American Rheumatism Association 1987 revised criteria for the
classification of rheumatoid arthritis. Arthritis Rheumatol. 1988;
31:315-324.
15.     Haier J, Nasralla M, Franco AR, Nicolson GL.  Detection of
mycoplasmal infections in the blood of patients with Rheumatoid Arthritis.
Rheumatol  1999; 38:504-509.
16.     Baseman J B, Tully JG. Mycoplasmas: sophisticated, re-emerging and
burdened by their notoriety.  Emerg Infect Dis 1997;  3:21-32.
17.     Nicolson GL, Nicolson NL. Diagnosis and treatment of mycoplasmal
infections in Persian Gulf War Illness-CFIDS patients.  Intern J Occup Med
Immunol Tox 1996; 5:69-78.
18.     Nicolson GL, Nicolson NL, Nasralla M.  Mycoplasmal infections and
Chronic Fatigue Illness (Gulf War Illness) associated with deployment to
Operation Desert Storm. Intern J Med 1998; 1:80-92.
19.     Nasralla M, Haier J, Nicolson GL.  Multiple mycoplasmal infections
detected in blood of Chronic Fatigue and Fibromyalgia Syndrome patients.
Eur J Clin Microbiol Infect Dis 1999; 18:559-565.
20.     Vojdani A, Choppa PC, Tagle C, et al.  Detection of Mycoplasma genus
and Mycoplasma fermentans by PCR in patients with Chronic Fatigue Syndrome.
FEMS Immunol Med Microbiol  1998; 22:355-365.
21.     Huang W, See D, Tiles J. The prevalence of Mycoplasma incognitus in
the peripheral blood mononuclear cells of normal controls or patients with
AIDS or Chronic Fatigue Syndrome.  J Clinical Microbiology 1998; 22: 355-365
22.     Choppa PC, Vojdani A, Tagle C, et al.  Multiplex PCR for the
detection of Mycoplasma fermentans, M. hominis and M. penetrans in cell
cultures and blood samples of patients with Chronic Fatigue Syndrome.  Mol
Cell Probes  1998; 12:301-308.
23.     Vojdani A, Franco AR.  Multiplex PCR for the detection of Mycoplasma
fermentans, M. hominis and M. penetrans in patients with Chronic Fatigue
Syndrome, Fibromyalgia, Rheumatoid Arthritis and Gulf War Illness.  J
Chronic Fatigue Syndr  1999; 5:187-197.
24.     Nasralla MY, Haier J, Nicolson GL. Determination of Mycoplasmal
infections in blood of 565 Chronic Fatigue Syndrome and Fibromyalgia
Syndrome patients detected by polymerase chain reaction. Intern J Med Biol
Environ 2000; 28(1): 15-23.
25.     Krause A, Samradt T, Burnmester GR.  Potential infectious agents in
the induction of arthritides.  Curr Opin Rheumatol  1996; 8:203-209.
26.     Midvedt T. Intestinal bacteria and rheumatic disease.  Scand  J
Rheumatol Suppl 1987; 64:49-54.
27.     Fox RI, Luppi M, Pisa P, et al.  Potential role of Epstein-Bar virus
in Sjögren's syndrome and rheumatoid arthritis.  J Rheumatol  1992;
32(Suppl):18-24.
28.     Tsai YT, Chiang BL, Kao YF, et al.  Detection of Epstein-Bar virus
and cytomegalovirus genome in white blood cells from patients with juvenile
rheumatoid arthritis and childhood systemic lupus erythematosus.  Intern.
Arch Allergy Immunol  1995; 106:235-240.
29.     Schaeverbeke T, Renaudin H, Clerc M, et al. Systematic detection of
mycoplasmas by culture and polymerase chain reaction (PCR) procedures in 209
synovial fluid samples. Rev Rheumatol  1997; 64:120-128.
30.     Furr PM, Taylor-Robinson D, Webster ADB.  Mycoplasmas and
ureaplasmas in patients with hypogammaglobulinemia and their roll in
arthritis: microbiological observation over twenty years. Ann Rheumatol Dis
1994; 53:183-187.
31.     Simecka JW, Ross SE, Cassell GH, Davis JK. Interactions of
mycoplasmas with B cells: production of antibodies and nonspecific effects.
Clin Infect Dis  1993; 17(Supp. 1):S176-S182.
32.     Cole BC, Griffith MM.  Triggering and exacerbation of auroimmune
arthritis by the Mycoplasma arthritidis  superantigen MAM.  Arthritis
Rheumatol  1993; 36:994-1002.
33.     Kirchhoff H, Binder A, Runge M, et al.  Pathogenic mechanisms in the
Mycoplasma arthritidis polyarthritis of rats.  Rheumatol Int 1989;
9:193-196.
34.     Mühlradt  PF, Quentmeier H, Schmitt E.  Involvement of interleukin-1
(IL-1), IL-6, IL-2 and IL-4 in generation of cytolytic T cells from
thymocytes stimulated by a Mycoplasma fermentans-derived product.  Infect
Immunol  1991; 58:1273-1280.
35.     Tilley BC, Alarcon  GS, Heyse SP, et al. Minocycline in rheumatoid
arthritis.  A 48-week, double-blind, placebo-controlled  trial.  Ann
Internal Med  1995: 122:81-89.
36.     Hawkins RE, Rickman LS, Vermund SH, et al. Association of Mycoplasma
and human immunodeficiency virus infection: detection of amplified
Mycoplasma fermentans DNA in blood.  J Infect Dis 1992; 165:581-585.
37.     Lo S-C, Dawson MS, Newton PB, et al.  Association of the virus-like
infectious agent originally reported in patients with AIDS with acute fatal
disease in previously healthy non-AIDS patients.  Am  J Trop Med Hyg  1989;
41:364-376.
38.     Blanchard A, Montagnier L.  AIDS associated mycoplasmas. Annu  Rev
Microbiol  1994; 48:687-712.
39.     Bauer FA, Wear DJ, Angritt P, Lo S-C.  Mycoplasmal fermentans
(incognitus strain) infection in the kidneys of patients with acquired
immunodeficiency syndrome and associated nephropathy: a light microscopic,
immunohistochemical and ultrastructural study. Human Pathol  1991; 22:63-69.
40.     Sloot N, Hollandt H, Gatermann S, Dalhoff K.  Detection  of
Mycoplasma spp. in bronchoalveolar lavage of AIDS patients with pulmonary
infiltrates.  Zentralbl  Bacteriol  1996; 284:75-79.
41.     Grau O, Slizewicz B, Tuppin  P, et al. Association of Mycoplasma
penetrans with human immunodeficiency virus infection.  J Infect Dis 1995;
172:672-681.
42.     Pollack JD, Jones MA, Williams, MV.  Clin Infect Dis  1993; 17(Suppl
1):S267-S271.
43.     Nir-Paz R, Israel S, Honigman A, Kahane I.  Mycoplasmas regulate
HIV-LTR-dependent gene expression.  FEMS Microbiol Lett  1995; 128:63-68.
44.     Kaneoka H, Naito S.  Superantigens and autoimmune diseases.  Jap J
Clin Med  1997;  6:1363-1369.
45.     Baseman JB, Reddy SP, Dallo SF. Am  J Respir Crit  Care Med  1996;
154:S137-S144.
46.     Cassell GH.  Infectious causes of chronic inflammatory diseases and
cancer.  Emerg Infect Dis  1998; 4:475-487.
47.     Kraft M, Cassell GH, Henson JE, et al.  Detection of Mycoplasma
pneumoniae in the airways of adults with chronic asthma.  Am  J Respir Crit
Care Med  1998; 158:998-1001.
48.     Gil JC, Cedillo RL, Mayagoitia BG, Paz MD.  Isolation of Mycoplasma
pneumoniae  from asthmatic patients.  Annu Allergy  1993; 70:23-25.
49.     Prattichizzo FA, Simonetti I, Galetta F.  Carditis associated with
Mycoplasma pneumoniae infections.  Clinical aspects and therapeutic
problems.  Minerva Cardioangiol 1997; 45:447-450.
50.     Fairley CKL, Ryan M, Wall PG, Weinberg J.  The organisms reported to
cause infective myocarditis and pericarditis in England and Wales.  J Infect
1996; 32:223-225.
51.     Busolo F, Camposampiero D, Bordignon G, Bertollo G.  Detection of
Mycoplasma genitalium and Chlamydia trachomatis DNAs in male patients with
urethritis using the polymerase chain reaction.  New Microbiol  1997;
20:325-332.
52.     Nicolson GL, Nicolson NL. Doxycycline treatment and Desert Storm.
JAMA 1996; 273:618-619.
53.     Nicolson GL. Considerations when undergoing treatment for chronic
infections found in Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Gulf
War Illnesses. (Part 1). Antibiotics Recommended when indicated for
treatment of Gulf War Illness/ CFIDS/FMS (Part 2). Intern  J Med  1998;
1:115-117, 123-128.
54.     Nicolson GL. The role of microorganism infections in chronic
illnesses: support for antibiotic regimens. CFIDS Chron 1999; 12(3):19-21.
55.     O'Dell JR, Paulsen G, Haire CE, et al.  Treatment of early
seropositive rheumatoid arthritis with minocycline: four-year follow-up of a
double-blind, placebo-controlled trial. Arthritis Rheumatol 1999;
42:1691-1695.
56.     Rea WJ, Pan Y, Johnson AR, Ross GH, et al.  Reduction of chemical
sensitivity by means of heat depuration, physical therapy and nutritional
supplementation in a controlled environment.  J Nutrit Environ Med 1996;
6:141-148.
57.     Bensoussan A, Talley NJ, Hing M, et al. Treatment of Irritable Bowel
syndrome with Chinese herbal medicine. JAMA 1998; 280:1585-1589.
58.     See D, Gurnee K, LeClair M. An in vitro screening study of 196
natural products for toxicity and efficacy.  J Am Nutraceut Assoc 1999;
2:25-39.
FIGURE LEGENDS
Figure 1A and 1B.  Incidence of increase in severity of signs and symptoms
in 300 chronic illness patients.  Severity of illness was scored using 118
signs and symptoms on a 10-point scale (0, none; 10 extreme) prior to and
after the onset of illness.  Scores were placed into 29 categories
containing 3-9 signs/symptoms and were recorded as the sum of differences
between values before and after onset of illness divided by the number of
questions in the category.  Changes in score values of 2 or more points were
considered relevant.  Patient groups were: CFS (p), FMS (p), GWI  (p),
Chronic illness patients without evidence of bacterial infection  (p).
Asterisk (*) indicates score = 0.
Table      1.  Summary of chronic illness patients' responses to antibiotic
therapy.
                Patients mycoplasma-positive or responding to therapy
GWI(reference) (17) (18)
Blinded, controlled study (Y/N) No No
Patients (n) 30  170
Mycoplasma-positive pts 47% 46%
Clinical Response* ND ND
Clnical Recovery* 78% 80%
CFS/ME/FMS (reference)     (54)
Blinded, controlled study (Y/N)     No
Patients (n)     30
Mycoplasma-positive pts     66%
Clinical Response*     80%
Clnical Recovery*     50%
RA (reference)       (35) (55)
Blinded, controlled study (Y/N)       Yes Yes
Patients (n)       219 46
Mycoplasma-positive pts       ND ND
Clinical Response*       54% 63%
Clnical Recovery*       ND 50%
*, Data only for mycoplasma-positive patients; ND, not determined.
Table   2.  Some nutritional supplements useful for chronic illnesses
(sources).
1. Vitamins
Multivitamins
Vitamin B Complex (Total B, Real Research; B complex, GNC)
Vitamin C
Vitamin E
CoQ-10
2. Mineral Salts
Zinc
Chromium
Magnesium
Selenium
3. Immune Enhancers
Whey protein (ImuPlus; Immunocal)
Ambrotose (Mannatec)
ACT-5 (James Mobb; Molecular Med)
Echinacea-C (NF Formulas)
NSC-100 (Nutritional Supply)
4. Natural Antibiotics/Antivirals
 Laktoferrin (Nutricology)
GK-17 (James Mobb; Molecular Med)
Olive Leaf Extract (Immunoscreen; Creation's Garden)
Colloidal Silver
Anti-B (Creaton's Garden)
5. Probiotics/Bacterial Support
Lactobacillus acidophilus capsules
Lactobacillus acidophilus mixtures plus FOS(fructoologosaccharides)
6. Other Dietary Supplements
Amino Acids (L-cysteine, L-tyrosine, L-glutamic acid,
3-hydroxy-L-tryptophan)
Tahitian Noni (Morinda)
Calm Colon (Samra)
Flaxseed Oil
Fish Oils
Malic Acid
L-carnitine

 una persona sana di mente possa giovarsi.
Tu che sei una persona sana di mente......leggiti questo:
.......Persino fra i militari USA che hanno partecipato alla guerra del
Golfo si è scatenata un'epidemia mortale (4.500 morti) procurata dai vaccini
inoculati (4 vaccinazioni)  prima di partire; altri 15.000 soldati sono
rimasti handicappati più o meno gravemente e circa altri  20.000 accusano
malattie le più varie.
Fra i militari Italiani e Francesi, che non hanno seguito quelle "pratiche
sanitarie", la "sindrome del Golfo" NON è comparsa.
Per depistare l'origine vaccinale, i medici militari hanno chiamato in causa
ipotetiche armi chimiche di Saddam, che come è noto non ha mai potuto usare
perché distrutte fin dai primi giorni di guerra.
[Ripostato da: Il Manifesto - 
http://www.mir.it/mani/
 ]
[
http://mir10.mir.it/mani/Quotidiano-archivio/31-Gennaio-1999/art22.html
]
31 Gennaio 1999
"Uno strano vaccino prima di partire, ora ci ammaliamo noi e le nostre
famiglie"
I militari Usa reduci dal Golfo denunciano il Pentagono, che risponde:
"Malattie inventate, sono psicopatici".
Il manifesto, dopo l'intervista del 24 dicembre 1998 al regista Alberto
D'Onofrio autore del documentario "La sindrome del Golfo" girato nelle
caserme Usa, continua la sua campagna contro l'oscuramento del video da
parte della Rai che lo ha prodotto.
Herberth Smith (veterano del Golfo) : "Hanno detto ai miei dottori civili
che io ero un pazzo e che fingevo di essere malato, che mi tagliavo ogni
notte per provocarmi l'anemia e che mi alzavo la temperatura corporea in
modo da provocarmi una febbre alta".
Dott. Esa : "I pazienti affetti da tale forma di disfunzione del sistema
immunitario hanno danni agli organi interni causati dai propri globuli
bianchi. Abbiamo scoperto che con cure molto aggressive come la
chemioterapia si può ridurre l'attività di quei globuli bianchi. Nel suo
caso la causa sembra essere quasi sicuramente una reazione ad un vaccino".
Dott. Pam Esa : "C'erano molti veterani che erano pronti a partire per il
Golfo ma poi non furono mai mandati in guerra. Questi soldati ricevettero
comunque il vaccino intramuscolare ma non lasciarono mai il Paese e molti di
loro si sono ammalati o hanno avuto figli con le tipiche deformazioni come
la Golden Hart Syndrome.
Ai veterani non è stato mai detto quali tipi di vaccini venivano loro
somministrati ed ho saputo che da una base militare sono sparite 10.000
pagine di documentazione relative a tali vaccini".
Anche in Italia si pone un problema simile: Vi sono centinaia di giovani
militari italiani che ogni anno si ammalano di strane malattie (meningiti,
leucemie, cancri, ecc.), e le autorità militari sanitarie cercano di
scaricare la colpa sul fatto che alcuni di loro (solo ¼ dei malati) sono
stati inviati in zone dette a rischio come il Kossovo e Bosnia ove per causa
della guerra le zone interessate sono piene di proiettili all'uranio
impoverito.
Questi militari è noto non hanno mai maneggiato personalmente quel tipo di
materiali, che sono sparsi sul terreno e che se fossero così pericolosi,
potremmo trovare le stesse malattie sulla popolazione civile ivi residente,
ma ciò non è avvenuto né avviene, evidentemente questi materiali non sono
cosi pericolosi come si vuol far intendere, per poter depistare l'attenzione
dai reali pericoli delle pluri vaccinazioni (35 vaccini) che quei poveri
militari hanno dovuto subire sulla loro pelle da quando sono nati.
Una circolare del Ministero della Difesa Italiano consegnata alla
commissione di indagine costituita dal governo in carica, contiene delle
disposizioni che fanno riflettere:..si proibisce agli investigatori di
effettuare indagini sulla popolazione autoctona, ma e solo sui militari
italiani !
Siccome è noto che l'uranio impoverito NON produce danni simili ed a breve
scadenza come invece avviene, si cercherà di indurre l'attenzione su altre
piste, (non quella vaccinale che ne è la causa) oppure non avendole si
invocherà la "ragion di stato" e si bloccherà ogni ricerca della verità.
"Sindrome dei Balcani" ora i vaccini fanno paura
La commissione della Difesa sui rischi dell'uranio indagherà anche sui sieri
protettivi - (di STEFANO CITATI)
----------------------------------------------------------------------------
----
ROMA - La "Sindrome dei Balcani" è per ora solo un'ipotesi, ma potrebbe
divenire una realtà, ingombrante come la "Sindrome del Golfo". In America
sono stati messi sotto accusa i "cocktail" di vaccini anti-botulinici,
iniettati nelle vene dei soldati per metterli al riparo da agenti chimici o
batteriologici che Saddam avrebbe usato nella guerra del '91. I vaccini
avrebbero innescato l'insorgere di patologie che hanno colpito circa 100mila
dei 700mila uomini impegnati nel Golfo, alcune di esse probabilmente legate
anche alla contaminazione da uranio impoverito. Ma i militari italiani non
sono mai stati vaccinati con questi "cocktail", bensì con ben più normali
sieri, come l'antitetanica o l'epatite A e B, perciò una sindrome simile a
quella che ha colpito i veterani americani è impossibile. Eppure la
possibilità che il "male dei Balcani" abbia fondamenti concreti esiste, e le
cause potrebbero essere - oltre all'uranio impoverito - proprio i comuni
vaccini con i quali i soldati italiani sono stati preventivamente protetti.
Dubbi, ipotesi e timori espressi finora e sempre più dalle associazioni di
tutela del personale militare finiranno al vaglio della commissione della
Difesa istituita dal ministro Mattarella per il caso uranio impoverito,
allargando e complicando il lavoro dei 6 esperti che dovrebbero dare in
primavera il responso sui rischi del DU (depleted uranium) e i possibili
legami con le malattie che stanno colpendo membri della missione di pace in
Bosnia.
Dopo le polemiche tra la Nato e il ministero della Difesa sull'ammissione
dell'uso di proiettili all' uranio impoverito in Bosnia, ieri l' Alleanza
Atlantica ha fatto sapere che "non esiste una vaccinazione standard della
Nato. Il tipo di vaccini somministrati ai militari prima di inviarli nei
teatri d'operazione vengono stabiliti dalle autorità militari nazionali
perciò la loro scelta dipende da paese a paese". L'elenco dei sieri
iniettati ai militari italiani che si recano all'estero è noto, gli
effetti - secondo alcuni - meno. Le associazioni che tutelano il personale
militare che hanno sollevato il caso uranio, stanno ora mettendo sotto
accusa proprio questi vaccini come causa scatenante delle malattie che hanno
colpito (e ucciso) in questi mesi alcuni sottufficiali. "Le reazioni alla
somministrazione e i tempi di reazione dell'organismo a questi sieri sono
stati sottovalutati dai vertici militari", sostengono all'Osservatorio per
la tutela delle Forze armate. "I vaccini sono comunque pericolosi, poiché
inibiscono le difese immunitarie", spiega il dott. Vanoli, che insieme al
professor Montanari M. ha redatto uno studio clinico sui rischi delle
vaccinazioni, consegnato allo Stato Maggiore della Difesa nel '96. Pur
dubbioso su un legame diretto tra l'abbassamento delle difese immunitarie e
l'intossicazione da uranio in Bosnia ("i tempi sono troppo brevi, i danni
prodotti dal DU vengono fuori solo dopo molti anni") l'esperto di vaccini
spiega che "certe malattie possono essere innescate da deficienze
immunitarie".
La successione clinica viene così descritta: "I vaccini provocano
l'indebolimento del sistema immunitario, portando anche a casi di diarrea;
questa produce perdita di flora batterica che produce acidosi (pH acido);
ciò favorisce tra l'altro la Candida Albicans, un fungo che si annida
naturalmente nell' intestino; la sua moltiplicazione, secondo gli ecologisti
clinici, può essere una delle cause di malattie croniche degenerative e
immunologiche, come i linfomi e la leucemia. "Potendo osservare le cartelle
cliniche dei militari malati, noteremmo un iter uguale per tutti: problemi
intestinali, problemi epatici e linfatici, sangue non depurato, sviluppo
della malattia", elenca Vanoli.
Il motivo principale della pericolosità dei vaccini risiederebbe nella
presenza nei sieri di "metalli pesanti, come alluminio e mercurio,
utilizzati stabilizzare e facilitare la veicolazione della soluzione, nonché
di formaldeide, che possono intossicare il sangue, soprattutto in soggetti
predisposti, ovvero con difese immunitarie deboli".
Per fugare i dubbi "sulle correlazioni tra malattie e vaccini si potrebbe
fare un'analisi statistica tra il numero di casi di leucemia nella
popolazione italiana e quelli tra il personale militare per stabilire se
rientrano nella "norma", solo che l'istituto di Sanità non raccoglie dati
sulle malattie degenerative, come appunto la leucemia".
Per questo ed altri gravi motivi richiediamo una attenta riflessione sui
processi di vaccinazione in uso qui anche in Italia che con la Francia sono
i soli stati della CEE ad averne l'obbligo.
Cerca di parlare con il dott. M. Montinari al Policlinico di Bari che
potrebbe anche farti conoscere il perche' ti sei ammalato in modo cosi'
grave !
--
G. Paolo Vanoli (I2VGP) Consulente in Scienza della Nutrizione e Medicine
Biologico Naturali - 
www.medicinaqualita.it


come ti e' stato chiesto piu' volte, ma sto' Montinari perche' queste cose
non le scrive su riviste scientifiche (serie!)
invece di farsi pubblicita' tramite uno spammone come te? (per giunta, cosi'
facendo, rischia di fare la stessa fine di simoncini!)
Ciao vanolone! Marius

 facendo, rischia di fare la stessa fine di simoncini!)
Temo che Montinari si stia demolendo da solo scrivendo libri demenziali  per
conto di case editrici sputtanatissime che trattano temi di magia e
sciocchezze varie.
Certo la grancassa di Vanoli completa l'opera di sputtanamento totale.
Spero che Vanoli non decida mai di fare pubblicita' a me.
Sarebbe la fine della mia gia' difficile carriera professionale :-)

vanoli ma non ti avevano arrestato???
Qualche anno fa ti ho visto da costanzo sei schifosamente brutto come la
morte.
Il tuo amico Montinari e tutti quegli alchimisti del policlinico non hanno
niente da spiegarmi mi hanno fatto gia tantissimi danni e visto che non sono
miliardario per fargli causa e vincerla ho deciso di dimenticarli.
Beviti pure tutto il piscio di tua madre tua nonna e tua sorella, se vuoi te
ne do anche del mio cosě vediamo se ti becchi anche tu la CFS. Sarebbe un
esperimento non male dai facciamolo per gli onori e la gloria entrerai nella
storia della medicina, ma quella vera perň.
Tu stai male ricoverati magari da Montinari
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