M.E. can occur in both epidemic and sporadic forms, over 60 M.E. outbreaks have been recorded worldwide since 1934. M.E. is an acutely acquired neurological illness initiated by a virus infection and there is very good evidence to suggest that the cause is an enterovirus (the same type of virus that causes polio).
M.E. can occur in both epidemic and sporadic forms. Over 60 M.E. outbreaks have been recorded worldwide since 1934.
M.E. is an acutely acquired neurological illness initiated by a virus infection. There is also good evidence to suggest the cause is an enterovirus (the same type of virus that causes polio).
This point of view is supported by history (ME epidemics have followed polio epidemics and serological studies have shown that communities affected by an outbreak of M.E. were effectively blocked (or immune) from the effects of a subsequent polio outbreak), incidence (correlation with a flu-like prodromic illness), symptoms (swollen lymph nodes, low-grade fever, sore throat), and similarities with other viral ailments, notably mononucleosis and post-polio syndrome. Research also supports a viral causation for the illness.
There is a history of recorded outbreaks going back to 1934, when an epidemic of what seemed at first to be poliomyelitis was reported in Los Angeles. A review of early outbreaks found that clinical symptoms were consistent in over sixty recorded epidemics of M.E. spread all over the world.
Although the illness we now know as Myalgic Encephalomyelitis has existed for centuries, for much of that time it was a relatively uncommon disease. Following the mass polio vaccination programs of the 1960’s cases of polio were greatly reduced and outbreaks of M.E. seemed to be similarly affected. It wasn’t until the late 1970’s that M.E. began (for reasons as yet not fully understood) its dramatic increase in incidence worldwide. Over 20 years later, M.E. is a worldwide epidemic of devastating proportions. Many people have died from M.E. and there are now a million or more people severely disabled by this epidemic.
Veteran M.E. specialist Dr Byron Hyde explains that:
[The] prodromal phase is associated with a usually short onset or triggering illness. This onset illness usually takes the form of either, or any combination, of the following, (a) an upper respiratory illness, (b) a gastrointestinal upset, (c) vertigo and (d) a moderate to severe meningitic type headache. These are only the most common onset illnesses or symptoms of which there are several. The onset illness is associated with either a low grade or subnormal temperature, headaches, sometimes persisting and accentuated by movement with intermittent attacks of vertigo or dizziness. Evidence of a previous immune insult [such as a recent immunisation] is found regularly in both epidemic and sporadic cases. The usual incubation period of the triggering illness is 4-6 days. The second and third phases of the illness are usually always different in nature from the onset illness and usually become apparent within 1-4 weeks.
There appears to be somewhat of an occupational bias towards teachers (students) and health care workers in the incidence of Myalgic Encephalomyelitis cases (and outbreaks). These higher risk groups do not work in environments which are more stressful than the average job, but these are jobs which require higher rates of immunisation than others. This relationship with inoculation is often seen in infectious illnesses.
The main period of infectivity of M.E. peaks at the time just before symptoms appear through to the initial acute phase of the illness (which lasts for several months or in some cases years). M.E. appears to be highly infective but also highly selective. Modes of transmission are thought to include: casual contact (respiratory), salivary transmission (eg. kissing), sexual transmission and transmission through blood products. There is also evidence that asymptomatic carrier of the illness may be able to pass the illness on to others for a brief period following their exposure to the illness. (During the recovery and/or chronic stages of the illness however M.E. does not appear to present a significant infective risk).
No real research into transmissibility (or more importantly on reducing infection rates) has been done by the Government despite ample evidence that this is an infectious disease. There have been many well-documented clusters or outbreaks of the illness, reports of 4.5% of people contracting the illness after blood transfusions (or after needle-stick injuries involving the blood of ME patients), evidence of the disease spreading through casual contact amongst family members and so on.
As Dr Elizabeth Dowsett explains: ‘The problem we face is that, in spite of overwhelming epidemiological and technical evidence of an infectious case, the truth is being suppressed by the government and the 'official' M.E. charities as 'too scary' for the general public.’
This pretence of ignorance on behalf of Government has had enormous consequences; only in the UK are people with ME directly banned from donating blood for example. So it is that the number of people infected with M.E. continues to rise unabated and largely unnoticed by the public.
Transmission of M.E. to monkeys has been successfully demonstrated and has produced central nervous system and parasympathetic nervous system injury in at least two separate sets of experiments; in 1934 where ‘cross sections of the spinal cord demonstrated numerous minute haemorrhages in the grey matter’ and in 1949-51 in the Adelaide, Australia epidemic of M.E. where a radiculitis of the sciatic nerve was demonstrated with small punctate lesions of the myelin sheath.
M.E. is an infectious neurological disease and represents a major attack on the central nervous system (CNS) by the chronic effects of a viral infection. A significant number of the world’s leading M.E. experts believe that M.E., like poliomyelitis, is caused by an enterovirus. (This includes doctors such as A. Gilliam, A. Melvin Ramsay and Elizabeth Dowsett, John Richardson of Newcastle-upon-Tyne, W.H. Lyle, Elizabeth Bell of Ruckhill Hospital, James Mowbray of St Mary’s, Peter Behan and also the brilliant Byron Hyde of Canada.) The evidence which exists to support this theory is compelling.
Enterovirus infections are able to cause:
An enterovirus would also explain the; age variation, sex variation, obvious resistance of some family members to the infection and the effect of physical activity (particularly in the early stages of the illness) in creating more long-term/severe M.E. illness in the host. There is also the evidence that; M.E. epidemics very often followed polio epidemics, M.E. resembles polio at onset, serological studies have shown that communities affected by an outbreak of M.E. were effectively blocked (or immune) from the effects of a subsequent polio outbreak, evidence of enteroviral infection has been found in the brain tissue of M.E. patients at autopsy, and so on.
M.E. expert Dr Elizabeth Dowsett writes about Myalgic Encephalomyelitis that: ‘This illness is distinguished from a variety of other post-viral states by an unique clinical and epidemiological pattern characteristic of enteroviral infection. Prompt recognition and advice to avoid over-exertion is mandatory.’
To read or download an extended and fully referenced version of the above text, please see the What is M.E.? page.
Despite popular opinion (and the vast amount of ‘CFS’ government and media propaganda) there is no link however between contracting M.E. and being a 'perfectionist' or having a ‘type A’ or over-achiever personality. M.E. also cannot be caused by a period of long-term or intense stress, trauma or abuse in childhood, becoming run-down, working too hard or not eating healthily. Myalgic Encephalomyelitis is not a form of ‘burnout,’ nervous exhaustion or nervous breakdown or the natural result of a body no longer able to cope with long-term stress.
Research also shows that it is simply not possible that M.E. could be caused by the Epstein-Barr virus, any of the herpes viruses (including HHV6), glandular fever/mononucleosis, Cytomegalovirus (CMV), Ross River virus, Q fever, hepatitis, chicken pox, influenza or any of the bacteria which can result in Lyme disease (or other tick-borne bacterial infections). These theories have been completely disproven with regard to M.E. M.E. is also not a form of chemical poisoning.
M.E. is undoubtedly caused by a virus, a virus with an incubation period of 4-7 days. This is an irrefutable fact. There is also ample evidence that M.E. is caused by the same type of virus that causes polio; an enterovirus. (Just as importantly, it must be noted that there are no 'holes' in the enteroviral theory, as with other theories.) The world's four most experienced M.E. experts ALL consider M.E. to be an enteroviral disease, which speaks volumes. What is needed now is enteroviral research involving genuine M.E. patients, unfortunately there is little interest or funding for such research with the current focus on finding endless conflicting causes for the heterogeneous patients that make up 'CFS.'
See: The outbreaks (and infectious nature) of M.E. section for more information. See also: A New and Simple Definition of Myalgic Encephalomyelitis by Dr Byron Hyde to read about why HHV6 and Epstein-Barr cannot be the cause of M.E. because they have (among other differences) entirely the wrong incubation periods. (A simple fact that should have been obvious decades ago.)
Dr Hyde is also very clear about the fact that M.E. is NOT caused by a retrovirus (including XMRV), as again, the incubation periods simply do not fit. This virus may cause some of the diseases commonly misdiagnosed as 'CFS' however, and may be one of many opportunistic co-infections seen in many different diseases (possibly including M.E.) involving immune weakness, but this has not yet been proven. See the Dr Byron Hyde page and XMRV, 'CFS' and M.E. by Sarah Shenk for details.
There is a lot of hype surrounding the recent XMRV 'CFS' research, and a lot of very slick press releases and marketing. All sorts of claims and promises and assumptions are being made (officially and especially unofficially by patients), which have very little or nothing at all to do with the type of research that has actually been conducted and what this research has actually shown.
These myths have an enormous potential to offer false hope to M.E. patients and to distract from the need for more advocacy to fund vital M.E. research and to demand that M.E. be separated from 'CFS.'
Some of the most common myths about XMRV and M.E. include the following:
MYTH: Evidence exists which suggests or shows that M.E. is caused (partially or completely) by XMRV infection, and this theory fits all the major facts of M.E. (with no big 'holes')
MYTH: The recent XMRV 'CFS' research was conducted on a distinct and 100% M.E. patient group. This research clearly separates M.E. patients from those with 'CFS.'
MYTH: The recent XMRV 'CFS' research shows promise in providing a unique test for M.E.
MYTH: Evidence exists which suggests or shows that anti-retroviral treatments (perhaps specific to XMRV) are the treatment breakthrough that M.E. patients have been waiting for, for so long. This type of treatment represents real hope (or certainty) of a cure for M.E. patients.
MYTH: XMRV is believed to be an important and absolutely vital scientific lead to follow, by all of the M.E. community.