A Postcard from Boston
Although on holiday I showed up to see what was going down at the AACFS conference. There were some highlights and some new 'bits' of information, to add to the old, but it was pretty much the same old faces.
Below I've tried to cover in detail the highlights and the New! bits, at least as I saw things.
In overview Nancy Klimas depicted current theory of the chain of events leading to CFS as: Genetic Predisposition >Triggering Event >Mediators (Immune Upregulation, Endocrine dysfunction, Neuroendocrine imbalance) > CFS persistance.
Many speakers spoke of the real need to subgroup patients currently under the CFS umbrella.
Finally a decent community based study has more carefully defined the prevalence of CFS. In the opening session a CDC epidemiologist announced that 2 in every thousand people have CFS (ie 0.2%). In women the rate is higher at between 3-4 in every thousand. By examining the prevalence of other common women's diseases, the CDC researcher concluded that CFS is a serious women's public health concern. "To put this into perspective with other health problems of women, CFS affects about a third the number of women with diabetes (900/100,000), but three times more women have CFS than HIV infection (125/100,000). CFS prevalence is 25 times the rate of AIDS among women (12/100,000), and is considerably higher than female lung cancer (43/100,000), breast cancer (26/100,000), and hypertension (20/100,000).". This is of particular importance because previously the CDC had estimated the rate of incidence was 50 times less frequent and had considered the illness as relatively uncommon, now they suggest that CFS is " a serious public health concern".
At these 'do's' they give an award called the Rudy Perpich Award. This year it was given to Dr Philip Lee, former US Assistant Secretary for Health. He'd flown in just for his acceptance talk . He thanked numerous other notable CFS researchers and patients for educating him on the disease. He was seemingly ardent in his speech that the name should be changed - he suggested the eponym Henderson/Shelokov. He said most physicians have no respect for the currrent name. He suggested too much research money was being spent on psychological issues and that there isn't enough biological research. He made comment about the British Royal Colleges report - saying he entirely agreed with the Lancet's Editorial analysis of it (ie that it was a waste of good money) in direct opposition to the BMJ 's stance (ie Wessley et al). He suggested the US needed a federal plan for CFS research. "This illness needs the same kind of focussed attention as is being put into AIDS," Lee said, "I don't know if we'll get 1.7billion (as is spent on AIDS) but we should be getting more than the 10 million that is being awarded to this illness now."
These were BIG things to be said, and it was good to hear. I only hope the powers that be were listening.
1) More on: Immune Activation
Nancy Klimas described the study she has wanted to do with CFS patients for years. Based on the evidence of abnormal function of lymphocytes and increased expression of pro-inflammatory cytokines in CFS, she is extracting lymph nodes analysing them and modifying them and reinfusing modified cells back into the patient. This is a therapy in trial with AIDS patients too.
In 14 CFS patients she found lymph nodes to be producing highly activated T cells (CD 4 & CD8) -the resultant supernatant soup was very antiviral in its activity. Once she'd expanded the cells (ie reproduced them in culture over 12 days) she then modified them to correct T cell levels and reinfused them back into the patients. She found that with T cell reduction, patients symptoms improved - cognition, "the works". She said it was safe and she was very excited about it and was hopefully moving to phase 2 trials in 1999. Therapy in the future would likely rely on multiple infusions.
The preponderance of activated T cells in the lymph nodes she said was even more than in peripheral blood!. All her findings are consistent with an a chronically activated immune system. In CFS, she said that the chronic immune activation is higher than in the setting of chronic hepatitis, and is more similar to that seen in some stages of AIDS.(This work supported by the CFIDS Assn, and the National CFIDS Foundation).
Eng Tann had extended his studies into new specific low titre auto antibody findings as reported in San Fransisco. In well known auto immune diseases like Lupus there is an increase in cell death (apotosis) which is associated with reduced auto antibody testing. What Tann showed in CFS was an increase in a particular type of auto antibody which should be associated with decreased cell death. Cell death is happening in CFS so he couldn't explain this anomaly with the expected findings in other auto immune diseases. The actual auto antibody he detected was different to the auto antibodies detected in other systemic illnesses - so he concluded that whilst he was getting these results, CFS was not auto immune as understood in other "classic" auto immune illnesses. Something is odd, but uniquely odd in other words. The assay he used was a newly developed process.
2) NEW!: HHV 6 Activation
For years research has looked at the HHV 6 virus and its relationship with CFS. To date the evidence hasn't been majorly convincing - in at least being causal . Konstance Knox and her team however took the view that tests are problematic if the situation is one of a reactivating nature. It is well known that in AIDS or bone marrow transplant recipients on immune suppressants, previously dormant immunologically 'controlled' viruses recur . Is this happening in CFS was their question. Could even persistence of it be happening in a subgroup? What they found was that CFS patients did change in their positivity to HHV6 and therefore it is crucial that immunological status needs appraising by multiple blood tests over periods of weeks or months. Out of a sample of 400 they estimated that 60-70% of CFS patients are either chronically activated, or more periodic in their expression. Interestingly in the course of the study they observed that many of the HHV 6 positive patients had central nervous system involvement in their disease. They found that those with CFS with recorded CNS involvement ( abnormal SPECT or MRI scans) tended to be more likely to have HHV 6 persistently activated. This fits because HHV 6 is highly neuroinvasive in nature, but the thing is that most people are infected with it and it remains dormant - the question is why is it now , reactivating and in many cases persisting?
(This study was funded solely by patient organisations: The CFIDS Association of America, and the National CFIDS Foundation)
3) More on: Dysregulated Anti-viral Pathway
Dr Bob Suhadolnik took the podium to further explain his work at Temple Uni on the pathway that kills virus's in humans. He stood bold and said that two years ago in San Fransisco he had presented preliminary work on something like under 10 patients - he jokingly quipped "how did I do that?" (meaning that no self respecting scientist would dare present work on such small numbers and actually claim anything). "Today I'm here to tell you that in the last two years that we have done three things required in science - 1) We've replicated the findings of a new lower molecular weight RNase L in CFS patients with a larger numbers of patients n=90 with a further 75 underway 2) CFS symptoms do correlate with these findings.3) Independent replication from another group (in Belgium) has confirmed our findings." (Komaroff later pointed out that a 4th requirement was needed, namely to compare the findings with other illnesses).
In CFS patients there is statistically significant increases in 1) RNaseL activity 2) bioactive 2-5A concentration 3) new 37kda RNaseL 4) interferon alpha , all from peripheral blood mononuclear cells.
The more ill the patient ,the worse the test results were. The dysfunction is more profound and complex than previously thought.
NEW! In another presentation by his PhD student, it was confirmed that the 37kda RnaseL was something new and not a breakdown product of the normal 80kda RnaseL. She also elegantly discovered that the 37kda RNaseL was not under the same regulation as the 80kda. (An aside here is that the drugs used in AIDS called protease inhibitors wipe out the 40kda breakdown product of the 80kda, but they have no effect on this new 37kdaRnaseL) NEW! In an in even niftier experiment she could demonstrate that in CFS patients it is the presence of the 37kdaRNaseL alone that is directly responsible for the elevated RNaseL activity that is found in CFS.
Therefore, key points:
- 37kDa is not under the same regulation as the normal 80kDa
- it appears that the 37kDa alone is causing the elevated RNaseL activity seen in CFS.
What is creating the 37kdaRnaseL? And where is it coming from? These questions remain unanswered (at least at this point).
These are profound and radical findings/abnormalities. Dr Bob couldn't emphasize this more. He is a man of intelligent compassion and it really showed, his parting comments were "Hopefully things will change as we learn more".
Two Q's were asked:
Have you looked at other diseases? Kenny replied that studies are underway, they have looked at Fibromyalgia and not found the 37kdaRNaseL.
Can you speculate on cause? Kenny replied, he doesn't think its genetic, he thinks it's virally induced.
4) Neuroendocrine Disturbances
NEW!: Greta Moorkens provided the first data on growth hormone abnormalities in CFS. Growth hormone is a hormone that kick in as we sleep and is vitally important for cell repair and cell maintenance .The nocturnal secretion of GH were shown to be half that cf controls. She gave GH therapy to 20 patients 6.7µg/kg/day for 12 weeks. Mean insulin growth factor-1 (IGF -1) increased during the 12mth of therapy. Other hormones remained stable. Levels of 6 amino acids (tyrosine, valine, tryptophan, phenylalanine , isoleucine and leucine) actually increased - she was unclear why this happened. Fat free mass increased as did total body water. Patients reported feeling better. In a related poster and in discussion time Paul Cheney spoke of his fear of using Growth Hormone but that he'd found a plant derived polypeptide which acts like GH, to be useful. IGF-1 normalised in an 'adaptogenic' fashion. Once again all this is in the halls of research at the moment - but interesting all the same.
The awful disturbed sleep that has been Moldofskys research interest for years - is truly that. He showed all sorts of 'stuff ups'- namely :overnight decline in NK cells (in both proportion and activity) - they "cut out" at around 3am, overnight increase in T cell proportions, a different diurnal and phase shifted overnight cortisol production, and a different and lower pattern of overnight prolactin release, a low GH peak at around 2am, and higher overnight alpha non -REM EEG recordings. All these disrupted hormones add up to sleep that doesn't do what it should for us. The phase shift of cortisol is advanced by about 1hour 45mins and likely why we can be up late at night, but can't wake up till late in the morning. All the abnormalities can account for the arousal disturbance we get throughout a night. In other words our circadian rhythm program is corrupted!
Ted Dinan gave a comprehensive overview of the dysregulated HPA axis. Release of cortisol (from adrenal gland) is blunted in CFS . Release of ACTH (from pituitary gland) is blunted. If he gave CRH (cortisol releasing hormone) cortisol and ACTH remained blunted. But if he gave DDAVP (a vasopressin hormone released from the hypothalamus) together with CRH he found that with this combination, cortisol and ACTH raised appropriately (this is NEW!) . The implication that I took from this is that the "stuff up" of the pituitary and the adrenal glands, is being propagated at the level of the hypothalamus. (this was a VERY complicated lecture and I may have got this wrong). He also showed that the adrenal gland itself is reduced in volume in CFS patients (this is in contrast to depression where this gland is found to expand).
5) NEW!: Cell Membrane Changes
Wilhelmina Behan reported on new findings of an abnormality of membrane ion channel function in a small group of ME patients from Glasgow. For proper cell function, each cell in your body requires effective operation of what is termed the "sodium-potassium pump" This pump keeps the cell in osmotic homeostasis - it is like a control gate keeping the right amount of these ions in or out of the cell .Normally sodium ion concentrations are high in the extracellular fluids but low in the cell and potassium is just the opposite, high in the cell and low in the extracellular fluids. ATPase is used as the carrier protein.
She had found evidence that these pumps weren't working as they should - she found them leaking (ie she found intracellular potassium lower, cellular potassium higher than normal, but overall total body potassium lower) . She postulated that such alterations could affect normal receptor sensitivity to neurochemicals and neurohormones such as acetylcholine, serotonin or other mono amines. This may account for the sensitivities to anything which alters ion channel function - including alcohol, quinine, anaesthetics and many drugs. Therapy to correct potassium levels may ? help, as it seems that CFS patients are losing potassium.
A question was asked, what can cause this? She answered, virus's or chemical exposure.
6) More on: Autonomic Problems
NEW! Pulse Pressure convergence on standing.Dr David Bell spoke of data he had been collecting which was showing a drop in pulse pressure over time whilst standing. [The pulse pressure is calculated by taking the difference of the systolic and diastolic measurement, eg., a person with a blood pressure measurement of 130/85 would have a pulse pressure of 45] The pulse pressure represents the ability of the body to circulate blood. When it drops essentially blood flow slows down. A low pulse pressure means that blood will not be circulated well . In normal people the pulse pressure remains fairly constant across all conditions, including when resting, tired or exercising. In his CFS patients the pulse pressures were showing convergence, simple faints show a very different pattern.
(In talking with David afterwards he explained how to do the test. It's simple and cheap . The patient lies down and BP and pulse are taken for 10 minutes. These readings are normal. The patient then stands still next to a wall. (most patients can't stand still because they automatically fidget which pumps blood) The BP is taken every 5 minutes for as long as the patient can stand for. In some patients the pulse pressure reduces to as low as 8mm of mercury - and they feel really bad at that point . "I tell them to sit down when they start feeling bad but some are so determined they even faint on me" he said. A reduction to 18mm is considered abnormal.)
NEW! The Natelson group reported that they were finding 2 disorders that were different dependent on severity .
- Severe patients had low stroke volume (stroke volume is the measure of venous blood returning to the heart) and low cardiac output. This suggests a low flow circulatory state. Their BPs and HR did not 'react' to stressors in the same way as the group of 'less severe' patients .
- The less severe patients displayed BP and HR variability and hyporeacted as in NMH and POTS
They suggested that the severe group had a low circulatory state (cause unknown) and the less severe group had normal blood flow but that its modulation was at fault (cause possibly neurally mediated ie from a defect in the brain).
In the less severe group they were able to detect lesions on MRI. Cognitive problems in both scenarios was seen as a consequence of lack of blood flow to the brain.
This same group also showed that CFS patients display abnormal BP and HR responses to both exercise stressors and cognitive stressors. Healthy people show increased BP and HR in both these situations. BP and HR changed differently in CFS patients. CFS patients showed a significantly lower changes in systolic pressure and lower HR responses. Since CFS patients have lower systolic BP and HR responses compared to their healthy counterparts, they suggest that patients may not be able to exhibit the expected range of responses required during these stressors and that this may , in part, be responsible for CFS patients reporting detrimental effects of psychological and physical stress/exertion.
A paediatrician called Julian Stewart demonstrated that 18/26 of his adolescent CFS patients had Postural Orthostatic Tachycardia (POTS) as assessed by Tilt table testing.
Another study by Mark Alexander from the Children's Hospital in Boston showed POTS in adolescence but they also did another NEW! neat thing. As well as measuring BP and HR they also measured brain blood flow velocity by Doppler monitoring of the middle cerebral artery. CFS patients had on tilting greater increases in HR, higher maximum HR, and larger decrease in cerebral artery blood flow velocity, but unchanged BP during the first 3mins of tilting cf controls. 6/26 displayed fainting, 15/26 had POTS. Therapy directed at POTS improved reported wellbeing - didn't 'cure' but roughly patients went from 4/10 to 8/10 in their scoring. This is the first study I've seen that documents the decreased brain blood flow whilst tilting. Doing SPECT or PET scanning simultaneous to tilting is what the Johns Hopkins team are also wanting to do.
7) Anti-Viral Therapy
4 study Ampligen review by William Strayer .It was convincing to me. The biological correlates eg the reductions in RNase L , 2-5A synthetase and alpha interferon matched improved patient status correlates eg treadmill score, or cognitive tests etc. The therapeutic benefit was shown to be lasting - once again this is pioneering stuff and still at phase 3 trialing. A question was asked about whether any variables seemed to predict response. Having the lower molecular weight RNase L did. Age, length of illness didn't.
So as you can see it is easy to see that EVERYTHING is related to everything else. 1, 2, 3 are connected , 4 could be a result of 1,2,3 or perhaps the cause of 1,2,3. 5 is an outcome as are the findings in 6. In practice the most easily measured and accessible aspects to the illness at the moment are related to 6. Because CFS is a continuum of illness the damages in each area in each individual are likely to be different - perhaps giving rise to the diversity of symptom expression seen in the illness. Because all of the systems are so interlinked, any intervention may effect all systems.
The 'story ' really hasn't changed, its just that more 'bits' are being uncovered/unpacked in the lab.
Ros has covered this section well but I wanted to add some extras "bits " I noted. These clinicians are our heroes and we all owe a lot to their fluid minds and dogged determination in recognising and treating this disorder over the last 15years.
B12 : use the hydroxy form, at night, up to doses of 5,000mcg. In terms of exercise, he doesn't recommend aerobic exercise, rather strengthening and stretching. He also suggested that light impact bouncing on a rebounder should theoretically aid the autonomic problems.
He asked his patients if they were stuck on a desert island and you could only choose one medication what would that be? The answer from most was Klonopin (NZ = Rivitril) - advantages - rapid in onset, normalises NMDA excitory toxicity.
B12 - not for deficiency, it effectively supports protein metabolism, serotonin metabolism , dopamine metabolism. A study at Vanderbilt Uni is showing that CFS patients are making antibody to B12. He uses 3,000mcg 2X weekly, up to a max 15,000mcg per week. With patients with abnormal ECGs he uses amphetamines. Ritalin 5-10mg twice a day. Dexidrine 5-20mg twice a day. Phentermine 15-30mg daily - all increase BP, good for hypersomulence. For allergies he recommended the new antihistamines. Ampligen he sees as the most promising therapy.
Also spoke of his dream : To see clinics available where patients can go to try relevent treatment strategies in controlled conditions . Its been a 'dream' for the last ten years - he hoped for the sake of patients that one day the dream would get *real* funding. He was encouraged by results using Ampligen for the subset testing positive for the 37kda RNaseL protein.
Doctor to Doctor Session
Only about 30 drs attended (pathetic eh?).
- Sleep - the first problem to sort out. Nancy Klimas tries 4-5 sleep meds then maybe orders a sleep study. She insists on keeping patients on the meds for the studies, despite what the labs want, because that is the condition under which the patient will be trying to sleep. Sleep studies will pick up narcolepsy and aberrant ECGs. She asks for the labs to look for restless legs too. Sleep apnea also needs ruling out. Generally Meds: Klonopin & low dose tricyclics. Lapp uses Melatonin.
- Pain - with regard to narcotic use. Lapp reported that patients report being able to think better and speculated that they likely block cytokine activity in the brain. He finds patients don't get addicted or need more. He uses Vicodin (synthetic codeine), up to 6 a day. Patients don't experience euphoria. For stonger relief he uses longer acting preparations like MS Contin, particularly at night.
- With regard to the use of stimulants eg Ritalin. There was concern raised about addiction and creating false highs and lows and the criticism received from colleagues in relation to prescribing them. Those using them said that patients didn't get addicted, and that if they helped it seemed to be like the prescription for ADD.
- NMH. The comment was made that oftentimes the treatment doesn't work as expected as in pure orthostatic hypotension. Generally the drs were starting with salt and fluid loading, then adding Florinef. For efficacy they trusted patient report. Tilt tabling made patients real sick and many didn't order them for this reason - they treated empirically. Some suggested using Midodrine (5-10mg 3X a day ) in combo with Florinef, for its vasoconstrictive qualities. Some noted that the therapy works for a while , then doesn't , so they take the patient on and off for better effect. Also they reported patients found compression hose useful, 30 - 40 mm pressure or even just tight stockings. Tilting bed head 5-10 degree up also reported as effective.
- SSRIs. These meds improve immune function. Nancy Klimas uses for this purpose in non depressed CFS patients. They also treat NMH too. She realises many patients are just intolerant - these are the toughest patients to treat. The side effect profile is reduction in gastric motility which she worried about in a patient with already reduced gastric motility, she suggested Zoloft had the least gastric effects. Dosages built up from even 1mg, to patient tolerance. Many drs reported the curious finding that the SSRIs sometimes make people sleepy rather than being activating.
- Diamox. This has been used for headaches but it lowers blood pressure but despite this on some patients it still helps, Lapp recommended a 'try and see' approach 125mg 2X a day.
- Dr Goldberg recommended an elimination diet to find foods that trigger intolerences. (Any intolerances feed the immune activation and potentially can aggravate NMH).
Discussion then revolved around the social problems that can arise. The problems of family members being hostile to sufferers as a result of looking well but being ill. One dr commented that the suicide rate amongst her patients had dropped over the past few years. She had had 1 patient and 2 spouses commit suicide in the last year. A psychiatrist noted that while Munchausen's syndrome by proxy may be the problem in a few rare cases, but that wrongfully accusing a family causes a great deal of harm.
A panel of 3 Ampligen patients (of Dr Dan Petersons & Cheneys) described their recoveries on the drug. The deal is though that these patients are paying big time for the drug and it is only available at 4 sites in the US and one in Belgium. This whole session was very emotional, hearing how peoples lives had been rebuilt - many of us were crying listening to the 3 patients tell of their stories. One of the speakers - a very eloquent lawyer said to me afterwards that he couldn't see how the FDA could not approve it, but he did roll his eyes and said "but you know the politics of this disease". Dr Dan Peterson who has administered the drug over 70 times said it was safe and is awaiting a time when it will finally become more widely available to those who need it.
Children and Adolescents
All the speakers agreed it was high time for a definition and better epidemiology in children. Bell and Lapp saw problems in the literature of the past because of the lack of differentiation between CF and CFS. Literature often quotes that 80% recover, Lapp suspected that only 20% of the children discussed actually had CFS. In his experience over the last 4 years, 4/20 children have improved. Bell suggested CFS does occur in children - his youngest had been 5yrs old. He suggested that under 12 the onset was more gradual, after 12 more acute. Karen Jordan suggested that children are more likely to have eye pain, girls - more sore throat and lymph node pain, boys - more memory impairment.
James Jones argued that CFS shouldn't be "diagnosed" in children because it will perpetuate the illness (yeah, right?). He also argued that failure to recover in children can be predicted by problem family dynamics ( again how presumptuous!!) (What does *not* diagnosing do to kids is my question??)
On the other hand psychiatrist Allan Gurwitt , like Bell and Lapp saw childhood CFS as a "major crisis in paediatrics". Any psychotherapy he did with patients was for grief, loss and fear ie. demoralisation not depression. He found children did not malinger - they were frustrated and mad. For parents he stressed that they had to learn when to advocate for their kids eg. course loads at school need to be appropriately adapted. Parents should help in teaching kids resting and pacing as a strategy. He'd found that adolescents had been pushed into adult roles prematurely but that most coped with this. Cohesive identity formation and socialisation were crucial aims in his approach.
I don't think the others were expecting the first wonderful presentation by pediatric psychiatrist Allan Gurwitt . He was first up and basically 'socked it' to the audience. He said his 'concerns' about the state of the field had made him decide to not to repeat his presentation on data on children , but to show how much iatrogenic damage the psychiatric profession had caused sufferers of this illness and how they continue to do so.
He said that psychiatrists can be helpful only if they really know about the illness. He relayed the story of a 28 year old female med student. She had asked that he not tell the med school that she had CFS. "She was scared not paranoid" he said. She felt ashamed for having CFS, a shame that had been induced by the medical profession itself because of the psychiatric slant that is so persuasively ingrained on the minds of doctors about CFS. This, he said vehemently, "had to stop". The history of this illness he said could be retitled "the morbid fascination with psychiatric study".
He thanked Leonard Jason for systematically going through the research of the past and pointing out the bias and flaws in much of the literature concerning CFS. He urged people to read Jasons' paper "Politics, Science and the Emergence of a New Disease: The case of CFS", By Jason et al. American Psychologist, 52 (9) 1997.
Over the years he has been appalled by:
- The repeated failure in literature to distinguish between CF & CFS. He exclaimed "this is just no longer acceptable". The conclusions about the illness have been all screwed as a result of this.
- The obsession with premorbid psychiatric history. He finds this bears no relevance to getting CFS, just as it bears no relevance to getting cancer.
- The almost routine readiness of physicians to send patients for psychiatric referral. He claimed patients should only need to see a psychiatrist when there is good reason. He sees CFS as being best handled by a primary care physician with psychosocial help where necessary.
He ended his passionate presentation by saying that we need to get away from the flawed research of the past that has so damaged patients and study of this illness needs to stay in the medical arena. He hoped that this conference would put psychiatry to rest and that future conferences would not in include such sessions.
From my perspective the next 2 speakers looked particularly stupid, Hickie discussed a possible genetic tendency for "fatigue" ( what did this have to do with CFS I thought?), Sharpe then asserted that psychiatric assessment was necessary as the accompanying depression is treatable, CBT provided collaborative problem solving, and that non forced exercise (this is a different bent on what he publishes) was useful.
The session ended with Jason pointing out 3 main criticisms of research. Namely the problems of 1) Selection of samples eg the UK definition, selects a different patient population 2) The 1994 Diagnostic criteria - the lack of constructs and operational definitions of symptoms - a lot rests on subjective interpretation. 3) The lack of consistency of the Instruments used particularly in psych based studies. He suggested what we use to measure, determines what we get and that CFS research has been thus distorted because of the variability of measures used in psychiatric instruments adopted in measuring it.
Gurwitt and Jason thankfully saved the day, I thought. I only hoped others saw it that way :).
One night there was a viewing of a film in-the-making about CFS, by CFS patient and filmmaker Kim Synder. It is GREAT... The real shame was that doctors didn't come and see the real story, the real patients... the real devastation..
In the film she documents the LA Hospital Epidemic of the 40s. She interviews some of the nurses effected who are now well into their '70s. They said they were a lot better but many said they had residual symptoms still. The Lake Tahoe epidemic is followed - interviewing Peterson and Cheney and their patients. David Bell and the people effected in Lyndonville in 1985 are interviewed.
It is a truthful if harrowing film, much like Oslers Web. She interviews the doctors who have fought for us and those who haven't - much of it reduced my friend and I to tears.
Recent footage of a severely ill student attending his graduation showed just how severe this illness can be. This young man could not do ANYTHING for himself. He was on jejunal feeding. To be moved from his bed, he is eleveted by a machine, moved onto a stretcher and then ambulanced everywhere. The cost of his care is astronomical (US$30,000/yr). A plea was made by the Conneticutt support gruop for financial assistance for his family.
I couldn't help thinking why weren't the 300 attendee doctors watching? Perhaps they were resting in the bar - a nice safe refuge....
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