A Night Of Unrest – Full talks by Australian Health Professionals on ME/CFS

Hi my name is Dr. Dianne Shanley. I’m a
clinical psychologist and the director of the psychology clinic at Griffith
University. Griffith University is also the home to the NCNED or the
National Centre of Neuro-immunology and Emerging Diseases. This Centre is leading
the research literature on ME/CFS or Chronic Fatigue Syndrome. One of my
interests is helping patients adjust to living with chronic illnesses, such as
ME/CFS. Patients with this disease often have challenges getting the practical,
financial and emotional support to help them cope with the illness, to improve
their quality of life, and to minimize any further deterioration. Many mecfs
patients struggle to accept that since getting the disease they have started to
react severely to things that they love, such as, exercising, socialising, working
and everyday items like, perfumes cleaning products, noise, food, and light. They can also have difficulty finding
practitioners who have training in the latest evidence relating to the illness.
Ketra is a patient of mine who has ME/CFS.
She lives in a nursing home due to her profound level of disability. This
video consists of a four-minute photo story of Ketra’s journey with ME/CFS
and it gives insight into how devastating this disease can be. It also
has short talks by the healthcare team who are helping Ketra to improve her
health and who spoke after the Gold Coast screening of the movie UNREST.
Thank you, I hope you enjoy. Hi my name is
Ketra, This is my story. I’ve always loved the water. In high school I can remember
the guidance counsellor saying, you’re good at science and love sailing, you should be
a marine biologist. After school I went to sea and did my
skipper’s tickets. Working as a first mate or chef, on luxury yachts for years,
I had a great life. I loved the travel and by
25 I’d sailed a lot of the world, from Istanbul, to the U.S,. Panama, and Brisbane.
And like most 25 year old female yacht crew
I knew my days at sea were numbered. You need to be young, very tanned, and
preferably blond for those jobs. No one stays young forever. I knew my life was
going to change dramatically in the next five years but I didn’t expect this. I’m
now 32 and I live in an aged care facility on the dementia ward. I spend
most days and nights in my room staring at the ceiling – resting. When I first got
sick with M.E. It was very confusing I looked healthy, and if I did nothing
I felt healthy, but any exertion would cause sore throats, headaches and
body-wide pain. Then I became sensitive to light, noise, smells, and most foods. I
had to stop walking. My heartrate would hit 220 just walking
to the bathroom, then after sitting or laying down, it would plunge to 40. I’d have
chills and then burning pain all over for hours after each trip.
I tried to so many things to get better, supplements, medications, IVs, everything
I could – but I got worse and worse. Thinking
became too hard. I couldn’t imagine colours. Words lost
their meaning. I just counted breaths to get through the pain. It was very tough,
but watching my mum get sick, was much harder. Knowing what she was about to
lose and seeing her go through the same illness cycle of hope, denial and
suffering, was really difficult. But now we’ve learnt to listen to our bodies. I
know that when my feet get cold it means I’ve overdone it. if I start to]
feel hyper or rushed I’ve also overdone it. I won’t take any
medication that makes my heart rate jump, as they aren’t good for me in the long
term. I’ve also learned about avoiding artificial and natural chemicals, scents,
noises, anything that triggers my symptoms – I avoid. And I meditate a lot.
The thing that’s helped the most though is heart-rate based pacing. I think that
anyone who’s newly diagnosed with M.E. or suspected of having exercise
intolerance should probably get a metabolic test and learn about the safe
zones and resting heart rates. I’m lucky that being in aged care, with lovely
carers and nurses, has meant that I’ve been able to rest enough, stay within my
safe zones of my heart rate, and to slowly improve. I can now let a little light
into my room and into my life. I can enjoy colors touch therapy and friends.
But aged care homes are not appropriate for M.E. patients. We need (extremely) quiet,
chemical-free areas. And we need people to accept this disease for what it is.
I wish my story was unique or even rare but it’s not, there are over 250,000
Australians with this disease, millions of people missing from their
lives around the world. And Jen Brea, an American woman, made the movie
documentary UNREST, which I decided to screen on the Gold Coast. Because, I’m bed-bound
and can’t walk. I asked for help from Kathy kindly answered my call, along
with my mother (Adrienne) we screened the movie
UNREST and I invited the health professionals that have helped me with
my health, to come and speak about the best ways to support patients now, along
with the researchers from the National Center of Neuro-immunology and
Emerging Diseases, about their latest breakthrough research.
Now we’re going to move into the speaker’s phase of the evening. Can I ask, to come to the stage, Professor Donald
Staines? Donald Staines is the co-director with
Professor Sonya Marshall-Gradisnik at the National Centre of Nueroimmunology
and Emerging Diseases at Griffith University. Please welcome Donald Staines. Well, thank you very much for that
introduction, and what a wonderful crowd we have here, this evening to see a truly
remarkable film. Perhaps it will be almost impossible to describe all of our
research, and our achievements in five or ten
minutes, so I will try and summarize that and maybe
there’ll be time for questions later. But first I’d like to acknowledge my
colleague and co–director Sonya Marshall-Gradisnik and also our wonderful team of
young researchers, some of whom are here this evening, who do just a fantastic job.
I would also like to acknowledge the many patients who have assisted with our
research, and who made blood samples available, and we couldn’t do that
without you. What I would like to do is just give a very brief summary of what
we set out to do and how far we have come. When we set out we wanted to understand
the pathology of this illness, we then wanted to develop a diagnostic test, and
then we wanted to develop candidate drugs that could be used in treatment. If
you have been following our research, and we have published, gosh
maybe 50-45-50, even more papers since about 2012, in the scientific literature.
And we take a very firm view, that it’s all about the science, and the litmus tests
for that ,are the publications that you get in peer-reviewed journals. Without making
it too complex, I would like to say right at the beginning that we believe this
will be found to be a treatable disease. What we haven’t got yet, is the complete
proof of the nature of that pathology. However we’ve come a long way, we now
understand that a group of receptors, or ion channels, which have really
relatively [recently] been discovered, by that I mean in
the last 15 years or so, and they have a critical role in allowing ions such as
calcium into the cells. Now without making again that too
complicated it’s absolutely critical to understand, that
ions like calcium are fundamental to how like calcium are fundamental to how
cells all through the body behave, and how they fulfill their functions. This
particular group of receptors or ion channels are called Transient Receptor Potential Ion Channels -a rather clumsy
name but there is a good reason for that, and they’re
located in the brain, and spinal cord, in the pancreas, in the heart, and the gut, in
the metabolic and hormonal systems, and just about everywhere in the body. And importantly
when they found [them] in the brain, it’s only the last few months, have there been
papers published about their location, in areas such as the brain and spinal cord.
Their main functional there is in support of the white matter, the supporting part
of these cells, that enables neurons to do their job. Now by isolating, or at
least, identifying these receptors in the white matter of the brain and spinal
cord we can get some insight into what the term Encephalomyelitis means.
Because you may be aware, there’s been some skepticism in the medical community
about that term, because normally you would expect that to be infection or
inflammation that’s really what the ITIS in that term means. However when those
cells being looked at in the brain, or different tests have been used, it’s been
a very evasive pathology to really understand. So it’s really not so much as
I said before about discovering a pathology of inflammation or infection or
even of neuro-degeneration such as multiple sclerosis and so on, but rather
a change in the homeostasis sort of a normal function of the white matter of
the brain and spinal cord in supportive neurons, so in other words they can’t do
their job properly. The other component about the term Myalgic Encephalomyelitis is that, these receptors are also heavily
engaged in nociception – making recognition of noxious stimuli
and pain, and aberrant stimulation of them, either suppression or stimulation,
may in fact be a root cause for why the pain is so severe in this illness. So
that’s some insight into the pathology. These receptors are also located in the
pancreas and they have a fundamental role in insulin fine-tuning, insulin
production and secretion and they’re also associated in other parts
of the body as I mentioned also, the genito–urinary system, the gut, and so on. And
other members of this family, have an important role in cardiac function.
Remember that for the heart to function properly there has to be the right
strength of contraction, there has to be the right rate of contraction, and there
has to be the right recovery period after each contraction, to allow the
heart to function normally. So it may be that they’re associated with this as
well. Because as we know, in some patients there is a very
severely disabling condition called P.O.T.S Postural Orthostatic Tachycardia
Syndrome. So the point I’m trying to make is that, we’re actually now beginning to
understand what this pathology is about. The second part I wanted to mention is
the development of a diagnostic test. That was our second aim, and we are well
advanced, we believe, in forming the basis for diagnostic test.
Clearly we’re very cautious in the terminology we use, all of the evidence
that we have, must be scientifically rigorous. But we’re moving forward in
being able to try and describe what are the changes to these critical receptors
and why do they occur. We believe that fundamentally there is a change in the
genes that transcribe these proteins that make up these receptors, and as it
turns out a particular receptor the TRPM3, which we’ve published, has the highest
number of isoforms, or different types of it, in the group, of any TRP receptor. And
that they are also widely and diversely located around the body
some of them having you would expect to have complementary or consistent activity some of them may actually be
antagonistic. So it’s a very, very complex thing, that we’re dealing with.
However the diagnostic test will be based primarily on the genetics of those
receptors, which also known as threat receptors, and Professor Pete Smith will talk
about that later I’m sure. So what happens, we believe, and in our
clinical experience – at least 60- 70 % of patients, as many mentioned in the film [UNREST]
become ill after an infection. And it doesn’t seem to matter what the infection is, it could be a virus, could
be bacteria, could be a parasitic disease, and they appear to recover somewhat from
the infection – but then some other catastrophic event happens. And by way of
speculation, we could say that, maybe just maybe, it’s that assault or threat of
that infection, that promotes expression of the wrong type of the proteins of the
receptors. In other words, abberrant receptors are produced, which is simply
not functional and our research has shown that there are less of these
receptors being expressed and they don’t work properly. So we believe that that’s a
fundamentally important concept to formulate a diagnostic, or at least a
screening test, and we’re working on that very hard at the moment. The third point
about what we set out to do, is to develop drug laws or to look at drugs
which may have a therapeutic benefit. This is a very tough job because there
are groups of receptors that have literally hundreds of drugs that have lignin’s
or molecules that impact on these receptors and signal them, one way or
another, sometimes inhibitory sometimes there stimulatory. It’s a very much an
mixed bag, in fact probably 60% of all drugs in use today, have an effect on the group
of receptors known as G-protein Coupled Receptors, and that’s just to illustrate
that the [TRPM] receptors which are not the same is that [G-Protien Coupled receptors]
that but let’s just say broadly speaking [similar] as receptors, means that
they are ammenable to drug intervention. but that’s going to be a terribly long haul,
to actually identify which drugs are going to produce which effects. Because
it’s becoming clear to us that not only are they clinical differences between
patients, but as we see in any one patient there can be the variation or the
clinical presentation, and that includes that cycle of relapse and recovery so
this is a very complex illness. But we think it can be explained. The
complexity is because the number of these [affected TRPM] receptors is probably
much greater than you might find in any other disease,
and that the nature of the changes in these receptors, is such that, a treatment
or drugs you might find a suitable for one patient, may not be suitable for
another. Anyway that’s not going to put us off it’s just another dimension of difficulty
that that we add to this. So I just want to finish on this point,
that I often hear people say it’s an incurable illness. Well as someone said
they might have thought that about diabetes at one stage, but by developing a
drug insulin, based on what occurs naturally in the body, then you may not
cure the illness, but people can lead a reasonably normal life. So that’s the
kind of scenario that we might envisage happening with this illness. So we don’t
believe in phrases such as incurable, we don’t believe that the barriers to
finding the suitable drug treatments are insurmountable we actually think there’s
every reason for optimism. Thank- you. Our next speaker is Dr. Georgina
Gibson. It gives me considerable pleasure to introduce
Georgina, who is actually a friend of our family. Georgina is a great cook, she is
also a general practitioner, from On The Park General Practice
Please welcome Dr. Georgina I can’t actually see all out there but I
know this lots of people I think it’s wonderful that we’re all here tonight
and it’s a huge credit to Ketra and Josh who got us all together to try and
understand more about this brutal illness I watched that film [Unrest} and my
heart sunk I’m sure some of you will be devastated by what you saw in that movie
tonight. But I also think that with the work that Don and Sonya are doing we
should feel very confident that there’s optimism. I felt embarrassed to be a
doctor hearing some of the stories on that movie and I think we as doctors
have to get much better at saying, as Jennifer Brea’s says in her Ted talk, I
don’t know, I can tell you’re sick, I don’t know what’s wrong with you and I’m
not even sure how I’m going to help you. but at least admitting we don’t
know, is a damn good start. Hopefully in years to come we’ll have
the treatment of ME/CFS as part of the medical curriculum. We certainly
don’t at the moment. I just wanted to mention, I think the goal of GPS is often
the one of filling in all the forms the forms we have to fill in and for our
universities and schools and work when patients with MECFS can’t work certain
exams need special consideration, then we have to also try and help our
patients get funded through Centrelink and applying for insurance – is the most
humiliating demoralizing experience for most patients with ME/CFS, to get any
things through Centrelink or an insurance company. It will be made so
much easier when Don comes up with the test – that we can do and write on the
form this is the score on this blood test. Right now that we’re left with very
little in ways of objective measurements of this condition but there is one test
that I learned not through Med. school or from journals but from my patients.
Thankfully my patients are sufficiently up to speed with MECFS treatments that
they’ve indicated to me that there is a site called the warn the Bateman Horne Center
in the US, who’ve developed a test that checks for orthostatic
intolerance, Don just mentioned this POTS- syndrome, Postural Orthostatic
Tachycardia Syndrome. Many MECFS patients suffer from it. At the end of the movie
when Jennifer’s dancing with her husband and she sort of wilts and collapsed
on the floor she was probably suffering from orthostatic intolerance. If she’d
been dancing probably bit faster she may not collapse when she did. I’m just going
to quickly run through a couple of slides because I appreciate most if you
aren’t doctors and you won’t be doing these tests on yourselves but I think those of
you who are patients should make sure that you do have this test done because
I think it’s a useful screening tool to compare how you’re traveling through the
journey of your illness. First of all when you’re going to do
the Ten Minute Lean tests, you need to educate your
GP, so I suggest you download the brochures that Josh did for me and bring them in so that you can prepare for the
test. My practice nurse does these tests now and they could be done in
about 15 minutes. Patients need to be prepared they’ve got
to have limited fluids to less than a litre over the previous 24 hours etc,
few medications they must avoid, it’s all on the website. Here are the photos that go
with it you’re going to lie your patient down
they’re going to be in comfortable clothing with their socks off and you’re going to
try and wait till their blood pressure and pulse stabilize. Then you’re going to
stand them up against the wall looking at their feet. Just ask them to lean on
the wall. I think that’s so they don’t fall over, then you’re going to monitor their pulse
and blood pressure every minute while they’re standing there, if they can
Last for the whole ten minutes. During that time look at their feet I think
this might be Adrienne’s feet, Ketra’s mother she obviously stood up
for a while and in no time at all that’s what her feet looked. like I think it was
two minutes of time but that sort of appearance that doesn’t happen in normal
people. People who have got, you know their autonomic nervous system
not working properly get this sort of an appearance this is the sort of varmint
chart that you know you might use to do a recording like this and these are the
sorts of findings that you’re looking at for unusually high change in systolic
blood pressure so the systolic blood pressure drops an unusual fall in
diastolic pressure sometimes narrator the blood pressure actually goes up but
what often is very significant is what’s called the pulse pressure the difference
between high blood pressure to systolic and the diastolic gets narrowed as Don mentioned POTS, we also get
this racing heart syndrome now I think the next slide might be
some figures of a real patient. Now isn’t that a shocking slide sorry to do
this to you, what I just want you to notice is some of the things highlighted in
red, the other thing is that the readings on this particular patient that
are abnormal that would indicate that she is suffering from POTS syndrome. The
most remarkable one of them is actually the last row where you see the change in
heart rate over time. She started with the resting heart rate of 62 and at the
10-minute mark she’d gotten up to 128 doing nothing except standing. That is not
normal. That’s what that looks like on a graph,
That was the systolic blood pressure, That’s what the heart rate
changes look like on a graph, so that sort of slides I’m going to show you. But
I hope that that’s just a little bit of hope and inspiration to people to at
least go and get their ME/CFS documented. Certainly whenever I’m
referring patients on to other healthcare providers, which is the role
of GPs, to sort of somehow try to coordinate all the other care providers
involved in a patient’s life, mentioning that this test has been done might just
get you over the line, and convince that health provider that this person is
absolutely genuine. So hopefully I’ll be able to take
questions later, if there are any thank you for listening. Next presenter is Mark Barrett, he is a
physiotherapist who is passionate about health and fitness is responsible for
metabolic testing, at Physiologic in Robina he uses cutting-edge technology to measure metabolism and exercise capacity and uses heart rate
monitoring to help his MECFS patients.
Please welcome Mark. Please welcome Mark. Thanks everyone and Thanks very much to Ketra, Adrienne and Josh for inviting me here tonight Hopefully I can shed some light for you. I thought I was talking for ten minutes, but then I realised it was five, so I’m going to zip through some slides here. You can see here a [CPET] test, these tests
are done on an exercise bike and basically we are measuring a number of physical variables, I’m won’t go into that too much, but from the data
collected from these [CPET/VO2 max] tests we can build some good educational pictures for
people. So this is the metabolism, metabolism energy of a healthy person:
We can see on the left, easy aerobic type exercise, moving across to the right
to more anaerobic exercise, and we can see how a person’s fuel burning, their fat/carbohydrate burning changes in that time. This is a graph of a pretty healthy, aerobically fit individual and we can see
good rates of fat and carbohydrate burning there. Another important thing we
do in the test Is measure some threshold
points, and those threshold points in a healthy person might appear at
a quite high intensity of exercise certainly running. Then in contrast to
this, we can see the aerobic metabolism of someone with MECFS and you can see
there’s a stark contrast there, much diminished ability to burn fat, much diminished
aerobic capacity and much more reliant on anaerobic metabolism when they work.
We also see that the thresholds can occur at much lower work rates. And it’s
important even for an athlete to not spend too much time above these
thresholds, but certainly important for someone with MECFS to to not go above above those thresholds. And we can see that is happening, much lower work rate.
So I guess when we analyze these graphs and compare the difference to healthy
individuals we have to really come up with a new definition for exercise,
because our standard definitions for exercise don’t really suit the MECFS
case. For example with anaerobic thresholds, it might take a
healthy individual running at quite a reasonable pace to reach that, threshold but someone with MECFS they do that, with activities of daily
living including, housework or even just personal hygiene
activities. So that makes us have to think very differently about what is
exercise for someone with MECFS. How do they manage that through the day when
when many of your daily activities become exercise, and then on top of that
we also have to consider that this person, is going to recover from exercise
much more slowly a much slower rate than and we traditionally recover from
exercise so we have to on top of building this new picture of what is
exercise, we also have to map in the recovery and that’s where we start to
bring in concepts like PACING: of doing activities and resting and doing
activities and resting and so on through the day. Now in terms of pacing and heart
rate we saw those thresholds, before that that we measured, in a test. Heart rate
monitors can be a useful too with pacing because you can set the heart rate
monitors to alarm when you go above certain thresholds and that’s giving you warning signs that you need to rest, or schedule in, rest and recovery. Heart
rate also can help define for a person when they are actually resting and
recovered so heart rate monitors can be useful there. And looking at rate data
retrospectively over time combined with things like activity and symptom logs
can help someone build a framework for themselves, a picture of what activities
they can get through in a day and how much rest they’re going to
require around those activities. I mean everyone wants to live a full life so
pacing is something that requires a lot of a lot of discipline on the part of
the person and it’s very difficult when you want to go out and do things, do
social things, do normal sort of daily living things that you’re missing.
So heart rate alarms can be a good way of keeping you in check and keeping you
honest and maybe even helping your carers keep you honest also. Then we come
to exercise therapy and I think you saw in the in the movie [Unrest] earlier that
exercise for a lot of people with MECFS is just not even possible. We have
to really, – exercise therapy, and talk of that, has to come with a warning that
it’s most important that any exercise therapy doesn’t actually make the person
worse because when they crash it can be for weeks or months. So whether a
person can exercise or not is really the first question. Then if they do exercise
and are embarking on some sort of exercise therapy those exercise programs
just need to be massively modified compared to what we see as a normal
exercise model. Loads need to be drastically reduced and by that I mean
the intensity of the exercise drastically reduced, to a point where
people might even start their exercise programs with exercises on the floor. The
interval of exercise, of a particular exercise set, needs to be
controlled and really marked recovery strategies need to be added. So again
recovery from an exercise set may be lying on the floor and certainly much
longer than we normally use in exercise programs. So when we’re dealing with
exercise we need very gentle programs that are really well thought out by exercise physiologists and physiotherapists, with a good
understanding of what’s going on with this condition. Because there is a very
high risk of symptom exacerbation and that can last for like I said weeks or
months and that’s definitely what we want to avoid. Thanks. Our next presenter is Professor Pete Smith, a leading Australian allergist and immunologist from Queensland allergy
services in Southport and Brisbane. He’s a professor in clinical medicine at Bond
and a clinic a specialist clinical collaborator at Griffith University
within the National Centre of Neuro- immunology and Emerging Diseases.
Please welcome Pete Smith. Thank you very much. This is and interesting mixture to be giving a talk at so,
(thank you, I do, I do, thank you very much) It’s very humbling to see such a film, so
thank you very much for the opportunity to be here. It’s great work and I look forward to make things better. Sometimes the
world lines up for bad things and that’s what these genes appear to do,
sometimes they line up to good things. And there’s been a really good alignment
of specialists and researchers and research students as well as clinicians and
patients, and the patient force has actually led us to a very interesting
place. I got asked to talk about immunology aspects, and I think it’s
like in the film, and doctors know nothing about this condition. We do know a little bit, but there’s a lot of information out there, and very small
numbers so what Professor. Staines has stressed we need to get good data, and we need to know where this is coming from this is critical for treating it. From my point of view there’s multiple overlapping symptoms of this disease and many different
phenotypes and from an allergy point of view. One of the interesting studies from the group, have found the Griffith, is that Mast cells, which are an allergy cell, get
activated and there’s more of them. We’re not even supposed to find you in
peripheral blood but in patients with ME/CFS, the team at Griffith have been able to identify them, have a couple of papers, It’s interesting aspect. But also
they interact with nerves. Nerves when they’re saying they’re in danger, tell these
mast cells, which are proficient immune cells to get involved in helping us.
We know mast cells get activated when we have a splinter or a mosquito bite, they
swell u , they itch, in the bloodstream it’s happening on the inside. I see
patients with non-allergic rhinitis and many of you will actually cringing your
seats as you see all these triggers, which is the Cincinnati Irritant index
scale. These typically hit a receptor called TRPV1 which we know is expressed great amounts in patients with chronic fatigue. And when the I’ve been Invited to have a chat to the team about, where on earth do we go looking for this(?), I thought V1 was getting involved but interestingly it forms dimers with
TRPA1 which picks up smoke and cold cold air. And TRPV1 is
increased in patients with irritable bowl the V1’s, any patients with knowledge of rhinitis, have brain fog and sensitivities to certain chemicals,
which Julie may mention, of odors and they have allergies or
hypersensitivities. Many allergists, when you, after one skin prick test say, ‘haven’t got allergies, you’re fine’ I’ve had patients being told they need to
should live in a bubble, which is hardly what, you wait several months to see
a specialist for. When we actually challenge the airways in patient, who are hypersensitive, we get ranges of pain, hyperalgesia. And depending on which
doctor you go to, they’re often very focused, and will see different
conditions, and you’ll have a various names for the condition
as well, depending on who you see. And getting the big picture is, we’re
still searching for that. When, Professor Staines mentioned, when nerves get activated all these neuropeptides effect blood vessel tone and there may be over release of these compounds, and they have been
found. These also affect other sensory nerves and effect of mast cells. So we
actually have complex clinical symptom set. And I’ve just drawn
these into bubbles, but these bubbles may be absent for some people and
some people may have a predominance of autonomic dysregulation, they might have,
hyperalgesia, chemical sensitivity or fog. So I was asked to come in, and the whole team will look at that, and they actually
decided okay let’s go have a look at TRP receptors, they look like a reasonable target. It hasn’t been looked at. And there’s 27 of them in humans, and
interestingly when they looked, the [NCNED] team looked, they found three just repeated that message, message. So they are there. And many of these ion channels are involved in thermo-detection,
chemical risk perception, nociception, and they are involved in the detection
of threat. And also the acetylcholine receptor’s involved in that threat response. But as you know, not every animal responds the same way to threat. We see many animals, deer in the headlight, and I’m sure many people in the room have seen this, we seen this we see withdrawing from the threat and saying it’s too hard, let’s remove ourselves. Some animals respond very differently, and in fact I’m sure, speaking to my patients and I listen to them: them they feel like that on the inside, but can only do that, so when they see threats going round, and you
have these mixed responses. I’m not trying to minimize or trivialize it. I’m trying to say, ‘I get it’. So at this stage we don’t have the answers and as Don said, we have hope,
we’re getting there ,we’re getting some real answers due to the great work of
great people. My clinical focus is looking at reducing the threat stimuli
and reduce the threat reactivity there are some chemical ways of doing this
decrease the ion channel activations and there are ways of doing that increased
resilience and part of that where appropriate is exercise training, correct
diet as part of reducing the threat and the N1 trials, the anecdotes, the
YouTube videos, are not the answers. We need good randomized control trials
based on genotype, that we’re actually in the process of doing. So that’s where I’d
like to sort of summarize, I believe. And say thank you to everyone tonight. Thank you. Thank you, our final presenter is Julie Albrecht who is a dietitian and nutritionist from Julie Albrecht & Associates at the Food Body Life Benowa,
her career spans 30 years, both practicing, lecturing, and consulting
about diet and health. She is passionate about helping people with food
intolerances allergies and sensitivities in chronic diseases.
Please welcome Julie. Thank you everyone, I must say I was also
humbled by that video and I’d like to say thank you to Ketra and Josh. I’ve had the really wonderful
opportunity of working with some wonderful patients who have taught me a
lot about this condition and encouraged me to broaden my mind, and how I’d look
to try and assist them in the journey and one of them. I think here this
evening is Rosie. Hi!, I think when I see a patient who presents like Rosie, did. . How many years ago …was it, 5 years now. It really makes me question about how we
go about, do our assessments. And I think it’s important that we actually take
some time to listen to these individuals and take some details about their
medical history and their symptom profile because we can learn a lot about
what those potential triggers are what those threats that Pete mentioned. We
need to look at their total body load with respect to every aspect of their
life, not only food but also their environment the time they spend
interacting with others, all can have a huge impact on their symptom presentation and
their recovery. And of course their environment from things like as, Pete talked about, about petro chemicals but things are subtle like curtains, people’s
clothings, their beddings, their mattresses, the dust in the room, all of
those things need to be taken into consideration. Acknowledging that people with
this presentation vary in their presentation, so we need to make
sure that we individualize our approach. And lastly then there’s the food. In some
patients we have challenges with major proteins whether it’s gluten or other
grains, problems possibly with dairy and soy and… naturally added chemicals as Ketra mentioned, all these take, to
investigate these, and to identify what a particular issue for a patient, takes
time. It takes a lot of persistence and assistance from their carers. And as I
mentioned before we also need to look at the environmental components that are in
their world and how they may influence their symptom presentation. And then the other challenge is, to make sure their diets nutritionally adequate, which for some
people we can’t actually have them have an adequate diet because their diets
are limited. We put foods back into their diet they end up with a reaction.
And then there’s another challenge of trying to supplement them appropriately
which they also react to. So it’s, it’s definitely a condition which makes you
thinking outside the box in relation to how you manage to support these
people in their journey to re-living and regaining their lives. I think one of the
things they taught me, in working with people with ME/CFS is that you
need to be quite particular about what you’re doing you need to pay particular attention to what they’re
telling me because a lot can be learned from them.
Sometimes it’s the simplicity of their lives that brings them on the journey to
recovery. I can definitely say that in Rosie’s life without her persistent and
caring mother she wouldn’t be where she is today, back now attending University
which is a far cry from where she was in a wheelchair, when I first saw her, the
nasogastric tube at her nose and with a head swung down, and the chair and unable
to communicate with me, so well done both of you. And the dogged persistence that
I’ve seen in them to keep all persisting to find the answers that suited Rosie to
have recovery I think is a wonderful lesson and not an easy journey to bear.
I just like to thank you for your time this evening and once again, all the best to all of you. Thank you. I did say that Dr. Dianne Shanley was due
to speak unfortunately she wasn’t able to be with us. We do have two slides
which I’ve been asked to speak to, Dianne Shanley is the director of the
Psychology [Health] clinic at Griffith University and is a practicing psychologist who
focuses on how to help people cope with being severely ill. So we have four bullet points here: The Role of Psychology ME/CFS, firstly to assist clients and recognizes that
they have a chronic disease. Assist clients and redefining their lives to
accommodate this disease. Assist clients to cope with the sometimes
tense debilitating emotions related to the disease. And assist clients and
managing the disruptions the disease causes to their work school and family
lives. If anybody is seeking more information we might just leave that
slide up there as we enter the question and answer period. (Questions have been condensed for brevity) in terms of testing, as we have heard,
is very heart-wrenching for, particularly GPs who have to deal with this
issue all the time, of enabling a diagnosis which will be accepted by the
economic, the health economic systems of healthcare. And it’s with all diseases it’s basically
saying, you don’t have it unless there is a test. We’re very confident that we have such a gold standard test and I can’t, don’t want to put a time on it, but
they’re not too distant future, we are well advanced in that now, and hopefully
that will be the major change that will enable the Medicare system, Centerlink, and so on, to more officially recognize the illness and to give us some benefit to
patients who have been struggling for so many years. . There is, as far as good randomized trials, what I mentioned in there, there is very little that’s done in good
randomized clinical trials with well-defined patient populations. There
are supplements that may help, having less information your body is better, but what
unfortunately does get pedalled, is ‘hope’ and ‘expectation’ and these things are very
often very expensive. If you’re doing something, make sure you are doing no harm. We’re talking about some of these ion channels and the way they might be activated, but
Professor Staines and I was having a chat before some of these, have you what we call
U-shaped kinetics, so what will block one block something at one dose, changes
it at the other, changes will actually irritate it, so you’ve got blocking and
irritation with the same compound. And when there’s changes, in
that receptor maybe – there’s a shift to the left or the right so that what is
normally helpful dose may be harmful. So my main messages is it make sure it’s got logic preferably do it in discussion with the doctor, have small
amounts, don’t try to do too much and if it’s not making a difference, move
away, until we get better good evidence, both ….. our adage in
medicine is do no harm. When you look at it really objectively in terms of
scientific benefit the proper properly conducted scientific studies two things
one is that supplements do not necessarily stay
beneficial and then secondly the amount of money that is spent on these is
just extraordinary for people with a very limited income. So I
think the way to look at this is, to is turn it around and say when we understand
the pathology, and we’re very close to that, and we can develop a
diagnostic test, tests there are differences within the pathologies to
then come up with properly conducted and probably derived chemicals and drugs
that will be specifically beneficial for that particular subcategory of illness.
And as I say they’re not too far away, but we’ve just got to keep at it. And I think that the other thing, to be really careful, that Pete raised before is that the
normal dose, may you may actually have and adverse response. I think of the
patients that I’ve worked with, that’s probably generally what I see and the
unfortunate thing is that they have often spent a lot of money by the time I get to see
them, so yes I think logic and getting some appropriate medical support
and guidance would be a good way forward. Can I just add too, that this enormous amount of money that gets spent on potentially lot of supplements that
might help, patients with ME/CFS are very vulnerable to magical cures. I actually think that with the work that Don’s doing there will be some hopeful treatments
in the very near future. In the meantime I suggest all that money gets put into
saving out for a motorised wheelchair and fantastic internet access
because that’s probably what saved you as a patient community, being able to talk
to each other on the internet and do research and don’t go in getting all the
quackery that’s out there. The amount of money invested in research
compared with other conditions is incredibly small in this illness and
part of that and I think this would be fairly widespread knowledge, is the
confusion and perhaps lack of clarity, that the funding bodies have had about
the illness, there simply, hasn’t been the evidence for them to say ‘this is
what the illness is’ and in fact I think as Nancy Klimas, the doctor from
Florida mentioned, it was about having a name for it, what kind of illness is this, and for many years people looked at autoimmunity we know
it’s not an autoimmune condition, they thought of may have been a mystery virus
and a lot of time was spent and energy and money spent on trying to diagnose a
mystery virus which was never found so what we believe we are saying is a
very unusual manifestation of a genetic mechanism which is causing a change in
these receptors so that they become essentially dysfunctional, now in that
sense, this is really a standalone illness, so until medical funding bodies
that research funding bodies the world come to understand that this
is a novel illness, you know, we haven’t got a category for this illness
before, and we’re seeing this for the first time, even though it’s been around
for decades, if not longer, then maybe that will send the message and the
impetus to the research funding bodies that it is time to change and
research funds should come into this illness. I’d just like to add a little bit
to that the team at Griffith (university) have done remarkable work, Don, was publishing 50 publications, a
good academic that it might be doing two three publications a year, they’re
putting out ten in that unit, they have fought for, sought hard, worked hard and
achieved good funding, they could certainly do with more and as a public,
as a group, if you’re making it into this condition –
yes services – having young care I think is a point that was made by Ketra,
getting good patient care and facilities should be an emphasis of a group that’s
politically active. I think medical research and attention
to the condition, as a real condition and be dam proud that this team at Griffith
are actually leading the world in this condition It is a challenging, seeing somebody
like this, is a good hour plus of work just on a first touching base,
going out there – I personally don’t have time, I finish work after 10
12 hours a day and work a day and find it very hard to actually sit down and
think beyond that. At Emerge Australia, we have asked patients to put forward
recommendations of doctors that will treat the condition, that they have found
to be helpful. Most of us feel we have never been
validated and it’s hard to go to doctors or professionals of all sorts that just
don’t believe you, that think you are a malingerer or a hypochondriac,
so tonight and seeing so many professionals for the medical side of
things come, it just gives me hope that we will be validated and that
something can be done to help us because the services that we need are important
to help people have a better life.


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