Saturday, June 25, 2005

Frustrations of CFIDS/CFS/ME

Glad to have met Jean (in Canada I think) through the comments at my main blog ME AND OPHELIA. Jean has suffered from CFIDS for two years. I totally identify with her post entitled Frustrations.

UPDATE: I am taking the liberty of copying the post here incase the link to Jean's blog becomes broken or the post gets deleted:


Although I try to maintain a positive outlook, there are times when I am just really pissed off & frustrated. Having this illness has changed my life completely. I am no longer the same person I was. I think the two things that are the hardest to deal with are: the isolation and the feeling of uselessness or not accomplishing anything. These are a struggle every day.

I used to be a very active person. I went out a lot with friends & family, I catered parties for friends and threw fun "do's", I travelled, I worked out regularly and was fit, I lived. Now, I find that I rarely go out, I'm lucky if I can go outside for a short walk, I'm deconditioned and I feel alone.

I have family & friends who care about me but they have lives. And these lives have continued while mine has sort have come to a standstill. Some friends no longer ask me to do things because they automatically assume that I will not be up to it. Maybe I can't do the type of socializing I was able to before, but I still want to interact with people in some way, still want to live some sort of life. I'm not dead.

I had a career, I worked hard & was appreciated for my efforts. Now that I can't work, I sometimes feel like I no longer accomplish anything of value. It has made me realize how much emphasis this society places on work, making money, success. How can an ill person be a success?

Well, I think that I am doing something really important right now. I'm trying to take care of myself the best I can. This is my full-time job. I'm believing that one day I will be better in some way and that these are my circumstances at this point in time. Maybe I will never be the same as before but I think that will be okay because no matter what type of improvement I have in the future, I will be so thankful for it. Having this illness has taught me a lot of things about myself. That I can still have hope no matter what is thrown across my path. That I am useful to those in my life - I can teach them what I'm learning every day. That I am stronger than I ever thought.

experiment in writing... 22/06/2005 21:31 Lady X

Wednesday, June 08, 2005

Six week aggressive rest programme

Last week, I started a six week rest programme that has taken me two years to organise. It did not get off to a good start on June 1, too many unexpected interruptions and a few more things to take care of. So I am counting this week as a warm up to fine-tune the routine and start it properly next Tuesday. It's hard because it is so lonesome and boring. Cried the first few days. You have to psyche yourself up for such a solitary, sedentary, no talking, no nothing existence.

Food cupboard, fridge and freezers have right amount of ingredients to manage well. Tried and tested it over the past six weeks. Some days I make simple sandwiches with fresh greens and ham and have devised ways to prepare food for each day. Too long and complicated to explain.

In the past, I have resisted sleeping during the day as I sleep well at night. Now, each day I unplug phone and return to bed and sleep 2pm - 4pm. At night I go to bed before 11pm and get up when Ophelia wakes.

From the moment we awake, the programme begins which means total rest for five minutes every 30 minutes, even after sleeping. Here is how it works, using a timer around neck and switching tasks. No visitors. No unnecessary talking on phone. No lifting, carrying or even watering plants. Brush teeth after food laying down (don't need water using dry electric brush and beaker). Walk down steps to post box only every 2-4 days.

Wake and get up, let Ophelia out, drink cold water, bathe, dress - rest- get up prepare food (in stages) rest - eat - rest - computer - rest - get up and prepare food (in stages) - rest - eat - read - rest - read - rest - prepare food (in stages) - rest - eat - rest - watch TV - rest - sit up outside in noon sun 10 minutes - rest - computer - rest ... and so it goes on throughout the day and night every 30 minutes ... eating five times a day.

30 minutes computer time includes reading emails, checking newsfeed, reading blogs and tracking news - by which time it does not stretch to writing a post - so it is taking all day to squeeze in getting a draft together. Next week, I shan't be replying to emails or leaving comments. No phone calls or lifting Ophelia for a cuddle.

Today, I had my haircut. It is straight and simply pulled back into a hair tie. Hairdresser visited here. It feels good to have a real short pony tail again. Easier to manage, wash and brush. Must go now. More on this later. Meanwhile, here is Patrick's cat Pixel - the same cat posted at my personal blog me and ophelia a few days ago. Just like Ophelia, except for the stripes. I talk to Ophelia and tell her how beautiful she is. No ball games for next seven weeks. Hope she does not get bored with our ribbon on a stick game.

Pixel in the Sun

Sunday, June 05, 2005


Dr Betty Dowsett, who has been involved with ME research for 51 years, was clearly excited by the possibilities of the drug Pleconaril being a breakthrough in the prevention and/or cure for M.E.

More about Pleconaril later, courtesy the newsletter I have just received from Shropshire & Wrekin ME Support Group.

Meanwhile, here is a copy of an item published at the The One Click Group October 2004:

From Dr. E. G. Dowsett, Medical Adviser of the 25% ME Group UK


Since early January 2004, scraps of information about this event have been coming to me in bits and pieces via email and ME Group publications. Much of this was, as usual, a mere "whisper" without editing or substantial foundation. It seemed a waste of time to respond. However, Simon Lawrence of the 25% ME Group had a more critical approach and sent information about a consortium formed between a professor, with whose work I had long been aquainted, and a commercial laboratory concerned with providing a rapid diagnostic service for his unit. The agreement was between competitive technologies, Inc. - For the Rapid Assay of Human Enteroviruses and Professor Harley A. Rotbart (Professor of Paediatrics and Microbioligy, Infectious Diseases and Epidemiology in children) at a well known university and children's hospital in Denver, Colorado, USA. The aim was to prevent the unnecessary expense and trauma of sending children to hospital and providing the wrong treatment. This was substantial enough for me, because fortunately, I had been able to purchase his excellent text book on "Human Enteroviral Infections" published by the American Society of Microbioligy in 1995, and found that we are of the same heart and mind. I have followed his work ever since! There will be no disappointment with the research from his unit!


This is a "collective name" for 5 subgroups of a very large family of
Picornaviruses (Pico, tiny size) (RNA Ribonucleic Acid, their internal
genetic constitution) Polio, Coxsackie A and B viruses, Echovirus and their
viruses only number based (EV 68 - 78). They account for millions of
infections each year and have been recognised since antiquity (1500 BC), but most infections are subclinical (without symptoms) and simply induce natural immunity. As viruses, they are too small to replicate themselves and must enter a human cell, obliged to hand the job over to their human host. For this, they target mainly cells within the respiratory and intestinal tracts of human hosts and have evolved over the centuries to persist in a form that does not usually threaten the host or virus. Unfortunately, modern standards of culture (eg, sanitary habits and lack of breastfeeding) have almost destroyed this convenient alliance, so that, in modern times clinical disease has arisen due to social change rather than to any mutation of the viruses concerned. Nowadays, enteroviruses are clinically associated with over 20 distinct syndromes. These usually arise from spill over of infected blood from the intestinal tract or by direct access to the brain via the spinal nerve tracts. These well recognised syndromes resulting from such "accidents" are characteristically inflammatory in nature and include: Polio, Polio Encephalitis, Myalgic Encephalitis (affecting the brain stem), Meningitis, Myocarditis, Pericarditis, and Degenerative Heart Muscle Disease, Pleurodynia (Bornholm Disease), Rashes on Skin or Mucous Membranes, Eye and Ear Infections, Vestibulitis (affecting balance), Gastroenteritis, Hepatitis, Pancreatitis, Juvenile Onset Diabetes, Urinary Tract Infections, Kidney Disease, Perinatal Enterovirus Disease and "cot death". The profusion and complexity of enterovirus infections is discouraging to scholars and leads to much apathy within the medical profession and mistreatment. They cling to a "psychological" explanation instead of questioning their local microbiology department!


(The study of disease in defined populations)

Any good clinical microbiologist such as Professor Rotbart, will have spent
some time on this and on working out how diseases spread and cluster into groups and how they can be defeated. Testing the drugs now being researched includes using the common cold viruses (Rhinoviruses which are also included in the Picornavirus family) to judge the effect. Many drugs, eg, Disoxaril, Enviroxime, Piradovir and Pleconaril have been tested on Rhinovirus infection and found to be effective. Research in Bulgaria has concentrated on ringing the changes by adding some of the drugs together and finding them to be synergistic (more active) or antagonistic (less active). These drugs can be used effectively to block the passage of the virus to the brain, if given early enough. Hence the wise collaboration between the clinical and commercial laboratories which provide a rapid (PCR) (Polymerase Chain Reaction) ready to read within 5 hours. These "capsid blocking" drugs*** provide a perfect fit into the minute chamber through which the live virus must pass into the cell. The dimensions are the same for all enteroviruses yet examined. Thus, nature has, by some miracle, provided us with a ready made "natural" means of cure! At the same time, vaccines have been
produced, but not yet used against coxsackie B viruses. These can prevent a whole variety of enterovirus diseases, and, (using rapid PCR) we can anticipate which virus strains will be coming next year to prevent further infections in baby nurseries and in school children, in the future.

Jane Colby and I have studied over 6000 members of the UK school population from 1990 - 1995 and discovered that ME is by far the commonest cause of longterm sickness absence in pupils - while school teachers are also the commonest sufferers worldwide from ME.

(International survey in 2002 -2003), school children are the epicentre of
the distribution of this disease to their friends, relatives and outside
contacts. If the American multicentre placebo controlled randomised trial of PLECONARIL in neonatal disease is successful, what a chance we have to treat, stop and prevent enteroviral illness now! Please talk to your MP as soon as possible about why similar studies are not being carried out within the UK despite large amounts of money being provided!!

*** The "Capsid" is the virus coat which has to be discarded before the virus can reproduce. "Capsid Blocking Drugs" prevent this from taking place.



Wednesday, June 01, 2005

Fundraising for Dr John Gow's research into ME at University of Glasgow, UK

Last week I emailed fellow ME sufferer Von a copy of the below report from the Hindu Times about Dr Gow's research because it looked hopeful.

Von said the news of Dr Gow's research had been circulating the ME community. She said everyone is excited about the news.

Shortly afterwards, I emailed Von a copy of a news report [copied here below] about the research funding crisis Dr Gow and his team were facing. I asked Von to please let me know if there was any fundraising going on, as I'd like to donate.

Von emailed me back with the following copy. [Yesterday I posted a cheque c/o University of Glasgow Research to the address given here below]


Dr Gow has kindly sent me some more details of his research and how to donate to his trials. Please distribute as widely as possible. Regards, Lara.

Thank you for your interest in our research on CFS/ME. If you would like to send a donation to help us continue our research we would be extremely grateful. Please send a cheque directly to myself at the address below and made payable to "The University of Glasgow" and my secretary will ensure that the cheque goes into our research account. The University will, of course, send you a receipt.

I have attached a copy of the abstract which I presented both orally and in poster form in Japan in February 2005. We have submitted the data for publication in a peer-reviewed journal and hope to have the data published later this year.

The University of Glasgow patented the novel biomarkers and triple drug treatment on Feb 1st 2005 "Materials and Methods for Diagnosis and Treatment of Chronic Fatigue Syndrome" application number GB 0502042.5

We have generated a "gene signature" of patients with CFS/ME but we emphasise that we require extensive further trials, including a larger number of patients with CFS/ME and controls (healthy controls and patients with a variety of disorders), of the diagnostic test prior to the test becoming widely available.

Thank you again for your interest in our work.

Kind regards,
Dr John W Gow

Senior Lecturer in Clinical Neuroscience
University Dept. of Neurology
Southern General Hospital
1345 Govan Rd
Glasgow, G51 4TF

Tel: 44 (0)141 201 2465
Fax: 44 (0)141 201 2993

Whole-Genome (33,000 genes) Affymetrix DNA Microarray Analysis of Gene Expression in Chronic Fatigue Syndrome

Gow JW, Cannon C, Behan WMH, Herzyk P, Keir S, Riboldi-Tunnicliffe G, Behan PO & Chaudhuri A.

University of Glasgow Department of Neurology, Southern General Hospital, 1345 Govan Rd, Glasgow G51 4TF, Scotland, UK. email:

Background: Chronic fatigue syndrome (CFS) is a complex disorder characterised by persistent fatigue, musculoskeletal pain and post-exertional malaise. The mechanism of fatigue in CFS is not known and as no reliable diagnostic test is available, misdiagnosis is common and treatment regimes vary. As CFS symptoms are multi-systemic and are often preceded by infections, gene expression in peripheral blood mononuclear cells (PBMC) was examined. The study was carried out to determine if any characteristic changes in biochemical pathways could be identified. This would identify biomarkers and provide a rational basis for targeted pharmacotherapy.

Methods: Whole human genome DNA microarray analysis was performed on RNA isolated from PBMC. Affymetrix HG-U133 (A+B) DNA chips which include probe sequences for the entire human genome, 33,000 genes, were used. Eight male patients with CFS (18-54 years, mean 36 years) and seven age-matched male healthy controls (22-58 years, mean 34 years) were included in the initial microarray study. An additional twenty patients with CFS and twenty age and sex matched controls were recruited for RT-PCR and western blot assays in order to verify the microarray data for a number of putative biomarkers.

Findings: Iterative group analysis of the differentially expressed genes indicate that in CFS: (a) there is a shift of immune response with preferential antigen presentation to MHC class II receptors, downregulation of the MHC class I system with a consequential suppression of Natural Killer cells and ĄT-cell receptors, (b) increased cell membrane prostaglandin-endoperoxide synthase activity with downstream changes in oxygen transport and (c) macrophage activation with phagocytosis of apoptotic neutrophils.

Interpretation: A comprehensive map of gene expression has been generated by whole-genome DNA microarray assay for patients with CFS. Several biomarkers have been identified by the microarray assay and confirmed by RT-PCR and western blot analysis. Functional changes affected by altered gene regulation offer an explanation of the fatigue experienced by patients with CFS. Western blot/ELISA assays of key biomarker genes can be used to support the clinical diagnosis and identify candidates for treatment trials in CFS.

Abstract S7-03/P2-19 (oral and poster presentations) In: International Conference on Fatigue Science, Karuizawa, Japan, February 9-11, 2005

Dr John Gow's research into ME hit by cash crisis

Copy of a report from the Glasgow Evening Times May 25, 2005:

DR JOHN GOW is leading the ground-breaking research on the illness ME at Glasgow University

PIONEERING research by Glasgow scientists which could lead to a cure for ME is under threat from a lack of funding.

A team at Glasgow University has made a genetic discovery which could change the lives of patients with the debilitating condition.

But the ground-breaking work - which is a year from completion - will halt within weeks unless extra cash is found.

Dr John Gow, leading the research, said: "As it stands I will not be able to continue my research beyond the end of May.

"I face having to let my research assistant go by then, which means the team will be broken up and momentum with the research will be lost.

"It would be a great loss for the university and for ME patients."

His plight has been taken up by Alex Fergusson, Tory MSP for Galloway.

Mr Fergusson said: "It's entirely unacceptable that the Executive seems prepared to see this grind to a halt, when we may be just a year away from a life-changing diagnostic test and cure for ME."

Dr Gow believes ME is caused by a gene malfunction which prompts the immune system to "work overtime", making patients excessively tired.

He says a cocktail of drugs could be used to switch off the defective genes, allowing patients to lead normal lives.

The drugs have still to be tested but Dr Gow believes his research is a big step forward.

He is waiting to hear about an application for an additional grant.

Dr Neil Abbot, of ME charity Merge, said Dr Gow's work was "absolutely crucial" and called for more funding for it.

Dr Gow's funding comes from the Executive via Scottish Enterprise.

A Scottish Enterprise spokeswoman said: "This could be an exciting opportunity for Scotland and in 2003 we offered an award to Glasgow University to develop this technology further.

"The project is at an interesting stage of its development and we continue to work with Glasgow University to try to help it achieve a commercial outcome."


•ME (Myalgic Encephalopathy) is also known as Chronic Fatigue Syndrome, Post Viral Fatigue Syndrome and Yuppie Flu.

•Symptoms include extreme tiredness, muscle pain, sensitivity to noise and light, severe headaches, digestive problems and disturbed sleep patterns.

•ME is notoriously difficult to diagnose. Doctors arrive at a diagnosis by a process of elimination, which can take up to six months.

•ME can last for anything between a few months and many years.

•As no cure exists, treatment involves managing the condition by finding a balance between activity and rest.

•For years it was debated whether ME was really an illness. It finally gained full medical acceptance in 2002.

ME/CFS/CFIDS: Scientists 'unlock ME genetics'

Copy of BBC report May 28, 2005:

No test currently exists for chronic fatigue syndrome.

Scientists have identified thousands of genes which appear to play a role in chronic fatigue syndrome (CFS).

A team from Glasgow University found a particular pattern of genetic activity among 50 people with the condition.

They hope their work, which is still in its early stages, could lead to a diagnostic test and new treatments.

CFS - or myalgic encephalomyelitis (ME) - used to be dismissed as "yuppie flu" and has been widely recognised as a disease only in recent years.

Gene signature

Lead researcher Dr John Gow said: "It is another year's development before it becomes an accepted diagnostic test and, similarly, we need to do some trials with therapy before that becomes widely available. But it is exciting."

By looking at the whole genome of about 50 people with chronic fatigue syndrome, they discovered certain genes that were different to those seen in healthy people of a similar age and sex.

Dr Gow said: "We have identified genes which were up-regulated compared with genes in normal healthy individuals, suggesting we could possibly have a diagnostic test for this syndrome which doesn't exist at the moment."

But he said they needed to check that this "gene signature" was specific for chronic fatigue syndrome by looking at more people with the condition, which would take a year or so.

Colleagues at the same university are also looking at targeting treatments towards the faulty biochemical pathways caused by the overactive genes in chronic fatigue syndrome.

Future hope

These drugs are already on the market for other conditions, so if they are proved to be useful in chronic fatigue syndrome, they could be given to patients in the near future.

"Our work has given us clues as to which pathways are up- or down-regulated and we know which drugs activate different pathways, so we think we can find drug treatments that will be beneficial to patients," Dr Gow said.

"Having said that, it really needs to go through proper trials before these drugs become widely available."

A spokesman from Action for ME said: "We are very interested to know and explore more."

He said it was good that work such as this was being carried out into chronic fatigue syndrome.