Merry Christmas Everyone. Enter recovery phase.

We pretty much all know the behavioral ways to recover from or reduce the length of a crash or flare are pretty simple. Depending on how hard you've been hit they consist of things like cutting down activities (just say No!), reducing stimulation (turning off TV, music, turning lights down), getting to bed earlier, and reducing stress (meditation, visualization, stopping catastrophic thought patterns).
The question this resource asks is whether we can do better than just waiting out a crash? There are certainly no guidelines on how to do that but some ideas are out there. First check out suggestions on how to recover from a crash from Hip, a patient who has studied the disease extensively, then from a blog by a PhD, and finally from a survey taken from the ME/CFS/FM communities.
................. 

 

From PEM Busters for Physical Exertion

1. Creatine hydrochloride - 2 grams 
2. Citrulline - 1000 mg 
3. Branched-chain amino acids (BCAA) - 5 grams 
4. CoQ10 - 800 mg 
5. Sodium bicarbonate - ¼ teaspoon (1.5 grams) 
6. Catalase - 600 mg (taken after exercise) 
7. D-ribose - (5 grams three times daily) 

All the above should help reduce PEM from physical exertion. These supplements might be particularly efficacious at preventing PEM if taken an hour or so before doing some unavoidable physical exertion.

RATIONALE: PEM Busters Work in Part by Neutralizing Lactate or Reducing its Production 

PEM Busters for Mental Exertion (eg: hectic social or professional events):

• Prednisone at a dose of 20 mg or so taken 4 hours before the event. Some ME/CFS patients have vouched this works very effectively and reliably (though others report ill effects from this corticosteroid drug). See this thread. But also see the warning in this post (which cautions against using prednisone for any extended period of time, and warns that the PEM protective effects do not work for the whole day, they seem to wear off after about 6 to 8 hours).

From Mitochondrial Dysfunction, Post-Exertional Malaise and ME/CFS by Lucy Duchene -for ME/CFS/FM patients with mitochondrial dysfunction

Recovery from prostration fatigue

• Vitamin B-1 (thiamine) (100 mg twice a day)
• Vitamin B-2 (riboflavin) (100 mg) 
• Biotin (5 mg twice a day) 

Postponing build-up of lactic acidosis

• Time-release guaifenesin (600-800 mg) 82

Dr. Goldstein's "Resurrection Cocktail"

Dr. Goldstein's "Resurrection Cocktail" is a different kind of crash buster. It was an IV push that helped to get really sick patients - people who are essentially in a severe crash all the time - out of their beds. It was not a cure - just a temporary aid - but it did get them going for a time.

• Ketamine
• IV ascorbate
• IV lidocaine
• IV thyrotropin- releasing hormone (which raises all biogenic amines plus acetylcholine)
• Nimotop
• Neurontin

Find out more about his "Resurrection Cocktail" and why he chose the ingredients he did.

Further details and associated research papers for each supplement are available on Cort Johnson's Blog Forum from where I copied this extract.  Cort Johnson's research summaries and explanations are highly respected in the chronic illness community by patients, researchers, pharmaceutical and health supplement industries and doctors.... especially doctors who are also patients.

Unfortunately the only way to get the prescription and IV services described above is to go to an alternative medicine practitioner who is also a General Practitioner (Doctor) or an ME/CFS expert specialist.  Mainstream medicine provides no treatment at all and the ME/CFS specialists are difficult to find unless you are able to travel overseas and attend a specialised clinic.  A naturopath or osteopath may be able to service some of these recommendations.  Lyme disease experts usually have a background in ME/CFS and fibromyalgia as well as tick-borne diseases.  Good Luck and Happy New Year.

It's just Miss Milo and me

2 Cops Quit Over Tactics At Standing Rock North Dakota

My ADRA1A gene on Chromosome 8 is "nearly significant"

A research paper published recently by the NCNED in Queensland, Australia has found a nearly significant prevalence of the presence of a gene mutation on the ADRA1A gene. I happen to have the problem allele (GG) according to my 23andme results and so do 75% of people who have responded in ME/CFS Australia Facebook group.

Showing my raw data for SNP rs2322333:

The specific physiological implications of ADRA1A are mainly involved in smooth muscle contraction. This is required for vasoconstriction of blood vessels throughout the body including the skin, gastrointestinal system, genitourinary system, kidney and brain. It is also involved in the glycogenolysis and gluconeogenesis of adipose tissue in the liver, in addition to enabling secretions from sweat glands. These above processes have been associated with symptomatology of CFS/ME. Hence, the differential expression of ADRA1A may explain particular clinical phenotypes of CFS/ME.

It is associated with processes that result in the release of Ca2+into the cytoplasm and contributes to a slow after depolarizing current (sADP) in neurons which means they are talking about electrical signals in the nervous system.  It is also associated with a decrease in gene expression of various mRNAs . The minor allele (AA) may also have a key role in ligand selectivity but I do not know what that is and I have not got the minor allele anyway.

Johnston, S., Staines, D., Klein, A., & Marshall-Gradisnik, S. (2016). A targeted genome association study examining transient receptor potential ion channels, acetylcholine receptors, and adrenergic receptors in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis. BMC Medical Genetics, 17, 79. http://doi.org/10.1186/s12881-016-0342-y

This bothers me. What will happen December 5th?

Water Protectors try to Clear 1806 Bridge met with Water Cannons, Tear Gas, Concussion Grenades & Rubber Bullets from Unicorn Riot on Vimeo.

Hey Jannette, where have you been?

A simple recipe for Lyme by Jannette Dann

Basic ingredients

An Aussie tick with Lyme
Insufficient medical care
Co infection of the ticks choice
A Goverment in denial

Please note all ingredients can easily be found in Australia just see your local area for more details .


Method

1. Firstly get bitten by a tick ( can be substituted with other lyme carrying animals) be careful with this one as often you won't feel it , but it is the base upon all other ingredients rely.

2. Seek insufficient medical care , this step is easy as it is widely available within Australia and doctors are very good at helping you complete this step of this recipe for disaster .

3 Chuck in some roughly conceived misdiagnosis

4. Now mistreat .... Be liberal with this as is recommended by our government

5. Now to add your own special ingredient to make this your signature dish , choose your co infections and this will determine the outcome of you toxic soup of Lyme.

6. Now that your immune system is mush , let simmer for decades all of the above in your now compromised immune system. Then keep adding slowly more misdiagnoses and incorrect treatments to ensure you get the full benefits they have to offer.

7 . Garnish with your yearly income and the grated fragments of your life

Evidence of Lyme Disease in Australia was discovered in 1992 but "they" still debate it?

#UNCOVERED - Lyme disease found in Australia 25 years ago! The LDAA are fortunate to have been provided with this video and further supporting evidence of 1992 research.
-

"We knew we had a break through as recently as about a week ago [1992] when we discovered that the microbe that we have been characterising is actually structurally very similar if not identical to the 'classical Lyme' disease [Borrelia burgdorferi] causing agent".
-

In 1992 ABC's The 7.30 Report aired a story highlighting how scientist Michelle Wills with little funding and tentative support discovered Borrelia sp. in Australian ticks.
-

The Department of Health’s specialist medical adviser, Dr Gary Lum,has continually argued that there is NO EVIDENCE of 'classical Lyme' ever being found in Australia. As a result nothing has been done to help the thousands of Australians that have become sick after tick bites.
-

Michelle's discovery of Borrelia was confirmed by US Professor of Microbiology & Molecular Genetics, Alan Barbour who had worked with Wihelm Burgdorfer who discovered Lyme disease.
-

So... WHY wasn't this research from the 90's ever followed up? More on that story later.
-

Click on the picture link below to watch this ground breaking report. It will blow you away how in 1992 locally acquired Lyme was known, yet ignored.

https://www.facebook.com/LymeDiseaseAustralia/posts/1370426006331225

Once every 6 to 8 years they come en masse

I'm sorry I did not get a video a few days before this day when there were heaps more. The Caper White's were everywhere because they mingle their genes once in a while coming from the other side of the Divide.

Let the Geisha Girl Flower and the butterflies will come

Lymphoma drug Rituximab for MEcfs

Dr. Øystein Fluge is Chief Physician in the Department of Oncology at Haukeland University Hospital, University of Bergen, Norway.  He received his medical degree in 1988 from the University of Bergen and has specialized in oncology since 2004.  He has conducted research at the Surgical Institute and Department of Molecular Biology, University of Bergen and has been funded as a Research Fellow by the Norwegian Cancer Society.

In 2004, Dr. Fluge and his colleague, Dr. Olav Mella, a neurologist at the same institution, noticed that a patient’s ME/CFS symptoms improved substantially while undergoing chemotherapy treatment for a concurrent diagnosis of lymphoma.  This was followed by a pilot study in 2009 with positive results. In 2011, Dr. Fluge, Dr. Mella, and their colleagues published a randomized double-blind placebo-controlled trial of rituximab in 30 ME/CFS patients demonstrating that  two-thirds of the intervention group experienced moderate to major improvements in their ME/CFS symptoms. For a medical condition with no disease-modifying treatments, this was a ground-breaking study. Currently, they are in the midst of attempting to replicate their results in a larger Phase III multi-center study in Norway.

The above was Dr Fluge's bio from the recent IACFS/ME Conference outline.

I was just wondering if you've got any of Dad's cancer/immune suppression/B cell depletion drugs still lying around?  I guess you think I'm joking.  Which drug ending in mab did he use?  It's just that by the time they figure out how to cure this thing and release the drug to the impoverished masses via Medicare, I could be dead.

Went to Coles for the first time in ages today.  I've been ordering groceries online since I couldn't walk straight, was dizzy and my heart was pounding after moving my body, even lifting an arm.  I did use the new wheelie walker at home but at the Golden Beach shops/doctors I only used a walking stick or just went ultra slow.  I only went out when I had no choice. I've had problems with breathing too as you know.  The first three things have just vanished more or less overnight when I started taking Jarrow Formula's sublingual Methyl B-12 which is not the same thing as what you can buy at the chemist because of the type of B12.  I have been taking it for 2 weeks I suppose and I am sure my brain is working a bit better too and I'm not falling asleep all the time. I do not know how much that 2 weeks has altered my serum B12.  I guess it may not show up as "Low" on the blood test I requested on Thursday but I am heading to another new doctor next week to find out.

I have read that people are getting neurological (including dementia) symptoms from low B12 even before it reaches the cut-off point for too low that the pathology labs set as standard.  I wish they would do something about that because the doctors set their standard by the pathology labs.  My doctor recently ran some blood tests but they were the same old ones and even if anything was slightly raised I would not be told.  I just got the standard reply "no action necessary".  It was hard enough to get an actual figure for my blood glucose 3 month average which was a well-controlled 6.2, one point up from last time.  What I mean to say is that if low B12 is going to be the explanation for my decline this year, then it will not be forthcoming from my regular doctor.  I'm doing this myself.  It also ties in with my MTHFR gene mutations.

My boys have moved on

S moved into a share house today and left the granny flat bottom floor rental where he has had more stability than ever before.  He was living alone and he was keen to take Milo when I go to Melbourne.  It is back to a share house situation with 3 people so this is a different kettle of fish for both Milo and my son but he has been feeling the urge to get in amongst it rather than be holed up watching TV from the bed because the place was too small for lounge furniture.  He did not even have an oven so he has actually ruined my Christmas present for him which he no longer needs.  I'm keeping it now,  but I am not telling you what it is.  He badly wants towels and socks which is not what he said another time when even he thought it was time for a "decent" Christmas present this year.  However we are all broke and in debt so it will not be much of a towel he'll be getting.

S says that one of the renters at the new place in North Lakes is a bikie and an unrelated statement to me indicated that he already knows that this move will only be temporary however the lease is for 6 months.  The aim of the move is to be closer to Connor especially now that his mother has drug problems that are becoming impossible to hide.  In fact poor old Connor does not know where his Mum is.  She was with him at his other Nana's place for a short while but not any more.  I have no idea if she has let her place in Noosaville go.

I just thought that I would post some photos of where he lived for most of this year and last. Where he first made Mulberry jam and ate BBQ food almost daily.  Solar sales and associated travel to towns between Tasmania and Northern Territory seemed to make it interesting from my viewpoint but even that has dwindled out to be replaced with the sale of education packages that promote recognition of prior learning for a man called (I always forget this strange name).



My other boy with his adopted family, a cute kitten, and his own son moved out of "The Domain" gated community and into the rental shown here earlier this year.  Later there was another addition to the household...  Kerry's problem dog which until this time had remained in the country.  This is the kind of dog that is going to bail you up.  But it was a neighbour's dog that killed the kitten and they kept that knowledge from Cohen who still is not doing a full day at school, just a half a day.





As usual, I will have to finish this some other time.

CFS is still a mystery

Chronic Fatigue syndrome better known as Myalgic Encephalomyelitis, is now thought to be a metabolic dysfunction with the result that not enough energy is being produced.  There is mounting evidence to suggest that the blood metabolites of CFS patients are very different from the products of metabolism in healthy controls (Naviaux et Al, Davis; Fluge and Mella.....)
In humans, energy comes from the complete oxidation of glucose to carbon dioxide and water. The digestive system does the first part, it produces glucose, glycerol and fatty acids, and amino acids (Myhill et al)


Impaired digestion is going to result in impaired energy production at a very base level (eg iron-deficient anaemia) and these problems are usually ruled out by running a few blood tests.  At the next step in energy
production is when the glucose and lipids are fed into the blood stream where, together with oxygen bound to haemoglobin in erythrocytes (red blood cells), they are transported to every cell in the body (MYHILL et al).  Those with CFS are
tested to determine if the lungs and circulatory system are functioning correctly and if so then it can be assumed that the energy deficit is coming from problems with cellular respiration and ATP production.  Without ATP, there is no energy!!!
With a little ATP formation there is a little energy and with the required level of ATP production there is more than enough energy to cover the functions of everyday living.  The problems in people with CFS are caused by not having enough ATP to produce the
energy required for maintaining a healthy body at the cellular level and in terms of the energy requirements of movement.  Unfortunately for patients, it seems as if the energy required to move is the first kind of problem they notice or at least the desire for a lot more sleep
(why can't I keep up with my peers and pull all-nighters?).  Others notice too and the word "lazy" can be the first accusation that motivates patients to seek help (if they are old enough).  The accusers cannot see the extra effort that is required to hear through all the background
noise that they can effortlessly block out for instance.  Without enough energy, everything becomes harder than it was.  Similarly without enough sleep. 

For people with CFS, the energy deficit is coming from within single cells even though they are being supplied with adequate oxygen and nutrients because their digestive system and circulatory systems are working with no sign of malfunction. 
The cellular performance is mostly invisible to others so the words "invisible disease" are used to describe the condition and for some unknown reason, testing for mitochondrial function is rarely considered unless your doctor happens to specialise in CFS.  The
 functioning or dysfunctioning of the energy producers called mitochondria seems like an obvious place to start for someone who is complaining about life-altering fatigue unless they have a known existing condition which would explain it.
Scientists have known about the structure within cells that handles ATP production for a long time and they called
the ATP energy producers "mitochondria".  Another way of looking at it is by thinking about your metabolism.  Someone with a fast metabolism makes lots of ATP energy and quickly enough to keep the supply going.  A slow metabolism is usually what is blamed
for people putting on weight and some people have the privilege of watching their own metabolic rate change over the years.  Mitochondria and metabolism go hand-in-hand; so that when you see a CFS study talking about patients having a hypometabolic disorder
 or having a slow (hypo means slow) metabolism, you will know why.  But even that seems to give the wrong idea because the kind of 'slow' the recent studies are talking about is designed for creatures who are going into a low-powered state "on purpose" as a matter of survival.
As a result of detecting a threat, which is quite often a lack of food supply triggering something like calorie restriction (not getting enough carbs usually).  This means that the CFS patients body is going into an altered state as a matter of survival,
after detecting a threat to life itself as in the state of dauer.  Your body is doing what it can to help when you have CFS and you had best follow its lead for now until further research uncovers what the threat to survival is.  Some are saying that the persistent threat is biotoxins and until
the threat is eliminated (aka cleaning up the environment or leaving the environment), the body will continue to protect itself in this strange way (Erikson & .  ............)  This means that the initial virus or trauma that appeared to trigger the CFS is totally incidental to the continuing
symptoms.  An infection for example, may well have been the event that triggered the need for more ATP which the body could not supply but it was an overloaded body system in the first place as a result of something even more sinister, like mould.  Black mould that is not
visible because it is on the inside of the wall or inside a pipe.

The other main theory seems to involve chronic, stealth or reactivating viruses and bacteria like EBV, mycoplasmas, Borreliosis to name a few and perhaps we can throw in the bugs we call probiotics because microbiome changes (Ref in Evernote I hope) are also noted in people with
CFs as compared to healthy controls and some have even suggested that feeding ourselves live bacteria is risk-taking behaviour when it is taking place in people who have dysfunctional immune systems (reference, I forgot). Others are explaining psychological
and neurological symptoms
 by the fact that evidence of many of these invaders including worms are being found in the brain and central nervous system. Similarly the heart and sexual organs.  These microinvaders are hiding in biofilm and plaques and they have been photographed under the microscope,
especially the spirochaetes (cork-screw-shaped bacteria)

References:
J Clin Exp Med. 2009; 2(1): 1–16.
Published online 2009 Jan 15.
PMCID: PMC2680051
Chronic fatigue syndrome and mitochondrial dysfunction
Sarah Myhill, Norman E. Booth, and John McLaren-Howard.

Not finished

Formation of biofilm Video

Ernie continues: Our research funded studies at New Haven University have destroyed the spirochetes and biofilm (cysts) of Lyme disease with cannabidiol at 10 mmol /cc concentrations. (corrected)

Positive subjective anecdotal improvement statements by many patients who had failed with prolonged antibiotics indicate the possible potential use for chronic Lyme disease sufferers.

Dr. Ernie Murakami M.D. Clinical Associate Professor Emeritus, UBC.
B.A. Bacteriology and Immunology ,UBC.

Dr Eva Sapi in 2010




The findings to date seem to me to indicate that Lyme Borreliosis is our modern-day syphilis in that both spirochetes will eventually progress to dementia or insanity of some other form if other organs continue to function.  A few researchers are trying desperately to prove that Alzheimer's is actually a biofilm infection.  I believe that the currently available antibiotics are unable to eliminate many infections completely because the bacteria change form in order to survive in spite of the threat as Dr. Eva above states. Our current antibiotics focus on killing the spirochaetal form which obviously reduces their number in the body and reduces the toxin load on the body however the surviving infection is no longer in spirochaetal form, if it ever was, immediately after antibiotic treatment, it is surviving in a form that enables the body to function better until the antibiotic threat has passed.  I was treated for a couple of other forms by way of alternate antibiotics and antimicrobial herbs taken in conjunction with the forms that were killing the form that originally invaded the body but I suspect that if there are also multiple pleomorphic forms known about already then we have not yet even discovered the antibiotic that will cure a late stage borrelial infection especially if you include other opportunistic bacteria within the umbrella of LYME disease (which they are not).  I mean that the world is desperate for a new kind of antibiotic because what we have got ain't workin' (so why bother trying again?) as a cure.  If anything, they are driving the infection underground (or in the joints or in tooth sockets) and swap their destructive behaviour for a state which is more self-preserving.  Kind of like the metabolic state our human body will go into when its survival is threatened  as seen in those with ME/CFS according to Fluge and Mella.  [The parallels are strikingly obvious when your Targin first kicks in but that's a joke...on me].  I am trying to say that morphed borrelia are less of a threat to human functioning than active feeders and breeders I think, so a year or so of better health is celebrated until the threat of antibiotics has passed which allows the destructive form to re-emerge Mum.  I'm sorry.  The other theory of my relapse is progressive vitamin B12 deficiency....but that's only my theory.  No doctor to date will even let me experiment.  It is just a vitamin for God's sake!!! And I have documented evidence of problems with it in the past.  I just managed to think up my next post didn't I?

A few good people out there doing "useful" research

Dr Patrick McGeer

Ernie Murakami said "Dr Pat McGeer is a class mate from Medical School, a director of Murakami Center for Lyme and is Head of Neurological Research at UBC. He and associates have done research on Alzheimer patients and on post mortem found live spirochetes on biopsy specimens from brain tissue.The Borrelia burgdorferi organism was reproduced in BSK fluid media and found to actively invade rat and human cells.  (Journal of Neuroinflammation, Sept 2008). He is world renown in his research and still continues his work in Neurological diseases. His work supports the theory that Chronic Lyme Disease is an infection and not a syndrome. "

Wiki says 

In August 2012, McGeer and his wife Edith founded Aurin Biotech Inc., following indications that the Aurintricarboxylic acid (ATA) complex inhibit activation of the Complement system. Since activation of the complement system is implicated in a number of diseases (see Complement system#Role in Disease), these indications suggested that ATA could be an effective treatment for these diseases. Aurin ^[2] was founded to explore the efficacy of using ATA and related compounds in the treatment of these diseases. The particular focus is on diseases that are caused or exacerbated by aberrant complement activation. Low molecular weight components of the aurintricarboxylic acid complex have been shown to be non-toxic and orally effective.

Pat McGeer is working with Ernie now or as well but what's this I see?  The Gold Coast Neuroimmune research investigating me/cfs has found calcium 2++ ion transport problems in those with me/cfs and it seems it can be cured by this ATA so they have the treatment already even though it is being used for something else at present?  Nothing would surprise me but the research has to be done first and I know nothing about the Complement system nor how it relates to Ca 2++ enzyme problems until I click on those links.  Not doing that now.   I reinstalled windows 10 as a clean install with this tool from microsoft that is actually working

Ernie Murakami is thought of by me as the cannabis man.   There is a lot more to him than that.   I have no idea if CBD oil has got anything to do with the complement system or calcium transport from an electrical point of view.  They may not be related at all, but Ernie seems to have had to deal with a lot of controversy  because of his interests in medical marijuana and now he is retired and offers his services to patients around the world while investigating cannibidiol or CBD.  He is a rare breed of doctor and he really should be at the top of this page because he is nice to everyone!!! He answers questions on his Facebook page and posts information knowing that it is the patients who are hungry for it even though our Governments are lagging in even making the product legal.  The essential oil cannot yet be patented as it is because it is a herb so they make it illegal unless you buy their version which is usually not a whole product but one that has been scientifically manipulated, divided in half at least.  The THC is usually removed by pharmaceutical companies trying to package it for a start.  Who knows what happens and will happen to it over the years but most people who have had no success with conventional medicine tend to go back to natural medicines particularly food and herbs.  I don't think that will ever change.  They could make a futuristic movie about people breaking out of controlled environment cities to pursue medicines in what had survived in the wild that will counter the sick city syndrome with live food.  Maybe nature always comes back if left to itself.  Is that an opiate meandering thought?  Take no notice of it.

Dr. Ernie Murakami M.D. Clinical Associate Professor Emeritus UBC

About Dr. Murakami

Dr. Ernie Murakami became involved in Lyme Disease while in his practice based in the rural community of Hope, British Columbia. 
Through his practice, he developed two new methods of tick removal, one which was the Blister Method; the injection of a pre-measured mixture of Xylocaine and Adrenaline directly beneath the jaw of the tick. This method is used today, primarily in Medical offices and by Emergency physicians. The second method was the Drinking Straw and Single Knot Method, in which the attached tick is placed inside the straw, with the straw held at a 45 degree angle. A suture string is placed under the straw, directly in contact with the mouth of the wood tick. A single knot is applied. Constant alternating releasing pressure is applied upwards away from the skin and the tick releases itself intact, from the host. This technique was accepted by the Compensation Board and the Justice Institute for the training of ambulance and first-aid personnel and is in full use today. 

These techniques were at the time, being taught by Dr. Murakami to other Physicians at International Conferences. During the times spent at these clinics, he became familiar with the treatment of Lyme, both long term and short term, as well as the split theories surrounding the treatment of Lyme. One fraction believed that only 3 weeks of treatment was adequate at any level, despite the fact that this had been disproven, while the other half believed that long term treatment was required to eradicate the Cystic form of the disease, based on biological fact. 

Dr. Murakami became intrigued with the disease as to the epidemiology with his first case of confirmed Lyme Disease in Agassiz, BC at the Federal Penitentiary. This patient showed the typical bulls-eye rash that developed soon after being infected. A second case intrigued him further when another patient from Hope, BC was confirmed to have a typical rash and a positive Eliza serology. Both these patients responded to three weeks of antibiotic treatment.

Subsequent to these cases, Dr. Murakami began receiving referrals from other physicians due to his keen interest in Lyme and his approach to medicinal treatments, both in the removal of the ticks and his successful treatments of the disease. He soon found himself to be a rare physician; willing to acknowledge, diagnose and treat the symptoms of Lyme disease in British Columbia. This was a stand very few other doctors were willing to make. 

Since that time, Dr. Murakami has offered his personal experiences as a physician treating Lyme patients to others in the medical field by speaking at seminars and conferences. His lectures are met with both interest and disbelief and the center of much controversy. News articles soon began to surface as patient after patient would give testimony to Dr. Murakami's somewhat "miraculous" assistance in treating some long-suffering patients of Lyme's, where a history of mis-diagnosis and denial existed prior. Reports began surfacing about the lack of knowledge that exists among the medical communities, both here in Canada as well as the US. 

Today, Dr. Murakami is retired from his regular practice. His keen interest and his willingness to explore a very controversial topic has surrounded him with much media attention and discord among the medical community. He remains true to his Hippocratic Oath however, and offers this site as a base of information to both patients, possible sufferers and doctors alike.

Contacting Dr. Murakami

Dr. Murakami can be spoken to regarding possible Lyme infection by following this procedure only.

Download and print out the Health Questionnaire.
Complete it as best you can
Fax the completed questionnaire to the toll-free number at               1-866-259-2320     
He will then go through the questionnaire and contact you to discuss with you over the phone. All inquiries are handled on a priority sequence basis.
Dr. Murakami does not charge for his opinions. You may, however, make a donation towards the Society.

Thank you for your cooperation in making this procedure as seamless and responsive as possible. We are working diligently to try to streamline his work load so he can be of service to more patients.

Reproduced from Dr. E. Murakami Centre for Lyme
Research, Education & Assistance Society

Getting back to the National Centre for Neuroimmunology and Emerging Diseases (NCNED), Gold Coast campus of Griffith University, they have just this week released a summary of their published research and they seem to be going ahead in leaps and bounds.  I have some recollection that they are tied with Simaron Research and not everyone trusts that latter's motives these days.  Actually I am not sure who they are tied up with but they are receiving Australian backing too. 

October 18, 2016

NCNED is pleased to release the following update of world first discoveries this year in CFS/ME:

• NCNED discovered significant associations of transient receptor potential (TRP) ion channel families from CFS/ME patients.
• NCNED discovered significant reductions in TRPM3 receptors on the cell surface of natural killer (NK) cells and B cells from CFS/ME patients.
• NCNED discovered significant reductions in intracellular calcium as well as stored calcium in NK cells from CFS/ME patients. 
• NCNED discovered significant changes in intracellular calcium-regulated genes from NK cells as well as cell signalling changes that are important for NK cell function and cytokine production in CFS/ME patients.
• NCNED aimed to determine if all these changes in NK cells were due to dysfunction of the TRPM3 receptors located on the cell surface of these cells. 
• NCNED now reports that the significant reduction in NK activity as well as changes in intracellular signalling is associated with low intracellular calcium ions in NK cells through the impairment of TRPM3 ion channels. 
• NCNED highlights these significant findings as the inability to allow sufficient calcium ions to move inside the cell with dysfunctional TRPM3 receptors.
• Importantly the significant dysregulation of TRPM3 receptors NCNED has identified is not confined to NK cells. TRPM3 receptors are located on nearly all cells in the body.  The dysfunction of TRPM3 NCNED has identified suggests this receptor is involved in CFS/ME pathology. 

 We thank every participant, donors, the Stafford Fox Medical Research Foundation, Mr Douglas Stutt, the Alison Hunter Memorial Foundation, the Queensland Government, the Mason Foundation and Change for ME.Without your support these pivotal studies would not have been possible. 

We are continuing to explore every possible pathway for successful therapeutic interventions.  As our research continues we would also like to announce our latest published paper below. 

• Nguyen T, Johnston S, Clarke L, Smith P, Staines D, Marshall-Gradisnik S: Calcium mobilisation in natural killer cells from Chronic fatigue syndrome/Myalgic encephalomyelitis patients is associated with transient receptor potential melastatin 3 ion channels. Clin Exp Immunol 2016.

I've got more to include so check back here. 

Kelly has my genome sequence

Kelly Gaunt, along with her research partner Kristina Gemayel are the real people behind what has come to be called the Nancy Klimas ME/CFS Gene Study which is a huge exercise in data collection enabling people to contribute their own genetic information on a voluntary basis. Genomics is a popular place to be in medicine so that getting people on board if any interesting patterns emerge, should not be problem for further detailed research.  With metabolomics, genomics and microbiomics at the forefront of modern-day research, at least these kinds of studies are attracting attention.  We need attention!!  Crowd-sourcing for genetic data is a brand new concept too and there were only a few little teething problems with this "RedCap" Platform that the girls set up so they deserve congratulations I do not know how much the girls will be involved with data analysis if at all but like the data collection much will be automated. Let's hear from Kelly.

Kelly describes her role in the project as follows: 

What is your background? 

I am currently a third year medical student at Nova Southeastern University that was awarded a research fellowship. Prior to medical school, I worked at the Institute for Neuro Immune Medicine as a Research Associate, where I primarily worked on the CDC Multi-Site Clinical Assessment for Chronic Fatigue Syndrome Study. For undergraduate studies, I attended the University of Florida and graduated cum laude with a Bachelors of Fine Arts.

How did you get interested in this project?  

Even though I no longer worked at the INIM while in medical school, I still maintained contact with Dr. Klimas and her incredible staff. Last year when she and I were talking about possible summer projects, this project came about. From the beginning it seemed like such an exciting project. The idea of creating the first ever unique ME/CFS genetic database that is linked to online symptom questionnaires, will open up countless doors for future research discovery revolving around ME/CFS. Therefore, throughout the summer and over the course of the school year, myself and my research partner Kristina Gemayel, created the study IRB and generated the online RedCap platform where participants are able to upload their genetic information. Then, with the incredible support and man power from Nova Southeastern University Institute for Neuro Immune Medicine the project was able to launch.

What will you be doing for the next year with this project?

As a Research Fellow, I am able to fully dedicate this year to further development of this study. Our goal is to have over 10,000 participants, so one of my main priorities is global recruitment through the use of social media. Our thoughts are since ME/CFS affects people worldwide, we want to reach out and recruit the world! I am reaching out to any website or support group that is willing to listen. The beauty of this project is that every step of this project can be performed by the participant, on their computer in the comfort of their home and geographic location or physical ability is not a limitation.In addition to recruitment, I will be conducting preliminary pilot studies with the data we collect along the way to see if we are able to establish any early noteworthy trends.

How could this project help improve our understanding of ME/CFS? 

The intention of this database is to allow investigators the possibility of nearly limitless research opportunities, such as identifying biomarkers used for establishing diagnoses or correlations between symptom clusters and specific genetic SNPs. Due to the constellation of symptoms that exists among the ME/CFS community, establishing a more definitive diagnosis tool for physicians, will help alleviate the stress and time currently involved. As well as, hopefully lead to sub-grouping symptom categories for effective treatments. Read More

Kelly told #MEAction that they intended to subgroup the patient population by symptom commonalities and investigate any correlating gene mutations. They also hope to discover biomarkers to help assist in diagnosing ME.

My data was provided to them in the form of a zip file that 23andme provided.  23andme charged me for the service and I gave a copy of the results to Kelly and Kristina under the oversight of Nancy Klimas.  The initial contact for me was with a Facebook group that was formed well before data collection began.  The group itself is virtually inactive now because most people have uploaded their files and filled in their online questionnaire after an initial screening to identify suitable patients.

I have not yet received any further requests for information about my illness nor have I received any updates on the progress of the study as a participant.  I did not expect to be kept informed except by way of more general updates from the ME/CFS community itself (the grapevine) and the subsequent publishing of research papers when the study completes.  However, this study is still recruiting for participants until they find 10,000 volunteers so it may be a long wait for results.  They are also now looking for healthy (non ME/CFS) controls and my sister comes to mind.  Hint, hint.  Let me recruit you to 23andme if you do Zena under their referral plan.

Kristine Gemayel, like Kelly was awarded the position at the Institute for Neuro-Immune Medicine at Nova Southeastern University as a winner of the Blue Ribbon Foundations' student fellowship awards which places them in leading ME/CFS research facilities as assistants.  You may remember the Blue Ribbon Foundation as the not-for-profit group that funded the documentary "Forgotten Plague"

When Cort Johnson (of Health Rising) was discussing this study he made a comment about his results with reference to neanderthal genetic material.  It was the first thing that hit me in the face too when I got my 23andme results.  The report you receive includes the percentile rank of neanderthal DNA that you have compared to all other 23andme users.  His was 99 and mine was 85 because apparently 2.9% of my DNA being Neanderthal is a pretty high amount. Comments from others with high percentages of Neanderthal DNA trivially appeared to suggest that there was a high prevalence in the ME/CFS population and so my mind raced ahead.  And if being able to go into a state of dauer is a protection mechanism then perhaps we are calling on ancient genes to do so especially if you like to see ME/CFS as providing some sort of evolutionary advantage for the future as some of us would like to think. The mutations that enabled the generations to survive what comes....that sort of thing.  Probably wishful thinking. Survival isn't everything though and Neanderthal DNA is really only a "smidgen" of our total DNA variants according to 23andme information. 

If you would like to be involved in the MECFS gene study then please email here.  Just be warned that the girls may have already finished their part in the project.

There are many more people involved in other aspects of it.  Nancy Klimas is front and central and one to the right.  It is a big team.

Renovations that I am already appreciating

I am finally safe in the shower.  The other tiles were quite scary for me so I CAN put up with the grey quite easily.  Wednesday stuff.

Don't use the front door, lock it.

next door got a lump of concrete in the ground for her rail

They are extending the front as well as the side part where the rail will go

I don't need that, my knees work again remember, after 2 years without. It's my elbows this year and they are so bad.

Do not use till Friday

 Thursday stuff

Milo has not stopped being on red alert since then.  Wondering if I should drug her tomorrow., she is so jumpy now.

The guy that drove his car on Flora's side

The guy that told Flora to mind her own business

Sexy men can sit cross-legged - to my liking anyway, 3 of them

They made themselves at home

Use the front door but not the back door OK? See my new step which is not wide enough to set the walker on?

Flora's cemented in rail at her front door.  She has not stopped complaining.

I had to move my car, at first he parked on Flora's side again.

Friday stuff

wet concrete

Monday Turf

Before the soil is built up to concrete level

It is more uneven to walk on  under that nice-looking surface than before.
I should fill a few depressions before it takes root.

The big depression got filled up, no more bird bath

The water meter access pit is now level with the turf bit surrounding it

How is that soil down the side NOT going to get washed away in what could be a garden?
And how is Milo going to keep her paws clean?

Quite a few depressions still under that lot too that I should attend to but can't.
If that is mould on the concrete, shouldn't I be removing that too?

I guess the asbestos fence will be the next major intrusion

The outdoor rails didn't get fitted until a couple of weeks later so I hope you realise that these photos were added post post-date.

Do you still love me?

He is busy he says.

Yes mum lol

u sure? ISn't not wanting to chat, a sign that u don't really care?

I miss you so much and the way things used to be between us was sorta better than this. Cohen does not know me. I don't think you realise how much all this withdrawal into your own happy world is actually hurting me. OK, I've said it. Let me back in to your life pretty please. Where do you work?