This bothers me. What will happen December 5th?

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