Psychiatrists put their label on poorly understood & under-researched Biomedical Diseases

It seems that Psychiatrists have come up with a new ingenious way to divert more patients away from receiving proper biomedical treatment. In the new ICD11-PHC proposed publication, there are several new entries to include 'Health Preoccupation' and 'Bodily Distress Syndrome' to name but a few.

'Health Preoccupation' essentially enables a psychiatrist to decide at their discretion in the absence of biomedical tests or even a shred of evidence to say that a person is concerned beyond that of 'normality' about their 'percieved ill health'. Firstly one has to question how any psychiatrist can determine this seeing as many so called 'Somatoform Disorders' would actually apply to poorly researched and understood biomedical illnesses. Diagnosing individuals who have a physically debilitating disease with Health Preoccupation will restrict their access to appropriate health care and any medications that help provide symptom relief.

In the case of Myalgic Encepalomyelitis (M.E.) there are now hundreds to thousands of biomedical papers evidencing highly significant biomedical abnormalities. The fact that these abnormalities cannot yet be routinely evaluated using a clinically available blood test, as none are yet widely available. By employment of this classification this enables psychiatrists to subdue and abuse severely ill patients and keep neuroimmune patients within the realm of mental illness. I find it most interesting to note how frequently the DSM (Diagnostic and Statistical Manual of Mental Disorders) is revised and updated by psychiatrists. New diagnostic criterion does rarely require any objective evidence and psychiatry seems to have a general lack lustre approach to searching for objective biomedical diagnostics to support the presence of their invented disorders.

One wonders how long it will be before conflict between psychiatrists and neurologists will arise. With psychiatric acquisition of many biomedical diseases and the inferior and often deleterious treatment that arises from this. After all it seems that psychiatry has the greatest reach of any medical specialism - they want to be involved with the treatment of ever more diseases as they begin to classify previously biomedical diseases as having significant psychiatric components. Again evidence is almost entirely lacking for their unsubstantiated claims.

It seems that diagnosis of somatoform disorders are not of any use to patient nor doctor. Of course psychiatrists seem to have a chronic propensity to prescribe antidepressants at the drop of a hat, based on the premise that his will perhaps improve the 'mind body connection'. The medical community should go back in time to simply admitting that perhaps they just do not yet know the cause of a disease and further biomedical research is warranted. If they cannot find biomedical evidence of a patent's distress such as is the case with the NHS in M.E. you are not informed by your doctor that they simply do not understand the mechanisms behind the illness - but rather you are told that if you engage in Graded Exercise Therapy and Cognitive Behavioural Therapy and maintain a positive 'happy go lucky' mindset the prognosis for recovery is very good. This statement could not be further from the truth and so I have found out 5 and a half years on. In depth examination of the PACE trial reveals many flaws most noticeably modification of the primary endpoint definition of moderate improvement, seeing as improvement in levels of 'fatigue' where hardly significant when defined under the initial primary endpoint. 

I remember back to the time that I went up to St. Bartholomews NHS hospital for a consultation with the Wessley school's 'Immunology' man, Dr Murphy who puts on a great front by orchestrating the illusion that they are in fact interested in your blood work for any signs of a real illness. One would think that having the NHS pay for patients to see a consultant who is in fact not the slightest interested in his speciality within this group of patients would be a waste of NHS and therefore taxpayer money. Also evidently there is in reality no need to have psychiatrists run a most inefficacious non-evidence based GET and CBT service across the United Kingdom but rather it should be maintained by clinical psychologists. Useful symptom medications are not prescribed by any of these psychiatrists - after all the primary difference between the two groups is the ability to prescribe by the latter and not by the former. General Practitioners are licensed to prescribe many symptom medications for sleep and pain etc.

At Wessley's nest they also ask you 'Do you think that your illness is a real physical one?'. I decided to contact Dr. Murphy showing him my mitochondrial assay results. My generalised mitochondrial energy score was 0.17 with a healthy individual scoring from 1.0 to 2.0 This essentially means that I was operating anywhere from 17% to 8.5% of the function of a healthy person. These tests have now been further validated proving correlation of scores to that of physical functioning. See: http://www.ijcem.com/files/IJCEM1204005.pdf Unfortunately I did not receive any reply from Dr. Murphy to my letter.

Hemispherx Biopharma the company behind Ampligen are looking to create a test to assess cell free DNA, an indicator of tissue damage. This is essentially what Dr. Myhill and Dr. John-Mclaren Howard have pioneered in the field of ME. It is thought that levels of cell free DNA will correlate with physical incapacity in this disease. Other innovative work includes efforts to examine any correlations between NK cell function (perforin) and disease presence or state. My dream is that these tests will one day be used in conjunction to diagnose ME. I'm sure Simon Wessley is eagerly awaiting these developments. Unsubstantiated claims that this disease is a mental disorder will finally be put to rest and ME will join the ranks of epilepsy, Alzheimer's and Parkinson's disease in the realm of neuro-immunology.

The current state of affairs with ME would be significantly different if psychiatrists had rigorously investigated the use of potentially effective medical treatments other than simply antidepressants, CBT and GET. But the reality is they have not. Consequently patients have suffered enormously. Evidently if psychiatrists genuinely wanted to help people and take charge of developing therapeutics in this field they would have drafted in researchers from other specialities and would have instigated in depth research looking into the possibility of ME being an autoimmune disease - a concept new to ME which is now being fortified by the ongoing research with the B cell depleting agent, Rituximab.

I'm sure Simon Wessley has lightened the load on NHS finances, manipulating the perception of a disease that is in actuality so severe, so vastly underfunded and has such a great multiplicity of symptoms. It is only to the advantage of government with patients being too physically weak to come out in numbers to demonstrate against this disgusting affair. It is only when one in power gets ill with ME that they will soon realise what a terrible travesty this all is.

Trying to Remedy Unrefreshing Sleep in ME

This is just a quick post I will follow up with further links to studies when I have the time.

Things that can help some people with the paralyzing feeling left over from unrefreshing sleep. I have found that Pregabalin 300mg can increased Slow Wave Sleep Stages 3&4.

Also 5HT2a antagonists such as Risperidone inhibit only 5HT2a receptors at low doses (i.e. 0.5mg) a higher dose will cause side effects and not as selectively target the 5HT2a receptor and thus inhibit other receptors such as D2 etc.

I have found that Pregabalin 300mg combined with Risperidone 0.5 give the best results for reducing that dreadful feeling where you wake up feeling like you've had a seizure - like your head's been kicked around like a football (aka unrefreshing sleep). Take these an hour before you go to bed - you may need to use them in conjunction with a sedative med like low dose doxepin 6-10mg that does not interfere with deep sleep. I use this to get me to sleep. I would not use any benzodiazepines in conjunction with these deep sleep meds because benzos will reduces Stages 3&4 sleep. Zopiclone, zolpidem etc are okay because they do not reduce SWS.

In the near future more potent deep sleep inducing medications will become available in the form of 5HT2a inverse agonists such as Ketanserin. These could provide a safer alternative to Sodium Oxybate (Xyrem).

I have to say though unfortunately I seem to build tolerance to almost all medications and hence I would recommend to administer these drugs in a cyclical fashion, rotating them frequently or if an alternative is not available, coming off them for several days before going back on. This should reduce receptor downregulation to some extent.

Mechansims Behind Mitochondrial Dysfunction

Mitochondrial Permeation Transition Pore (MPTP)

I believe there is evidence that using the mitochondrial protocol consisting of methylb12, meta-folate, trimethylglycine is akin to trying to patch up a hole in the hull of the ship. Water is gushing in fast and wreaking havoc on board, we are using supplements simply as treatments to correct mitochondrial deficits internally , yet what we need to control is the perimeter of the mitochondria, also known as the MPTP (Mitochondrial Permeation Transition Pore). This controls the flow of molecules in and out of this structure.

One way to help make the mitochondria less permeable to many extracellular components such as excessive calcium influx (in many cases induced by glutamate transmission) is to reduce the permeability of the pore. Research shows the drugs such as the powerful immunosuppressant Cyclosporin A has a side effect of doing this. Also a drug with a high safety record is Trimetazidine, currently used to treat angina. It has been shown to increase levels of ATP and also reduce production of free radicals. I believe some synergy would occur using Trimetazidine in conjunction with a glutamate modulator. Or alternatively using Trimetazidine alongside the mitochondrial protocol could possibly enhance the efficacy of this treatment strategy.

I will provide references shortly when I get the time.

Death of 20 Year Old from ME Induced Immune Dysfunction

I am re posting this information in order to try and highlight the gravity of the situation that is ME. This disease needs to be investigated and treated by a branch of true 'medicine' that uses objective markers and not subjective findings as we find at present in psychiatry. Psychiatry has provided no useful answers for ME evidently because it is NOT a psychiatric disease. If psychiatry could help people with ME they would be more than willing to accept help from doctors in this field such as the highly acclaimed professors Wessley and White.

Note: It is important to remember that Ms. Morgan did not die from ME
or CFS directly, but rather from associated complications. This is an
important difference in science and medicine even though in human
terms it means little because the end result is what is more
important. For example, in terms of science, no one dies directly from
AIDS, they die from AIDS-related diseases and conditions. Or when
someone dies from a gunshot wound the actual death is from the
specific associated trauma. If it were the bullet that was the actual
cause of death then everyone who had ever been shot would die - and
that doesn't happen.
Letchworth 20-year-old’s sudden death caused by dysfunctional immune system
By Nick Gill
Tuesday, April 17, 2012
1:33 PM

A CORONER investigating the death of a 20-year-old woman who died
suddenly in her bed has recorded a verdict of natural causes.
An inquest into the death of Tara Morgan was held today (Tuesday),
after she was found dead at her home in Abbotts Road, Letchworth GC,
in September last year.
Speaking at Hatfield Coroner’s Court, deputy coroner Graham Danbury
described the situation when Tara was found dead by her two brothers,
James and Aaron, on Sunday, September 4, 2011.
He said: “There was no response when she was called a few times. Both
of her brothers went to get her up and they found her in bed. The
ambulance service arrived but were unable to revive Tara, who was
pronounced dead on their arrival and probably had been for some time.”
The former Woolgrove and The Valley school pupil was taken to Lister
Hospital where her death was recorded.
Dr Rajiv Swamy, consultant pathologist for the North and East
Hertfordshire Trust, said her death was probably caused by a
dysfunctional immune system, after Tara had been unwell for a couple
of weeks prior to her death.
Tara, who was born with a learning disability, had a history of
headaches, muscle aches, joint pains and a bloating of the abdomen.
“There is a history of being unwell for some time without a proper
robust reason,” said Dr Swamy.
He also said a toxicology revealed that fluid had gathered in fluid
sacs in the lungs, with white blood cells and blood found.
“A parasitic infection would have triggered an allergic reaction and
this is probably the reason we had a lot of white cells,” said Dr
Swamy.
He added that Tara’s death could be related to chronic fatigue
syndrome, a disorder defined by persistent fatigue.
Tara’s mother, Amanda Lovering, sobbed during the inquest and said “I
could have stopped it” after hearing about the presence of lice.
But responding, Dr Swamy said: “I want to reassure you that with the
lice infection the body did respond to it appropriately. I do not
believe that was the direct cause of her death.
“It has affected the immune system but that had been dysfunctional for
quite some time. I’m at a loss other than this possibility to explain
what happened to your daughter.”
Summing up, Mr Danbury said: “This is a case of something in the body
going wrong over quite some time. In the light of what Dr Swamy has
told us, I will record a verdict in respect to the death of Tara as
respiratory and cardiac arrest due to autonomic neuropathy.”
Tara, an avid Luton Town supporter, had been studying child care at
North Hertfordshire College at the time of her death.

Medical Intervention for Someone in Crisis

My Reality

Through my journey with having experienced the extreme struggles of trying to survive with severe ME, this disease has been relentless and 'good days' need to be clearly defined. From my perspective my days don't vary any great deal - there is always significant muscle weakness, cognitive impairment and all the other many symptoms which at present my memory evades me.

Of the many many interventions I have tried to improve the outcome of my illness, none seem to induce any noticeable benefit relatively quickly (as in minutes or hours, not days) other than that but a few. As outlined in many studies into neuroinflammation that affects the brain and Central Nervous System, these regions are seperated from the rest of the body by the Blood Brain Barrier (BBB) [2]. Within this separate compartment, the environment is patroled by microglia: the resident macrophages of the brain and spinal cord. It is quite probable that in ME microglia are chronically activated in a state where they respond to some form of viral or other infection that they are unable to neutralise. This activation induces significant up regulation of pro-inflammatory cytokine production: Il-1a, Il-1b and TNF-a. It must not be forgotten that blood tests for the aforementioned cytokines will most often show no abnormalities due to the compartmentalisation of the immune system behind the blood brain barrier. Doctors by and large do not seem capable of understanding ME simply because the pathology is complex compared to diseases such as rheumatoid arthritis, where elevated levels of TNF-a often show up on blood tests [6] due to the location of the inflammation in the synovial fluid that has access to the peripheral circulation.

Chronic sustained production of these cytokines results in neuronal degeneration [1]. Activated microglia produce profound levels of Glutamate, an excitotatory neurotransmitter, or when in abundance may be referred to as an excitotoxin [5]. This induces an increase in the concentration of intracellular calcium ions, which subsequently has many detrimental effects on the cell inducing apoptosis (programmed cell death).


Getting some relief from acute paralysing symptoms

Seeing as neuroinflammation and subsequent up regulated glutamate production is most likely present, I tried various strategies to see if I could improve some of the most disabling, paralysing symptoms of this disease.

The medication 'Flupirtine', an NMDA receptor antagonist and potassium channel opener has given me significant relief from some of the most crippling symptoms such as complete muscle weakness and visual and auditory excitation. This drug is not readily available in the UK at present, but has been used in other European countries for quite some time primarily as a non-opiate non-NSAID pain killer. It reduces the effect of glutamate on neurons and thus reduces excitation A compound structurally akin to Flupirtine and that is available in the UK under prescription and at present licensed and indicated for epilepsy is 'Retigabine'. This however can be prescribed off-label for a variety of conditions to include ME. For safety, Liver Function Tests should be performed intermittently to ensure hepatic enzymes are within the normal range and not grossly elevated.

'Memantine' a mild NMDA receptor antagonist, used in Alzheimer's disease can reduce the effect of glutamate in stimulating neurons via blockade of the NMDA channel. This drug has some other effects on other receptors such as D2, 5HT3 and Nicotonic Acetylcholine receptors of which D2 agonism may provide benefit for symptoms of Restless leg syndrome and Periodic Limb Movement Disorder.

Currently due to the recent deterioration of my condition and failure to improve on a concoction of D-ribose, Carnitine, Manganase, Zinc, Selenium, Ascorbic Acid, Omega 3 (2 grams daily), Malic Acid, Methylcobalamin (Subcutaneous), Metafolate (6mg daily), S-Adenosyl Methionine (Sam-e) and Magnesium Sulphate (Subcutaneous) I have instigated and maintained a regime of glutamate down regulation that has been of great therapeutic value:

Daily, I take:

Flupirtine - instant release capsule 100 mg every 6 hours.
Memantine - 20 mg at 7:00 and 20mg at 19:00 hours.

I have found that if symptoms put you at breaking point and the above combination does not provide sufficient relief, in emergencies I intermittently use low doses (0.5 to 1mg) of Clonazepam (Rivotril), a long acting benzodiazepine GABA-a agonist. GABAergic drugs have the ability to indirectly down regulate the N-Methyl D Aspartic Acid (NMDA) receptor - the receptor that receives and induces the effects of glutamate. I have not found tolerance to be an issue if this medication is not used every day, but only rarely as needed. I have not found I have incurred any tolerance to the Flupirtine and Memantine combination - this does not seem to be a problem with these drugs when used chronically over extended periods.

Of course, the above medications may not be suitable for everyone due to the extreme chemical sensitivities present for many sufferers.

Disclaimer: These medications must only be tried under the supervision of a qualified medical professional. If you need further information about who can prescribe them please contact me.



The only more natural alternaitves that seem to be of any efficacy from personal experience are Lithium Orotate - this is not a prescription drug and does not have the toxicity issues that are present from the prescription only Lithium Carbonate, which is used at very high doses.

With Lithium Orotate, 5 to 15 mgs may be of quite to some use when in an acute crisis.

Sun Theanine, a patented specially processed high purity form of the amino acid L-Theanine can increase the synthesis of GABA. GABA has inhibitory effects on the glutamatergic system [8]

In ALS, also known as Lou Gehrig's disease, the drug 'Riluzole' is employed and has the capacity to indirectly down regulate glutamate. Therefore the effect of glutamate on motor neurons is drastically reduced and this can improve symptoms such as muscle weakness [7].


Rituximab & B Cell Depletion Therapy

It is interesting to note that elevated levels of IL-8 can induce the differentiation and growth of B cells. Work done by the Whittemore Peterson Institute observed a trend for various cytokines to be elevated in so called XMRV+ subjects - in other words I think for the time being these patients should simply be considered as well defiend severe ME patients due to the controversy surrounding XMRV. However there was a trend for IL-8 to be quite substantially elevated in this group. With the recent findings demonstrating the benefits of employing B cell depletion therapy using the monoclonal antibody Rituximab, it would seem logical that autoimmunity may arise at least in part from the dysregulation of IL-8. In various autoimmune diseases upregulation of IL-8 seems to be prominent [3] [4].

I do hope that the information obtained from this post may help those ME patients in desperate need for some form of effective medical intervention. Evidently there are only but less than a few doctors in the UK that know how to effectively help patients. Even then I do not have confidence in their ability to help patients in an acute crisis that may endanger their survival. If you have any questions please feel free to contact me.


References

[1] Wood, Paul (2003). Neuroinflammation: Mechanisms and Management. Humana Press.

[2] Hamilton RD, Foss AJ, Leach L (2007). "Establishment of a human in vitro model of the outer blood–retinal barrier". Journal of Anatomy 211 (6): 707–16. doi:10.1111/j.1469-7580.2007.00812.x. PMC 2375847. PMID 17922819. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2375847.

[3] Deregulated production of interleukin-8 (IL-8) in autoimmune thyroid disease studied by newly developed IL-8 radioimmunoassay. PMID: 8003701

[4] Regulation of IL-6 and IL-8 Expression in Rheumatoid Arthritis Synovial Fibroblasts: the Dominant Role for NF-κB But Not C/EBPß or c-Jun¹ http://www.jimmunol.org/content/165/12/7199.abstract

[5] Manev H, Favaron M, Guidotti A, and Costa E. Delayed increase of Ca²⁺ influx elicited by glutamate: role in neuronal death. Molecular Pharmacoloy. 1989 Jul;36(1):106-112. PMID 2568579.

[6] Elevated TNF receptor plasma concentrations in patients with rheumatoid arthritis. PMID: 1318122 http://www.ncbi.nlm.nih.gov/pubmed/1318122

[7] Riluzole prolongs survival and delays muscle strength deterioration in mice with progressive motor neuronopathy (pmn) PMID: 11090865

[8] Enhanced activity of GABA receptors inhibits glutamate release induced by focal cerebral ischemia in rat striatum. PMID: 17531382

I decided to start this blog fuelled by the most desperate of my struggles. And that is to try to scratch the surface of the medical community and make them finally wake up and hear the music. We have no voice, because of the very paralysing nature of the illness that afflicts us, we have ME. 


ME, the acronym for Myalgic Encephalomyelitis is a devastating neuro-immune disease, as evidenced in part, at least with regard to the neurological characteristics by the World Health Organisation as am ICD-10 classification. However various immunological abnormalities have also been found. Physiological abnormalities are evidenced through hundreds of biomedical papers.