The blood volume paradox in ME/CFS & POTS

Posted on 08/03/2016 by wames

Health Rising blog post: The Blood Volume Paradox in Chronic Fatigue Syndrome (ME/CFS) and POTS by Cort Johnson, 29 July 2016.

Kunihisa Miwa, a Japanese ME/CFS researcher, has been on something of a roll. Through no less than five studies he pioneered the small heart findings in chronic fatigue syndrome (ME/CFS). Systrom basically validated Miwa’s finding in his large study of people with unexplained exercise intolerance – some of whom had ME/CFS.

The Exercise Intolerance in ME/CFS, POTS and FM Explained?

Miwa appears to be something of a lone wolf; his ME/CFS studies were either authored just by him or by one other person. Miwa may not be working with a lot of researchers, but he’s certainly up to date; he refers to ME/CFS as ME in this and other papers, and the patients in this study had to meet not the Canadian Consensus Criteria, but the International Consensus Criteria developed in 2011.

Miwa recognized that the small hearts he found in his chronic fatigue syndrome (ME/CFS) patients were likely due not to some defect but to reduced blood flows. If the heart, like any other muscle, doesn’t work out it won’t grow, and the heart needs blood, and lots of it, to work itself into shape.

In this study (ME/CFS=8, HC=5) people Miwa examined some factors – renin (plasma renin enzymatic activity), aldosterone and antidiuretic hormone (ADH) – that affect blood volume. He also also did an echocardiograph and examined the effects of desmopressin – an ADH replacement – to see if it helped.

Results

The study confirmed… “that the vast majority of the patients with ME had a small heart shadow….and their cardiac function was actually impaired with a low cardiac output.”

As before Miwa found evidence of a smaller than usual heart (LV end-diastolic diameter) and reduced output (stroke volume index, cardiac index) in the ME/CFS patients. Mean blood pressure was also lower. More importantly, the factors designed to increase blood volume such as renin enzymatic activity (p<.06), aldosterone (p<.02), and ADH (p<.004) were significantly lower or nearly significantly lower (p<.05) in the ME/CFS patients.

The Low Blood Volume Paradox

Low blood volume has been a recognized issue in ME/CFS since Streeten and Dr. Bell nailed it way back in the year 2000. In fact the Streeten-Bell study – done on 15 randomly selected ME/CFS patients – may have described postural orthostatic tachycardia syndrome (POTS) before it showed up in the literature. Streeten and Bell found reduced blood pressure, reduced blood volume, increased norepinephrine levels and excessive tachycardia upon standing. (This study appears to precede any studies on POTS. If so, chronic fatigue syndrome may have birthed POTS.)

Demonstrating another overlap with ME/CFS and POTS Miwa’s findings mimic those of a 2005 POTS study (reduced blood volume, aldosterone and plasma renin activity).
Streeten would go on to show way back in 2001 that blood pooling in the veins as well as low blood volume was preventing sufficient amounts of blood from getting to the heart. Military antishock trousers were reportedly quite effective in reducing the problem.

(Military antishock trousers are inflated with a pump. They don’t seem to have ever be suggested as a viable treatment option but do indicate that blood pooling the veins is very important is very important). The excessive tachycardia, Streeten believed, was an attempt to increase blood flows to the brain.

Jump forward 15 years and David Systrom shows up with a large study years in the making which shows that unexplained fatigue associated with exercise is characterized by reduced preload (blood flows to the heart), reduced blood volume and blood pooling in the veins; i.e. exactly the same problem Streeten and Miwa found but being applied to a much larger set of patients.

Systrom suggested that problems with the veins were more important than blood volume but Hurwitz’s large study suggested that blood volume was most important factor in the low cardiac output found in ME/CFS. About half the patients in Hurwitz’s study had low blood volume and they were the sickest.

The fact that POTS, ME/CFS and some other disorders were included in Systrom’s study indicates this problem is present in an array of diseases. Miwa describers the tachycardia in POTS in the same way that Streeten did – as a reaction to the low blood levels reaching the heart. We know now, though, that POTS is more complicated than once thought, and that autoimmune processes targeting the receptors that effect heart rates are involved as well. .

Low blood volume appears to be common, though, in both ME/CFS and POTS. Ordinarily, low blood volume should trigger the renin-angiotensin-aldosterone system and ADH (vasopressin) to increase it, but in what’s called the renin-aldosterone paradox, both these systems appear to poop out in ME/CFS and POTS.

The Renin Aldosterone Paradox

Miwa doesn’t posit a clear answer to the renin-aldosterone paradox but suggests that central nervous system/HPA axis and “structural or functional brain abnormalities” are to blame. The top of the HPA axis chain – the hypothalamus – is part of the limbic system in the lower brain. It links the nervous and endocrine systems together via the pituitary gland. (The hypothalamus also regulates our circadian rhythms (and thus sleep) and the autonomic nervous system.

ADH (vasopressin) is produced in the hypothalamus and then carried into the blood via the pituitary gland. Aldosterone is produced by the adrenal glands in response to angiotensin II, ACTH, potassium or via messages from the stretch receptors in the heart that blood pressure has fallen.

Dr. Bateman’s Big Picture

In her talk “the Big Picture and ME/CFS” Dr. Bateman proposed a similar scenario. First, she focused on the Zinn’s findings from the Stanford Symposium which suggested that people with ME/CFS were asleep when they were awake, and awake when they were asleep. The Zinn’s proposed a “limbic encephalopathy” – a brain disorder concentrated in the lower regions of the brain – was present.

Dr. Bateman echoed that idea noting that the Japanese had found inflammation in the lower part of the brain, and that a Rhomberg test – an indicator of deep brain issues – is often positive in ME/CFS/FM.

Then she noted a bevy of hormones including ADH (vasopressin) are produced in the lower part of the brain. With his functional or structural brain abnormalities Miwa appears to be positing that this area is producing the low blood volume, and perhaps the vein problem in ME/CFS.

Treatment

Miwa proposes the use of desmopressin, a drug not often associated with ME/CFS. Desmopressin is a synthetic analogue of vasopressin. Vasopressin, which is decreased in both ME/CFS and POTS, increases blood vessel “tone” and blood pressure. Desmopressin doesn’t increase blood vessel tone but it does increase blood volume. It’s most frequently used in diabetes insipidus and for night-time bed-wetting.

The IACFS/ME Primer doesn’t mention desmopressin but a 2012 study found that desmopressin significantly reduced the heart rate in POTS patients. The authors of the POTS study found desmopressin effective in the short term, but would not recommend its daily use until further studies had been done. They did say it’s been proven safe for children with night-time bedwetting problems.

One risk of daily use is hyponatremia – low blood sodium concentrations – which might be exacerbated by the large amounts of water some patients drink. The authors concluded that desmopressin is

highly effective at acutely decreasing orthostatic tachycardia and standing tachycardia in patients with POTS, and this was associated with an improvement in symptom burden in these patients. Longer-term studies are needed to assess this therapy.

That’s significantly better than the finding that fludrocortisone – another drug commonly used in orthostatic intolerance – was no better than placebo.

New Studies
Researchers have been showing more interest in blood volume enhancement as of late. Medow’s study quantifying the effects of saline on ME/CFS should be out this year, and he just got a nice NIH grant to examine the effectiveness of oral rehydration salts in increasing blood volume in ME/CFS.

Oral rehydration salts (ORS) were developed by the World Health Organization to combat diseases such as cholera. They are cheap, easy to make and surprisingly effective.

Medow states in the grant that he believes that the ORS may bemore effective than IV saline infusions in increasing blood volume and improving blood flows to the brain.

Conclusions

We’ve made some progress since Bell and Streeten identified the low blood volume, problems with the veins, and rapid heart rates 15 years ago in ME/CFS. We know that smaller than usual hearts are also present in ME/CFS and POTS and people with idiopathic exercise intolerance (who have not been diagnosed with ME/CFS). Researchers are taking a deeper look at blood volume, and we know that the inflammation in the lower brain may have something to do with it.

If Dr. Bateman is right further brain studies will highlight this area. We should know in the next year or so.

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Gender differences in CFS

Posted on 08/03/2016 by wames

Research abstract:

BACKGROUND AND OBJECTIVES:
Chronic fatigue syndrome (CFS) is a chronic condition that predominantly affects women. To date, there are few epidemiologic studies on CFS in men. The objective of the study was to assess whether there are gender-related differences in CFS, and to define a clinical phenotype in men.

PATIENTS AND METHODS:
A prospective, cross-sectional cohort study was conducted including CFS patients at the time of diagnosis. Sociodemographic data, clinical variables, comorbid phenomena, fatigue, pain, anxiety/depression, and health quality of life, were assessed in the CFS population. A comparative study was also conducted between genders.

RESULTS:
The study included 1309 CFS patients, of which 119 (9.1%) were men. The mean age and symptoms onset were lower in men than women. The subjects included 30% single men vs. 15% single women, and 32% of men had specialist work vs. 20% of women. The most common triggering factor was an infection. Widespread pain, muscle spasms, dizziness, sexual dysfunction, Raynaud’s phenomenon, morning stiffness, migratory arthralgias, drug and metals allergy, and facial oedema were less frequent in men. Fibromyalgia was present in 29% of men vs. 58% in women. The scores on physical function, physical role, and overall physical health of the SF-36 were higher in men. The sensory and affective dimensions of pain were lower in men.

CONCLUSIONS:
The clinical phenotype of the men with CFS was young, single, skilled worker, and infection as the main triggering agent. Men had less pain and less muscle and immune symptoms, fewer comorbid phenomena, and a better quality of life.

Gender differences in chronic fatigue syndrome, by Faro M, Sàez-Francás N, Castro-Marrero J, Aliste L, Fernández de Sevilla T, Alegre J [Article in English, Spanish] in Reumatol Clin. 2016 Mar-Apr;12(2):72-77 [Epub 2015 Jul 17]

 

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Mixed results for MitoQ in FM & CFS study

Posted on 08/02/2016 by wames

Research abstract:

Fibromyalgia (FM), myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS) are disorders with similar symptom constellations including pain, fatigue, cognitive problems and sleep disturbance, among others.

These multi-system illnesses have many known abnormalities, few reliable treatment options and unknown causes. Oxidative stress has been linked to disorder severity, suggesting anti-oxidants may be of benefit. Coenzyme Q10 (Q10) has been shown to improve symptoms and biomarkers of FM, and ME/CFS if taken in combination with another coenzyme. However, Q10 is poorly absorbed by mitochondria.

MitoQ is a mitochondria targeted Q10 analog with superior absorption and accumulation by mitochondria in vivo. The current study tested the effect of 6-weeks of daily oral MitoQ (20mg) on FM and ME/CFS with two randomized, blinded, placebo-controlled crossover studies. A third open label cohort contributed data but did not receive placebo.

Results suggest MitoQ may reduce pain and increase working memory in FM. Further investigation in a more controlled environment is warranted.

The influence of Mitoq on symptoms and cognition in fibromyalgia, myalgic encephalomyelitis and chronic fatigue, by Cort Johnson & Joshua Grant

[This article has NOT been officially peer reviewed and is the opinion of the authors. Comments can be made publicly or privately on either Mendus.org or HealthRising.org]

Mendus is a platform to encourage people with health conditions share experiences, interact with research scientists, generate research questions and initiate research studies.

Founder Joshua Grant says:

We had a great turnout for the MitoQ study. Though not everyone finished, 144 people contributed data. Newcomers can still complete the study but I wanted to inform you that an official report is freely accessible here.

There were encouraging and disappointing results. MitoQ seems to work quite well for fibromyalgia, lowering pain and improving memory. For ME/CFS the higher dosage (those who also had placebo) showed no effects that could not be explained by placebo. However, our open label cohort (Group3) showed huge effects with the lower dose. You can read much more about our interpretation in the discussion section of the paper.

Did MitoQ mend us? by Cort Johnson, 8 Aug 2016

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Lower level of dynamic postural control in CFS & FM

Posted on 08/02/2016 by wames

Research highlights:

  • Fibromyalgia and chronic fatigue syndrome showed a lower level of postural control in gait initiation.
  • There was no significant difference between fibromyalgia and chronic fatigue syndrome in dynamic postural control.
  • Fibromyalgia patients showed a higher K value compared to the controls.

Research abstract:

BACKGROUND: Impaired postural control has been reported in static conditions in chronic fatigue syndrome and fibromyalgia, but postural control in dynamic tasks have not yet been investigated. Thus, we investigated measurements from a force plate to evaluate dynamic balance control during gait initiation in patients with chronic fatigue syndrome and fibromyalgia compared to matched healthy controls.

METHODS: Thirty female participants (10 per group) performed five trials of gait initiation. Center of pressure (CoP) trajectory of the initial weight shift onto the supporting foot in the mediolateral direction

(CoPX) was analyzed using General Tau Theory. We investigated the hypothesis that tau of the CoPX motion-gap (τCoPx) is coupled onto an intrinsic tauG-guide (τG) by keeping the relation τCoPx=KτG, where K is a scaling factor that determines the relevant kinematics of a movement.

FINDINGS: Mean K values were 0.57, 0.55, and 0.50 in fibromyalgia, chronic fatigue syndrome, and healthy controls, respectively. Both patient groups showed K values significantly higher than 0.50 (P<0.05), indicating that patients showed poorer dynamic balance control, CoPX colliding with the boundaries of the base of support (K>0.5).

INTERPRETATION: The findings revealed a lower level of dynamic postural control in both fibromyalgia and chronic fatigue syndrome compared to controls.

TauG-guidance of dynamic balance control during gait initiation in patients with chronic fatigue syndrome and fibromyalgia by O Rasouli, AK Stensdotter, AL Van der Meer in J Clin Biomech (Bristol, Avon) Vol 37, August 2016, pp 147–152  [Epub ahead of print]

 

 

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CFS – is the biopsychosocial model responsible for patient dissatisfaction and harm?

Posted on 08/01/2016 by wames

Article extracts:

In 1977 George Engel wrote about the need for an ‘integrated approach’ in medicine that moved the focus beyond biological mechanisms of disease to include all pertinent aspects of illness presentation, setting out a ‘biopsychosocial model’.1

Around the same time, McEvedy and Beard asserted that the disease ‘benign myalgic encephalomyelitis’, described by Ramsay at the Royal Free Hospital, London, was nothing more than a case of ‘mass hysteria’.2 In the 1980s, doctors combined theories of neurasthenia, hysteria, and somatoform illness, to reconstitute ME as ‘chronic fatigue syndrome’. Psychiatrists argued that CFS was best understood using a biopsychosocial (BPS) framework, being perhaps triggered by viral illness (biology), but maintained by certain personality traits (psychology) and social conditions (sociology).3

Although the BPS model holds much utility in understanding ‘illness’ in a wider context, many sufferers of CFS reject the notion that their illness is psychologically or socially derived. Significant numbers of patients report difficult interactions with doctors that leave them feeling dissatisfied, disbelieved, and distressed.

In this article, we question whether or not the BPS model generates ‘harms’ for CFS patients, and we ask if other, alternative approaches might be more preferable to both patients and GPs…

CONCLUSION: INVOLVING PATIENTS AND EMPOWERING GPS
Many CFS patients report that they wish to be cared for by GPs in primary care, rather than psychiatrists in specialist centres.

CFS patients ranked the professionals they want to manage their condition, putting GPs as first choice (1502 votes), with psychiatrists last choice (15 votes).10 However, in a survey of attitudes to CFS among English GPs, Bowen and colleagues found that many GPs lack confidence in making a diagnosis (48%) or in treating patients (41%).13

Scepticism and a lack of awareness and training among GPs concerning CFS may well explain some of the patient dissatisfaction highlighted in patient surveys, as well as explain delays and error in diagnosis. However, it is also arguable that the biopsychosocial approach of challenging the nature of the illness, and seeking to intervene with psychotherapy to challenge patients’ illness beliefs may also play a part in generating distress for patients with CFS.

In order to minimise iatrogenesis, GPs require better training in how to diagnose CFS and communicate with patients with CFS; GPs should not seek to impose a biopsychosocial model of illness on a patient. Models of illness should not supplant the ‘lived experience of illness’ or subjugate the expert status of the patient as ‘witness to their condition’. Nassir Ghaemi, critical of the biopsychosocial model, suggests doctors should consider alternative clinical approaches, such as Karl Jaspers’ ‘method-based’ or William Olsen’s ‘medical humanist’ model’.14

Such models might be used by GPs to:

  • inform patients of the absence of known aetiology in CFS (rather than speculating around psychogenic causes);
  • inform patients that there are explanations for some CFS symptoms (for example, the IOM report of biomedical evidence);
  • offer patients treatments such as CBT, but inform patients that these therapies do not work for all (rather than suggesting the patient controls outcomes);
  • offer alternative interventions and support, such as counselling and community care (rather than just referral to CFS clinics); and
  • accept the legitimacy of the patient account (rather than seeking to challenge patients’ illness beliefs).

Such differences of approach may seem subtle, but arguably represent a more pragmatic approach, which we recommend for general practice. It is probable that harm could be minimised by adopting a more concordant model that includes patients’ preferences in treatment and management.

Chronic fatigue syndrome: is the biopsychosocial model responsible for patient dissatisfaction and harm?, by Keith J Geraghty & Eneesz Esmail,  in British Journal of General Practice vol. 66 no. 649 437-438 [Published 1 August 2016]

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Intestinal cell damage & systemic immune activation in people with sensitivity to wheat

Posted on 08/01/2016 by wames

Research abstract:

Objective:  Wheat gluten and related proteins can trigger an autoimmune enteropathy, known as coeliac disease, in people with genetic susceptibility. However, some individuals experience a range of symptoms in response to wheat ingestion, without the characteristic serological or histological evidence of coeliac disease. The aetiology and mechanism of these symptoms are unknown, and no biomarkers have been identified. We aimed to determine if sensitivity to wheat in the absence of coeliac disease is associated with systemic immune activation that may be linked to an enteropathy.

Design: Study participants included individuals who reported symptoms in response to wheat intake and in whom coeliac disease and wheat allergy were ruled out, patients with coeliac disease and healthy controls. Sera were analysed for markers of intestinal cell damage and systemic immune response to microbial components.

Results: Individuals with wheat sensitivity had significantly increased serum levels of soluble CD14 and lipopolysaccharide (LPS)-binding protein, as well as antibody reactivity to bacterial LPS and flagellin. Circulating levels of fatty acid-binding protein 2 (FABP2), a marker of intestinal epithelial cell damage, were significantly elevated in the affected individuals and correlated with the immune responses to microbial products. There was a significant change towards normalisation of the levels of FABP2 and immune activation markers in a subgroup of individuals with wheat sensitivity who observed a diet excluding wheat and related cereals.

Conclusions: These findings reveal a state of systemic immune activation in conjunction with a compromised intestinal epithelium affecting a subset of individuals who experience sensitivity to wheat in the absence of coeliac disease.

Significance of this study:

What is already known on this subject?
Some individuals experience a range of symptoms in response to the ingestion of wheat and related cereals, yet lack the characteristic serological or histological markers of coeliac disease.

Accurate figures for the population prevalence of this sensitivity are not available, although estimates that put the number at similar to or greater than for coeliac disease are often cited.

Despite the increasing interest from the medical community and the general public, the aetiology and mechanism of the associated symptoms are largely unknown and no biomarkers have been identified.

What are the new findings?
Reported sensitivity to wheat in the absence of coeliac disease is associated with significantly increased levels of soluble CD14 and lipopolysaccharide-binding protein, as well as antibody reactivity to microbial antigens, indicating systemic immune activation.
Affected individuals have significantly elevated levels of fatty acid-binding protein 2 that correlates with the markers of systemic immune activation, suggesting compromised intestinal epithelial barrier integrity.

How might it impact on clinical practice in the foreseeable future?
The results demonstrate the presence of objective markers of systemic immune activation and gut epithelial cell damage in individuals who report sensitivity to wheat in the absence of coeliac disease.

The data offer a platform for additional research directed at assessing the use of the examined markers for identifying affected individuals and/or monitoring the response to treatment, investigating the underlying mechanism and molecular triggers responsible for the breach of the epithelial barrier, and evaluating novel treatment strategies in affected individuals.

Intestinal cell damage and systemic immune activation in individuals reporting sensitivity to wheat in the absence of coeliac disease, by Melanie Uhde, Mary Ajamian, Giacomo Caio,
Roberto De Giorgio, Alyssa Indart, Peter H Green, Elizabeth C Verna, Umberto Volta,
Armin Alaedini in Gut [Published Online 25 July 2016]

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Interdisciplinary group treatment may improve quality of life in CFS/ME

Posted on 07/29/2016 by wames

Research highlights:

  • Interdisciplinary group treatment may improve quality of life in CFS/ME.
  • Psychological Flexibility (PF) has applied utility in the treatment of CFS/ME.
  • Changes in PF activity/occupational engagement suggest greatest benefit in CFS/ME.

Research  abstract:

Objective: Psychological Flexibility (PF) is a relatively new concept in physical health. It can be defined as an overarching process of being able to accept the presence of wanted/unwanted experiences, choosing whether to change or persist in behaviour in response to those experiences. Associations between processes of PF and quality of life (QoL) have been found in long-term health conditions such as chronic pain, PF has not yet been applied to Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME).

Methods: Changes in PF, fatigue severity and QoL were examined in one hundred and sixty-five patients with CFS/ME engaged in a six-week outpatient interdisciplinary group treatment programme. Participants were assessed using a series of self-report measures at the start of the start (T1) and end of a six-week programme (T2) and at six months follow up (T3).

Results: Significant changes in PF and QoL were observed from pre-treatment (T1) to post treatment follow-up (T2 and T3); changes in fatigue severity were observed from T1 to T3 only. Controlling for fatigue severity, changes in the PF dimension of activity/ occupational engagement were associated with improvement in QoL at six month follow up (T3) but not at six weeks post programme (T2).

Conclusion: Findings indicate an interdisciplinary group treatment approach for people with CFS/ME may be associated with improved QoL, processes of PF and fatigue severity, supporting a link between PF and long term health conditions. Results highlight links between PF and patient QoL in CFS/ME and the value of interdisciplinary treatment approaches in this patient population.

Enhanced psychological flexibility and improved quality of life in chronic fatigue syndrome/ myalgic encephalomyelitis, by Sarah Densham,Deborah Williams, Anne Johnson, Julie M. Turner-Cobb in Journal of Psychosomatic Research Vol 88, Sep 2016, Pp 42–47 [Published online: July 2016]

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Non-restorative sleep in FM & CFS

Posted on 07/29/2016 by wames

Prohealth blog post, by Celeste Cooper, 21 May 2016: “Wake Up Sleepy Head” – Non-Restorative Sleep in FM and CFS

“Are you deprived?”

Disordered sleep is prevalent in both fibromyalgia and chronic fatigue syndrome/ myalgic encephalomyelitis. Sleep deprivation can affect your mental, physical, emotional, and spiritual health. Lack of restorative sleep weakens the immune response leaving us more susceptible to other diseases and disorders.

I understand only too well the effects of insomnia and disordered sleep. Sometimes, many times, despite doing everything right, a road block occurs and we literally lose our map to life. This is why I think it is important, in light of the more recent research, that we all have a sleep study, so integrative therapies can be implemented.

What is a sleep disorder?

Sleep disorders are characterized by different circumstances. Sleep apnea, for instance, is an obstructive sleep disorder and can co-exist with FM and CFS/ME. When this happens a person is deprived of oxygen, which is needed for cellular metabolism and energy.

Disordered sleep, meaning that the normal cycles of sleep are not present, not maintaining sleep, and delayed sleep onset have been consistently reported by fibromyalgia (FM) and chronic fatigue syndrome (CFS/ME) patients.

Here is a link from About.com that has a really good explanation of the sleep cycles, though these seem to be changing. One thing we expect in science is that nothing remains the same.

Many of us seldom, if ever, enter deep stages of sleep, so I am including a link regarding slow wave sleep (SWS, which may in the future be defined as one stage).

It seems to me, anecdotally and according to some studies, people with non-restorative sleep, an overlapping symptom between FM and CFS/ME, have a disordered or disrupted sleep cycle. As if that is not enough, there are other co-existing conditions that seem to cluster with both FM and CFS/ME, such as teeth grinding (bruxism), periodic limb movement (PLM), TMJ, sleep starts, and delayed sleep phase (inability to fall or maintain sleep). These can and do play a role in sleep quality, and I am advocating that an assessment for myofascial trigger points, RLS and PLM be included in the proposed diagnostic criteria for FM and a better explanation for “jaw pain.”

Sleep deprivation can impede healing and interfere with our body’s immune system, not to mention agitation and sleep deprivation psychosis. This might explain why so many of us have difficulty fighting off viruses and recovering from trauma, including the micro-trauma we experience in our everyday lives that is repaired during normal sleep.

So what do we do?

According to the Wikipedia link, it seems alcohol (I am assuming not too much, though they don’t state such), THC, SSRIs, and possibly Xyrem can promote slow wave sleep (SWS), and benzodiazepines, such as Klonopin, can inhibit SWS.

I bring up Klonopin specifically because it is often prescribed to help with the periodic limb movement (PLM) seen in the FM and CFS/ME patient. This leads me to conclude that the treatment for PLM may also be an aggravating factor for lack of SWS. Other treatment suggestions for PLM include sleeping pills, anti-seizure medications and narcotic pain killers. On the flip side, I have heard that the addition of a benzodiazepine such as Ativan (Lorazepam) might help with myofascial trigger point relaxation. Don’t give up, continue to work with your doctor to find the right treatment for you. People with hypertension know the trial and error involved in finding the right blood pressure medication; the same holds true for us. Not only are we genetically different, we all have our own grocery cart of co-existing conditions.

If I didn’t learn anything else from this investigation, it is that your best bet is to find a good sleep specialist that understands FM and CFS/ME. You and he/she can work together.

There is something you can do to promote your circadian rhythm, which is
orchestrated by two markers, melatonin concentration and core body temperature. Have a bedtime ritual.

A Helpful Acronym for Sleep Hygiene ©

Schedule bedtime and stick to it
Limit physical activity before bedtime
Use comfort measures
Meditate (count those lambs)
Breathe
Eliminate stress and food (including caffeine 2-3 hours prior to bedtime)
Remember nothing—clear your mind (journal your to-do list so you can let go)

*(Excerpt from the book, copyrighted material)

I hope you will take a minute to stop by Arthritis Today (link below) and leave a comment regarding restless leg syndrome, sleep disruption and assessment in diagnosis of fibromyalgia.

More detailed information of good sleep hygiene is provided in the book.

Harmony and Hope, Celeste

Resources:

Arthritis Today. Restless Leg Syndrome Linked to Fibromyalgia by Jennifer Davis (accessed, 11/18/10)
http://www.arthritistoday.org/news/restless-leg-syndrome-fibromyalgia097.php

Cooper and Miller. Integrative Therapies for fibromyalgia, Chronic Fatigue Syndrome and Myofascial Pain: The Mind-Body Connection. Healing Arts Press: Vermont, 2010.

A. R. Gold, F. Dipalo, M. S. Gold, and J. Broderick, “Inspiratory airflow dynamics during sleep in women with fibromyalgia,” Sleep 27, no. 3 (2004): 459–66.

M. Irwin, J. McClintick, C. Costlow, M. Fortner, J. White, and J. C. Gillin, “Partial night sleep deprivation reduces natural killer and cellular immune responses in humans,” Federation of American Societies for Experimental Biology 10, no. 5 (1996): 643–53.

M. Irwin, J. McClintick, C. Costlow, M. Fortner, J. White, and J. C. Gillin, “Partial night sleep deprivation reduces natural killer and cellular immune responses in humans,” Federation of American Societies for Experimental Biology 10, no. 5 (1996): 643–53.

T. Kato, J. Y. Montplaisir, F. Guitard, B. J. Sessle, J. P. Lund, and G. J. Lavigne, “Evidence that experimentally induced sleep bruxism is a consequence of transient arousal,” Journal of Dental Research 82, no. 4 (2003): 284–88.

B. Kundermann, J. C. Krieg, W. Schreiber, and S. Lautenbacher, “The effect of sleep deprivation on pain,” Pain Research & Management 9, no. 1 (2004): 25–32.

M. L. Mahowald and M. W. Mahowald, “Nighttime sleep and daytime functioning (sleepiness and fatigue) in less well-defined chronic rheumatic diseases with particular reference to the alpha-delta NREM sleep anomaly,” Sleep Medicine 1, no. 3 (2000): 195–207.

H. Moldofsky, “The significance, assessment, and management of nonrestorative sleep in fibromyalgia syndrome,” CNS Spectrums 13, no. 3 (2008): 22–26.

M. K. Millott and R. M. Berlin, “Treating sleep disorders in patients with fibromyalgia: exercise, behavior, and drug therapy may all help,” Journal of Musculoskeletal Medicine 14 (1993): 25–28.

T. Kato, J. Y. Montplaisir, F. Guitard, B. J. Sessle, J. P. Lund, and G. J. Lavigne, “Evidence that experimentally induced sleep bruxism is a consequence of transient arousal,” Journal of Dental Research 82, no. 4 (2003): 284–88.

A. Korszun, L. Sackett, Lundeen, E. Papadopoulos, C. Brucksch, L. Masterson, N. C. Engelberg, E. Hause, M. A. Demitrack, and L. Crofford, “Melatonin levels in women with fibromyalgia and chronic fatigue syndrome,” Journal of Rheumatology 26, no. 12 (1999): 2675–80.

H. K. Moldofsky, “Disordered sleep in fibromyalgia and related myofascial pain condition,” Journal of Clinical Dentistry, North America 45, no. 4 (2001): 701–13.

H. Moldofsky, “The assessment and significance of the sleep/waking brain in patients with chronic widespread musculoskeletal pain and fatigue syndromes,” Journal of Musculoskeletal Pain 15 Suppl. no. 13 (2007): [Myopain 2007 poster].

H. K. Moldofsky, “Disordered sleep in fibromyalgia and related myofascial pain condition,” Journal of Clinical Dentistry, North America 45, no. 4 (2001): 701–13.

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J. C. Rains and D. B. Penzien, “Sleep and chronic pain: challenges to the alpha- EEG sleep pattern as a pain specific sleep anomaly,” Journal of Psychosomatic Research 54, no. 1 (2003): 77–83.

E. R. Unger, R. Nisenbaum, H. Moldofsk, A. Cesta, C. Sammut M. Reyes, and W. C. Reeves, “Sleep assessment in a population-based study of chronic fatigue syndrome,” BMC Neurology 4, no. 1 (2004): 6.

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Celeste Cooper, RN, is a frequent contributor to ProHealth.  She is an advocate, writer and published author, and a person living with chronic pain. Celeste is lead author of Integrative Therapies for Fibromyalgia, Chronic Fatigue Syndrome, and Myofascial Pain and Broken Body, Wounded Spirit, and Balancing the See Saw of Chronic Pain (a four book series). She spends her time enjoying her family and the rewards she receives from interacting with nature through her writing and photography. You can learn more about Celeste’s writing, advocacy work, helpful tips, and social network connections at CelesteCooper.com

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Variable effects of clonidine treatment in CFS

Posted on 07/29/2016 by wames

Research abstract:

Clonidine, an α2-adrenergic receptor agonist, decreases circulating norepinephrine and epinephrine, attenuating sympathetic activity.

Although catechol-O-methyltransferase (COMT) metabolizes catecholamines, main effectors of sympathetic function, COMT genetic variation effects on clonidine treatment are unknown. Chronic fatigue syndrome (CFS) is hypothesized to result in part from dysregulated sympathetic function.

A candidate gene analysis of COMT rs4680 effects on clinical outcomes in the Norwegian Study of Chronic Fatigue Syndrome in Adolescents: Pathophysiology and Intervention Trial (NorCAPITAL), a randomized double-blinded clonidine versus placebo trial, was conducted (N=104).

Patients homozygous for rs4680 high-activity allele randomized to clonidine took 2500 fewer steps compared with placebo (P_interaction=0.04). There were no differences between clonidine and placebo among patients with COMT low-activity alleles. Similar gene-drug interactions were observed for sleep (P_interaction=0.003) and quality of life (P_interaction=0.018).

Detrimental effects of clonidine in the subset of CFS patients homozygous for COMT high-activity allele warrant investigation of potential clonidine-COMT interaction effects in other conditions.

Genetic variation in catechol-O-methyltransferase modifies effects of clonidine treatment in chronic fatigue syndrome, by KT Hall, J Kossowsky, TF Oberlander, TJ Kaptchuk, JP Saul, VB Wyller, E Fagermoen, D Sulheim, J Gjerstad, A Winger, KJ Mukama in the Pharmacogenomics Journal [online publication 26 July 2016]

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Long-Term Consequences of Cryptosporidium and Giardia Gastroenteritis

Posted on 07/28/2016 by wames

Research abstract:

Cryptosporidium and Giardia are protozoan intestinal parasites which may present as asymptomatic infections in humans or cause severe and prolonged diarrhea. Studies over the last two decades show an association between these two pathogens, and various sequelae after the parasite has been successfully eradicated either by medication or by the host immune system.

In endemic countries, Giardia infection has been associated with later wasting and poor cognitive function, while growth faltering, stunting, and reduced physical fitness have been shown after Cryptosporidium infections. More recently, outbreaks of Giardia and Cryptosporidium in non-endemic settings have shown association between infections with these pathogens and long-term sequelae including not only long-lasting abdominal symptom but also extra-intestinal symptoms such as chronic fatigue and joint pain.

More studies are needed to confirm these associations and determine mechanisms and causality in order to identify effective prevention and treatment alternatives.

Long-Term Consequences of Cryptosporidium and Giardia Gastroenteritis by Kurt Hanevik Protozoa (R Mejia, Section Editor) in Current Tropical Medicine Reports, pp 1–5 [published online: 22 June 2016]

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