Potential medication: Florinef

Regarding pharmacotherapy for POTS, UpToDate states ‘There have
not been long term, high quality trials testing the efficacy of any pharmacologic approach in POTS.All suggested medications are off label’, and ‘The optimal therapy of POTS is not established’.

The use of fludrocortisone as the first line of therapy for POTS has Grade 2C evidence (UpToDate).

Beyond this, studies specific to orthostatic intolerance in CFS found fludrocortisone to be no more efficacious than placebo for amelioration of symptoms (Rowe. et al, 2001). 

A 2011 RACGP review found this medication not effective and potentially harmful/damaging in ME/CFS, with serious side-effects
from long-term corticosteroid therapy (RACGP, 2011). 

The NICE 2007 guidelines (on which much of  the Australian guidelines are based) also explicitly state ‘ The following drugs should not be  used for the treatment of CFS/ME: mineralocorticoids (such as fludrocortisone)’. 

Regarding neuroendocrine function, as stated in the 2002 RACP quoted by the HPAU, impaired hypothalamic– pituitary–adrenal (HPA) axis activation has been shown in CFS (Level III-2).


Fludrocortisone works to raise blood pressure primarily by increasing blood volume, assumed to be a cause of POTS in CFS patients, as deconditioning or time in bed reduces blood volume.


2017 Me/Cfs Symposium highlights

Video link: OMF symposium on YouTube

Time stamps (care of Melbourne bioanalytics)

Full overview: http://scopeblog.stanford.edu/2017/08/25/at-symposium-researchers-and-patients-examine-molecular-basis-of-chronic-fatigue-syndrome/


(Note the colour coding appears to be reversed in this graphic)


More slides can be found as images here Myalgic encephalomyelitis post

Sex differencess

Women are affected by ME/CFS at much higher rates. Presumably the factors which lead to this may play a role in treatment response and recovery rates.

Recent metabolomics studies show a different pattern of disruption, with differences in the protein deficiencies and pathways affected between males and females. Similar to other autoimmune diseases like lupus, 80-90% of ME/CFS patients are women.

Women are, generally, physically smaller than men and our hearts and lungs are much smaller in size. Yet our anatomy makes added room to carry a fetus in order to create new human life.

Our smaller heart, lungs, and organs still have to be able to do everything a human male does – pump oxygen, circulate blood, run fast, think fast, be awake 16 hours a day – and have the necessary fuel to carry a child to term. We have to do double duty, on half the machinery. Women can do so much more on less because we also have higher baseline levels of the hormone estrogen. Oestrogen acts as a kind of messenger, carrying information between groups of our cells. Say we are stressed, or catch a flu, or get a vaccine – estrogen helps women have a more robust immune response. This more robust immune response is also thanks to steroid hormones known as glucocorticoids (or GCs).l, which are produced by the adrenal gland and are anti-inflammatory. They help regulate inflammation. This heightened female immune response also means that when our immune system sets out to fight off any foreign invader, such as a virus or bacteria, as women we also produce more of what are called antibodies, or fighter immune cells. That’s good BUT it can also be a problem. As women, when we produce more antibody fighter cells, we also produce more autoantibodies. Autoantibodies are rogue fighter immune cells that can mistakenly attack the body’s own tissue or organs, in what we refer to as friendly fire/ #autoimmunedisease.

When girls repeatedly face #toxicstress during the developmental years, over time, their stress response begins to be dysregulated. Glucocorticoids, or GCs, become less able to properly regulate a healthy, appropriate immune response, which leads to more inflammation. Boys immune systems become dysregulated in response to #toxicstress too — e.g. boys who face #ACEs are more likely to show decreases in brain matter volume in the caudate region of the brain — related to impulse control and behavior), whereas for women risk of autoimmunity is increased 20% for every ace score. Women develop Hashimoto’s thyroiditis at a rate of 10:1 compared with men. In lupus, that rate is 9:1. In Sjögren’s syndrome, 9:1. #AutoimmuneDisease is one of the top ten leading causes of death in women under the age of sixty-five. Women are also twice as likely as men to have chronic pain syndromes. Women with an ACE score of 3 are significantly more likely to have chronic pain syndromes including headaches, back and neck problems. Both boys and girls who grow up with #toxicstress demonstrate, on brain scans, fewer neural connections between the pre-frontal cortex (the decision-making center of the brain) and the hippocampus (area of the brain that helps us to make sense of our emotions and experiences). But, in girls who grow up with #toxicstress and #ACEs, another area of neural connectivity is affected. It goes offline. Synaptic connections between an area of the brain known as the amygdala (fear-and-alert center of the brain) and the pre-frontal cortex are also weakened. the risk that growing up with #toxicstress and #adversechildhoodexperiences will lead to neuroinflammatory diseases such as depression and anxiety disorders is, as with autoimmune disease, 2x as high for women as it is for men. Having experienced 6 categories of childhood adversity can take 20 years off your lifespan. #toxicstress each ace is 20% increased fish for women but only 10% for men. And girls face more #ACEs growing up in general. In fact, girls are 50% more likely to have experienced 5 or more categories of childhood adversity.

Anecdotally, CFS recovery, especially through exercise, seems more common amongst men. Perhaps men are originally affected at similar rates to women (without being diagnosed) but recover. Testosterone may play a role, given the role of muscle wasting, as testosterone makes it easier to build muscle. It may also be anti-inflammatory (ref). Menstruation may also play a maintaining role.

2015 study on gender differences in CFS: Only 9.1% of patients were men.

‘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.’
‘Men had less pain and less muscle and immune symptoms, fewer comorbid phenomena, and a better quality of life.’

‘More men reported an initial infectious process (26.9 versus 13.0%), while pregnancy-partum issues were precipitating factors in 11.3% of women.’

Ratios of male to female differ and differing case definitions confuse the issue even more so. A 2014 Norwegian study found the female to male incidence rate ratio of CFS/ME was 3.2 (75.4% women).

Metabolic features of me/cfs Naviaux 2016 study showed distinct patterns for males versus females. This could theoretically explain higher incidence of me/cfs in females, the above lower quality of life for females, and potential differences in treatment response.

Fluge and Mella found sex differences also:

Analysis in 200 ME/CFS patients and 102 healthy individuals showed a specific reduction of amino acids that fuel oxidative metabolism via the TCA cycle, mainly in female ME/CFS patients. Serum 3-methylhistidine, a marker of endogenous protein catabolism, was significantly increased in male patients.

‘Sex appeared to be an important factor in interpretation of the results, with significant reductions of mean serum levels of category II and III amino acids evident in female ME/CFS patients’

Infections reveal inequality between the sexes

Hormones also play a part. Oestrogen can activate the cells involved in antiviral responses, and testosterone suppresses inflammation. Some vaccines have been more effective in girls (TB), others have killed girls (measles in 1992).

‘Genetic factors may also guide how the sexes deal with infection. Meyaard studies a protein called TLR7, which detects viruses and activates immune cells. Encoded by a gene on the X chromosome, the protein causes a stronger immune response in women than in men. Meyaard suspects that this is because it somehow circumvents the process whereby one of the two X chromosomes in women is shut down to avoid overexpression of proteins.’

This is particularly interesting in light of the protein deficiencies found in women but not men by naviaux (above).

As a result of these differences, many ME/CFS researchers (such as the Armstrong lab in Melbourne Australia and Nauvieux with his suramin research) are now using a female only cohort to reduce variability.


There may also be a social dimension whereby men are more likely to be believed by doctors, family members and peers. See for example Women are dying because doctors treat us like men or the ABC podcast on the same topic. This article regarding the psychologisation of illness may also be of interest.

Swallowing & tachycardia

The ‘cardiac chronotropic response’ on swallowing is where there is an abrupt initial rise in heart rate on swallowing, slowed rise in heart rate, and then recovery. he acceleration is due to inhibition of vagal activity. ‘Deglutination tachycardia’ is the average resting heart rate beforehand compared with peak during swallowing.
In normies, ‘the contribution of each swallow is lower than that of the previous one’ and  the parasympathetic compensation actually causes HR to drop after. The mechanism of swallowing is designed to be completed quickly to allow the resumption of breathing. 
The ranges for heart rate rise found in the attached study were:
supine position (13.1 +/- 5.6 bpm)
standing position (8.5 +/- 3.8 bpm).
Thus in the normal population 95% of people’s HR raised:
laying flat 2-24bpm
Standing 1- 16bpm
In the study, tests were performed in the morning (as mine was), after 10 mins rest in supine position (from resting), each patient completed a single swallow, three swallows, and five swallows one at a time, and then 7-10 water swallows through a tube (like i did using a straw). This is shown in the attached image, 1 is deglutination tachycardia, 2 is the addition of each bpm for 2 heart beats, across 1,3,5 swallows.

This video documents a rise of 68-92 bpm, laying reclined. The following day sitting knees up in a crouch position, resting 59 went up to 94bpm, a raise of 36bpm). Once PEM improved, EG able to move more under 100bpm, the repeat test of 7 swallows of water elevated heart rate 20bpm only (Resting 63- peak 83- dropped back to 61). This return to bradycardia is noted as part of normal parasympethic compensation. 

In PEM for patients the sympathetic dominance can cause high heart rates and breathlessness when eating or drinking. Difficulties swallowing can also be an issue due to swollen glands, sinus congestion, muscle weakness, stress etc.

The parasympathetic nervous system slows heart rate through the action of the vagus nerve. The response relies on the vagus nerve, which may be lacking tone, or inflamed? in ME/CFS/fibro. Thus in PEM there is sympathetic dominance, the HR isn’t slowed by the parasympathetic response, the parsympathetic response may not occur and the heart rate may continue to elevate beyond the third swallow. This may likely be inflammation, as if it was just a lack of tone it would presumably be constant across time, not just in crashes. This seems to be readily documentable evidence of vagus nerve problems, specific to PEM.

IOM 2015 report

The 300 page IOM report ‘“Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Redefining an Illness” funded by the American National Academies of Medicine, written by a committee, is not without criticism. For the most part, its suggestion of the name ‘SEID, systemic exertion intolerance disorder’ has not been accepted by the ME/CFS community (primarily as its suggested criteria is too wide, conflates CFS, ME and would not exclude those with primary depression). However, the content was written by a respected committee, is evidence based and provides a thorough overview. Here is a snapshot of some good points (Taken from phoenix rising, Discussion in ‘Institute of Medicine (IOM) Government Contract‘ on phoenix rising, started by DanMEFeb 11, 2015).

About ME/CFS/SEID in general:

“The primary message of this report is that ME/CFS is a serious, chronic, complex, multisystem disease that frequently and dramatically limits the activities of affected patients. In its most severe form, this disease can consume the lives of those whom it afflicts. It is “real.” It is not appropriate to dismiss these patients by saying, “I am chronically fatigued, too.”

“The cause of ME/CFS remains unknown, although in many cases, symptoms may be triggered by an infection or other prodromal events such as “immunization, anesthetics, physical trauma, exposure to environmental pollutants, chemicals and heavy metals, and rarely blood transfusions.”

“Seeking and receiving a diagnosis can be a frustrating process for patients with ME/CFS for several reasons, including a lack of understanding of diagnosis and treatment of the condition among health care providers and skepticism about whether it is in fact a true medical condition. Less than one-third of medical schools include ME/CFS-specific information in their curriculum (Peterson et al., 2013), and only 40 percent of medical textbooks include information on the condition (Jason et al., 2010). Some studies on awareness of ME/CFS have found high awareness among health care providers, but many providers believe it is a psychiatric/psychological illness or at least has a psychiatric/psychological component (Brimmer et al., 2010; Jason and Richman, 2008; Unger, 2011).”

“ME/CFS can cause significant impairment and disability that have negative economic consequences at the individual and societal levels. At least one-quarter of ME/CFS patients are house- or bedbound at some point in their lives (Marshall et al., 2011; NIH, 2011; Shepherd and Chaudhuri, 2001). The direct and indirect economic costs of ME/CFS to society are estimated to be between $17 and $24 billion annually (Jason et al., 2008), $9.1 billion of which can be attributed to lost household and labor force productivity (Reynolds et al., 2004)”

“Although a variety of names have been proposed for this illness, the most commonly used today are “chronic fatigue syndrome,” “myalgic encephalomyelitis,” and the umbrella term “ME/CFS.” Reaching consensus on a name for this illness is particularly challenging in part because its etiology and pathology remain unknown (CFS/ME Working Group, 2002).”

“In addition to difficult interactions with health care providers, patients have reported several other ways in which the stigmatization of ME/CFS affects them, including financial instability (such as job loss or demotion), social disengagement, and feeling the need to hide their symptoms in front of others (Assefi et al., 2003; Dickson et al., 2007; Green et al., 1999).”

“Symptoms can persist for years, and most patients never regain their premorbid level of health or functioning (Nisenbaum et al., 2000; Reyes et al., 2003; Reynolds et al., 2004). The duration of ME/CFS and the potentially debilitating consequences of symptoms can be an enormous burden for patients, their caregivers, the health care system, and society.”

“Patients with ME/CFS have been found to be more functionally impaired than those with other disabling illnesses, including type 2 diabetes mellitus, congestive heart failure, hypertension, depression, multiple sclerosis, and end-stage renal disease.”

About fatigue:

“Regardless of what criteria are used, however, ME/CFS patients often have a level of fatigue that is more profound, more devastating, and longer lasting than that observed in patients with other fatiguing disorders. In addition, fatigue in ME/CFS is not the result of ongoing exertion, not lifelong, and not particularly responsive to rest (Jason and Taylor, 2002).”

“However, ME/CFS should not be considered merely a point on the fatigue spectrum or as being simply about fatigue. Experienced clinicians and researchers, as well as patients and their supporters, have emphasized for years that this complex illness presentation entails much more than the chronic presence of fatigue. Other factors, such as orthostatic intolerance, widespread pain, unrefreshing sleep, cognitive dysfunction, and immune dysregulation, along with secondary anxiety and depression, contribute to the burden imposed by fatigue in this illness.”

About PEM:

“As described by patients and supported by research, PEM is more than fatigue following a stressor. Patients may describe it as a post-exertional “crash,” “exhaustion,” “flare-up,” “collapse,” “debility,” or “setback.” PEM exacerbates a patient’s baseline symptoms and, in addition to fatigue and functional impairment (Peterson et al., 1994), may result in flu-like symptoms (e.g., sore throat, tender lymph nodes, feverishness) […]”

“PEM is worsening of a patient’s symptoms and function after exposure to physical or cognitive stressors that were normally tolerated before disease onset. Subjective reports of PEM and prolonged recovery are supported by objective evidence, including failure to normally reproduce exercise test results (2-day CPET) and impaired cognitive function. These objective indices track strongly with the presence, severity, and duration of PEM.”

“Many studies have demonstrated that pain is increased and prolonged after a physical stressor in ME/CFS subjects compared with healthy or sedentary controls. Similar to the evidence base for fatigue, reports of increased pain among ME/CFS subjects are consistent across maximal exercise tests (Davenport et al., 2011a,b; VanNess et al., 2010) and other physical stressors (Black et al., 2005; Nijs et al., 2010).”

About Sleep:

“It is clear, however, that people with ME/CFS universally report experiencing unrefreshing sleep, and further research will be important to determine whether there is a specific sleep abnormality common to ME/CFS patients or a heterogeneity of abnormalities that may define subsets of ME/CFS patients.”

“Despite the absence of an objective alteration in sleep architecture, the data are strong that the complaint of unrefreshing sleep is universal among patients with ME/CFS when questions about sleep specifically address this issue.”

“ME/CFS patients are more likely than healthy controls to experience sleep-related symptoms occurring at least half of the time and of at least moderate severity (see Figure 4-2) (Jason et al., 2013b). Although sleep- related symptoms also are reported by healthy persons and by chronically fatigued persons who do not fulfill ME/CFS criteria, a greater percentage of people fulfilling ME/CFS criteria report unrefreshing sleep, sleep distur- bances, and difficulties falling asleep or waking up early in the morning (Komaroff et al., 1996a; Krupp et al., 1993; Nisenbaum et al., 2004) relative to these other groups.”

About neurocognitive function:

“Impairments in cognitive functioning are one of the most frequently reported symptoms of ME/CFS. Patients describe these symptoms as debilitating and as affecting function as much as the physical symptoms that accompany this disease. During a survey of ME/CFS patients, descriptions of neurocognitive manifestations included, among others, “brain fog,” “confusion,” disorientation,” “hard to concentrate, can’t focus,” “inability to process information”.

“Collectively, the studies reviewed here support the notion that ME/CFS patients present with neurocognitive impairment. Slowed information pro- cessing, demonstrated by objective neuropsychological testing and potentially related to problems with white matter integrity, is one of the strongest neurocognitive indicators in support of a diagnosis of ME/CFS, particularly if there is evidence of normal functioning on untimed tests and impaired functioning on time-dependent tasks.”

About OI:

“There is consistent evidence that upright posture is associated with a worsening of ME/CFS symptoms, as well as the onset of other symptoms such as light-headedness, nausea, and palpitations. While there is variability in the reported prevalence of orthostatic intolerance in ME/CFS, heart rate and blood pressure abnormalities during standing or head-up tilt testing are more common in those with than in those without ME/CFS. Heart rate variability analyses demonstrate a sympathetic predominance of autonomic tone in those with ME/CFS, including during sleep.”

“Orthostatic intolerance can occur as an isolated syndrome or in association with a variety of other comorbid disorders, including ME/CFS (Benarroch, 2012). The most prevalent forms of orthostatic intolerance in the general population, as well as among those with ME/CFS, are POTS and neurally mediated hypotension (NMH), with delayed variants of orthostatic hypotension and orthostatic tachycardia also being seen.”

About Pain:

“Sufficient evidence shows that pain is common in ME/CFS, and its presentation supports the diagnosis. However, while pain worsens ME/CFS when present, there is no conclusive evidence that the pain experienced by ME/CFS patients can be distinguished from that experienced by healthy people or those with other illnesses. Further, pain may be experienced in many areas, and while comprehensively assessing a patient’s pain symptoms is a challenging task, it is not specific to ME/CFS.”

About Immune Impairment:

“Symptoms related to inflammation are reported frequently by ME/CFS patients. When attempting to convey their illness experience to healthy persons, many patients describe it as similar to a perpetual flu-like state (Maupin, 2014). Patients also report persistent or recurrent sore throats, tender/swollen cervical and/or axillary lymph nodes, muscle pain, achy joints without swelling or redness, headaches, chills, “feverishness” (but not necessarily meeting objective criteria for fever), and new or worsened sensitivities to certain substances (e.g., foods, odors, medications) (FDA, 2013).”

“One of the most consistent findings in ME/CFS subjects is poor NK cell function. Using K562 cells as target cells, 16 of 17 studies reviewed found poor function in subjects compared with healthy controls. However, this finding should be interpreted with caution as even the strongest of these studies are subject to methodological limitations discussed at the beginning of Chapter 4.”

“Low NK cytotoxicity is not specific to ME/CFS. It is also reported to be present in patients with rheumatoid arthritis, cancer, and endometriosis (Meeus et al., 2009; Oosterlynck et al., 1991; Richter et al., 2010). It is present as well in healthy individuals who are older, smokers, psychologically stressed, depressed, physically deconditioned, or sleep deprived (Fondell et al., 2011; Whiteside and Friberg, 1998; Zeidel et al., 2002).”

About Autoimmunity:

“In other studies, ME/CFS or postviral fatigue syndrome patients showed antibodies to smooth muscle (36 percent) (Behan et al., 1985), heat shock protein 60 (24 percent) (Elfaitouri et al., 2013), and endothelial antigens (30 percent) (Ortega-Hernandez et al., 2009). The only clinical trial targeting antibodies found moderate to marked clinical improvements in 10 of 15 subjects treated with rituximab, a B cell depleting antibody, and 2 of 15 placebo arm subjects at a single time point (Fluge et al., 2011). This, however, was a post hoc analysis as the trial failed to meet its primary endpoint. Currently, researchers in the United Kingdom and Norway are conducting further studies addressing this question (Edwards, 2013; Mella and Fluge, 2014).”

About Neueoendocrinic Function:

“Patients with ME/CFS may have relatively reduced overnight cortisol, 24-hour urinary cortisol, CRH and/or AVP, and ACTH levels compared with healthy controls. The current preponderance of evidence points to normal adrenal function in such patients and suggests a secondary (central) rather than a primary (adrenal) cause of reduced but not absent cortisol production at the level of the pituitary, the hypothalamus, or higher. Patients with ME/CFS may have defective serotonergic signaling in the brain, localized to the level of the hypothalamus or higher, resulting in downstream dysregulation that may play a role in ME/CFS. The exact mechanism is not clear.”

About Infection:

“The literature indicates a possible relationship between EBV and ME/CFS. The evidence suggests that ME/CFS can be triggered by EBV infection, but there is insufficient evidence to conclude that all ME/CFS is caused by EBV or that ME/CFS is sustained by ongoing EBV infection. Improved diagnostic techniques may reveal as yet undetected associations. Further research in this area is warranted to determine whether patients in whom disease was triggered by EBV or patients with evidence of an ongoing abnormal response to EBV represent clinically significant subsets of ME/CFS.
There is insufficient evidence for an association between ME/CFS and bacterial, fungal, parasitic, and other viral infections. These infectious agents may, however, be comorbidities, and their presence may reflect the presence of problems with immune function in these patients. Future research may clarify the role of these infections in this illness.”


gut studies

April 2017

Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome

(Study first of many by lipkin with multicentre colab with klimas, bateman and others, crowdfunded as part of the microbe discovery project, summary on sciencedaily))


Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome Ludovic Giloteaux,

The association of fecal microbiota and fecal, blood serum and urine metabolites in myalgic encephalomyelitis/chronic fatigue syndrome (increase in Clostridium spp. and a decrease in Bacteroides spp)


Here’s my (messy) cheat sheet of the bacterial changes found in me/cfs the above three studies and whether they’re increased or decreased. The right column is my personal results in relation to what’s expected (left column)

Testing available through Ubiome covers most of the mentioned bacteria with the exception of enterococcus, coprococcus, coprobacillus, and strain specific information. The ‘explorer kit’, available internationally, also includes metabolism details such as those below.



Brain Imaging: Lyme, ME, depression

This summary includes information on Single Photon Emission Computerized Tomography (SPECT) scans & MRI’s. Here are examples of normal spects,

normal SPECT

And a guide (from a primary CFS SPECT study) to brain regions in the SPECTS

note: it is standard for the SPECT to reverse left and right; this is labelled on the sheet

Swartz et al found hypofusion in areas 5, 2 & 6.
Mena & Villaneueva-Meyer found hypofusion in temporal lobes 1 & 2
Ichise et al found decreased radionuclide uptake mainly in 1,2/4,5, but also in 8, 3 & 6.

These are reversible and correlate with changes in clinical severity.


SPECT: In Lyme Disease, the most common finding is of heterogeneous hypoperfusion diffusely throughout the brain, similar to in Lupus, chronic cocaine abuse or other vasculitic inflammatory disorders. This pattern is different to primary depression or Alzheimer’s disease. Approximately 70% of patients with chronic Lyme disease will have multiple areas of hypoperfusion, but it cannot be used for diagnosis, as blood flow is rated relative to the cerebellum or deep grey matter which is presumed to be normal.

The above images are from hypobaric treatment where SPECT can be used as a marker of improvement.

From ‘looking at lyme‘:

SPECT scan of the brain before (A) and after (B) antibiotic brain specttreatment.

These transaxial images are from a 51-year-old man diagnosed with Lyme disease with a recent change in memory. Representative pretreatment images show hypoperfusion within the mid posterior and mid temporoparietal cortex bilaterally. Representative posttreatment images (14 months later) reveal improved perfusion to the posterior temporoparietal cortex bilaterally, correlating with improved symptoms. Perfusion within the remaining cerebral cortex, basal ganglia, thalamus, and cerebellum was normal.

MRI:  Looks similar to MS: Up to 40% of adults with Lyme disease may have small white matter hyperintensities suggestive of inflammation or areas of demyelination., but it should be noted that the number of hyperintensities increase with age – even among patients who do not have Lyme disease.

Youtube has many video tutorials on interpreting brain mri.


SPECT: Hyde considered an abnormal SPECT as well as an abnormal EEG or PET scan and/or neuropsychological abnormalities required for ME diagnosis, in particular decreased perfusion of blood in the left middle cerebral artery and the branches of the parietal lobes, present very early in the illness. He strongly emphasised vascular issues (moreso than PEM), and ‘difficulty concentrating and finding words, etc, problems sleeping, poor muscle functioning, trouble standing without exaggerated heart rates and dizziness, little ability to exert themselves, cold fingers, loose joints and gut problems’.

Screenshot (47)

EG “Intrinsic Functional Hypoconnectivity in Core Neurolocognitive Networks Suggests Central Nervous System Pathology in Patients with Myalgic Encephalomyelitis”, PMID: 26869373 or “Functional Neural Network Connectivity in Myalgic Encephalomyelitis

The ICC for ME notes SPECT abnormalities, however it specifies *with contrast*. Contrast can be reactive and cause side effects. Repeated SPECT scans done at the same medical center to allow for a fair comparison across images can track progress of treatment or disease progression.

ICC case study : Extensive areas of hypoperfusion are characteristic of ME… marked hypoperfusion in the lateral aspects of the temporal lobe, extending to the frontal and parietal lobes… extensive hypoperfusion in the limbic system involving anterior, medial and posterior cingulates. There is left temporal medial hypoperfusion that denotes hypofunction in the projection of the hippocampus. Both posterior cingulate and hippocampal hypofunction denote cognitive impairment. Finally, there is hypoperfusion in the occipital lobe.

Taken from Ireland ME which has good overview brain abnormality summary and study quotes.

brain areas

Medial temporal lobes (area 1) hypofusion seen in concussion, head injuries, hippocampus, memory impairment



Both hypo and hyperfusion is found in fibromyalgia.

Red: HYPOfusion, green: HYPERfusion

The images show the anatomical localization of peak significant differences between brain SPECT of patients with fibromyalgia and healthy subjects. Patients with fibromyalgia exhibited posterior hyperperfusion (red), including of the somatosensory cortex, and hypoperfusion (green) of frontal, cingulate, temporal, and cerebellar cortices. Images courtesy of the Journal of Nuclear Medicine


Severity was “positively correlated with bilateral parietal perfusion, including postcentral cortex. These clusters of correlation were included in the areas of significant hyperperfusion. [Severity] was also negatively correlated with perfusion of a left anterior temporal cluster, included in the areas of significant hypoperfusions. No other clinical correlation was observed with regional cerebral blood flow.”

Compared with healthy controls, patients with fibromyalgia exhibited posterior hyperperfusion, including of the somatosensory cortex, and hypoperfusion of the frontal, cingulate, temporal, and cerebellar cortices in particular, the temporal hypoperfusion including the polar and mediobasal cortices.

Positive correlations (both on left) represent hyperfusion, negative (right) represents hypofusion- ie low blood flow.


Brain perfusion abnormalities in patients with fibromyalgia “are independent of the patient’s anxiety and depression status and correlate with the clinical severity of the disease, expressed by the disability and evaluated by the FIQ total score.”

shows increased activity in the thalamus and basal ganglia (study)

below- here is an example of normal basal ganglia flow, the basal ganglia is in the centre
(note the rest may be abnormal as this woman had tremors.
note- basal ganglia abnormalities may also occur with lupus).


This same region is relevant for ADD: people with Anxious ADD show the hallmark ADD signature of low prefrontal cortex activity (image on the right) combined with overactivity in the basal ganglia (image on the left)—a region of the brain that allows for smooth integration of emotions, thoughts, and physical movement.



One review found differences between cfs & depression spects, with significantly more defects in the occipital lobe in depression; fischler found major depression showed significantly lower left superofrontal regional perfusion, in line with previous reports

while note: its normal to see more activity in the right than the left temporal lobe, with slightly larger left than right volume; this assymetry may be more pronounced in depression

depression            depression brain scan

depression         e7e6d170266384b583dfb80ba97875d9





severe anxiety neurosis revealed hyperactive prefrontal cortices and basal ganglia in technetium-99m-hexamethylpropyleneamineoxime brain perfusion single photon emission computed tomography images. (a) Transverse view, (b) sagittal view, (c) right lateral view of three-dimensional Talairach cortical perfusion report, (d) extracted basal ganglia and thalamus by “Neurogam” processing, (e) color scale for (c and d):


See: Brain perfusion single photon emission computed tomography in major psychiatric disorders: From basics to clinical practice


On CFS vs Depression, and CFS neurology scans in general:

spect textbook neurology.png

NOTES: my results ‘ischemia

‘A mild-moderate symetrical reduction uptake in the posterior tempero-parietal cerebral cortex is seen. There is a sparing of the posterior cingulate and the visual association cortex. Normal perfusion within the basal ganglia and the cerabellum… Bilateral mild to moderate posterior tempero-parietal cortical hypoperfusion’.

The ICC for ME says: ↓ reduced blood flow in temporal lobes may contribute to memory and cognitive impairment & fatigue

Hyde mentions abnormalities in the parietal lobe and the left middle cerebral artery: The middle cerebral artery is the largest branch of the artery that supplies a portion of the frontal lobe and the lateral surface of the temporal and parietal lobes, including the primary motor and sensory areas of the face, throat, hand and arm, and in the dominant hemisphere, the areas for speech. Low blood flow in the temporal and parietal lobes likely results from not enough blood coming through the cerebral artery.
There was no hyperperfusion, as seen in PTSD or fibromyalgia, or hypofusion in the superofrontal lobes, as seen in depression. Brain stem was not reported on; this is used to differentiate depression & ME. FND/conversion disorder expects abnormal functional but normal structural imaging, as I have, but is a debatable clinical entity.
This does not rule out lyme which shows a similar pattern, abnormalities in perfusion to various areas of the brain, most notably the frontal, temporal, and parietal lobes- those these may be asymmetrical?
I have orthostatic intolerance, which can be linked to low blood volume. I was well hydrated, and as I was laying down, this may be of negliable significance, especially as only some regions of the brain were affected

The ICC also states: Greater source activity and more parts of the brain are utilized in cognitive processing, which supports patients’ perception of greater effort… These observed pathological changes are consistent with neurological disorders but not psychiatric conditions…


The parietal lobes involves sensation and perception and integrates sensory input, primarily with the visual system. Neurons in the parietal lobes receive touch, visual and other sensory information from a part of the brain called the thalamus. The thalamus relays nerve signals and sensory information between the peripheral nervous system and the cerebral cortex. The temporal lobes are involved in high-level auditory processing such as selective listening, language recognition of words, and Mathematical Computation! Problems include the inability to recall the correct names of everyday items, difficulty in making exact movements, inability to perform complex tasks in the proper order

The temporal lobes play an important role in organizing sensory input, auditory perception, language and speech production, language comprehension, as well as memory association and formation. Structures of the limbic system, including the olfactory cortex, amygdala, and the hippocampus are located within the temporal lobes. Damage to this area of the brain can result in problems with memory, understanding language, and maintaining emotional control. This is also important for facial recognition and regulating fight or flight!

The frontal lobes are involved in reasoning and personality expression is fine! The posterior cingulate is between the frontal and parietal lobes and is considered part of the default mode network, a group of brain structures that are more active when an individual is not involved in a task that requires externally-focused attention, also implicated in moral judgments


fig-29-05brain diagram amygdala 416


Hypoperfusion Neuro-SPECT ↓ regional blood flow (rCBF), ↓ absolute cortical blood flow ↓ hypoperfusion in brainstem distinguishes ME from depression ↓ further reduction in cerebral blood flow after exercise; Greater involvement of the brain correlates with greater severity

Review: Stan Tatkin Attachment Podcast

Following up on the previous blog detailing attachment, here is a summary of the podcast interview by Stan Tatkin. (listen here, or see http://stantatkin.com/).

Stan Tatkin returns and serves up another awesome dose of relationship advice through the lens of adult attachment. From how relationships impact your health, to helping your triggered or upset partner, to dealing with an avoidant partner.

Allostatic load is the price we pay for adaptation, neurobiological wear and tear
cardiovascular, neuroimmune, inflammation

Chronic health issues have a correlation with insecure attachment
good stress occurs when there is a solution/end to a problem
interpersonal stress is both acute and chronic, and takes toll on brain, body, and nervous system. A good marriage extends life, in a terrible marriage, we die sooner.
EG: not trusting- feeling betrayed- feeling abused- feeling neglected- feeling misunderstood- not getting anything done- fighting with no repair- take a toll
interpersonal stress the most common and likely to age, poor health, feeling crap
insecurity and unsafety.

We take things personally when our nervous system memories result in us being flooded. the important thing in a connection is that both people have a common/mutual interest of shortening the distress, to get to relief
move through distress as quickly and efficiently as possible
this requires the person who has the urge to defend or explain, asking tell me what i did, i wasn’t aware, you’re right in order to relieve the person who is aroused or threatened and waiting to see if you’re friendly or unfriendly

Secure attachment requires accepting the other as is… taking full responsibility for one’s own faults. It makes no sense to choose but not accept/to want to change and find fault.

a secure environment/milieu allows both to be free to be themselves, accepted as they are;
yet there is a requirement to take responsibility for the things i do that get in the way of secure attachment, such as island behaviour, wave behaviour, plain rude behaviour

Secure functioning isn’t ‘love’- its safety and security, with agreement and loyalty.

Avoidants can be considered as an ISLAND
to get them on board; avoidants need to be in touch with their original longing-
to give and receive coregulation, validate and reassure others, and ask for their own needs

Attachment leaves the avoidant/island encumbered by an overwhelming amount of interpersonal stress. The feel relief when they leave, and auto regulate, skipping over missing the other person. Object constancy is missing and out of sight out of mind-
alone they feel relief. Untethered. HOWEVER their eating changes, sleep changes, addictive behaviours- the island is not okay, not independent.
it’s important to assume and to speak to the dependency, loss, as the ‘island’ is actually very needy with unmet infant dependency needs
they may be annoyed that you’d suggest they’d have a problem. Yet after separation, there can be acting out, reunion causes behaviour, cancelling, coming late.
the avoidant/island is ensconced in memory of relationship trauma, of being exploited, interrupted, not allowed to be separate but not allowed to depend, misunderstood, expected to perform for others but not for them, etc. don’t poke the bear.
For the island, to be held and talked to be intrusive, they feel caught, trapped, demanded upon. Catch and release, loosen sooner than expected to deamplify the behaviour. Proving won’t hurt them as they anticipate- talk to them like they will love and miss you, and slowly increasing the window of tolerance, like titration

For anxious WAVES it can be hard to have confidence- as they fear they are too much, a pain in the butt, fear rejection, withdraw, afraid they will be alone, can’t do this by myself

Both have FEAR: the island scanning for being taken advantage of: wave scanning for withdrawal and punishment

It’s important for the wave to see the island is actually more inept, developmentally delayed, less well defended; socially and emotionally inept, tense, unable to relax or let go… The wave is actually more able to hold things together

eye contact to regulate, after or during conflict, to get the other adult to soften
(book gabler matay pure orientation)
babies who were intruded upon by an invasive parent
joint attention on a third object. Amplify pleasure, baby looks at her. Comment. Then connect. Amplify through third thing as a bridge. parallel play can help, but too much creates a loneliness that is quite profound, being in the room and not relating to me is different to being not in the room, withdrawn, isolating, disturbing. Worse than not being here.

Lead with relief
use eye contact and touch to reach out
to help calm them down and sooth them
to know you’re safe and that you’re on their team

SECURITY FREES UP RESOURCES otherwise used for chronic anxiety, planning to run, cling, etc. development moves when there are resources. Massive insecurity or trauma interrupts it. Relationship constantly threatening and may not exist tomorrow- tremendous resource drain. Acceptance of each other allows space, resistance ties up resources

WIRED FOR DATING: we subconsciously choosing emotionally unavailable partners. We pick familiars. Recognition, until we metabolise the experiences- organise them- learn to handle them inside oneself- challenges until we learn how, mastered them

The important question:
DOES THIS PERSON WANT TO PLAY: two person systems, on the same page, fully engaged, wants to be here, messed up is ok.
Requires collaboration, cooperation, justice, mutual agreement, fairness, sensitivity, aiming for me and for them, mutual, fair, agreed upon

If not invested. Doesn’t see, doesn’t care to see what they’re doing, doesn’t matter to them what their partner thinks, doesn’t matter whether this is a secure functioning relationship, then said goodbye.



50-75% of CFS meet ME/CFS criteria, and less again meet the ICC definition of ME. This discrepency results in the variance in prevalence estimates (0.2-6.4%)

Beyond this, a number of studies have attempted to break the heteogenous group of ‘CFS’ down into sub-components. This has been done via genes, microbiome, or by secondary symptoms.

According to Jason & Zinn (2015), secondary symptoms of ME might include symptoms within immune, neuro-endocrine, autonomic, and pain domains. ‘Despite the reported lower prevalence of these domains, these secondary symptoms are nonetheless found with enough frequency in the literature to utilize them for patient subtyping, such as, ME-immune, ME-autonomic, ME-neuroendocrine, ME-pain, or ME-combination’.

‘Glucocorticoid sensitivity was greater among ME/CFS patients overall compared to healthy controls and between ME/CFS GC-Hypersensitive (red circle) compared to ME/CFS GC-Typical (blue circle; p’s ≤0.05)’… ‘Mild hypocortisolism and enhanced negative feedback to glucocorticoids were observed in several studies of GC responses in ME/CFS [3, 49]. The presence of both the GC-Typical and GC-Hypersensitive subgroups within our ME/CFS cohort thus aligns with the observed heterogeneity of HPA-related differences in these previous reports.’

Exercise & gene expression: two subgroups of patients with CFS can be identified by gene expression changes following exercise. The larger subgroup showed increases in mRNA for sensory and adrenergic receptors and a cytokine. The smaller subgroup contained most of the patients with CFS with orthostatic intolerance, showed no postexercise increases in any gene and was defined by decreases in mRNA for α-2A.  Postexercise increases for four genes meet published criteria as an objective biomarker for CFS and could be useful in guiding treatment selection for different subgroups.

Immunity weirdness

I’m investigating strange immune reactions, such as coldsore/ulcer outbreaks from SB probiotics, and a failure to seroconvert antibodies. Here’s some info about immunity  (Phoenix Rising):

T cells are T lymphocytes, a type of white blood cell found in the blood and in the lymph system, that mature in the thymus gland. T cells are part of the adaptive immune system. T helper cells (Th) help other cells in the immune system to respond appropriately to threats. 

T cells start out as naive T cells, and then they get converted to the types that are needed depending on the requirements of the body. There are two types of helper T cells, Th1 and Th2. Th1 cells act by activating macrophages so that they can attack bacteria that are inside the macrophages. So Th1 cells are formed when the best approach for defending the body is to activate the macrophages. This is called “cell-mediated” immunity. The weapons of the Th1 system include cytotoxic T cells and Natural Killer (NK) cells (low in ME/CFS). On the other hand, for bacteria that are extracellular, i.e. not inside macrophages, the better approach is to make antibodies that will attach to the bacteria. Its weapons include eosinophiles (Eos), polymononuclear cells (PMN), and antibody secreting cells (Ab). This is called “humoral” or “antibody mediated” immunity. 

Antibodies are made by B lymphocytes, which turn into plasma cells. In order to help them to act, Th2 lymphocytes are needed. 

In the presence of a virus, cancer, yeast, or intracellular bacteria (like mycoplasma or chlamydia pneumonia), a cytokine called Interleukin 12 activates Th1. In the presence of normal bacteria, parasites, toxins, and allergens, Interleukin 10 (IL-10) triggers the production of Th2.

In stress and ME/CFS, Th2 dominates (although Th1 may dominate in the gut, with th3). When they are Th2 activated, they no longer have the defense mechanisms to protect or keep dormant things caught in the past. They cannot suppress or control them anymore, and the EBV, chlamydia pneumonia, mycoplasma, rickettsia, CMV, etc. reactivate. There is also not a good defense against viruses or fungi, including yeasts. These infections that are found in ME/CFS because the immune system is not able to effectively defend against them, because of the shift to Th2.
The cause of this shift is not agreed upon. Allergies may be a sign of a very early or inherent th2 domination. There may be a role of stress, high cortisol suppressing inflammation, low glutathione causing low b12 and HPA disruption with low ATCH & low cortisol, or viruses may disturb neurotransmitter receptors. Viruses, especially herpes viruses like EBV, CMV and HHV6, make cytokine proteins that mimic IL-10 and cause a Th2 shift. Zinc deficiency may be associated with lowered Th1 activity.

Vit D is a TH2 promotor. MS is a TH1 dominant condition.

Astragalus may shif the immune response back toward Th1, as does Lactobacillus paracasei. Heat killed saccromyces cereviseae induces a th1 response Study. Mouth ulcers are causes by th1 Study. Herpes simplex is a ‘delayed type hypersensitivity’ reaction based on th1 as well, Quoting: “HSV lesions demostrate a prevailing Th1 pattern in which the induction of MCH-II on epidermal cells and the activation of CD8+ T cells through IL-12 and IFN-y are particularly important in the control of recurring infections”.

More to come, regarding testing: 
t1/t2- t lymphocytes- helper/suppressor ratio
Secretory IgA
Low IgG