Frontiers in Pediatrics: Blood volume status in ME/CFS correlates with the presence or absence of orthostatic symptoms (2018) Van Campen et al

Kalliope

Kalliope

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Frontiers in Pediatrics: Blood volume status in CFS/ME correlates with the presence or absence of orthostatic symptoms


Introduction: Conflicting data have been published on the reduction of circulating blood volume in adults with Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). The aim of the present study was to compare blood volumes based on the presence or absence of orthostatic symptoms.

Conclusions: Adults with ME/CFS had a significantly lower blood volume if they had a clinical suspicion of OI compared to those without a clinical suspicion of OI, as well as a significantly lower blood volume compared to the expected value. The data suggest that accounting for symptoms of OI could enhance the detection of the subset with reduced blood volume.
 
At 12 participants, it's a really small study, but good on the authors for looking at something basic and useful. They say there have been conflicting data on blood volumes in PwME, unfortunately a 12 participant study is not going to settle the matter once and for all.

Lots of questions that hopefully the full text will answer. The link says that the paper has been provisionally accepted and that the full paper will be published soon.

Blood volume comparisons:
The reference blood volume (presumably equivalent to that of a healthy control) seems to have been 70 ml/kg

The 12 participants averaged 59 ml/kg
The 4 participants without OI averaged 66 ml/kg
The 8 participants with a clinical suspicion of OI averaged 56 ml/kg

Even with this small sample, differences were significant.

We really need this study done on lots more PwME, including tracking what happens as soon as people get ME, so that we know when the OI/low blood volume starts. It's not rocket science but I would have thought we need to know this basic stuff.
 
strategist said:
The question I have, is the finding of low blood volume a consequence of low activity levels or directly caused by the illness?
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Just going on my own experience, it is directly caused by the illness, as OI started straight away for me, it was one of the first symptoms.

I also simply wasn't inactive enough during the first few months (maybe even years) after onset to induce deconditioning.

It is one reason why I am so dismissive of the deconditioning claim, at least as a primary feature. It is certainly possible, maybe even probable, that secondary deconditioning occurs. But it also true that it is very difficult for the patient to avoid that happening, or do much about when it does.
 
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Sean said:
Just going on my own experience, it is directly caused by the illness, as OI started straight away for me, if was one of the first symptoms.

I also simply wasn't inactive enough during the first few months (maybe even years) after onset to induce deconditioning.
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Exactly the same here.
Then, after a couple of years or so, the fainting stopped and the postural orthostatic tachycardia started.
If OI and low blood volume are linked, what about POTS and low blood volume?
I'm speculating that I first got low blood volume, this lead to OI, which finally morphed into POTS as an adaptive response.
 
I can't think of a way low activity could lead to low blood volume. I never knew what it was, but I had OI right from the start. In those days, they spoke about the hypothalamus being affected so that temperature control and so on were bad. I don't know if that is the same as dysautonomia or a separate thing. If it is I hope it isn't lost as it is a real problem for me.

I was not deconditioned for decades, not until I became housebound.
 
Now I'm curious how that relates to findings of reduced liver volume.

It seems to follow that with lower blood volume, the liver would shrink since it doesn't need to filter as much. Does that make sense?
 
I’m not sure.

I do know fasting affects liver size, and seeing as how the metabolics of PwME can look similar to that what you see in healthy people during prolonged fasting there might be a connection there, possibly the liver is a good temporary fuel source for the body?
 
Looking through the Liver Perspective, although i am not sure this is directly related :


Quantitative measurement of human tissue hepatic blood volume by C15O inhalation with positron-emission tomography.
Taniguchi H1, Masuyama M, Koyama H, Oguro A, Takahashi T.
Author information

Abstract
In order to estimate the tissue liver function, tissue hepatic blood volume was measured quantitatively and non-invasively using C15O inhalation in conjunction with positron-emission tomography. Fifty-eight patients with normal liver function, 14 patients with chronic hepatitis, 28 patients with hepatic cirrhosis, and 4 patients with obstructive jaundice were studied by positron-emission tomography scan after the single breath inhalation of 20 mCi of high specific activity 15O-labeled carbon monoxide. The mean tissue hepatic blood volume was significantly greater in patients with normal livers than in patients with chronic hepatitis or hepatic cirrhosis (mean: 20.5, 18.2, and 16.1 ml per 100 cm3, respectively, p = 8.6 x 10(-8)). Tissue hepatic blood volume (tHBV) correlated with the reaction of the mesenchymal system and protein synthesis, because there was a potent correlation between tHBV and hepatic fibrosis. In normal livers, we were able to demonstrate significant differences in tissue hepatic blood volume among liver segments.
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strategist said:
The question I have, is the finding of low blood volume a consequence of low activity levels or directly caused by the illness?
Click to expand...
What makes you think of linking the 2? I haven’t heard of blood volume being tied to physical conditioning before
 
Well its anecdotally a well known trait with ME that a bad patch is associated with peeing a lot. Also a high ESR reading (erythrocyte sedimentation rate: so long time is thick blood) is associated with low blood volume, Dr Paul Cheney documented this years ago.

This may be because kidney filtration is based on reuptake which is an active process requiring metabolic energy input. It stands to reason that if your kidneys have less energy they become less effective and your water leaks out but proving the association with OI and ME empirically is another matter and deserves to be done properly I feel sure.

At first before diagnosis I was susceptible to OI and on one occasion fainted because of it and knocked myself cold in the process and was mildly concussed. Since then I have been very careful standing up and since diagnosis (ten years later) I treat it by making an effort to drink plenty of fluid and minerals.

Nevertheless I read a story of one guy with ME being told by doctors that he was making himself ill because he was drinking too much and giving himself hyponatremia. I was tested for that myself on one occasion but it was normal.
 
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Sean said:
Just going on my own experience, it is directly caused by the illness, as OI started straight away for me, it was one of the first symptoms.

I also simply wasn't inactive enough during the first few months (maybe even years) after onset to induce deconditioning.

It is one reason why I am so dismissive of the deconditioning claim, at least as a primary feature. It is certainly possible, maybe even probable, that secondary deconditioning occurs. But it also true that it is very difficult for the patient to avoid that happening, or do much about when it does.
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But without the deconditioning narrative, how can we blame the patients?
 
Moderator note: Merged thread


I noticed there was no thread for this study when I was working on the discussion of orthostatic intolerance in UARS below and seemed like it probably deserved one. The pathway to orthostatic intolerance via hypovolemia in UARS seems relatively straightforward (repeated negative intrathoracic pressure during effortful inspiratory flow limitation → atrial stretch → ANP release → sodium and water excretion → hypovolemia), the question is: why do only some UARS patients have orthostatic intolerance? And why do only some ME/CFS patients (who I’m proposing are UARS patients, as you’ve probably realized by now) have hypovolemia? I'm hypothesizing that the compensation for ANP-mediated volume loss becomes impaired following limbic sensitization to inspiratory flow limitation in some individuals:
nataliezzz

Post in thread 'Sleep-disordered breathing (UARS/OSA) and orthostatic intolerance'



Here is the section of the recent clinician's round table hosted by Renegade Research where I discuss sleep-disordered breathing and orthostatic intolerance. I go into a bit more detail there on how orthostatic intolerance could fit in with Dr. Gold's theory (limbic sensitization/stress response to inspiratory flow limitation driving symptoms in sleep-disordered breathing patients) and why orthostatic intolerance typically emerges along with unrefreshing sleep/fatigue/etc. Specifically, I posit a two-part process:

1) Increased ANP → sodium & water...
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It looks like the abstract contains an error:

Abstract:
Twenty consecutive adults with ME/CFS participated in the study
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Text:
Due to the high cost of the blood volume measurements (3500 USD) and the loss of funding for these studies, patient enrollment was limited to the first 12 individuals.
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There’s no control group, and the studies they cite that had control groups and more participants for the most part found no differences between ME/CFS and controls.
 
Utsikt said:
It looks like the abstract contains an error:
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Lol yeah.
Utsikt said:
There’s no control group, and the studies they cite that had control groups and more participants for the most part found no differences between ME/CFS and controls.
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Here's the discussion of the studies:
Only a limited number of studies on blood volume have been performed in those with ME/CFS. Streeten and colleagues found in 12 female CFS patients that the RBC volumes were lower than that of female control subjects, but found in contrast that plasma and whole blood volumes were not significantly different from control subjects (6). Farquhar identified no significant difference in blood volume between ME/CFS patients and simultaneously studied age-matched controls (4), although there was a non-significant trend toward lower blood volume in those with ME/CFS. Hurwitz and colleagues examined 56 with ME/CFS (30 more severely affected and 26 non-severely affected). Total blood volume, erythrocyte volume, and plasma volume were not significantly different from 21 sedentary controls (5). However, when recalculating the reduction from ideal volumes, the percent total blood, plasma, and RBC volumes were all significantly lower in those with ME/CFS than in sedentary controls and also lower in those with severe ME/CFS compared to less severely affected individuals. Of interest, the mean absolute blood volume in our patient population (59 ml/kg) was mid-way between the values for those with severe ME/CFS (57 ml/kg) and non-severe ME/CFS (61 ml/kg) reported by Hurwitz et al. Newton et al. (16) found no significant difference for whole blood volumes between 41 with CFS and 10 healthy controls, but 68% of those with ME/CFS had a RBC volume below 95% of the expected mean volume for healthy individuals. Thirty-two percent had a normalized plasma volume below the lower limit of normal of 95%, suggesting a difference in the degree of reduction between plasma and RBC volumes.
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But importantly:
None of these studies classified participants according to the presence or absence of orthostatic intolerance.
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