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Maintenance of Chronic Fatigue Syndrome (CFS) in Young CFS Patients Is Associated with the 5-HTTLPR

Messages
16
Location
Norway
For those who think all is just well in Norway, think again. Certain people will always find (invent) a BPS explanation no matter what the findings are.

Here they have a genetic variation correlating to CFS prognosis. As the the faithful members of the "church of BPS" they are, they couple their genetic findings to mental health, and argue that therefore mental health is a maintaining factor of CFS! These guys are supposed to be the "experts in Norway" apart from Fluge &Mella.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0140883

Abstract
Earlier studies have shown that genetic variability in the SLC6A4 gene encoding the serotonin transporter (5-HTT) may be important for the re-uptake of serotonin (5-HT) in the central nervous system. In the present study we investigated how the 5-HTT genotype i.e. the short (S) versus long (L) 5-HTTLPR allele and the SNP rs25531 A > G affect the physical and psychosocial functioning in patients with chronic fatigue syndrome (CFS). All 120 patients were recruited from The Department of Paediatrics at Oslo University Hospital, Norway, a national referral center for young CFS patients (12-18 years). Main outcomes were number of steps per day obtained by an accelerometer and disability scored by the Functional Disability Inventory (FDI). Patients with the 5-HTT SS or SLG genotype had a significantly lower number of steps per day than patients with the 5-HTT LALG, SLA or LALA genotype. Patients with the 5-HTT SS or SLG genotype also had a significantly higher FDI score than patients with the 5-HTT LALG, SLA or LALA genotype. Thus, CFS patients with the 5-HTT SS or SLG genotype had worse 30 weeks outcome than CFS patients with the 5-HTT LALG, SLA or LALA genotype. The present study suggests that the 5-HTT genotype may be a factor that contributes to maintenance of CFS.

Depending on the localization of the 5-HTT relative to the 5-HT autoreceptors, this might decrease or increase the 5-HT signaling in the CNS. Hence, genetic variability in the gene encoding the 5-HTT has consequences that may be associated with mental health. Previous data have demonstrated that the S allele of the 5-HTTLPR may be linked to depression [22,23] and suicidality in relation to stressful life events [22]. Earlier studies also suggest that the S allele of the 5-HTTLPR is associated with neurocognitive impairment [24] and bipolar disorders [25]. In addition, variation in the 5-HTT gene SLC6A4 may modulate attention to threat [26], anxiety, negative affect and fear [10–12]. Moreover, the SS and SLG genotype seems to be associated with higher neuroticism [11], and a more serious symptomatic profile in patients who suffers from posttraumatic stress disorders [10]. Ultimately, it has also been suggested that the 5-HTT SS and SLG genotype may be associated with increased neuroplasticity making individuals more susceptible to environmental influences [13]. Hence, psychosocial aspects, bullying and stressful life events may have a more pronounced impact on adolescents with the 5-HTT SS and SLG genotype than other individuals. These data, together with the observations of the present study, indicate that the 5-HTT SS and SLG genotype may be a factor that contributes to the maintenance of CFS.
 

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia
Classic example of trying to spin a negative result into a positive one.

Only ~26% of the patients had the genotype they claim contributes to the maintenance of CFS. The P-value for the comparison of 5-HTT genotype in patients vs healthy controls was 0.55.


Significus.jpg

From: http://statistically-funny.blogspot.com.au/2014/03/if-at-first-you-dont-succeed.html
 

msf

Senior Member
Messages
3,650
Ah, the neuroticism that is a famous component of neurasthenia!

Morons.
 

SOC

Senior Member
Messages
7,849
Classic example of trying to spin a negative result into a positive one.

Only ~26% of the patients had the genotype they claim contributes to the maintenance of CFS. The P-value for the comparison of 5-HTT genotype in patients vs healthy controls was 0.55.
And of course we don't know what their patient cohort really was, so it's not even clear whether the 26% of the people with the genotype have simple chronic fatigue or the neuroimmune illness ME/CFS.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
And of course we don't know what their patient cohort really was, so it's not even clear whether the 26% of the people with the genotype have simple chronic fatigue or the neuroimmune illness ME/CFS.
Quite. I suspect that simplistic diagnostic criteria quite frequently confuse depression with CFS and vice versa, and does not address the core symptom of ME. So if they are not careful they will wind up with a large part of the cohort being depression.

Please note the first link is to the full paper. If I have the energy I might read it.
 

Sidereal

Senior Member
Messages
4,856
As far as I remember from the many papers churned out by this psychobabble group in Norway, they have made up their own case definition for paediatric CFS (three months of fatigue, that's it).
 

Sidereal

Senior Member
Messages
4,856
In accordance with previous studies of Caucasians or European Americans indicating a general 5-HTT SS or SLG genotype frequency of about 25% [6,10], the same genotype frequency was 26% in the patients and 21% in the controls. Thus, the 5-HTT genotype cannot explain why some individuals develop CFS. Interestingly however, we found that CFS patients with the 5-HTT SS or SLG genotype had a more pronounced reduction in physical and psychosocial functioning than patients with the 5-HTT LALG, SLA or LALAgenotype. This suggests that patients with the 5-HTT SS or SLG genotype have a less favorable 30 weeks outcome than patients with the 5-HTT LALG, SLA or LALA genotype.
 

Sidereal

Senior Member
Messages
4,856
Moreover, earlier in-vivo positron emission tomography studies have provided evidence that the SS and SLG subjects may display decreased expression of 5-HTT in the midbrain [21]. The result is a reduced 5-HT re-uptake, and a higher concentration of extracellular serotonin. This might have two possible consequences: 1) either increased negative feedback as a result of more available 5-HT near the presynaptic autoreceptors, or 2) increased signaling because of a higher concentration of 5-HT near the postsynaptic receptors of the cell membrane.

Depending on the localization of the 5-HTT relative to the 5-HT autoreceptors, this might decrease or increase the 5-HT signaling in the CNS.

These two possibilities could help explain why some here keel over from serotonergic drugs and supplements while others benefit.
 
Messages
16
Location
Norway
As far as I remember from the many papers churned out by this psychobabble group in Norway, they have made up their own case definition for paediatric CFS (three months of fatigue, that's it).

Yes they insist on using what they call "a broad case definition":

A broad case definition of CFS, requiring three or more months of unexplained, disabling fatigue worsened by physical or mental exertion, was applied
 

Sidereal

Senior Member
Messages
4,856
Or this association occurred due to chance like so many other similar small scale studies of genetics of this nature.

Well, this study didn't investigate serotonergic meds so there is no "association". This is just my personal speculation based on the biological mechanisms outlined and the range of reactions you see to these meds in the population at large.