This is not about LDN; I took a gummy bear of CBD/THC for the first time in years. I have never taken LDN. This is about attribution of improvement due to ingestion of a substance, a med for instance.
I have FM for 27 years now, and not ME/CFS by Institute of Medicine diagnostic criteria (I don't have orthostatic hypotension or cognitive dysfunction severely (ie more than half the time).
I wanted to add that my FM pain came back after I wrote the post along with the weather clouding up.
So, in my humble opinion, or at least for me, my mood (I would term how I feel as a form of mood) is like the weather (depending where on the planet you live).
For me, I could devise my personal objective outcome measures of improvement. (This would be leaving the house every day, driving to a trail for a walk, talking in person to someone for two hours without PEM, or flare up. Being able to do cognitive tasks after 2pm).
So, stratification of research subjects by levels of impairment and perhaps symptomatology for objective outcome of improvement is key.
Again, the fallacy of post hoc ergo...."after this therefore because of this" does not prove causality.
I am aware this wasn’t about LDN.
My ESR rate has significantly declined. This is true of others.
The use of low-dose naltrexone (LDN) as a novel anti-inflammatory treatment for chronic pain
https://link.springer.com/article/10.1007/s10067-014-2517-2
Association with general markers of inflammation
As clinical research of LDN is still in its infancy, we do not have studies in humans that parallel the work performed in animal models. However, some indirect evidence supports the concept of LDN as a novel anti-inflammatory. In the initial pilot study of LDN in fibromyalgia [
15], baseline erythrocyte sedimentation rate (ESR) was a significant predictor of clinical response to LDN. ESR is a commonly employed clinical test that is sensitive to both chronic and acute inflammatory processes [
33]. In our study, individuals with greater ESR at baseline experienced a greater drop in pain when taking LDN, despite that fact that FM is not considered to be a classic inflammatory disorder, and ESR values were in the normal to high-normal range.
We have now collected more data on the relationship between baseline ESR and LDN (38 individuals with fibromyalgia in total). Aggregating across studies (Fig.
2), we see that fibromyalgia patients with greater ESR levels at baseline tend to have greater pain reduction when taking LDN (left pane;
r = 0.58,
p = 0.0001). In contrast, there is no association between baseline ESR and pain reduction during placebo administration (right pane;
r = 0.06,
p = 0.744). Each participant received both LDN and placebo in a blinded fashion. The difference in correlations is significant (
z = 2.52,
p = 0.012), suggesting that the clinical effect of LDN may be physiologically associated with the reduction of inflammation. Unfortunately, as we collected ESR only as a screening blood test (to exclude major inflammatory disease), we did not measure ESR at the end of the LDN condition and therefore cannot determine if LDN responders had a significant decrease in their ESR.
Reduced Pro-Inflammatory Cytokines after Eight Weeks of Low-Dose Naltrexone for Fibromyalgia
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5489802/
3.2. Main Results
In our primary analyses, we found the following inflammatory plasma markers to be significantly reduced at Drug compared to BL: IL-1β, IL-1Ra, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12p40, IL-12p70, IL-15, IL-17A, IL-27, IFN-α, TGF-α, TGF-β, TNF-α, and G-CSF ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5489802/table/biomedicines-05-00016-t002/']Table 2). The concentrations of these cytokines are presented, for each two-week block, in Figure 1. In addition, as a demonstration of individual cytokine levels over the study period, we present each individual’s TNF-α concentrations for the entire study period in Figure 2. We also found a significant reduction of FM-associated pain (15%), and overall symptoms (18%) at Drug compared to BL.
4. Discussion
The goal of this study was to test if LDN administration is associated with reduced markers of inflammation in FM. We found that, after eight weeks of LDN administration, plasma levels of a range of broadly pro-inflammatory cytokines were decreased. In addition, we found that participants reported less pain and symptoms following LDN. Combined, these results support the hypothesis that LDN may help chronic pain conditions, such as fibromyalgia, by acting as an atypical anti-inflammatory medication.
FM is not a classical inflammatory or immune-mediated condition, but the immune system is thought to be a part of its complex pathophysiology [9,17]. However, existing literature on inflammatory abnormalities in FM was insufficient to allow us to predict which specific cytokines would respond to LDN [18]. Therefore, we examined a large array of cytokines. After correcting for multiple comparisons, we found that the cytokines most suppressed by LDN are known to promote nociception, allodynia, and hyperalgesia, including TNF-α, IL-1β, IL-2, IL-6, IL-15, and IL-17 [19,20].
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