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Could oral / topical Minoxidil help CFS?

borko2100

Senior Member
Messages
156
Some time ago I remember applying big amounts of Minoxidil topically for hair growth and coincidentally my CFS improved by a large degree around that time - I had much more energy and some of my symptoms disappeared almost completely for a few months, then they came back later. I know that a significant amount of the topical minoxidil got absorbed because I experienced hair growth in unexpected places, like my hands.

It seems strange how a hair loss drug could help CFS, but it turns out Minoxidil is a potassium channel opener and increases blood flow in general, things that seem like might be helpful for CFS. It is likely a coincidence, but maybe not, who knows. I need to do an experiment again and see if I improve again. If anyone wants to experiment, it seems like a safe drug to try for a month or two. Just beware of the unwanted hair growth that might occur. Thankfully it goes away completely a few months after you stop taking it.

Has anyone noticed something similar? What about oral minoxidil has anyone taken it?
 

datadragon

Senior Member
Messages
389
Location
East Coast, USA

Interesting that you found relief from your CFS using minoxidil and posted. Robert Phair believes that IL-1a may be stuck on (turned on) in those with CFS and one possible way to target that would be a reduction in IL-1a to break the cycle and suggested it may not require ongoing use. I have some research I put together on hair loss and one interesting finding is that Minoxidil treatment downregulated IL-1α expression by 0.3433-fold compared with untreated cells (P = 0.001) in human kerantinocytes. Keratinocytes are the primary type of cell found in the epidermis, the outermost layer of the skin. In humans, they constitute 90% of epidermal skin cells. If it helped you then perhaps its also helping in other types of cells and this should be mentioned to Robert Phair.

Minoxidil Downregulates Interleukin-1 Alpha Gene Expression in human keratinocyte Cells​

Higher concentration of inflammatory cytokine IL-1α (which increases C-reactive protein levels) is a potent inhibitor of hair follicle growth that causes inhibition as a secondary response. Although IL-1α is prominent in skin wounding repair and inflammatory responses, it is actually downregulated during the anagen (growth) phase of hair cycles. Minoxidil treatment downregulated IL-1α expression by 0.3433-fold compared with untreated cells (P = 0.001). https://pubmed.ncbi.nlm.nih.gov/30034189/
 

borko2100

Senior Member
Messages
156
Very interesting theory. It could well be that it indeed affects this cytokine at a systemic level too (given that enough is absorbed after topical application or taken orally). Maybe the improvements I had were due to immunomodulatory effects.
 

datadragon

Senior Member
Messages
389
Location
East Coast, USA
Very interesting theory. It could well be that it indeed affects this cytokine at a systemic level too (given that enough is absorbed after topical application or taken orally). Maybe the improvements I had were due to immunomodulatory effects.

Yes I would imagine that would be the case. They were studying hair loss and so were testing only the effect on human kerantinocytes. If the IL-1a cytokine is confirmed to be on and not shutting off, then this would be a far less problematic potential solution to try initially as far as side effects as one option. My personal experience was in using Rogaine 5% minoxidil foam which had less negative effects than the solution such as far less dryness. I stopped using when I felt that I was overinhibiting inflammation and tested as such since the research is showing its only when its overactive it will affect the hair growth, and so I would vote that its effects are at a systemic level.
 

hapl808

Senior Member
Messages
2,000
I have no idea what any of this means and my brain is off, but I've noticed that when I use Nizoral for my newfound seborrheic dermatitis on my face, I feel much less brain fog for an hour or two. I think it downregulates IL-1 or something, so is that the same mechanism being discussed here? I've always been confused by it. First I thought washing my face did it, but it only happens when I use Nizoral.
 

borko2100

Senior Member
Messages
156
I have no idea what any of this means and my brain is off, but I've noticed that when I use Nizoral for my newfound seborrheic dermatitis on my face, I feel much less brain fog for an hour or two. I think it downregulates IL-1 or something, so is that the same mechanism being discussed here? I've always been confused by it. First I thought washing my face did it, but it only happens when I use Nizoral.
There might be something to it. Nizoral is used as a hair loss product as well.
 

datadragon

Senior Member
Messages
389
Location
East Coast, USA
I think it downregulates IL-1 or something, so is that the same mechanism being discussed here?
Looks like the active ingredient of Nizoral (Ketoconazole) may work on IL-1A signaling. Ketoconazole, a potent but transient inhibitor of adrenal steroid hormone biosynthesis, inhibited IL-1 alpha induced increases in plasma corticosterone. When ketoconazole at 40 or 60 mg/kg was given l h prior to IL-1«,the IL-1«induced rise in plasma corticosterone was completely abolished. https://pubmed.ncbi.nlm.nih.gov/2369744/

One study demonstrated a 6% incidence of Acute respiratory distress syndrome (ARDS) in patients receiving ketoconazole 200 mg/d (n = 35) versus 31% on placebo (n = 36) (p < 0.01). Another study demonstrated a 15% incidence of ARDS in patients receiving ketoconazole 400 mg/d (n = 26) versus 64% on placebo (n = 28) (p < 0.002), and showed a statistically significant decrease in mortality in the ketoconazole group (15%) versus placebo (39%) (p < 0.05). https://www.researchgate.net/public...ention_of_Acute_Respiratory_Distress_Syndrome

Regarding Dr Phairs latest video about IL-1
This article confirms IL-1 can induce production and release of more IL-1, a process described as an autoinflammatory loop. Anakinra is a bio-engineered form of the naturally occurring interleukin-1 receptor antagonist (IL-1ra) that blocks the action of interleukin-1. It is routinely used in patients with autoimmune and inflammatory disorders and MAS. Within the IL-1 family of cytokines, several inhibitory mechanisms are in place to prevent runaway inflammation induced by IL-1α or IL-1β. The main mechanism is the IL-1 receptor antagonist (IL-1Ra), which blocks the IL-1R1 and prevents binding of IL-1α and IL-1β. In contrast to JAKinibs, anakinra will not directly block the IFN-STAT1/STAT2 pathway critical for host defense against viral infections. Third, in contrast to tocilizumab (an IL-6 inhibitor), it targets and inhibits the core mechanism in the pathogenesis of MAS, namely the hyperactive inflammasome loop https://ccforum.biomedcentral.com/articles/10.1186/s13054-020-03166-0

This one metions neutralization of IL-1α inhibits the antiviral activity of IFN-γ by 90%, whereas no inhibition of type I IFN activity was observed. Indeed, the antiviral activity of IFN-γ depends largely on the basal level of NF-κB, which is maintained by constitutively expressed IL-1α. https://www.sciencedirect.com/science/article/pii/S1568997221000227#s0070
 
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datadragon

Senior Member
Messages
389
Location
East Coast, USA
Vitamin K2 affected the expression of proinflammatory cytokines during inflammation and infection, the MK-7 form of vitamin K2 is able to dose dependently inhibit TNF-a, IL-1a, and IL-1b gene expression. Vitamin K has been shown to act as an anti-inflammatory by suppressing nuclear factor B (NF-B) signal transduction and to exert a protective effect against oxidative stress by blocking the generation of reactive oxygen species . https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6747195/