Could oral / topical Minoxidil help CFS?

[borko2100]

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]

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]

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]

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.

 

[Mary]

@borko2100 , @datadragon - I'm tagging Dr. Phair here so hopefully he'll take a look at this thread. His PR user name is @HTester . You could also send him a PM to get his attention if you wanted. I find this thread quite interesting!

 

[hapl808]

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]

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]

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

 

[datadragon]

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/