Prurigo Pigmentosa (PP) is a skin rash that can establish itself when people transition to a ketogenic diet. If you want to know how it looks like then you’ll find plenty of examples on Google.
Obviously people who are affected by PP want to know what to do about it but also want to know what causes it.
In the following article where a dermatologist describes some background, the link with ketosis is very strong. Various cases that all lead to higher ketone production are affected by PP. There is some thought that there is inflammation triggered.
Linking the observations
Although what I’ll show in this article is in no way proven, the links are quite strong to suspect that I’m close to the reality. Just through observation we can find the following associations
- One of the things noted is that the affected areas often the areas where people produce more sweat.
- Asians seem to be more easily affected
- Case reports reveal that anti-biotics resolve/ammeliorate PP
- Ketosis is a necessary factor
The anti-biotics is already a strong indicator that it could be bacteria related. What is unique about ketosis are the metabolites that are produced which are acetoacetate, acetone and beta-hydroxybutyrate.
Acetoacetate is furder metabolised into acetone and beta-hydroxybutyrate. beta-hydroxybutyrate is confined in our blood and requires endothelial transfer via specific transporters. This doesn’t coincide well with the affected areas in the skin.
So acetone seems to be a good candidate to look into. It is the product that is known for the ‘keto-breath’ and evaporates easily. The affected areas are also on the upper skin, from the liver upwards.
OK, let’s see if there is a connection between bacteria and acetone. The article above described an inflammatory response to bacterial folliculitis.
The histologic presence of follicular bacterial colonies supports the theory that prurigo pigmentosa may be a reactive inflammatory response to bacterial folliculitis.
Looking into bacterial folliculitis we find the bacteria Staphylococcus aureus (Sa) popping up as a resident on our skin.
Bacterial folliculitis. This common type is marked by itchy, white, pus-filled bumps. It occurs when hair follicles become infected with bacteria, usually Staphylococcus aureus (staph). Staph bacteria live on the skin all the time. But they generally cause problems only when they enter your body through a cut or other wound.
What are the effects of acetone on Sa?
With Staphylococcus aureus and Streptococcus pyogenes, acetone washed forearms had 2- to 510-fold more organisms than the control arm (P = 0.0008 and 0.08, respectively). Similar results were noted with ether (average 1:62, P = 0.005). Candida albicans increased 2- to 200-fold (average 1:37, P = 0.002). This effect did not occur with Escherichia coli and Pseudomonas aeruginosa (P = 0.8). To determine the time required for natural replenishment of the antimicrobial substances, bacteria were applied 2, 3, and 5 hours after washing with acetone.
Wow, in this experiment they used acetone to wash away the anti-microbial substances! Acetone makes these bacteria on the skin thrive.
“SURVIVAL OF PATHOGENIC MICROORGANISMS ON HUMAN SKIN” (short link)
I found a second experiment from 1965 where acetone increased bacterial count in a similar way.
“Antibacterial action of human skin. In vivo effect of acetone, alcohol and soap on behaviour of Staphylococcus aureus.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2093882/?page=3
This establishes a clear link between acetone and bacterial growth, specifically Sa as the one that is very comfy on our skin.
Acetone and the skin
Those 2 papers applied acetone on the skin. Is the acetone really excreted through sweat when in ketosis? In the next paper they looked at skin acetone evaporation and found it in correlation with ketosis with emissions in the range of 0.00 to 2.70 ng/cm2/h in the studied patients.
“Feasibility of skin acetone analysis in patients with cardiovascular diseases” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6141450/
With certainty we see that anti-biotic treatment works due to the case reports. Probably not any kind of anti-biotic works, depending on the type of bacteria that is triggering the PP. Although everything seems to point to Sa, it would be a good guess to start with but until there is clear proof by sampling and analysis, we can’t say this for sure.
You could also try to treat it first through sun exposure. Sun exposure makes your skin produce vitamin D3. This results in the endogenously produced anti-biotic cathelicidin.
“The vitamin D–antimicrobial peptide pathway and its role in protection against infection” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821804/
If you are afraid of the sun or have no ability to expose your affected areas to the sun then vitamin D supplementation is also effective at increasing cathelicidin. I would recommend the sun though because this provides a much higher production of vitamin D.
After supplementation with 4000 IU/d oral vitamin D for 21 days, AD lesional skin showed a statistically significant increase in cathelicidin expression from a median of 3.53 relative copy units (RCU) before supplementation to a median of 23.91 RCU postsupplementation
“Administration of oral vitamin D induces cathelicidin production in atopic individuals” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2659525/
It counteracts the biofilm that the bacteria produce to protect themselves. This biofilm has also been linked with impeded wound healing.
The helical human cathelicidin LL-37 was tested against S. aureus, and was found to exhibit effective anti-microbial, anti-attachment as well as anti-biofilm activity at concentrations in the low μg/ml range.
“LL-37-Derived Peptides Eradicate Multidrug-Resistant Staphylococcus aureus from Thermally Wounded Human Skin Equivalents” https://aac.asm.org/content/58/8/4411
“PS-302 Human Cathelicidin Antimicrobial Peptide Ll37 Influences Staphylococcus Epidermidis´ Biofilm-associated Gene-expression And Biofilm Mass On A Medical Devise Surface” https://adc.bmj.com/content/99/Suppl_2/A220.3
“Natural and synthetic cathelicidin peptides with anti-microbial and anti-biofilm activity against Staphylococcus aureus” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3397408/
I’ve also scanned a few fora to see what people have tried and found helpful. They are listed here if I could find a reasonable link with either acetone or the bacteria since those 2 components are for sure involved.
- black seed oil (can also cause skin irritation)
- dandelion tea
- vitamin C (topical cream and/or oral intake)
“Anti-microbial effect of Nigella sativa seed extract against staphylococcal skin Infection” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219874/
“Characterisation of antimicrobial extracts from dandelion root (Taraxacum officinale) using LC-SPE-NMR.” https://www.ncbi.nlm.nih.gov/pubmed/25644491
“Immunomodulatory and Antimicrobial Effects of Vitamin C” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6798581/
As blood ketones go higher, the correlation with acetone seems to change in such a way that there is a higher increment in acetone. This study but also others I’ve seen indicate this. But the correlation doesn’t matter so much. Important to know is that as BHB goes up, so does acetone. So if you are affected, you could reduce your BHB levels while treating the bacterial issue or temporarily get off the ketogenic diet completely. You can still go low carb but just not in the ketogenic state.
“Acetone as biomarker for ketosis buildup capability – a study in healthy individuals under combined high fat and starvation diets” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4471925/
With this piece of information I hope whoever is effected now has a good idea what to do. If all turns out to be correct then first of all you are dealing with a bacterial infection in the skin. That is priority one to resolve.
Secondly, you are probably short in vitamin D. So get sun exposure or at least supplement.
You could combine vitamin D with anti-biotic treatment to get the best result.
If all else fails then there is always the possibility to reduce the ketone production but that doesn’t help you get rid of the bacterial infection.
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