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The Seborrheic Dermatitis thread
@jaj I have answered you in the other thread, but I feel that this info might help here as well since it's about seb derm and ALDH.
So I have explained above that I suspected a vE deficiency as per the blood results. With further investigation, I found that the lab value given on this test are highly unusual ; 12.1 - 20.3 ug/ml.
As per google and as per my french lab the usual value for vE are : 5-6 to 15-17 ug/ml. Their seem to be lots of variation between labs on this one so not sure that the "proper range" is known at all.
Anyway, so as per my french lab and the ranges I have found on google I'm no deficient at all. This would make sense to me but IDK.
So I'm coming to what I wanted to share with you : Now that I recall correctly, I think that I had a skin reaction to vitamin C as well. We know that vitamin C could reduce ALDH right ? I wonder if vitamin E could do the same ? Did you or Dr Smith investigated this already ?
I find it strange that both "anti oxydant vitamins" seems to worsen my seb derm. If I refer to my toxicology classes, vitamin C should recycle vitamin E, thus both make a great ROS scavenger team. Not sure how I should interpret the worsening of SD when using both - HERX ? Slowed ALDH thus excess aldehydes ? This SD is a true chinese puzzle
Garrett Smith has linked to published manuscripts that indicate Vitamin E slows both ADH and ALDH.
I've been trying a Vitamin E supplement myself lately, based on results from a Spectracell test indicating deficiency, and it seems to bring on symptoms of Vitamin A toxicity like sore aching muscles and joints, headaches, and a weird sensation I've been getting in my sinuses after going on a low Vitamin A diet.
The user @rockarolla has posted many times about the "dark side" of antioxidants. I believe the basic message is that they suppress an appropriate immune response. I wasn't sure what to make of that commentary for a while, but I'm starting to come around to the same opinion after reading more about the pro-oxidant effects of Vitamin C. Namely, it appears that nutritional antioxidants like Vitamin C and Vitamin E can suppress ROS signaling, which was thought to be a good thing because ROS is associated with inflammation, but this seems now to be a case of killing the messenger rather than the root of the problem that is sparking the ROS production in the first place.
I'm not sure where endogenous antioxidants like glutathione and alpha lipoic acid fall, but I'm guessing their function is going to be inherently different from antioxidants like C and E due to the fact that they are produced by our own bodies. Of course, most animals do produce their own Vitamin C endogenously, so I think in humans Vitamin C only becomes problematic when it's supplemented beyond what you would normally be able to get from food (which is going to be a pretty small amount if you eat only locally sourced foods in season in temperate climates).
Glancing at nutrition tables, it seems like you're unlikely to get much Vitamin C or E unless you're eating foliage and/or eating extracted oils, both of which I would say are pretty unnatural in a pre-agricultural context. Vitamin E seems to be closely associated with unsaturated fats because its primary purpose is to prevent the oxidation of those fats, so you probably wouldn't expect to eat or need much Vitamin E unless you were ingesting a bunch of PUFAs.
Our endogenously produced antioxidants seem to be sulfur-based, which would make a lot of sense if the baseline human diet was heavy in meat.
Lowering levels of retinoic acid is what will improve seb derm, one could be following a low vitamin A diet for 2 years and see little benefit if their liver stores are still high. People that try out a low vitamin A diet for a few months and then claim it's not helpful don't understand its purpose. If one has Hypervitaminosis A then one should follow a low vitamin A diet until they have normalized their liver levels, regardless of it it's improving their health noticeably or not. If one doesn't have Hypervitaminosis A there's really no point in following a strict low vitamin A diet.
To ensure a low vitamin A intake one needs to strictly avoid fortified foods and dairy products that contain any fat as well as fruit and vegetables containing significant beta-carotene. Even small amounts of dairy products are allowed if they are low fat. Because of the need to often avoid vitamin A long term there needs to be as few rules as possible. As long as one consumes a diet that is low in mcg RAE serum retinol will reduce over time. Regular consumption of legumes and fish is very important IMO and all food groups except dairy play a role in a nutritionally sound diet but at the same time there's no need to eat a whole foods diet.
H2O2 works, is it stinging a lot when you apply it? Use a towel or tissues to remove any sebum from the area and then use a spray bottle to apply 6% H2O2. It can look worse for a day before it heals.
My seb derm did improve quickly but it was still there. What changed at the start was how frequently I needed to use H2O2.
Your vitamin D is quite low. I don't recommend any supplementation of E or D or anything but you should definitely try to sunbathe when you can. Sunbathing seemed to help with seb derm on my chest too. Hypervitaminosis A depletes vitamin E so even if there are other factors lowering E reducing A should help.
I think you mean 581 mcg/L?
From my experience of worsening skin, it related to aldehydes rather than retinoic acid. However, I have not had a SD diagnosis and mine may be more rosacea. I had it when I was vA toxic and it has flared up again post covid, where I have become very aldehyde intolerant again. These facts pushed me to look at the NAD deficiency work, as NAD is the ALDH cofactor.
However, the aldehyde and the retinoic acid theories do not seem to be mutually exclusive to me. They are both grounded in vA toxicity. Why not both. ALDH enzymes could fluctuate with a build up of aldehydes creating a skin sensitivity and then a sudden rush of retinoic acid flairing it up. Just a thought.
Tim’s experience is pretty good evidence that the cause of SD (at least for some) is rooted in vA toxicity. VA just adds a large extra aldehyde burden on the body. This then converts to the very nasty retinoic acid. Mat, your serum vA is still very high. This is a sure sign of vA toxicity. Low serum retinol doesn’t indicate no vA toxicity (can be trapped in liver) but high serum retinol does indicate too much.
@wavygravygadzooks Yeah you're right I believe that I've read something about vE slowing ALDH. This would fit the aldehydes overload induced by it thus the worsening of seb derm @jaj you're right.
Also, I agree that it's pretty hard to have the RDA vE without seed oil. So not sure how this would be possible without it, except by eating buckets of nuts, mango or olives. And the PUFA/vE link is also very much understandable as per the instability of PUFAs.
Again, I don't doubt that hyper vA is very much a cause of seb derm. I have observed that many people who went on accutane for acne developp SD after. So no doubt on that. But yes, I feel that there might be more to it, and that the model I explained at the start of the thread is still very much on the table and it include vA in it. It is for sure a very strong aldehydes source too.
@tim-2 I corrected it - I meant 581 ng/ml so yeah same thing. At the start of the vA journey it was less but +/- similar. On my French lab this value is on the "lower side" of the range so I assumed it was a low serum, but I guess it is not after reading you. What would you consider "out of the hyper vA range" ? I'm aware that low serum vA doesn't exclude hypver vA (liver stellar cell storage) but I guess that if from that point of 581 ng/ml in 6 month of low vA (so 1year total) I see my serum fall down significantly, it will mean that store are depleted. And then I guess I'll be able to assess if yes or no vA is driving my SD.
Yeah that is what I'm following regarding the diet. No fortified food in France or very very little and if so, clearly indicated (and I eat whole food anyway). Regarding the vD yeah I've tried some supps in the past to raise it but felt nothing. I do try to expose myself to the sun but I feel It will resolve itself with proper exposure (like now) but once the liver/deeper cause are resolved.
Regarding the H2O2 - I've used it in the past for some days and it worked but then stop working. I have no explanation for it... I started again today exactly like you said. I don't feel much of a "sting" sensation, but I can see that it "does something" tho it's very short lived. At what frequency did you apply it ? 1x every night ?
When I was listening to a bunch of Morley Robbins talks, I remember him claiming that excessive Vitamin C led to the production of hydrogen peroxide (I think by oxidizing iron?), and that Vitamin A was involved in "cleaning up" that hydrogen peroxide. I haven't read anything since then about an interaction between Vitamin A and hydrogen peroxide, but it's something you might look into if it seems like H2O2 has benefits for SD and you're not sure why... Maybe H2O2 applied to the affected skin somehow depletes local stores of Vitamin A?
But yes, I feel that there might be more to it, and that the model I explained at the start of the thread is still very much on the table and it include vA in it. It is for sure a very strong aldehydes source too.
The main sources of aldehydes are formaldehyde from pectin consumption and acetaldehyde from alcohol consumption. Aldehydes from retinoid metabolism are present in much smaller amounts. Grams vs micrograms. The most toxic retinoid is an acid but it's not toxic because it's an acid. Even when one is fasting the endogenous production of formaldehyde is much higher than any other source of aldehydes.
What would you consider "out of the hyper vA range" ?
I think it was @orion that posted a helpful graph showing serum retinol dynamics. I think it's best to be below 40 mcg/dL. Normally the body is quite resistant to having a serum retinol much above 50 in order to protect itself. 58 can indicate severe Hypervitaminosis A where the body can no longer totally control the serum retinol level and retinoic acid is at toxic levels. It may take years for you to get to 40.
Regarding the H2O2 - I've used it in the past for some days and it worked but then stop working. I have no explanation for it... I started again today exactly like you said. I don't feel much of a "sting" sensation, but I can see that it "does something" tho it's very short lived. At what frequency did you apply it ? 1x every night ?
What percentage H2O2? 6% on seb derm stings a lot for a few minutes and the seb derm will become very red before it heals.
The main sources of aldehydes are formaldehyde from pectin consumption and acetaldehyde from alcohol consumption. Aldehydes from retinoid metabolism are present in much smaller amounts. Grams vs micrograms. The most toxic retinoid is an acid but it's not toxic because it's an acid. Even when one is fasting the endogenous production of formaldehyde is much higher than any other source of aldehydes.
Yes. For me, alcohol and fruits (as well as legumes but less so I think) will worsen my SD. Fasting also will worsen my SD.
Like @jaj said, I dont think that aldheydes overload and hypervA are mutually exclusive. Maybe they can "nurture" each other somehow. Maybe they work in tandem to generate SD.
A little bit like what I'm doing now at work, experimenting on Tau wt alone vs Tau wt TDP43 wt and the impact on alzheimer disease. Both mutation will damage the mitochondria, but both at the same time will make even more damage in a "synergy way".
IDK. Maybe you're right and it's vA only. I guess we'll see how I will report !
What would you consider "out of the hyper vA range" ?
I think it was @orion that posted a helpful graph showing serum retinol dynamics. I think it's best to be below 40 mcg/dL. Normally the body is quite resistant to having a serum retinol much above 50 in order to protect itself. 58 can indicate severe Hypervitaminosis A where the body can no longer totally control the serum retinol level and retinoic acid is at toxic levels. It may take years for you to get to 40.
Noted. If you are right, indeed I'm far from it.
Regarding the H2O2 - I've used it in the past for some days and it worked but then stop working. I have no explanation for it... I started again today exactly like you said. I don't feel much of a "sting" sensation, but I can see that it "does something" tho it's very short lived. At what frequency did you apply it ? 1x every night ?
What percentage H2O2? 6% on seb derm stings a lot for a few minutes and the seb derm will become very red before it heals.
10%. It does become very red, then improve yes but in an incomplete way. I can see it does something, but short lived. That is why I wanted to know the frequency at where you applied it ? 1x per day ? 2x per day ?
Maybe I need to do it for several days before seeing more improvment.
@mat may I ask if there are specific areas where do you get SD? I get it almost exclusively on eyebrows and between, looks like wearing glasses irritates this area somehow, but what exactly is the mechanism of this mechanical stimulation, more sebum production, more cell renewing .. ?
Right before going on low vit A my SD was at it worst affecting other areas of the face. On my last serum test vitamin A was below the range, I don't remember if I had SD at that time. Also not sure if Accutane toxicity would appear on vitamin A test.
Quote from grapes on February 24, 2022, 12:25 am@mat may I ask if there are specific areas where do you get SD? I get it almost exclusively on eyebrows and between, looks like wearing glasses irritates this area somehow, but what exactly is the mechanism of this mechanical stimulation, more sebum production, more cell renewing .. ?
Right before going on low vit A my SD was at it worst affecting other areas of the face. On my last serum test vitamin A was below the range, I don't remember if I had SD at that time. Also not sure if Accutane toxicity would appear on vitamin A test.
I get it on the side of the nose + on the cheeks up until the eyebrow limit (a little bit like the butterfly shaped lupus) as well as forhead, scalp, ears, beard. Mine is very bad.
Not sure of the specific mechanism that will generate the lesion at X or Y spot. But seems plausible that glasses will generate more irritation thus more lesions.
So basically, you're saying that you have lower vA value than what @tim-2 said (< 40 mcg/dL) and still have SD ? For how long have you followed the diet until you reach this value (how much is it by the way?) and did you noticed improvment in the SD area at least ?