Psoriasis And Seborrheic Dermatitis Are Both Caused by Antibiotics Induced Fungal Overgrowth
If you are one of those close-minded people who thinks that psoriasis is something entirely different than seborrheic dermatitis and surely not curable with fluconazole you may want to avoid reading this article.
In this post I will present you a testimonial of one seborrheic dermatitis sufferer who shared his experiences with his diagnosis and how it developed following the antibiotics treatment.
His words speak for themselves and if you know how stubborn and health destroying the yeast and fungal infections can be you will think twice next time you get strep throat and your doctor will prescribe you penicillin or amoxicillin which both support the fungal growth immensely.
Here is the testimonial of the above mentioned seborrheic dermatitis sufferer:
I came down with strep throat about three weeks ago and ended up getting the antibiotic called amoxicillin. I took it for 3 days and got a rash the following day. The rash didnt bother me cause I just thought it was a side effect. After the rash went away I started getting patches of dry skin and flaky eye brows right away. I went to the dermatologist and he said it was seborrheic dermatitis. But that wasnt the only symptom I got. I started getting fungus on my toe as well as heartburn, nausea, and a metallic taste in my mouth when I would eat. Im just really confused on what has happened and need help. After doing research I believe it has something to do with my gut.
by user #195623
OK, we don’t know what was that first rash he developed.
Maybe it was a fungal infection of the skin and maybe it was some kind of allergy or skin toxicity caused by amoxicillin or its metabolites.
And it doesn’t really matter, because all his symptoms if they would appear spontaneously and one at a time during the life they could be caused by a lot of different causes. But since they appeared all in a short period of time after the treatment with antibiotics the chances are that all problems share one cause.
Was that cause a fungal infection?
I am sure it was that!
It is fungal infection!
Fungus (and antibiotics induced dysbiosis) impaired intestinal peristalsis and fermentation leads to gas production and its release “the shorter way out”.
You know, if the gas is produced in the first part of the small intestine it is way easier for that gas to get out through the stomach (burping or slow gas release without even you noticing it) than releasing the gas as farts.
The gas produced in the upper part of the small intestine pushes against the stomach sphincters and this allows the stomach acid to go up into the esophagus.
This causes the heartburn!
Long-term leaking of the stomach acid this way decreases the pH in the mouth which causes the tooth decay!
Especially during the sleep when we lie and stomach acid can easily leak into the esophagus and mouth.
In some people this problem is so huge that they can’t sleep without having a few pillows under their head and upper part of the back in order to avoid acid leak out of the stomach.
And what causes that nausea?
The toxic gas (containing the nitrogen metabolites) produced by bacteria and fungi in the small intestine activates probably the chemoreceptors found in the stomach and this leads to nausea. It is the same as if you ate spoiled food (food in advanced stage of fungal and bacterial degradation). Because the process of rotting of food is nothing else what goes in your digestive tract if your body does not make enough stomach acid, pepsin, pancreatic enzymes, disaccharidase,…
Still don’t believe that Seborrheic dermatitis is a yeast/fungal infection?
Then read the next abstract of the study:
Seborrheic dermatitis is a subacute or chronic disease of the skin, affecting the seborrhea afflicted areas and presenting with erythema and desquamation. The inflammatory reaction towards the fungi Malassezia spp. is considered to have a basic etiologic connection with this disease.
The purpose of the present study was to monitor the therapeutic effects of the anti-fungal drug fluconazole in patients with seborrheic dermatitis. We compared two study groups of patients: Group I–27 patients with seborrheic dermatitis stage I, II and III, treated with fluconazole, 50 mg/day for two weeks. As topical therapy we applied clobetasol propionate 0.05% ointment. After the completion of the therapeutic course, 85% of the patients in this group were clinically cured and their symptoms faded away. Fifteen percent of the subjects in this group–mainly stage III seborrheic dermatitis patients, showed partial but significant clinical improvement. The specific fungal test for Malassezia spp. on Dixon agar was negative in 93% of the cases in this group.
Group II–eleven patients with similar clinical indexes were treated with fluconazole 50 mg/day only, for the same time period. The therapeutic results in this group were also satisfactory–31.5% of the patients were cured and 68.5% showed clinical improvement. In 74% of the patients the specific test for Malassezia spp. was negative after treatment. Fluconazole treatment in patients with seborrheic dermatitis proves to be successful, effective and safe.
Interesting results, what do you think?
50 mg of fluconazole daily for two weeks and a strong corticosteroid – 0.05% clobetasol propionate – applied topically, cured 85% of patients!
As you probably know topically applied corticosteroids are one of the worst things for your skin and that’s probably why the researchers in Group II used only 50 mg of fluconazole per day as a treatment of Seborrheic dermatitis.
This treatment cured 31.5% of patients and 68.5% of patients showed a clinical improvement. If you do a math actually 100% of people improved or were cured using only low dose fluconazole for two weeks.
Fluconazole is hard on the liver so it is not a drug you would want to take for a long time but this study proved that antifungal drugs can cure Seborrheic dermatitis.
We still have a lot of natural choices when fighting the fungal and yeast infections.
You can also use Nystatin but it’s up to you to decide if it is natural enough for you. In some countries it is sold as an over-the-counter antifungal as – cream, oral suspension or tablets.
There was also another study researching the fluconazole effects on Seborrheic dermatitis.
Sixty-three patients with mild-to-moderate SD were randomly allocated to receive either oral fluconazole 300 mg in a single dose per week or placebo, for 2 weeks. Twenty-seven patients taking fluconazole and 23 patients taking placebo completed the study and were analyzed. The SD area severity index (SDASI) score and the patient’s subjective assessment of pruritus and burning sensation were evaluated before and after treatment. Both the investigator and the patients were blinded to treatment.
A statistically significant improvement in SDASI score after treatment compared with baseline was obtained with fluconazole (p=0.01) but not with placebo. However, the difference between the treatment groups was not statistically significant (p>0.05). Subjective improvements in symptoms, such as pruritus and burning sensation, were observed in both groups but no statistically significant differences versus baseline were seen.
The results of this study indicate that fluconazole provides marginal and statistically insignificant benefit for the therapy of SD. However, larger studies using different dosages and/or durations of fluconazole therapy may provide a rationale for systemic use of fluconazole in SD.
I think that the biggest problem why there wasn’t better results is the design of that study itself.
Taking one 300mg dose of fluconazole per week for two weeks is not enough to get good results in my opinion.
I believe that most people involved in that study had Seborrheic dermatitis for a long time and it is not possible to eliminate the fungal infection and allow the body to recover in 2 weeks using only 600mg of fluconazole in two divided doses.
Especially considering the fact that fluconazole has not particularly long elimination half-life (considering the reason for what purpose it is taken):
Oral forms (capsule and solution) are quickly absorbed and bioavailability is nearly complete (about 90%). Plasma protein binding is low (11 to 12%) and fluconazole circulates as active drug. Distribution is extensive throughout the tissues and allows the treatment of a variety of systemic fungal infections. The average elimination half-life (t1/2) of 31.6 +/- 4.9h is long, with a minimum of 6 days needed to reach steady-state; thus, a loading dose (equal to double the maintenance dose) is recommended. The metabolism of fluconazole is not qualitatively or quantitatively significant. The main route of elimination is renal.
Fungal Psoriasis affecting the Lips
In 2012 the Indian doctors published a case study describing the case of 16 year old girl diagnosed with plaque psoriasis on her lips.
A 16-year-old unmarried woman presented with recurrent cracking of the lips indicated by the appearance of grayish white flakes since
October 2004, which, in due course, shed off leaving behind an apparently normal mucous membrane. Chewing roasted corn treated
with salt and lemon (bhutta) initially caused the lesions. Ever since, it has been a cause of its exacerbation. She never had any relief
with either systemic or topical treatment.
There was a positive history of psoriasis in her mother.
The clinical examination did not reveal any evidence of skin and/or nail psoriasis/psoriatic arthropathy or any other systemic
abnormality. Blood examination including total and differential leukocyte count, complete hemogram, and liver and renal function tests
Biopsy of the representative lesion was subjected to serial sections.
Submucosal vessels were dilated and congested. Periodic-acid-Schiff (PAS) stain revealed fungal hyphae and spores within the parakeratotic
layer. Colonies of Gram-positive cocci were also demonstrated on the surface of the mucosa. She was administered combination therapy,
comprising topical tacrolimus (0.1%) ointment and calcipotirol hydrate (50 μg/g) plus betmethasone dipropionate (0.5 mg/g) twice a day
for 7 days. A single bolus dose of fluconazole 450 mg orally was also administered. The response to treatment was favorable and the lesions
showed regression (Figure 3).
What I am especially interested in is that the submucosal “vessels were dilated and congested.” Isn’t that something very close to what I have been saying all that time from the start of this blog in 2013?
Here is the link to my article “My Psoriasis Cause Theories”.
Sure, there are the facts and thoughts in my old blog posts which are not as important as my further research but it has been almost 4 years since then so naturally, now I know more and I can connect the dots more straightforwardly.
You should imagine the smallest vessels in this picture as very tiny tubes which are just about 5-10 micrometers wide (red blood cells are about 8 micrometers wide) so just one red blood cell can flow through it at a time. And even the one RBC have to change the shape to get through the smallest micro-vessels (capillaries).
If you want to know how did I prove impaired blood flow in psoriasis plaque read my article “Glucose Levels In the Blood From Psoriasis Plaques”.
Psoriasis-like disease exists in plants, too. You can read about it in my article “The Viral, Fungal And Bacterial Cause Of Psoriasis”.
Fungal infections are responsible directly or indirectly in myriads of diseases.
Think about it!
1) Zisova LG. Fluconazole and its place in the treatment of seborrheic dermatitis–new therapeutic possibilities. Folia Med (Plovdiv). 2006;48(1):39-45.
2) Cömert A, Bekiroglu N, Gürbüz O, Ergun T. Efficacy of oral fluconazole in the treatment of seborrheic dermatitis: a placebo-controlled study. Am J Clin Dermatol. 2007;8(4):235-8.
3) Debruyne D, Ryckelynck JP. Clinical pharmacokinetics of fluconazole. Clin Pharmacokinet. 1993 Jan;24(1):10-27.
4) Virendra N. Sehgal, MD; Shruti Sehgal, MDS; Prashant Verma, MD; Navjeevan Singh, MD; Farhan Rasool, MD. Exclusive Plaque Psoriasis of the Lips: Efficacy of Combination Therapy of Topical Tacrolimus, Calcipotriol, and Betamethasone Dipropionate. SKINmed. 2012;10:183–184