Im sure some of you here have read about this "cure" before. Dr. Maebashi National Akita Hospital in Japan. I am going to give it a whirl because I also suffer from the dreaded, very painful condition know as sternocostaclavicular hyperstotosis, basically its severe swelling, pain and distruction of the clavical joints, what our US Dr.s refer to as psoriatic arthritis. I get pustular psoriasis on hands, feet, and have widespread plaques. I have tried many food alterations with great success in the past, it always returns.

This Dr. states that there is high prevelance of psoriasis in people who smoke ciggaretts. How many people here smoke?
He claims you need to quit to eliminate the body of this immune dysfunction. The body typically breaks out with psoriasis when strep strikes. Antibiotics can mess up the gut flora, making us biotin resistant. The treatment is B vitamin Biotin, and a probiotic agent Clostridium butyricum Miyairii, which a company was trying to get FDA approval for, they named it CDACTIN-OI. I don't know what this Dr. suggests as far as purity, brand, and dose of either of these for effective treatment. I am going to email him. I was going to do this last year but dropped the ball because I couldnt get my hands on the Clostridium butyricum Miyairii.
Here is some info from an article a patient of his wrote that attended one of his lectures. She was treated and is cured and reportedly has been for years now.

The patients had metabolic abnormalities and subsequent immune dysfunction as a result of biotin deficiency. Biotin plays an important role as a coenzyme of various enzymes related to the metabolism of glucose, fatty acids and branched-chain amino acids. Thus, its deficiency causes serious metabolic abnormalities and adversely affects immune function. In fact, low serum biotin concentration, impaired glucose metabolism, reduced serum levels of fatty acids and abnormal composition of serum amino acids were observed in the patients. Other features of the patients include increased serum levels of 2-globulin and -globulin, an increased IgA level ,a marked increase of helper T lymphocytes, reduced numbers of suppressor T lymphocytes. ( These indicate abnormalities of immune function.) Also, an inverse correlation between helper T cells/suppressor T cells and serum biotin concentration was observed.

(This means that biotin deficiency is implicated in the occurrence of immune dysfunction.) In cases with severe bone lesions, there occurred an increase of Th1/Th2 in T lymphocytes.

In accordance with the concept, rats fed on a biotin-deficient diet showed similar skin and bone disorders, metabolic abnormalities and immune dysfunction. These findings suggested the possible therapeutic efficacy of biotin to the patients.


Treatment

Nonsteroidal anti-inflammatory drugs are of no effect to correct the eruptions, although the patients might be temporally free of the chest pain , and immune issues, plaques or pustuals. Their long-use may be associated with rapidly developing arthropathy, because occurrence of immune dysfunction and inhibition of the synthesis of prostaglandins relating to bone remodeling.
Oral administration of biotin to the patients alleviates chest pain after 1~2 weeks and almost eliminated within 4 weeks. Abnormal bone shadows on radiographs shows normal figures after 2 to 3 years administration, if the bone damages are not advanced. Pustular eruptions and plaques disappear usually on the palms after 3 to 4 months and on the soles after 5 to 7 months. All of the biochemical and metabolic abnormalities were corrected soon. Immune dysfunction normalizes within 2 years. Complications, such as diabetes mellitus and IgA nephropathy, were also improved in a short time.

In the patients, frequent episodes of severe constipation or diarrhea were observed prior to the occurrence of the disease. Serum biotin concentration remained to be low and unchanged even after oral administration of the vitamin. Since biotin is mainly produced by microflora in the intestine and absorbed from the intestine into the circulation. It is, therefore, suggested that biotin deficiency may be attributable to the proliferation of harmful microflora in the intestine to digest or to degrade the vitamin. However, supplementary administration of a probiotic agent, Clostridium butyricum Miyairii, to the biotin treatment significantly increased serum biotin concentration and maintained the concentration high enough to improve clinical manifestations and other disorders including complications, because the probiotic agent prevents the proliferation of the harmful microflora in the intestine and intensifies the therapeutic action of the vitamin with no evidence of hematological, renal and hepatic toxicity. Supplementation of other probiotic agents such as Lactobacillus showed poor therapeutic effectiveness to the biotin treatment.