Health Boards
Mon-16-07-2012, 19:01 PM
That psoriasis is called an autoimmune disease is already known for decades. We must realize ourselves that that suggests more than it clarifies.
It suggests that we understand the disease as we know both cellular and humoral events in the immune system. These are, however, only reactions, reactions of the immune system, not the cause of disease.
The auto antigens to which the psoriasis-specific T lymphocytes are aimed are still not defined and that isn't different for many autoimmune diseases.
Both for the pathogenesis as for the treatment this knowledge delivers little because it doesn't tell anything about the root cause of this disorder. Of course we can paralyze the immune system with immunosuppressors, but that gives always great risk's. We do not have the immune system, for nothing and the suppression of it can lead to other serious diseases.
Naviaux, director of the Mitochondrial and Metabolic Disease Center at the University of California mentions in The Spectrum of Mitochondrial Disease dozens of degenerative diseases that are wholly or partly based on mitochondrial mutations (6).
Various abnormalities of the citric acid cycle are then listed, but also M Alzheimer, M. Parkinson M.S., SLE, R.A and many others. Some of which are known under the generic name: auto-immune disease.
In 2004 a thesis appears on the above, citing NHR Litjens at Leiden University which deals on the effects of fumarate (7).
In vitro cell cultures were incubated with various components of the citric acid cycle and fumaarzuuresters. The efficacy of MEF (Mono-ethylfumarate) was negligible, DMF was a good second and MMF (monomethylfumarate) was most active. MMF is a substance that is not itself available as a medicament. This substance is formed in the intestine by demethylation of DMF, according to Litjens.
Previously Nieboer et al (8) in a clinical trial already had found that MEF in itself does not have an antipsoriatic effect.
That Schweckendieck healed himself in 1959 of psoriasis with the help of fumaarzuuresters, as in the thesis is stated, is not entirely correct. Schweckendieck accomplished this result with fumaric acid (9). To achieve his goal Schweckendiek had to use doses in grams, with unpleasant gastrointestinal complications. Later he carried on using fumaarzuuresters, stating that the difference between the acid and its esters is gradual, not essential, according to Schweckendiek.
Following the in vitro study, Litjens continued his studies in various groups of healthy volunteers and psoriasis patients over time. It was only aimed at examining the influence of the fumaarzuuresters, in particular of DMF. MMF which results from the hydrolysis of DMF, is intracellular further hydrolysed to fumaric acid, and then ends up in the citric acid cycle "as a fuel".
It follows that the stimulation of the citric acid cycle is that of having a regulatory effect on the immune system, in particular, to certain characteristics of psoriasis cells in the skin (T lymphocytes and dendritic cells) and on the cytokynebalance.
In the next paragraph below titled "DMF versus MEF" is the literal text of the thesis cited, showing that stimulation of the mitochondria according Litjens the purpose of the fumarate treatment.
This is based on the above finding and is also very obvious, but curiously we find nowhere this link back into the summary or in the hypothesis of this thesis.
There the author only repeats the usual classification of psoriasis as an autoimmune disease.
Regarding the side effects of this treatment in the final conclusion is said: "The adverse reaction profile of the fumarate-therapy is usually mild and temporary, the fumarate-herapy can therefore be seen as a safe anti-psoriasis therapy which can be used for a long term."
It suggests that we understand the disease as we know both cellular and humoral events in the immune system. These are, however, only reactions, reactions of the immune system, not the cause of disease.
The auto antigens to which the psoriasis-specific T lymphocytes are aimed are still not defined and that isn't different for many autoimmune diseases.
Both for the pathogenesis as for the treatment this knowledge delivers little because it doesn't tell anything about the root cause of this disorder. Of course we can paralyze the immune system with immunosuppressors, but that gives always great risk's. We do not have the immune system, for nothing and the suppression of it can lead to other serious diseases.
Naviaux, director of the Mitochondrial and Metabolic Disease Center at the University of California mentions in The Spectrum of Mitochondrial Disease dozens of degenerative diseases that are wholly or partly based on mitochondrial mutations (6).
Various abnormalities of the citric acid cycle are then listed, but also M Alzheimer, M. Parkinson M.S., SLE, R.A and many others. Some of which are known under the generic name: auto-immune disease.
In 2004 a thesis appears on the above, citing NHR Litjens at Leiden University which deals on the effects of fumarate (7).
In vitro cell cultures were incubated with various components of the citric acid cycle and fumaarzuuresters. The efficacy of MEF (Mono-ethylfumarate) was negligible, DMF was a good second and MMF (monomethylfumarate) was most active. MMF is a substance that is not itself available as a medicament. This substance is formed in the intestine by demethylation of DMF, according to Litjens.
Previously Nieboer et al (8) in a clinical trial already had found that MEF in itself does not have an antipsoriatic effect.
That Schweckendieck healed himself in 1959 of psoriasis with the help of fumaarzuuresters, as in the thesis is stated, is not entirely correct. Schweckendieck accomplished this result with fumaric acid (9). To achieve his goal Schweckendiek had to use doses in grams, with unpleasant gastrointestinal complications. Later he carried on using fumaarzuuresters, stating that the difference between the acid and its esters is gradual, not essential, according to Schweckendiek.
Following the in vitro study, Litjens continued his studies in various groups of healthy volunteers and psoriasis patients over time. It was only aimed at examining the influence of the fumaarzuuresters, in particular of DMF. MMF which results from the hydrolysis of DMF, is intracellular further hydrolysed to fumaric acid, and then ends up in the citric acid cycle "as a fuel".
It follows that the stimulation of the citric acid cycle is that of having a regulatory effect on the immune system, in particular, to certain characteristics of psoriasis cells in the skin (T lymphocytes and dendritic cells) and on the cytokynebalance.
In the next paragraph below titled "DMF versus MEF" is the literal text of the thesis cited, showing that stimulation of the mitochondria according Litjens the purpose of the fumarate treatment.
This is based on the above finding and is also very obvious, but curiously we find nowhere this link back into the summary or in the hypothesis of this thesis.
There the author only repeats the usual classification of psoriasis as an autoimmune disease.
Regarding the side effects of this treatment in the final conclusion is said: "The adverse reaction profile of the fumarate-therapy is usually mild and temporary, the fumarate-herapy can therefore be seen as a safe anti-psoriasis therapy which can be used for a long term."