Psoriasis Severity is Correlated With the Fibrinogen Levels
From the beginning of this blog I claim that psoriasis is caused by low oxygen levels in the body and skin. I say the cause or at least huge contributing factor is thick blood what causes bad blood flow mostly in the microvessels which are naturally so narrow that even one red blood cell must be really flexible to go through it.
Fibrinogen – inflammation and thick blood
What role does the fibrinogen play in psoriasis pathogenesis?
Well, fibrinogen is a glycoprotein synthesized in liver which is converted to fibrin by thrombin during the coagulation process. Fibrin together with the platelets form the blood clot during some injury like when you cut your finger.
Fibrin is your friend in cases like acute injury but sometime may become an enemy because a lot of fibrin formation leads to thickening of the blood and even thrombosis. Thick blood caused by high generation of fibrin strands is by some researchers suspected as the underlying factor contributing to many diseases like CFS, fibromyalgia, depression, anxiety, worsening of eyesight, tinnitus, fungal infections of the skin, nail fungus, Crohn’s disease, bad digestion, …
The authors of one study in Turkey measured the inflammatory markers and associated hypercoagulability in patients with psoriasis.
The scientists concluded that “although not reaching statistical significance, the fibrinogen levels for the study group were higher” than in control group.
The scientists were clever enough to point out that fibrinogen levels were higher in psoriatics even though statistically were not high enough.
And that’s why we should not believe in statistics so much.
Because you need to look at the whole problem more closely and in broad terms. We need to check also the other blood clotting factors like – antithrombin-III which inactivates the serine protease enzyme – thrombin.
And guess what? The results in study showed that antithrombin-III levels in psoriatics were significantly lower.
Also the activity of protein S and protein C – the two vitamin K dependent glycoproteins involved in anticoagulation was found to be lower in psoriatics. 
In summary psoriatics have:
- higher fibrinogen: increase the chance to form a clot
- lower antithrombin-III: increase the chance to form a clot
- lower protein C: increase the chance to form a clot
- lower protein S: increase the chance to form a clot
And suddenly we got 4 different glycoproteins involved in coagulation cascade which blood levels in psoriatics predispose them to increased blood clotting.
One very interesting fact found in this study is that fibrinogen levels positively correlated with folic acid levels and negatively with antithrombin-III.
Another fact is that psoriatics had significantly lower levels of folic acid in their blood than the controls.
This is actually an interesting information since there are some people (like those with CFS – Chronic Fatigue Syndrome) who claim that folic acid makes them feel bad. This may be caused by increase in fibrinogen and decrease in antithrombin-III which can possibly lead to worsening of the oxygen transport to the brain and whole body.
However folic acid may greatly help with the detoxification so some sort of detox or die-off reaction is also possible.
Inflammatory markers in psoriatics treated with Enbrel
In another study from 2011 the authors measured the inflammatory markers in psoriatics treated with etanercept (patients know this drug under its trade name as Enbrel).
Note: Etanercept blocks TNF-Alpha which is blamed by mainstream medicine for being the cause of psoriasis or at least major mediator of psoriasis inflammatory pathways. However the effects of etanercept on immune system are very serious and in 2008 the FDA issued the black box warning due to a lot of serious (and even fatal) infections in people treated with this drug.
The authors measured the blood levels of inflammatory markers and their association to the PASI (Psoriasis Area and Severity Index).
Some of the measured markers were neutrophils, fibrinogen, ferritin, high-sensitivity C-reactive protein (hs-CRP) and erythrocyte sedimentation rate (ESR). The levels of 41 psoriatics were checked before and after 3 months of taking etanercept 50 mg twice per week.
Actually all inflammatory markers were reduced after treatment. Two of them even correlated with PASI: fibrinogen and hs-CRP. Of the 41 patients, 19 (46.3%) reduced their PASI level of 75%.
The authors concluded that inflammatory markers like hs-CRP and “to a lesser extent” fibrinogen and ESR can be used as part of assessing the disease severity and response to treatment.
Small intestine and TNF-alpha
- What causes the TNF-alpha production?
- How does inflammatory state can cause psoriasis?
The answer on the first question is: TNF-alpha production is usually caused by endotoxins leaking to blood from small intestine. High amounts of endotoxins are found in the small intestine because of bad liver function – low bile flow.
The answer to the second question is: inflammation cause coagulation of blood and thick blood is hard to pump through the microvessels. Then we end up with poor oxygenation of the tissues, poor nutrient delivery to the tissues as well as poor waste removal of the tissues.
Bacterial and fungal toxins (from root canal teeth, intestines and also hidden in tissues) as well as viruses interfere with the energy production and block many (inter-) cellular processes.
The cells without oxygen can not produce energy (ATP) what makes the organs struggle in every single task. The organs which can’t do their job make the symptoms we call DISEASES.
1) Ozlem Karabudak, Rifat Eralp Ulusoy, Alev Akyol Erikci, Emrullah Solmazgul, Bilal Dogan and Yavuz Harmanyeri. Inflammation and Hypercoagulable State in Adult Psoriatic Men. Acta Derm Venereol 2008; 88: 337–340.
2) Kanelleas A, Liapi C, Katoulis A, Stavropoulos P, Avgerinou G, Georgala S, Economopoulos T, Stavrianeas NG, Katsambas A. The role of inflammatory markers in assessing disease severity and response to treatment in patients with psoriasis treated with etanercept. Clin Exp Dermatol. 2011 Dec;36(8):845-50.