Alcohol Is Not As Bad For Psoriasis As You Think
Alcohol is considered to be a risk factor for psoriasis but most people do not know why and how it may induce or worsen psoriasis.
Now let me explain that…
Alcohol directly does not cause psoriasis but at the same time it may significantly worsen it. Endotoxemia is perhaps the worst acute problem caused by alcohol consumption.
The biggest part in psoriasis development in most people is probably the liver function.
Liver is a major “biochemical factory” so when you drink any alcohol and your psoriasis worsen, become more red or itchy it is the most likely a fault of the liver.
As I said above “alcohol is considered to be a risk factor for psoriasis”. I said “considered” because the science claims that there’s not enough evidence whether alcohol consumption is a risk factor for psoriasis. 
I have to agree with that.
You know, maybe those who drink excessive amounts of alcohol do that because they feel anxious about their psoriasis or cause of psoriasis (which is a nervous system disorder) shares some underlying processes with anxiety disorders which many people cope with by drinking alcohol.
In other words, if somebody started drinking alcohol after he developed psoriasis then alcoholism should not be considered as a cause of psoriasis rather then the result of psoriasis-induced low self-esteem anxiety.
However, generally speaking, I can tell you that everything what places a burden on the liver is indeed a risk factor for a disease. Not only for psoriasis but actually for any chronic degenerative disease.
Is there a connection between alcohol and psoriasis?
Yes, study on 100 patients with chronic plaque psoriasis concluded that in male patients heavy drinking at level which is detrimental to health was found more commonly in those with severe psoriasis. However, in women excess alcohol intake does not correlated as much with the severity of psoriasis as in male patients. 
Another study examined 1987 patients (due to whatever the diagnosis was present) for the presence or absence of psoriasis and alcohol consumption. The incidence of psoriasis in patients who regularly consumed alcohol was 5,3% compared to non-drinkers 0,7%.
Epidemiological evidence suggests that patients with moderate to severe psoriasis have an increased incidence of alcohol-related diseases and mortality. This appears to be unique to psoriasis compared with other autoimmune diseases.
The excessive consumption of alcohol may significantly contribute to inflammation, cardiovascular disease and depression. 
Endotoxins, alcohol and psoriasis
Endotoxins are undoubtedly a big cause of inflammation and chronic inflammatory diseases like diabetes, chronic hearth failure, periodontal diseases and others. [8, 9, 10]
That is why we should always look for a possible cause or source of endotoxins like small intestine inflammation or dental infection in every developed chronic degenerative disease.
Alcohol significantly affects the liver and intestinal health which may affect the levels of circulating endotoxins in the whole blood.
Higher levels of circulating endotoxins are observed in alcohol-abusing patients. 
Patients with minor (A1; n=27), more pronounced (A2; n=13), cirrhotic alcoholic liver disease (A3; n=18), and non-alcoholic cirrhosis (NC; n=6), and 15 healthy control persons (HC) were included in the study.
All groups of alcohol abusers had significantly elevated endotoxin plasma levels with a considerable portion of ‘bound’ endotoxin. Conversely, the endotoxin binding capacity was markedly diminished, mainly in patients with more advanced liver disease (A1: 85.8% of the control value [non-significant vs. controls]; A2: 25.4% [p<0.05]; A3: 43.6% [p<0.02], NC: 43.2%).
The endotoxin-binding capacity is diminished in patients with alcoholic and non-alcoholic cirrhosis, as well as in less advanced alcoholic liver disease. Reduced endotoxin binding may contribute to the adverse effects of endotoxemia.
If there is a lot of endotoxins circulating in the blood the endotoxin-binding capacity of the whole blood is markedly diminished which means more systemic inflammation.
In another study the levels of endotoxins in patients with alcoholic liver cirrhosis were found to be significantly higher than in patient with non-alcoholic liver cirrhosis.
Plasma endotoxin concentration was measured in 85 patients with alcoholic liver disease (alcoholic cirrhosis (n = 64), alcoholic hepatitis without cirrhosis (n = 11), fatty liver (n = 10), and in patients with non-alcoholic cirrhosis (n = 15]. Endotoxin concentration was determined with an improved chromogenic substrate assay, using individual standard curves for each plasma sample. In patients with alcoholic cirrhosis the mean endotoxin concentration was significantly higher than in patients with non-alcoholic cirrhosis (p less than 0.05). In addition, distinctly higher endotoxin concentrations (greater than 20 pg/ml) were more frequently observed in patients with alcoholic cirrhosis than in non-alcoholic cirrhosis (34.4 vs. 14.3%, p less than 0.05). Mean endotoxin concentration was not significantly higher in cirrhotics with ascites or esophageal varices as compared with the subgroup without ascites or esophageal varices. The endotoxin concentration did not correlate with serum bilirubin, prothrombin concentration or serum enzyme activities. In patients with alcoholic liver disease, however, endotoxin concentration revealed a negative correlation (p less than 0.05) with the concentration of high density lipoprotein cholesterol. On admission endotoxin concentrations in alcoholics with fatty liver were similarly elevated as observed in alcoholic cirrhosis. In six out of 12 patients with fatty liver or alcoholic hepatitis, in whom a second sample of plasma was investigated after 6 to 8 days, endotoxemia was no longer detectable; in the remaining patients, the endotoxin concentration decreased markedly. The results indicate that, irrespective of the stage of liver disease, alcohol abuse favours the development of endotoxemia. They support the hypothesis that gut-derived endotoxins might play a role in the initiation and aggravation of alcohol-induced liver disease.
The endotoxin concentration did not correlate with serum bilirubin or prothrombin concentration but negatively correlated with the levels of high density lipoprotein. This means that the higher the levels of endotoxins in the blood the lower levels of “good” cholesterol circulate in the blood. 
It is almost sure that “gut leakage in persons with chronic alcohol misuse leads to endotoxaemia, which might contribute to the development of alcoholic hepatitis or cirrhosis.” 
It was already proved that endotoxin-binding capacity (amount and potency of proteins which significantly attenuate the inflammation by binding the endotoxins) of whole blood is reduced in persons with intestinal permeability and in those who consume excessive amounts of alcohol.
In alcoholics the concentration of endotoxin binding factors (LPS binding protein and sCD14) that modify the action of endotoxins on target cells (mostly macrophages) are increased. 
Endotoxin antagonists, such as bactericidal/permeability-increasing protein and high-density lipoprotein, were increased in the pre-cirrhotic stages, whereas a significant reduction of the latter was observed in cirrhosis. Low-density lipoprotein remained unchanged. The elevation of binding factors in the pre-cirrhotic stages of alcoholic liver disease might attenuate the effects of endotoxaemia, whereas in cirrhosis the reduction of high density lipoprotein, to which large quantities of endotoxin bind, may contribute to its pro-inflammatory effects.
Chronic alcohol consumption leads to endotoxemia which is considered a major causal factor in development of alcoholic liver disease.
Patients with alcoholic liver disease exhibit a mild endotoxemia and a marked decrease in endotoxin-neutralizing capacity (ENC).
The levels of TNF-alpha, IL-6, sICAM and sCD14 were found to be significantly elevated in this study. 
The levels of IL-10 were elevated only in patients with cirrhotic alcoholic liver disease.
Elevated levels of endotoxin correlate with acute excessive alcohol ingestion. No gender differences were observed.
Does not matter if you are a man or a woman, alcohol significantly increases the amount of endotoxins in blood of both sexes.
Acute alcohol intoxication rather than severe ALD [Alcoholic Liver Disease] results in significant endotoxemia. The limited capacity of plasma to neutralize endotoxin in liver injury seems to be an important factor in ALD which may be responsible for the release of endotoxin-induced mediators, such as cytokines, as well as s-ICAM-1, that are relevant in the pathogenesis of ALD.
The scientists concluded that acute alcohol consumption rather than chronic alcoholic liver disease results in endotoxemia and inflammation!
You can read more about the inflammation, endotoxins and how the body recognize them in my blog post LDN for Psoriasis: Good Treatment But Still Not a Cure.
Relevancy of data on alcohol and psoriasis
Factors affecting the data gathered from psoriatics drinking alcohol:
- do they started drinking before the onset of psoriasis?
- does the person also smoke or stopped smoking which may induce psoriasis as well?
- levels of anxiety in psoriatics?
– Alcohol may be just a calming drug and might not be fully responsible for severity of psoriasis.
- type of alcohol the person drink?
– Red wine has a lot of histamine in it as well which creates strong inflammation itself.
– Wine has sulfites in it.
- The quality of alcohol?
– Sugar cane rum will be probably less toxic than whiskey made from (molded) grains.
As I already mentioned above, psoriasis causes social isolation and low self-esteem which many people cope with by drinking alcohol. This is true especially in severe cases of psoriasis.
Therefore we can not claim that alcohol caused their psoriasis if they developed it before they even started drinking alcohol.
However, drinking alcohol further worsen psoriasis so psoriatics may become the alcoholics since they cope with low self-esteem the way they drink even more… which worsen they psoriasis even more…a vicious circle.
But don’t forget that anxiety or in other words low stress tolerance is often caused by inflammation (like OCD/PANDA/Streptococcus pyogenes…) which is usually induced by endotoxins.
This low stress tolerance puts a huge burden on your adrenal glands and causes a lot of adrenaline release.
This adrenaline overload may desensitize the adrenergic nervous pathways (beta-2 adrenergic receptors) which are so heavily involved in pathophysiology of many “autoimmune” considered diseases.
Psoriasis and asthma are just two of them.
Psoriasis, as we already know already, is not a direct result of alcohol abuse since it is common in people who never drank alcohol.
On the other hand, there is a group of alcohol abusing psoriatics who developed psoriasis after a significant period of alcohol abuse.
Because acute alcohol intoxication induces endotoxemia which leads to release of inflammatory mediators. The chronic inflammation (as some people drink excessive amounts of alcohol on a daily basis) leads to liver dysfunction (fatty liver, cirrhosis) – low bile flow, problems with protein synthesis and overall homeostasis – iron and copper regulation. Both of those will create significant problems with oxidative stress if not regulated properly by the liver.
Alcohol also depletes and impairs absorption of the minerals and vitamins – especially vitamin B9 (folate), B6, B1 (thiamine) and vitamin A. 
Add to that magnesium and zinc which even those with perfect diets have troubles to get enough.
How to reverse alcohol induced (endotoxin->inflammation) liver damage?
Let’s be honest…
Not every liver damage can be fully reversed and everything needs time…
Lecithin (choline), B-complex, Artichoke Leaf Extract are the basic supplements needed.
Minerals like magnesium, zinc and even calcium (if your digestion is a mess and have poor tooth health).
Then there are very effective supplements like Silymarin, N-Acetylcysteine, vitamin C as supportive antioxidant supplements and proteolytics enzymes like Bromelain and Serrapeptase.
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