Psoriasis and Type 2 Diabetes is Caused by TNF-alpha

Do you know what causes type 2 diabetes?


Well, first we should define what is the type 2 diabetes.

If it is high blood sugar then the science knows exactly what causes it – inflammation is the major cause!

TNF-alpha as the major inflammatory messenger induces the symptoms of diabetes. No wonder that high blood glucose is so common in psoriatics. Psoriasis responds quite well to drugs and supplements which decrease the TNF-alpha production or attenuate the effects of TNF-alpha on the body.

Scientifically said the “Insulin resistance” is actually what causes the type 2 diabetes – this fact is well known and even mainstream medicine doctors will tell you this.

But what is actually the insulin resistance caused by?

Insulin resistance “is partially caused by the cytokine tumor necrosis factor-α (TNF-α), which is produced in inflammatory fat tissue in muscle, liver, and adipose tissue.”[4]

Abdominal fat tissue releases a lot of inflammatory adipokines (cytokines) one of which is TNF-alpha.[4]

Aspirin as one drug of the group of salicylates is known to lower the blood sugar levels in high doses and these effects were documented before the insulin came on the market.[1]

The scientists tested the effects of insulin on rate of glucose uptake by cells and high blood sugar using the TNF-alpha which is known to induce the pathways we call type 2 diabetes.[1]

In the next picture you can see how TNF-alpha, Insulin and Aspirin affect the glucose uptake into the cells.


You can see that Insulin extremely increases the glucose uptake into the cells, TNF-alpha very significantly decreases the effects of Insulin on glucose uptake and addition of Aspirin in presence of TNF-alpha and Insulin significantly increases the effects of Insulin on glucose uptake. Aspirin alone increases the glucose uptake by cells only slightly.
Image Source: Zhanguo Gao, Aamir Zuberi, Michael J. Quon, Zigang Dong and Jianping Ye. Aspirin Inhibits Serine Phosphorylation of Insulin Receptor Substrate 1 in Tumor Necrosis Factor-treated Cells through Targeting Multiple Serine Kinases. The Journal of Biological Chemistry 278, 24944-24950. July 4, 2003

What increases the TNF-alpha levels in the body?

Endotoxins also called lipopolysaccharides – the parts of dead bacteria – as I have already mentioned many times in my previous posts. Generally, I would consider that infection with any type of pathogen will increase the levels of inflammatory TNF-alpha.

However, there were some scientific studies which suspected that infection with – Plasmodium yoelii and Plasmodium chabaudi (two types of parasites which cause malaria like symptoms in rodents) – may paradoxically lower the blood sugar levels, however it was revealed that the those pathogens lower the blood glucose levels via the increased secretion of insulin.[2]

The effect of these pathogens on insulin secretion was documented in mice study by administration of human recombinant TNF (rTNF) which caused an increase in blood sugar levels. The scientists “conclude that the hypoglycaemia of malaria is not caused by increased levels of TNF, which may in fact be beneficial, but is secondary to a hyperinsulinaemia that is probably stimulated directly by products of the parasite.”[3]

You can read about more about the infection – type 2 diabetes connection in my previous post “Insulin Resistance is caused by Infection” which mentions the 73 years old study published in Journal of the American Medical Association.

TNF-alpha and blood glucose levels in humans

In one study the researchers were trying to find out how the anti-TNF therapy affects the blood glucose levels.

The previous studies were limited in both the time and dosages of the drugs because of toxicity of the anti-TNF drugs.

Therefore the people involved in this particular study were the rheumatoid arthritis and Crohn’s disease patients who were on anti-TNF-alpha drugs for their diagnoses other than type 2

There is still another 320 words in this article!

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