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Hello guys! Today I bring a very complex issue and on which I have had a lot of interest in lately, so for me turned out to be a pleasure to write this post because I acquired knowledge that for me until then was unknown, and now I can share them with you. I believe many people still do not know or do not understand the relationship between obesity and cancer, am I right?
So I will try to make a link between the two issues in a way that everyone can understand. I believe that today, even with so many scientific studies, we cannot say that we know everything that happens with the cells in the presence of obesity, but we have enough information to know that there is a strong link between them, obesity and cancer. A normal cell may suffer changes in the DNA of genes, and we call this phenomenon of genetic mutation. The cells whose genetic material has been altered, were given wrong instructions for their activities. These changes can occur in specific genes called proto-oncogenes, which in principle are inactive in normal cells, but become active cells and transform in oncogenes responsible for the malignant transformation of normal cells. These cells begin to multiply uncontrollably, have the power to create angiogenesis (formation of new blood vessels) to nourish, acquire the ability to detach from the tumor and reach the surrounding tissue. Reach the inside of the blood vessels or lymphatic system and spread to distant organs where they initiated the call metastasis. Understanding how cancer can arise, gives us a sense that we are totally unprotected and at its mercy!
But I have good news, you can change that thought. Our body is 100% prepared to fight the different agents who come in contact with our body, through natural mechanisms and can be said that throughout life, we produce many of these altered cells, but the body's natural defense enables us to stop this process. OK, but what makes obesity a risk factor for cancer?
The adipokine is a protein produced by adipose tissue (fat cells), and of these cytokines have several endocrine and metabolic functions, and participate in inflammation and immune system reset process. Obesity is characterized as a chronic inflammation state and this low level inflammation responds proportionally to the increase of body fat mass, or higher production of proinflammatory cytokines. Some studies show that this chronic inflammation is linked to hypoxia (low oxygen concentration) that is augmented with hypertrophy of the fat cells by compressing the blood vessels that are responsible for oxygen transport. A cytokine that has a strong connection to all this is the TNF-alpha, which belongs to the group of pro-inflammatory cytokines. Studies show that their development is associated with insulin resistance, lipid metabolism and apoptosis. In the body of an obese person the process starts with increased body fat, which go beyond the normal, healthy value enters a metabolic disorder. Existing necrosis tissue, production of adipokines proinflammatory TNF-alpha (inflammation indicator) increases, which in turn activates the immune system, causing the body's own defense mechanisms to be activated in adipose tissue since there is an warning that something is wrong at that location. At this time the immune system no longer focus on taking care of diseased cells which may be present throughout the body, becoming vulnerable to the emergence or aggressive cancer cells.
As we know, other diseases are associated with obesity and we can say that the trigger for many existing diseases, is the metabolic disorder caused by obesity.
Now, I leave a question to you: When do we leave the speech that we have no time to take care of our own health, that doing exercise is boring and that eating junk food is better than maintaining a healthy diet? We already know that fighting obesity is far beyond the aesthetic, and the old speech "I am happy so" no longer has to be accepted when it goes beyond a matter of health and quality of life.
Bibliography (Click to read more):
VUCENIK I STAINS P. J. Obesity and cancer risk: evidence, mechanisms, and recommendations. New York Academy of Sciences. 2012: 37-43.
C. Oeffinger K, BAXI S. S, D FRIEDMAN N., S. C. MOSKOWITZ Solid Tumor Second Primary Neoplasms: Who is at risk, what can we do ?. National Institutes of Health. 2013; 40 (6): 676-689.