Iron in the Promotion and Initiation of Cancer How Free Iron Accelerates Predisposing Insulin Resistance

Abstract

Juan Ariel Jara Guerrero

Iron is physiologically essential to life, but biochemically it is harmful because of its evident -but unappreciated- oxidative and inflammatory tissue power when it accumulates, is dosed in excess, or is free; and that because, after entering the body, unlike any other metal, its elimination is almost non-existent in man; thus, metal is a powerful promoter of chronic degenerative diseases, from diabetes, neurodegeneration to cancer, through extensive coronary and cardio-cerebrovascular disease; modifying its clinical expressivity and accelerating its severity.

Iron is a powerful oxidizing and inflammatory agent, and its accumulation causes and promotes the proliferation of cancer cells in particular, both in animals and in humans. Free and accumulated iron triggers a powerful uncontrolled Cell Proliferation, permanently feeding the survival of the neoplastic cell.

After more than 50 years of experimental and preclinical studies, it is clearly demonstrating the carcinogenicity of iron; and this is also proven in humans, from breast cancer and endometrium, in women, to cancer of the colon-rectum, prostate, and pancreas in men.

In Western men and women, the reductions in iron deposits have an important anti-tumor and preventive effect for the development of cancer or diabetes, two entities biologically interrelated by the states of Resistance to Insulin, an inflammatory state that favors the development of malignant neoplasms, and can accelerate its aggressiveness.

It is the chronic excess of insulin or its Tissue Resistance, the biological event and the clinical syndrome that increases the cancerous power of excess iron, both silent epidemics in modern man. Moderate increases in body iron levels increase the risk of acquiring cancer, and raise the level of their mortality. And its deficiency or chelation in vivo decreases the Tumor growth (Wang F, Elliott RL, Head JF: Inhibitory effect of deferoxamine mesylate and low iron diet on the 13762NF rat mammary adenocarcinoma Anticancer Res. 1999 Jan-Feb; 19 (1A): 445-50). If excess iron mediates and increases the risk of cancer associated with Insulin resistance, any subject with this syndrome can minimize any associated health risks (and their increased risk of cancer), avoiding iron-rich diets and donating blood with regularity; Iron is the metal that causes “exponential” and punctual mutations and fusion of genes through chromosomal translocations, constituting the greatest risk factor for human carcinogenesis.

Iron is physiologically essential for life but biochemically dangerous. Chronic accumulation of iron causes pantropic organ damage and excess body iron play an important role in carcinogenesis, coronary artery disease, neurodegenerative disease, stroke and inflammatory disorders. Iron is very slowly excreted from humans once it is absorbed into the body.

The significance of iron excess has been markedly underestimated, despite the fact that iron overloading disorders are as common place in the US white population.

Iron-overload and catalytic iron promotes activation of oxidative responsive transcription factors and pro-inflammatory cytokines that increase cancer extension and aggravate them. There is accumulative evidence for iron as a carcinogenic metal in epidemiological, clinical, animal, and cell culture studies. The role of iron in various cancers, such as colorectal and liver cancer was demonstrated. Recent advancements on the molecular mechanisms of iron carcinogenesis evolved the Insulin-resistance generation and promotion, fisiopatologic condition that is not only permissive, but may be generated cancer and promoting it. Unlike other nutritional metals, iron is highly conserved: toxicity due to excess iron can occur either acutely after a single dose or chronically due to excessive accumulation in the body from diet. In vivo studies have demonstrated that an iron deficiency induced by either feeding a low iron diet injecting the iron chelator deferoxamine mesylate decreases tumor growth (Wang F, Elliott RL, Head JF: Inhibitory effect of deferoxamine mesylate and low iron diet on the 13762NF rat mammary adenocarcinoma Anticancer Res. 1999 Jan-Feb;19(1A):445-50). Iron supplementation has at times proven ineffective and even detrimental to health.

Thus, iron excess may mediate the increased cancer risk associated with insulin resistance and heme-rich diets, and subjects who are insulin resistant can minimize any health risk associated with iron overload by avoiding heme-rich flesh foods and donating blood regularly. The energy that sustains cancer cells derived preferentially from glycolysis depends on the gene p53 deficiency-iron induced. This nutrient is postulated to contribute to the initiation of cancer in vivo, but iron overload initiates and sustain cancer development if chronic infection or insulin resistance conditions are present. Cancer cells require considerably more iron than normal cells. Since iron catalytic can induce driver point mutation and create fusion genes through chromosomal translocations, iron overload is one of the most important risk factors in human carcinogenesis. Because free iron may play a catalytic role in “spontaneous” mutagenesis, moderately elevated iron stores increased overall risk for cáncer.

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