2 replies to this topic

[brotherx]

Hi,

is just came across this article - and thought it might be interesting for you as well!

Cheers Alex


"
Iron & Cancer

Nutrition Action Health Letter

09-17-08

Originally Published:20080901.

Do lower levels of iron in the body mean less cancer? Iron can damage tissues by creating free radicals, but previous studies that looked at iron and cancer risk were inconsistent.

To answer the question, researchers randomly assigned 1,300 middle-aged men with peripheral artery disease to one of two groups. (Arteries going to their arms, legs, kidneys, or stomach were clogged.)

The "iron-reduction" group donated blood every six months for an average of four years, while the "control" group didn't donate. (The study was designed to see if reducing iron levels could lower the risk of heart attacks and stroke, which it didn't.)

During the study, cancers (lung, prostate, colon, and others) were diagnosed in 60 men in the control group, but in only 38 in the iron-reduction group. And among participants who were diagnosed with cancer, those in the iron-reduction group were only half as likely to die.

And regardless of which group the men were in, those who were diagnosed with cancer had higher iron levels in their blood than those who weren't diagnosed with cancer. Ferritin (the protein that stores most iron in the body) averaged 127 nanograms per milliliter in those diagnosed with cancer and 76 ng/mL in those who weren't.

What to do: The results of this study are so striking-especially because the risk of cancer began to drop after just one blood donation-that they need confirmation. And even if other studies bear out these findings, it's unclear if they also apply to women or to older people.

Nevertheless, it's worth checking your multivitamin to make sure it doesn't contain more iron than you need. Current daily targets (for food and supplements combined) are 8 milligrams for men and postmenopausal women and 18 mg for premenopausal women."

source:http://www.lef.org/news/LefDailyNews.htm?NewsID=7329&Section=Disease

[s123]

Not only too much but also too little iron causes oxidative stress because iron is needed to make antioxidant enzymes (catalase and peroxidases). Also the kind of iron is important, heam-iron causes colon cancer, so it's better to take some other form of iron like the Fe3+ that you find in vegetables.

Also, I read today that maybe calorie restriction could change iron metabolism (in mitochondria).
Frontiers in Bioscience 13, 6554-6579, May 1, 2008; The mitochondrial free radical theory of ageing – Where do we stand?

A dramatically increased risk of liver cancer (hepatocellular carcinoma) in individuals with cirrhosis due to iron overload in hereditary hemochromatosis has been well documented. However, the relationship between dietary iron and cancer risk in individuals without hemochromatosis is less clear (11). Several epidemiological studies reported associations between measures of increased iron status and the incidence of colorectal cancer or the occurrence of precancerous polyps (adenomas), but the associations were not consistent. Dietary iron intake appears to be more consistently related to the risk of colorectal cancer than measures of iron status or iron stores (33, 34). Increased red meat consumption has been associated with an increased risk of colorectal cancer, but there are a number of potential mechanisms by which increased meat consumption could affect cancer risk other than increasing iron intake. For example, increased red meat consumption increases the secretion of bile acids, which can be toxic to colonic cells, and increases exposure to carcinogenic compounds generated when meat is cooked (35). Increased iron in the contents of the colon, rather than increased body iron stores, could increase the risk of colon cancer by exposing colonic cells to potentially damaging reactive oxygen species derived from iron-catalyzed reactions, especially in the presence of a high fat diet. Although this possibility is presently under investigation, the relationship between dietary iron intake, iron stores, and the risk of colorectal cancer remains unclear.

http://lpi.oregonsta...iron/index.html

[Mind]

There was a presentation at UABBA about heme vs. non-heme iron indicating the heme-iron was not good.

Here is the abstract link

Mitochondrial dysfunction, oxidative stress and apoptotic cell death are fundamental mechanisms that drive mammalian aging. Iron (Fe) mediated redox chemistry is particularly important because of its role in mitochondrial oxidative phosphorylation and other life-sustaining functions. Perturbation of mitochondrial Fe homeostasis causes a decline in mitochondrial function and plays a significant role in various neuromuscular degenerative diseases, as well as age-related tissue dysfunction. Hence, we investigated whether non-heme Fe accumulates in mitochondria with advancing age and furthermore, whether Fe overload causes mitochondrial oxidative damage and mitochondrial dysfunction. Specifically, our study investigated whether non-heme Fe levels increased over the course of aging in the quadriceps muscle interfibrillar mitochondria (IFM) and subsarcolemmal mitochondria (SSM) of Fischer 344 x Brown Norway rats. We also assessed mitochondrial susceptibility to apoptosis by measuring mitochondrial permeability transition pore (mPTP) openings and mitochondrial RNA oxidative damage. Furthermore, we investigated whether perturbation of mitochondrial Fe homeostasis differs between post-mitotic myofibers and mitotically active tissue, such as that found in the liver.

This study made several significant and novel findings. In particular, we determined for the first time that (i) non-heme Fe levels increase significantly with advancing age in mitochondria (IFM and SSM) of quadriceps muscle and liver tissue; (ii) levels of mitochondrial RNA oxidation increase during the aging process and correlate with mitochondrial levels of non-heme Fe; (iii) mitochondrial Fe is associated with an increased susceptibility of mPTP opening, possibly via the increased oxidative damage that occurs in mitochondria with age; and (iv) significant biochemical and physiological differences exist between skeletal muscle mitochondrial subpopulations (IFM and SSM), in terms of trace metal handling and functional parameters. Our study provides new insights into the role of mitochondrial Fe dyshomeostasis in cellular aging. Our findings also suggest that mitochondrial non-heme Fe represents a potential novel target for targeted interventions to slow aging. This research was supported by grants from the National Institute of Health to CL (AG17994 and AG21042) and a University of Florida Claude D. Pepper Older Americans Independence Center NIH grant (1 P30 AG028740).