Nienna said:
anarkist said:
latest from our friends at SOTT
"Another possible factor mentioned in the study may come as a surprise: a decrease in smoking.
Although smoking has been shown to increase risk for a host of other health problems — including cardiovascular disease, stroke, lung cancer and other cancers — it oddly has been linked to a decreased risk of developing thyroid cancer, the study said.
It's good to know that "science" is talking about this, but you may want to read two articles on SOTT that show that a lot of what "science" says about smoking causing various illnesses is not entirely true. Or, even, false.
I have been thinking about this recently. When I wrote that article on tobacco, I was under the impression that all associations with different cancers (especially lung cancer) could be explained by miscalculation, researcher bias, or generally less-health conscious lifestyles of smokers.
But now I actually think there is probably some merit to the link between smoking and lung cancer in research. To be clear, I am not saying that smoking
causes lung cancer. Only that it may exacerbate a present lung cancer caused by other factors.
My line of thought is that it is related to glutathione upregulation. The increased glutathione in smokers is well established, and glutathione is generally presumed to be a good thing (all of the time). The problem is, when we start to examine cancer cell metabolism, antioxidants are not always beneficial in large amounts.
Otto warburg showed last century that cancer cells revert to a primitive state of metabolism called glycolysis. This is normally the first stage of properly functioning energy/ATP production. It yields pyruvate, 2 NADH and 2 ATP. Pyruvate is then fed through to the next stage by being converted to Acetyl CoA by an enzyme called pyruvate dehydrogenase (PDH). This process continues through to the TCA cycle and oxidative phosphorylation to produce a maximum amount of energy. In short, NADH is oxidised to NAD+, which can then be recycled through the process again. But when there are a lack of resources available to the cell (low oxygen, low CO2, low pyruvate dehydrogenase, low B vitamins, excess estrogen and lactate), the cell can no longer complete all steps of this respiration process. So instead, the cell converts pyruvate to lactate, and continually repeats this low-energy yielding process.
When this happens long term (in other words, when there is too much glycolysis and not enough oxidative phosphorylation), the cell becomes OVERLY reduced (too many electrons). This basically means that there are too many NADHs, and not enough NAD+. The ratio between NADH/NAD+ is also well established in the research (longevity, health, etc), and high NAD+ is generally considered good sign that mitochondria are working efficiently. Even in the presence of oxygen, the cell continues to run through this anaerobic metabolic process (which may be due to PDH issues). This is called the "Warburg effect", and is present in all cancer cells.
So in this state, some antioxidants may actually "feed" the cancer cell. According to this framework, cancer is a state where there is not enough of an oxidising agent (or enzyme constituents etc) to complete full cellular respiration. Therefore, adding in reducing agents like glutathione may actually increase the growth of the cancer by added fuel to the fire, so to speak. There is also some interesting research which suggests that cancer cells may use glutathione to neutralise free radicals aimed at destroying the cell, or evade tagging. Here is an exerpt below:
For the new study, published in Science Translational Medicine, Martin Bergö, a cell biologist at the University of Gothenburg’s Sahlgrenska Cancer Center in Sweden, and his colleagues decided to look at melanoma because rates have been increasing and because the cancer is known to be sensitive to the effects of free radicals. They fed the antioxidant N-acetylcysteine (NAC) to mice that had been genetically engineered to be susceptible to melanoma. The per-weight dose they gave the mice was consistent with what people typically consume in supplements. Although the treated mice did not develop more skin tumors than similar mice that had not been fed the antioxidants, they developed twice as many tumors in their lymph nodes, a hallmark of the spread of cancer—a process called metastasis. When the researchers added NAC or a form of vitamin E to cultured human melanoma cells, they confirmed that the antioxidants improved the cells’ ability to move and invade a nearby membrane.
Antioxidants may bolster protection of these dangerous cells. Bergö and his colleagues found higher levels of glutathione, an antioxidant made by the body, inside metastatic tumor cells in treated mice compared with untreated mice. The treated mice also had a higher ratio of glutathione to glutathione disulfide, the molecule that glutathione becomes after it neutralizes free radicals. These findings suggest that when the body is given extra antioxidants, its tumor cells get to keep more of the antioxidants that they already make themselves. The cells can store the surplus, improving their ability to survive damage. This idea is supported by work that shows some genes that drive cancer growth turn on other genes that make intrinsic antioxidants.
The substances may help cancer cells in other ways, too. Previous research has suggested that glutathione affects the activity of a protein called RhoA, which helps cells move to different parts of the body. “If you were to select one protein that is known to be involved in [cell] migration, RhoA is it,” Bergö explains. He and his colleagues confirmed that the extra glutathione in the treated mice caused levels of RhoA to increase in their metastatic tumors. In their 2014 lung cancer study they also found that antioxidant supplements caused lung tumor cells to turn off the activity of a well-known cancer-suppressing gene called p53; its inactivation is believed to drive metastasis. And Schafer’s work has shown that antioxidants help migrating breast cancer cells survive when they detach from the extracellular matrix, the network of proteins surrounding cells.
These molecular investigations shed light on the large human trials that have implicated antioxidants in cancer. It is possible that the supplements did not triggercancer but rather accelerated the progression of existing undiagnosed cancers, making later discovery of the disease likely.In other words, it “could be that while antioxidants might prevent DNA damage—and thus impede tumor initiation—once a tumor is established, antioxidants might facilitate the malignant behavior of cancer cells,” Schafer says.
Hence, increased levels of glutathione in smokers is probably a good thing for many... however if you already suffer from lung cancer, there is a possibility that the extra glutathione induced by cigarettes is enabling cancer cells to thrive and avoid detection.
