by Barbara Minton
A simple substance found in food appears to reverse the harmful effects of smoking, a finding that can bring cheer to anyone who smokes or loves someone who does. Lung cancer is the leading cause of cancer related death in the U.S., and 85 to 90% of lung cancer cases are associated with tobacco use, so this discovery is a very big deal. Tobacco components promote the initiation and growth of lung tumors through their toxic effects on genes as well as through biochemical modulation of signaling pathways that regulate cell proliferation and survival. Inositol seems to stop these processes dead in their tracks.
Inositol is a naturally occurring nutrient grouped with the B complex of vitamins, even though it is not officially recognized as a vitamin and no RDA has been set. Like the B vitamins, inositol is water soluble and as a result is not stored very well in the body. Even though approximately 4 grams a day are naturally produced from glucose in the kidneys, this amount does not meet the body's needs, and more must be obtained from the diet.
Two famous researchers discovered inositol prevents cancer
Dr. Lee Wattenberg, known as the father of chemoprevention, searched for several decades starting in the 1970`s to find naturally occurring compounds that could theoretically prevent cancer and applied scientific methodologies to research his discoveries. After testing several molecules, he found inositol showed great promise. Using various study models he was able to demonstrate that inositol could prevent lung cancer. It had previously been documented that a poor diet increased the chances for cancer to occur, but Dr. Wattenberg was among the first to show that a common nutrient could actually prevent cancer, a truly empowering discovery.
A few years later, Dr. Abdul Kalam Shamsuddin, known as the father of IP6 (inositol hexaphosphate), also showed that inositol was able to prevent cancer, demonstrating the preventive value of the compound with colon cancer. Research by Dr. Shamsuddin revealed that inositol affects health in several ways, largely because it is in all human cells and is a major component of cell linings or membranes where it facilitates communication between the various organelles and molecules in the cell signaling process.
Why don`t cigarette companies hand out a bottle of inositol with each carton of cigarettes?
Some bright young executive at one of the major tobacco companies has probably had the idea to boost sales by telling everybody that inositol, an inexpensive supplement, could prevent lung cancer. But for the cigarette companies to buy into the idea would mean an acknowledgement that cigarettes do cause cancer. Such an acknowledgement would create immense legal liability for any company making and selling cigarettes.
Inositol provides many other benefits in to the body
Inositol is a critical nutrient for hair growth. It helps prevent hardening of the arteries and is important in the formation of lecithin and in the metabolism of fats and cholesterol. Inositol has a calming effect on the brain and has been used successfully at high doses as a treatment for psychiatric disorders such as depression, bipolar, obsessive-compulsive, and panic. Inositol is also used for insomnia, retinopathy, bulimia nervosa and binge eating. It is beneficial for diabetic neuropathy, brain seizures, and for normalizing cholesterol and triglyceride levels.
Symptoms of deficiency are arteriosclerosis, constipation, hair loss, high blood cholesterol, irritability, mood swings, and skin eruptions. The consumption of large amounts of caffeine usually results in inositol deficiency. As coffee consumption was often accompanied by cigarette smoking, this shortage of inositol may have been a critical factor in the cases of smoking induced lung cancer so prevalent during the time when smoking was in style.
Research continues to refine knowledge of the mechanisms by which inositol works
Inositol is a natural compound and therefore not able to be patented by drug companies, so there is little incentive for studies of it. However, some dedicated researchers are continuing to study the effects of inositol, trying to determine the specific mechanisms by which it prevents lung cancer in cigarette smokers. Here are summaries of the abstracts from the most recent research. It is truly amazing, or maybe criminal is a better word, that the smoking public has not been made aware of these results which date back steadily to the time of Drs. Watterberg and Shamsuddin.
The most recent studies are based on those that have gone before in an effort to refine the knowledge of how inositol affects pathway activation in the development of lung cancer. The phosphatidyl-inositol-3-kinase-AKT pathway is emerging as an important regulator of tumor cell survival.
Researchers at Boston University Medical Center have observed a significant increase in activation of another pathway, phosphatidylinositol 3-kinase (PI3K), in the bronchial airway of smokers with lung cancer and dysplastic lesions, suggesting that PI3K is activated in the airway before a tumor beings. (1) Further, these researchers found that when PI3K is decreased in the airway of high risk smokers by the use of inositol treatments, their dysplasia is regressed. They also noted the PI3K pathway was inhibited by inositol in vitro, and concluded that the deregulation of the PI3K pathways in the bronchial airway epithelium of smokers is an early, measurable and reversible event in the development of lung cancer.
Meanwhile, scientists at the National Cancer Institute in Maryland also studied the pathways through which genes are damaged by tobacco smoking and the pathways that regulate cancerous cell proliferation and survival. (2) After a review of data, they described the cell surface receptors and other upstream components required for tobacco carcinogen-induced activation of the Akt and mTOR pathways and the positive effects of inositol and other treatments upon them.
In Biochemical Pharmacology, December 2008 researchers reported inositol potentiating appropriate cell death. This effect correlated with down-regulation of various gene products that mediate cell survival, proliferation, metastasis, and invasion, all known to be regulated by NF-kappaB (a transcription factor that enhances production of inflammatory mediators). Inositol blocked NF-kappaB activation induced by cigarette smoke.
Cancer Epidemiology Biomarkers and Prevention, August 2006 reported a clinical study conducted to assess the safety, tolerability, maximum tolerated dose, and potential chemopreventive effects of inositol in smokers with bronchial abnormal cell development. Smokers between the ages of 40 and 74 participated in dose escalation ranging from 12 to 30 grams per day of inositol for a month to determine the maximum dose tolerated, which turned out to be 18 grams per day. Ten new subjects were then enrolled to take the maximum tolerated dose for 3 months. Side effects, when present, were mild and mainly gastrointestinal in nature. A significant rate of reduction in abnormal cells was observed (91% compared to 48% in the controls). A significant reduction in systolic and diastolic blood pressure by an average of 10mm Hg was also observed after taking 18 grams per day of inositol for a month or more.
Researchers acknowledged that chronic exposure of mice and rats to cigarette smoke affects T-cell responsiveness which may account for the decreased T-cell proliferative and T-dependent antibody responses in humans and animals exposed to cigarette smoke. In a study reported in the Journal of Pharmacology and Experimental Therapeutics, April 2000 researchers sought to discover the mechanism by which cigarette smoke affects T cell function. They found that spleen cells from animals with chronic nicotine exposure have depleted inositol stores and a decreased ability to raise intracellular calcium levels. Their results suggest that chronic smoking causes T cell energy reduction and inactivity by impairing pathways and depleting stored inositol resulting in a diminished level of inositol-sensitive calcium.
Mice were fed a diet supplemented with inositol and exposed for 5 months to a mixture of sidestream and mainstream cigarette smoke, in a study reported in Carcinogenesis, July, 1999. In the animals fed the control diet alone, the average number of manifest lung tumors was 2.1. In the animals given the control diet plus an inositol mixture, the number of manifest lung tumors was 1.0. Researchers concluded that the inositol constitutes an effective prevention regimen against the initiation of tobacco induced lung tumors.
(1) Airway PI3K pathway activation is an early and reversible event in lung cancer development. Gustafson AM et al. Sci Tranl Med. 2010 Apr 7;1(26):26ra25.
(2) The role of the Akt/mTor pathway in tobacco carcinogen-induced lung tumorigenesis. Memmott RM, Dennis PA. Clin Cancer res. 2010 Jan 1;16(1):4-10.