Is there a way to mitigate the damage caused by smoking cigarettes? Preliminary research is showing the answer to this question may be yes, and the result could be a financial blockbuster to anyone able to patent a form of it.
A compound made in the human body, known as inositol, is showing favorable results against several facets of damage from smoking cigarettes. Clinical trials are now being conducted under the auspices of the National Cancer Institute, and some have already been completed, though the results have not been publicized.
Components of tobacco have been long known to spur the initiation and growth of lung tumors and other negative effects through their ability to affect genes and to alter signaling pathways in favor of those leading to cell proliferation and cancer growth. The free reign of this process has led to a statistic that says up to 90% of lung cancer cases are associated with tobacco usage. Researchers are studying the ability of inositol to end this free reign.
How Inositol may Help Those Who Smoke
Inositol is a simple carbohydrate often classed with B vitamins, but it is not technically a vitamin. It occurs in several forms, with myo-inositol being the most prominent and widely occurring in nature. Inositol is also found in many foods, especially cantaloupe and citrus, in the form of inositol hexaphosphate (IP6). However, in this bound state, it is not bioavailable to any great degree.
The basic premise behind the clinical trials on inositol is that although the body naturally produces 4 grams of inositol every day from glucose in the kidneys, this small amount is not enough to stand up to the threat posed by cigarette smoking. But when inositol levels are increased beyond what the body naturally makes, there is power in numbers, and inositol can exert a protective affect.
This premise became apparent in a study back in 1996 when animals chronically treated with nicotine exhibited a loss of ability to produce inositol. It is backed up by research in 2006 that found inositol to be safe at the maximum tolerable limit of 18 grams per day, leaving a wide range to be used for therapeutic purposes.
Since the 1996 study, researchers have continued to add to the growing knowledge base that supports the theories now being tested in clinical trials.
- In 1999, mice exposed to cigarette smoke and treated with a combination of supplemental inositol and dexamethasone (a synthetic glucocorticoid) developed less than half the number of lung tumors as mice not treated. The researchers of this study concluded that inositol is an effective prevention against initiation of tobacco induced lung tumors.
- In 2000, researchers studying the connection between cigarette smoke and T cell function found that animals chronically exposed to cigarette smoke have depleted stores of inositol. They concluded that smoking results in T cell energy reduction, and impairment in critical pathways is the depleting factor.
- In 2008, inositol was found to initiate apoptosis (programmed cell death) and down-regulate genes that sponsored proliferation, invasion and metastasis of cancerous cells, and to block a transcription factor that is activiated by cigarette smoke.
- In a review of data published in 2010, researchers from the National Cancer Institute in Maryland outlined the components necessary for activating noted pathways and the positive effect of treatment with inositol.
- In that same year, researchers identified a reduction in the P13K pathway as an early event in lung cancer development, and found that it could be mediated by inositol.
- Shortly after, researchers at Boston University Medical Center discovered that the P13K pathway was actually activated in the airways of smokers before a tumor begins to form. This team also found that when inositol treatment was given, abnormal development and growth regressed.
- In 2013, researchers in China found that a higher inositol phosphate (IP7) is turning out to be a key cellular signaling molecule. They reported that cigarette smoke extract and nicotine reduces levels of IP7 in white blood cells, leading to a cascade of negative events. However these events were sidestepped by increasing IP7. The team concluded that modifying white cell death provides a strategy and therapeutic target for the treatment of tobacco-induced chronic obstructive pulmonary disease.
It seems clear by now that inositol plays a major role in protecting smokers, and it is safe even at doses up to 18 grams. This begs the question of why the smoking public has not been alerted to these discoveries. Is it possible that this information is being suppressed until a drug version gets the green light from the FDA?
The fact that inositol is already being referred to as a ‘drug’ in the National Cancer Institute’s coverage of the ongoing clinical trials suggests that this is what is happening.