Monthly Archives: April 2010
A recent publication appeared in the April 7th issue of Science Translational Medicine concerning a novel approach to lung cancer prevention through detection of the oncogenic pathway, PI3K, and effective prevention of lung cancers with myo inositol. This study represents the emergence of epigenomics and nutritional medicine into mainstream medicine. It also represents a supreme opportunity for us to examine how the upregulation (switching-on) of a gene is directly related to a nutrient that acts as part of the whole. The study had two important aspects that were elegantly merged.
First was that the researchers were able to identify a gene that upregulated (switched on) the cancer-related pathway PI3K, in people with lung cancer. 90% of lung cancers occur in people who smoke, used to smoke, or had significant exposure to second-hand smoke. Of all those smokers, only 10-20% of them ultimately develop lung cancer. In the past, lung cancer had been diagnosed using invasive procedures that are usually only utilized when the cancer has already progressed enough to produce symptoms. At this stage both the treatment and prognosis are grim. As the press releases stated, the gene(s) that upregulate the PI3K pathway are detectable in the airways of smokers long before the cells become cancerous. This offers a novel approach to identifying those at high risk of lung cancer.
Second, the researchers were able to identify what they call “a lung cancer chemopreventive agent” that down-regulates, or “turns off” the expression of the PI3K pathway-inducing genes. The “chemopreventative agent” that they refer to is the semi-essential nutrient, myo-inositol.
Before you run out to the health food store to get your bottle of inositol, there are two important considerations. First, the cancer-promoting PI3K pathway also plays some very beneficial roles in our physiology. For example, it is likely involved in the formation of long term memories in a process called Long Term Potentiation (LTP). Chemicals that inhibit the PI3K pathway have been found to stop the expression of LTP. The PI3K pathway is also involved in normal cell growth and development.
Second, myo-inositol is formed naturally in the gut when various species of bifidobacteria convert phytic acid, (found in grains, nuts, seeds, brewer’s yeast, and many vegetables) into myo inositol. Bifidobacteria are an example of the good bacteria that have recently become part of the new nutriceutical digestive drink craze. Myo inositol facilitates several cellular functions like proper metabolism of cholesterol and transmission of neurotransmitter signaling of serotonin. I use inositol (along with other appropriate supplements) in my practice in some cases of depression, insomnia and fibromyalgia when there are obvious signs of digestive issues. I’ve found that if a person is actually low in inositol, they respond very quickly small doses (500-1000mg) with improved sleep and mood. Ultimately this is a sign of imbalanced gut bacteria which must be addressed in order for the person to become healthy again. Some practitioners use large doses of inositol for insomnia. It works but because large doses may be too inhibitory of the PI3K pathway, I don’t think it’s making the patient healthier…it’s just using too much of the substance to knock them out.
A couple other interesting facts: EPA, the omega-3 fat found in fish oil, improves the absorption of myo inositol in the gut which may partly explain why fish oil helps with depression. Phytic acid intake (as mentioned above, phytic acid is the precursor to myo inositol) is associated with lower risk of colon cancer and also switches off the PI3K pathway in the colon. There are several studies suggesting that colon cancer is also associated with the upregulation of the PI3K pathway.
Candida albicans, a yeast that commonly occurs in the gut, can use myo inositol as its primary food source. Overgrowth of this yeast can significantly alter bioavailability of myo inositol creating a scenario in which it would compete with its host, the human, for the nutrient. Giving a person myo inositol in a situation like this might initially help with symptoms but will ultimately lead to more yeast overgrowth in the gut making the situation worse.
Interestingly, many pathogenic species such as Salmonella prevent the production of myo inositol and produce more toxic and inflammatory byproducts of phytic acid. These organisms can survive in the gut in smaller numbers that don’t produce an all out infection. It’s possible that constant, low-level persistence of these pathogenic organisms could result in a functional, myo inositol deficiency.
Since overgrowth of some pathogenic bacteria and yeast can halt or alter the production of myo inositol, here are the questions we should be asking:
- Is the expression of PI3K a functional deficiency of myo inositol?
- Is it possible that gut dysbiosis (depleted colonies of beneficial bifidobacter and overgrowth of candida) can result in a deficiency of myo inositol and ultimately lead to an increase in cancers related to the PI3K pathway?
- How can we establish ideal ranges for myo inositol?
- At what level can PI3K be suppressed without negatively impacting its physiological benefits?
- Is it possible that the demographic with a high exposure to cigarette smoke has a higher incidence of upper respiratory infections which ultimately require more frequent use of antibiotics than the general population? Would this lead to reduced bifidobacter species and candida overgrowth in the gut resulting in a functional deficiency of myo inositol?
As with vitamin D and sunlight, will conventional medicine decide to replace myo inositol with a pill or will it strive to treat the root of the problem and create the conditions in which we evolved to give rise to its natural occurrence and create a healthier individual?by