What is “Personalized Medicine” and why are the medical profession and pharmaceutical industry moving toward making it the new paradigm for medical treatment?

Personalized medicine refers to determining the most effective course of treatment based on a patient’s biochemical constitution, which, in turn, is determined by his/her gene profile. Why is this approach gaining popularity? Consider just one area in which it may be very effective: medication side effects.

How often have you seen/heard ads that start by describing the health benefits of a particular drug only to end with a frightening description of its numerous potential side effects? Who experiences those reactions and how can they be avoided? Identifying slight differences in the biochemistry of individuals in a population, governed by their individual gene profiles, may provide the answers.

Similar to having different reactions to drugs, individuals also respond differently to environmental toxins. A recent study seems to support a role for personalized medicine in predicting and improving those responses.

Smoker Signals

Most people would probably tell you that inhaling the particles present in cigarette smoke will not improve your health, especially the health of your lungs. But not many would be aware that only 15% of smokers actually develop emphysema associated with chronic bronchitis (also known as chronic obstructive pulmonary disease or COPD).

The question is why such a surprisingly low number? You’ve probably already guessed the broader answer: gene profile. But a group of investigators recently set out to uncover more of the specifics, like which gene/genes is/are responsible and how do variations in gene structure make one person susceptible to smoke and another relatively resistant?

Nrf2 Protein Power

The investigators were aware of reports that identified a significantly lower level of a specific protein in the tissues of patients with COPD, as compared to healthy people. This protein, known as Nrf2, is often referred to as a redox-sensitive protein and controls a cellular system for detoxification.

Nrf2 is activated in cells under oxidant stress, for example, lung tissues exposed to high levels of toxic free radicals like those produced by cigarette smoke. Once Nrf2 is activated, it transports to the nucleus of the cell and turns on numerous genes (over 100) responsible for protecting cells from toxic insults.

The investigators theorized that individuals whose lung tissues respond to cigarette smoke with a robust activation of the Nrf2 protein are less susceptible to COPD than those with little or no Nrf2 activation. They tested their hypothesis with a mouse model of COPD.

Of Mice and Nrf2

The investigators used a strain of mice that developed COPD in response to a six-month exposure to cigarette smoke. In one experiment, they microscopically examined lung tissue from the mice and found similar pathological changes to lung tissue taken from human COPD patients.

The subjects of a separate experiment were completely lacking in the gene necessary for the production of Nrf2. This group exhibited more pronounced development of COPD and the tissues of the lung were more diseased.

These findings supported the researchers’ hypothesis of a direct correlation between the capacity to produce Nrf2 and preventing COPD in cigarette-smoke exposed mice. In other words, if the gene was absent (or functioning poorly), the individual exposed to cigarette smoke would develop the disease.

Boosting Nrf2 Response

Next, the investigators experimented with synthesizing a nutrient/chemical, a triterpenoid known as CDDO-IM, which, when fed to mice, acts as a potent activator of Nrf2. Now, they wondered whether pre-treating mice with this nutrient would protect them from the damaging effects of cigarette smoke and, moreover, if the mice would be more resistant the more Nrf2 their cells produced.

So, in another experiment, one group of mice was fed a diet containing CDDO-IM while the diet of a comparable group was lacking this Nrf2 activator. The CDDO-IM group developed significantly less lung tissue pathology from exposure to cigarette smoke than their counterparts. These results seem to imply that specific nutrients can help boost the cell-protective Nrf2 response and prevent, or at least improve, the symptoms of a toxin-induced disease.

Back to Personalized Medicine

The results from the above experiments, as well as observations from human reactions to drugs and environmental toxins, indicate a genetic capacity for cell protection against a variety of threats and their tissue-damaging effects.

Unfortunately, some of us are more susceptible to certain potentially toxic substances than others due to genetic differences. These differences manifest themselves not only in the ability to respond, but also in the strength of the response. Working from an individual’s genetic profile, personalized medicine could provide targeted treatment.

For example, prescribing nutrients that appear to activate the Nrf2-controlled detoxification cellular system could potentially support a more robust response. Some of these include sulforaphane, present in cruciferous vegetables (broccoli, Brussels sprouts), as well as other plant compounds such as lipoic acid.

In other words, a diet containing plenty of vegetables, whole grains, and fruits may promote a genetically more efficient detoxification system, helping to prevent a variety of diseases.

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