Home / Juvenon Health Journal / The Case for Personalized Medicine 1/09

 

Juvenon Health Journal volume 8 number 1 january 2009

the case for personalized medicine
By Benjamin V. Treadwell, Ph.D.

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 resveratrolcurcumin, green tea extract, garlic and 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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Research Update

A team of investigators, from Johns Hopkins University, Tohoku University and Dartmouth Medical School, recently conducted a series of experiments concerning the biochemical events and genetics involved in the development of chronic obstructive pulmonary disease (COPD). The group reported their findings in “Targeting Nrf2 with the triterpenoid CDDOimidazolide attenuates cigarette smoke-induced emphysema and cardiac dysfunction in mice,” published in the January 6, 2009 issue ofProceedings of the National Academy of Sciences (PNAS).

First the team wanted to determine why some (approximately 15%), but not all heavy smokers develop COPD. Previous work had shown that the protein Nrf2 was noticeably deficient in tissues taken from patients who developed COPD.

Nrf2 is an important protector, which is normally produced by cells. It acts as a transcriptional factor, activating the transcription and expression of a specific set of detoxification genes. The researchers proposed that an Nrf2 deficiency would lead to damage in cells exposed to toxins such as cigarette smoke.

Using a mouse model of the human disease, the investigators observed a correlation between Nrf2’s absence and the development of cigarette-smoke-induced COPD. They also found that they could stimulate production of Nrf2 with a synthesized nutrient/chemical, triterpenoid CDDOimidazolide (CDDO-IM). Feeding mice a diet containing CDDO-IM, as compared to a diet without it, prior to prolonged exposure to cigarette smoke, reduced the damage to the mouse lung tissue.

The results of this study suggest that the reason some smokers develop COPD, and others do not, is related to the capacity of their cells to produce sufficient amounts of the cell-protector, Nrf2, in response to exposure to toxins, such as cigarette smoke. They also imply that artificially increasing Nrf2 and activating the detoxification genes could lessen or prevent COPD damage.

Read article abstract here.

This Research Update column highlights articles related to recent scientific inquiry into the process of human aging. It is not intended to promote any specific ingredient, regimen, or use and should not be construed as evidence of the safety, effectiveness, or intended uses of the Juvenon product. The Juvenon label should be consulted for intended uses and appropriate directions for use of the product.

Ask Ben

Dr. Treadwell answers your questions about Juvenon™ Cellular Health Supplement

question: My doctor recently gave me a list of supplements I needed  to consider. On the list were Acetyl Carnitine and R-Lipoic Acid, strikingly similar to Juvenon, which I already take. My question is what is the difference between R-Lipoic Acid and Alpha Lipoic Acid, if any?  My doctor even underlined the “R” to make sure I got that instead of another type.  – G 

answer: The Juvenon lipoic acid contains what is commonly referred to as a racemic mixture, a 50:50 blend of the R (also known as R+) and S isomers. Both are active as antioxidants.

For the most part, only the R+ form of lipoic acid is made by and found in our bodies. Furthermore, the R+ form is the isomer that is used by the enzymes of the mitochondria for the conversion of food metabolites to energy. The S form cannot substitute in these reactions.

Virtually all of the human studies, going back some 35 years, have utilized the racemic mixture with great results and a good safety record. No study, to date, has actually proven that either the racemic preparation or the R+ form is more effective for human health. However, there is evidence to indicate the R+ isomer becomes unstable when isolated from the S isomer, forming unnatural polymerized products.

Juvenon may offer a product with the R+ form in the future, but only if/when it is proven to be safe and superior.

Benjamin V. Treadwell, Ph.D., is a former Harvard Medical School associate professor and member of Juvenon’s Scientific Advisory Board.

 

Creative Commons LicenseThe Case for Personalized Medicine 1/09 by Juvenon is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. If you are interested in more in-depth information on this topic, please contact us.


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