Part 2 Nutrigenomics: The Science of How Food Interacts With Our Genes

At this point, it may be worth asking, what do free radicals and antioxidants have to do with our genes? This seems like a simple environmental issue: eat more antioxidants to balance out the free radicals. Alas, the situation is not quite so simple. Often times, external antioxidant consumption is unable to keep up with free radical production. However, the cell has developed an extraordinary way to keep up with the myriad of free radicals that the body is exposed to. According to several studies, including a 2007 study in the journal Clinical Interventions in Aging Medical, the genome can produce specific antioxidant enzymes that break down free radicals in immense quantities, far more than external antioxidants (Rahman et al).


This all sounds well and good. But these antioxidant enzymes require an initiation of sorts — they aren’t simply active all the time. In fact, according to a 2013 review article in Oxidative Medicine and Cellular Longevity, intermittent activation of these enzymes complexes are preferable to continued activation (Hyun-Ae Soe et al). Thus we find our main question: how do we effectively and efficiently activate these enzyme complexes at the appropriate times? You guessed it, with broccoli, and, more specifically, with sulforaphane.


Sulforaphane has, along with various other phytochemicals, been shown to activate the Nrf2 pathway


According to a 2013 study on cancer prevention, this is how it works: Sulforaphane, the compound in broccoli, interacts with another compound called Keap1. Once Keap1 is activated, a subsequent compound, Nrf2, accumulates in the nucleus of the cell. Nrf2 is what we call a transcription factor, it helps express specific genes along the genome. In the case of Nrf2, the gene for Antioxidant Response Element (ARE) is activated. This is where the magic happens. The ARE spurs a release of several of the aforementioned enzyme complexes, ultimately preventing large amounts of free radical damage to the biological system (Kensler et al).


The bottom line of all this is that, while not containing many antioxidants of their own, the phytonutrients in broccoli enhance our body’s ability to produce antioxidants when necessary, and thus serves as a highly efficient guard against the dastardly effects of free radicals.


Now that we have our baseline biology covered, let us move to the macroscale and figure out with this may mean for human health.


In recent years, many aspects of human health have been connected to the Nrf2 pathway. The list is lengthy and includes topics such as general inflammation, mental health disorders, gastrointestinal diseases, and arthritis to name a few. However, I would like to focus on three areas in particular: obesity, cancer, and neurodegenerative diseases.


Let’s start with obesity


The excess body mass accumulated in the form of fat tissue causes detrimental effects on an obese individual’s health. How might the Nrf2 pathway impact obesity? The article cited previously, “The Role of Nrf2: Adipocyte Differentiation, Obesity, and Insulin Resistance” published in the Journal of Oxidative Medicine and Cellular Longevity covers this topic well. According to its findings, the precise biochemical relationship between the Nrf2 pathway and obesity is unclear. When you feed both wild-type mice (normal mice) and Nrf2 KO mice (mice in which the Nrf2 gene pathway does not work) a high fat diet, inconsistent results ensue. Notice, however, that the gene pathway was completely knocked out in these cases. Subsequently, the researchers concluded, “intermittent Nrf2 activation reduces total body weight and fat tissue content under HFD (high fat diet) conditions”. This is consistent with the idea that bioactive compounds in food may be the ideal modulator of the Nrf2 pathway, and, even more, that this may stem from its antioxidant effects, according to the authors (Hyun-Ae Soe et al).


In regards to a cancer, a similar, albeit different mechanism is thought to be at play


 In a 2014 study published in the journal Topics in Current Chemistry, the authors stated, “sulforaphane is a potent inducer of Nrf2 signaling and blocks the formation of dimethylbenz[a]anthracene-evoked mammary tumors in rats as well as other tumor types in various animal models”. Translated into English, this is a good sign. Ultimately, the authors concluded, “the overall potent and multimodal actions of sulforaphane makes it appealing to use in both preventive and therapeutic settings” (Kensler et al).


Finally, in an article titled “Nrf2-regulation in brain health and disease: implication of cerebral inflammation” published in the journal Neuropharmacology, authors concluded: emerging evidence suggests that Nrf2, in addition to its antioxidant functions, may also play an important role in regulating inflammation in the brain” (Sandberg et al). Moreover, depression is often cited to be a result of cerebral inflammation. As an article in the journal Psychoneuroendocrinology states, “A causative relationship between inflammation and depression is gradually gaining consistency” (Martín-de-Saavedra et al).


I digress for a moment: the subject of the Nrf2 pathway and antioxidant regulations invoke temptations of radical conclusion, even with certain causal relationships. It should be understood that the sheer number of individual molecular pathways in human physiology surpasses our comprehensive abilities at this point in time.

Evidently, nutritional science is complicated; yet, it has immense promise. Nutrigenomics, including broccoli, sulforaphane, and the Nrf2 pathway, as an example, is just one of the many ways in which the foods we eat are being evaluated for human health.

Looking to the future, I will actively search and simultaneously wait with patience for what may emerge in the scientific literature. Until then, I, as well as you, should stay curious, yet questioning — the foods we eat are far more powerful, and biochemically active than once thought — a concept which will only advance with time.

Source: By: Jonah Stavsky  The Commentator

Date:  November 12, 2017


Nutrigenomics Institute is not responsible for the comments and opinions included in this article




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