NIH to test glycine supplementation in mice!
Followers of this blog are no strangers to the idea of glycine supplementation—as with sweetamine—to eliminate excess inflammation. And there is also plenty of peer-reviewed research to back up glycine’s anti-inflammatory role. Then again, even if most of the conditions that make people sick and die these days—heart disease, cancer, etc—are now know to be tied to chronic inflammation, no claims as to glycine’s ability to prevent such diseases can yet be made, because this must be proven through peer-reviewed published studies on lab animals over years and on real people over decades of time. Toward that end, the National Institute on Aging—one of the National Institutes of Health (NIH)—has just decided to give us a good start by setting up a multi-center study on glycine supplementation in mice, using a protocol designed by yours truly.
Last September, I submitted an application to the NIA’s Interventional Testing Program (ITP). It is like submitting a grant application to the NIH, except that the Sponsor (myself, in this case) does not involve his own institution in the research directly: The entire study is performed at 3 study centers: at the University of Michigan, the University of Texas, and the Jackson Labs in Maine, by NIA-funded scientists, according to the protocol proposed by the sponsor. Every year, the NIA selects up to 5 dietary interventions that are hypothesized to extend the lifespan of the mice and/or delay the onset of age-related diseases. The Sponsor, however, has access to all the data generated, participates in the analysis of the data and is a co-author on resulting published studies.
Of course, the NIA’s decision to run the glycine supplementation experiment does not mean there will results overnight. Even intermediate results on the delay of age/inflammation-related conditions are likely at least two years away, but it’s a great start!
Here is the paragraph—taken straight from my application—which explains my rationale for why it’s a good idea to supplement the diet with glycine:
Physiological role of glycine
As a free amino acid, glycine’s major role appears to be mediated mainly through the glycine receptor, which is a gated chloride channel. Until relatively recently, glycine receptors were thought to be restricted to neurons, as receptors for glycine as an inhibitory neurotransmitter in the central nervous system. Over the last two decades, the same glycine receptor has been identified in a host of other body cell types, especially macrophages from all tissues and endothelial cells (Yamashina et al., 2007). Glycine is thus emerging as essentially a plasma membrane voltage regulator, maintaining the resting potential of cells by keeping these chloride channels sufficiently open to allow the influx of adequate amounts of chloride ion. Thus, cells such as macrophages—the mediators of inflammation—are less prone to activation, a phenomenon which is initiated by cellular depolarization via the opening of calcium channels and the influx of calcium. (Zhong et al., 2003). As most major lifespan-impacting diseases in our society (e.g., cancer, cardiovascular disease, diabetes) seem to stem from some sort of chronic inflammation, it is reasonable to hypothesize that this may be due to widespread low-grade deficiency of glycine in body fluids, and that supplementation with glycine might prevent the onset of many conditions rooted in chronic inflammation and associated with age.
Of course, we can all enjoy the benefits of glycine supplementation right now, and turn almost any diet into an anti-inflammatory diet with one daily serving of sweetamine!
Joel Brind, Ph.D. Jan 26, 2014