Nutrigenetics Case Study: GSTT1

I have a client who is GSTT1 null type, which means he completely lacks this enzyme function, and as a result is not a good conjugator of glutathione to toxins.  Clinically, this is showing up as high levels of toxic, heavy metals, especially arsenic, lead, and mercury. 

The glutathione s-transferases (“GSTs,” including; GSTA; GSTM; GSTP; and GSTT) comprise a family of genes involved in Phase II detoxification, and specifically in the conjugation of toxins to GSH (Hollman, Tchounwou, & Huang, 2016).  Each class has a specific function, and GSTT has been found to play a role in the development of cancer (Hollman et al., 2016). According to Hollman et al. (2016), studies have found that GSTT1 null type is also a risk factor for the development of type 2 diabetes due to the fact that pancreatic beta cells are subject to high levels of oxidative stress.  It is also associated with inflammation, peripheral neuropathy, and cardiovascular disease (Hollman et al., 2016).  This is interesting, because when my client first came to me he had peripheral neuropathy and glucose dysregulation.  Further GSTT1 null type is associated with reduced antioxidant defense and impaired heavy metal detoxification (Penes, Weber, & Paun, 2017), which was exactly what I was seeing in my client.  

Research suggests that individuals who lack GSTT1 should reduce exposure to GSTT1 substrates as much as possible.  These include methyl bromide, chlorodinitrobenzene, and trans-stilbene oxide (Penes, Weber, & Paun, 2017).  Further, supplemental antioxidant support in the form of vitamins A, C, E, selenium, and lycopene, and supplemental omega-3 fatty acids may be beneficial (Penes, Weber, & Paun, 2017).  In particular, vitamin C may play a compensatory role in GSTT1 null types, and studies have found that vitamin C is more likely to be depleted in individuals with this genotype as a result (Schrawtz, 2014).  This means that my client’s need for vitamin C may be increased well beyond the current RDA.  Finally, as my client has other, functioning glutathione enzymes, anything that induces the production of glutathione, including the precursors cysteine (NAC), glutamine, and glycine, may be helpful (Penes, Weber, & Paun, 2017).  

References:

Hollman, A. L., Tchounwou, P. B., & Huang, H. C. (2016). The association between gene-environment interactions and diseases involving the human GST superfamily with SNP Variants. International journal of environmental research and public health, 13(4), 379.

Penes, N. O., Weber, B., & Paun, S. D. (2017). Role of genetic polymorphism in nutritional supplementation therapy in personalized medicine. Romanian journal of morphology and embryology 58(1), 53.

Schwartz, B. (2014). New criteria for supplementation of selected micronutrients in the era of nutrigenetics and nutrigenomics. International journal of food sciences and nutrition, 65(5), 529-53