Glycine is a neurotransmitter for which elevated levels have been observed to correlate with inflammation. From the literature, it has been demonstrated that glycine has an immunomodulatory role – inhibiting, as well as stimulating, pro-inflammatory cytokine production and synthesis. However, it is not clear which inflammatory processes stimulate the increased synthesis of glycine. The studies below are a sampling of the research pertaining to glycine’s connection to the immune system.
- Carmans, et al. (2010), discussed that glycine has been shown to modulate peripheral immune cell responses. Glycine modulates macrophage effector functions implicated in central nervous system inflammation by stimulating TNF-α production by macrophages. The authors also noted that glycine levels are increased in several neuroinflammatory disorders, such as amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS).
- Hasegawa, et al., (2010) found that glycine can inhibit NF-κB activation and IL-6 production in human arterial endothelial cells, suggesting that it may exhibit anti-inflammatory effects during endothelial inflammation.
- It was reported by Almanza-Perez, et al., (2010) that glycine can regulate the production of inflammatory cytokines, including TNF-α and IL-6, through peroxisome proliferator-activated receptors (involved in energy balance) in adipocytes.
Glycine’s correlation with inflammation should be considered when examining a neurotransmitter report. Identifying and ruling out potential immune contributions is an important aspect of determining the root cause of a patient’s symptoms and imbalances observed in urinary neurotransmitter tests.