{Reference Type}: Journal Article
{Title}: The relationship between equol production status and normal tension glaucoma.
{Author}: Himori N;Uchida K;Ninomiya T;Nagai M;Sato K;Tsuda S;Omodaka K;Nakazawa T;
{Journal}: Int Ophthalmol
{Volume}: 44
{Issue}: 1
{Year}: 2024 Jun 27
{Factor}: 2.029
{DOI}: 10.1007/s10792-024-03225-3
{Abstract}: <B>OBJECTIVE: </B>Equol is metabolized by intestinal bacteria from soy isoflavones and is chemically similar to estrogen. Dietary habits, such as consumption of soy products, influence equol production. A relationship between glaucoma and estrogen has been identified; here, we investigated the relationship between equol production status and glaucoma in Japan.<BR><B>METHODS: </B>We recruited 68 normal-tension glaucoma (NTG) patients (male to female ratio 26:42, average age 63.0 ± 7.6 years) and 31 controls (male to female ratio 13:18, average age 66.0 ± 6.3 years) from our hospital. All women included were postmenopausal. Urinary equol concentration was quantified with the ELISA method. MD was calculated based on the Humphrey visual field. The association between MD and equol was analyzed with Spearman's rank correlation coefficient. The Mann-Whitney U test was used to compare the equol-producing (> 1 μM) and non-producing (< 1 μM) subjects. We also investigated the association between equol and glaucoma with a logistic regression analysis.<BR><B>RESULTS: </B>There was a significant association between equol and MD (r = 0.36, P < 0.01) in the NTG patients. Glaucoma, represented by MD, was significantly milder in the equol-producing subjects than the non-equol producing subjects (P = 0.03). A multivariate analysis revealed the independent contributions of equol, cpRNFLT, and IOP to MD (P = 0.03, P = 0.04, and P < 0.01, respectively).<BR><B>CONCLUSIONS: </B>Our results suggest that equol, acting through estrogen receptor-mediated neuroprotective effects, might be involved in suppressing the progression of NTG. This result also adds to evidence that glaucoma may be influenced by lifestyle.