Similarly, increased Ranolazine dihydrochloride oxidative stress correlated with shorter telomere Pneumocandin B0 length in a study of insulin resistance and hypertension. Moreover, it has been suggested that telomere length might serve as a biomarker of cumulative exposure to oxidative stress and a prognostic indicator for risk of late-life diseases. The hypothesis that white blood cell telomere length is associated to morbidity or mortality has recently been tested, but the results have been conflicting. Interestingly, it has been shown that maternal diet influences the aortic telomere length through changes in DNA single stranded breaks, antioxidant capacity, and oxidative stress in rat pups. Oxidative stress has been suggested to play a role in the etiology of anxiety disorders, and support for the involvement of oxidative stress in the regulation of anxiety-like behavior in rodents has been observed in several studies. Shorter telomere length has been observed in other psychiatric diseases, including mood disorders and schizophrenia, and in schizophrenia patients with poor treatment response. Importantly, oxidative stress has been shown to be involved in the etiology of these disorders. Another intriguing putative mechanism involves adult neurogenesis, which has been shown to be involved in mental health and illness. It was recently shown that deficient neurogenesis correlates with reductions in telomere length in adult subependymal zone neural stem cells. Due to the lack of longitudinal studies, it is not known whether telomere shortening is a cause or a consequence of stress. A recent work in mice suggests that stress over a period of six months leads to accelerated telomere shortening in stressed, but not in the control mice, and even increased telomere length was observed in some control groups. In humans, telomere lengthening has been observed in a subset of individuals in two epidemiological studies in which samples were taken approximately 10 years apart. In both studies the telomere length at the follow-up was proportional to the telomere length at the baseline, with those individuals with the shortest telomeres to start with showing no difference or increase in the telomere length.