chronic overnutrition (ie overeating) results in activation of the IKKBeta/NF-kappaB complex, increase NF-kappaB transcription and inflammation. This leads to ER (endoplasmic reticulum) stress
elevated FFA (free-fatty acids) shown to produce inflammation and insulin resistance through endoplasmic reticulum stress. The main target in this pathway is IKK-Beta overexpression.
sleep disruption is a major symptom in those with PTSD. There is no greater stress than combat. The majority of research on PTSD is done on combat veterans
stress results in shrinkage of the hippocampus of the brain. This would result in deficiency in serotonin and thus contribute to many of the symptoms found in those with PTSD.
Always remember to evaluate cortisol in post stress psychiatric disorders. normallzation of cortisol can resolve psychiatric condition indicating that the underlying etiology is adrenal in nature.
Relapsing remitting MS patients found to have in increased 8OHdG, reduced glutathione, reduced glutathione to oxidized glutathione ratio, super oxidized disumutase, glutathione reductase, and global oxidative stress. In contrast, decreased total antioxidant capacity, oxidized glutathione, glutathione perioxidase, and glutathione transferase were found in relapsing remitting MS patients.
Stress decreases the innate immune response. This is critical in the battle against cancer. Specifically, low NK activity is found in stress individuals with cancer.
Astaxanthin at 20 mg found to reduce oxidized LDL and other oxidative stress biomarkers as assessed by Malondialdehydy, SOD, Isoprostane, and TAC. The dose was 20 mg for 12 weeks. This higher dose was associated with minimal side effects--red stools.
Sex steroid hormones are primarily responsible for sex difference in adult HPA function; androgens inhibit whereas estrogens
enhance HPA axis activation after a stressor
the PVN contains relatively high levels of AR (Bingaman et al., 1994; Zhou et al., 1994) and ERβ (Alves et al., 1998; Hrabovszky et al., 1998; Somponpun and Sladek, 2003) but is essentially devoid of ERα
the nonaromatizable androgen DHT and the nonselective ER ligand E2 influence HPA
reactivity by acting on neurons within or surrounding the PVN
inhibitory action of DHT is detectable at both the level
of hormone secretion as well as PVN c-fos mRNA expression
the inhibition can be mimicked by the DHT metabolite
3β-diol and by the subtype selective ERβ agonist DPN
E2 acts to enhance HPA reactivity
the ability of the ER antagonist tamoxifen, but
not the AR antagonist flutamide, to block the inhibitory actions of DHT, speaks to the intracellular mechanism by which this
inhibitory signal might be transduced.
that is because the interaction with the DHT metabolite is not with the AR, but with the ER-beta.
the DHT metabolite 3β-diol and the ERβ-subtype-selective agonist DPN suppressed ACTH, corticosterone, and c-fos
mRNA responses to restraint stress in a manner similar to DHT
metabolism of DHT to
3β-diol and subsequent binding to ERβ can be inhibitory to HPA reactivity, and this is one possible mechanism for the action
of DHT.
Our data also suggest that E2 enhances the reactivity of the HPA axis to stress by acting on or near neurons of the PVN
the actions of E2 appear to be through an ERα-dependent mechanism
these studies suggest that ERβ, within the male hypothalamus, acts to inhibit the HPA axis and that the inhibitory
effects of DHT may be, at least in part, via its intracellular conversion to 3β-diol and subsequent binding to ERβ