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--- home:diseases:anxiety [08.13.2019] – [Evidence of infectious cause] sallieq
+++ home:diseases:anxiety [01.26.2020] – [Research into various drug effects] sallieq
@@ Line 101: / Line 101: @@
 Interviews of patients with other diseases are [[home:patients:patient_interviews|also available]].
+===== Evidence of infectious cause =====
+Mark Lyte of the Texas Tech University School of Pharmacy noticed that lab mice dosed with //Campylobacter jejuni//, bacteria that are commonly a cause of food poisoning, were more anxious than control mice. After several experiments, Lyte’s team concluded that the vagus nerve, which extends into the colon, was probably transmitting the news of a gut infection to the brain areas involved in emotions. Reporting their results in the August 2007 //Brain, Behavior and Immunity//, the team also conjectured that the anxiety often exhibited by victims of bowel disorders may operate on the same network, which is not under conscious control:
+<blockquote>Infection and inflammation lead to changes in mood and cognition. Although the "classic" sickness behavior syndrome, involving fatigue, social withdrawal, and loss of appetites are most familiar, other emotional responses accompany immune activation, including anxiety. Recent studies have shown that gastrointestinal bacterial infections lead to enhanced anxiety-like behavior in mice. The bacteria-induced signal is most likely carried by vagal sensory neurons, and occurs early on (within 6h) during the infection. These signals induce evidence of activation in brain regions that integrate viscerosensory information with mood, and potentiate activation in brain regions established as key players in fear and anxiety.
+//**L.E. Goehler** et al.//(({{pubmed>long:17428636}}))</blockquote>
+Further, Neufeld //et al.// showed that germ-free mice exhibited reduced anxiety-like behavior as well as significant neurochemical changes in the brain compared to specific-pathogen-free mice. (({{pubmed>long:21054680}}))
+The frequency with which patients of certain Th1 diseases also experience anxiety(({{pubmed>long:8818377}})) (({{pubmed>long:18774427}})) (({{pubmed>long:18774427}})) (({{pubmed>long:9361174}})) (({{pubmed>long:15569892}})) (({{pubmed>long:7883407}})) (({{pubmed>long:9707157}})) (({{pubmed>long:12011605}})) (({{pubmed>long:11391746}})) may also suggest a single underlying cause.
+<blockquote>
+It is my opinion that early and prominent symptoms of Th1 disease are psychological which have been interpreted as anxiety, depression, insomnia, learning disabilities etc. These symptoms like physical ones are exacerbated during effective treatment of Th1 [diseases].
+By understanding this, one can lessen some of the impact of those symptoms, just as one can with the physical symptoms. Not knowing why one is 'suffering' increases the stress of the situation which then, actually intensifies the problem. By understanding, one can remain more relaxed which lessens the intensity and supports recovery. Also, by accepting the temporary limitations imposed, it is again less stressful and more beneficial for recovery.
+//**Greg Blaney, MD**// </blockquote>
+===== Research into various drug effects =====
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+ findings suggest that a low dose of THC produces subjective stress-relieving effects in line with those commonly reported among cannabis users, but that higher doses may non-specifically increase negative mood.  [[https://www.sciencedirect.com/science/article/abs/pii/S037687161730220X?via%3Dihub|effects of delta-9-THC on responses to the Trier Social Stress Test (TSST)Link]]
+baseline symptoms of depression (but not anxiety or stress) appeared to be exacerbated across time/tracked sessions. [[http://example.com|https://www.sciencedirect.com/science/article/pii/S0165032718303100?via%3Dihub Link]]
+Perhaps most well-studied is the role the CeA plays in unconditioned and conditioned fear generation (Ciocchi et al., 2010, Li et al., 2013, Tye et al., 2011), fear extinction, and conditioned inhibition (Amano et al., 2010), as well as conditioned orienting responses to emotionally salient stimuli (El-Amamy and Holland, 2007, Groshek et al., 2005).  [[https://www.cell.com/neuron/fulltext/S0896-6273(14)00017-8?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627314000178%3Fshowall%3Dtrue|The central amygdala Link]]
+the mechanisms by which stress increases amygdala-dmPFC synaptic strength and generates anxiety-like behaviors are not well understood. Here, we show that the mouse basolateral amygdala (BLA)-prelimbic prefrontal cortex (plPFC) circuit is engaged by stress and activation of this pathway in anxiogenic. [[https://www.cell.com/neuron/fulltext/S0896-6273(19)31090-6?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627319310906%3Fshowall%3Dtrue|Functional coupling between the amygdala and the dorsomedial prefrontal cortex Link]]
 ===== Notes and comments =====

home/diseases/anxiety.txt · Last modified: 09.14.2022 by 127.0.0.1