<html><div class=“mainarticle”>Related articles:</html> Anti-anxiety agents and antidepressants, Stress<html></div></html>

Anxiety or anxiety disorder is a common co-morbidity of patients sufferings from chronic inflammatory diseases. Like all inflammatory diseases, anxiety disorder is caused by the Th1 pathogensThe community of bacterial pathogens which cause chronic inflammatory disease - one which almost certainly includes multiple species and bacterial forms. and may temporarily increase during periods of immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed.. Cognitive dysfunctionThe loss of intellectual functions such as reasoning; memory loss; and other neurological abilities that is severe enough to interfere with daily functioning. can be managed using the generic strategies for managing immunopathology, and should resolve over the course of the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. (MP).

Anxiety can be subtle or debilitating or both. Some patients may not possess the presence of mind to know they're suffering from anxiety. It often does not occur to Marshall Protocol (MP) patients, even in the midst of severe anxiety, that their emotional state may be a product of the disease process.

Patients suffering from anxiety may wish to modify their dose of antibiotics or take an anti-anxiety agent.

Management of symptoms

Anxiety can and should be managed just like other symptoms. The following strategies and therapies may limit or help manage the anxiety a patient experiences

Another option is to consider how one can manage stress.

Continued stress will… interfere with the restoration of health even on the MP. If one has endeavoured to manage stress better but one's condition continues to deteriorate than something else is going on. If other medical problems have been ruled out, then, a chronic infection is very likely….

Early on, distress can and does exacerbate symptoms. Patients with better coping skills and support do better. As one improves, one experiences less or no distress in response to stressors.

Greg Blaney, MD

Finally there's certain evidence that olmesartan (Benicar)Medication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. may be useful against stress disorders. A National Institutes of Health paper says an important stress hormone, ANGII, and by extension stress disorders, could be managed by the use of ARBs, of which olmesartan is one.1)

Patients experiences

When I am in the midst of herxing my emotions tell me that I have always been herxing, always will, with no end in sight. I know many of us have that psychological response.

John McDonald

The physical stuff seems a bit more manageable than the anxiety stuff, as physical flares are tangible and come and go quickly by comparison. I guess the good news is that if you are hitting this aspect already, then you must certainly be working on healing there so it can't all be a bad thing.

For me, after working the minocycline brake/gas pedals as per MP, distraction is a great compatible non-drug tool that is easy to manage. Instead of allowing focus to remain in the areas that enlarge anxiety, respond with action that requires focus elsewhere when the claws of anxiety dig deep into your soul.

Experiment around and find what works best for you. Low energy/low risk/high return activities for me include games, puzzles, calling a trusted friend, curling up with a worthy book, handwork/crafts. Your list may be different. The main idea is to arm yourself with ample distraction actions and get adequate rest to help the MP medications and your immune system win the big battle.

Janet Foutin

Use the 'relaxation/meditation stuff.' I found that relaxing (sleeping) to loud rock music helped me through the darkest years.

Trevor Marshall, PhD

Patient interviews

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<html> <div class=“patientinterviewboxl”> <div class=“patientinterviewimage”></html><html></div> <div class=“patientinterviewtext”> <div class=“patientinterviewname”></html>Doreen V. (patient's mother)<html></div></html>

autism, ADHD, depression, severe anxiety, chronic fatigue syndrome (CFS)

Read the interview


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Interviews of patients with other diseases are 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:

Infection and inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. 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.2)

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. 3)

The frequency with which patients of certain Th1 diseasesThe chronic inflammatory diseases caused by bacterial pathogens. also experience anxiety4) 5) 6) 7) 8) 9) 10) 11) 12) may also suggest a single underlying cause.

It is my opinion that early and prominent symptoms of Th1 diseaseAny of the chronic inflammatory diseases caused by bacterial pathogens. 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

Research into various drug effects

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. 13) effects of delta-9-THC on responses to the Trier Social Stress Test (TSST)

Baseline symptoms of depression (but not anxiety or stress) appeared to be exacerbated across time/tracked sessions. Journal of Affective Disorders 14)

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). The central amygdala Link 15)

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. Functional coupling between the amygdala and the dorsomedial prefrontal cortex Link


===== Notes and comments =====


Brain Behav Immun. 2008 Mar;22(3):354-66. Epub 2007 Oct 24. Campylobacter jejuni infection increases anxiety-like behavior in the holeboard: possible anatomical substrates for viscerosensory modulation of exploratory behavior. Goehler LE, Park SM, Opitz N, Lyte M, Gaykema RP. Department of Psychology, University of Virginia, Charlottesville, VA 22904, USA. goehler@virgina.edu Abstract The presence of certain bacteria in the gastrointestinal tract influences behavior and brain function. For example, challenge with live Campylobacter jejuni (C. jejuni), a common food-born pathogen, reduces exploration of open arms of the plus maze, consistent with anxiety-like behavior, and activates brain regions associated with autonomic function, likely via a vagal pathway. As yet, however, little is known regarding the interface of immune sensory signals with brain substrates that mediate changes in behavioral states. To address this issue, we challenged mice with either C. jejuni or saline, and 7-8h later assessed anxiety-like behavior using the open holeboard, and used immunohistochemical detection of the protein c-Fos as an activation marker in the brain. C. jejuni treatment was associated with increased avoidance of the center regions of the holeboard, compared to saline-treated controls. Exposure to the holeboard induced activation in multiple brain regions previously implicated in anxiety-like behavior, including the lateral septum (LS), paraventricular (PVN) and dorsomedial hypothalamic nuclei (DMH), basolateral and central nuclei of the amygdala (BLA, CEA), bed nucleus of the stria terminalis (BST) and periaquiductal grey (PAG), compared to homecage controls. In C. jejuni-treated animals c-Fos induction also occurred in autonomic regions, as previously reported. The PVN, BLA, parts of the BST, medial prefrontal (mPFC) and anterior cingulate responded to both C. jejuni treatment and the holeboard, suggesting a role for these regions in the enhanced anxiety-like behavior observed. In saline-treated animals, anxiety-like behavior was predicted by activation in the CEA and BLA, whereas in C. jejuni-treated animals, c-Fos expression in the BST predicted the degree of anxiety-like behavior. These findings implicate the PVN, amygdala and BST as interfaces between gastrointestinal pathogenic challenge and brain regions that mediate behavioral responses to stress, and reinforce these nuclei as anatomical substrates by which viscerosensory stimuli can influence behavior.

PMID: 17920243

Mice raised in environments without any bacteria were far more likely to take risks than mice that had a normal mix of microbes, Sven Pettersson, a cellular microbiologist at the Karolinska Institute in Stockholm and the Genome Institute of Singapore, discovered with his colleagues. Mice generally skulk around in shadows and stay close to walls, but that behavior may not be the mice’s idea alone.

Mice raised in a sterile environment were much bolder, literally going out on a ledge more often than mice reared with bacteria in their bellies, Pettersson’s team reported in the Feb. 15 Proceedings of the National Academy of Sciences. Bacteria-free mice were also more active overall than their bacteria-laden counterparts. Inoculating bacteria-free newborn mice with intestinal bacteria reversed the changes in behavior. But restoring gut bacteria in adult bacteria-free mice did not change the rodents’ behavior, indicating that whatever bacteria do to the brain, they do it early in life. Bacteria’s presence or absence affected how the mice used certain brain chemicals and genes involved in brain development. Taken together, the results indicate that intestinal bacteria somehow shape the brain and make mice more anxious — or cautious, depending how you look at it, Pettersson says.

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