Answer: Yes and no. Is the bug truly the root cause? I believe most of you are aware that the nasty bugs are secondary to poor internal terrain.
Our team recognizes 5 main mechanisms that drive most diseases. One we call thrive vs survive. A subset of this mechanism is the more commonly recognized phrase, "fight or flight." I believe if you dissect the two phrases, you will agree that you "fight or flight" to thrive and, in this case, survive. Thus thrive vs survive is a higher-order driver (more of a root-cause)
When you think about PTSD, emotional trauma, and other afflictions particularly impacting our military and veterans, you think of brain conditions. Brain trauma of all types may lead to depression and anxiety but also to more severe neurological and neurodegenerative conditions.
Dr. Trempe and I explained this process in a paper we published in Frontiers Aging Neuroscience.
Here is the abstract for this paper. However, the purpose of this blog is to explore beyond the brain for individuals affected by traumatic brain-centric events.
Abstract: The path to sporadic Alzheimer’s is a tragic journey beginning prior to birth and ending in the most dreaded disease of society. Along the disease path are a myriad of clues that portend AD, many of which are complaints of seemingly unrelated conditions from chronic migraines, mood disorders, eye diseases, metabolic syndromes, periodontal diseases, hormonal and autoimmune diseases. Properly treating, not just managing, these diseases prior to onset of dementia, may significantly reduce dementia incidences.
Current high levels of health complaints reflect a state of generalized poor health and compromised immunity. During the mid-Victorian era, people were long-lived yet healthy, suffering from chronic diseases at one-tenth the rate of peoples today. It’s our poor health, at any age that increases susceptibility to chronic diseases and Alzheimer’s. Infection is involved in many cases of Alzheimer’s and other neurodegenerative diseases but is also implicated in many chronic conditions.
Scientists seeking causation recognize that Alzheimer’ is multifactorial and systemic—not “brain only.” To slow, stop and reverse the AD epidemic, identification and reversal of causal factors must occur across the entire life spectrum of humans. This approach considers enhancing the immune status of our bodies and brains, and controlling inflammation and infection throughout the entire age spectrum.
Infection is a causal factor, but the root cause is multi-factorial and immune health related. Pasteur stated it best when acknowledging the work of Bernard in 19th Century France, “The seed is nothing, the soil is everything.”
For the very curious, in this paper I highlight a 70 year study - impossible for anyone to do routinely as it covers more than an entire adult lifespan. The conclusion of the study is quite remarkable - but obvious when you "peel the onion" back to the most basic mechanisms of disease. Feel free to write to me for an explanation if the paper isn't clear.
Now back to the point of this blog wrt H pylori causing stomach ulcers.
This paper caught my attention because, before (and long after - by doctors in denial) the connection between h pylori and stomach ulcers was made, stress was considered the key root cause. Since our understanding, the concept of stress as causal has pretty much disappeared. But should it have? After all, one key disease mechanism is "Thrive vs Survive" which also encompasses stress.
Objective
To investigate the effect of military stress on immune response and Helicobacter pylori stomach infections.
Methods
In this prospective, observational study, the Symptom Checklist-90 questionnaire was completed by military recruits before and following a 3-month basic training programme. H. pylori immunoglobulin (Ig)G levels, C14-urea breath-test values and levels of cortisol, catecholamine, and certain humoral and cellular immune responses were measured before and after the basic training.
Results
For 60 military recruits, somatization (development of unexplained medical conditions), depression and paranoid ideation scores were significantly increased after, compared with before, basic training. Post-training H. pylori IgG detection revealed three additional cases of H. pylori infection. Post-training C14-urea breath-test values were significantly higher than before training – thus suggesting higher levels of H. pylori colonization in the stomach.
Post-training cortisol and catecholamine levels were increased, while serum IgG levels were decreased; complement component (C)3 and C4 levels remained unchanged. Post-training CD4+ and CD8+ T-cell percentages and the CD4+/CD8+ ratio were significantly reduced compared with before training. Serum interleukin (IL)-2 levels were lower and IL-10 levels were higher following training and there was a significant decrease in the IL-2/IL-10 ratio.
Conclusion
Military stress may reduce humoral and cellular immune responses and may aggravate the severity of H. pylori infection.
Lewis note: They do not appear to be including the impact of heavy physical activity as a contributor - but they should. However, it's clear that the scoring does show emotional stress.
Introduction:
The army is a distinct occupational group and its members are at high risk of mental health problems. Recruits often undergo military and survival training in extremely harsh environments that make great demands on physical and mental strength. In addition, troops deployed in war zones face near-constant threats from opposing combatants. Such stresses cause psychological and pathophysiological changes,1,2 and have been identified as a primary reason for non-battle casualties in military personnel.3
Helicobacter pylori infection is one of the most common infections in humans worldwide. It is a substantial cause of chronic active gastritis, peptic ulcers and other stomach diseases that are closely correlated with gastric carcinoma and lymphoma.4–6 H. pylori has been categorized by the World Health Organization as a Class I carcinogen.7–9 Emerging epidemiological data show that H. pylori infection (and peptic ulcers resulting from H. pylori infection) are correlated with infectivity of the bacteria, and also with the host’s genetic profile and immune status, in addition to the microenvironment in the gastrointestinal tract.4
4. Backert S, Clyne M. Pathogenesis of Helicobacter pylori infection. Helicobacter 2011; 16 Suppl 1: 19–25. [PubMed] [Google Scholar]
Lewis note: When the h pylori igg test was readily available, I ran over 2,000 tests. NO ONE had a zero level - or undetected - IgG antibody level. This means that the organism is in everyone, but controlled by immunity. Anything that can compromise immunity opens the possibility that the bug may opportunistically multiply.
This summary explains how stressors cause H pylori infections to manifest clinically.
Stress is a nonspecific adaptive bodily response that can be stimulated by various internal and external events or social and psychological factors. It is recognized as an important cause of serious health problems. Psychological stress has been demonstrated to:
inhibit immune function,
increase the body’s susceptibility to infection and
play a substantial role in a variety of diseases.17,18
Anecdotal evidence and clinical observation have also suggested that exposure to psychological stress can affect disease outcomes in:
immune-related disorders, such as viral/bacterial infections and chronic autoimmune diseases.17,19,20
Interactions between the components of the HPA axis that produce cortisol and catecholamine, and which affect the sympathetic nervous system, also impact on immune regulation.21
17. Kemeny ME, Schedlowski M. Understanding the interaction between psychosocial stress and immune-related diseases: a stepwise progression. Brain Behav Immun 2007; 21: 1009–1018. [PubMed] [Google Scholar]
18. Melinder C, Udumyan R, Hiyoshi A, et al. Decreased stress resilience in young men significantly increases the risk of subsequent peptic ulcer disease - a prospective study of 233 093 men in Sweden. Aliment Pharmacol Ther 2015; 41: 1005–1015. [PubMed] [Google Scholar]
19. Godbout JP, Glaser R. Stress-induced immune dysregulation: implications for wound healing, infectious disease and cancer. J Neuroimmune Pharmacol 2006; 1: 421–427. [PubMed] [Google Scholar]
20. Kanno T, Iijima K, Abe Y, et al. Peptic ulcers after the Great East Japan earthquake and tsunami: possible existence of psychosocial stress ulcers in humans. J Gastroenterol 2013; 48: 483–490. [PubMed] [Google Scholar]
21. Smith SM, Vale WW. The role of the hypothalamic-pituitary-adrenal axis in neuroendocrine responses to stress. Dialogues Clin Neurosci 2006; 8: 383–395. [PMC free article] [PubMed] [Google Scholar]
Epidemiological data show that the presence of H. pylori infection is closely correlated with the immune response and microenvironment in the gastrointestinal tract.4,9
H. pylori infection is a substantial cause of numerous gastrointestinal diseases that are closely associated with gastric carcinoma and lymphoma.6
In patients with gastric ulcers, a synergistic relationship between H. pylori infection and stress is associated with ulcer recurrence, 22–24, but this relationship remains unclear.
In one study, H. pylori colonization was significantly higher in the stomachs of psychologically stressed BALB/c mice than in those of control mice, and the increased H. pylori colonization was thought to be mediated by a stress-related decrease in the mucosal immune response.10
6. Marshall BJ, Windsor HM. The relation of Helicobacter pylori to gastric adenocarcinoma and lymphoma: pathophysiology, epidemiology, screening, clinical presentation, treatment, and prevention. Med Clin North Am 2005; 89: 313–344. [PubMed] [Google Scholar]
7. Roesler BM, Rabelo-Gonçalves EM, Zeitune JM. Virulence factors of helicobacter pylori: a review. Clin Med Insights Gastroenterol 2014; 7: 9–17. [PMC free article] [PubMed] [Google Scholar]
8. Watari J, Chen N, Amenta PS, Fukui H, et al. Helicobacter pylori associated chronic gastritis, clinical syndromes, precancerous lesions, and pathogenesis of gastric cancer development. World J Gastroenterol 2014; 20: 5461–5473. [PMC free article] [PubMed] [Google Scholar]
9. Sepulveda AR. Helicobacter, Inflammation, and Gastric Cancer. Curr Pathobiol Rep 2013; 1: 9–18. [PMC free article] [PubMed] [Google Scholar]
10. Guo G, Jia KR, Shi Y, et al. Psychological stress enhances the colonization of the stomach by Helicobacter pylori in the BALB/c mouse. Stress 2009; 12: 478–485. [PubMed] [Google Scholar]
22. Yamamoto N, Sakagami T, Fukuda Y, et al. Influence of Helicobacter pylori infection on development of stress-induced gastric mucosal injury. J Gastroenterol 2000; 35: 332–340. [PubMed] [Google Scholar]
23. Budzynski J, Klopocka M. Brain-gut axis in the pathogenesis of Helicobacter pylori infection. World J Gastroenterol 2014; 20: 5212–5225. [PMC free article] [PubMed] [Google Scholar]
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