H. pylori is a gram-negative spirochete bacteria that may reside in the stomach or first part of the small intestine. To proliferate it requires an acidic environment—nestling into the rich mucosa of the stomach. To survive the harsh pH of the stomach, H. pylori releases an enzyme called urease. This enzyme can be detected on breath testing and is considered the Gold Standard test to determine active infection.
Another caveat of urease is that it breaks down the waste product urea into ammonia and bicarbonate. These two alkaline compounds protect the bacteria from the acidic stomach secretions by neutralizing the mucous around it. Due to this protective layer and the depths H. pylori burrows, the bacteria may be difficult to detect with traditional testing.
The prevalence of H. pylori cannot be ignored. An estimated 50% of the population may have the infection; with advanced age risk of infection increases (1). Infection with H. pylori is commonly known to be an etiological factor in GERD and peptic ulcers and may predispose to gastrointestinal cancers. However, symptoms may be more insidious—vague post-prandial sweating, weakness, pallor, autonomic symptoms, and neurocognitive symptoms (2).
While H. pylori leads to local inflammation of the mucosa, the global effect on digestion can be reductions of stomach acid. Because of this, protein digestion may be greatly hindered in those with infection. This may lead to key amino acid deficiencies as well as hindered B12 absorption, which requires an acidic stomach to activate intrinsic factor. Yet another effect of H. pylori infection is its ability to disrupt mucosal adhesion molecules leading to a compromised gut barrier (2).
Autonomic dysfunction may result from H. pylori infection in part via the connection between the gut and the autonomic nervous system—the enteric nervous system. In a 2004 study of over 100 patients with atypical chest pain and heart rate variability, a positive association between H. pylori infection and cardiovascular symptoms was found (3).
Could there be a link between H. pylori infection and the autonomic dysfunction seen in CFS and POTS?
Small intestinal bowel overgrowth is common place in both CFS and fibromyalgia. Many suggest it is a causative mechanism in fibromyalgia. The hallmark sign of SIBO is excessive hydrogen gas produced by the bacterial colonies. This gas can also be measured on breath testing. Bacterial gas production irritates the mucosa and promotes symptoms of IBS. To add insult to injury, H. pylori thrives on hydrogen gas—proliferating with the help of other bacterial species. In a large study (n=6,476) H. pylori infection was significantly prevalent in GERD patients as well as those with GERD and IBS (4).
Yet another consequence of H. pylori infection is over production of tumor necrosis factor-alpha; TNF-a. This molecule plays a key role in CFS pathogenesis as it promotes systemic inflammation, sickness behaviors, and disrupts immune surveillance of pathogens. H. pylori induces TNF-a which is believed to be one mechanism in its role in cancers (5). In CFS, undiagnosed infection may promote the vicious cycle of immune dysregulation and inflammation via TNF-a.
Summary of H. pylori Effects:
- Disrupts intestinal barrier to promote leaky gut
- Increases TNF-a
- Decreases stomach acid
- Increases norepinepherine
- Promotes food sensitivities (gluten, casein, lactose)
- Depletes vitamin B12
- Disrupts normal neurotransmitter balance between serotonin, melatonin, tryptamine
- Depletes arginine
According to Dr. Amy Yasko (2), chronic H. pylori infection is prevalent in her autism and chronic illness patients. To date, no studies have looked at the incidence of H. pylori infection and chronic fatigue syndrome. One study suggested this infection was statistically significant in a cohort of fibromyalgia patients. However, the researchers utilized inaccurate testing methods (6). The jury is still out.
Have you been tested for H. Pylori? Let us know in the comments.
1 Pounder RE, Ng D. (1995) The prevalence of Helicobacter pylori infection in different countries. Aliment Pharmacol Ther. 9 Suppl 2:33-9. http://www.ncbi.nlm.nih.gov/pubmed/8547526
2 Yasko, A. & Mullan, N. (2012) Gastrointestinal Balance and Neurotransmitter Formation. Autism Science Digest, Issue 04. http://www.scribd.com/doc/98433639/Gastrointestinal-Balance-and-Neurotransmitter-Formation
3 Budzyński J, et al. (2004) Eur J Gastroenterol Hepatol. 2004 May;16(5):451-7. Autonomic nervous function in Helicobacter pylori-infected patients with atypical chest pain studied by analysis of heart rate variability. http://www.ncbi.nlm.nih.gov/pubmed/15097036
4 Yarandi SS, Nasseri-Moghaddam S, Mostajabi P, Malekzadeh R. (2010) Overlapping gastroesophageal reflux disease and irritable bowel syndrome: increased dysfunctional symptoms. World J Gastroenterol. 16(10):1232-8. http://www.ncbi.nlm.nih.gov/pubmed/20222167
5 Yea SS, Yang YI, Jang WH, Lee YJ, Bae HS, Paik KH. (2001) Association between TNF-alpha promoter polymorphism and Helicobacter pylori cagA subtype infection. J Clin Pathol. 54(9):703-6. http://www.ncbi.nlm.nih.gov/pubmed/11533078
6 Akkaya N, et al (2011) Helicobacter pylori seropositivity in fibromyalgia syndrome. Clin Rheumatol. 30(11):1519-20. Epub 2011 Sep 9. http://www.ncbi.nlm.nih.gov/pubmed/21904815