Helicobacter pylori, or better known as H. pylori, is a bacteria popularly associated with gastrointestinal problems like leaky gut, peptic ulcers, and gastritis. In the gut, H. pylori can bury itself in the GI mucosa, where the body’s immune cells cannot readily reach and fight it. The bacteria then destroys the lining that protects the stomach from harsh acids, making it susceptible to irritation, sores, or ulceration. There other species in the Heliobacter genus such as H. hepaticus and H. bilis which have been linked to liver infections and even liver and biliary cancer. Among all the known species, H. pylori is the most widely studied.
It is estimated that H. pylori affect two-thirds of the world’s population. However, many are oblivious to it because the bacterial infection is often asymptomatic. Therefore, it is possible to acquire it during childhood, via ingestion or via contact with infected fecal matter, and only know about it as an adult. But just because you are not experiencing any tummy issues, you can’t be sure you’re safe from all the trouble it brings. In addition, you could be a carrier that passes it on without ever noticing symptoms yourself! As most people know, the digestive and biliary systems are closely linked. So it is not a surprise that H.pylori poses a significant risk to your gallbladder too.
So How Exactly Does H.Pylori Affect the Gallbladder?
1. It contributes to the formation of gallstones.
The relationship between H.pylori and gallbladder diseases, specifically gallstones, is controversial due to conflicting studies and inconclusive reports. However, there is enough evidence to show that the bacterial population of H.pylori increases the risk of developing cholesterol-type gallstones. There are different mechanisms responsible for this condition, but recent studies have highlighted the role of H.pylori.
According to a study published by the World Journal of Surgical Oncology, H.pylori releases a protein similar to an aminopeptidase enzyme which sets the stage for gallstone formation. This enzyme has cholesterol crystallization promoting abilities. Therefore, the presence of H.pylori can contribute to the formation of gallstones and serve as a starting point for infection around which a stone can develop. Aside from releasing proteins, it also produces soluble antigens that can lead to irregularities in the cycling of conjugated bile acids. This may result in the abnormal transit time of bile acids.
Aside from the reasons mentioned above, H.pylori’s impact on the overall immune system indirectly contributes to lithiasis or stone formation.
2. H. Pylori aggravates gallbladder inflammation.
There are numerous known causes of chronic cholecystitis. One of them is the presence of bacterial infection in the biliary system. Various studies have shown that H. pylori are correlated with gallbladder inflammation through the exact mechanism that it contributes to the development of different gastrointestinal diseases.
Lab tests prove that in an H. pylori-infected gallbladder, the cells lining the gallbladder are destroyed, with swollen mitochondria and dilated endoplasmic reticulum. These are crucial parts of the cell needed for energy and the production and transport of proteins.
Rapid decrease in cell division, cell rupture, and cell death are all effects of H.pylori infection. The toxic factors in H pylori can activate factors inhibiting cell proliferation and ultimately lead to the death of cells.
Exposure of gallbladder cells to H. pylori also activates inflammatory cells in three ways: via cellular immunity, humoral immunity, and autoimmunity.
3. H. pylori increases the risk of developing gallbladder tumors and gallbladder cancer.
H.pylori’s role in inflammation leads to another gallbladder complication in which the bacteria contributes to the development of tumors and cancer of the gallbladder.
It is hypothesized that H.pylori plays a crucial role in developing benign tumors and the higher prevalence of adenomyomatosis (GAM). GAM, also called adenomyomatous hyperplasia of the gallbladder, involves the wall thickening of the gallbladder wall, cholesterol accumulation, cholesterol crystallization, and enlargement of the gallbladder. Though GAM is usually asymptomatic, this condition can be an initial stage of developing gallbladder cancer.
On the other hand, gallbladder cancer is characterized by chronic inflammation brought about by the presence of H.pylori. This leads to DNA damage, cell death, and modulated enzyme activities. In 1994, the International Agency for Research on Cancer declared that Heliobacter pylori infection is associated with the development of stomach cancer. Aside from stomach and gallbladder cancer, H.pylori has been linked to non-Hodgkin’s lymphoma.
What other organs do H. pylori affect?
Aside from the gastrointestinal tract and the gallbladder, other closely related organs within the biliary system, like the liver and pancreas, can also be severely affected by the proliferation of H. pylori.
Experiments in animal models have proven that the Heliobacter species can cause hepatitis, liver cancer, and severe damage to the immune system. H.pylori colonization is also a known culprit in pancreatic cancer.
In the biliary system, H.pylori has been implicated in diverse conditions such as skin diseases, coronary artery disease, autoimmune diseases, and growth retardation in children.
How Do We Prevent H.Pylori?
They say an ounce of prevention is worth a pound of cure. And since the sources of H.pylori are contaminated food and water, unclean and shared utensils, and activities that may cause fecal matter to be ingested (eating with dirty hands, contaminated food preparation, etc.), cleanliness and sanitation are crucial.
Is H. Pylori Contagious?
Yes, it is. And considering its prevalence and the fact that it is easily spread with intimate contact through saliva, sharing cups, etc., it is best to assume that we are part of the two-thirds who already have the bacteria in our system. In that case, what do we do?
The most common route taken by medical practitioners is the prescription of antibiotics, specifically the ‘triple therapies’. It consists of omeprazole, amoxicillin, and clarithromycin for 10 days, subsalicylate, metronidazole, and tetracycline for 14 days, and lansoprazole, amoxicillin, and clarithromycin for another 10 days. Years ago, the reported cure rates were as high as 85-90%. However, with the increasing rise of bacterial resistance, the failure rate of the standard medical therapy has been increasing. Therefore, it is important to follow directions rather than choosing to take one or parts of the prescribed protocol. Ask your doctor if you have issues with any part of the program and discuss the consequences and possibilities of alternatives.
H.Pylori Natural Treatment
Aside from standard pharmaceutic solutions, there are also natural ways to support the eradication of H. pylori.
- Zinc-Carnosine – There is a plethora of benefits from taking Zinc Carnosine. In support of reducing H. pylori infection, it reduces inflammation, helps the body heal ulcers, supports a healthy mucosal lining, and prevents free-radical damage to cells. Zinc carnosine’s antibacterial ability also provides added protection from more bacterial invaders. If you’re unsure what to take, try Zinc-Carnosine Complex with PepZin GI – 120 ct.
- Probiotics – Taking probiotics is especially important if you have taken antibiotics as it kills both good and bad bacteria. Taking supplements helps restore the normal GI flora by replenishing good bacteria.
- Enzyme and HCl Therapy – Since H.pylori alters and reduces stomach acidity, supplementation with Digestive Enzymes will help in increasing nutrient absorption. Some studies even state that some enzymes present in World Nutrition Vitalzym Hybrid Veggie Capsules (available on Amazon) can be used for cancer therapy and as a general treatment for digestive diseases. On the other hand, HCl therapy helps suppress or prevent the regrowth of the bacteria.
- Black Cumin Seed Oil – Black seed cumin is rich in antioxidants and anti-inflammatory compounds to help address the H.pylori symptoms. It is also a strong antibacterial oil that can help protect the body from further bacterial infections.
1.Abayli, B., Colakoglu, S., Serin, M., Erdogan, S., Isiksal, Y. F., Tuncer, I., … & Demiryurek, H. (2005). Helicobacter pylori in the etiology of cholesterol gallstones. Journal of clinical gastroenterology, 39(2), 134-137.
2.Boscak, A. R., Al-Hawary, M., & Ramsburgh, S. R. (2006). Adenomyomatosis of the gallbladder. Radiographics, 26(3), 941-946.
3.Chang, A. H., & Parsonnet, J. (2010). Role of bacteria in oncogenesis. Clinical microbiology reviews, 23(4), 837-857.
4.Chen, D. F., Hu, L., Yi, P., Liu, W. W., Fang, D. C., & Cao, H. (2008). Helicobacter pylori damages human gallbladder epithelial cells in vitro. World Journal of Gastroenterology: WJG, 14(45), 6924.
5.ERDEN, E., & KIYAN, M. (2010). Evaluation of the presence of Helicobacter species in the biliary system of Turkish patients with cholelithiasis. Turk J Gastroenterol, 21(4), 421-427.
6.Maurer, K. J., Carey, M. C., & Fox, J. G. (2009). Roles of infection, inflammation, and the immune system in cholesterol gallstone formation. Gastroenterology, 136(2), 425-440.
7.Pandey, M. (2007). Helicobacter species are associated with possible increase in risk of biliary lithiasis and benign biliary diseases. World journal of surgical oncology, 5(1), 94.
8.Pandey, M., Mishra, R. R., Dixit, R., Jaiswal, R., Shukla, M., & Nath, G. (2010). Helicobacter bilis in human gallbladder cancer: results of a case-control study and a meta-analysis. Asian Pac J Cancer Prev, 11(2), 343-347.
9.Raderer, M., Wrba, F., Kornek, G., Maca, T., Koller, D. Y., Weinlaender, G., … & Scheithauer, W. (1998). Association between Helicobacter pylori infection and pancreatic cancer. Oncology, 55(1), 16-19.
10.Risch, H. A. (2012). Pancreatic cancer: Helicobacter pylori colonization, N‐Nitrosamine exposures, and ABO blood group. Molecular carcinogenesis, 51(1), 109-118.
11.Zhou, D., Guan, W. B., Wang, J. D., Zhang, Y., Gong, W., & Quan, Z. W. (2013). A comparative study of clinicopathological features between chronic cholecystitis patients with and without Helicobacter pylori infection in gallbladder mucosa. PloS one, 8(7), e70265.