H.pylori infection has affected up to 4.4 billion individuals worldwide, based on a study in 2015.[1]
Regionally, prevalence is around forty-five per cent in China[2] and over fifty per cent in South Korea. Estimates in Hong Kong have one in two people infected acutely or previously as a child.[3]
This prevalence rate differs globally, with rates around forty per cent in the USA and as low as twenty-five per cent in Australia.[4]
How come so many people have had this, and I’ve never heard of it?
There are a few reasons.
Most of the time, the higher prevalence rates are in developing countries, with the African continent estimated to have up to an eighty per cent infection rate.[5]
Eight out of ten people!
On other occasions, H.pylori can be asymptomatic, or people have it but don’t know it.
It’s easy to catch H.pylori, and we often catch it when we are children![6]
Primary methods of transmission of H.pylori are via contaminated food, such as raw, unwashed vegetables, contaminated water and humans!
Yep, one of the most common ways children pick up the bacteria is through kissing or sharing a glass with a family member.[7]
This form of transmission is not as common as it used to be but is always a consideration in children who show digestive symptoms with H.pylori infection.
Unexpectedly to most, milk is also one of the common ways children pick up H.pylori.[8]
Most of the time, people who have it from childhood remain asymptomatic, but thirty per cent of people develop symptoms and feel unwell.
H.pylori can make people extremely unwell.
And this is what this article is exploring. H.pylori can be one of the leading causes of active gut issues in the upper part of the digestive system. It’s not just functional symptoms, though.
Many governments throughout Asia, including Japan, China and South Korea, cover eradicating H.pylori.[9]This coverage is because it can cause peptic ulcers or stomach ulcers and, in worse cases, gastric cancer.[10]
The research and discovery of what H.pylori does to us led to a Nobel prize in 2005.
The story of how the researchers got there is almost better than the prize itself.
Dr Barry Marshall, an Australian gastroenterologist, was at the centre of what is now one of the most famous modern-day self-experiments.
The story started in 1984. Dr Marshall found himself arguing with sceptics for years, trying to convince them of his hypothesis that H.pylori was a pathogenic bacteria that made people sick. Unfortunately, at the time, no animal models could prove that H.pylori was causing gastritis or inflammation in the stomach lining.
In his own words, Dr Marshall says, “if I was right, then anyone was susceptible to the bug and would develop gastritis and maybe an ulcer years later.”
At a loss on how to prove this to his peers, Dr Marshall decided to give himself a brew containing H.pylori, and after five days, his appetite decreased, and the bloating and fullness worsened. Dr Marshall also found his breath worsened, and as the days continued, he began vomiting.
Immediately, his next move was to get an endoscopy or a camera into his stomach to investigate what was happening. Lo and behold, his whole stomach lining was severely inflamed. This account was the first confirmed case of H.pylori, causing inflammation and digestive problems!
This n=1 case study was, of course, the beginning of the long journey to H.pylori, now one of the most chronic infections in the world.[11]
All because Dr Marshall and his colleagues wouldn’t give up on their hypothesis.
So where does that leave us now with H.pylori, and why do you need to know about it?
Symptoms of H.pylori primarily present when the bacteria has been living in the stomach for a long enough time to cause inflammation. Commonly, these symptoms are abdominal pain, especially in the upper abdomen, nausea, decreased appetite, fullness and bloating.
One of the main symptoms that often bring people into the clinic is the appearance or worsening of dyspepsia or indigestion.[12] This indigestion can cause fullness after eating, nausea, heartburn and bloating.
One of the ways that H.pylori lives in your stomach is also the cause of indigestion and gut symptoms you experience.
As I’ve been learning more about the bacteria that live within us, I’ve found myself amazed on many occasions at how adaptive they are and the lengths they go to set up a colony within a host. In this case, of course, the host is our stomach.
H.pylori is an excellent example of this. The acid in the gastric juice in the stomach is one of the most essential and effective immune barriers to bacteria coming into the body from the outside world.
H.pylori doesn’t just bypass this barrier, but it lives there too! It does so by releasing an enzyme called urease that decreases the acidity in the stomach.
This enzyme is so powerful at reducing stomach acidity that it enables H.pylori to take residence in the stomach.[13] To date, it is the only bacteria that can colonise the stomach in such a way.[14]
Once in the stomach, the bacteria then swim through the protective mucus lining on the stomach, a significant part of the immune defence, and latches onto the stomach lining, where the inflammation begins.
Wonderment aside, this inflammation in the stomach lining and the diluted, more alkaline environment is the beginning of not only some of the gut issues we’ve discussed above, such as bloating and indigestion, but also malabsorption issues.
Especially when it comes to absorbing protein, vitamin B12 and iron.[15]
You can read about the importance of amino acids and protein intake in another article on the website. Suffice to say that most people’s dietary intake is already down on minimum numbers, and throw in the low acidic environment, and we have a double problem.
Whilst the article above goes into more detail, running low on amino acids, and being unable to get them into the bloodstream basically makes the protein you get from your diet nutritionally benign. Protein only becomes nutritionally valuable when the stomach acid and the enzymes in the stomach break the protein up into its parts, the amino acids.
These amino acids are the building blocks of hormones such as insulin and essential brain chemicals such as serotonin.
On a vitamin and mineral level, evidence suggests H.pylori contributes to vitamin B12 deficiency,[16] lower vitamin C levels in the blood[17] and Vitamin A.[18]
The low stomach acid caused by the presence of H.pylori also affects the immune system.
We touched on the role of stomach acid in blocking bacteria from the outside world from entering the body and how H.pylori dilutes it to colonise itself.
But what effect does this have on the immune system?
Unfortunately, the less acidic the gastric juice, the higher the chances of many different bacterial and gut-oriented infections sneaking into the body through the gut leading to more issues.[19]
Now, this can also mean that opportunistic bacteria from the mouth can also get into the small intestine along with other gram-negative bacteria and contribute to SIBO or small intestinal bacterial overgrowth.[20]
All from one bacterial infection.
But that’s not all.
H.pylori interferes with the hormones created in your gut that manage hunger and your metabolism.
Or at least this is a hypothesis that’s yet to be proven. Once again, if you’d like to read more about the hormones that manage and control your appetite, go ahead.
Let’s start with H.pylori and the hormone ghrelin. Ghrelin’s primary function is to stimulate your appetite and breakdown of glucose and fat storage.[21]
Whilst the extent of H.pylori’s influence on ghrelin is still to be confirmed, one study showed that people who were positive for H.pylori infection had lower circulating ghrelin levels than those who tested negative.[22]
This hormonal influence also has significant consequences on how the body deals with sugar, so definitely a watch this space situation.
It doesn’t end there, though, as leptin, considered a partner in crime to ghrelin, has been increased in H.pylori patients.[23]
Why is this important?
One of leptin’s primary functions is to manage how the energy from your food is used, initiating satiety and thereby influencing weight loss.[24]
When leptin increases in the body, we see poorer fullness signals, overeating and increased total body mass.[25]
The cascade of metabolic issues continues as H.pylori also seems to influence insulin resistance.
There are seemingly a few ways this happens, which we won’t go into for the sake of brevity. Still, it’s safe to say that the research into the connection between these hormones and H.pylori is building to the point where even non-alcoholic fatty liver disease is associated with the infection.[26]
Reading an article like this can be scary as it always seems like you could be one of those people with H.pylori.
I’m here to tell you that you may not, and you can take a test for it. Your medical doctor can raise blood and breath tests for the urease exams we discussed earlier. Our clinic can also raise a sensitive stool exam to look for more chronic cases of H.pylori along with other markers of the function of your digestion, such as the state of your stomach acid.
Rest assured, I’ll be doing another in-depth article about the treatment options for H.pylori infections when the time is right!
Hope this helps xx
References
[1] Hooi JKY, Lai WY, Ng WK, et al. Global Prevalence of Helicobacter pylori Infection: Systematic Review and Meta-Analysis. Gastroenterology. 2017;153(2):420-429. doi:10.1053/j.gastro.2017.04.022
[2] Ren S, Cai P, Liu Y, et al. Prevalence of Helicobacter pylori infection in China: A systematic review and meta-analysis. J Gastroenterol Hepatol. 2022;37(3):464-470. doi:10.1111/jgh.15751
[3] https://www.med.cuhk.edu.hk/press-releases/cuhk-announces-worlds-first-meta-analysis-on-prevalence-of-helicobacter-pylori-infection, viewed Thursday 15th September, 2022.
[4] Hooi JKY, Lai WY, Ng WK, et al. Global Prevalence of Helicobacter pylori Infection: Systematic Review and Meta-Analysis. Gastroenterology. 2017;153(2):420-429. doi:10.1053/j.gastro.2017.04.022
[5] Hooi JKY, Lai WY, Ng WK, et al. Global Prevalence of Helicobacter pylori Infection: Systematic Review and Meta-Analysis. Gastroenterology. 2017;153(2):420-429. doi:10.1053/j.gastro.2017.04.022
[6] Kayali S, Manfredi M, Gaiani F, et al. Helicobacter pylori, transmission routes and recurrence of infection: state of the art. Acta Biomed. 2018;89(8-S):72-76. Published 2018 Dec 17. doi:10.23750/abm.v89i8-S.7947
[7] Gisbert JP, Arata IG, Boixeda D, et al. Role of partner’s infection in reinfection after Helicobacter pylori eradication. Eur J Gastroenterol Hepatol. 2002;14(8):865-871. doi:10.1097/00042737-200208000-00009
[8] Zhang YY, Xia HH, Zhuang ZH, Zhong J. Review article: ‘true’ re-infection of Helicobacter pylori after successful eradication–worldwide annual rates, risk factors and clinical implications. Aliment Pharmacol Ther. 2009;29(2):145-160. doi:10.1111/j.1365-2036.2008.03873.x
[9] Cho JH, Jin SY. Current guidelines for Helicobacter pylori treatment in East Asia 2022: Differences among China, Japan, and South Korea. World J Clin Cases. 2022 Jul 6;10(19):6349-6359. doi: 10.12998/wjcc.v10.i19.6349. PMID: 35979311; PMCID: PMC9294908.
[10] Crowe SE. Helicobacter pylori Infection. N Engl J Med. 2019;380(12):1158-1165. doi:10.1056/NEJMcp1710945
[11] Marshall B. Helicobacter pylori–a Nobel pursuit?. Can J Gastroenterol. 2008;22(11):895-896. doi:10.1155/2008/459810
[12] Fischbach W, Malfertheiner P. Helicobacter Pylori Infection. Dtsch Arztebl Int. 2018;115(25):429-436. doi:10.3238/arztebl.2018.0429
[13] Celli JP, Turner BS, Afdhal NH, et al. Helicobacter pylori moves through mucus by reducing mucin viscoelasticity. Proc Natl Acad Sci U S A. 2009;106(34):14321-14326. doi:10.1073/pnas.0903438106
[14] Celli JP, Turner BS, Afdhal NH, et al. Helicobacter pylori moves through mucus by reducing mucin viscoelasticity. Proc Natl Acad Sci U S A. 2009;106(34):14321-14326. doi:10.1073/pnas.0903438106
[15] Hudak L, Jaraisy A, Haj S, Muhsen K. An updated systematic review and meta-analysis on the association between Helicobacter pylori infection and iron deficiency anemia. Helicobacter. 2017;22(1):10.1111/hel.12330. doi:10.1111/hel.12330
[16] Kaptan K, Beyan C, Ural AU, et al. Helicobacter pylori–is it a novel causative agent in Vitamin B12 deficiency?. Arch Intern Med. 2000;160(9):1349-1353. doi:10.1001/archinte.160.9.1349
[17] Waring AJ, Drake IM, Schorah CJ, et al. Ascorbic acid and total vitamin C concentrations in plasma, gastric juice, and gastrointestinal mucosa: effects of gastritis and oral supplementation. Gut. 1996;38(2):171-176. doi:10.1136/gut.38.2.171
[18] Zhang ZW, Patchett SE, Perrett D, Domizio P, Farthing MJ. Gastric alpha-tocopherol and beta-carotene concentrations in association with Helicobacter pylori infection. Eur J Gastroenterol Hepatol. 2000;12(5):497-503. doi:10.1097/00042737-200012050-00004
[19] Obradovic M, Sudar-Milovanovic E, Soskic S, et al. Leptin and Obesity: Role and Clinical Implication. Front Endocrinol (Lausanne). 2021;12:585887. Published 2021 May 18. doi:10.3389/fendo.2021.585887
[20] https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0036-1584014, viewed Friday 16th September 2022.
[21] Young ER, Jialal I. Biochemistry, Ghrelin. [Updated 2022 Jul 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK547692/
[22] Nweneka CV, Prentice AM. Helicobacter pylori infection and circulating ghrelin levels – a systematic review. BMC Gastroenterol. 2011;11:7. Published 2011 Jan 26. doi:10.1186/1471-230X-11-7
[23] Roper J, Francois F, Shue PL, et al. Leptin and ghrelin in relation to Helicobacter pylori status in adult males. J Clin Endocrinol Metab. 2008;93(6):2350-2357. doi:10.1210/jc.2007-2057
[24] Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007;8(1):21-34. doi:10.1111/j.1467-789X.2006.00270.x
[25] Obradovic M, Sudar-Milovanovic E, Soskic S, et al. Leptin and Obesity: Role and Clinical Implication. Front Endocrinol (Lausanne). 2021;12:585887. Published 2021 May 18. doi:10.3389/fendo.2021.585887
[26] Abenavoli L, Milic N, Masarone M, Persico M. Association between non-alcoholic fatty liver disease, insulin resistance and Helicobacter pylori. Med Hypotheses. 2013;81(5):913-915. doi:10.1016/j.mehy.2013.08.011
