A recent study from Italy (1) has identified a relationship between the bacteria that causes stomach ulcers and heart disease. H Pylori is a bacteria that can colonize the lining of the stomach and remain there for a lifetime unless diagnosed and eliminated with antibiotics. This bacteria was demonstrated to be a major cause of stomach ulcers by two physicians ( Dr. Barry Marshall and Dr. Robin Warren) who won the Nobel Prize for their finding.
Atherosclerosis the formation of plaque in the walls of arteries, is in large part an inflammatory process (2,3). The coronary arteries supply oxygenated blood to heart muscle and heart valves. A heart attack (myocardial infarction) occurs when a plaque ruptures or tears, sending debris downstream in a coronary artery. That debris and/or the exposed ruptured plaque causes a blood clot that obstructs blood flow to a portion of the heart and if the clot remains untreated a heart attack (muscle damage) occurs within minutes to hours. This process can also result in a fatal abnormal heart rhythm (ventricular fibrillation).
A major source of inflammation that is known to contribute to atherosclerosis and heart attacks is infection (2). Many patients suffer heart attacks following an acute infection or severe emotional stress. Inflammation is involved in forming plaques, creating unstable plaques, causing plaque to tear or rupture and inflammation is involved in the dynamic process that leads to a heart attack (3). To quote the authors of this study:
Ischaemic heart disorders are the consequence of an atherosclerotic process. A concomitant cause of atherosclerosis is inflammation. Infections represent the single most frequent determinant of inflammation. In case of H pylori infection, the organism colonises the human stomach for life (if infection is not properly treated); therefore, the trigger is continuous and inflammation lasts for a lifetime.
The authors of this study found that a certain subset of H Pylori bacteria carry a protein that is similar to two or more very important and essential proteins in heart muscle. Those proteins are called human tropomyosin and cardiac ATPases. Both types of proteins are essential to the ability of the heart muscle to pump blood through the heart.
The authors postulate a mechanism called molecular mimicry. Because H Pylori proteins are very similar to certain proteins in the heart, colonization or infection in the GI tract by H Pylori results in an immune response directed against these foreign proteins which are very similar to proteins in heart muscle. The immune system”mistakes” these heart muscle proteins for the foreign proteins in H Pylori and mounts an immune response against the heart muscle. The study found that patients infected with certain H Pylori strains had higher circulating levels of inflammatory markers and BNP . BNP is associated with heart failure, (loss of heart muscle contracting ability) and loss of heart muscle function results in a poorer prognosis in patients with coronary artery disease.
Thus this study supports a direct link between bacterial infection in the GI tract and heart disease, mediated through the immune system.
This sort of molecular mimicry has been recognized in medicine as it relates to two very well known diseases caused by infections with a species of streptococcus (as in strep throat). Those diseases are rheumatic heart disease (also called rheumatic fever) and glomerulonephritis, Either of these can occur as a complication of strep infections, ergo the importance of diagnosing and treating strep throat.
H Pylori represents one of many examples of the interplay between bacteria in our GI tract, the immune system and disease causation. Intestinal dysbiosis (imbalance between healthy and disease causing bacteria that reside in our gut) has been associated with a multitude of disease processes including obesity, diabetes, psychiatric disorders and cancer (5,6,7,8,9,10).
An essential component of this process is the entry of foreign proteins or other antigens (immune stimulants) across the gut wall into the body where the immune system gets activated. Intestinal Permeability is a term that describes the ability of substances to cross the GI barrier (intestinal wall) and enter the circulation (blood or lymph glands). I have discussed this before. There are many potential causes of increased intestinal permeability (leaky gut) including small intestinal bacterial overgrowth (a specific kind of dysbiosis) dietary sources such plant lectins and saponins found in grains and legumes, stress, sleep deprivation and medications such as NSAIDS. When an individual suffers from leaky gut (increased intestinal permeability) the probability that toxic substances can enter the blood stream increases. Endotoxin (produced by pathogenic bacteria in the gut) has been related to many inflammatory disease processes wreaking havoc when it penetrates the intestinal barrier.
Intestinal permeability, auto-immune disease, molecular mimicry, and gut dysbiosis are topics often discussed in the Paleo community. These topics represent physiologic processes that relate to humans deviating from our evolutionary habits, diets and lifestyles.
References are below.
(1) Cross-sectional Study: CagA–positive Helicobacter pylori Infection, Acute Coronary Artery Disease and Systemic Levels of B-type Natriuretic Peptide Journal of Clinincal Pathology. 2014;67(3):251-257.
(2) 11. Epstein SE, Zhou YF, Zhu J. Infection and atherosclerosis: emerging mechanistic paradigms. Circulation 1999;100:e20–8.
(3) Ross R. Atherosclerosis: an inflammatory disease. N Engl J Med 1999;340:115–26
(4) Mayr M, Kiechl S, Mendall MA, et al. Increased risk of atherosclerosis is confined to CagA-positive Helicobacter pylori strains: prospective results from the Bruneck study. Stroke 2003;34:610–5.
(5) Diabetes, obesity and gut … [Best Pract Res Clin Gastroenterol. 2013] – PubMed – NCBI
(6) Involvement of gut microbiota in the de… [Gut Microbes. 2012 Jul-Aug] – PubMed – NCBI
(7) Crosstalk between the gut microbiota a… [Clin Microbiol Infect. 2012] – PubMed – NCBI
(8) [The role of gut microbiota in… [Postepy Hig Med Dosw (Online). 2013] – PubMed – NCBI
(9) [Research advances in th… [Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2013] – PubMed – NCBI
(10) The gut microbiota, obesity and insulin resi… [Mol Aspects Med. 2013] – PubMed – NCBI
Thanks for the post! this is very interesting. Would you then recommend to try to treat H Pylori? I heard there is no definitive treatment and that one needs to take a huge cocktail of antibiotics. not sure what’s the right thing to do 🙂
I do not routinely treat H pylori because of the nature of my practice but there are effective treatments that usually require multiple antibiotics and sometimes more than one course of treatment. It is worth pursuing for many reasons. Go to PubMed and search “H Pylori AND antibiotics” and you will find plenty of information. The treatment protocols have become more refined. As usual, probiotics during and after an course of antibiotics are likely beneficial. Plenty of fermented foods as a regular part of the diet can only be helpful.