While gut health and heart disease may seem unrelated at first glance, it turns out that the friendly bacteria living in our intestines may offer more benefits to our health than we ever imagined.
Over the last several decades, the research investigating the role that infection plays in heart disease has been mounting. Studies have found:
- An association between common systemic infections and heart disease (1)(2)(3)
- An association between gut infection and heart disease (4)(5)
Isn't dietary cholesterol the real cause of heart disease?
Even though cardiovascular disease is the leading cause of death worldwide, the jury is still out as to what exactly causes heart disease. (6) Popular opinion will tell us that the obvious cause for heart disease is a diet that is high cholesterol and in saturated fats.
But what happens when we look at traditional diets that were free of modern, processed conveniences? We find whole foods that are rich in both cholesterol and saturated fats. We also find no incidence of heart disease. (7)(8)
Still not convinced?
The latest medical literature reveals that there are many routes to heart disease, and that too many egg yolks is not necessarily one of them. In fact, for all the cholesterol in egg yolks, they are surprisingly protective. (9)(10)
If it is not cholesterol and saturated fats that lead to the buildup of atherosclerotic plaque, then what is the cause?
So far, the research points to several risk factors. A risk factor is something that increases a person's chance of getting a disease. Risk can be found in diet, lifestyle, or family history.
The risk factors for heart disease cover a wide spectrum of people and lifestyles. One thing that all heart disease risk factors have in common is oxidative stress. Oxidative stress happens on a cellular level. Excessive oxidative stress leads to the breakdown of cells and to tissue damage.
How does oxidative stress show up in the blood vessels? One way is in the form of atherosclerotic plaque. Atherosclerotic plaque is made up of:
- Immune cells, which play an important role in the inflammatory process
- Cell debris, which are pieces of cell from cells that have died
- Crystalline cholesterol (11)
When tissue becomes damaged, it becomes inflamed. If this goes on for too long, you see an ongoing vicious cycle of inflammation, leading to tissue damage, which in turn causes more inflammation, and so on.
Inflammation leads to the development and build up of plaque. The most recent studies on heart disease have found that inflammation is more related to heart disease than elevated levels of cholesterol! (12)(13)
How Leaky Gut Can Increase the Risk for Heart Disease
When we talk about the relationship between the digestive system and heart disease, we are really talking about another repercussion of a leaky, or permeable, gut lining.
Once the lining of the gut wall becomes permeable, something called an endotoxin can get into the bloodstream. Endotoxins are found in the cell wall of many disease-causing bacteria. When these bacteria die, the endotoxin is released.
Three things to remember about endotoxins and their role in heart disease:
1. Our immune system reacts strongly to endotoxins. When detected, the immune system will send out the message to begin an inflammatory response.
2. Endotoxins, which are pieces of disease-causing bacteria, can become lodged in human tissue and remain there for years, continually igniting an immune response.
3. Endotoxins, being pro-inflammatory, generate oxidative damage.
Endotoxins have been found in atherosclerotic plaque. These endotoxins are gut-derived. What this means is that a leaky gut lining allowed endotoxins to escape into the bloodstream. Based on this information, you would think that those with chronically leaky guts, or full-blown celiac disease, would be at higher risk for heart disease. And you would be correct. Studies show an increase risk of heart disease in celiac patients. (14) (15)
But anyone can have a leaky gut, not just those people with celiac disease. These are just some of the ways the gut wall can become permeable, or leaky:
- In times of stress, such as over-work or from lack of sleep
- When we over-eat
- From physical trauma
- During a gut infection
- After a bout of food poisoning
How Fermented Foods Can Reduce The Risk of Heart Disease
The relationship between infection and heart disease is so pronounced that one large trial even examined how effective an antibiotic may be in treating heart disease! (16) The antibiotic focused on fighting an infection caused by one single organism. At the end of the study, researchers found that it was unsuccessful in preventing heart disease or reducing the overall risk for heart disease. However, it furthered investigation into both prebiotic and probitoic therapy. (17)(18)(19)(20)
A prebiotic is a soluble fiber that feeds and nourishes the friendly bacteria living in our intestinal tract. Most of these bacteria have made their home in the lower end of the digestive tract, or what is commonly known as the large intestine.
A probiotic is a supplemental form of healthy bacteria. Usually, a probiotic offers one or several strains of healthy bacteria. While this is a good start, your gut is populated with a wide range of beneficial bacteria!
Fermented foods offer the best range of beneficial bacteria that can reduce inflammation, combat disease-causing microorganisms, and heal a permeable gut wall. When we eat fermented foods that are naturally rich in beneficial bacteria, we can bring balance to an unhealthy inner ecosystem and even reduce our risk of heart disease.
1. P. Libby, et al. Roles of infectious agents in atherosclerosis and restenosis: an assessment of the evidence and need for future research. Circulation. 1997; 98: 4095 - 4103.
2. K.J. Mattila, et al. Role of infection as a risk factor for atherosclerosis, myocardial infarction and stroke. Clin Infect Dis. 1998; 26: 719 - 734.
3. M. Kalayoglu, et al. Induction of Macrophage Foam Cell Formation by Chlamydia pneumoniae. J Infect Dis. 1998; 177 (3): 725 - 729.
4. The importance of the gastrointestinal system in the pathogenesis of heart failure. Eur Heart J. 2005 Nov; 26 (22): 2368 - 2374.
5. S. von Haehling, et al. The emerging role of the gut in chronic heart failure. Current Opinion in Clinical Nutrition & Metabolic Care. 2008 Sept; 11 (5): 632 - 639.
6. W Rosamond, et al. Heart disease and stroke statistics 2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2007; 115: e69 - e171.
7. Peter Bjerregaard, et al. Low incidence of cardiovascular disease among the Inuit: what is the evidence? Atherosclerosis. 2003;166: 351 - 357.
8. S. Lindeberg, et al. Apparent absence of stroke and ischaemic heart disease in a traditional Melanesian island: a clinical study in Kitava. J Intern Med. 1993 Mar; 233 (3): 269 - 275.
9. Fernandez ML. Dietary cholesterol provided by eggs and plasma lipoproteins in healthy populations. Curr Opin Clin Nutr Metab Care. 2006; 9(1): 8-12.
10. KL Herron, et al. High intake of cholesterol results in less atherogenic low-density lipoprotein particles in men and women independent of response classification. Metabolism. 2004 Jun; 53 (6): 823 - 30.
11. E. Latz, et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature. 29 April 2010; 464 (7293): 1357-1361.
12. I. Ikonomidis, et al. Inflammatory and non-invasive vascular markers: the multimarker approach for risk stratification in coronary artery disease. Atherosclerosis. 2008;199: 3 - 11.
13. P Barath, et al. Detection and localisation of tumor necrosis factor in human atheroma. Am J Cardiol. 1990; 65: 297 - 302.
14. M. Curione, et al. Prevalence of Coeliac Disease in Idiopathic Dilated Cardiomyopathy. The Lancet. 1999; 354: 222 - 223.
15. J.F. Ludvigsson, et al. Nationwide cohort study of risk of ischemic heart disease in patients with celiac disease. Circulation. 2011 Feb; 123 (5): 483 - 490.
16. T.D. Cook, et al. Azithromycin for the secondary prevention of coronary heart dis- ease events. The WIZARD study: a randomized controlled trial. JAMA. 2003; 290: 1459 - 1466.
17. R. Burcelin, et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes. 2007; 56: 1761 - 1772.
18. M.W. Schwartz, et al. Toll like receptor-4 mediates vascular inflammation and insulin resistance in diet-induced obesity. Circ Res. 2007; 100: 1589 - 1596.
19. P.L. Ogra, et al. In vivo effects of bifidobacteria and lactoferrin on gut endotoxin concentration and mucosal immunity in Balb/c mice. Dig Dis Sci. 2004; 49: 579 - 589.
20. A. Mazur, et al. Inulin attenuates atherosclerosis in apolipoprotein E-deficient mice. Br J Nutr. 2006; 96: 840 - 844.
For more by Donna Gates, click here.
For more on natural health, click here.
HuffPost Lifestyle is a daily newsletter that will make you happier and healthier — one email at a time. Learn more