It’s safe to say you are interested in gut health. That’s why you are here, right?
I suspect you want to find out more about leaky gut. Well, let’s try and decipher the evidence that is currently out there without getting too technical.
Leaky gut…you hear it being bantered about a lot. It’s the new buzzword in gut health, particularly in the wellbeing niche. The truth is the average medical professional doesn’t generally recognise leaky gut as a legitimate ailment.
Let’s look at the evidence and see who is right and who is wrong – it’s not strictly black and white.
What is leaky gut?
Food is broken down, and the nutrients are absorbed into the digestive tract. These nutrients are then transported around the body to your organs. The walls of the gastrointestinal tract are essential in protecting your body. They act as a barrier, controlling what does and doesn’t enter your bloodstream.
Our gut wall is made up of cells that form tight junctions. There are minute gaps in the junctions to let water and essential nutrients to cross into the bloodstream and tissues on the other side. But these gaps are tiny enough to block the movement of harmful substances such as bacteria and toxins.
This cellular set up is called intestinal permeability and describes how substances move across the intestinal barrier.
Leaky gut is also referred to as increased intestinal permeability or hyperpermeability. This is because the tight junctions of the intestinal wall become loose and form cracks or holes. That makes the gut more permeable, allowing partially digested food, bacteria, and toxins to pass from the gut into the bloodstream. Hence the term leaky gut.
It’s thought that when the gut is extra permeable and bacteria and toxins enter the bloodstream, this initiates extensive inflammation and triggers an immune system reaction in some people.
Why the controversy?
We mentioned that leaky gut isn’t recognised as a medical diagnosis by ‘conventional’ practitioners. In fact, there is a base of medical professionals that deny it exists.
However, supporters claim leaky gut is the fundamental cause of a broad range of conditions and modern health problems. Some of these include migraines, food sensitivities, mental health problems, autism, and chronic fatigue syndrome, just to mention a few.
One of the problems facing medicine today regarding this issue is insufficient scientific studies that reference ‘leaky gut syndrome.’ And if you know someone in a health profession, they will be adamant about the need for scientific evidence to prove the existence of a condition before it is recognised by most of the profession. Hence the reluctance to claim it as a condition.
This reluctance is also due, in part, to the fact that intestinal permeability is real – everyone has it. The average person could argue that because we all have it, why does it only affect a small portion of people?
Surprisingly, some health professionals agree that increased intestinal permeability exists in certain chronic diseases (Visser, Rozing, Sapone, Lammers, & Fasano, 2009) (Arrieta, Bistritz, & Meddings, 2006).
Presently, science is unsure as to whether it’s an outcome of chronic disease or the cause of chronic disease.
The sceptics claim that increased intestinal permeability is a chronic disease symptom rather than the disease’s underlying cause (Odenwald & Turner, 2013).
There are animal studies on coeliac disease, type 1 diabetes, and IBS that identify increased intestinal permeability before developing these chronic diseases. This clearly supports the theory that leaky gut is involved in the development of illness (Hall & Batt, 1991) (Meddings et al., 1999) (Odenwald & Turner, 2013). But, while animal studies are reasonable for studying human disease, they are not perfect. When conditions are linked to a leaky gut in humans, it doesn’t always mean it’s causative.
To make things a little muddier, a small-scale study found intestinal permeability in people with coeliac disease returned to normal in over 85% of people who followed a gluten-free diet for more than 12 months. This finding suggests that abnormal intestinal permeability responds to gluten ingestion, rather than the cause of the coeliac disease (Duerksen, Wilhelm-Boyles, & Parry, 2005).
There is not enough conclusive scientific evidence to prove that a leaky gut is the underlying cause of all chronic diseases. However, there is evidence that it’s present in several chronic conditions.
Therefore, the interesting question is whether a leaky gut is the CAUSE of chronic diseases, specifically autoimmune diseases. Another good question to be asked of science is whether leaky gut may cause problems elsewhere in the body.
What do we know about Leaky Gut?
It still remains a bit of a medical mystery, but here is a rundown of what we know.
What causes it?
Zonulin is a protein and the only known factor that regulates intestinal permeability (Fasano, 2012). When it’s triggered in genetically vulnerable people, it can possibly lead to leaky gut. The two elements that trigger its release are certain bacteria in the intestines and gluten (Fasano,2011).
However, there is some opposition to the above finding. Some studies have demonstrated that gluten only activates zonulin to increase hyperpermeability in certain conditions – such as coeliac disease or irritable bowel syndrome. Not just anyone who is genetically prone (Sander, Cummins, Henshall, & Powell, 2005) (Sapone, Lammers, & Casolaro, 2011).
The truth is, there are likely multiple contributing factors that increase intestinal hyperpermeability.
Studies have indicated that a diet high in sugar, especially fructose, has been shown to harm the intestinal wall’s barrier function (Bischoff, et al., 2014) (Spruss & Bergheim, 2009). This can cause temporary harm and allowing the passage of toxins and bacteria into the bloodstream.
There is also evidence that long-term use of non-steroidal anti-inflammatory drugs such as ibuprofen can increase intestinal permeability and contribute to leaky gut (Bjarnason & Takeuchi, 2009) (Groschwitz & Hogan, 2009) (Hollander, 1999). The long-term use of these drugs has also been known to be implicit in other gastrointestinal disorders.
Excessive alcohol intake (Ferrier, et al., 2006) (Groschwitz & Hogan, 2009) and chronic stress (Konturek, Brzozowski, & Konturek, 2011) have also been shown to contribute to various gastrointestinal disorders, including leaky gut.
Chronic inflammation is not only reported to be caused by leaky gut, but there is emerging evidence to suggest that it may contribute to leaky gut syndrome (Hietbrink, et al., 2009). These findings lead us to ‘overall gut health.’ When the balance between harmful bacteria and good bacteria is disrupted, and the population tips favoring harmful bacteria, it can adversely affect the intestinal wall’s barrier function, causing leakage (Arrieta, Bistritz, & Meddings, 2006) (Bischoff, et al., 2014).
Who Gets Leaky Gut?
All these contributing factors effectively amount to the modern lifestyle. So everyone is at risk.
We all have some degree of leaky gut, as this barrier is not entirely impenetrable. It shouldn’t be; we need it for our survival.
But, hyperpermeability does not automatically equal disease. The liver and kidneys are also protective mechanisms that defend us against harmful toxins. If these two organs are in perfect working condition, the leaky gut symptoms won’t be present. Genes also play a role. But there is a lot more to understand.
What hasn’t been proven?
Advocates of leaky gut have argued that it’s linked to a broad range of conditions, including autism, mental health problems, and cancer. All of these assertions are yet to be demonstrated by science.
There are conflicting studies regarding gut permeability and autistic children. A few studies indicate the children have increased gut permeability. But there are more investigations categorically showing the direct opposite. There is also no evidence to show that a leaky gut is present before the start of autism. This indicates there’s no evidence that it’s a causal component of autism.
Evidence is available to suggest that bacteria penetrating the gastrointestinal barrier may play a part in mental health disorders such as depression and anxiety. But additional investigation is required to prove any potential causative factor. (Bested, Logan, & Selhub, 2013) (Evrensel & Ceylan, 2015).
There is presently no scientific proof for the claim that leaky gut syndrome causes cancer.
What we know for sure…
Leaky gut is a condition in which bacteria and toxins pass through small junctions in the intestinal wall into the bloodstream.
Various medical professionals reject that leaky gut exists, but there is growing evidence to substantiate that increased intestinal permeability is real and present in several autoimmune disorders.
However, there isn’t enough evidence to conclude that leaky gut syndrome is the underlying cause of the diseases where it is present.
What can we do about Leaky gut?
Research into intestinal hyperpermeability is in the early years, and most of what is known is speculated from animal studies. There is evidence emerging to suggest that preventing intestinal hyperpermeability involves doing the same things that promote good health overall – eating a diet full of healthy foods and exercising (Durk, et al., 2019). Take a look here if you would like to find out more about how exercise improves your gut health.
Although leaky gut syndrome is not an official medical diagnosis, there are actions you implement to improve your gut health and decrease your chances of having the consequences of intestinal hyperpermeability.
The main aim of the interventions is to increase the number of beneficial bacteria.
5 Tips to Support a Healthy Gut
Increasing the beneficial bacteria in your gut can improve your gut health overall, most likely preventing intestinal hyperpermeability. It also supports your overall health, so if something gets through, the body has the defences to protect itself.
1. Limit your sugar
Harmful bacteria thrive on sugar. It is their food of choice. Excessive sugar intake has been known to harm the gut barrier function.
2. Decrease your alcohol intake
Alcohol has been proven to be detrimental to the intestinal wall and destroy beneficial bacteria.
3. Limit the use of NSAID
It is known that long term use of these drugs is detrimental to the intestinal wall and increase gut permeability.
4. Eat fermented food
Fermented foods such as plain yogurt, kimchi, and kombucha are well known to contain probiotics. In moderation, these can improve your gut health environment.
5. Eat Plenty of high Fibre Foods
Gut Performance® has the right type of fibre, which acts as a prebiotic, to supply the beneficial bacteria with the sources they need to improve your gut health. Taking just one scoop daily will give you a significant boost to your fibre intake.
Let us know via our Gut Performance® Instagram page and #gutperformance how you prepare your daily Gut Performance® dose. We love to hear how Gut Performance® has taken your gut health to the next level.
Arrieta, M. C., Bistritz, L., & Meddings, J. B. (2006). Alterations in intestinal permeability. Gut, 55(10), 1512-1520. DOI:. https://doi.org/10.1136/gut.2005.085373
Bested, A. C., Logan, A. C., & Selhub, E. M. (2013). Intestinal microbiota, probiotics, and mental health. Gut pathogens, 5(1). doi:https://doi.org/10.1186/1757-4749-5-3
Bischoff, S. C., Barbara, G., Buurman, W., Ockhuizen, T., Schulzke, J. D., Serino, M., . . . Wells, J. M. (2014). Intestinal permeability – a new target for disease prevention and therapy. BMC Gastroenterology, 14. doi:https://doi.org/10.1186/s12876-014-0189-7
Bjarnason, I., & Takeuchi, K. (2009). Intestinal permeability in the pathogenesis of NSAID-induced enteropathy. Journal of Gastroenterology, Suppl 19, 23-9. Retrieved 2020, from https://pubmed.ncbi.nlm.nih.gov/19148789
Duerksen, D. R., Wilhelm-Boyles, C., & Parry, D. M. (2005). Intestinal permeability in long-term follow-up of patients with celiac disease on a gluten-free diet. Digestive diseases and sciences, 50(4), 785-90. Retrieved 2020, from https://link.springer.com/article/10.1007/s10620-005-2574-0
Durk, R. P., Castillo, E., Marquez-Magana, L., Grosicki, G. J., Bolter, N. D., Lee, C. M., & Bagley, J. R. (2019). gut Microbiota Composition is Related to Cardiorespiratory Fitness in Healthy Young Adults. International Journal of Sprot Nutrition and Exercise Metabolism, 29(3), 249-253. DOI: 10.1123/ijsnem.2018-0024
Evrensel, A., & Ceylan, M. E. (2015). The Gut-Brain Axis: The Missing Link in Depression. Clinical psychopharmacology and neuroscience, 13(3), 239-244. doi:https://doi.org/10.9758/cpn.2015.13.3.239
Fasano, A. (Jan, 2011). Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiology Review, 91(1), 151-175. Retrieved 2020, from https://pubmed.ncbi.nlm.nih.gov/21248165/
Fasano, A. (2012). Intestinal permeability and its regulation by zonulin: diagnostic and therapeutic implications. Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association, 10(10), 1096-1100. doi:https://doi.org/10.1016/j.cgh.2012.08.012
Ferrier, L., Berard, F., Debrauwer, L., Chabo, C., Langella, P., Bueno, L., & Fioramonti, J. (April, 2006). Impairment of the intestinal barrier by ethanol involves enteric microflora and mast cell activation in rodents. American Journal of Pathology, 168(4), 1148-54. Retrieved 2020, from https://pubmed.ncbi.nlm.nih.gov/16565490/
Groschwitz, K. R., & Hogan, S. P. (2009). Intestinal barrier function: molecular regulation and disease pathogenesis. The journal of allergy and clinical immunology, 124(1), 3-22. doi:https://doi.org/10.1016/j.jaci.2009.05.038
Hall, E. j., & Batt, R. M. (1991). Abnormal permeability precedes the development of a gluten-sensitive enteropathy in Irish setter dogs. Gut, 32(7), 749-53. Retrieved 2020, from https://pubmed.ncbi.nlm.nih.gov/1906829/
Hietbrink, F., Besselink, M. G., Renooij, W., de Smet, M. B., Draisma, A., van der Hoeven, H., & Pickkers, P. (2009). Systemic inflammation increases intestinal permeability during experimental human endotoxemia. Shock, 32(4), 374-8. Retrieved 2020, from https://pubmed.ncbi.nlm.nih.gov/19295480/
Hollander, D. (1999). Intestinal permeability, leaky gut, and intestinal disorders. Current Gatroenterological Reports, 1(5), 410-6. Retrieved 2020, from https://pubmed.ncbi.nlm.nih.gov/10980980/
Konturek, P. C., Brzozowski, T., & Konturek, S. J. (2011). Stress and the gut: pathophysiology, clinical consequences, diagnostic approach, and treatment options. Journal of Physiology and Pharmacy, 62(6), 591-9. Retrieved 2020, from https://pubmed.ncbi.nlm.nih.gov/22314561/
Meddings, J. B., Jarand, J., Urbanski, S. J., Hardin, J., & Gall, D. G. (April, 1999). Increased gastrointestinal permeability is an early lesion in the spontaneously diabetic BB rat. Americal Journal of Physiology, 276(4). Retrieved 2020, from https://pubmed.ncbi.nlm.nih.gov/10198339/
Odenwald, M. A., & Turner, J. R. (2013). Intestinal permeability defects: is it time to treat? Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association, 11(9), 1075-1083. doi:https://doi.org/10.1016/j.cgh.2013.07.001
Sander, G. R., Cummins, A. G., Henshall, T., & Powell, B. C. (2005). Rapid disruption of intestinal barrier function by gliadin involves altered expression of apical junctional proteins. FEBS Lett, 579(21), 4851-5. Retrieved 2020, from https://pubmed.ncbi.nlm.nih.gov/16099460/
Sapone, A., Lammers, K. M., & Casolaro, V. (2011). Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity. BMC Med, 9(23). doi:https://doi.org/10.1186/1741-7015-9-23
Spruss, A., & Bergheim, I. (2009). Fructose and intestinal barrier: potential risk factor in the pathogenesis of nonalcoholic fatty liver disease. Journal of Nutritional Biochemistry, 20(9), 657-62. Retrieved 2020, from https://pubmed.ncbi.nlm.nih.gov/19679262/
Visser, J., Rozing, J., Sapone, A., Lammers, K., & Fasano, A. (2009). Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms. Annals of the New York Academy of Sciences, 1165, 195-205. doi:https://doi.org/10.1111/j.1749-6632.2009.04037.x