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How do you permanently heal leaky gut?

Leaky gut is the result of structural damage in the intestines. With the gut permeability been compromised, most individuals experience a series of symptoms, not solely digestive. To heal leaky gut permanently a structured multidisciplinary approach is needed.

Leaky gut: is a digestive track with a compromised permeability (like a hose with holes).

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The Intestinal Immune System

The reason why leaky gut symptoms are not exclusively digestive are due to gut’s double role:

• digest and absorb nutrients

• host part of the immune system

The immune system in the gut has the delicate role of balancing between: Tolerating or Reacting to the foods it comes in contact with. The evolutionary benefit of this role is the following:

Foods we consume may be degraded or containing toxins and thus be poisonous to the body. In these cases the activation of the immune system can kill the pathogenic substances and protect us.  This process is mediated through a series of steps leading to the increase of intestinal permeability.

Unfortunately in certain people the same reaction is triggered not only by toxins but also by regular foods. In these cases after the consumption of the “trigger food” the individual experiences a reaction such as: foggy brain, bloatedness, diarrhea, stomach cramps, increased heart rate, running nose, anxiety, irritability. Reducing gut permeability (i.e. healing leaky gut) can make previous “trigger foods” tolerable again.

 

Our gut wall consists of just one cell thick epithelial tissue (Sturgeon, C. and Fasano, A., 2016). The space between each epithelial cell is called tight junction. The following tests can be used to identify leaky gut.

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Lactulose/Mannitol test

The test that has been used the longest for detecting leaky gut is the lactulose/mannitol urine test. The test is simple: after an overnight (12 hour) fast you collect the urine then have a solution of lactulose & mannitol and 6 hours later you collect the urine again.

Mannitol enters the body through the epithelial cell membrane, while lactulose goes through the tight junctions (FlemIng, S.C. et al., 1990)

The loss of absorptive areas ➛ ↓ the absorption of mannitol.

The loss of mucosal integrity ➛ ↑ lactulose absorption.

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An elevated lactulose: mannitol ratio indicates the presence of leaky gut. The test is available from many labs including Genova Diagnostics. The results can be affected by the use of  NSAIDS, alcohol and according to Dr. Alesio Fasano the results are very sensitive to the collection process and thus may not be reliable when done outside a lab.

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3 stool markers of leaky gut (α1-Antitrypsin – sIgA – calprotectin)

α1-Antitrypsin

is a protein of the liver. When detected in stool (sourced from the intestines) it indicates a severe case of intestinal permeability and thus is not a sensitive enough marker of leaky gut (Biancone, L. et al., 2003)

sIgA

is part of the immune system and functions as a tag for substances that need to be excreted.

Calprotectin

is a protein linked with intestinal inflammation. It is used to distinguish between IBD & IBS (Leblhuber, F., et al., 2015).

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3 blood markers of leaky gut (Zonulin – LPS – DAO)

Zonulin

Zolulin is a protein responsible for the modulation of tight junctions (Sturgeon, C. and Fasano, A., 2016).

↑ levels of Zonulin ➛ Opening of tight junctions ➛ influx of dietary & microbial antigens in the blood

The 2 main triggers of Zonulin release have been found to be:

  1. Bacteria: including Eschericha coli, lab E. coli, virulent E. coli, and Salmonella typhi (El Asmar et al. 2002)
  2. Gliadin: a protein found in gluten (Clemente, M et al., 2003)

Elevated levels of Zonulin have been linked in the literature (Sturgeon, C. and Fasano, A., 2016) to:

  1. autoimmune conditions such as Type 1 Diabetes, Celiac Disease, Multiple Sclerosis, Intestinal Bowel Diseases
  2. metabolic disorders such as: Obesity & PCOS
  3. Asthma
  4. Coronary Heart Disease
  5. Systemic infections
  6. Gluten Sensitivity
  7. Necrotizing Enterocolitis
  8. Brain cancer (Skardelly, M et al., 2009) by altering the integrity of the Blood Brain Barrier.

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Lipopolysaccharide Bacterial Endotoxin

Lipopolysaccharide (LPS) is a component of the wall of gram-negative bacteria (Trent, M.S et al., 2006) responsible for the activation of the innate immune system. LPS has 3 regions. Lab tests measure the lipid A region which is also known as endotoxin. Germ-negative bacteria live in the lumen of the gut but should not be found in the blood. Detection of LPS endotoxins in the blood is a sign of leaky gut.

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DAO

Dunwoody Labs measures the levels of DAO enzyme in their intestinal permeability test. DAO is responsible for the break down of histamine. Histamine while necessary for good gut health when elevated can cause problems. Low levels of DAO thus is also a sign of leaky gut. Genetic polymorphisms in the AOC1 gene (which encodes the DAO enzyme) can impair the body’s ability to produce the DAO. Those with low levels can check their genetic burden using the table below.

source: Opus23

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The future of leaky gut testing

While not currently available for the general public I-FABP is a marker of gut permeability used in laboratories. Intestinal fatty acid binding protein (I-FABP), is a marker of early enterocyte cell death (Derikx, J.P. et al., 2010)

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How to support a leaky gut?

When it comes to supporting leaky gut I like to split the nutrients in 2 categories:

  1. the ones affecting the mechanisms that cause the problem (these are the ones that ultimately will heal the intestines)
  2. the ones that suppress the symptoms – commonly referred to as anti-inflammatory (these are the ones that should help ameliorate the symptoms)

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Avoid trigger foods

While I consider elimination diets not a good idea long-term in the short run it is important to remove any trigger foods to control inflammation. IgG food intolerance tests can be very useful for that matter.

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Probiotics

I consider the use of probiotics the most potent yet the most tricky in implementation among all interventions. Certain probiotic strains have been found to induce cell proliferation in gut cells:

Bifidobacterium breve R0070 & Lactococcus lactis R1058, when taken together, seem to have synergistic effects and both can be found in the Jarrow-Dophilus EPS. (Grimoud, J. et al., 2010 *)

Some others that were shown to suppress inflammation induced by LPS levels are:

  1. Bifidobacterium longum subsp. Infantis, Bifidobacterium longum, Bifidobacterium bifidum, Lactobacillus rhamnosus – in the order mentioned (Laetitia, R. et al., 2013)
  2. Lactobacillus reuteri strain, ATCC PTA 6475 – available from Biogaia. (Thomas, C.M. and Versalovic, J., 2010)
  3. Bifidobacterium infantis 35624 (Groeger, D. et al., 2013)

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* The French study by Julien Grimoud is a goldmine of information.

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Mushrooms

Edible & medicinal mushrooms have been shown to activate & modulate the  immune system in the gut acting this way as anti-inflammatory in LPS toxicity.  A. bisporus, C. cibarius and L. deliciosus (Saffron Milkcap mushroom) are mushroom extracts available in supplemental form (Moro, C. et al., 2012).
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Berberine

Berberine is an alkaloid found in some plants shown to inhibit the inflammatory effects of LPS (Mo, C. et al., 2014, Wu, Y.H., et al., 2012). Berberine has been shown to interact with 57 genes, so cross-checking polymorphisms related to other symptoms is worth doing.

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Other agents

Quercetin & CoQ10 were also shown to have anti-inflammatory effects in  LPS toxicity (Abd el-gawad, H.M. and Khalifa, A.E., 2001). Fish Oils were shown to restore intestinal integrity by increasing DAO enzyme concentration in the gut (Liu, Y. et al., 2012).

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L-glutamine

L-glutamine acts as fuel for intestinal cells (Larson, S.D, et al., 2007), and to that extent supplementation can benefit a leaky gut. Gradually building the dosage from as little as 2.5 gr per day to 20 gr should be a safe way to avoid adverse reactions. I have not seen any studies demonstrating the benefits of L-glutamine supplementation for leaky gut however it does support overall intestinal health.

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Larazotide acetate

Larazotide acetate is a protein shown to inhibit Zonulin production without any adverse effects (Paterson, B.M et al., 2007). Alba Therapeutics an Indian pharmaceutical company is in the process of developing a drug with this protein.

 

Frequently Asked Questions

Many individuals suffering from leaky gut, experience food sensitivities. The easiest way to deal with food sensitivities is to adopt an elimination diet. While this initially is a good idea as inflammation goes down, long term they cause problems.

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That’s why in my opinion:

  1. While elimination diets (i.e. FODMAP, low oxalate, low histamine diets) remove foods that cause reactions, the reason why the reaction was there are 1st place stays. The same foods that
  2. Most chronically ill patients have restricted diets: the body is not able to renew the epithelial tissue in the gut leading to poor gut integrity ➛ increased gut permeability  ➛ food sensitivities.
  3. Diversity in gut flora is positively associated with health: A diverse gut flora supports gut integrity.

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Can Candida cause Leaky Gut?

Candida can cause intestinal imbalances and sequentially leaky gut. As candida symptoms overlap with other GI tract issues it is worth testing for candida prior to following a protocol.

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How do you permanently heal leaky gut?
Reverse Vitiligo
How to fix Histamine Intolerance?

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References

Abd el-gawad, H.M. and Khalifa, A.E., 2001. Quercetin, coenzyme Q 10, and l-canavanine as protective agents against lipid peroxidation and nitric oxide generation in endotoxin-induced shock in rat brain. Pharmacological research, 43(3), pp.257-263.

 

Biancone, L., Fantini, M., Tosti, C., Bozzi, R., Vavassori, P. and Pallone, F., 2003. Fecal α1-antitrypsin clearance as a marker of clinical relapse in patients with Crohn’s disease of the distal ileum. European journal of gastroenterology & hepatology, 15(3), pp.261-266.

 

Clemente, M.G., De Virgiliis, S., Kang, J.S., Macatagney, R., Musu, M.P., Di Pierro, M.R., Drago, S., Congia, M. and Fasano, A., 2003. Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function. Gut, 52(2), pp.218-223.

 

Derikx, J.P., Luyer, M.D., Heineman, E. and Buurman, W.A., 2010. Non-invasive markers of gut wall integrity in health and. World J Gastroenterol, 16(42), pp.5272-5279.

 

El Asmar, R., Panigrahi, P., Bamford, P., Berti, I., Not, T., Coppa, G.V., Catassi, C. and Fasano, A., 2002. Host-dependent zonulin secretion causes the impairment of the small intestine barrier function after bacterial exposure. Gastroenterology, 123(5), pp.1607-1615.

 

FlemIng, S.C., Kapembwa, M.S., Laker, M.F., Levin, G.E. and Griffin, G.E., 1990. Rapid and simultaneous determination of lactulose and mannitol in urine, by HPLC with pulsed amperometric detection, for use in studies of intestinal permeability. Clinical chemistry, 36(5), pp.797-799.

 

Grimoud, J., Durand, H., De Souza, S., Monsan, P., Ouarné, F., Theodorou, V. and Roques, C., 2010. In vitro screening of probiotics and synbiotics according to anti-inflammatory and anti-proliferative effects. International journal of food microbiology, 144(1), pp.42-50.

 

Groeger, D., O’Mahony, L., Murphy, E.F., Bourke, J.F., Dinan, T.G., Kiely, B., Shanahan, F. and Quigley, E.M., 2013. Bifidobacterium infantis 35624 modulates host inflammatory processes beyond the gut. Gut microbes, 4(4), pp.325-339.

 

Laetitia, R., Paul, A., Marinescu, D., Shao, W. and Prakash, S., 2013. Effect of probiotics Lactobacillus and Bifidobacterium on gut-derived lipopolysaccharides and inflammatory cytokines: an in vitro study using a human colonic microbiota model. Journal of microbiology and biotechnology, 23(4), pp.518-526.

 

Larson, S.D., Li, J., Chung, D.H. and Evers, B.M., 2007. Molecular mechanisms contributing to glutamine-mediated intestinal cell survival. American Journal of Physiology-Gastrointestinal and Liver Physiology, 293(6), pp.G1262-G1271.

 

Leblhuber, F., Geisler, S., Steiner, K., Fuchs, D. and Schütz, B., 2015. Elevated fecal calprotectin in patients with Alzheimer’s dementia indicates leaky gut. Journal of Neural Transmission, 122(9), pp.1319-1322.

 

Liu, Y., Chen, F., Odle, J., Lin, X., Jacobi, S.K., Zhu, H., Wu, Z. and Hou, Y., 2012. Fish oil enhances intestinal integrity and inhibits TLR4 and NOD2 signaling pathways in weaned pigs after LPS challenge. The Journal of nutrition, 142(11), pp.2017-2024.

 

Mo, C., Wang, L., Zhang, J., Numazawa, S., Tang, H., Tang, X., Han, X., Li, J., Yang, M., Wang, Z. and Wei, D., 2014. The crosstalk between Nrf2 and AMPK signal pathways is important for the anti-inflammatory effect of berberine in LPS-stimulated macrophages and endotoxin-shocked mice. Antioxidants & redox signaling, 20(4), pp.574-588.

 

Moro, C., Palacios, I., Lozano, M., D’Arrigo, M., Guillamón, E., Villares, A., Martínez, J.A. and García-Lafuente, A., 2012. Anti-inflammatory activity of methanolic extracts from edible mushrooms in LPS activated RAW 264.7 macrophages. Food Chemistry, 130(2), pp.350-355.

 

Paterson, B.M., Lammers, K.M., Arrieta, M.C., Fasano, A. and Meddings, J.B., 2007. The safety, tolerance, pharmacokinetic and pharmacodynamic effects of single doses of AT‐1001 in coeliac disease subjects: a proof of concept study. Alimentary pharmacology & therapeutics, 26(5), pp.757-766.

 

Skardelly, M., Armbruster, F.P., Meixensberger, J. and Hilbig, H., 2009. Expression of zonulin, c-kit, and glial fibrillary acidic protein in human gliomas. Translational oncology, 2(3), pp.117-120.

 

Sturgeon, C. and Fasano, A., 2016. Zonulin, a regulator of epithelial and endothelial barrier functions, and its involvement in chronic inflammatory diseases. Tissue Barriers, p.e1251384.

 

Thomas, C.M. and Versalovic, J., 2010. Probiotics-host communication: Modulation of signaling pathways in the intestine. Gut microbes, 1(3), pp.148-163.

 

Trent, M.S., Stead, C.M., Tran, A.X. and Hankins, J.V., 2006. Invited review: diversity of endotoxin and its impact on pathogenesis. Journal of endotoxin research, 12(4), pp.205-223.

 

Wu, Y.H., Chuang, S.Y., Hong, W.C., Lai, Y.J., Chang, G.J. and Pang, J.S., 2012. Berberine reduces leukocyte adhesion to LPS-stimulated endothelial cells and VCAM-1 expression both in vivo and in vitro. International journal of immunopathology and pharmacology, 25(3), pp.741-750.

How to fix Histamine Intolerance

How to fix Histamine Intolerance?

Histamine is a hormone involved in digestion, immune & nervous system function. Anti-histamine drugs for asthma, they are also prescribed to those with food allergies. Improving digestive health and in particular, the gut microbiome and intestinal integrity can help you fix histamine intolerance.

 

What is histamine intolerance?

Histamine intolerance results from an imbalance between accumulated histamine and the capacity to break it down. The symptoms are due to histamine’s relation with the immune system. Histamine activates immune cells (basophils & mast cells) while causing blood vessels to dilate so that immune cells can be quickly transferred to kill pathogens.

Histamine Intolerance Symptoms

Histamine Intolerance is a fire alarm 🚨 turned on in the immune system, because of a breakdown in the endocrine system.

How is histamine broken down?

Like all hormones, histamine needs to be eliminated from the body when it has done its job. While it is broken down by a few different enzymes (HNMT, NAT1,2 & DAO), it is the DAO (ref) responsible for the breakdown of ingested histamine.

Histamine Intolerance Detoxification pathways

Can histamine cause digestive problems?

Gastrointestinal problems are very common among those with histamine intolerance. While histamine is necessary for proper gut function excess levels can cause digestive complications. Below are a few findings, highlighting the link between histamine intolerance and gut health:

a. all 4 histamine receptors H1R-H4R are found in the digestive tract and they have excitatory actions there (ref).

b. In a study conducted in Italy, 13 out of 14 subjects (with food intolerances) reported benefits in at least 1 food after DAO supplementation (ref).

c. The capacity of both histamine breakdown pathways: HNMT and DAO have been reported to be reduced in those with food intolerances (ref).

Enzymatic activities of HNMT and DAO in individuals with histamine intolerance

d. Elevated levels of histamine in the brain have been shown to suppress appetite (ref).

e. 30-55% of individuals with digestive disorders, including IBS, IBD, and Chron’s Disease have histamine intolerance (ref).

Diet can help histamine intolerance in 2 ways: i. reduce histamine load ii. support histamine breakdown.

Histamine intolerance foods to avoid

Those with histamine intolerance will benefit by avoiding 2 categories of foods:

a. Those that contain histamine

b. those that can cause the release of histamine in the body, although they don’t contain histamine (ref)

 

Histamine intolerance diet

The fresher the food the lower it is in histamine.

 

Histamine intolerance supplements

Vitamin C supplementation has also been shown to reduce histamine levels (ref), while B6 supplementation is also beneficial as it acts as a co-factor in DAO production (ref).

 

Drugs that cause histamine intolerance

It should probably come as no surprise that medication can also mess up your levels of histamine. Drug intake, especially long-term, should be considered in the interpretation of histamine intolerance symptoms and DAO concentrations (ref).

 

Can hormonal imbalance cause histamine intolerance?

Histamine levels are positively correlated with estrogen, while progesterone and testosterone levels are negatively correlated in women and men respectively. Women are more likely than men (ref) to suffer from histamine intolerance possibly due to the fluctuations in sex hormones during the menstrual cycle and menopause.

Histamine and estrogen have a bidirectional relationship.

Histamine has been shown to stimulate, in a dose-dependent manner, the synthesis of estradiol (E2) (ref). As estradiol levels are responsible for painful uterine contractions of primary dysmenorrhea, through the increase of prostaglandin F2α, histamine can also be considered a contributing factor. Estrogen also influences histamine’s action. During the mid-cycle, when ovulation occurs and estrogen peaks, a significant increase in the occurrence of wheal and flare is observed due to histamine (ref). Progesterone on the other hand stabilizes histamine levels (ref).

During pregnancy, DAO concentrations in the body may increase by as much as 500%, due to the production of DAO by the placenta (ref), which may well explain the reduction in food intolerances women experience during this period (ref).

Histamine increases libido (ref), which is why antihistamine medication needs to be considered when treating sexual dysfunction.

Blood sugar regulation and histamine intolerance

The link between histamine and diabetes goes back to 1950 (ref). Plasma histamine was shown to reduce after insulin administration in diabetic rats (ref). Given the positive correlation between diabetes and histamine intolerance (ref), stabilizing sugar levels should be of high priority in those with histamine symptoms.

In pancreatic beta cells, the activation of histamine 3 receptors (H3R) was shown to:

a. inhibit insulin secretion (ref)

b. reduce glucagon production in a non-hyperglycemic state (ref).

 

Can histamine cause breathing problems?

Histamine release is involved in seasonal allergies. A recent novel clinical trial (ref) has shown that the inhalation of small dosages of CO2 can suppress the symptoms of seasonal allergies.

Histamine and Carbon Dioxide 1

Histamine and Carbon Dioxide 2

CO2 can suppress histamine release in mast cells by increasing intracellular Calcium levels (ref). While no studies so far have tested the use of breathing exercises to suppress seasonal allergies, it is well documented and clinically confirmed that certain breathing exercises can increase the levels of CO2 in the body. Based on that it is well worth considering using CO2 Breathing Therapy for histamine intolerance.

 

How to test for histamine intolerance?

Prior to treating any condition, it is wise to confirm its presence first. The symptoms of histamine intolerance overlap with those having intestinal permeability and gut dysbiosis. By measuring the levels of DAO enzyme in your blood you can assess your body’s capacity to break down histamine and thus indirectly the presence of histamine overload.

When DAO levels are below <10 U/mL (ref1, ref2) the probability of histamine intolerance is high.

 

Histamine Intolerance🚦 • Serum DAO: 🔴 <3U/mL, 🟠 <10U/mL, 🟢 >10U/mL

 

Labs that offer this service in 🇬🇧 UK are Smart Nutrition (link) and Invivo Clinical, and in 🇦🇺 AUS: ImmunoPro (link).

23andme results & histamine intolerance

23andme results can be useful in identifying potential blockages in the pathway of histamine. At the same time, it is dangerous to drive conclusions solely from one’s genetic makeup, let alone one gene. In many cases, a person may have no SNPs in the gene that produces the DAO enzyme (AOC1 gene) and at the same time experience histamine-like reactions after the consumption of red wine for instance. The case below is such an example.

The woman is in her mid-40s, vegetarian with a more or less healthy lifestyle. She carries only 1 homozygous polymorphism in the AOC1 gene which has been shown to be beneficial.

SNPs for Histamine Intolerance

Source: Opus23

 

While there seems to be no burden on the production of DAO if you look at the entire pathway you will see that she carries SNPs in the HNMT and MAOB genes. Both of which can tax DAO’s function.

Histamine Genetic Pathway

Source: Opus23

 

How can this information be useful? 

For this woman supporting the function of HNMT and MAOB can help with histamine symptoms. For HNMT methylation support as well Salacia Oblonga (ref)  can be used while for MAOB vit B2.

 

MAOB SNP agent interactions

Source: Opus23

 

FAQ

Do Antihistamines reduce histamine?

Antihistamine tablets can be life-saving in times of crisis. At the same time if one doesn’t deal with what causes the reaction at 1st place she/he is trying to put off a fire by removing the battery from the fire alarm.

 

References

Breunig, E., Michel, K., Zeller, F., Seidl, S., Weyhern, C.W.H.V. and Schemann, M., 2007. Histamine excites neurones in the human submucous plexus through activation of H1, H2, H3 and H4 receptors. The Journal of physiology, 583(2), pp.731-742.

 

Casale, T. B., Onder, R. F., Berkowitz, R. B., & Korenblat, P. E. (2018). Nasal Carbon Dioxide Used As Needed in the Symptomatic Treatment of Seasonal Allergic Rhinitis. The Journal of Allergy and Clinical Immunology: In Practice, 6(1), 183-189.

 

Hemilä, H., 2014. The effect of vitamin C on bronchoconstriction and respiratory symptoms caused by exercise: a review and statistical analysis. Allergy, Asthma & Clinical Immunology, 10(1), p.58.

 

Hollis, T.M., Kern, J.A., Enea, N.A. and Cosgarea, A.J., 1985. Changes in plasma histamine concentration in the streptozotocin-diabetic rat. Experimental and molecular pathology, 43(1), pp.90-96.

 

x Kuefner, M.A., Schwelberger, H.G., Weidenhiller, M., Hahn, E.G. and Raithel, M., 2004. Both catabolic pathways of histamine via histamine-N-methyltransferase and diamine oxidase are diminished in the colonic mucosa of patients with food allergy. Inflammation Research, 53, pp.S31-S32.

 

x Malmlöf, K., Zaragoza, F., Golozoubova, V., Refsgaard, H.H.F., Cremers, T., Raun, K., Wulff, B.S., Johansen, P.B., Westerink, B. and Rimvall, K., 2005. Influence of a selective histamine H3 receptor antagonist on hypothalamic neural activity, food intake and body weight. International journal of obesity, 29(12), pp.1402-1412.

 

x Manzotti, G., Breda, D., Di Gioacchino, M. and Burastero, S.E., 2015. Serum diamine oxidase activity in patients with histamine intolerance. International journal of immunopathology and pharmacology, p.0394632015617170.

x Maintz, L. and Novak, N., 2007. Histamine and histamine intolerance. The American journal of clinical nutrition, 85(5), pp.1185-1196.

 

Nakamura, T., Yoshikawa, T., Noguchi, N., Sugawara, A., Kasajima, A., Sasano, H. and Yanai, K., 2014. The expression and function of histamine H3 receptors in pancreatic beta cells. British journal of pharmacology, 171(1), pp.171-185.

 

Nakamura, T., Yoshikawa, T., Naganuma, F., Mohsen, A., Iida, T., Miura, Y., Sugawara, A. and Yanai, K., 2015. Role of histamine H 3 receptor in glucagon-secreting αTC1. 6 cells. FEBS open bio, 5, pp.36-41.

 

Oda, Y., Ueda, F., Utsuyama, M., Kamei, A., Kakinuma, C., Abe, K. and Hirokawa, K., 2015. Improvement in Human Immune Function with Changes in Intestinal Microbiota by Salacia reticulata Extract Ingestion: A Randomized Placebo-Controlled Trial. PloS one, 10(12), p.e0142909.

 

Pini, A., Obara, I., Battell, E., Chazot, P.L. and Rosa, A.C., 2016. Histamine in diabetes: is it time to reconsider?. Pharmacological research, 111, pp.316-324.

 

Strider, J. W., Masterson, C. G., & Durham, P. L. (2011). Treatment of mast cells with carbon dioxide suppresses degranulation via a novel mechanism involving repression of increased intracellular calcium levels. Allergy, 66(3), 341-350.

 

 

Probiotics for Rhinitis

Probiotics for Rhinitis

Nasal health depends on the bacterial ecosystem in our nasal cavity. For this reason, probiotics can support both pulmonary and nasal inflammatory conditions including rhinitis.

 

Similar to all orifices in your body, the nose hosts bacteria that ideally serve a symbiotic relationship with their host: YOU. Similar to your gut flora your nasal flora is unique to you and is affected as much by genetic and environmental factors. In contrast, however, with our gut flora, the ones in our nose (as well as those in the vagina and mouth) are not directly affected by nutrition. Consecutively in order to support we have 2 options:
1. Direct administration of probiotics [ref]

2. Oral consumption of lozenges that will affect the proximal nasal ecosystem.

 

As far as probiotics go, Lactococcus lactis [ref1, ref2], Lactobacillus sakei [ref] & staphylococcus epidermidis [ref]  have been tested with positive outcomes. Unfortunately at the moment not all of them are commercially available.

 

If you are dealing with chronic nasal or pulmonary inflammatory conditions and need help you can reach out to me via the contact page.

 

References:

Abreu, N. A., Nagalingam, N. A., Song, Y., Roediger, F. C., Pletcher, S. D., Goldberg, A. N., & Lynch, S. V. (2012). Sinus microbiome diversity depletion and Corynebacterium tuberculostearicum enrichment mediates rhinosinusitis. Science translational medicine, 4(151), 151ra124-151ra124.

 

Bianco, M. R., Ralli, M., Modica, D. M., Amata, M., Poma, S., Mattina, G., & Allegra, E. (2021, December). The Role of Probiotics in Chronic Rhinosinusitis Treatment: An Update of the Current Literature. In Healthcare (Vol. 9, No. 12, p. 1715). MDPI.

 

Cleland, E. J., Drilling, A., Bassiouni, A., James, C., Vreugde, S., & Wormald, P. J. (2014, April). Probiotic manipulation of the chronic rhinosinusitis microbiome. In International forum of allergy & rhinology (Vol. 4, No. 4, pp. 309-314).

 

Cho, D. Y., Skinner, D., Lim, D. J., Mclemore, J. G., Koch, C. G., Zhang, S., … & Woodworth, B. A. (2020, April). The impact of Lactococcus lactis (probiotic nasal rinse) co‐culture on growth of patient‐derived strains of Pseudomonas aeruginosa. In International forum of allergy & rhinology (Vol. 10, No. 4, pp. 444-449).

 

Endam, L. M., Alromaih, S., Gonzalez, E., Madrenas, J., Cousineau, B., Renteria, A. E., & Desrosiers, M. (2020). Intranasal application of Lactococcus lactis W136 is safe in chronic rhinosinusitis patients with previous sinus surgery. Frontiers in Cellular and Infection Microbiology, 10, 440.

 

Schwartz, J. S., Peres, A. G., Endam, L. M., Cousineau, B., Madrenas, J., & Desrosiers, M. (2016). Topical probiotics as a therapeutic alternative for chronic rhinosinusitis: a preclinical proof of concept. American journal of rhinology & allergy, 30(6), e202-e205.