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07429 247 672

Gut Health

Gut Health

IBS used to be considered an umbrella term for any unexplained digestive disturbance but now there is a much greater understanding and more comprehensive approach to addressing this condition.

How can clinical research shape the current Nutritional Therapy protocols helping clients manage their symptoms.

IBS – Low Stomach Acid?

Clinical research has been carried out in many different aspects of digestive health and I would like to look specifically at the affect that low stomach acid may have on IBS symptoms.

In my practise there has been a significant increase in the clients I have with digestive health problems. They usually come in with some other symptoms but we always end up at the Gut.

I often find that clients with gut health problems lead extremely stressful lives, they don’t eat regularly, they don’t relax at all, they certainly do not concentrate on what they are eating or choosing to eat and they ALL have low stomach acid. Life is fast and furious and they are not coping with it. My clients are not digesting life so therefore may not be absorbing their nutrients.

Low stomach acid is on the increase and some of the symptoms of this are nutrient deficiency, anaemia, allergies, osteoporosis, protein mal digestion, dysbiosis

Gastric acid is necessary for the breakdown of our food and to kill bacteria we can assume that if it is not at optimum levels the environment of the Small intestine may be changed.

  • Small intestine Bacterial Overgrowth (SIBO) is generally defined as the presence of more colony forming units/ml of small intestine aspirate (1.2). It could be distinguished into two qualitative types; bacterial overgrowth with upper respiratory tract flora and with Gram negative bacteria respectively (3)

*The first type generally due to the failure of the gastric acid barrier. The second is associated with the failure of intestinal clearance and the Gram negative bacilli and are usually found making the small intestinal flora intestinal like.

- In a healthy stomach 99% of ingested bacteria are killed within 5 minutes.

- When the gastric acid barrier fails, bacteria from the mouth and upper respiratory tract can colonise the lower gut (4)

The production of stomach acid is necessary for the prevention of Helicobacter Pylori, candida proliferation in the gut, breaking down proteins , extracting B12, killing bacteria and more.

There is evidence that treatment with Proton Pump Inibitors (PPIs) such as omiperazole are responsible for bacterial overgrowth in 53% of patients, against 17% of patients treated with Cimetidine (5).

When the gastric acid barrier falls contaminating bacteria are mainly composed of upper respiratory tract flora (6.7) eg. Lactobacillus and streptococci.

Gram negative bacilli, E coli, Klesbsiella sp and proteus sp. Represent 10-30% of patients treated with PPI (8)

Low gastric acid can also affect B12 production. The absence of or reduced gastric acid may lead to an insufficiency in B12 as gastric acid is necessary for the pepsin that breaks down the animal protein in foods. If this is not fully functioning then the B12 cannot be extracted.

Vitamin B12 absorption may be reduced as a result of binding B12 – intrinsic factor complex to the cell wall of bacteria colonising the small intestine.

Bacteria colonising the small intestine of hypochlorhydric subjects cannot absorb or metabolize vitamin B12 making it unavailable to the host. (9)

Other symptoms of IBS that may be as a direct result of low stomach acid is the production of gas from fermenting foods. If food reaching the stomach is not broken down properly by stomach acid and digestive enzymes then they will reach the Small intestine where they will start to ferment and create gas. This can be embarrassing for the client as there is often an unpleasant odour that accompanies the flatulence that is created by the gas. There may also be bloating and discomfort.

Up to 96% of patients with IBS complain of bloating and gas related symptoms which is therefore considered a supportive symptom for the diagnosis of IBS. (10.11)

Low Stomach Acid – Coeliac Disease?

It may be of interest to look at Coeliac disease as a symptom of low stomach acid if the client is genetically predisposed.

If the Small Intestine has an over proliferation of bacteria could one of the possible scenarios be the creation of an environment that encourages gluten sensitivity and or full blown celiac disease?

Malabsorption syndrome is more frequently seen in patients with an overgrowth of colonic rather then Gram positive bacteria, localised upstream of the distal ileum. This condition is related to the bacterial metabolism of nutrients in lumen of the Small intestine and to be the direct damage of enterocytes, with a following loss of absorption surface. Infact carbohydrate malabsorption may be due both to bacterial fermentation of these substrates and to the damage to the enterocyte brush border, caused by bacterial enzymes (12)

Poor folate and B12 status is associated with hypersysteinemia in coeliacs and may therefore represent an increased risk of Cardio vascular disease and osteoporotic fractures. (13)

There is much duality with symptoms in both SIBO and Coeliac disease. Malabsorption of nutrients creating a myriad of symptoms with both.

There also seems to be villus atrophy in clients who have either.

Does one lead to the other or is it just two different areas of disease showing very similar outcomes.

Is it any wonder then that GPs struggle with diagnosing digestive issues, without the research it can be difficult to work out exactly what is going on.

Protocols

  1. Stomach Acid Testing.

  2. Refer clients for celiac testing as appropriate. New Saliva testing may be useful.

  3. May be useful for clients to check for genetic markers for celiac disease.

  4. Bowel testing – for IGA, bacterial overgrowth and parasites.

  5. If celiac – Gluten free diet. Explaining the importance of checking labels of foods and products. Also how important it is not have even the smallest amount of gluten getting into your system.

  6. Supplementing nutrients as the body will be depleted in both situations.

  7. Mineral replacement again due to malabsorbtion.

  8. Check B12, Folate, Iron levels.

References

1. ] King CE, Toskes PP. Small intestine bacterial overgrowth. Gastroen-

terology 1979;76:1035–55.

[2] Toskes PP. Bacterial overgrowth of the gastrointestinal tract. Adv

Intern Med 1993;38:387-407.

[3] Husebye E. The pathogenesis of gastrointestinal bacterial over-

growth. Chemotherapy 2005;51:1-22.

(4) parody A et al 2009

(5) Thorens J, Froehlich F, Schwizer W, et al. Bacterial overgrowth

during treatment with omeprazole compared with cimetidine: a

prospective randomised double blind study. Gut 1996;39:54–9.

(6) Snepar R, Poporad GA, Romano JM, et al. Effect of cimetidine and

antacid on gastric microbial flora. Infect Immun 1982;36:518–24.

[7] Sharma BK, Santana IA, Wood EC, et al. Intragastric bacterial

activity and nitrosation before, during, and after treatment with

omeprazole. Br Med J 1984;289:717–9.

[8] Fried M, Siegrist H, Frei R, et al. Duodenal bacterial overgrowth

during treatment in outpatients with omeprazole. Gut 1994;35:23–6.Endocrinol Metab 2007;92:4180–4.

(9) (Evenepoel p.2001).

[10] Longstreth GF, Thompson WG, Chey WD, et al. Functional Bowel

Disorders Gastroenterology 2006;130:1480–91.

[11] Spiller R, Aziz Q, Creed F, et al. Guidelines for the management of

Irritable Bowel Syndrome. Gut 2007;56:1770–98.

insulin resistance syndrome. Hepatology 2002;35: 373–9.

motor complex of normal subjects and patients with bacterial over-

growth of the small intestine. J Clin Invest 1977;59:1158–66.

[12] Toskes, PP, Giannella, RA, Jervis, HR, et al. Small intestinal mu-

cosal injury in the experimental blind loop syndrome. Light- and

electron-microscopic and histochemical studies. Gastroenterology

1975;68:1193–203.

(13) . ( DickeyW.et al 2008)