This article first appears in Nutrition Practitioner Journal vol 12, issue 1 Spring 2011
Angela Walker BScNut.Med. mBANT NTCC CNHC
Functional Laboratory tests are an extremely useful tool for the nutrition practitioner who takes a functional model approach. This case study involves an amateur runner with digestive issues, often referred to as ‘Runners Diarrhoea’ (RD), that were inhibiting her ability to train for a marathon. Digestive disturbances including RD are relatively common amongst long distance runners, yet the underlying causes remain unclear. Prior to presenting at my clinic, various nutritional strategies had been trialled, all unsuccessful in resolving RD. The use of functional laboratory tests enabled identification of underlying imbalances and a targeted digestive and nutrition support programme, which led to significant improvement in the RD.
Runners Diarrhoea (RD) is characterized by frequent, loose bowel movements during or immediately after a run. It is most common in long-distance or marathon runners1. While it is a relatively common problem amongst runners, the aetiology is not fully understood.
In one study at an event of 119 competitors 81% of responders had gastrointestinal symptoms, 61% reported lower gastrointestinal symptoms2. In a larger survey of 707 marathon runners, over 1/3 experienced an urge to defecate during and immediately after running3. A pubmed search for ‘Runners Diarrhoea’ brings up only 29 articles. Of course it may be that the term is too colloquial, but at least one author reviewing the topic has stated that very little is available in the literature compared to other ailments experienced by endurance athletes and given the prevalence.4
While a precise understanding of the aetiology remains elusive a number of potential underlying causes have been proposed, these are summarise in Table 1. Effects of increased sympathetic activity, dehydration, nutritional factors, hormonal changes and underlying infection or dysbiosis and the main areas which are thought to lead to RD.
Table 1 Proposed etiology of Runners Diarrhoea
|Increased sympathetic activity 1: reduced splanchnic blood flow (by up to 80%)5,6||Intestinal mucosa dysfunction7
|Increased sympathetic activity 1: suppresses parasympathetic activity||Reduced parasympathetic activity means decreased gut tone, accelerating transit time3|
|Increased sympathetic activity 2: triggers release of gastrin & motilin3||Directly contributes to diarrhoea when exercise intensity is high 3|
|Nutritional Factors 1; sports drinks with glucose concentration in excess of 7 to 10% cause increase osmotic pressure in gastrointestinal (GI) tract drawing water into tract and creating diarrhoea3||“Dumping Syndrome” 3|
|Nutritional Factors 2: High dietary intake of fibre and high glycemic index foods can have same effect on osmotic pressure in GI as above3||“Dumping Syndrome”3|
|Hormonal changes 1. Cortisol, adrenalin & noradrenaline may all be elevated after marathon 4
|Exact effect unknown, but GI symptoms may be correlated with lower post race cortisol and or noradrenaline and higher potassium levels 4|
|Hormonal Changes 2. Elevation of certain gut hormones including Vasoactive Intestinal Peptide (VIP), gastrin and secretin. All believed to provide increased metabolic support of increased fuel demands4||Effect of these hormones may also be as vasodilation and increased motility4|
|Consider infections3 and consider that RD can signify a “stress test for the colon”.8||Hypothesis is that aerobic exercise can stress colon to the stage where is reveals an underlying disorder, imbalance or infection.|
|Dehydration.||Exacerbates reduced blood flow 1,3
Electrolyte and fluid imbalance can cause irritation to colonic smooth muscle and mucosa.3
|Effect of persistent pounding in a long distance race causes churning in intestine9||Stool liquefies|
|NSAIDS3||Can contribute to GI bleeding, can be used inappropriately by athletes3|
Sally is a 31 year-old Caucasian female of a slim, light build.
Sally was hoping to train for a marathon and was regularly running a 12k circuit, however on most training runs she experienced a cramping pain that would come in waves after approximately 30 minute, she would feel the need to defecate, would have to stop and experienced diarrhoea. If she ran first thing in the morning on an empty stomach there would be no digestive problems, but this was unrealistic for every training run and the problem was inhibiting her from training for a marathon. Her primary health concern was to resolve these digestive issues so that she could pursue her running ambitions.
Sally was referred to me by a chiropractor, he had already worked with her to optimise hydration and to improve diet, adding whole grains, fruit, vegetables and including a good protein source with meals. He had also ordered an IgG4 assay which showed only a mild positive for crab. Timing of meals had been explored and a small snack of seeds 2 hours included before each run. Non of these strategies improved the RD symptoms.
Health History (key points)
Sally had suffered (self diagnosed) Irritiable Bowel Syndrome (IBS) during her 20’s. She had experience pain and cramps after meals. These issues improved as she started to exercise and eat more frequently.
Skin problems (acne) had persisted for a number of years leading to two courses of Roaccutane 7 and 5 years previous to the consultation. Prescribed the antibiotic Minocin since 2006 for acne. Prescribed Yasmin birth control pill for skin in 2006.
Insomnia on and off since early teens, still persisted at times and didn’t sleep well.
Current Digestive Health
Bowel movements 2 or 3 times a day and rarely constipated. They could be loose or formed, colour varied, occasional mucous. On occasion she had a cramping pain in middle of stomach and to right hand side and passed mucous. Whilst running, before onset of RD, pain was experienced in the same location (i.e. middle and right hand side) and described as a ‘grinding’.
Minocin (Minocycline antibiotic) and Yasmin (combination birth control pill)
Current Diet & Lifestyle
- Breakfast: Cereal with milk, plus two pieces of fruit
- Lunch: salad with tinned tuna
- Dinner: salad with salmon or fish cakes.
- Fruit as snacks
- Caffeinated drinks daily and alcohol two or three times a week
Sally experienced more bloating with salad-based meals. Sally was quite conscious about low fat foods and as a result essential fatty acid sources were limited as no oils or dressings used with salads.
As already noted, she ran 12K three times a week and had a stressful and demanding job in Public Relations.
A zinc taste test was undertaken during the initial consultation: furry tongue, dry taste, reasonably strong after a few seconds, but not described as metallic.
As previously stated an IgG 4 test of 30 foods ordered by the referring clinician revealed only a mild response to crab.
Having reviewed the case history, we ordered a comprehensive stool test that uses PCR technology to identify microbes by DNA. The rationale for this was to identify underlying imbalance within the GI tract.
A blood spot fatty acid test was also ordered. Early studies on acne indicated lower levels of linoleic acid in the skin surface lipids of sufferers10. Coupled with the low dietary fat intake and knowing the role of essential fatty acids in the gastric epithelium, an assessment of fatty acid levels was felt to be important.
Figure 1: Stool Test Result
Figure 2: Fatty Acid test result
Summary of abnormal findings
- H Pylori
- Elevated anti-gliadin sIgA
- Low Pancreatic Elastase
- Low levels of linoleic and gamma linolenic acids
Interpretation of the case under the Functional Model
(This section will focus only on the most relevant aspects of this case)
Digestion/absorption / Elimination
Occasional mucous stool and on-going loose stool suggest a degree of digestive imbalance.
Helicobacter pylori is a bacterium that primarily affects the stomach inhibiting normal proliferation of the gastric mucosal cells, furthermore, it can release bioactive factors that inhibit the ability of the parietal cells to produce hydrochloric acids (HCl)11. Normal secretion of gastrin, which stimulates release of HCl from parietal cells and stimulates gastric motility may also be inhibited. H.pylori could have been asymptomatic, but given the presence of some bloating it was felt to be relevant in this case and possible that the H pylori infection could be inhibiting normal digestive potency, therefore inhibiting optimal absorption.
Fecal pancreatic elastase is considered an accurate measure of pancreatic enzyme output12. Combined with the presence of H pylori and its inhibition of stomach acid, it would appear that Sally’s digestive potency is reduced, this may be contributing to bloating after certain meals, loose stools, low nutritional status as well as RD.
Despite long term (4 year) use of an antibiotic, the predominant bacterial populations were good on the test results. However opportunistic bacteria (Klebsiella) yeast and the parasite Blastocystis were present, indicating a dysbiotic state. Stool studies to investigate for parasites, pathogenic and opportunistic bacteria is suggested as part of a comprehensive assessment of RD 4 (see Table 1). Furthermore, one hypothesis is that aerobic exercise can stress the colon to the extent that underlying imbalances or disorders can be revealed 3. This interpretation may apply in the current case; a dysbiotic state, while not creating symptoms in every day life, but the symptoms are revealed once stressed from an extended run.
Anti Gliadin sIgA is a marker for gluten sensitivity and is elevated in the test results. Gliadin is known to induce zonulin release, opening up the tight junctions on the intestinal epithelium, increasing intestinal permeability 14. While gluten remains in the diet there will be a continued irritation to the gastrointestinal tract.
Toxic by products of bacterial and yeast overgrowths create and additional toxic load for the liver (15,16). These can also contribute to intestinal hyperpermeability.
Inflammation & Defense
Inflammation markers on the test are low but it could be expected that continued exposure to gluten from the diet as well as toxic by products from yeast and bacteria and presence of parasites would create an inflammatory state. Inflammation is involved in the pathogenesis of acne 17,18. The laboratory testing has identified low Linoleic and Gamma Linolenic acid levels, given their role in membrane phospolipids, eicosanoids 19, and connection to acne5, re-establishing these levels will be important to improve gastric epithelial function and reduce skin inflammation.
A key role of the essential fatty acids is cellular membrane structure and fluidity 19, in this capacity they are also involved in cell receptors. Table 1 described the possible factors involved in RD, which include hormone imbalance. Optimising cell receptor function, via the required essential fatty acids may therefore be of benefit.
Structure and repair
As has already been mentioned, the essential fatty acids have a key structural role, in particular the omega 6 fatty acids may have a restorative effect on the intestinal epithelial cells through the COX pathways 20. The fact that these are depleted will have implications for optimal digestive function.
The NICE guidelines for H Pylori treatment is a 7 day course consisting of proton pump inhibitor (PPI) with two antibiotics either metronidazole 400mg and clarithromycin 250mg OR amoxicillin 1g and clarithromycin 500mg 21. However these protocols are not always effective and come with concerns regarding antibiotic resistance 22,23. Given the ongoing antibiotic use and in discussion with Sally, a botanical approach was first tried for H Pylori.
A tailored 4 R programme with additional essential fatty acids:
- Digestive enzymes before each meal
- Botanical anti microbial formula 2 caps bid (per 2 caps: tribulus terrestris 24 400mg , sweet wormwood 25 300mg, caprylic acid 25 300mg, berberine 25 200mg, grape seed extract 26 200mg, barberry 27 100m, bearberry (cranberry) 21 100mg, black walnut 100mg). (30 days in total)
- Botanical formula to target H Pylori 2 caps bid (Vitamin C 28 500mg, Deglycyrrhizinated licorice DGL 29 1500mg, Mastic Gum 30 1000mg, Methylmethioninesulfonium “vitamin U” 200mg, Zinc-carnosine 31 75mg) (30 days in total)
- Oil of Oregano to target yeast 32 30mg pd
- Gamma Linoleic Acid 500mg pd
- Gluten Free diet
- Sally was coached to introduce more variety (fresh fish rather than tinned), wider range of vegetables, less raw salad, inclusion of seeds and nuts each day as well as for salad dressings. The need to continue phasing a small snack 2 hours before each run and to maintain hydration was empahsised. She was also coaching to chew more thoroughly.
4 week follow up
- Week 1 of programme: no different, possibly worse
- From week 2 onwards, definite improvement. Still experienced ‘feeling’ but no need to stop run
- Skin felt clearer
- Bowel movements more solid.
- All of the improvements were despite an extremely stressful period at work.
Ceased botanical formulas & oil of oregano. Continued with rest of programme
Follow up test results
Figure 3: Microbial Profile Result
Summary of findings:
- H Pylori, Yeast & Blastocystis no longer present
- Predominant bacteria all low (mainly in 2nd quintile), due to the anti-microbial botanical formulas used, which will have a non-discriminatory effect on gut microflora.
- Parasites (taxonomy unknown). The test sensitive and often traces of parasite are identified with taxonomy unknown, this generally means the parasite is not likely to be a human pathogen and is probably transient.33
Follow Up Consultation (2 months)
- Sally described improvement as 80 to 90%. She hasn’t had to stop any runs at all for a bowel movement, although has had ‘the feeling’ in her stomach. Planning to run half marathon later in the year.
- Daily bowel movements and digestive function improved
- Skin improved and noticeably smoother
- Gluten avoidance is 100% during week but only 90% at weekends
- Energy levels improved but would like to have more energy
Revised nutrition & supplement programme
The maintenance strategy is to support the natural defences from pathogenic bacteria, yeasts and parasites. The programme goals are to re-establish healthy microflora population, support gut immune defences and epithelial function.
Comprehensive Bifidobacterium strains 30 billion CFU’s per day
- Prebiotic formula of chicory inulin, oligofructose, larch arabinogalactan and purified yeast beta-glucan. 5g per day. Prebiotics can help healthy populations of bifidobacterium (and other comensal probiotic strains) to flourish34 beta glucans may also have an immune supportive role against bacterial and parasitic challenges. 35
- Continue to avoid gluten. Recommended a digestive enzyme which includes Glucoamylase to support gluten digestion for use at weekends when needed
- Essential fatty acid blend of omega 3, 6 & 9
- A multi vitamin and mineral was added
The stool test revealed significant dysbiosis. Parasites, pathogenic bacteria, opportunistic bacteria don’t always lead to symptoms. In this case, although a history of digestive issues and (certainly from a nutritional therapy perspective) below optimal current daily digestive function existed, the symptoms weren’t bothersome for the client until they intensified during high intensity running resulting in RD. Once the gut dysbiosis improved, evidenced by the follow up stool test, the symptoms improved by 80 to 90%. The hypothesis that aerobic exercise can stress the colon and reveal underlying imbalances would appear to be a valid interpretation in this case. The client is very happy with her progress and we are continuing to work on the maintenance programme to enable her to successfully pursue her marathon ambitions.
1. Mayo Clinic. Runner’s Diarrhea. How can I prevent it? Available from: http://www.mayoclinic.com/health/runners-diarrhea/AN00376. [Accessed September 2010]
2. Worobetz & Gerrard (1985) Gastrointestinal symptoms during exercise in Enduro athletes: prevalence and speculations on the aetiology. NZ Med. J. 98 (784) pp 644-6
3. Keeffe et al (1984) Gastrointestinal symptoms of Marathon Runners. Western Journal of Medicine. 141 (4) pp 481-484.
4. Ho (2009) Lower Gastrointestinal distress in endurance athletes. Current Sports Medicine Reports 8 (2) pp 85-91
5. Cohen et al (2006): Marathon-Induced ischemic colitis why running is not always good for you. Am J Emerg Med. Feb 27 (2) pp 255
6. King & Avery (2010): Marathon Induced Colitis. Available from http://www.surgisphere.com/SurgRad/issues/volume-2/1-january-2011-pages-1-112/154-original-article-marathon-induced-colitis.html. [Accessed 21st March 2011]
7. Ho (2009) Lower Gastrointestinal Distress in Endurance Athletes. Current Sports Medicine Reports 8(2) pp 85-91
8. Swain (1993) Exercise-induced diarrhea: when to wonder. Medicine and Science in Sports And Exercise Vol. 26(5) pp 523-526
9. Simon & Kennedy (2004) Gastrointestinal Problems in Runners. Current Sports Medicine Reports 3 pp 112-116
10. Downing, D.T. Stewart, M.E. Wertz, P.W. and Strauss, J.S. (1986) Essential fatty acids and acne. Journal of American Academy of Dermatology 14(2 Pt 1); 221-5
11. eMedicine. Helicobacter Pylori Infection. Available from http://emedicine.medscape.com/article/176938-overview. [Accessed 21st March 2011]
12. Takeda et al (2002) Fecal elastase-1 test: clinical evaluation of a new noninvasive pancreatic function test Rinsho Bylori (article in Japanese) 50(9) pp 893-8.
13. Swain (1993) Exercise-induced diarrhea: when to wonder. Medicine and Science in Sports And Exercise Vol. 26(5) pp 523-526
14. Lammers et al (2008) Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3. Gastroenterology. 135(1) pp194-204.
15. Lord & Bralley (2008) Laboratory Evaluations for Integrative and Functional Medicine. 2nd Ed. Metametrix Institute
16. Thomas Sult (2005) Clinical Approached to Gastrointestinal Imbalance. Textbook of Functional Medicine. Ed Jones & Quin. Institute for Functional Medicine.
17. Webster (2002) Acne vulgaris. BMJ 325 pp475-9
18. Cordain (2005) Implications for the Role of Diet in Acne. Semin Cutan Med Surg 24 pp 84-91
19. Calder & Grimble (2002) Polyunsaturates fatty acids, inflammation and immunity. European Journal of Clinical Nutrition Vol 56 (Sup3) pp 14-19
20. Ruthig & Meckling-Gill (2001) N3 and n6 fatty acids stimulate restitution by independent mechanism in the IEC-6 model of intestinal wound healing. Journal of Nutritional Biochemistry 13 pp 27-35
21. Dyspepsia: Managing dyspepsia in adults in primary care. August 2004. Available from http://guidance.nice.org.uk/CG17/Guidance/pdf/English [Accessed 15th November 2010]
22. Fuccio et at 2008. Treatment of Helicobacter pylori infection. BMJ 2008; 337