The use of functional laboratory testing in a case of Runner’s Diarrhoea

This article first appears in Nutrition Practitioner Journal vol 12, issue 1 Spring 2011

Angela Walker BScNut.Med. mBANT NTCC CNHC

Abstract

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.

 

Introduction

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

Mechanism	Effect
Increased sympathetic activity 1: reduced splanchnic blood flow (by up to 80%)5,6	Intestinal mucosa dysfunction7 Malabsorption (and hence evacuation) Cellular injury necrosis and erosions leading to bloody stool Increased membrane permeability
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

 

Case background

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’.

 

Current Medications

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.

 

Other assessments

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.

 

Laboratory Evaluations

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.

 

Test Results

Figure 1: Stool Test Result

Figure 2: Fatty Acid test result

 

Summary of abnormal findings

• H Pylori
• Yeast
• Blastocystis
• Klebsiella
• 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.
Detoxification/biotransformation

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.
Communication

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.

 

Nutrition Programme

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 2^nd 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

 

Summary

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.

 

 

 

 

References

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. 2^nd 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

 

Nutrient and Toxic Elements*

Selecting the right specimen to measure nutrient and toxic elements* can be a bit of a minefield. What specimens are most relevant for nutrient and toxic elements for an individual case? For many elements, the likelihood is that no one specimen is optimal, as each specimen has its own strengths and weaknesses and often multiple specimens are more appropriate for the most comprehensive assessment.

When it comes to the toxic elements, the question is often asked, should specimens be taken with or without a challenge? Metametrix have recently change the reference ranges on the urine so that ranges are now provided for both challenged / chelated and non challenged specimens, providing clinicians with even more data to make their clinical judgements.

The Metametrix interpretation guide offers more detail on specimens all element assessments and provides a concise yet comprehensive overview of both; definitely recommended as a read and a great reference point.

The interpretation guide as well as new sample test reports with the new reference ranges can be found at http://www.nutritiongeeks.co.uk/cp8.php under Improved Metametrix Elements Profiles

Angela Walker BSc Nut Med mBANT CNHC registered

Technical Advisor, Nutrition Geeks

 

 

Definitions:

* The definition here of elements is the form of the chemical element found in the human body, either nutrients (i.e. minerals) or toxic metals, usually complexed to proteins or other biological macromolecules.

 

Statin Drugs, Cholesterol and Heart Disease: Myth versus Reality

We’re delighted to introduce our first ever guest ‘post’, from By Dicken Weatherby, N.D. and Donald R. Yance, MH, CN. Dicken will be speaking at the upcoming BANT seminar we are hosting on 29th October, read on for a taster of what to expect!

© michelangelus - Fotolia.com

Pfizer and Merck are continuing their efforts to have the commonly prescribed Statin medications Lipitor and Mevacor approved for over the counter use. Currently these drugs are made available in the US only with a physician’s prescription. In the US, the Food and Drug Administration or FDA has turned down three times Merck’s application to make Mevacor, one of the first statin drugs, available without a prescription. The panel that made this decision the third time raised concerns that patients would turn to statin drugs instead of seeking a physician’s care. It’s good news that the FDA isn’t giving the green light to widespread over-the-counter drug use despite the heavy sway of advertising that would have people believe statin drugs are a safe panacea for preventing cardiovascular disease. We know most of you reading this already understand the misinformation being foisted on the public regarding statin drugs, but we thought we’d take this opportunity to review some the myths and the realities behind this issue so you can properly consult with your patients and clients.

Dispelling some of the myths regarding statin drugs, cholesterol and heart disease:

MYTH 1

“High cholesterol (and LDL) is the number-one cause of heart disease in the West.”

Wrong. High cholesterol is among the risk factors for heart disease, but is not the leading risk factor. The most prevalent risk factor is low HDL, along with small LDL particles, which commonly occur together. In fact, of every 100 people with coronary heart disease, 60-70 will have low HDL and small LDL particles, but fewer than 30 will have high LDL. If this is the case, why do we not hear more about low HDL and small LDL particles? The answer is simple: because treating these is not as profitable for drug companies. But just wait—when a profitable drug becomes available to treat this more prevalent risk factor for heart disease, we can expect to hear about an “epidemic” that will justify billions of dollars in new drug expenditures.^1-4

What qualifies as low HDL? National guidelines say it is a level of less than 40 mg/dL for men and less than 45 mg/dL for women.⁵ In fact, a level of less than 60 mg/dL is probably very significant.⁶ HDL is already a standard measure in everyday cholesterol panels. Small LDL particles, on the other hand, need to be measured specifically. The medical world focuses on statin therapy for LDL, while the most prevalent risk factor for heart disease goes untreated in the great majority of cases.

MYTH 2

“If I take a statin agent, I won’t have a heart attack.”

This is simply untrue. Lowering cholesterol (even to rock-bottom levels) reduces, but does not eliminate, the risk of heart attacks. Many heart attacks still occur in people with low cholesterol levels, whether or not they take cholesterol-lowering drugs.⁷ We must consider that there are other risk factors for heart disease besides cholesterol, such as small LDL particles, low HDL, high fibrinogen, high homocysteine, and high insulin levels. Results from the most recent National Health and Nutritional Survey show that 47 million US adults have metabolic syndrome (low HDL, high triglycerides, high blood pressure, excess abdominal fat), which substantially heightens the risk of heart disease even in the presence of low cholesterol levels.⁸

MYTH 3

“I feel fine and my stress test was normal. My doctor says I don’t have heart disease.”

This is among the most widely propagated fallacies spread by many primary care physicians and even cardiologists. First, lack of symptoms should not be reassuring, as most heart disease is silent—without symptoms and undetectable by conventional means such as electrocardiograms and cholesterol testing. Second, stress testing is a miserable failure for screening asymptomatic people. Most future deaths and heart attacks, in fact, occur in people with normal stress tests (when symptoms are not present). The net result of this misperception is that most future heart-attack victims are walking around feeling fine and unaware of their risk.⁹ Cholesterol can be high, low, or in between, but all too frequently fails to shed light on this murky situation.

Cholesterol: the lipid with a bad reputation

Hyperlipidemia refers to elevated blood levels of lipids (fats), including cholesterol and triglycerides. Most people with hyperlipidemia have no symptoms. However, hyperlipidemia is a contributing factor associated with an increased risk of coronary heart disease (CHD), a thickening or hardening of the arteries that supply blood to the heart muscle. CHD, in turn, can result in angina pectoris (chest pain), a heart attack, or both.  Although hyperlipidemia is considered a risk factor to heart disease, it is one of many risk factors and what actually causes hyperlipidemia is a debatable issue.  It not as simple as foods that contain cholesterol, elevate lipids.

Another important risk factor, which has been largely overlooked, is the oxidation of low-density lipoprotein (LDL) cholesterol caused from a lack of antioxidant-rich foods, herbs, and nutrients and/or a large intake of foods and chemicals that contains damaging free radicals.  Chronic inflammation also contributes to oxidative stress and an increase in CHD.  When LDL cholesterol oxidizes, it promotes atherosclerosis by a process referred to as the macrophage-foam cell mechanism, particularly in the presence of stressors, like cortisol and insulin.  Cortisol and insulin together act as a dynamic duel causing all kinds of disruptions including an increased oxidative and inflammatory state.  These are the real underline causes to chronic disease.  Inflammation is also involved in the process of LDL oxidation and contributes to the development of vascular disease. ^10-13 Ideally LDL levels should be kept under 120 mg/dL and you should monitor your patients for oxidative activity, especially lipid peroxidation.

The production of C-reactive protein is an essential part of the inflammatory process, and the measurement of this substance reflects the level of inflammatory activity deep within the body. It appears that certain conditions create a state of excessive inflammation within the circulatory system. High C-reactive protein levels are evidence of this type of inflammation. ^14-17 Ideally it is best to keep C-reactive protein levels below 0.55 mg/L in men and 1.5 mg/L in women. Please note that the reference ranges above refer to the High Sensitivity CRP or hs-CRP test.

Multiple risk markers for atherosclerosis and cardiovascular disease act in a synergistic way through inflammatory pathways.  The following lists the different factors that have been identified as risk factors for CHD and arterial damage:

1. Elevated CRP
2. Elevated LDL
3. Excess Insulin
4. Low HDL
5. High Glucose
6. Nitric Oxide Deficit
7. Excess Triglycerides
8. Low Free Testosterone
9. Excess Fibrinogen
10. Excess Homocysteine
11. Hypertension
12. Low Vitamin K
13. Excess Cholesterol

There are many key inflammatory biochemical risk markers for cardiovascular disease; in particular, the role of three basic cell types affected by these risk markers (endothelial cells, smooth muscle cells, and immune cells), the crucial role of inflammatory mediators, nitric oxide balance in cardiovascular pathology, and the use of nutrients (flavanoids, carotenoids, sterols, vitamin C and E, Omega 3 fatty acids etc.) to circumvent several of these inflammatory pathways. Most of the above risk markers for cardiovascular disease have a pro-inflammatory component, which stimulates the release of a number of active molecules such as inflammatory mediators, reactive oxygen species, nitric oxide, and peroxynitrite from endothelial, vascular smooth muscle, and immune cells in response to injury. Nitric oxide plays a pivotal role in preventing the progression of atherosclerosis through its ability to induce vasodilation, suppress vascular smooth muscle proliferation, and reduce vascular lesion formation. Nutrients such as arginine, antioxidants (OPCs, vitamins C and E, lipoic acid, selenium, glutathione), and enzyme cofactors (vitamins B2 and B3, B6, B12, folate, zinc) help to elevate nitric oxide levels and may play an important role in the management of cardiovascular disease. Other dietary components such as DHA/EPA from fish oil, tocotrienols, vitamins B6 and B12, and quercetin contribute further to mitigating the inflammatory process.  ¹⁸

Within the broad range of cholesterol levels from 180 to 240 there is little to no evidence that this alone correlates with heart disease. Below 180 there is increased risk of hemorrhagic stroke, depression, and suicide. Above 240 there is increased risk of cardiovascular disease and ischemic stroke. Over age 70, elevated cholesterol and cardiovascular events no longer correlate. All told, total serum cholesterol alone is a poor indicator of cardiovascular disease. Half of all heart attack patients have normal total cholesterol levels.

So, not only do statin drugs have their inherent drawbacks, but in some ways they are treating a fabricated problem based on misunderstood and misrepresented “research”. As natural health care providers, we know that we must be wary of the current cholesterol hysteria, we must be able to explain the real evidence, and we must help our patients understand the facts so they can make educated health choices.

Dicken Weatherby, ND is originally from Oxfordshire in the UK and is based in Ashland, Oregon USA. A graduate of the National College of Natural Medicine, Dicken is author of the bestselling book Blood Chemistry and CBC Analysis-Clinical Laboratory Testing from a Functional Perspective. He has self-published seven other books in the field of alternative medical diagnosis, has created numerous information products, and runs a number of successful Web sites including http://www.FMTown.com, an online membership community for practitioners interested in Functional Medicine and Functional Diagnosis. Dr. Weatherby is the creator of the “Foundations of Functional Diagnosis Training Program” at www.FunctionalDiagnosis.com and the “Foundations of Functional Blood Chemistry Analysis” Training Program at www.BloodChemistryTraining.com.

 

Donald R. Yance, CN, MH, RH is an internationally known herbalist and nutritionist. He is the founder and medical director of the Centre for Natural Healing in Ashland, Ore. Through extensive research and clinical practice, he has developed his Triphasic system, which forms the cornerstone of his clinical approach. Donald is the founder and formulator of Natura Health Products, and founder and president of The Mederi Foundation, whose programs promote health education and clinical research on the use of natural medicine, with an emphasis in the field of integrative oncology.

This article was also published in the BANT newsletter September 2011

 

 

 

References

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2. Stampfer MJ, Krauss RM, Ma J, et al. A prospective study of triglyceride level, low- density lipoprotein particle diameter, and risk of myocardial infarction. JAMA. 1996 Sep 18;276(11):882-88.
3. Lamarche B, Tchernof A, Moorjani S, et al. Small, dense low-density lipoprotein particles as a predictor of the risk of ischemic heart disease in men: Prospective results from the Quebec Cardiovascular Study. Circulation. 1997 Jan 7;95(1):69-75.
4. Kuller L, Tracy P, Arnold A, et al. Nuclear magnetic resonance spectroscopy of lipoproteins and risk of coronary heart disease in the cardiovascular health study. Arterioscler Thromb Vasc Biol. 2002 Jul 1;22(7):1175-80.
5. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the third report of the national cholesterol education program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III). JAMA. 2001 May 16;285(19):2486-97.
6. Gotto AM, Brinton EA. Assessing low levels of high-density lipoprotein cholesterol as a risk factor in coronary heart disease. J Am Coll Cardiol. 2004 Mar 3;43(5):717-24
7. van Lennep JE, Westerveld HT, Van Lennep HW, Zwinderman AH, Erkelens DW, van der Wall EE. Apolipoprotein concentrations during treatment and recurrent coronary artery disease events. Arterioscler Thromb Vasc Biol. 2000 Nov;20(11):2408-13.
8. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA. 2002 Jan 16;287(3)356-9.
9. Taylor AJ, Merz CN, Udelson JE. 34th Bethesda Conference: “Can atherosclerosis imaging techniques improve the detection of patients at risk for ischemic heart disease?” J Amer Coll Cardiol. 2003 Jun 4;(11)41:1860-2.
10. Rifai N, Ridker PM, Inflammatory markers and coronary heart disease. Curr Opin Lipidol 2002      Aug;13(4):383-9.
11. Albert CM, et al, Prospective study of C-reactive protein, homocysteine, and plasma lipid levels as predictors of sudden cardiac death. Circulation 2002 Jun 4;105, (22):2595-9.
12. Bermudez EA, Ridker PM, C-reactive protein, statins, and the primary prevention of atherosclerotic cardiovascular disease. Prev Cardiol 2002 Winter;5(1):42-6.
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Welcome to Nutrition Geeks

Welcome to the blogsite of Nutrition Geeks.

At Nutrition Geeks we are serious about providing you with the best functional laboratory tests and research driven nutritional supplements formulated by professionals for professionals.

A new approach to healthcare is emerging which looks at the underlying causes of dysfunction rather than symptoms and named disease. Referred to as Functional Medicine or Integrative Medicine, this approach focuses on identifying and addressing nutritional, metabolic and gastro-intestinal imbalances as well toxin effects that underlie chronic disease.

Who we work with

We offer functional laboratory tests, nutritional supplements and education to clinicians and healthcare professionals in the UK and Europe.

For clinicians and health care professionals we can take you from investigation of underlying issues with our functional laboratory tests through to clinical solutions via our research driven nutritional supplements. We also have a wealth of education resources available on laboratory evaluations, functional medicine and nutritional supplements.

For members of the public and patients we can offer the testing services and nutritional supplements as long as you are already working with a clinician or health care professional.

What is our role?

Laboratory Testing: All laboratory work is undertaken by Metametrix Clinical Laboratory in Atlanta, US. We are the appointed exclusive UK distributor for Metametrix as well as distributing to select European countries. Once a test has been completed, the results will be made available to the ordering clinician. Nutrition Geeks do not have access to any of the test results. All patients must therefore speak to their clinician or healthcare professional for their test results.

If patients don’t have a clinician,  you can search for one of our registered clinicians through the find a clinician tool. Alternatively you can speak to one of our own clinicians through Nutrition Geeks Clinic.

Supplements: Our supplement range from Designs for Health is designed by professionals for professionals. They are exclusive to Nutrition Geeks in the UK and are only available through a clinician or healthcare professional. Nutrition Geeks cannot advise on supplements, you must speak to your clinician or healthcare professional regarding how long to take supplements for and dosage.