Flaxseed for Heart Healthy Nutrition
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Written by John H. Maher, D.C.   
Tuesday, 27 May 2008 16:46

The use of flaxseed in food and beverages, functional foods and dietary supplements has risen dramatically. Such increased popularity is related to the increasingly recognized benefits of flax’s rich omega-3 fatty acid, lignans (powerful phytonutrient phytoestrogens/antioxidants) and fiber content.

A typical flax profile is approximately 40 percent fat, being mostly omega-3 as alpha linolenic acid (ALA); 28 percent dietary fiber; 21 percent protein; 4 percent mineral ash; and 6 percent carbohydrates.1

And all the plant sources (see chart) are richer in omega 6 than omega 3, none having flax’s most desirable 3 to 1 omega-3 to omega-6 ratio.3


ALA is converted in the body to eicosapentaenoic acid (EPA) and, to a much lesser extent, docosahexaenoic acid (DHA).4,5 EPA and DHA, as such, are found abundantly in fish oil. Both of these longer chain omega 3 fatty acids are known for their salubrious effects on cardio-vascular health.6 However, flaxseed has also demonstrated impressive support for its heart health promoting benefits.


ALA Improves Heart Health


Below is a small list of scientific studies supporting the benefit of a high ALA diet derived from plant sources.

Supplementation with 8g/day ALA resulted in significantly lower systolic and diastolic blood pressure levels. There was observed a hypotensive effect of ALA, which may constitute another mechanism accounting, in part, for the apparent cardio-protective effect of this n-3 fatty acid.7

To get an idea how omega-3 ALA rich flaxseed is compared to other ALA rich foods, the following should be instructive.

One and a half tsp. of ground flaxseed supplies 1,000 mg of ALA in 40 calories. One half tsp. of flaxseed oil supplies the same 1,000 mg ALA in 20 calories.

To get the same 1,000 mg of ALA, the following amounts of other sources are needed:

• Five walnut halves, providing 70 calories;

• two tsps. canola oil, garnering 80 calories;

• one tbs. of wheat germ or soybean oil, with 120 calories;

• two ounces salmon, herring, albacore, two ounces of sardine, rainbow trout, or eel, adding 100 calories;

• 9-12 ounces of most other fish, adding 300 calories or more;

• 5 cups cooked broccoli, providing 220 calories;

• 10 cups cooked spinach, with 280 calories;

• ¾ cup soy nuts, adding 285 calories and

• ¼ cup rice bran oil, tipping the scales at 480 calories.2

To compare the effects of ALA to EPA + DHA on cardiovascular risk markers in healthy elderly subjects, a randomized double-blind nutritional intervention study was done on thirty-seven mildly hyper-cholesterolemic subjects (fourteen men and twenty-three women, aged between sixty and seventy-eight years). During a run-in period of three weeks, subjects consumed an omega 6, oleic acid-rich (LN) diet. The following six weeks, ten subjects remained on the control diet, thirteen subjects consumed an ALA-rich diet (6.8 g/day) and fourteen subjects an EPA/DHA-rich diet (1.05 g EPA/day+0.55 g DHA/day). The researches concluded, in the European Journal of Clinical Nutrition, that, in healthy elderly subjects, ALA might affect concentrations of LDL-cholesterol and apoB more favorably than EPA/DHA.8

The Health Professionals Follow-up Study reported in the British Medical Journal a one percent increase in ALA as a percent of total calories was associated with a 40 percent risk reduction in non-fatal coronary heart disease.9

A 2001 article in the Journal of Nutrition Health and Aging noted that both Crete and Japan have the greatest life expectancy among the peoples of the first world. They also enjoy the highest levels of dietary ALA and the lowest intakes of saturated fat.10

The Lyon Diet Heart Study included as participants those patients who had survived a myocardial infarction (MI). The experimental group consumed a typical Mediterranean-style diet rich in ALA. The controls enjoyed diets low in ALA, typical of the Standard Amercan Diet (S.A.D.). Those in the experimental ALA group had a 75 percent reduction in non-fatal myocardial infarctions, and a 70 percent reduction in death from all causes compared to the S.A.D. group.11

A number of studies have focused on the health benefits provided specifically by flax.

Women who consumed 50g of milled flax a day (1/8 cup) for four weeks garnered total blood and LDL-cholesterol level reductions of 9 percent and 18 percent, respectively.12

The Journal of Nutrition reported, in 2004, that two ways ALA may protect the heart are through (1) improvements in abnormal heart rhythms and (2) a reduction of blood platelet stickiness and resultent.13

Also in 2004, data from the Nurses Health Study demonstrated the higher the ALA intake, the lower the plasma concentrations of C-reactive protein (CRP).14 The year following, the European Journal of Clinical Nutrition reported that a diet high in ALA dramatically decreased CRP in men and women with high cholesterol levels.15 In 2005, the American Heart Association presented studies showing ALA lowers C-reactive protein (CRP), an even more important biomarker of inflammation.

Indeed, lowering C-reactive protein may be as important as reducing LDL cholesterol for heart attacks and stroke prevention.16 Fifty percent of all strokes and MI in the United States and Canada happen to persons with normal cholesterol findings. Twenty percent of all major cardiovascular events happen to folks with no major risk factors!17

Even more recently, the American Journal of Physiology-Heart and Physiology Circulation shared that, in rabbits with hypercholesterolemia, dietary flaxseed inhibited vascular contraction and atherosclerosis formation.18

Lanzmann and Petithory, in a review of studies focusing on flax and ALA, concluded that this ALA rich essential fatty acid (EFA) source may reduce ventricular fibrillation.19

The above research is leading to a consensus that flaxseed has very beneficial effects in the prevention of cardiovascular disease.20,21 It is apparent, even from this briefest of introductory reviews, that the cardio-protective benefits of a flaxseed rich diet comes from numerous salubrious mechanisms. Furthermore, this research also demonstrates these many benefits despite differences in study populations, length of follow-up, outcomes, and methods of statistically analyzing the study data.



At the present time, there is no Recommended Dietary Allowance (RDA) for EFA’s in the U.S. However, the National Academy of Sciences’ Institute of Medicine (IOM) recommends 1.6g/day of ALA for men and 1.1g/day for women.22


Excellent Source of Dietary Fiber

Numerous health benefits are derived from consuming ALA in flax. Not to be overlooked is flaxseed’s dietary fiber content of about 28 percent, which grants added health benefits. The American Dietetic Association has cited fiber’s "significant impact" on obesity, cardiovascular disease and type 2 diabetes prevention and management.23

Flax has a ratio of soluble to insoluble fiber that can vary in a ratio of between one part soluble to four parts insoluble, to fourparts to six parts, respectively.24 Insoluble dietary fiber supports healthy elimination and colon health, and may even have protective effects against colon cancer.25 The soluble dietary fiber fraction of flax is found primarily as mucilage gums, which have been shown to play a role in lowering serum cholesterol levels.26

John H. Maher, D.C., oversees physician and consumer education for BioPharma Scientific, creators of NanoGreens10. Dr Maher maintained an active chiropractic practice for 25 years. He has taught nutrition to health professionals nationally for the past 15 years. Dr. Maher is past post-graduate faculty of NYCC Academy of Anti-Aging Medicine, a Diplomate of the College of Clinical Nutrition, and a Fellow of the American Academy of Integrative Medicine. To learn more, visit





4)       Harper, CR, Edwards, MJ, DeFilipis, et al. 2006. Flaxseed oil Increases the Plasma Concentrations of Cardioprotective (n-3) Fatty Acids in Humans. J.Nutr. 136:83.

 5)       Burdge, GC, Wootton, SA. 2002. Conversion of alpha-linolenic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic acids in young women. Brit. J.Nutr. 88:411-420.


7)       Paschos GK, Magkos F, Panagiotakos DB, Votteas V, and Zampelas A, Dietary supplementation with flaxseed oil lowers blood pressure in dyslipidaemic patients. European Journal of Clinical Nutrition (2007) 61, 1201–1206.

 8)       Goyens P L L and Mensink R P, Effects of alpha-linolenic acid versus those of EPA/DHA on cardiovascular risk markers in healthy elderly subjects. European Journal of Clinical Nutrition (2006) 60, 978–984.

 9)       Ascherio, A., Rimm, E.B., Giovannucci, E.L., et al. 1996. Dietary fat and risk of coronary heart disease in men: Cohort follow-up study in the United States. Br.Med. J. 313:84-90.

 10)     Renaud, S., de Lorgeril, M., Delaye, J. et al. 1995. Cretan Mediterranean diet for prevention of coronary heart disease. Am. .J Clin.Nutr. 61(Suppl):1360S-7S.


12)    Cunnane, S.C. et al. 1995. Nutritional attributes of traditional flaxseed in healthy young adults. Am. J. Clin.Nutr. 61(1):62-68.

 13)    Lopez-Garcia, E, Schulze, MB, Manson, JE, et al. 2004. Consumption of n3 fatty acids is related to plasma biomarkers of inflammation and endothelial activation in women. J. Nutr. 134:1806-1811.

 14)    Ibid 13

 15)    Bemelmans,W.J.E., Lefrandt, J.D., Feskens, E.J.M. et al. 2004. Increased alpha-linolenic acid intake lowers C-reactive protein, but has no effect on markers of atherosclerosis. Eur. J. Clin. Nutr. 58:1083-89.

 16)     American Heart Association. Inflammation, Heart Disease and Stroke: The Role of C Reactive Protein. October 26, 2005.

 17)     Simopoulos, A.P. 1999. Essential fatty acids in health and chronic disease. Am. J. Clin. Nutr. 70(Suppl):560S-569S.

 18)    Dupasquier C.M.C., et al, Effects of dietary flaxseed on vascular contractile function and atherosclerosis during prolonged hypercholesterolemia in rabbits Am J Physiol Heart Circ Physiol 291: H2987-H2996, 2006

 19)     Lanzmann-Petithory,D. 2001. Alpha-linolenic acid and cardiovascular diseases. J. Nutr.Health Aging. 5(3):179-183.

 20)    Renaud SC, Lanzmann-Petithory D. 2002.The beneficial effect of a-linolenic acid in coronary artery disease is not questionable (letter). Am. J. Clin.Nutr. 76: 903-904.

 21)    Vos E, Cunnane SC. 2003. a-Linolenic acid, linoleic acid, coronary artery disease, and overall mortality (letter). Am. J. Clin.Nutr. 77: 521-522.

 22)     Anon. Dietary Reference Intakes for Energy, Carbohydrates, Fiber, Fat, Protein and Amino Acids (Macronutrients). 2002. National Academy of Sciences, Institute of Medicine, Health and Human Service’s Office of Disease Prevention and Health Promotion (U.S.).

 23)    American Dietetic Association. 1997. Health implications of dietary fiber—Position of American Dietetic Association. J. Am. Diet. Assoc. 971157-1159.  

 24)    Hadley,M., Lacher, C.,Mitchell-Fetch, J. 1992. Fiber in Flaxseed. Proc. Flax Inst. 54:79-83

 25)    Ibid. 24

26)    Ibid 24


The Whey to Enhancing Glutathione
Written by John H. Maher, D.C.   
Saturday, 08 September 2007 10:57

GLUTATHIONE is widely found in all forms of life nad plays an essential role in the health of organisms, particularly aerobic ones. In humans, animals, and plants, glutathione is the predominant non-protein sulfhydryl group and functions most especially as an antioxidant, keeping its own sulfhydryl (-SH) groups and related proteins in a reduced (non-oxidized) condition.1, 2

Though there are undoubtedly multiple functions for glutathione yet to be appreciated, we do know that glutathione is:

• a co-factor for the glutathione peroxidases, which are crucial selenium-containing antioxidant enzymes.

• a co-factor for glutathione S-transferases, enzymes which are involved in the detoxifi cation of xenobiotics, including carcinogens.

• involved in the regeneration of ascorbate (Vitamin C) from its oxidized form, dehydro-ascorbate.3

Glutathione, itself, is a non-essential nutrient composed of three amino acids: glutamic acid, glycine and cysteine or, more exactly, the tripeptide L-gamma-glutamyl-L-cysteinylglycine. Availability of cysteine is a limiting factor in the liver’s synthesis of glutathione.

Chronic functional glutathione defi ciency is associated with immune disorders, an increased incidence of cancer and, in the case of HIV disease, probably accelerated pathogenesis of the disease.4, 5

Acute manifestations of functional glutathione defi ciency can be seen in those who have taken an over-dosage of acetaminophen (Tylenol). A vital role of glutathione is the maintenance of a normal redox state of the liver. An overdose of acetaminophen leads to its metabolism into large quantities of N-acetyl-benzoquinoneimine (NABQI) in the liver. NABQI depletes hepatic glutathione stores, placing an enormous oxidative stress on the liver, leading to liver failure.6


N-acetyl-L-cysteine (NAC) is integral to the treatment of acetaminophen overdose. This is due mainly to its ability to regenerate liver stores of glutathione. NAC is a bioavailable delivery form of L-cysteine, which serves as a major precursor to the antioxidant glutathione, but its half-life is only thirty minutes.7,8 Therefore, its use as a supplement to enhance glutathione levels is limited.

Alpha Lipoic Acid

Alpha-lipoic acid (ALA), which is synthesized in mitochondria and also requires L-cysteine, appears to participate in the recycling of glutathione.9 There is extensive animal work showing that lipoic acid, by supporting glutathione levels, can exert signifi cant protective effects against oxidant damage related to ischemia-reperfusion injury.10 More research may be needed to further elucidate these mechanisms and determine whether these results will apply in humans.

Reduced Glutathione

Glutathione, as such, is present in the diet in amounts usually less than 100 milligrams daily. It does not appear that much of the oral intake is absorbed from the intestine into the blood, at least in humans. However, there is an occasional study that does show an increase in circulating glutathione after oral administration of reduced glutathione.11,12,13,14 There is greater evidence that glutathione may be absorbed into the enterocytes, where it may help repair damaged cells.15 Patents have been submitted for reduced glutathione in a liposome claiming enhanced absorption.16

Organic L-Selenomethionine

Glutathione formation requires an adequate level of selenium. Selenium belongs to the sulfur group of elements which includes oxygen, tellurium and polonium. It is an essential trace element in human and animal nutrition. L-selenomethionine or L-selenocysteine are selenoproteins necessary to the endogenous production of glutathione peroxidases (GSHPx 1-4).17,18

There appears to be an inverse relationship between coronary heart disease and selenium intake. The possible anti-atherogenic activity of selenium may be accounted for, in part, by its antioxidant activity. Glutathione peroxidase may protect low density lipoprotein (LDL) from oxidation, thereby inhibiting atherogenesis and platlet aggregation. (Lipoperoxides impair prostacyclin synthesis and promote thromboxane synthesis).19

Undenatured Whey Protein and Colostrum

Undenatured whey and colostrum proteins’ antioxidant, detoxication and immunological effects are in no small part likely related to the glutamylcysteine groups which act as the substrate for glutathione (GSH) synthesis. These cystine groups needed for the intracellular conversion to cysteine are in whey and colostral sub-fractions.20 However, this highly bioavailable, double bonded cystine portion is very thermo-labile. Denaturization by heat will, therefore, greatly inhibit the ability of whey proteins to act as precursors to GSH synthesis, though not affecting the biological value (BV) of whey as a protein nutrient, as such. 21


Reduced glutathione is the major endogenous antioxidant and detoxication peptide. Its hepatic production and intracellular levels may be enhanced in the following ways:

• NAC, 200 mg, 3 or 4 times daily

• Reduced glutathione, in liposome: 50-200 mg, once or twice daily

• Selenium, which is abundant in garlic, onion, broccoli, whole grains and, most especially, Brazil nuts, has an optimal daily dosage at perhaps 200 mcg a day.22

• Whey protein, undenatured, 10-15 gm, 1 to 3 times a day

• Colostrum, whole, 2 gm, 1 to 3 times a day.

A palatable functional food formula of undenatured whey and/or colostrum, combined with some of the above nutraceuticals, may be both the most clinically effi cacious and nutritionally complete way to enhance endogenous glutathione production.

John H. Maher, D.C., oversees physician and consumer education for BioPharma Scientifi c, creators of Nano- Greens10. Dr Maher maintained an active chiropractic practice for 25 years. He has taught nutrition to health professionals nationally for the past 15 years. Dr. Maher is past post-graduate faculty of NYCC Academy of Anti-Aging Medicine, a Diplomate of the College of Clinical Nutrition, and a Fellow of the American Academy of Integrative Medicine. To learn more visit

The Many Clinical Faces of Protein Deficiency
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Written by Dr. Howard F. Loomis, D.C.   
Saturday, 08 September 2007 10:09

If the Chiropractic Profession were to “Discover the Secret” of improving protein digestion and assimilation, it could transform the health care marketplace almost overnight! That is not an exaggeration. Almost impossible to detect in its early stages with ordinary lab tests such as blood work, protein deficiency is behind many of the most persistent chief complaints for which patients enter your office. I estimate that at least 90 percent of all my female patients were protein deficient. The percentage was much lower for males, but especially significant in chronic back problems. Just examine the following list of clinical possibilities:


Hemoglobin and almost all of the factors involved in blood clotting are proteins. The photoreceptors in the eye responsible for vision are proteins. The neurotransmitters dopamine (alertness chemical) and serotonin (calming chemical) are proteins.

Protein defi ciency accounts for a large amount of infant mortality among malnourished children because specifi c antibodies against infection cannot be formed. Antibodies exhibit exactly the same chemical and physical properties of the plasma gamma globulins which are responsible for the body’s natural immunity to invasive agents. (See Table 2)


As extensive as the list in Table 1 is, it does not include fatigue and the often-heard complaint of being sick and tired of being sick and tired. This is so commonplace that it is usually ignored or even joked about by doctors and patients alike. When serious diagnostic investigations are made, the test results are usually normal and the patient is informed that nothing is wrong. Obviously the patient should be relieved that nothing serious is involved. But, without resolution of the vague symptomatology, their frustration lingers and they seek other means of treatment. Often many of these also fail but at a high price, since the expense must be covered out-of-pocket.

The medical profession is fi nding out that the old “try this and if it doesn’t work, we will do something else” routine has worn thin. By 1994, patient visits to so-called alternative health care providers were beginning to outnumber visits to medical providers. The economic “pinch” has gradually become stronger and now is driving the medical revolution toward alternative methods.

A cursory examination of the symptoms listed in Table 1 indicates that the allopathic approach in these conditions fails because they do not have anything to measure and, therefore, treatment with prescription drugs becomes hit-or-miss on a symptomatic basis. Obviously, it has been mostly miss. Once objective evidence of a disorder can be established, medicine’s track record improves. But, without objective evidence of pathological signifi cance, a vaccine or drug cannot be developed for the “sick and tired of being sick and tired“ syndrome. This should be good news to all who practice without the benefi t of pharmaceuticals. It means the patient is not diseased, and you will be able to help.

The answer for this common malady may lie within the body’s inability to handle stress (be it mechanical, nutritional, or emotional). Fortunately, the body handles all stress in a very predictable manner. Hans Selye was known for his landmark research that identifi ed the effects of stress on the human body. He found that stress, regardless of its source (chemical, mechanical, or emotional), always elicited a specifi c response. He called this process the General Adaptation Syndrome, and it consisted of the following stages:

• Alarm reaction to any stress;

• Resistance to or compensation for that stress;

• Exhaustion, if the stress is too strong or is maintained too long;

• The stages of disease, degeneration and, fi nally, death followed.

Symptoms do not occur until the body can no longer compensate for the stress being applied to it. And there can be no pathological fi ndings until the body reaches the stage of disease.

So the question is, what is lacking in a body in which symptoms are being manifested but is not yet evidencing alterations on objective tests such as blood, urine, X-ray, or MRI?

One obvious answer is that the body is not being supplied with adequate nutrients to nourish the organs responsible for the symptomatic pattern. Each organ and organ system is responsible for doing its part in maintaining, within narrow limits, the body temperature, pH, volume of extracellular fl uid, and the concentration of dissolved substances within that fl uid. This continuing process is called homeostasis. Seldom is homeostasis taken into consideration when deciding on a therapeutic course of action. Yet, if you can defi ne the price the body is paying to maintain homeostasis, you will know exactly how to solve the problem of “sick and tired of being sick and tired”!

As we turn our attention now to solving the riddle of being sick and tired, we can be sure of one thing: the body will maintain homeostasis or die. It maintains it all the time, everytime, and it does it with protein.

Despite all the claims made for the many combinations of vitamins, minerals, amino acids, and herbal extracts, the simple truth is that protein is the primary nutrient needed to maintain normal body functions. I didn’t say the others are not important. I said that, without protein, the others are totally irrelevant. To understand this seemingly outrageous statement, it is necessary to look at how the body uses protein to maintain the extracellular fl uid.

If detecting subclinical protein defi ciencies were easy, there would be no need for this article, because a big part of your formal education would have centered on correcting this insidious problem. I say “insidious” because blood tests for plasma proteins are usually normal outside of advanced disease states. Since homeostasis must be maintained ALL THE TIME and AT ALL COST, the body will catabolize its own tissues to maintain normal plasma protein levels in the blood. Consequently, the blood levels only drop when the body is exhausted. This results in protein defi ciency states going undetected until serious tissue damage has resulted. This brings us back to our basic premise: If protein defi ciency is undetectable in its early stages, then the only sign we have to go on is the symptom of an organ or organs being unable to meet the demands placed on it/them to maintain homeostasis.

Tissue catabolism for the purpose of maintaining homeostasis results in the sensation of fatigue and, if the condition continues uncorrected, the patient eventually becomes sick and tired of being sick and tired. Fortunately for us all, there are tissues the body will not tear down to use as protein sources, such as the heart and brain. Unfortunately, protein defi ciency can, and usually does, continue for long periods of time before a diagnosis of a specifi c disease process can be made.

While plasma proteins serve a host of important functions, it is important to remember that they are not used by the cells as metabolic fuel. Accordingly, they must be viewed quite differently from most other constituents of plasma such as glucose and cholesterol, which use the proteins as a vehicle for transport but are used by the cells.


Functions of Plasma Proteins

The functions of the plasma proteins (which remain in the blood and are not used by the cells), are as follows:

• The concentration of plasma proteins determines the colloidal osmotic pressure of the blood. In other words, it maintains fl uid balance between the blood, tissue fl uid, and the cells. Defi ciency results in the symptom of cold hands and feet.

• Plasma proteins act as buffers to help maintain acid-base balance. The body must always maintain acid-base balance, but stress in either direction will result in indigestion. Indigestion results from either the inability to spare adequate acidity to produce suffi cient stomach acid or the inability to spare adequate alkalinity to activate the pancreatic enzymes. This relationship has been discussed in many of my previous articles over the past fi fteen years.

• Plasma proteins bind and transport many critical compounds, such as lipids, hormones, vitamins, and minerals. Many nutritional problems can be laid at the doorstep of inadequate plasma proteins. Inability to perform these functions can result not only in nutritional defi ciencies, but endocrine dysfunctions as well.

• Plasma proteins bind and detoxify potentially dangerous drugs and other toxic substances. Therefore, a body catabolizing itself to maintain adequate plasma protein levels can and does result in the symptoms of toxicity. One of these, obviously, is fever; but before an elevated temperature becomes necessary come the sensations of being sick and tired!

• As the body’s means of transporting nutrients and waste products, the plasma proteins can be at the root of many blood test deviations.


The Most Prominent Chiropractic Finding

The appearance of Pottenger’s saucer (the so-called anterior dorsal complex) invariably heralds a digestive problem and adrenal stress. Adrenal exhaustion and plasma proteins go hand in hand and result in the syndrome of being sick and tired of being sick and tired. Understanding protein digestion and assimilation will increase your clinical confi dence because homeostasis is a constant on which you can depend.



Howard F. Loomis, Jr., DC, President of Enzyme Formulations ®, Inc., has an extensive background in enzymes and enzyme supplementation. As president for fi fteen years of 21st Century Nutrition® (now the Loomis Institute ® of Enzyme Nutrition), he has forged a remarkable career as an educator, having conducted over 400 seminars to date, in the United States and internationally, on the diagnosis and treatment of food enzyme defi ciency syndromes. Dr. Loomis welcomes your comments or questions through the Loomis InstituteTM at 6421 Enterprise Lane, Madison, WI 53719 or by phone at 1-800-662-2630.


Syndrome X and C-reactive Protein
Written by David Seaman, D.C., M.S., D.A.B.C.N., F.A.C.C.   
Saturday, 08 September 2007 09:51

Syndrome X is most easily viewed as a Pre-Diabetic State,as it is characterized by hyperinsulinemia and hyperglycemia. Syndrome X can initially exist without symptoms and, as it progresses, symptoms such as fatigue can develop, which are considered a “normal” part of aging, rather than the outcome of a pathological state.

Metabolic features of syndrome X:1  

1. Increased production of pro-infl ammatory mediators: C-reactive protein (CRP), nuclear factor kappa-B (NF-kB), tumor necrosis factor (TNF), and free radicals

2. Increased platelet aggregation—platelet hyperaggregability

3. Reduced degradation of fi brin

4. Tonic vasoconstriction; reduced vasomotor regulation

5. Promotes a pro-thombotic state

6. Promotes greater infarct size

7. Leads to heart disease and stroke

As outlined above, there are numerous pro-infl ammatory factors involved in syndrome X. Perhaps the most well studied is C-reactive protein. CRP was discovered seventy years ago when scientists were studying the human infl ammatory response. It was initially characterized as an acute-phase mediator that was released during infection and trauma. However, we now know that CRP can be released chronically as part of an ongoing subclinical pro-infl ammatory state. Consider the diverse functions of CRP in the pathogenesis of heart disease.



Patients need to understand that dietary changes are the most important component for reducing the expression of syndrome X. In addition, supplements to help reduce the pro-inflammatory state include a multivitamin, magnessium, fish oil, vitamin D, and botanicals such as ginger, tumeric, and garlic.

Pro-inflammatory aspects of CRP:2

1. Localizes in atherosclerotic intima, but not normal intima

2. Induces the production of adhesion molecules

3. Reduces endothelial derived relaxing factor, which is also known as endothelial-nitic oxide

4. Induces the production of plasmin inhibitors which lead to increased fi brin deposition

5. Triggers the oxidation of LDL-cholesterol

6. Mediates the uptake of LDL by macrophages

7. Blunts normal endothelial vasoreactivity

8. Recruits circulating monocytes into the arterial wall, and their subsequent activition

9. Stimulates complement activiation


When I was in chiropractic college, as part of our training, we did blood tests on our patients, and CRP and ESR were part of the panel. Back in those days (1986) the CRP we tested for was never elevated unless there was overt trauma or infection or, perhaps, rheumatoid arthritis. Otherwise CRP was never elevated.

In recent years, a new high sensitivity CRP (hsCRP) has been developed, which can be used as a screening test for patients.3 Ridker indicates that many physicians screen for hsCRP, because it is associated with a markedly increased risk of myocardial infarction, stroke, peripheral arterial disease, and sudden cardiac death, even among apparently healthy individuals with low levels of LDL-cholesterol.2

What about musculoskeletal conditions? Most medical and chiropractic physicians have been taught that osteoarthritis (OA) is a non-infl ammatory condition caused by mechanical wear and tear. Recent research would suggest otherwise, and is consistent with most clinical presentations of osteoarthritis; that is, several joints hurt, but one may be most pronounced and perhaps associated with previous injury. We tend to forget that other joints also hurt, which takes our mind away from viewing OA, more correctly, as a systemic condition.4



In this regard, research suggests that increasing levels of CRP can predict the emergence and severity of osteoarthritis.5,6

If you decide to measure hsCRP in your offi ce, the typical interpretation is as follows: less then 1mg/L is low risk for heart disease prediction/expression; between 1-3 mg/L refl ects moderate risk; and between 3-10 mg/L suggests high risk. Greater than 10 suggests an acute phase response and, thus, a re-test in 3 weeks.3 In terms of diet, it appears that the following are associated with elevated CRP: syndrome X, low fi ber diet, low magnesium intake, low omega-3 intake, trans-fat intake, low micronutrient intake, and reduced sleep.7-15

The key to understanding elevated CRP is that it is a marker for dietary imbalances that create a pro-infl ammatory state. Syndrome X is a signifi cant metabolic driver of elevated CRP and numerous other pro-infl ammatory mediators. The dietary approach to syndrome X focuses on foods with a low glycemic index and low glycemic load, which means vegetables, lean animal products, fruits, and nuts.

Patients need to understand that dietary changes are the most important component for reducing the expression of syndrome X. In addition, supplements to help reduce the pro-infl ammatory state include a multivitamin, magnesium, fi sh oil, vitamin D, and botanicals such as ginger, turmeric, and garlic.


Dr. Seaman is the Clinical Chiropractic Consultant for Anabolic Laboratories, one of the fi rst supplement manufacturers to service the chiropractic profession. He is on the postgraduate faculties of several chiropractic colleges, providing nutrition seminars that focus on the needs of the chiropractic patient. He is also a faculty member at Palmer College of Chiropractic Florida, where he teaches nutrition and subluxation theories. He can be reached by e-mail at This e-mail address is being protected from spambots. You need JavaScript enabled to view it .



  1. Dandona P, Aljada A, Chaudhuri A, Mohanty P, Garg R. Metabolic Syndrome - A Comprehensive Perspective Based on Interactions Between Obesity, Diabetes, and Inflammation. Circulation 2005; 111:1448-54
  2. Ridker PM. Rosuvastatin in the primary prevention of cardiovascular disease among patients with low levels of low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein: rationale and design of the JUPITER trial. Circulation. 2003; 108: 2292–2297
  3. Ridker PM. C-reactive protein. A simple test to help predict risk of heart attack and stroke. Circulation. 2003:108:381-e85
  4. Aspden RM, Scheven BA, Hutchison JD. Osteoarthritis as a systemic disorder including stromal cell differentation and lipid metabolism. Lancet. 2001:357:1118-20.

5.      Pearle AD, Warren RF, Rodeo SA. Basic science of articular cartilage and osteoarthritis. Clin Sports Med.  2005; 24:1-12

  1. Sharif M et al. Elevated serum C-reactive protein levels in osteoarthritis. Brit J Rheumatol  1997; 36:140-49
  2. Ajani UA, Ford ES, Mokdad AH. Dietary fiber and C-reactive protein: findings from national health and nutrition examination survey data. J Nutr. 2004; 134:1181-5.
  3. Lopez-Garcia E, Schulze MB, Manson JE et al. Consumption of (n-3) fatty acids is related to plasma biomarkers of inflammation and endothelial activation in women. J Nutr. 2004; 134:1806-11
  4. Ma Y, Griffith JA, Chasan-Taber L et al. Association between dietary fiber and serum C-reactive protein. Am J Clin Nutr 2006;83:760–66.
  5. King DE Mainous AG, Geesey ME, Woolson RF. Dietary magnesium and C-reactive protein levels. J AM Coll Nutr. 2005; 24L3):166-71.
  6. Church TS, Earnest CP,  Wood KA, Kampert JB. Reduction of C-reactive protein levels through use of a multivitamin. Am J Med. 2003;115:702–707.
  7. Lopez-Garcia E, Schulze MB, Meigs JB et al. Consumption of trans fatty acids is related to biomarkers of inflammation and endothelial dysfunction. J Nutr. 2005; 135(3):562-66.
  8. Pfutzner A, Forst T. High-sensitivity C-reactive protein as cardiovascular risk marker in patients with diabetes mellitus.  Diabetes Technol Ther. 2006; 8(1):28-36.
  9. Dandona P, Aljada A, Chaudhuri A, Mohanty P, Garg R. Metabolic Syndrome - A Comprehensive Perspective Based on Interactions Between Obesity, Diabetes, and Inflammation. Circulation. 2005; 111:1448-54.
  10. Meier-Ewert HK, Ridker PM, Rifai N et al. Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk. J Am Coll Cardiol. 2004; 43(4):678-83.
Excuse me, can we talk about poop?
User Rating: / 5
Written by Dr. Rodger Murphree, D.C.   
Saturday, 08 September 2007 09:27

Not necessarily the Best Topic for a Cocktail Party, I agree. However, for over 40 million Americans who have been diagnosed with irritable bowel syndrome (IBS), bowel movements are an important topic. Some experts report that irritable bowel syndrome affects approximately 10–20 percent of the general population. Irritable bowel syndrome is characterized by a group of symptoms in which abdominal pain or discomfort is associated with a change in bowel pattern, such as loose or more frequent bowel movements or diarrhea, and/or hard or less frequent bowel movements or constipation. Gender plays a clear role, as more than 80 percent of IBS patients are women between twenty and fifty-five years old. The financial burden of IBS is high. In the United States, IBS results in an estimated $8 billion in direct medical costs and $25 billion in indirect costs annually.

The criteria for diagnosing IBS is based on the newly modified Rome criteria (Rome II criteria) as the presence for at least twelve weeks (not necessarily consecutive) in the preceding twelve months of abdominal discomfort or pain that cannot be explained by a structural or biochemical abnormality and that has at least two of following three features: (1) pain is relieved with defecation, and its onset is associated with (2) a change in the frequency of bowel movements (diarrhea or constipation) or (3) with a change in the form of the stool (loose, watery, or pellet-like).

Some people with the disorder have constipation (IBS-C). Some have diarrhea (IBS-D). And some alternate back and forth between constipation and diarrhea (IBS-A). IBS symptoms result from what appears to be a disturbance in the interaction between the gut or intestines, the brain, and the autonomic nervous system that alters regulation of bowel motility (motor function) or sensory function.

Research has shown that the cause of IBS is related to neuroendocrine immune system dysfunction (brain and stomach hormones). This connection is largely mediated by the neurotransmitter serotonin. The brain and gut are connected through the neuroreceptors 5-hydroxytriptamine-3 (5-HT3) and 5-hydroxytriptamine- 4 (5-HT4). These serotonin receptors regulate the perception of intestinal pain and the GI motility (contractions that move food through the intestinal tract). Therefore, serotonin controls how fast or how slow food moves through the intestinal tract. In fact, there are more serotonin receptors in the intestinal tract than there are in the brain. Ninety percent of serotonin receptors are in the intestinal tract.  

Research suggests that IBS patients have extra sensitive pain receptors in the gastrointestinal tract, which may be related to low levels of serotonin. Decreased levels of serotonin may help explain why people with IBS are likely to be anxious or depressed. Studies show that 54-94 percent of IBS patients meet the diagnostic criteria for depression, anxiety, or panic disorder.

Restoring optimal levels of serotonin has been the focus of traditional drug therapy.

Zelnorm, a 5-HT4 receptor agonist, which was once hailed as “the drug” for IBS-C (IBS with frequent constipation), has recently been pulled from the market for its association with heart attacks and stroke. The percentage of patients taking Zelnorm that had serious and life-threatening side effects was ten times higher than the percentage of patients taking a placebo.

Even before this drug was recalled due to cardiovascular risks, many experts warned that this drug was dangerous for its other potential side effects, including severe liver impairment, severe kidney impairment, bowel obstruction, diarrhea, constipation, abdominal pain, headaches, abdominal adhesions, gallbladder disease, and back pain.

Lotrinex (Alosetron), a 5-HT3 agonist, is prescribed for IBS-D. Within eight months of being on the market, reports of ischemic colitis (a life endangering situation in which the blood supply to the intestines is blocked) began to grow each day. Lotrinex was responsible for at least four deaths, probably many more. Many who took the drug reported severe abdominal pain from constipation. The drug was taken off the market. It is now back and available with strict prescribing guidelines. An editorial in The British Medical Journal suggests that as many as 2 million Americans will be eligible for the drug under the new guidelines. According to previous reported side effects, this would result in 2,000 cases of severe constipation, almost 6,000 cases of ischemic colitis, 11,000 surgical interventions, and at least 324 deaths.

Antispasmodics (Levsin, Levsinex, Bentyl, Donnatal, etc.) are routinely prescribed for the treatment of IBS symptoms.

Potential side effects include bloating; blurred vision; clumsiness; constipation; decreased sweating; dizziness; drowsiness; dry mouth; excessive daytime drowsiness (“hangover effect”); feeling of a whirling motion; headache; light-headedness; nausea; nervousness; rash; hives; diffi culty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; agitation; confusion; diarrhea; diffi culty focusing eyes; disorientation; exaggerated feeling of well-being; excitement; fainting; fast or irregular heartbeat; hallucinations; loss of coordination; loss of taste; memory loss; muscle pain; pounding in the chest; severe or persistent trouble sleeping; trouble urinating; unusual weakness; very slow breathing; vision changes; and vomiting.

Why in the world would someone prescribe this crap? (Pun intended.) It is absurd to suggest that individuals with IBS have a drug defi ciency. IBS is not a disease; it is a symptom of a compromised gastrointestinal system. Using potentially dangerous drugs to reduce symptoms, while ignoring natural and often more effective approaches, is typical of what is wrong with “cookbook” (symptom-focused) medicine.   

Reversing IBS with nutritional therapy

I fi nd that IBS usually disappears rather quickly once my patients correct their poor eating habits (increase fi ber, reduce simple sugars, caffeine and junk foods), uncover any hidden allergies when present, including gluten intolerance (Celiac disease), boost optimal stress coping chemicals (serotonin, magnesium, B-vitamins, etc.), restore bowel ecology (probiotics), and take digestive enzymes with their meals.


To boost serotonin levels, I recommend patients take the amino acid responsible for making serotonin, known as 5- hydroxytryptophan (5HTP). Patients should take 300-400mg a day with food.

Digestive enzymes

Most digestion and absorption takes place in the small intestine and is regulated by pancreatic enzymes (digestive) and bile. The pancreas aids in digestion by releasing proteolytic enzymes, which help break down proteins into amino acids. Natural digestive enzymes are found in raw fruits and vegetables. Processed foods are usually devoid of digestive enzymes. Over consumption of these processed foods can lead to digestive enzyme defi ciencies. This may then lead to malabsorption and/or intestinal permeability syndrome (bloating, gas, indigestion, diarrhea, constipation, and intestinal infl ammation). To ensure proper digestion and absorption, I recommend taking pancreatic enzymes with each meal.


I always recommend people take a good optimal daily allowance multivitamin/mineral formula. Patients with IBS have depleted their stress coping chemicals and this not only leads to IBS but also prevents them from beating IBS. It is a vicious cycle that can only be broken by taking adequate amounts of essential vitamins and minerals. The mineral magnesium, which is involved in over 300 bodily processes, is particularly important for reversing the symptoms of IBS-C. Magnesium helps relax the smooth muscle of the colon (natural laxative) allowing normal bowel movements. While a diet high in nutritious fiber is important, magnesium is even more important. A magnesium defi ciency not only causes constipation but can also lead to heart disease, mitral valve prolapse (MVP), depression, anxiety, chronic muscle pain, headaches, migraines, fatigue, and many other unwanted health conditions. Those with IBS-C may need up to 1,000mg of magnesium each day. While those with IBS-D, may need less than 500mg. I recommend patients begin with 500mg of magnesium a day.


The human intestines are inhabited by billions of benefi cial bacteria. These bacteria, which are mostly located in the colon, aid in digestion by fermenting substances that were not digested in the small intestine and by breaking down any remaining nutrients.

A healthy intestinal tract contains some 2-3 lb. of bacteria and other microorganisms, such as yeast, that normally don’t cause any health problems.

However, when the intestinal tract is repetitively exposed to toxic substances (antibiotics, steroids, NSAID’s, etc.), these microorganisms begin to proliferate and create an imbalance in the bowel flora. Harmful organisms, like yeast and some normally dormant bacteria, begin to overtake the good bacteria. This is known as intestinal dysbiosis.

IBS and small-intestinal bacterial overgrowth may share similar symptoms. One study showed that 78 percent of IBS participants had small-intestinal bacterial overgrowth. To aid in digestion and prevent intestinal dysbiosis, patients with IBS should take probiotics (Lactobacillus and Biidobacterium) on a daily basis.

This approach isn’t guaranteed to solve every case of IBS. However, in the majority of my patients, symptoms improve to such a point that, within a few weeks, we can focus on more important topics, like, “Who is going to win American Idol?”


Rodger Murphree, D.C., has been in private practice since 1990. He is the founder and past clinic director for a large integrated medical practice located on the campus of Brookwood Hospital in Birmingham, Alabama. He is the author of Treating and Beating Fibromyalgia and Chronic Fatigue Syndrome, Heart Disease What Your Doctor Won’t Tell You, and Treating and Beating Anxiety and Depression with Orthomolecular Medicine. He can be reached at or This e-mail address is being protected from spambots. You need JavaScript enabled to view it or 1-205-879-2383.


1.Bodemar G, Ragnarsson G. [Irritable bowel syndrome. Survey of definitions, differential diagnosis and pathogenesis]. Lakartidningen. 2001 Feb 14;98(7):666–71.2.FDA Announces Discontinued Marketing of GI Drug, Zelnorm, for Safety Reasons,” published on 3/30/07 via the U.S. Food and Drug Administration Web site ( Accessed 3/30/07.3.“FDA Public Health Advisory, Tegaserod maleate (marketed as Zelnorm)” published on 3/30/07 via the U.S. Food and Drug Administration Web site ( Accessed 4/3/07.4.“Novartis Stops Zelnorm Marketing, Sales on Heart Risk,” by Eva von Schaper. Published 4/2/07 via ( Accessed 4/2/07.5.Sandler RS. Epidemiology of irritable bowel syndrome in the United States. Gastroenterology. 1990;99:409-415.6.Thompson WG, Longstreth G, Drossman DA. Functional bowel disorders and Functional abdominal pain. In: Drossman DA, Corazziari E, Talley N, Thompson WG, Whitehead W, eds. Rome II: The Functional Gastrointestinal Disorders. 2nd ed. McLean, VA: Degnon Associates, 2000:351-375. 7.Goldberg PA, “Modification ofvisceral sensitivity and pain in irritable bowel syndrome by 5-HT3 antagonism (ondansetron).” Digestion Nov-Dec 1996:57(6):478-83.8.Saggioro A. Probiotics in the treatment of irritable bowel syndrome. J Clin Gastroenterol. 2004 Jul;38(6 Suppl):S104–S106.9. Monthly Prescribing Reference. Prescribing Reference Inc.  New York, NY. October 2006.




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