Print Page  |  Contact Us  |  Sign In  |  Join ACAM
ACAM Integrative Medicine Blog
Blog Home All Blogs

Curcumin for Inflammatory Bowel Disease: A Review of Human Studies

Posted By Administration, Friday, July 8, 2011
Updated: Friday, April 18, 2014


Case study from the Alternative Medicine Review (AMR) - the official journal of the American College for Advancement in Medicine (ACAM)

by Rebecca A. Taylor, PharmD, MBA, BCPS and Mandy C. Leonard, PharmD, BCPS


OBJECTIVE: To evaluate the use of curcumin in inflammatory bowel disease. DATA SOURCES: ALTMEDEX, Comprehensive Database of Natural Medicines, MEDLINE/PubMed were searched from January 1980 through May 2009 using the terms curcumin, turmeric, ulcerative colitis, Crohn’s disease,
Curcuma longa, Curcuma domestica, Indian saffron, inflammatory bowel disease. Data was limited to human trials. References of identified articles were reviewed. DATA SYNTHESIS: Data evaluating the use of curcumin in inflammatory bowel disease (including ulcerative colitis and Crohn’s disease) is limited to two studies comprising data for only 99 patients. Curcumin in conjunction with mainstream therapy, consisting of sulfasalazine (SZ) or mesalamine (5-aminosalicylic acid [5-ASA] derivatives) or corticosteroids was shown to improve patient symptoms and allow for a decrease in the dosage of corticosteroids or 5-ASA derivatives. In one small study of 10 patients, some patients even stopped taking corticosteroids or 5-ASA. CONCLUSIONS: Although two small studies have shown promising results, all authors conclude
that larger-scale, double-blind trials need to be conducted to establish a role for curcumin in the treatment of ulcerative colitis. In addition to improving results when used in conjunction with conventional medications for UC, curcumin may pose a less-expensive alternative. (Altern Med Rev 2011;16(2):152-156)


Turmeric, used as a spice in curry powders and mustard, is known scientifically as Curcuma longa or Curcuma domestica. The perennial herb has multiple ingredients, including curcuminoids, the most active ingredients for medicinal use. These curcuminoids, comprising the yellow-pigmented fractions of turmeric, include diferuloylmethane (curcumin I), demethoxycurcumin (curcumin II), bisdemethoxycurcumin (curcumin III), and the recently discovered cyclocurcumin. The major components of commercial curcumin are curcumin I (77%), curcumin II (~17%), and curcumin III (~3%). Curcumin is also known by many synonyms and translated into various languages around the world; in Tibetan language it is known
as Gaser, in Swahili it is known as Manjano.

Curcumin has well-documented historical use in Chinese, Hindu, and Ayurvedic medicine. Curcumin has been used for a variety of disorders, from respiratory conditions to dyspepsia to malignancy. To date, no studies in animals or humans have discovered significant toxicity related to curcumin, even at very high doses.

Mechanisms of Action

Much is known about the molecular targets and interactions of curcumin with receptors, growth and transcription factors, cytokines, enzymes, and genes. Curcumin is often cited as pleiotropic, meaning it has the ability to interact with many cell targets. For the purposes of this discussion, curcumin’s molecular targets will be confined to those involved in gastrointestinal inflammation. Curcumin has been shown to inhibit the activity of lipoxygenase4 or binding to phosphatidylcholine micelles, thereby inhibiting lipoxygenase I. Of note in gastrointestinal disorders, curcumin has been found to inhibit the activation of various transcription factors that play a key role in inflammation, cell survival and proliferation, and
angiogenesis. These include nuclear factor-kappaB (NF-kB), activated protein-1 (AP-1), signal transducer and activator of transcription (STAT) proteins, peroxisome proliferator-activated receptor-gamma (PPAR-γ), and β-catenin. Inflammatory stimuli activate one of three independent mitogen-activated protein kinase (MAPK) pathways leading to activation of the p44/42 MAPK, JNK, or p38 MAPK pathway.
Cyclooxygenase-2 (COX-2) proteins are crucial to the inflammation cascade and have been linked to
certain cancers. There are several ways in which curcumin inhibits COX-2, both directly and indirectly. Curcumin downregulates the expression of COX-2, most likely through the downregulation of NF-kB that is required for COX-2 activation. In cancer cells, curcumin exerts anti-inflammatory and growth-inhibition by inhibiting expression of interleukin-1beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α).


Curcumin studies in animals show it is rapidly metabolized, conjugated in the liver, and excreted in the feces with minimal amounts found in the urine. A 40 mg/kg intravenous dose of curcumin given to rats resulted in complete plasma clearance at one hour post-dose, showing its rapid metabolism; data in humans is inconclusive. A phase I clinical trial conducted on 25 patients with precancerous lesions showed oral doses of 4, 6, and 8 g curcumin daily for three months yielded serum curcumin concentrations of only 0.51 ± 0.11, 0.63 ± 0.06, and 1.77 ± 1.87 µM respectively, indicating poor absorption of straight curcumin. In this study serum levels peaked one and two hours post-dose and declined rapidly.

Inflammatory Bowel Disease (IBD)

Inflammatory bowel disease is a chronic immune disorder that involves an overactive immune component in the intestinal mucosa. IBD is divided into two major categories, ulcerative colitis (UC) and Crohn’s disease (CD). The two diseases have a fair amount of overlap, including presenting symptoms, quality of life issues, and treatments. Patients with IBD often have symptoms of abdominal pain, cramping, diarrhea, rectal bleeding, urgency, nausea, fever, and weight loss. Major differences of the two types of IBD are listed in Table 1.11 Proctitis is ulcerative colitis confined to the rectal area.

Certain cytokines have been associated with IBD, including TNF-α, IL-1, IL-6, IL-8, and others. Targeted drug therapies, specifically infliximab, have been successful in treating IBD. Infliximab is an anti-TNF-α monoclonal antibody that has been extensively studied in myriad inflammatory disorders, including CD and UC. Widespread use of infliximab is limited because of adverse effects, cost, and the emergence of antibodies that result after multiple administrations.

Most recently, the role of NF-kB in IBD has been elucidated. Colon biopsies in IBD patients with active disease show increased levels of NF-kB p65 protein (a member of the NF-kB family of proteins). The amount of NF-kB p65 in the tissue samples correlated with the severity of intestinal inflammation. This increased expression of NF-kB results in an increased ability to secrete inflammatory cytokines, such as
TNF-α, IL-1, IL-6, IL-12, and IL-23, the latter of which are directly responsible for mucosal damage in IBD. TNF-α is also able to up-regulate the production of NF-kB, resulting in a cyclical feedback loop of inflammation.

Table 1. Differential Diagnosis of Ulcerative Colitis and Crohn's Disease


 Diagnosis and Staging of IBD in Clinical Studies

Ulcerative colitis is diagnosed through a colonoscopy, while the severity of symptoms can be rated on a number of severity index scales. Although several endoscopic indices are available to characterize the severity of ulcerative colitis, those currently used in clinical trials are not uniform. Hanai and colleagues, in the double-blind study discussed below, did not disclose their specific methodology for endoscopic index. The Clinical Activity Index (CAI) was used to assess UC severity in this same study. A CAI of ≤4
indicated remission, whereas a CAI ≥5 indicated relapse. A Crohn’s disease activity index (CDAI) is
often used to evaluate disease severity in CD – as was the case in the small pilot study discussed below.

Clinical IBD Studies
Small Pilot Study

Holt and colleagues conducted a small, open-label, pilot study of curcumin in five patients with ulcerative colitis/proctitis and five patients with Crohn’s disease. Five patients with ulcerative proctitis, who were currently using 5-aminosalicylic acid (5-ASA) compounds and corticosteroids (four of five patients were on corticosteroids + 5-ASA compounds), were given 550 mg curcumin twice daily for one month, then 550 mg three times daily for the second month. The five patients with Crohn’s disease received curcumin at a dose of 360 mg orally three times daily for one month and then 360 mg four times daily for an additional two months. Patient characteristics and demographics are reported in Table 2.

Patients were assessed at baseline and after two months of curcumin via hematological, biochemical, and inflammatory analysis (C-reactive protein [CRP] and erythrocyte sedimentation rate [ESR]) as well as sigmoidoscopy and biopsy. Subjective analysis was via a self-reported symptom diary. In the ulcerative
proctitis group, all five patients had significant improvement. Two patients stopped taking 5-ASA compounds, two reduced 5-ASA dosages, and one stopped corticosteroids entirely. Although only four of five CD patients completed the study, they also experienced a reduction in CDAI scores, ESR, and CRP. The Crohn’s disease group also reported symptomatic improvements of fewer bowel movements, less diarrhea, and less abdominal pain and cramping. In the absence of a clearly stated primary endpoint, it was considered to be the symptom diary. Based on the symptom diary (p<0.02), all patients improved from baseline after two months and inflammatory markers decreased to normal limits. The authors recommended larger scale, double-blinded, placebo-controlled trials in the future.

Table 2. Patient Characteristics and Medications at Study Entry


Adapted from: Holt PR, Katz S, Kirschoff R Curcumin therapy in inflammatory bowel disease; a pilot study. Dig Dis Sci 2005;50:2191-2193.

5-ASA = 5-aminosalicyllic acid

SZ = sulfasalazine

6-MP = 6-mercaptopurine

Double-blind, Placebo-controlled Trial

Hanai and colleagues conducted a randomized, multicenter, double-blind, placebo-controlled trial of curcumin plus sulfasalazine (SZ) or mesalamine compared to placebo plus SZ or mesalamine in 89
patients with UC. After a four-week washout period, subjects were randomly assigned to a six-month regimen of either placebo (n=44) or curcumin 1,000 mg after breakfast and 1,000 mg after dinner (n=45) in combination with SZ (1-3 g/ day; median 2 g/day) or mesalamine (1.5-3 g/day; median 2.25 g/day). The inclusion and exclusion criteria were extensive (Table 3).

Patients were followed during treatment and for six months after the treatment ended; patients received only SZ or mesalamine during the six-month follow-up. Seven patients requested to be excluded, leaving 82 evaluable patients. The relapse rate was significantly higher in the placebo group (20.5% [8/39]) than in the curcumin-treated group (4.7% [2/43]). Curcumin also suppressed disease-associated CAI and endoscopic index (EI) scores. The mean CAI in the curcumin group was improved from 1.3 to 1.0 at six months (p=0.38), while CAI in the placebo group increased from 1.0 to 2.2 (p=0.0003). Patients in the curcumin group also had significantly improved EI (1.3 to 0.8 [p=0.0001]), while EI values in the placebo group showed no significant improvement. The authors provided only before- and after-treatment data,
despite assessments every two months. There was a statistically significant (p=0.049) difference between the percentage of patients with recurrence at six months in the curcumin (4.44 [95% confidence interval (CI) 0.54-15.15]) compared to the placebo (15.15 [CI 8.18-32.71]) group. This difference was not significant at 12 months.

Side effects reported by study subjects included abdominal bloating, nausea, hypertension (one patient), diarrhea, and elevated γ-guanosine triphosphate (GGTP) levels (one patient). This latter patient was a heavy drinker. With the exception of the patient that experienced hypertension, no patient discontinued curcumin therapy due to side effects.

Only two of 43 patients treated with curcumin in combination with SZ or mesalamine relapsed during six months of therapy; whereas, eight of 39 patients who received placebo with SZ or mesalamine relapsed during the same period. Although this difference was not statistically significant, the authors postulate curcumin may have an effect on suppressing relapse. The authors drew three major conclusions: (1) curcumin had better clinical efficacy over placebo in the prevention of relapse, (2) curcumin significantly improved the CAI and EI, and (3) curcumin was well-tolerated. The authors, stating their results might have
been better had they used a higher dose of curcumin, recommend that future studies use dosages greater than 2 g/day.

Table 3. Inclusion and Exclusion Criteria in Hanai Study


Precautions and Contraindications

Patients with gallstones or bile duct obstructions should use curcumin with caution, primarily due to curcumin’s ability to cause gallbladder contractions. In a randomized, double-blind, cross- over study involving 12 healthy volunteers, 20 mg curcumin produced as much as 29-percent reduction in gallbladder size, indicating gallbladder contraction (statistically different than placebo). A subsequent study indicated
that doses of 40 and 80 mg curcumin produced 50- and 72-percent decreases in gallbladder volume, respectively.

Because curcumin inhibits platelet aggregation in vitro and in animal studies, it is theorized it could be additive in effect to antiplatelet medications such as aspirin, clopidogrel, and non-steroidal anti-inflammatories (NSAIDS).18,19 In a mouse model, 100 mg/kg curcumin or 25 mg/kg aspirin resulted in 60- or 61.1-percent protection from thrombosis, respectively. The concomitant use of curcumin and
anticoagulant or antiplatelet medications should be approached with caution.


Although this review discusses just two clinical studies of inflammatory bowel disease, the uses of curcumin far exceed the scope of this article. Curcumin shows promise in treating myriad disorders. It has recently been studied, at wide-ranging daily dosages of as little as 20 mg and as much as 12 g, for ailments such as psoriasis, colorectal cancer, renal graft function, pancreatitis, dyspepsia, and chronic anterior uveitis, to name a few. Larger-scale, prospective studies are needed to confirm its effect for IBD. Curcumin has an advantageous safety profile as well as low relative cost, making it an attractive option for IBD patients.

1. Goel A, Kunnumakkara AB, Aggarwal BB. Curcumin as “curecumin”: from kitchen to clinic. Biochem Pharmacol 2008;75:787-809.
2. Jurenka JS. Anti-inflammatory properties of curcumin, a major constituent of Curcuma longa: a review
of preclinical and clinical research. Altern Med Rev 2009;14:141-153.
3. Hanai H, Sugimoto K. Curcumin has bright prospects for the treatment of inflammatory bowel disease. Curr Pharm Des 2009;15:2087-2094.
4. Skrzypczak-Jankun E, Zhou K, McCabe NP, et al. Structure of curcumin in complex with lipoxygenase and its significance in cancer. Int J Mol Med 2003;12:17-24.
5. Began G, Sudharshan E, Appu Rao AG. Inhibition of lipoxygenase 1 by phosphatidylcholine micelles-bound curcumin. Lipids 1998;33:1223-1228.
6. Shishodia S, Singh T, Chaturvedi MM.  Modulation of transcription factors by curcumin. Adv Exp Med Biol 2007;595:127-148.
7. Cho JW, Lee KS, Kim CW. Curcumin attenuates the expression of IL-1beta, IL-6, and TNF-alpha as well as cyclin E in TNF-alpha-treated HaCaT cells; NF-kappaB and MAPKs as potential upstream targets. Int J Mol Med 2007;19:469-474.
8. Sharma RA, Steward WP, Gescher AJ. Pharmacokinetics and pharmacodynamics of curcumin. Adv Exp Med Biol 2007;595:453-470.
9. Ireson C, Orr S, Jones DJ, et al. Characterization of metabolites of the chemopreventive agent curcumin in human and rat hepatocytes and in the rat in vivo, and evaluation of their ability to inhibit phorbol esterinduced prostaglandin E2 production. Cancer Res 2001;61:1058-1064.
10. Cheng AL, Hsu CH, Lin JK, et al. Phase I clinical trial of curcumin, a chemopreventive agent, in patients with high-risk or pre-malignant lesions. Anticancer Res 2001;21:2985-2900.
11. Friedman S, Blumberg RS. inflammatory bowel disease. In: Fauci AS, Braunwald E, Kasper DL, Hauser SL, eds. Harrison’s Principles of Internal Medicine. 17th ed. Columbus, OH: McGraw-Hill Professional; 2008:1886- 1898. content.aspx?aID=2883197
12. Papadakis KA, Targan SR. Role of cytokines in the pathogenesis of inflammatory bowel disease. Annu Rev Med 2000;51:289-298.
13. Atreya I, Atreya R, Neurath MF. NF-kappaB in inflammatory bowel disease. J Intern Med 2008;263:591-596.
14. Hanai H, Iida T, Takeuchi K, et al. Curcumin maintenance therapy for ulcerative colitis: randomized, multi- center, double-blind, placebo-controlled trial. Clin Gastroenterol Hepatol 2006;4:1502-1506.
15. Holt PR, Katz S, Kirschoff R. Curcumin therapy in inflammatory bowel disease: a pilot study. Dig Dis Sci
16. Rasyid A, Lelo A. The effect of curcumin and placebo on human gall-bladder function: an ultrasound study. Aliment Pharmacol Ther 1999;13:245-249.
17. Rasyid A, Rahman AR, Jaalam K, Lelo A. Effect of different curcumin dosages on human gall bladder. Asia Pac J Clin Nutr 2002;11:314-318.
18. Srivastava KC, Bordia A, Verma SK. Curcumin, a major component of food spice turmeric (Curcuma longa) inhibits aggregation and alters eicosanoid metabolism in human blood platelets. Prostaglandins Leukot Essent Fatty Acids 1995;52:223-227.
19. Srivastava R, Dikshit M, Srimal RC, Dhawan BN. Anti-thrombotic effect of curcumin. Thromb Res 1985;40:413-417.
20. Srivastava R, Puri V, Srimal RC, Dhawan BN. Effect of curcumin on platelet aggregation and vascular prostacyclin synthesis. Arzneimittelforschung 1986;36:715-717.

Tags:  inflammatory bowel disease 

Share |
PermalinkComments (0)

Detox - What Does that Mean?

Posted By Administration, Tuesday, June 28, 2011
Updated: Friday, April 18, 2014

IStock_000004322112Small Crop Duster

by Marsha Nunley, MD

I have gone through many changes on my journey to health: gluten-free/dairy-free diet, limited alcohol, no processed foods, bio identical hormones, many, many supplements, meditation, yoga, etc. and for me, doing a detox is the last frontier. I think I have resisted because I did not really understand and honestly, it seemed a bit daunting. Juice, shakes, and limiting food intake? Really, I love my food and because I have adrenal issues, I am used to eating frequently. Yes, I pretty much eat whole organic foods and even try to get in as many raw foods as possible, but I do love a good steak every now and then. (Sushi does not count on a raw food diet.) So let’s explore the reasons we should consider doing a detox every six months (or at least annually).

In medical school, I learned about detoxification that occurs in the body to remove waste – a part of normal bodily processes. We also learned about how the body metabolizes drugs and other foreign invaders. The assumption seemed to be that the body had a system that would readily get rid of whatever it needed to, when it needed. Not much was taught about augmenting the process of detoxification. In medicine, it is referred to as a metabolic process. To your average physician, drugs and toxins are metabolized (not detoxified), so detoxification in the sense of patient treatment is not something that your average physician will be interested in or familiar with necessarily. Not to criticize, just to let you know that if you try and talk to your family doc about detox, you will probably be met with a questioning look and dismissed. I think it is really that most doctors are simply not aware of the burden we are putting on our bodies’ detoxification capabilities.

Toxins can be classified as inner toxins, which are generated within the body, or outer toxins, which are toxins that enter the body from the outside. Inner toxins come from the body’s normal metabolic processes and from invaders, such as an infection. So where do outer toxins come from? Read this article from the Environmental Working Group about a study where they tested volunteers for 210 chemicals (San Francisco Chronicle, 2004).

“There are more than 75,000 chemicals licensed for commercial use; more than 2,000 new synthetic chemicals are registered every year; the Environmental Protection Agency has tallied close to 10,000 chemical ingredients in cosmetics, food and consumer products. The 210 we were tested for are just a few of the industrial chemicals in our world. We can surmise that the actual number of manufactured chemicals in our bodies is far greater than our results show. Very few of these chemicals were in our environment, or our bodies, just 75 years ago.

In 1998, U.S. industries reported manufacturing 6.5 trillion pounds of 9,000 different chemicals, and in 2000, major American companies — not even counting the smaller ones — dumped 7.1 billion pounds of 650 different industrial chemicals into our air and water.”

We are living in a sea of toxins and there is good evidence that it is affecting our health in a major way. Many chronic conditions such as arthritis, chronic fatigue, fibromyalgia, elevated cholesterol and triglycerides, depression, and on and on are related to our toxic world. These chemical toxins are stored in fat in the body and are likely a major contributing factor to the obesity epidemic in the U.S. and the world.
We are living in a different world from our parents and grandparents. Clearly, regular augmentation of the body’s detoxification process is essential for us to remain healthy and vital. Even though it’s not easy, I am putting regular detoxification into my health regimen and encourage you to do the same. I am currently a week into a 21-day detox. I will keep you posted on how it goes.

Good resources on detox and toxicity in our world:

Cleanse Your Body, Clear Your Mind. by Jeffrey Morrison, MD
Essential Cleansing. by Brenda Watson
Healing Digestive Illness. by Russell Mariani
Detoxify or Die. by Sherry Rogers
Environmental Working Group

Dr. Marsha Nunley is a Texas native who moved to California in 2000. She earned her medical degree from the University of Texas at San Antonio and is Board Certified in Internal Medicine. She currently practices Internal as well as Functional Medicine in San Francisco and Oakland, California. Dr. Nunley is also an expert in menopause, andropause and bio-identical hormone therapies. She has completed specialty training in Geriatric Medicine, Palliative Care, and Pain Management, and is also certified in the new area of Aging Medicine through the American Academy of Anti-Aging and Regenerative Medicine. She has completed an Associate Fellowship in Integrative Medicine at the University of Arizona, where she explored the benefits of mind-body medicine, chiropractics, acupuncture, homeopathy, craniosacral therapy, hypnotherapy, and energy healing. Visit Dr. Nunley's website at:

This post has not been tagged.

Share |
PermalinkComments (0)

Anti-Aging Lifestyle Prolongs Life

Posted By Administration, Wednesday, June 22, 2011
Updated: Friday, April 18, 2014

by Andrea Purcell, ND

In a study published in the Journal of Internal Medicine, researchers in Sweden have studied 900 men over the last 50 years and have come up with predictors of longevity. Of all of the subjects, 111 lived to 90 and had the following predictors:

  • They did not smoke
  • Moderate coffee intake < 2 cups
  • Good socio-economic status by age 50
  • Engaged in good physical work capacity at age 54
  • Low Cholesterol at age 50

In another study by the National Institutes of Health on 400,000 people showed that those who ate high fiber diets were 22% less likely to die over a nine-year period. The average American consumes 15 grams of fiber daily. Recommendations are 25g/day for women and 38g/day for men. Fiber is beneficial for heart health, respiratory and infectious disease, and cancer. Fiber’s benefits come from vitamins, micro-nutrients, and antioxidants which assist the body in detoxification and are present in whole grains, especially rice bran.

Consider Brown or Black Rice:

Most of us have heard of brown rice but black? Black rice also called forbidden rice, is nutty and chewy and filled with anthocyanins (same antioxidant found in blueberries.) This antioxidant rich food comes with all of its bran layers intact, and the black rice bran has more antioxidants per spoonful compared to blueberries along with less sugar, more fiber and more vitamin E. So go on cook up a pot tonight!

Note from Dr. P:

Reducing toxicity and body cleansing from the inside out are essential for longevity. Fiber is an essential component of this especially rice bran found in brown or black rice. Chlorophyll found in dark leafy greens is also essential in cleansing the body while providing fiber. Drop the coffee and have 2 cups of green tea instead and we have a winning combination.

Move your body! As we age we lose muscle due to inactivity and loss of hormones, this results in loss of mobility, strength and balance. In the words of Jack LaLanne “Let exercise be your king and nutrition be your queen and then you have a kingdom” Stay Healthy, Keep Moving!

-Be Happy, Healthy, & Holistic

This post has not been tagged.

Share |
PermalinkComments (0)

Hydration Nation

Posted By Administration, Tuesday, June 21, 2011
Updated: Friday, April 18, 2014


by John Gannage, MD, MCFP, DH

This article, as the warm weather arrives, is intended to provide guidance to those committed to physical activity as part of a healthy lifestyle. In the shorter term, the information will assist the prevention of electrolyte disturbances from exercise and improper fluid replacement which are common, and which can be dangerous. Long term, owing to the relationship between chronic mineral depletion and chronic disease, the article is also pertinent.

As a personal anecdote, I continue to play hockey at least twice a week in the winter months, and have found that, as I have optimized my detoxification metabolism and overall fitness, I actually sweat to a much greater degree. In recent years, this had led to a different kind of challenge for me - post-exertion fatigue and severe headaches. In fact, I was often wiped out into the next day after a particularly vigorous session, and for a while floundered trying to find the correct formula to prevent such debilitating episodes.

The answer lies in proper hydration - before, during and after exercise - with the understanding that when it comes to hydration and exercise, the rules are different compared to a non-athletic general population. My mistakes were too much plain water intake, risking low blood sodium concentration (hyponatremia), and inadequate pre-loading (i.e. entering exercise well hydrated) with fluid AND electrolytes, particularly sodium. Also, the widely available sport drinks didn't work well with me - I have since read (at that MSG is used as a flavour enhancer (not good for headache sufferers or anyone else) in some sports drinks, but have yet to confirm this.

I have had better success with a sport drink product named “e-load”, developed by a Toronto Sports Medicine specialist, Dr. Doug Stoddard. I like the formula for its sodium content and its “anti-bonking” effects. Not to be understated, it has had a huge impact on my life and allowed me to perform better, more vigorously and with longer endurance, while negating all of the previous post-exertion adverse effects. Simply, it kept me in the game.

Let it be known that dehydration is the most common performance-sapping mistake that athletes make, but it's also the most preventable. Here are some guidelines to help athletes stay well hydrated. Remember that everyone sweats differently (in sweat volume and sodium content - in fact I am likely a “high-salt sweater”) and therefore needs vary as to fluid and salt requirements before and during exercise. A general recommendation is 1 gram of sodium per hour of intense exercise.


Hydrate before exercise begins.

Drink 2-3 cups (475-700 ml) of fluid 2-3 hours before exercise to allow excess fluid to be lost as urine. This may mean drinking the evening before for early AM exercisers. About one-half hour before exercise, drink 5-10 oz (150-300 ml). Use a sports drink with adequate sodium content, as indicated below.

Drink during exercise.

Most athletes find it helpful to drink every 10 to 20 minutes during a workout. Heavy sweaters can benefit from drinking more often (e.g., every 10 minutes) and light sweaters should drink less often (every 20+ minutes).

Ingest sodium before and during exercise.

Sodium lost in sweat must be replaced during exercise. That's one reason why a good sports drink is better than plain water. Before a long endurance activity, increasing dietary salt 10 -25 grams for the few days prior is helpful.

Use weight as your guide.

The best way to determine if you'd had enough to drink during a workout is to check to see how much weight you've lost. Minimal weight loss means that you've done a good job staying hydrated. Remember that weight loss during an exercise session is water loss, not fat loss, and must be replaced.


Don't rely solely on water.

For the athlete, drinking large amounts of water is not only unnecessary, but can be downright dangerous. Drinking water alone keeps you from replacing the electrolytes lost in sweat (and from ingesting performance-boosting carbohydrates that help you train longer and stronger). Bloated stomach, swollen fingers and ankles, a bad headache, and confusion are warning signs of hyponatremia, a harmful electrolyte disturbance that can occur due to excessive water intake.

Don't gain weight during exercise.

A sure sign of too much fluid intake is weight gain during exercise. If you weigh more after your activity than you did before, that means that you drank more than you needed. Be sure to cut back for the next time.

Don't restrict salt in your diet.

Ample salt (sodium chloride) in the diet is essential to replace the salt lost in sweat. Because athletes sweat a lot, their need for salt is much greater than for non-athletes. During non-activity (or for the sedentary), I recommend a teaspoon of sea salt for every 2 litres of purified water - consumed daily.

Don't use aspirin, ibuprofen and other non-steroid anti-inflammatories
These medications increase the risk of hyponatremia in athletes, and should be avoided.


Drink adequate amounts of fluid designed for exercise, and enter your activity well hydrated while finding a drinking routine that suits your individual needs. (On the day of a hockey game, I'll drink 3.5 litres of sport drink - totalling the before, during and after fluid consumption.)

Disclaimer: The information contained in this article is for educational purposes only. One should always seek the personalized advice from a qualified practitioner before making the dietary and behaviour changes listed, as the needs and medical status of individuals are highly variable.

This post has not been tagged.

Share |
PermalinkComments (0)

Lowering Cholesterol Without Statin Medications

Posted By Administration, Monday, June 20, 2011
Updated: Friday, April 18, 2014

by Allan Magaziner, DO

Just last week, the FDA issued yet another warning regarding the use of  a statin medication, this time Simvastatin, which is frequently prescribed to lower cholesterol levels.  They noted that there is a significant risk of muscle damage (myopathy) in those patients taking high dose Simvastatin (brand name: Zocor).  In addition, the FDA warned against taking this drug along with some commonly utilized anti-fungal, antibiotic and cardiac medications.

I have always been critical of the use of high dose and, often, low dose, statin use especially in light of the numerous alternative treatments that are extremely effective.  In fact, in my previously published book, The All-Natural Cardio Cure, I highlighted many of the problems with statin drugs such as Zocor (Simvastatin), Lipitor (Atorvastatin), and Crestor (Rosuvastatin) and presented many effective options.  

Do all people with high cholesterol levels require cholesterol-lowering medications?  Of course not.  Drew, a 48 year old male, consulted with me when  struggling with seasonal allergies and a long history of sinus problems.  After a thorough evaluation, his cholesterol level was found to be high at 255 (with a normal range of 120-199) and the “bad” LDL cholesterol was also elevated at 184 (normal <99).   

Rather than starting him on a statin to lower his cholesterol, he was placed on an anti-inflammatory diet and I recommended the use of natural supplements including red yeast rice, plant sterols and omega-3 fatty acids.  

Within three short months, Drew’s lipid profile was greatly improved.  His latest total cholesterol had declined to a normal level of 177, while the LDL also fell to 101. Best of all, perhaps, Drew’s energy was better than ever, he felt his immune system was far stronger, he had not been sick at all and his allergy symptoms were completely gone...and all of this without any statin medications or any other prescription medicines!   

Drew is one of hundreds of patients who have been successfully treated at the Magaziner Center for Wellness for high cholesterol without the use of statins or other medications. 

In my opinion, statins should not be taken as first line therapy and should be used only as a last resort.  We have plenty of effective options…let’s use them. 

For more information about lowering your cholesterol level or other cardiac risk factors, contact the Magaziner Center for Wellness at 856-424-8222.

This post has not been tagged.

Share |
PermalinkComments (0)

Sickness Syndrome Depression - The Link Between Seasonal Allergies, Inflammation, and Depression

Posted By Administration, Wednesday, June 8, 2011
Updated: Friday, April 18, 2014


by Gina Nick, NMD, PhD

A recent article in the New York Times discusses several large studies that link seasonal allergies to  depression and anxiety. The cause is an increase in inflammatory cytokines that lower serotonin levels.  This is a classic example of Sickness Syndrome Depression, a condition identified years ago and finally gaining media attention.  We often see cases of wrongly diagnosed anxiety and depression at our practice where patients are prescribed antidepressant medications instead of being treated for Sickness Syndrome Depression. To learn more about the syndrome click here. One treatment that is not yet mentioned on the site but that we have recently been using successfully in practice to treat Sickness Syndrome Depression and other psychiatric illnesses with an inflammatory component is BRM4 by Daiwa Health Development- an immunomodulator that alters levels of inflammatory cytokines throughout the body. The effective dosage is 4 capsules three times per day for 4 weeks, and then 4 capsules per day thereafter.

In health and healing,

-Dr. G

This post has not been tagged.

Share |
PermalinkComments (0)

Ease Anxiety Naturally

Posted By Administration, Monday, June 6, 2011
Updated: Friday, April 18, 2014


by Andrea Purcell, ND

In this fast paced life anxiety is presenting itself in many different forms. Patients will describe nervousness, irritability, edginess, heart palpitations, difficulty breathing, hurriedness, and inability to turn off the mental motor. These are just a few descriptions that I hear daily in private practice. Stress is present, people become overwhelmed by it and then get stuck in an anxiety cycle that leads to sleeplessness and becomes very difficult to get out of.

Here are a few tools that can be used on a daily basis to help re-boot our nervous system and break the fight or flight cycle.

The top three-lifestyle ways to soothe anxiety are physical exercise, breathing exercises, and meditation.

Physical exercise has physical in the name so we forget how much it helps our mental health. Daily exercise can lift our moods, influence our food choices, which influence our moods, and act as a mental stress reliever. It helps us get out of our heads, and allows us to take a mental health break.

Deep breathing increases the amount of oxygen in the blood which acts to boost our immune system and give us more energy. It also calms down the sympathetic nervous system and in turn decreases our adrenalin output. So we feel like there is less of an emergency all the time. Breathing abdominally is better than chest breathing. I recommend the “breathing in a box technique”. Inhale slowly for 4 counts, hold your breath for 4 counts, exhale for four counts, and hold for four counts. And repeat. The slower you do it, the more you can focus on the air entering, moving through, and exiting your body. Posture is important! Sit up straight with your shoulders down and pulled back, align your neck over your spine and breathe. Poor posture promotes shallow breathing and more anxiety.

Meditation is a daily practice just like exercising and breathing. Many patients say that they have difficulty completely emptying their mind and find this practice hard to do. My recommendation is to get yourself a tape that will take you through a very short say 1 minute meditation to begin and then expands as you practice your meditation muscle. The Chopra Center has free online meditations; they gradually introduce a new-comer to meditation.
You do have to subscribe to their free online library.

Supplements to use when you are overwhelmed:
Rescue remedy by Bach flower
Calms forte –homeopathic remedy for an over stimulated nervous system.
Double bag of chamomile tea
L-theanine – found in green tea it has calming properties. 200mg capsule, 1-2 capsules usually help take the edge off.

Note from Dr. P
Stress is here to stay, so we all need to get a game plan that works for us to manage stress on a regular basis. I recommend calendaring everything, yes, even exercise. Items on your calendar will not get pushed to the side they will get done with everything else. Every woman I know has a daily list of items to accomplish that is greater than what is humanly possible. Have the immediate list and then the list that can be done over more time. I call it my doing “now” list and my “not” doing now list.
Another stress reduction tip is to be present! The gift is in the present! The present is all we have, so enjoy it, soak it up like a good piece of Italian bread in garlic and oil, ummm, that will help diffuse the anticipation of what is next on the to do list.
Finally, if you find that you just can’t keep it together, and that your day is running you instead of you running your day, there could be other factors that need to be evaluated by a trained professional. You may have a hormonal imbalance and need good council by an integrative doctor. So get the help, get balanced, and get on with your life!

-Be Happy, Healthy & Holistic

This post has not been tagged.

Share |
PermalinkComments (0)

Case Study - Neuroendocrine and Immune Contributors to Fatigue

Posted By Administration, Friday, June 3, 2011
Updated: Friday, April 18, 2014

Marni N. Silverman, PhD, Christine M. Heim, PhD, Urs M. Nater, PhD, Andrea H. Marques, MD, PhD, and Esther M. Sternberg, MD
Central fatigue, a persistent and subjective sense of tiredness, generally correlates poorly with traditional markers of disease. It is frequently associated with psychosocial factors, such as depression, sleep disorder, anxiety, and coping style, which suggest that dysregulation of the body's stress systems may serve as an underlying mechanism in the maintenance of chronic fatigue (CF). This article addresses the endocrine, neural, and immune factors that contribute to fatigue and describes research regarding the role of these factors in chronic fatigue syndrome as a model for addressing the biology of CF. In general, hypoactivity of the hypothalamic-pituitary-adrenal axis, autonomic nervous system alterations characterized by sympathetic overactivity and low vagal tone, as well as immune abnormalities, may contribute to the expression of CF. Noninvasive methods for evaluating endocrine, neural, and immune function are also discussed. Simultaneous evaluation of neuroendocrine and immune systems with noninvasive techniques will help elucidate the underlying interactions of these systems, their role in disease susceptibility, and progression of stress-related disorders.
Fatigue comes in various forms. Acute fatigue is a normal, protective mechanism in healthy individuals, is usually linked to a single cause, and is often relieved by rest or life-style change (ie, diet, exercise, rest, stress management). Rarely is it associated with long-term cognitive dysfunction, a state that most often returns to baseline after rest and recovery. However, chronic fatigue (CF) is considered maladaptive or pathologic, lasts 6 months or more, adversely affects physical and mental function, and may have multiple and unknown causes. Generally, no relief is gained from usual restorative measures aimed at relieving fatigue [1]. CF is especially apparent in individuals with chronic disease, such as autoimmune diseases (rheumatoid arthritis [RA], multiple sclerosis, systemic lupus erythematosus [SLE]), psychiatric disorders (major depressive disorder [MDD]); neurologic disorders, eg, stroke; cancer (during and after treatment); and idiopathic chronic multisymptom illnesses, eg, chronic fatigue syndrome [CFS] and fibromyalgia (reviewed in [2]). Peripheral fatigue is observed in chronic diseases associated with muscle wasting and inflammation or joint abnormalities, as often occurs in RA and SLE, myasthenia gravis, and cardiorespiratory diseases. Peripheral fatigue can be attributed to organ-system dysfunction and usually is not associated with cognitive loss.
Central fatigue generally correlates poorly with traditional markers of disease [2] and is frequently associated with other psychosocial factors, such as depression, sleep disorder, anxiety, and coping styles [3,4], which suggests that dysregulation of the body's stress systems may serve as an underlying mechanism of CF. Indeed, there appears to be an intricate interplay between the neural, endocrine, and immune systems in regulating the body's response to stress and the maintenance of homeostasis.

That the nervous and immune systems communicate with each other in a bidirectional manner is well established (reviewed in [5-12]). There are 2 main pathways by which psychogenic stress is relayed from the brain to the body: (1) via the hypothalamic-pituitary-adrenal (HPA) axis with the resultant release of glucocorticoids (cortisol in humans and primates; corticosterone in rodents) and (2) via the sympathetic nervous system (SNS), with the resultant release of catecholamines (noradrenaline and adrenaline). These neuroendocrine stress systems coordinate the response of many other physiologic systems to a stressor, including the immune and cardiovascular systems, as well as energy production and/or utilization and behavior, therefore, bringing the physiologic systems back to homeostasis [13].
However, maintenance of homeostasis during an immune challenge involves activation of the immune system, resolution of the challenge, and protection of the host against potentially detrimental inflammatory processes. Relevant to the latter, interleukins (IL) and/or cytokines (tumor necrosis factor [TNF]-α, IL-1, and IL-6 in particular) activate the same stress pathways to coordinate an appropriate immune response [5,6,12]. Cytokine receptors have been detected at all levels of the HPA axis, and, therefore, each level can serve as an integration point for immune and neuroendocrine signals [5]. In turn, glucocorticoids negatively feedback onto immune cells to suppress the further synthesis and release of innate proinflammatory molecules. Glucocorticoids also shape immunity by influencing immune cell trafficking to sites of inflammation and alter downstream adaptive immune responses by causing a shift from cellular (Th1 inflammatory) to humoral (Th2 anti-inflammatory) type immune responses [14,15]. Therefore, in contrast to the traditional view of glucocorticoids as immunosuppressant hormones, a more accurate view is that they are immunomodulatory hormones that stimulate as well as suppress immune function, depending on glucocorticoid concentration, type of immune response, immune compartment, and cell type. Glucocorticoids also play an important role in the regulation of the SNS. In addition to subserving permissive effects on relevant synthetic enzymes and receptors for catecholamines, endogenous glucocorticoids restrain SNS responses under resting conditions and after stress [16].
In addition to HPA axis-immune interactions, there is strong evidence for interactions between the immune system and the autonomic nervous system (ANS) (SNS and parasympathetic nervous system [PNS] pathways) and peripheral nerves. Whereas, circulating hormones, such as glucocorticoids, regulate immunity at a systemic level, neural pathways regulate immunity at a local and regional level. The SNS and peripheral nervous system innervate immune organs, where sympathetic influences can be both pro- and anti-inflammatory, depending on the type of adrenergic receptor to which the catecholamine binds [8,9]. Neuropeptides released from peripheral nerves, such as substance P, tend to be proinflammatory [7]. Locally released norepinephrine or circulating epinephrine also affect lymphocyte trafficking, proliferation, function, and cytokine production. With regard to the peripheral nervous system, both afferent and efferent parasympathetic activities have been shown to be immunomodulatory. Whereas, afferent vagal fibers express IL-1 receptors on paraganglia cells situated in parasympathetic ganglia [12], efferent vagal fibers have been shown to exert anti-inflammatory action via the release of acetylcholine [10, 11]. Therefore, the vagus nerve also serves as a source of negative feedback on the immune system, with the brain being an integral relay station.
Dysregulation of any of these stress systems can lead to dysregulation of multiple physiological and behavioral systems, which leads to a maladaptive response to stress [13-17]. Indeed, dysregulation of neural-immune interactions is described in many stress-related disorders, including inflammatory, autoimmune, metabolic, and cardiovascular disease, as well as psychiatric and somatic disorders.
The capacity of proinflammatory cytokines to cause changes in behavior, including symptoms of fatigue, psychomotor retardation, anorexia, anhedonia, hyperalgesia, somnolence, lethargy, muscle aches, cognitive dysfunction, and depressed mood, has led to the suggestion that proinflammatory cytokines may contribute to the behavioral features of depression [18,19] as well as somatic disorders, such as CFS and fibromyalgia [20].
The first indication that inflammation may induce psychosomatic symptoms came from research about depression. There is a strong similarity between neurovegetative symptoms (anorexia, sleep disturbance, psychomotor retardation, fatigue, and pain) of depression and inflammation-induced sickness behavior [21]. Indeed, cytokine-based immunotherapy (interferon [IFN]-α) induces 2 distinct behavioral syndromes: a neurovegetative syndrome, which appears early, persists, and is minimally responsive to classical antidepressants; and a mood-cognitive syndrome, characterized by depressed mood, anxiety, and cognitive dysfunction, which appears later and is responsive to classic antidepressants (ie, selective serotonin reuptake inhibitors [SSRIs]) [22]. Moreover, differential clustering of mood-cognitive and neurovegetative syndromes is observed in patients with cancer. Indeed, cancer-related fatigue does not respond well to antidepressants, which suggests that it is not exclusively a mood or behavioral problem. [23]. Of note, cancer-related fatigue has also been associated with elevated inflammatory biomarkers and impaired HPA axis function [24,25].
It appears that these 2 categories of symptoms are mediated by different biological mechanisms. For example, dopaminergic pathways may play a more prominent role relative to other monoamine neurotransmitters (serotonin, norepinephrine) in the neurovegetative subset [3,22]. In support of this notion, Meeusen et al [26] proposed a central fatigue hypothesis and suggested that an increase in the brain ratio of serotonin to dopamine is associated with feelings of tiredness and lethargy, which accelerates the onset of fatigue, whereas, increased dopamine levels favor improved performance through the maintenance of motivation and arousal.
Given the role of corticotropin-releasing hormone (CRH) in behavioral and HPA-axis activation, it has been hypothesized that defective central CRH synthesis and/or release may also contribute to symptoms of fatigue [27]. Indeed, abnormal central CRH pathways have been detected in various chronic disease states with a fatigue component, including SLE, multiple sclerosis, RA, fibromyalgia, and CFS [2,27]. Moreover, both psychogenic and immune stressors can induce similar neuroendocrine and neurotransmitter changes in the brain, therefore, sensitizing the brain to subsequent stressors, and, hence, inducing a state of increased stress vulnerability as seen in various psychiatric and psychosomatic disorders [28].
In the next section, we discuss how hypoactivity of the HPA axis, ANS alterations characterized by sympathetic over-activity and low vagal tone, as well as immune abnormalities, may play a role in CFS.
A diagnosis of CFS requires that an individual displays severe CF for more than 6 months without a defined cause (with all other medical conditions being excluded), as well as the presence of 4 of the following 8 symptoms: myalgia, arthralgia, sore throat, tender nodes, cognitive difficulty, headache, postexertional malaise, or sleep disturbance [29]. (See Clauw later in this supplement.)
HPA Axis
A substantial body of research on the pathophysiology of CFS has focused on dysregulation of the neuroendocrine systems. The HPA axis is the key neuroendocrine system that adapts the organism to various challenges, including emotional, physical, chemical, and immune stressors. These stressors have been associated with risks for developing CF. The secretion of glucocorticoids from the adrenal cortex results in multiple metabolic, behavioral, and immune regulatory responses that help the organism adapt to such challenges. Dysregulation of these regulatory functions may be causally associated with symptoms of CFS. Thus, insufficient glucocorticoid signaling has been associated with increased immune activation and inflammatory responses, potentially promoting symptoms of fatigue, malaise, somnolence, myalgia, and arthralgia (reviewed in [13,17]).
Dysfunction of the HPA axis, characterized by lower than normal cortisol secretion, is one of the hallmark biological features of CFS, although the literature is somewhat inconsistent. Poteliakhoff [30] first described attenuated basal plasma cortisol levels in patients with CFS. After these initial observations, Demitrack et al [31] reported lower than normal cortisol excretion in patients with CFS. Results of several subsequent studies confirmed lower than normal cortisol levels in plasma or saliva [32-39], flattened cortisol diurnal secretion [38-40], and decreased urinary free cortisol secretion in patients with CFS [41-44].
However, results of a substantial number of studies failed to identify hypocortisolism in CFS (eg, reviewed in [45-46]). Similarly, results of an array of endocrine challenge studies revealed signs of hypocortisolism in CFS, including enhanced negative feedback inhibition of the pituitary [47-50] or mild adrenal insufficiency [31,51], although results are inconsistent [45,46]. Results of a recent study found decreased glucocorticoid sensitivity of immune cells in persistently fatigued adolescent females [52], which suggests decreased cortisol signaling, consistent with the idea of a lack of cortisol effects contributing to CFS. However, in vitro studies on glucocorticoid sensitivity are also inconsistent [53]. Of note, glucocorticoid sensitivity was shown to be regulated in a tissue- and cell-specific manner (reviewed in [6]).
There may be important subgroups of patients with CFS, depending on etiologic pathways or clinical features. Heim et al [54], for example, demonstrated, in a population-based sample, that only those patients with CFS who reported childhood traumatic experiences exhibited low cortisol levels compared with well controls, whereas patients with CFS and without a history of severely stressful circumstances had normal cortisol levels. Thus, it is plausible that several of the neuroendocrine features of CFS covary with risk factors other than illness state and reflect a vulnerability to develop CFS in response to challenge [54]. Of note, hypocortisolism, as reported in patients with CFS, has been observed in animal models of early life stress (reviewed in [55]). Thus, CFS could be conceptualized as a disorder of adaptation that is promoted by developmental risk factors.
Some researchers have suggested that hypocortisolism in CFS might be a consequence of having the disorder, because low cortisol secretion has been associated with illness features, for example, inactivity [56]. In addition, the stress of symptoms themselves, such as fatigue, sleep and mood disturbances, and pain, can contribute to the further dysregulation of biological stress pathways, which lead to a positive feed-forward cascade. Whether or not hypocortisolism is a cause or a consequence of CFS remains to be evaluated in longitudinal studies. Perhaps it is both.
A number of studies examined the involvement of the ANS in the pathophysiology of CFS. The rationale for these studies is based on the observation that several symptoms of CFS, namely fatigue, dizziness, diminished concentration, tremulousness, and nausea, could be explained by autonomic dysfunction. In addition to the neuroendocrine system, the ANS is another key regulation system that adapts the organism to challenge. Thus, autonomic dysregulation could further trigger symptoms of CFS in response to challenges that disturb homeostasis.
Initial studies found an increased prevalence of neurally mediated hypotension and orthostatic intolerance in patients with CFS, measured by using a prolonged standing or a head-up tilt table test [57-64]. However, results of several studies failed to find differences between CFS and control groups regarding dysautonomia [65-68].
Another line of research in the study of ANS alterations in CFS has focused on cardiovascular autonomic measures. Results of most studies found increased heart rate measures in CFS, both at rest and in response to challenge [65,69-74]. Increased heart rate and/or reduced heart rate variability (HRV) is in accordance with other studies that reported low vagal tone [69,75-77] or general sympathetic overactivity [62,78-80], although inconsistent results exist (reviewed in [46]). Whether or not there are subgroups with CFS and altered autonomic function based on etiologic factors or illness features is unknown. Sympathetic overactivation, in concert with low glucocorticoid signaling, may contribute to an overactive immune system, particularly in response to challenge, which may lead to symptoms of CFS.
Immune System
Many findings suggest that infectious agents (viral and bacterial infections) and immunologic dysfunction (eg, inappropriate production of pro- and anti-inflammatory cytokines) may play a role in the pathophysiology of at least some cases of patients with CFS (reviewed in [81-83]). Indeed, persistent postinfection fatigue has been well documented [84]. Results of early studies showed that many individuals with CFS had evidence of enhanced antibody responses to Epstein-Barr virus (EBV). However, subsequent reports showed that many patients with CFS lacked evidence of EBV reactivity, although they displayed elevated antibody titers to a number of other viral agents. Interestingly, acute viral infection studies found that initial infection severity was the single best predictor of persistent fatigue [85]. Taken together, results of these studies suggest that, although some cases of CFS may be triggered by an infectious agent, the chronic symptoms of this syndrome are unlikely to be caused by an active infection.
Results of other studies indicated signs of immune disturbance in patients with CFS, especially in the form of elevated proinflammatory cytokine levels [86,87], such as IL-6 and TNFα in serum and cerebrospinal fluid [88,89]. Consistent with these findings, increased in vitro inflammatory cytokine release has been reported in stimulated peripheral blood mononuclear cells of patients with CFS [90]. Other indices of cytokine-mediated immune alterations that have been reported in patients with CFS include increased levels of auto-antibodies, decreased natural killer cell activity, high levels of type 2 cytokine–producing cells, activated T lymphocytes, CD19+ B cells, neopterin (a marker of activated cell-mediated immunity), and activated complement [91-94]. In addition, alterations in the expression of genes involved in immunity have been detected [95]. However, despite multiple indications of immune system activation in CFS, the best-replicated immunologic findings in this disorder are suppression of several immune functions, especially natural killer cell activity and mitogen-induced lymphocyte proliferation [94-96]. Nonetheless, these multiple findings need to be interpreted in light of a meta-analysis [81] that found no evidence for clear immune abnormalities in CFS.
Interestingly, results of a recent and robustly designed study by Raison et al [97] showed that fatigue not only in its severe and chronic form, as in CFS, but also in its milder forms, is associated with increased inflammation, as indexed by elevated plasma C-reactive protein levels and white blood cell count, even after adjusting for depressive status. This study further supports the notion that the symptom of fatigue, rather than a diagnosis of CFS itself, may be what is clinically associated with inflammation. In addition, childhood traumatic experiences appear to be an important risk factor for a hypocortisolemic profile in CFS [54], and adults with a history of childhood trauma exhibit elevated markers of inflammation, even in the absence of depression [98]. Moreover, patients with depression and childhood trauma show even higher levels of inflammation than with either risk factor alone [98,99]. Whether immune status is different in patients with CFS, with or without a history of childhood trauma, remains to be determined.
In summary, chronic (pathologic) fatigue can be attributed to hypoactivity of the HPA axis; ANS alterations characterized by sympathetic overactivity and low vagal tone; and immune abnormalities, including reduced cellular responses and enhanced inflammation and humoral responses. CFS is an exemplar, but not the only example, of fatigue conditions, with these associations. Disparate findings among various studies may be because of (1) differences in methodology, recruitment, and analysis; (2) comorbidities, including depression and/or other chronic diseases; (3) lack of an epidemiologically comparable control group; and (4) biological changes not present in all cases of a heterogeneous disorder, such as CFS, but rather related to particular symptoms or risk factors of the disorder. The latter indicates the importance of grouping by symptom subtypes rather than an arbitrarily defined disorder. Indeed, different symptom categories of CFS may be mediated by different biological mechanisms, as seen in cytokine-induced depressive symptomatology [22]. To help elucidate a “molecular signature” for clinical sub-types within a heterogeneous disorder, noninvasive methods for evaluating neural, endocrine, and immune function are available without causing further pain or distress, which could confound outcome measures of interest.
Measurement of hormones, cytokines, and neuroactive substances has frequently posed a problem for clinicians and investigators because of the need to perform invasive tests, such as drawing blood. Noninvasive and ambulatory methodologies of neural, endocrine, and immune biomarker collection can overcome several limitations intrinsic to invasive methods, reducing the stress triggered by collection of samples and allowing a wider application to community-based settings. Collection of sweat and saliva and measurement of HRV are noninvasive methods that can be applied to evaluate neuroimmune interactions. Ultimately, simultaneous evaluation of neural and immune systems with noninvasive techniques will help elucidate the underlying interactions of these systems and their role in disease susceptibility and progression of stress-related disorders.
HPA Axis: Salivary Cortisol
Because (1) the HPA axis is a self-regulated dynamic feedback system and (2) cortisol is secreted in a pulsatile fashion, single time-point measures of cortisol cannot be used to accurately interpret HPA axis function. An adequate assessment of HPA axis function requires multiple serial sampling (to test basal activity and circadian profiles) or dynamic testing by using pharmacologic or psychologic challenges (to test reactivity and/or feedback sensitivity). More recently, the salivary cortisol response to awakening has received considerable scientific attention and has been shown to be sensitive to detect HPA axis dysregulation related to stress and disease, including CFS [39,100]. When collected in the context of such sampling protocols, cortisol can be reliably measured in saliva as an index of HPA axis function [101].
The majority of circulating cortisol is bound to corticosteroid-binding globulin, which inactivates the biological actions of cortisol. Only the free fraction of cortisol is biologically active and can bind to glucocorticoid receptors to influence gene expression and protein synthesis. In saliva, only the free fraction of cortisol can be measured. Free cortisol measures in saliva reliably reflect the amount of free cortisol circulating in the blood stream [101]. In studies that focus on the actions of cortisol in target systems, it is advantageous to measure the free and biologically active fraction of cortisol. However, for studies that focus on assessment of total cortisol output of the adrenal gland or ratios of bound versus unbound cortisol and corticosteroid-binding globulin activity, blood measures are necessary. These differences must be considered when interpreting data from salivary cortisol studies.
ANS: Salivary α-Amylase and Heart Rate Variability
Because the transfer of norepinephrine from blood to saliva takes approximately 1 hour [102], which is too long for accurate assessment of stress-induced changes, salivary α-amylase (sAA), a digestive enzyme, has become an emerging biomarker for stress as an indicator of SNS activity. Both the sympathetic and parasympathetic branches of the ANS innervate the salivary glands, where SNS stimulation increases protein secretion and PNS stimulation increases salivary flow rate [103]. sAA has repeatedly been found to increase in response to physical stress or exercise, as well as psychological stress, and also correlates with plasma norepinephrine responses to those same stressors, although to a lesser extent to psychosocial stress (reviewed in [104]). sAA concentration can also serve as an index for pathologic dys-regulation of the ANS in specific clinical and subclinical conditions, such as anxiety and somatic disorders [104]. One important caveat of measuring sAA is that, in the presence of stress and SNS activation, the PNS is inhibited, which leads to reduced salivary flow rate, and hence, decreased saliva production. Therefore, stress-induced increases in sAA could be confounded with parallel decreases in salivary volume, thereby increasing sAA concentration.
Evaluation of the ANS can also be performed noninvasively through measurement of HRV. The heart is under tonic control by parasympathetic influences. Heart rate is characterized by beat-to-beat variability, which also implicates vagal dominance, because the sympathetic influence on the heart is too slow to produce rapid beat-to-beat variability. HRV is a term that describes variations of both instantaneous heart rate and the interval between consecutives beats. A prominent circadian variation in HRV, with significant increases during the night and decreases during the day, is observed in healthy individuals. Results of previous studies showed that this increase in nighttime HRV is blunted by acute stress and that decreased HRV is associated with increased overnight urinary cortisol and increased proinflammatory cytokines and acute-phase proteins [105]. Decreased HRV, indicative of reduced parasympathetic-vagal tone, is an independent risk factor for morbidity and mortality.
Neural and Immune Biomarker Profiles: Cutaneous Sweat Patch
Another noninvasive and nonstressful approach to evaluating neural and immune systems is through collection of sweat via a 24-hour cutaneous sweat patch. In our initial validation studies, we showed that immune biomarkers, such as proinflammatory cytokines, in sweat were tightly correlated with plasma levels in healthy women [106]. In addition, we have shown that a population of women with MDD in remission exhibited elevated sweat levels of proinflammatory cytokines, sympathetic neuropeptides (neuropeptide-Y), and pain-related neuropeptides (substance P, calcitonin gene–related peptide) but decreased parasympathetic (vasoactive intestinal peptide) neuropeptide levels relative to controls, which strongly correlated with plasma levels [107]. This pattern is consistent with a shift in MDD from parasympathetic to sympathetic tone and an underlying proinflammatory state that could account for enhanced susceptibility to conditions known to be comorbidly expressed with MDD, including cardiovascular disease, osteoporosis and diabetes. Moreover, biomarker levels strongly correlated with symptoms of depression and anxiety, which indicate functional significance of these biomarker profiles. A similar biomarker profile was reported in pain- and fatigue-related syndromes [2].
Ultimately, these noninvasive methodologies could provide a “molecular signature” for clinical subtypes within a heterogeneous disorder to be used for (1) diagnostic and prognostic purposes; (2) earlier intervention in asymptomatic conditions; (3) optimization of individualized treatment regimens; (4) patient monitoring in remote areas and in large-scale epidemiologic settings; (5) monitoring patients in whom invasive methodologies are unfeasible, especially vulnerable populations, including pregnant women, infants, children, and the elderly; and (6) to shed light on mechanisms that underlie individual vulnerability or resiliency to develop stress-related diseases and/or disorders.
In summary, CF states have been shown to be attributable to a dysregulation of stress systems, including hypoactivity of the HPA axis, ANS alterations characterized by sympathetic overactivity and low vagal tone, and immune abnormalities, such as reduced cellular responses and enhanced inflammation and humoral responses. Hypocortisolemia may develop through reduced synthesis or depletion of HPA-axis hormones, receptor downregulation, and/or increased negative feedback sensitivity [108]. Fries et al [108] proposed that the phenomenon of hypocortisolism may occur after a prolonged period of hyperactivity of the HPA axis because of chronic or traumatic stress, in which this “switch“ may prevent possible deleterious effects of excessive glucocorticoid exposure. CFS and related pain and fatigue disorders may then be interpreted as a maladaptive overadjustment, in which the HPA axis is then functioning at an alternate, more stress-sensitive steady state [109]. Interestingly, the consequences of insufficient glucocorticoid signaling, including hyperactive SNS activation and enhanced inflammation, result in similar deleterious effects to that of hyperactive glucocorticoid signaling, such as altered metabolic, cardiovascular, immune, neurologic, and behavioral functions [17], including the potentiation of fatigue and related symptoms. Given the complex nature of fatigue, with its many physiologic and behavioral risk factors and correlates, the most effective therapeutic strategy may require multimodal action. The simultaneous evaluation of a large array of neural, endocrine, and immune biomarkers, when using noninvasive methodologies, may help inform the design of more effective pharmacologic therapeutic interventions to be used along with nonpharmacologic interventions, such as cognitive-behavioral therapy. It may also inform clinicians of mechanisms by which these interventions act and how successful they are in altering the neuroendocrinologic and immunoregulatory aspects of fatigue.
Contributor Information
Marni N. Silverman, Section on Neuroendocrine Immunology and Behavior, National Institute of Mental Health, National Institutes of Health, Rockville, MD.
Christine M. Heim, Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA.
Urs M. Nater, Department of Clinical Psychology and Psychotherapy, University of Zurich, Switzerland, Centers for Disease Control and Prevention, Atlanta, GA.
Andrea H. Marques, Genetic Epidemiology Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, MD.
Esther M. Sternberg, Section on Neuroendocrine Immunology and Behavior, National Institute of Mental Health, National Institutes of Health, Integrative Neural Immune Program, 5625 Fishers Lane (MSC-9401), Rockville, MD 20852.
1. Guymer EK, Clauw DJ. Treatment of fatigue in fibromyalgia. Rheum Dis Clin N Am. 2002;28:367–378.
2. Swain MG. Fatigue in chronic disease. Clin Sci (Lond) 2000;99:1–8. [PubMed]
3. Demmyttenaere K, De Fruyt J, Stahl SM. The many faces of fatigue in major depressive disorder. Int J Neuropsychopharmacol. 2005;8:93–105. [PubMed]
4. Bower JE. Behavioral symptoms in patients with breast cancer and survivors. J Clin Oncol. 2008;26:768–777. [PMC free article] [PubMed]
5. Silverman MN, Pearce BD, Biron CA, Miller AH. Immune modulation of the hypothalamic-pituitary-adrenal (HPA) axis during viral infection. Viral Immunol. 2005;18:41–78. [PMC free article] [PubMed]
6. Silverman MN, Sternberg EM. Neuroendocrine-immune interactions in rheumatoid arthritis: mechanisms of glucocorticoid resistance. Neuroimmunomodulation. 2008;15:19–28. [PMC free article] [PubMed]
7. Sternberg EM. Neural regulation of innate immunity: a coordinated nonspecific host response to pathogens. Nat Rev Immunol. 2006;6:318–328. [PMC free article] [PubMed]
8. Elenkov IJ, Wilder RL, Chrousos GP, Vizi ES. The sympathetic nerve–an integrative interface between two supersystems: the brain and the immune system. Pharmacol Rev. 2000;52:595–638. [PubMed]
9. Nance DM, Sanders VM. Autonomic innervation and regulation of the immune system. Brain Behav Immun. 2007;21:736–745. [PMC free article] [PubMed]
10. Tracey KJ. Physiology and immunology of the cholinergic anti-inflammatory pathway. J Clin Invest. 2007;117:289–296. [PMC free article] [PubMed]
11. Thayer JF. Vagal tone and the inflammatory reflex. Cleve Clin J Med. 2009;76:S23–26. [PubMed]
12. Goehler LE, Gaykema RPA, Hansen MK, Anderson K, Maier SF, Watkins LR. Vagal immune-to-brain communication: a visceral chemosensory pathway. Auton Neurosci. 2000;85:49–59. [PubMed]
13. Chrousos GP. Stress and disorders of the stress system. Nat Rev Endocrinol. 2009;5:374–381. [PubMed]
14. McEwen BS, Biron CA, Brunson KW, et al. The role of adrenocorticoids as modulators of immune function in health and disease: neural, endocrine and immune interactions. Brain Res Brain Res Rev. 1997;23:79–133. [PubMed]
15. Dhabhar FS. Enhancing versus suppressive effects of stress on immune function: implications for immunoprotection and immunopathology. Neuroimmunomodulation. 2009;16:300–317. [PMC free article] [PubMed]
16. Kvetnansky R, Pacak K, Fukuhara K, et al. Sympathoadrenal system in stress: interaction with the hypothalamic-pituitary-adrenocortical system. Ann NY Acad Sci. 1995;771:131–158. [PubMed]
17. Raison CL, Miller AH. When not enough is too much: the role of insufficient glucocorticoid signaling in the pathophysiology of stress-related disorders. Am J Psychiatry. 2003;160:1554–1565. [PubMed]
18. Raison CL, Capuron L, Miller AH. Cytokines sing the blues: inflammation and the pathogenesis of depression. Trends Immunol. 2006;27:24–31. [PubMed]
19. Dantzer R, O'Connor JC, Freund GG, Johnson RW, Kelley KW. From inflammation to sickness and depression: when the immune system subjugates the brain. Nat Rev Neurosci. 2008;9:46–57. [PMC free article] [PubMed]
20. Maes M. Inflammatory and oxidative and nitrostative stress pathways underpinning chronic fatigue, somatization and psychosomatic symptoms. Curr Opin Psychiatry. 2008;22:75–83. [PubMed]
21. Maes M, Yirmaya R, Noraberg J, et al. The inflammatory and neuro-degenerative (I&ND) hypothesis of depression: leads for future research and new drug developments in depression. Metab Brain Dis. 2009;24:27–53. [PubMed]
22. Capuron L, Miller AH. Cytokines and psychopathology: lessons from interferon-α. Biol Psychiatry. 2004;56:819–824. [PubMed]
23. Cleeland CS, Bennett GJ, Dantzer R, et al. Are the symptoms of cancer and cancer treatment due to a shared biologic mechanism? A cytokine-immunologic model of cancer symptoms. Caner. 2003;97:2919–2925.
24. Bower JE. Cancer-related fatigue: links with inflammation in cancer patients and survivors. Brain Behav Immun. 2007;21:863–871. [PubMed]
25. Miller AH, Ancoli-Israel S, Bower JE, Capuron L, Irwin MR. Neuroendocrine-immune mechanisms of behavioral comorbidities in patients with cancer. J Clin Oncol. 2008;26:971–982. [PMC free article] [PubMed]
26. Meeusen R, Watson P, Hasegawa H, Roelands B, Piacentini MF. Central fatigue: the serotonin hypothesis and beyond. Sports Med. 2006;36:881–909. [PubMed]
27. Clauw DJ, Chrousos GP. Chronic pain and fatigue syndromes: overlapping clinical and neuroendocrine features and potential pathogenic mechanisms. Neuroimmunomodulation. 1997;4:134–153. [PubMed]
28. Hayley S, Merali Z, Anisman H. Stress and cytokine-elicited neuroendocrine and neurotransmitter sensitization: implications for depressive illness. Stress. 2003;6:19–32. [PubMed]
29. Fukada K, Straus SE, Hickie I, et al. The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group. Ann Intern Med. 1994;121:953–959. [PubMed]
30. Poteliakhoff A. Adrenocortical activity and some clinical findings in acute and chronic fatigue. J Psychosom Res. 1981;25:91–95. [PubMed]
31. Demitrack MA, Dale JK, Straus SE, et al. Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome. J Clin Endocrinol Metab. 1991;73:1224–1234. [PubMed]
32. Hamilos DL, Nutter D, Gershtenson J, et al. Core body temperature is normal in chronic fatigue syndrome. Biol Psychiatry. 1998;43:293–302. [PubMed]
33. MacHale SM, Cavanagh JT, Bennie J, Carroll S, Goodwin GM, Lawrie SM. Diurnal variation of adrenocortical activity in chronic fatigue syndrome. Neuropsychobiology. 1998;38:213–217. [PubMed]
34. Strickland P, Morriss R, Wearden A, Deakin B. A comparison of salivary cortisol in chronic fatigue syndrome, community depression and healthy controls. J Affect Disord. 1998;47:191–194. [PubMed]
35. Cevik R, Gur A, Acar S, Nas K, Sarac AJ. Hypothalamic-pituitary-gonadal axis hormones and cortisol in both menstrual phases of women with chronic fatigue syndrome and effect of depressive mood on these hormones. BMC Musculoskelet Disord. 2004;5:47. [PMC free article] [PubMed]
36. Gur A, Cevik R, Nas K, Colpan L, Sarac S. Cortisol and hypothalamic-pituitary-gonadal axis hormones in follicular-phase women with fibromyalgia and chronic fatigue syndrome and effect of depressive symptoms on these hormones. Arthritis Res Ther. 2004;6:R232–238. [PMC free article] [PubMed]
37. Roberts AD, Wessely S, Chalder T, Papadopoulos A, Cleare AJ. Salivary cortisol response to awakening in chronic fatigue syndrome. Br J Psychiatry. 2004;184:136–141. [PubMed]
38. Jerjes WK, Cleare AJ, Wessely S, Wood PJ, Taylor NF. Diurnal patterns of salivary cortisol and cortisone output in chronic fatigue syndrome. J Affect Disord. 2005;87:299–304. [PubMed]
39. Nater UM, Maloney E, Boneva RS, et al. Attenuated morning salivary cortisol concentrations in a population-based study of persons with chronic fatigue syndrome and well controls. J Clin Endocrinol Metab. 2008;93:703–709. [PubMed]
40. Nater UM, Youngblood LS, Jones JF, et al. Alterations in diurnal salivary cortisol rhythm in a population-based sample of cases with chronic fatigue syndrome. Psychosom Med. 2008;70:298–305. [PubMed]
41. Cleare AJ, Blair D, Chambers S, Wessely S. Urinary free cortisol in chronic fatigue syndrome. Am J Psychiatry. 2001;158:641–643. [PubMed]
42. Cleare AJ, Miell J, Heap E, et al. Hypothalamo-pituitary-adrenal axis dysfunction in chronic fatigue syndrome, and the effects of low-dose hydrocortisone therapy. J Clin Endocrinol Metab. 2001;86:3545–3554. [PubMed]
43. Jerjes WK, Peters TJ, Taylor NF, Wood PJ, Wessely S, Cleare AJ. Diurnal excretion of urinary cortisol, cortisone, and cortisol metabolites in chronic fatigue syndrome. J Psychosom Res. 2006;60:145–153. [PubMed]
44. Scott LV, Dinan TG. Urinary free cortisol excretion in chronic fatigue syndrome, major depression and in healthy volunteers. J Affect Disord. 1998;47:49–54. [PubMed]
45. Cleare AJ. The neuroendocrinology of chronic fatigue syndrome. Endocr Rev. 2003;24:236–252. [PubMed]
46. Nater UM, Heim C, Raison CL. Chronic fatigue syndrome. In: Aminoff MJ, Boller F, Swaab D, editors. Handbook of Clinical Neurology. Elsevier; Amsterdam: (3rd series.). In press.
47. Gaab J, Huster D, Peisen R, et al. Low-dose dexamethasone suppression test in chronic fatigue syndrome and health. Psychosom Med. 2002;64:311–318. [PubMed]
48. Segal TY, Hindmarsh PC, Viner RM. Disturbed adrenal function in adolescents with chronic fatigue syndrome. J Pediatr Endocrinol Metab. 2005;18:295–301. [PubMed]
49. Jerjes WK, Taylor NF, Wood PJ, Cleare AJ. Enhanced feedback sensitivity to prednisolone in chronic fatigue syndrome. Psychoneuroendocrinology. 2007;32:192–198. [PubMed]
50. Van Den Eede F, Moorkens G, Hulstijn W, et al. Combined dexamethasone/corticotropin-releasing factor test in chronic fatigue syndrome. Psychol Med. 2008;38:963–973. [PubMed]
51. Scott LV, Medbak S, Dinan TG. The low dose ACTH test in chronic fatigue syndrome and in health. Clin Endocrinol (Oxf) 1998;48:733–737. [PubMed]
52. ter Wolbeek M, van Doornen LJ, Schedlowski M, Janssen OE, Kavelaars A, Heijnen CJ. Glucocorticoid sensitivity of immune cells in severely fatigued adolescent girls: a longitudinal study. Psychoneuroendocrinology. 2008;33:375–385. [PubMed]
53. Visser J, Lentjes E, Haspels I, et al. Increased sensitivity to glucocorticoids in peripheral blood mononuclear cells of chronic fatigue syndrome patients, without evidence for altered density or affinity of glucocorticoid receptors. J Investig Med. 2001;49:195–204.
54. Heim C, Nater UM, Maloney E, Boneva R, Jones JF, Reeves WC. Childhood trauma and risk for chronic fatigue syndrome: association with neuroendocrine dysfunction. Arch Gen Psychiatry. 2009;66:72–80. [PubMed]
55. Heim C, Ehlert U, Hellhammer DH. The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders. Psychoneuroendocrinology. 2000;25:1–35. [PubMed]
56. Cleare AJ. The HPA axis and the genesis of chronic fatigue syndrome. Trends Endocrinol Metab. 2004;15:55–59. [PubMed]
57. Bou-Holaigah I, Rowe PC, Kan J, Calkins H. The relationship between neurally mediated hypotension and the chronic fatigue syndrome. JAMA. 1995;274:961–967. [PubMed]
58. Rowe PC, Bou-Holaigah I, Kan JS, Calkins H. Is neurally mediated hypotension an unrecognised cause of chronic fatigue? Lancet. 1995;345:623–624. [PubMed]
59. Tanaka H, Matsushima R, Tamai H, Kajimoto Y. Impaired postural cerebral hemodynamics in young patients with chronic fatigue with and without orthostatic intolerance. J Pediatr. 2002;140:412–417. [PubMed]
60. De Lorenzo F, Hargreaves J, Kakkar VV. Possible relationship between chronic fatigue and postural tachycardia syndromes. Clin Auton Res. 1996;6:263–264. [PubMed]
61. Schondorf R, Benoit J, Wein T, Phaneuf D. Orthostatic intolerance in the chronic fatigue syndrome. J Auton Nerv Syst. 1999;75:192–201. [PubMed]
62. Stewart J, Weldon A, Arlievsky N, Li K, Munoz J. Neurally mediated hypotension and autonomic dysfunction measured by heart rate variability during head-up tilt testing in children with chronic fatigue syndrome. Clin Auton Res. 1998;8:221–230. [PubMed]
63. Stewart JM, Gewitz MH, Weldon A, Munoz J. Patterns of orthostatic intolerance: the orthostatic tachycardia syndrome and adolescent chronic fatigue. J Pediatr. 1999;135:218–225. [PubMed]
64. Yataco A, Talo H, Rowe P, Kass DA, Berger RD, Calkins H. Comparison of heart rate variability in patients with chronic fatigue syndrome and controls. Clin Auton Res. 1997;7:293–297. [PubMed]
65. Duprez DA, De Buyzere ML, Drieghe B, et al. Long- and short-term blood pressure and RR-interval variability and psychosomatic distress in chronic fatigue syndrome. Clin Sci (Lond) 1998;94:57–63. [PubMed]
66. Jones JF, Nicholson A, Nisenbaum R, et al. Orthostatic instability in a population-based study of chronic fatigue syndrome. Am J Med. 2005;118:1415. [PubMed]
67. LaManca JJ, Peckerman A, Walker J, et al. Cardiovascular response during head-up tilt in chronic fatigue syndrome. Clin Physiol. 1999;19:111–120. [PubMed]
68. Poole J, Herrell R, Ashton S, Goldberg J, Buchwald D. Results of isoproterenol tilt table testing in monozygotic twins discordant for chronic fatigue syndrome. Arch Intern Med. 2000;160:3461–3468. [PubMed]
69. Freeman R, Komaroff AL. Does the chronic fatigue syndrome involve the autonomic nervous system? Am J Med. 1997;102:357–364. [PubMed]
70. Karas B, Grubb BP, Boehm K, Kip K. The postural orthostatic tachycardia syndrome: a potentially treatable cause of chronic fatigue, exercise intolerance, and cognitive impairment in adolescents. Pacing Clin Electrophysiol. 2000;23:344–351. [PubMed]
71. Naschitz JE, Rozenbaum M, Rosner I, et al. Cardiovascular response to upright tilt in fibromyalgia differs from that in chronic fatigue syndrome. J Rheumatol. 2001;28:1356–1360. [PubMed]
72. Streeten DH, Thomas D, Bell DS. The roles of orthostatic hypotension, orthostatic tachycardia, and subnormal erythrocyte volume in the pathogenesis of the chronic fatigue syndrome. Am J Med Sci. 2000;320:1–8. [PubMed]
73. van de Luit L, van der Meulen J, Cleophas TJ, Zwinderman AH. Amplified amplitudes of circadian rhythms and nighttime hypotension in patients with chronic fatigue syndrome: improvement by inopamil but not by melatonin. Angiology. 1998;49:903–908. [PubMed]
74. Winkler AS, Blair D, Marsden JT, Peters TJ, Wessely S, Cleare AJ. Autonomic function and serum erythropoietin levels in chronic fatigue syndrome. J Psychosom Res. 2004;56:179–183. [PubMed]
75. Cordero DL, Sisto SA, Tapp WN, LaManca JJ, Pareja JG, Natelson BH. Decreased vagal power during treadmill walking in patients with chronic fatigue syndrome. Clin Auton Res. 1996;6:329–333. [PubMed]
76. Sisto SA, Tapp W, Drastal S, et al. Vagal tone is reduced during paced breathing in patients with the chronic fatigue syndrome. Clin Auton Res. 1995;5:139–143. [PubMed]
77. Stewart JM. Autonomic nervous system dysfunction in adolescents with postural orthostatic tachycardia syndrome and chronic fatigue syndrome is characterized by attenuated vagal baroreflex and potentiated sympathetic vasomotion. Pediatr Res. 2000;48:218–226. [PubMed]
78. De Becker P, Dendale P, De Meirleir K, Campine I, Vandenborne K, Hagers Y. Autonomic testing in patients with chronic fatigue syndrome. Am J Med. 1998;105:22S–26S. [PubMed]
79. Pagani M, Lucini D, Mela GS, Langewitz W, Malliani A. Sympathetic overactivity in subjects complaining of unexplained fatigue. Clin Sci (Lond) 1994;87:655–661. [PubMed]
80. Boneva RS, Decker MJ, Maloney EM, et al. Higher heart rate and reduced heart rate variability persist during sleep in chronic fatigue syndrome: a population-based study. Auton Neurosci. 2007;137:94–101. [PubMed]
81. Lyall M, Peakman M, Wessely S. A systematic review and critical evaluation of the immunology of chronic fatigue syndrome. J Psychosom Res. 2003;55:79–90. [PubMed]
82. Lorusso L, Mikhaylova SV, Capelli E, Ferrari D, Ngonga GK, Ricevuti G. Immunological aspects of chronic fatigue syndrome. Autoimmun Rev. 2009;8:287–291. [PubMed]
83. Klimas NG, Koneru AO. Chronic fatigue syndrome: inflammation, immune function, and neuroendocrine interactions. Curr Rheumatol Rep. 2007;9:482–487. [PubMed]
84. Jones JF. An extended concept of altered self: chronic fatigue and post-infection syndromes. Psychoneuroendocrinology. 2008;33:119–129. [PubMed]
85. Hickie I, Davenport T, Wakefield D, et al. Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens: prospective cohort study. BMJ. 2006;333:575. [PMC free article] [PubMed]
86. Patarca-Montero R, Antoni M, Fletcher MA, Klimas NG. Cytokine and other immunologic markers in chronic fatigue syndrome and their relation to neuropsychological factors. Appl Neuropsychol. 2001;8:51–64. [PubMed]
87. Patarca R. Cytokines and chronic fatigue syndrome. Ann N Y Acad Sci. 2001;933:185–200. [PubMed]
88. Borish L, Schmaling K, DiClementi JD, Streib J, Negri J, Jones JF. Chronic fatigue syndrome: identification of distinct subgroups on the basis of allergy and psychologic variables. J Allergy Clin Immunol. 1998;102:222–230. [PubMed]
89. Straus SE, Dale JK, Peter JB, Dinarello CA. Circulating lymphokine levels in the chronic fatigue syndrome. J Infect Dis. 1989;160:1085–1086. [PubMed]
90. Cannon JG, Angel JB, Abad LW, et al. Interleukin-1 beta, interleukin-1 receptor antagonist, and soluble interleukin-1 receptor type II secretion in chronic fatigue syndrome. J Clin Immunol. 1997;17:253–261. [PubMed]
91. Mawle AC, Nisenbaum R, Dobbins JG, et al. Immune responses associated with chronic fatigue syndrome: a case-control study. J Infect Dis. 1997;175:136–141. [PubMed]
92. Skowera A, Cleare A, Blair D, Bevis L, Wessely SC, Peakman M. High levels of type 2 cytokine-producing cells in chronic fatigue syndrome. Clin Exp Immunol. 2004;135:294–302. [PMC free article] [PubMed]
93. von Mikecz A, Konstantinov K, Buchwald DS, Gerace L, Tan EM. High frequency of autoantibodies to insoluble cellular antigens in patients with chronic fatigue syndrome. Arthritis Rheum. 1997;40:295–305. [PubMed]
94. Whiteside TL, Friberg D. Natural killer cells and natural killer cell activity in chronic fatigue syndrome. Am J Med. 1998;105:27S–34S. [PubMed]
95. Steinau M, Unger ER, Vernon SD, Jones JF, Rajeevan MS. Differential-display PCR of peripheral blood for biomarker discovery in chronic fatigue syndrome. J Mol Med. 2004;82:750–755. [PubMed]
96. Bounous G, Molson J. Competition for glutathione precursors between the immune system and the skeletal muscle: pathogenesis of chronic fatigue syndrome. Med Hypotheses. 1999;53:347–349. [PubMed]
97. Raison CL, Lin JMS, Reeves WC. Association of peripheral inflamma-tory markers with chronic fatigue in a population-based sample. Brain Behav Immun. 2009;23:327–337. [PubMed]
98. Danese A, Moffit TE, Pariante CM, Ambler A, Poulton R, Caspi A. Elevated inflammation levels in depressed adults with a history of childhood maltreatment. Arch Gen Psychiatry. 2008;65:409–415. [PMC free article] [PubMed]
99. Pace TW, Mletzko TC, Alagbe O, et al. Increased stress-induced inflammatory responses in male patients with major depression and increased early life stress. Am J Psychiatry. 2006;163:1630–1633. [PubMed]
100. Clow A, Thorn L, Evans P, Hucklebridge F. The awakening cortisol response: methodological issues and significance. Stress. 2004;7:29–37. [PubMed]
101. Kirschbaum C, Hellhammer DH. Salivary cortisol. In: Fink G, editor. Encyclopedia of Stress, Volume 3. Academic Press; San Diego, CA: 2000. pp. 379–383.
102. Kennedy B, Dillon E, Mills PJ, Ziegler MG. Catecholamines in human saliva. Life Sci. 2001;69:87–99. [PubMed]
103. Baum BJ. Principles of saliva secretion. Ann NY Acad Sci. 1993;694:17–23. [PubMed]
104. Nater UM, Rohleder N. Salivary alpha-amylase as a non-invasive biomarker for the sympathetic nervous system: current state of research. Psychoneuroendocrinology. 2009;34:486–496. [PubMed]
105. Thayer JF, Sternberg EM. Beyond heart rate variability: vagal regulation of allostatic systems. Ann NY Acad Sci. 2006;1088:361–372. [PubMed]
106. Marques-Deak AH, Cizza G, Eskandari F, et al. Measurement of cytokines in sweat patches and plasma in healthy women: validation in a controlled study. J Immunol Methods. 2006;315:99–109. [PubMed]
107. Cizza G, Marques AH, Eskandari F, et al. Elevated neuroimmune biomarkers in sweat patches and plasma of premenopausal women with major depressive disorder in remission: the POWER study. Biol Psychiatry. 2008;64:907–911. [PMC free article] [PubMed]
108. Fries E, Hesse J, Hellhammer J, Hellhammer DH. A new view of hypocortisolism. Psychoneuroendocrinology. 2005;30:1010–1016. [PubMed]
109. van Houdenhove B, van den Eede F, Luyten P. Does hypothalamic-pituitary-adrenal axis hypofunction in chronic fatigue syndrome reflect a “crash” in the stress system? Med Hypoth. 2009;72:701–705.


This post has not been tagged.

Share |
PermalinkComments (0)

Bran Cancer Risk from Cell Phone Use

Posted By Administration, Thursday, June 2, 2011
Updated: Friday, April 18, 2014


by Nalini Chilkov, LAC, OMD

A scientific report released Tuesday by the World Health Organization concludes radio frequencies and electromagnetic fields – including those routinely emitted by mobile phones – are “possibly” carcinogenic to humans.

The World Health Organization and its subsidiary investigative panel, the International Agency for Research on Cancer, or IARC, stated today what many scientific studies have been suggesting for decades: that there is a possible connection between mobile phone use and malignant brain tumors.  Dr. Jonathan Samet, who heads IARC’s Working Group of 31 international scientists from 14 countries, made the announcement at the conclusion of the group’s week-long meeting in Lyon, France.

“The working group classifies the radio and electromagnetic fields as possibly carcinogenic to humans; that is within the classification used by the International Agency for Research on Cancer,” he said.

The group advised that, because five billion people around the world currently use mobile phones, therefore, much further research in the subject is needed.  The report places at most risk those with the greatest use of cell phones and exposure to other sources of radiation. ”We also carefully consider the sources of exposure of populations to radio frequency electromagnetic fields, the nature of these fields as they come from various devises, including wireless phones, and we look carefully at the physical phenomenon by which exposure to such fields may perturb biological systems and lead to cancers,” he said.

The IARC working group had gathered in France for the past eight days, reviewing all previous studies done on electromagnetic radiation’s effects on humans and animals over the past decade.

Health advocacy groups that have been warning of possible cell phone-cancer links are praising the WHO pronouncement.

Camilla Rees, the founder of a U.S. based group called Electromagnetic Health, says she is pleased but said much more needs to be done. ”They focused on brain cancer, and brain cancer includes a relatively small number of people.  But we only have had this technology for about 15 years and most carcinogens will take several decades before they develop into a cancer.  Early indicators from scientists are projecting a tsunami of brain cancer unless we do something to educate people to lower their exposure,” she said.

Rees says there are many other health effects of radiation, including damage to human cell tissue, that the World Health Organization has yet to recognize. But for now, she believes the most urgent need is to begin a campaign to protect children from the effects of electromagnetic fields, and in  particular, from cell phones.

“What microwave radiation does in most simplistic terms is similar to what happens to food in microwaves, essentially cooking the brain,” said Dr. Keith Black, chairman of neurology  and world class brain surgeon at Cedars-Sinai Medical Center in Los Angeles. “So in addition to leading to a development of cancer and tumors, there could be a whole host of other effects like cognitive memory function, since the memory temporal lobes are where we hold our cell phones.” Dr Black recommends using ear buds or texting to keep the cell phone away from the head.

While wireless carriers instruct users to keep cell phones a certain distance from their heads, such as Apple’s iPhone 4 safety manual that says to keep the device at least 15 millimeters from the body, CTIA – The Wireless Association noted that WHO’s announcement does not mean that cell phones cause cancer. In addition, the association denounced WHO’s results since it “did not conduct any new research, but rather reviewed published studies.”

This post has not been tagged.

Share |
PermalinkComments (0)

My Kid has ADD/ADHD

Posted By Administration, Tuesday, May 31, 2011
Updated: Friday, April 18, 2014


by Matt Angove, ND, NMD

No doubt, genetic susceptibility plays into the whole ADHD paradigm but that goes for everything. Whatever your state of being, good or bad has to do with how you bathe your genes.

I find it to be a modern day miracle that more people aren’t suffering from ADHD, depression, anxiety disorders, bipolar, schizophrenia, and the like considering the laboratory derived concoctions we douse our bodies with daily.

Before you put your child on Ritalin, a compound that has marked similarities to amphetamines and actions consistent with cocaine, just dampened somewhat, let us consider our options.

Let us Consider

Consider the Red No. 40, Yellow No. 5, MSG, aspartame, Splenda, partially hydrogenated oils, high fructose corn syrup, soybean oil (Is there anything in a box it is not in?), caffeine (Monster drinks, Red Bull, Soda, coffee), phosphorus (soda pop) and refined sugars.

Consider the refined foods and naked grains they are consuming.

Consider the hormone buffed and corn stuffed meats they are putting on their sandwiches.

Consider the hours of reckless television and video games that are being sprayed across their eyes and mind.

If you or your child is consuming items such as JELL-O, Lucky Charms, Pop-Tarts, Butterfinger bars, Skittles, Hostess Twinkies or Frito-Lay Doritos, to name a few, you should fully expect marked neurological dysfunction.  It is only natural!!!

Nutritionally based therapies for ADHD can be EXTREMELY beneficial!!!  Understand that 8-10% of school age children are considered to be in this spectrum.  So, there are plenty of children who are suffering and in most cases, I would suggest needlessly.

Available therapies


Avoidance of possible food sensitivities (start with gluten, refined sugars, dairy, chocolate, citrus, peanuts, eggs, soy) –an elimination and reintroduction diet may be in order.

Elimination of synthetic sweeteners, colors and whatever isn’t FOOD from the diet.

Evening Primrose oil coupled with Fish Oil

Flaxseed oil with Vitamin C

Nutrient optimization ( Magnesium, Zinc, Calcium, Iron, Potassium, B vitamins)


Amino acid combination’s (as monitored by your health provider)

Lifestyle is High Style

You have to realize that getting ADHD under control isn’t an overnight affair.  Just like any other chronic condition, you must set forth and live out a lifestyle conducive to the sustaining of life.  I know it is not easy.  Our current available knowledge state has given everyone the opportunity for abundant health.  However, the societal pace rarely allows us to utilize and practice that knowledge.

You simply have to choose what lane you want to live in.

This post has not been tagged.

Share |
PermalinkComments (0)

Gluten Free - The Latest Fad Diet

Posted By Administration, Wednesday, May 25, 2011
Updated: Friday, April 18, 2014


by Andrea Purcell, ND

The shocking news in 2003 was that 1 in 133 people had celiac disease. Celiac disease is a genetic intolerance to gluten contained in wheat, rye, and barley. Eating and cooking gluten free means consuming a whole food diet devoid of gluten containing grains.

Celiac disease once considered rare, is now a common autoimmune disease afflicting 1 in 133 people. If you or a loved one has Celiac disease there is a good chance that first and second-degree relatives have the diagnosis as well. As a medical necessity, there are three groups of people who should avoid gluten.

*Any person with a diagnosis of Celiac disease.

*Any person with an allergic reaction to wheat as determined either by an IgG or an IgE blood test.

*Any person with gluten sensitivity.

Many people are sensitive to wheat and/or gluten but do not have the diagnosis of celiac disease. Sensitivities can cause symptoms such as skin reactions, congestion in the throat, ears, or sinuses, digestive upset, or other body inflammation such as fatigue and aching joints. A recent study in 2010 found that people could lose their tolerance to gluten as they age. These people are not born with the genetic intolerance commonly seen with celiac disease but are developing the intolerance later on in life. This suggests a weakening of digestive function due to repeated exposure to gluten, which can cause leaky gut, toxin exposure, antibiotics, medications, and even vaccines.

The information about gluten and the awareness around celiac disease seems to have thrown the nation into a gluten free frenzy. Many people are eating gluten free as a type of fad diet. These people have heard that gluten is bad and have chosen to avoid it as a way to be healthy. As the awareness builds so does the variety of gluten free products. It is easier than ever to find gluten free cake, cookie, brownie mixes, breads, need I say more? Even if you are going gluten free filling your day with these will not bring you closer to health. Moving towards a plant-based diet however, will.


Cooking Gluten Free…

For those first diagnosed with Celiac disease the act of cooking and eating initially becomes very stressful. Learning a few tried and true recipes that you know you can whip up in a flash will be extremely helpful.

The first thing you should do when you find out that you need to eat gluten free is to focus on a plant based diet. This includes vegetables, fruits, nuts, seeds, and lean proteins. These foods will become the foundation of your daily food plan.

Experiment with alternative grains such as brown rice, wild rice, quinoa, amaranth, buckwheat, sorghum, and teff.

There are many benefits to home cooking. You have complete control over what you eat and the quality of ingredients, plus there will always be leftovers for lunch the next day, hooray!

Baking Gluten Free…

Cooking is one thing and baking is another. The general rule of thumb for mastering any gluten free baked good recipe is to experiment with the recipe at least three times. The first will be a flop, the second will be better, and you will try a different flour, moisture ingredient or sweetener, and by the third try you will be satisfied. Then you can actually bring the finished product to a social gathering. Making a bread or cupcake with one type of flour is not recommended, the success in baking gluten free comes from mixing the flours. You can mix bean flour with a gluten free flour to help with the texture. In gluten free baking many things can come out dry and crumbly so items must be added that create more moisture. These items could be mashed banana, tofu, honey, eggs, pumpkin, or xantham gum. In order to succeed you must experiment with a variety of flours. Become familiar with the tastes and textures of the alternative flours, then you can combine them. Once you master the moisture content, then you can experiment with the level of sweetness. Many recipes just have you add plain old white sugar but I prefer stevia, agave, brown rice syrup, honey or a combination of two sweeteners to reduce the calorie and sugar content of the recipe.

Note from Dr. P

In order to determine if you are sensitive to gluten you can do this simple experiment at home. Avoid all gluten for 14 days. This means all gluten. Read labels carefully because many items contain hidden gluten such as cereals, deli meats, and canned soups. After 14 days reintroduce gluten containing foods 1-2x daily for three days in a row. Observe your body for any signs of gluten sensitivity that I listed above. Looking for healthy gluten recipes? Get my book!


-Be Healthy, Happy, & Holistic

This post has not been tagged.

Share |
PermalinkComments (0)

You Have a Right to Make Healthy Choices!

Posted By Administration, Wednesday, May 18, 2011
Updated: Friday, April 18, 2014

It's no secret that pesticides are harmful to humans and the environment. According to the National Institutes of Health, pesticides are linked to diabetes, Parkinson's Disease, cancer and more. Below is a letter from the Environmental Working Group that invites you to sign their petition to urge the FDA not to cave in to the chemical agribusiness's campaign to limit the public's information to pesticides.

Dear Friend,

Since 1991, the U.S. Department of Agriculture has been testing fresh produce for pesticide residues and releasing the findings. Environmental Working Group analyzes these detailed technical reports to produce our Shopper's Guide to Pesticides. But this year, the USDA may cave in to an industry campaign to alter the results and give consumers less information. That's bad news for us all.

Chemical agribusiness interests have launched an expensive all-out campaign to silence EWG and deny you information you need to make healthy choices. Just last year, nearly $200,000 of taxpayers' money was used to support a misinformation campaign run by the Alliance for Food and Farming, a pro-agricultural chemicals lobby dedicated to combating pesticide critics like EWG.

Chemical agribusiness interests want to suppress the truth about pesticides. We can't let them get away with it. USDA officials need to hear that you want the truth, all of it and nothing but. Please join the more than 36,000 people who have called on USDA to not cave in to industry.

Click here to sign our petition that tells USDA officials to not cave to industry pressure and to stop funding industry's disinformation campaigns!

The evidence linking pesticides to health problems -- such as increased risk of cancer -- is overwhelming. New studies show that pesticide exposure may lead to developmental delays and lower IQs in children. Last year, the President's Cancer Panel recommended that consumers avoid foods with pesticide residues.

Instead of kowtowing to industry groups like the Alliance for Food and Farming, the USDA and other federal agencies should compile and analyze more information about pesticides. Industry spin should not drive disclosure of critical information about pesticides in our food. If you want to know whether your kids' lunch boxes contain fruits and veggies high in pesticide residues, take action today!

Click here to sign our petition today. It's unpalatable that your tax dollars fund disinformation about pesticides in food.

Thank you for standing with EWG against the pesticide lobby.


Ken Cook
President, Environmental Working Group


This post has not been tagged.

Share |
PermalinkComments (0)

Saffron - Research Shows Anti-Cancer Activity

Posted By Administration, Tuesday, May 17, 2011
Updated: Friday, April 18, 2014


by Nalini Chilkov, LAC, OMD


Saffron, Crocus sativus, also known as Hong Hua in Traditional Chinese Herbal Medicine, has been used both as a culinary spice and as a medicinal botanical on many continents throughout history for over 3,000 years. Recent research demonstrates that a component of saffron, a orange-red colored carotenoid called crocetin shows promise as an anti-cancer agent. Saffron also contains other carotenoids including zeaxanthin, lycopene, and various alpha- and beta-carotenes

According to researcher Fikrat Abdullaev, who is so impressed with saffron’s multiple medicinal properties that he suggests there be a new scientific discipline called “saffronology”

Considerable scientific evidence has suggested that plant-based dietary agents can inhibit the process of carcinogenesis effectivelySince cancer is the most common cause of death in the world population, the possibility that readily available natural substances from plants, vegetables, herbs, and spices may be beneficial in the prevention of cancer warrants closer examination. Saffron in filaments is the dried, dark red stigmata of Crocus sativus L. flowers and it is used as a spice, food colorant, anda drug in medicine. A growing body of research has demonstrated that saffron extract itself and its main constituents, the carotenoids, possess chemopreventive properties against cancer.

Studies show that crocetin, only one of several carotenoids found in saffron, acts affects four important functions in cancer cells:

  • inhibiting nucleic acid (DNA and RNA) synthesis (affecting gene expression, growth and replication)

  • enhancing anti-oxidative system (acting as a free radical scavenger and reducing oxidative stress)

  • i

    nducing apoptosis – promoting normal cell death

  • hindering growth factor signaling pathways (growth inhibition)


These are the characteristics of a valuable anti-tumor, anti-cancer therapeutic agent.



Here is the abstract of the recent study

Crocetin: An Agent Derived from Saffron (Hong Hua) for Prevention and Therapy for Cancer

Cancer is one of the leading causes of death in the United States and accounts for approximately 8 million deaths per year worldwide. Although there is an increasing number of therapeutic options available for patients with cancer, their efficacy is time-limited and non-curative. Approximately 50-60% of cancer patients in the United States utilize agents derived from different parts of plants or nutrients (complementary and alternative medicine), exclusively or concurrently with traditional therapeutic regime such as chemotherapy and/or radiation therapy. The need for new drugs has prompted studies evaluating possible anti-cancer agents in fruits, vegetables, herbs and spices. Saffron, a spice and a food colorant present in the dry stigmas of the plant Crocus sativus L., has been used as an herbal remedy for various ailments including cancer by the ancient Arabian, Indian and Chinese cultures. Crocetin, an important carotenoid constituent of saffron, has shown significant potential as an anti-tumor agent in animal models and cell culture systems. Crocetin affects the growth of cancer cells by inhibiting nucleic acid synthesis, enhancing anti-oxidative system, inducing apoptosis and hindering growth factor signaling pathways.

Gutheil WG, et al. Kansas City Veterans Affairs Medical Center, 4801 Linwood Boulevard, Kansas City, MO 64128, USA. Curr Pharm Biotechnol. 2011 Apr 5. Source: PubMed

Prior Studies include:

Oost, Thorten K. et al Discovery of Potent Antagonists of the Antiapoptotic Protein XIAP for the Treatment of Cancer J. Med. Chem., 2004, 47 (18), pp 4417–4426

FIKRAT I. ABDULLAEV Cancer Chemopreventive and TumoricidalProperties of Saffron (Crocus sativus L.) Laboratory of Experimental Oncology, National Institute of Pediatrics, Mexico City 04530, Mexico Cancer Lett. 1991 May 1;57(2):109-14.Antitumour activity of saffron (Crocus sativus). Nair SC, Pannikar B, Panikkar KR. Amala Cancer Research Centre, Kerala, India

Asian Pac J Cancer Prev. 2009;10(5):887-90.Crocin from Kashmiri saffron (Crocus sativus) induces in vitro and in vivo xenograft growth inhibition of Dalton’s lymphoma (DLA) in mice. Bakshi HA, Sam S, Feroz A, Ravesh Z, Shah GA, Sharma M.

Exp Oncol. 2007 Sep;29(3):175-80. Crocin from Crocus sativus possesses significant anti-proliferation effects on human colorectal cancer cells.

Aung HH, Wang CZ, Ni M, Fishbein A, Mehendale SR, Xie JT, Shoyama CY, Yuan CS. Tang Center for Herbal Medicine Research, The Pritzker School of Medicine, University of Chicago, Chicago, IL 60637, USA.

This post has not been tagged.

Share |
PermalinkComments (0)

High-Dose Vitamin C for People with Cancer: A Promising Adjunct to Mainstream Cancer Treatment

Posted By John C. Pittman, MD, and Mark N. Mead, MSc, Monday, May 16, 2011
Updated: Friday, April 18, 2014

It may come as a surprise to learn that most people with cancer do not die from the disease itself, but from life-threatening infections such as sepsis.  A great many cancer sufferers also die from chronic inflammatory problems that are associated with the disease, such as cancer cachexia.  A recent report published in the March 2011 Journal of Translational Medicine presents a powerful argument for using intravenous (IV) vitamin C in the context of life-threatening infections and cancer.  The authors report that IV vitamin C has been effective in directly treating cancer as well as in helping to reverse chronic inflammation and stave off life-threatening infections in these patients.

Vitamin C is the most widely used single-nutrient supplement in the United States, and has long been lauded by the general public for its supposed powers to treat many ills, from colds to cancer, from herpes to heart disease.  Back in the 1970s, two-time Nobel Prize winner Linus Pauling did much to bolster the vitamin’s profile by touting it as an immune-enhancing and tumor-killing therapy.  Pauling asserted that the anti-cancer potential of vitamin C depended on getting the proper dosage, and toward the end of his life, he further emphasized that vitamin C was best combined with various other anti-cancer agents that worked synergistically with the vitamin.

Dr. Pauling was among the first scientists to recognize that it’s impossible to attain the therapeutically optimal level of vitamin C by taking the vitamin orally—that is, in the form of the standard vitamin C pills or tablets.  On one hand, it's virtually impossible for people to overdose on oral vitamin C, since the body only assimilates a certain quantity through the mouth and then stops allowing it to build up.  On the other hand, this prevents health care professionals from being able to achieve the blood levels that have been linked with killing tumors.  One solution, of course, is to use intravenous (IV) vitamin C.

With IV vitamin C, you can bypass the digestive system and thus circumvent the body’s normally tight regulation of vitamin C levels.  As researchers recently reported in a recent issue of the Proceedings of the National Academy of Sciences, IV vitamin C generates hydrogen peroxide which will destroy primitive cells like bacteria, viruses and cancer cell, and this in turn leads to the shrinkage of aggressive tumors—including ovarian, pancreatic and brain tumors—in laboratory animals.   Despite the very high levels of vitamin C used in these studies normal cells appear to be completely unharmed by the therapy.  The researchers stated that it’s feasible to intravenously boost levels of vitamin C in humans to the same levels used in the mice.

Indeed, numerous studies have suggested that high-dose IV vitamin C may help eliminate cancer, even when combined with conventional treatments.  For example, in a report for the August 8th 2010 issue of Cancer Chemotherapy and Pharmacology, Dr. Mark Levine, chief of the U.S. National Institutes of Health's Molecular and Clinical Nutrition Section, concluded that exposing tumors to vitamin C made them more vulnerable to the killing effects of at least four widely used chemotherapy drugs.  Previously, Dr. Levine had published research with mice suggesting that IV doses of vitamin C could one day reduce the size of malignant tumors in people.

Dr. Levine’s findings confirm what we have been seeing for the past 15 years at the Carolina Center for Integrative Medicine.  On numerous occasions, we have observed that IV vitamin C enabled patients with advanced cancers to respond to chemotherapy drugs to which they had previously failed to respond.  We therefore believe that it can enhance the effectiveness of cancer chemotherapy and pave the way for therapeutic success.  In a recent issue of PloS One, Dr. Levine concluded that high-dose IV vitamin C is in wide use by integrative practitioners and that “high dose intravenous vitamin C appears to be remarkably safe. Physicians should inquire about IV vitamin C use in patients with cancer [and] chronic, untreatable, or intractable conditions…”

A Short History of Vitamin C Therapy
Vitamin C has long been the most widely used dietary supplement, and much of the initial excitement surrounding this vitamin can be traced back to studies conducted in the 1970s by Dr. Pauling and his Scottish colleague Ewan Cameron, MD. The scientists published two studies that demonstrated an approximate quadrupling in survival in “terminal” cancer patients who received vitamin C by a combination of IV and oral routes.  These findings were subsequently replicated by a clinical trial in Japan.  In addition, the Scottish and Japanese clinical studies found significant improvements in the quality of life for cancer patients receiving high-dose vitamin C.

A chemist by training, Dr. Pauling had publicly questioned the adequacy of the Recommended Daily Allowance (RDA) for vitamin C, and he suggested that taking gram doses of vitamin C—that is, 1000 milligrams (mg) or more—could be effective in the prevention and treatment of colds.  At the time, the RDA was a mere 45 mg per day, an amount considered sufficient to prevent scurvy, the classic disease of vitamin C deficiency. (Today, the RDA is 90 mg per day for men, and 75 mg per day for women.)

Pauling took the controversy up another notch when he proposed daily doses of 5 to 30 grams—5000 to 30,000 mg—for the treatment of advanced cancers.  To this day, the very mention of Pauling’s vitamin C research still sparks heated arguments among medical professionals, oncologists in particular.Clinical studies of the potential therapeutic value of high-dose vitamin C began in Scotland in 1971.  The findings from these early investigations were dramatic indeed.  In addition to the aforementioned three studies showing a four-fold increase in survival, one other study of 100 “terminal” cancer patients showed a nearly six-fold increase in survival for patients with advanced cancer.  

To date, six out of a total of seven clinical studies have concluded that high-dose vitamin C did increase survival in patients with advanced cancers. Many of these patients also noted significant improvements in their energy levels, pain reduction, appetite, and other measures of quality of life. Understandably, these findings attracted much media attention and ignited an explosion of public interest in using vitamin C for cancer therapy.  Many thousands of cancer patients began self-prescribing the vitamin.  At the same time, however, some scientists sharply criticized Pauling’s research on the grounds that his early studies were not randomized controlled clinical trials, the “gold standard” of medical research.  For this reason, the studies’ findings were deemed unreliable or preliminary at best.Controlled clinical trials are indeed the best way to assess the true value of any proposed treatment strategy.  In the case of vitamin C, the ideal study would randomly assign cancer patients to receive either vitamin C or a placebo (a substance having no biological or therapeutic activity), and to do so without the patients knowing which one they were receiving.

In the late 1970s, researchers from the Mayo Clinic did conduct two randomized clinical trials, but alas, these studies only focused on oral, not intravenous, vitamin C.  In the first study, the cancers were too far advanced to reasonably expect any intervention to affect the outcome. (the average survival for all patients was only 51 days).  In the second trial, there was no difference in survival for colorectal cancer patients who received the high-dose oral vitamin C.  Strangely, neither study adhered to Dr. Pauling’s recommended protocol for achieving “bowel tolerance”—that is, in order to prevent diarrhea, the oral dose was supposed to have been increased gradually over time.

Because neither of the Mayo Clinic studies provided vitamin C in oral form, they have no bearing on the issue of whether high-dose IV vitamin C can be an effective treatment for advanced cancers.  Thus the jury is still out on vitamin C as a potential cure for cancer, and no one has adequately tested Pauling’s hypothesis with the appropriate controlled clinical trial design. 

Intravenous Vitamin C May Be Essential
In order to achieve the doses that have a therapeutic impact, as noted earlier, it seems necessary to use intravenous (IV) vitamin C.  The original protocol recommended by Drs Pauling and Cameron involved a 10-day course of IV vitamin C in which the vitamin was given as a slow-drip infusion of 10 grams sodium ascorbate. After this, vitamin C was given orally in the form of a syrup, at a dose of 2.5 grams every 6 hours for a total dose of 10 grams per day.  This strategy enables patients to avoid the diarrhea that otherwise accompanies vitamin C doses in excess of 6 to 7 grams per day.   Subsequent studies used oral and intravenous doses ranging from10 to 30 grams per day.

The recommended dose for IV vitamin C has steadily increased over the past two decades, and physicians continue to report striking benefits.  In the March 2008 issue of Puerto Rico Health Sciences Journal, researchers reported that, “only by intravenous administration, the necessary [vitamin C] levels to kill cancer cells are reached in both plasma and urine.”  By giving the vitamin intravenously, one can readily achieve the blood levels (at least 20 mM) that have been reported to selectively kill tumor cells.   In at least two clinical trials now in progress, scientists are trying to determine the safety, tolerability, best therapeutic dose, and other key aspects of using IV vitamin C.

The power of this approach has been well documented in mainstream medical journals.  In March 2006, the Canadian journal CMAJ (Canadian Medical Association Journal) told the story of three patients with advanced cancer who had received IV vitamin C.  One was a 49-year-old man with “terminal” bladder cancer who had declined chemotherapy. Nine years after receiving the deadly prognosis, he was still alive and apparently free of cancer. Another patient, a 66-year-old woman, had an aggressive lymphoma with an extremely poor prognosis. After IV vitamin C, her disease went into remission and she was alive and well 10 years later.  In a third case, IV vitamin C was given to a 51-year-old woman with kidney cancer that spread to her lungs.  Two years later, she had a normal chest X-ray, and a pathologist confirmed the findings.  

Why did these patients succeed where others have not?  It could be that the secret is in the dosage.  Only two controlled clinical trials of vitamin C have been done, and both used oral vitamin C rather than the IV route.  But oral doses can never achieve the high blood levels provided by IV methods, the levels necessary for killing cancer.  Dr. Levine recently demonstrated that, indeed, only IV vitamin C can achieve the desired blood levels.  The reason for this is that your kidneys will get rid of vitamin C as fast as your gut can absorb it.  With the IV approach, the blood levels are immediately elevated, and it takes much more time for the kidneys to eliminate the excess. Thus, for an extended period, you’re able to expose cancer cells in your body to the levels that can make a difference.

Dr. Levine also confirmed that vitamin C is metabolized to hydrogen peroxide.  Unlike normal cells, cancer cells lack the internal defenses to protect themselves from this highly unstable and reactive ( compound.  As a result, they die.  (Many chemotherapy agents operate, in part, through a similar mechanism.  Green tea, resveratrol, and artemisinin may have similar effects; taken in combination, these natural agents may reach levels of peroxide lethal to malignant tumors.) These days, IV vitamin C doses may range from 10 grams to as high as 300 grams per day (300,000 mg!), though most doses are in the range of 30 to 80 grams per day.  The optimal strategy, as designed by Dr. Hugh Riordan, includes certain other nutrients, such as alpha lipoic acid.  

The good news is that, in contrast with conventional chemotherapy, IV vitamin C is not a particularly expensive therapy. If you have cancer, talk to your Integrative Medicine physician about IV vitamin C.  Preliminary reports from a clinical trial in Kansas City indicate that giving IV vitamin C prior to chemotherapy can dramatically reduce the toxicity of those treatments while bolstering the tumor-killing impact of the chemo.  

John C. Pittman, MD, is the Medical Director of the Carolina Center for Integrative Medicine in Raleigh, NC, and is certified by the American Board of Clinical Metal Toxicology.  Mark N. Mead, MSc, serves as the Center’s Integrative Medicine Research Consultant.


  • Ichim TE, Minev B, Braciak T, Luna B, Hunninghake R, Mikirova NA, Jackson JA, Gonzalez MJ, Miranda-Massari JR, Alexandrescu DT, Dasanu CA, Bogin V, Ancans J, Stevens RB, Markosian B, Koropatnick J, Chen CS, Riordan NH.  Intravenous ascorbic acid to prevent and treat cancer-associated sepsis?  J Transl Med. 2011; 9:25

  • Duconge J, Miranda-Massari JR, Gonzalez MJ, Jackson JA, Warnock W, Riordan NH.  Pharmacokinetics of vitamin C: insights into the oral and intravenous administration of ascorbate. P R Health Sci J. 2008; 27(1):7-19.

  • Padayatty SJ, Riordan HD, Hewitt SM, Katz A, Hoffer LJ, Levine M. Intravenously administered vitamin C as cancer therapy: three cases.CMAJ. 2006; 174(7):937-42.

  • González MJ, Miranda-Massari JR, Mora EM, Guzmán A, Riordan NH, Riordan HD, Casciari JJ, Jackson JA, Román-Franco A.  Orthomolecular oncology review: ascorbic acid and cancer 25 years later. Integr Cancer Ther. 2005; 4(1):32-44.

  • Riordan HD, Riordan NH, Jackson JA, Casciari JJ, Hunninghake R, González MJ, Mora EM, Miranda-Massari JR, Rosario N, Rivera A.  Intravenous vitamin C as a chemotherapy agent: a report on clinical cases. P R Health Sci J. 2004; 23(2):115-8.

  • Block KI, Mead MN.  Vitamin C in alternative cancer treatment: historical background.  Integr Cancer Ther. 2003;2(2):147-54.

This post has not been tagged.

Share |
PermalinkComments (0)

Food Allergy and Disease

Posted By Administration, Friday, May 13, 2011
Updated: Friday, April 18, 2014


by Matt Angove, ND, NMD

Food allergies are no doubt becoming a bigger and bigger part of our lives.  Unfortunate indeed for food lovers everywhere.  But  to be fair to our body, it can only be dragged through so much before its ability to continue in pristine rhythm gets interrupted.

How do we get allergies to food?

Allergies to foods are generated by an over-reactive immune system coupled with a porous digestive tract.  What happens is that small undigested protein particles, namely polypeptides and peptides of food pass through the intestinal wall into the blood stream and are recognized by the immune system as an invading factor.  This occurs because the genetic make up of the food proteins doesn’t belong to you.

The immune system is actually doing precisely what it was engineered to do.  However, this overactive arm of the immune system against food proteins actually makes us more susceptible to cancer.   The immunoglobulins that cause the allergic symptoms, actually depress the production of  your bodies own immune cancer killers.  Most notably, natural killer cells and tumor necrosis factor.   What you end up with is an imbalance in the immune system.

Imbalances in the immune system not only create opportunity for cancer but also a host autoimmune and inflammatory conditions.

There are many ways to check for food sensitivities.  The gold standard is to limit a food category (i.e. dairy products) for a certain period of time.   After that time has elapsed you then reintroduce that food category in its purest form (i.e. glass of milk) to your diet.


Cut out dairy for 4 weeks and then at 4 weeks drink 8 ounces of milk at breakfast, lunch and dinner.  If you had any symptoms previous to cutting out the dairy write them down and notice if any symptoms disappeared and then notice if any symptoms reappeared upon adding dairy back in.

Something to note is that allergic reactions to food are not always instant and can show up days later.  This makes it all the more important to take note of your symptoms during this time period.

You may also get blood tests to check for food sensitivities.  These tests also allow you to see your allergic intensity to specific foods.

Most Common Food Allergies

The most common allergenic foods are milk, wheat, eggs, corn, peanuts, non-organic soybeans, chicken, and shellfish.

This post has not been tagged.

Share |
PermalinkComments (0)

When Medicine Fails...A Holistic Approach to Allergies, Chronic Fatique, Fibromyalgia, & Chronic Pain

Posted By Administration, Thursday, May 12, 2011
Updated: Friday, April 18, 2014



ACAM member Charles Scott, DC, wrote the book When Medicine Fails... A Holistic Approach to Allergies, Chronic Fatigue, Fibromyalgia, and Chronic Pain. Within its pages reveals a synthesis of Dr. Scott's 25 years of clinical experience as a holistic nature doctor. This book presents proven, comprehensive and highly effective holistic approaches to the major chronic, degenerative diseases that plague mankind.

Dr. Scott is the founder of Scott Chiropractic and Wellness Center in Odessa, Texas. His holistic clinic focuses on helping patients become pain free, healthy and optimally functional. Among his services and therapies he provides are: nutritional programs, allergy elimination techniques, applied kinesiology (AK), and detoxification.

Visti Dr. Scott's website at:

This post has not been tagged.

Share |
PermalinkComments (0)

Natural Migraine Relief

Posted By Administration, Wednesday, May 11, 2011
Updated: Friday, April 18, 2014


by Andrea Purcell, ND

Twelve percent of Americans suffer from migraines. Women are affected three times more than men. Of migraine sufferers 98% rely on acute treatment and symptom suppression.

Natural Integrative medicine asks the question, why? Why does this person suffer with migraines? Typically, the cause is different for each person.

Integrative medicine is effective as a preventative therapy for migraine sufferers and works the best through identifying the underlying cause of the migraines. Successful treatment is more likely if we determine each individual’s cause of migraines.

Every person’s biochemistry is unique and individualized care is the only way to ensure successful treatment.


1) Triggers: Many things can trigger Migraines; food, stress, environment, wherein the patient is hypersensitive to these stimuli and it initiates a headache.

2) Histamine release: This most often happens in allergic patients wherein some allergen causes a release of histamine and triggers constriction and head pain. Often an avoidance of environmental and food allergens as well as anti-histamines can prevent this migraine. The herb Butterbur works as a natural anti-histamine and will help these migraine patients.

3) Lack of energy production from brain cells: Recent data has confirmed that some migraine sufferers actually cannot produce adequate energy from brain cells to meet the demands, which results in vasospasm. Supplements such as CoQ10, Magnesium, Riboflavin (vitamin B2), and d-ribose can be beneficial in these patients.

4) Dietary allergens: Food allergens should be determined via IgE (acute) and IgG (delayed) allergy testing. Avoiding allergic foods can decrease body inflammation, eliminate triggers, and prevent migraines long term.

Note from Dr. P:

If you have migraines or know someone who does this is a terrible disease. Especially since conventional medicine only suppresses the acute symptoms with drug therapy. Symptom suppression is fine short term but isn’t it better to find out why the cycle is continuing and what you can do about it? This is where Integrative Medicine shines, as we work to uncover the underlying cause and the unique biochemistry of the individual.

Tags:  migraines 

Share |
PermalinkComments (0)

Patch Up Your Menopause

Posted By Administration, Friday, May 6, 2011
Updated: Friday, April 18, 2014


by Shira Miller, MD

You are at the top of your game.  Why not stay there?  

Menopause causes permanent hormone deficiencies which accelerate the aging process, make you feel old, and increase your risk of chronic diseases.  The good news is that it doesn’t have to be that way.  Believe it or not, menopause is already a luxurious experience for many proactive and well-informed men and women.  Yes, even after Mother Nature quits, you can keep your mind, body, and sex life healthy as you age!

This is the premiere post of the “Patch Up Your Menopause” blog, where I will teach you how the hormone deficiencies caused by menopause and male menopause can be, and need to be, safely patched up with bio-identical hormone replacement therapy.  My unique concierge wellness and anti-aging practice, The Integrative Center for Health & Wellness, uses bio-identical hormones and a cutting-edge, science-based, holistic approach to help educated and motivated men and women stay healthy and productive as they age.  

As both menopause and male menopause occur at different ages for different people and may have inconspicuous symptoms, the sooner you know about them the better, especially if you are over 40.

What are your thoughts about menopause and male menopause?

To your luxurious menopause!


Tags:  menopause 

Share |
PermalinkComments (0)

Prolotherapy for Pain

Posted By Administration, Friday, May 6, 2011
Updated: Friday, April 18, 2014

Medical innovations are transforming the science of pain management.

Many South Jersey sports fans remember several years back to when former Flyer Simon Gagne was benched mid-season due to severe post-concussion symptoms, including debilitating head, neck and shoulder pain. Gagne, his coaches and the fans all wondered if he would ever return to the ice.

Dr. Scott Greenberg of the Magaziner Center for Wellness and Anti-Aging in Cherry Hill had also suffered from severe head and neck pain for more than a decade. None of modern medicine’s advanced treatments worked—until he discovered prolotherapy, a nonsurgical, holistic procedure that Greenberg says stimulates the body’s own ability to heal.

Greenberg cured himself by injecting an irritant directly into the affected area, causing his immune system to react and heal the damaged tissue or tendon. Then, he went to work on Gagne—who eventually went on to play in the 2010 Stanley Cup Finals—and many other professional athletes and South Jersey residents of all ages.

Chronic pain is a condition that affects many people. Many hope at most to merely manage that pain, whether with over-the-counter painkillers like Motrin or Tylenol or narcotics like oxycodone. But pain-management specialists in South Jersey say there are better ways. These include everything from plasma injections to tiny needle-pricks to attack muscle spasms, to interdisciplinary treatments that target psychosomatic symptoms. The results, say local doctors, have been entirely revolutionary revolutionary.

“Chronic use of anti-inflammatory medications can actually make joint problems worse,” Greenberg says. “It’s well documented that they accelerate arthritis, they’re not good for kidneys and liver, they can cause ulcers. They block the healing processes that happen in the body. Instead of masking pain, we want to cure the pain.”

Greenberg does this by seeking out the source: damaged tissue, joints, muscles, nerves, ligaments or tendons. In many cases, he says, prolotherapy can be the solution. “Patients that have tried chiropractic, epidural steroids, nerve blocks and even surgery, can be cured by prolotherapy and platelet-rich plasma treatments,” Greenberg says. Greenberg makes several injections to the damaged area with either a prolotherapy solution or platelet-rich plasma taken directly from the patient’s own bloodstream. Treatment can be effective in as little as a few months or up to a year, depending on the extent of the problem. These therapies can even treat post-concussion symptoms such as dizziness and loss of balance, for which there is no traditional medical remedy. Greenberg says he’s also found success treating cumulative pain problems, too, such as arthritis, tendinitis and carpal tunnel syndrome.

One of the more unique pain management treatments currently available is biopuncture, in which patients are injected with natural, FDA-regulated homeopathic products that stimulate the immune system to promote natural healing. This practice, popularized in Europe, is gaining steam in the United States.

Locally, Dr. Polina Karmazin and Dr. Robert Davis of Integrated Family Medicine in Voorhees are among just a handful of physicians in the country trained to administer the treatment, which can help with everything from localized pain and arthritis to bronchitis and the flu. After a consultation and evaluation, each patient receives a customized treatment targeted to their specific condition.

Thanks to the positive response from South Jersey patients, including 610-WIP radio personality Angelo Cataldi, biopuncture is surging in popularity. “This year, we have been seeing a number of new patients with a serious interest in biopuncture,” says Davis.

Adds Karmazin: “With biopuncture, the healing effect comes from within your body, as opposed to some conventional drugs that tend to simply suppress the symptoms or potentially cause significant side effects.”

As interest in the treatment grows, Davis warns that biopuncture is not the cure-all some may be looking for, but it certainly has a place in pain management.

It has also been indicated for a broad range of other purposes. For one, he notes, “Biopuncture is a great, natural way to prevent and treat colds. Of course, nothing can truly replace the flu shot, but biopuncture is a safe and gentle therapy that can modify a patient’s illness and shorten its duration and intensity.”

However, as people age and cope with life-threatening diseases like cancer, the nature of pain management changes focus. Dr. Stephen Goldfine, chief medical officer for Samaritan Hospice in Marlton, must often address the chronic pain associated with end-of-life care, and his approach is more than physical.

“What I try to bring to the table is looking at the whole person,” Goldfine says. “I really look at who that person is and then try to handle the physical pain as well as the spiritual and emotional side. I even engage with chaplains, who will come in and help me hold spiritual counseling.”

Goldfine finds that, in his patients, physical pain is often compounded by depression. “Looking at a life-threatening illness, the depression can be overwhelming, which turns up the volume on the pain,” he says.

So, he partners with specialists including psychologists, psychiatrists and social workers, to work with clients on things like setting goals for the future. “This is a way we create hope,” Goldfine says. As well, he notes, anti-depressants can also be helpful, taken along with traditional counseling.

Treating both physical and emotional pain is the key to truly improving quality of life for patients—both in palliative care and elsewhere. “We don’t focus on death,” Goldfine concludes. “We focus on our patients living their life.”

Source: Twining, Stephanie. 

Pain, Pain, Go Away. South Jersey Magazine. May 2011 Issue.


Tags:  pain  prolotherapy 

Share |
PermalinkComments (0)

Autism and the Environment: An Undeniable Link

Posted By Administration, Friday, April 29, 2011
Updated: Friday, April 18, 2014


by Allan Magaziner, DO

I just returned from the annual meeting of the American College for Advancement in Medicine (ACAM), on whose Board I serve. As always, I left excited about the many advances being made in the field of integrative medicine. 

At the conference, there was much discussion about the impact of the environment on a person’s health and wellbeing. I felt compelled to touch on this topic here immediately as April is Autism Awareness Month and, in my professional opinion, there is no way to deny the link between environmental factors and the appearance – and, often, the severity – of autism and related disorders. 

Consider this alarming finding from a recent study of 10 newborn children: Upon birth, the average person has already been exposed to more than 200 chemicals. In fact, when the cord blood of these infants was analyzed, 287 different chemicals were identified…at birth!  

This is incredibly dangerous since, at birth, the blood-brain barrier is not yet developed so these chemicals are not blocked in any way and therefore can adversely impact brain function. 

So what does this have to do with autism? 

There’s been an increase in recognition of autism over the last 10 years – presently one out of every 90 children have some form of the disorder, which is a condition that causes difficulties with perception, thought, language, behavior and sociability. 

To really understand autism, we need to look at what has changed during this period of rapid diagnosis of the disorder. We know that genetics hasn’t changed. What has changed are environmental factors, including the increasing number of chemicals we are exposed to from pesticides, flame retardants, plasticizers, solvents, personal care products, medicines, artificial sweeteners and flavors. These varied factors have a clear impact on the expression of our genes. 

Each of us is biochemically different, which is why two brothers may have the same genes, but one may develop a disorder while the other never does – even if exposed to the same environmental factors in utero or beyond. Simply put, some people are predisposed to react to a chemical substance differently than others.

It has been found that many autistic children have a defect in their ability to excrete certain chemicals; therefore, they were more genetically susceptible to the chemicals’ effects. Many also have mitochondrial dysfunction and an inability to metabolize high levels of metals which results in neuro-inflammation, oxidative stress, impaired mitochondrial function and neurotransmitter imbalances.  They also often have liver toxicity and gastrointestinal problems. 

What does this mean for prevention of autism? 

While the cause of autism is still not clear, nobody can say definitively at this point that doing one thing or another will completely prevent the disorder. However, looking at the data and reviewing the common denominators in these children, what is clear is that there is an undeniable link between the chemicals found in our environment and autism. The best we can do – to help reduce the numbers and/ or the severity of cases – is to eliminate these chemicals from our lives as much as we can by eating a healthy diet of natural, unprocessed foods rich in vitamins and nutrients, rounding out our diets with nutritional supplements as advised by a healthcare professional and reducing our exposure to phthalates (like those in nail polish), organophosphates (often found in pesticides), PCBs, (found in plastic products including most baby bottles), solvents (found in furniture and new carpets) and heavy metals such as lead and mercury. These measures should, if possible, begin with the mom in the pre- or peri-conception time, at the latest, and continue with the birth of the child.

And what if my child has autism? 

At the Magaziner Center for Wellness, our goal is to help maximize a child’s potential by setting up an individualized program aimed at diagnosing and treating often hidden problems that may be impeding his or her development. We support the use of behavioral counseling and speech, physical and occupational therapies that are often recommended as part of the overall treatment regimen. 

We analyze each patient individually – because, as I’ve said before, each person is biochemically different and, even among those on the autism spectrum, not every treatment works for every person. We administer safe, nontoxic dietary supplements, antifungal agents, and dietary modifications. We also place great emphasis on the detoxification and evaluation and treatment of toxic metals, including mercury, lead, cadmium and aluminum. Treatment may also include improving digestion and assimilation and asking a child to avoid certain foods which could be harmful to his or her wellbeing. We often recommend hyperbaric oxygen therapy, which greatly increases oxygen uptake to the brain, nervous system, skeletal muscle, and all body tissues and has been been found useful in the treatment of the symptoms of autism.

What’s Next? 

While autism is still quite a mystery, great strides have been made in increasing the awareness of the disorder and uncovering some clues to its potential causes. With more research, increased commitment and willingness for doctors and patients alike to ask tough questions and demand a change in our environment, I am confident the next 10 years will yield much better news on this front than the previous decade has.

This post has not been tagged.

Share |
PermalinkComments (0)

Natural Treatments for Autoimmune Infertility Concerns

Posted By Administration, Thursday, April 28, 2011
Updated: Friday, April 18, 2014

by Fiona D. McCulloch, BSc, ND

Infertility is a reproductive disease which has an enormous impact on the quality of life for millions of patients. It affects 1 in 5 of all couples, and most patients undergo extensive diagnostic and treatment interventions on their journey to create a family. Infertility has a myriad of causes including endocrine disorders, gynecological disease, infectious disease, circulatory disease and aging and cellular health. Autoimmune disorders are also implicated in reproductive disorders and may especially play a role in unexplained cases of infertility.

It is known that autoimmune diseases such as diabetes, autoimmune thyroiditis and systemic lupus erythematosis are linked to decreased fertility. Other causes of infertility such as premature ovarian insufficiency, endometriosis and polycystic ovarian syndrome include autoimmune components. In many unexplained cases of infertility, inflammatory processes may be involved or antibodies may be directed against hormones, clotting factors, or reproductive tissues such as the ovaries or testes. The research into autoimmune infertility is just in its beginning, but as naturopathic physicians there are valuable tests and treatments we can provide to our patients who present either with known autoimmune disorders and difficulty conceiving, or with the ever enigmatic diagnosis of “unexplained infertility”.

The biological factors involved in autoimmune infertility are various. These include a multitude of cellular and inflammatory changes. Some of the most common factors are discussed below.


Endometriosis has many autoimmune components including elevated levels of cytokines, and T- and B-cell abnormalities. Peripheral monocytes are more active, and peritoneal macrophages are present in higher numbers with higher activity levels. This causes increased inflammatory cytokine release.

There are alterations in B-cell activity and an increased incidence of autoantibodies in women with endometriosis. Like classical autoimmune diseases, endometriosis has been associated with polyclonal B-cell activation, immunological abnormalities in T- and B-cell functions, increased apoptosis, tissue damage, multiorgan involvement, familial occurrence, possible genetic basis, involvement of environmental cofactors, and association with other autoimmune diseases. TNF-a, levels are elevated in the peritoneal fluid of patients with endometriosis. In women with endometriosis, TH2 mediated immunity humoral responses are commonly elevated.

A 2001 study found that 50% of endometriosis patients had autoantibodies to candida enolase. The same study found increased levels of these antibodies in patients with a list of other autoimmune conditions.

Autoimmune thyroid disease and infertility.

Thyroid diseases involving antithyroid antibodies have been correlated to infertility and increased pregnancy loss. Autoimmune thyroid disease, even in the absence of hypothyroidism has been associated with infertility and reduced response to fertility treatment. It has also been associated with gluten related autoimmunity. Autoimmune thyroid disease can lead to hypo or hyperthyroidism which can impact fertility and cause miscarriage.

Other Autoimmune Diseases and Fertility

Antinuclear antibodies (ANAs ) which have been associated with infertility can be present in conditions such as SLE, Sjogren’s syndrome, Raynaud’s syndrome, and can also be detected in women with a history of exposure to chemicals such as bisphenol-A.

Addison’s disease is associated with anti-ovarian antibodies which can reduce ovulatory function and cause premature ovarian failure in severe cases.

Patients with celiac disease may have multiple nutritional deficiencies that can lead to infertility. Celiac disease has been linked to recurrent miscarriage, pregnancy complication and infertility. A 2010 study found that between 5-10% of women with a history of stillbirth, recurrent miscarriage, intrauterine growth restriction, and infertility were seropositive for transglutaminase IgA compared to 1% of the control group. Latent celiac disease may be a major cause of unexplained infertility.

In approximately 20% of women with premature ovarian insufficiency(POI), autoimmune factors can be found. POI can be linked to autoimmune thyroid disease, Addison’s disease, or SLE or may have unknown etiology. Women may have antibodies against the ovarian tissues, or reproductive hormones such as FSH.

Antisperm antibodies are another cause of infertility. These can be present in either male or female patients. They are commonly found in males after vasectomy procedures, and their presence can make vasectomy difficult to reverse. Antisperm antibodies affect the ability of the sperm to penetrate the egg or reduce motility by attaching to the tail of the sperm . They have also been associated with antiphospholipid antibodies. Antisperm antibodies are generally produced by CD19+/5+ B cells and are associated with elevated natural killer cells and anti-dna antibodies.

Autoimmune blood clotting disorders

Disorders with increased antiphospholipid antibodies( APAs) including anti-cardiolipin antibodies cause a hypercoagulatory state in the blood and can be associated with reproductive failure and recurrent miscarriage. These antibodies can be found in systemic diseases such as SLE, or on their own.

Immunological Considerations for Patients with Reproductive Challenges

TH1/TH2 Ratios

A condition of TH1 cytokine dominance can be associated with the inability to conceive or maintain a pregnancy. In women with high TH1/TH2 ratios there is an increased incidence of pregnancy loss and infertility however for different autoimmune conditions the predominant immune pathway may differ.

Natural killer(NK) cells

Elevated peripheral NK cells are associated with many systemic autoimmune diseases but can also be found in women with unexplained infertility conditions. NK cells produce TH1 cytokines including TNF-alpha and Interferon gamma. These cytokines are normally involved in cellular toxicity directed at cancerous cells and viruses . If increased in early pregnancy, the presence of NK cells and their cytokines can disrupt the growth and development of the embryo. TNF-alpha works as a signal to other immune cells which then migrate to the uterus to attack the non-self invader which has been immunologically detected. A 1999 study found that in women who had repeated miscarriage, there was markedly increased NK cell cytotoxicity associated with a rise in CD56+CD16+ and a drop in CD56+ cells. Another special type of NK cell called uterine NK (uNK) cells have a protective immunosuppressive effect locally in the endometrium. Dysfunction of these cells has been associated with pregnancy loss

Homocysteine and Folate Metabolism

ciency and hyperhomocysteinemia are known to be risk factors for infertility and pregnancy complications. Errors in these pathways caused by genetic mutations have been associated with autoimmune diseases Patients with a mutation of the MTHFR gene have difficulty reducing 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate. 5- methyltetrahydrofolate is used to convert homocysteine to methionine by the enzyme methionine synthase. A 2010 study on a group of 71 Swedish and Finnish female patients with unexplained infertility found a higher incidence of folate metabolism polymorphisms compared to women in the general population. Folate receptor blocking autoantibodies have also been related to subfertility

Folate metabolism disorders can can lead to reduced cell division, inflammatory cytokine production, altered nitric oxide metabolism, increased oxidative stress, abnormal methylation reactions and thrombosis. This causes problems with folliculogenesis and implanting or maintaining a healthy pregnancy. In males, defects in this pathway can impair spermatogenesis.

Diagnostic testing in the naturopathic clinic

In addition to general and endocrine panels for infertility, consider testing for homocysteine, CRP, ESR, ANA panels, APA panels, PTT, Partial PTT, DHEA-S, TSH, Antithyroglobulin, Antithyroid peroxidase, HBA1C, CBC, diurnal cortisol, assessments for candida, and gluten sensitivity testing.

Clinically, I have found that optimal homocysteine levels should be 8mmol/L or below in patients with autoimmune infertility factors.

TH1 to TH2 ratios can be a very helpful tool for designing treatment plans. NK assays and testing for genetic variants of MTHFR are also available.

Conventional treatments:

These vary depending on results found and can include low dose aspirin, anti-coagulants, corticosteroids, IVIG, Lymphocyte immunization therapy (LIT) and TNF-alpha blockers. These are often combined with IVF or other assisted reproductive technologies.

Treatments in the naturopathic clinic

Some of the following treatment options may be considered after a thorough assessment determines specific autoimmune factors.

  1. To reduce TH1 dominant inflammatory responses in patients who require it, maritime pine extract (100mg bid), resveratrol ,(100mg bid) , and green tea EGCG (300mg catechins bid), . Maritime pine, and resveratrol also inhibit platelet aggregation and thrombosis,,. The antioxidant effects of these substances are also beneficial.
  2. Proline rich polypeptides such as those found in bovine colostrum may favour a shift towards TH1 and downregulate overactive TH2 responses.
  3. High quality omega 3 fish oil. 2 – 3g of EPA and DHA qd to aid with inflammatory and thrombotic disorders . A 2007 study on mice found that a ratio of 23:14 EPA :D HA decreased tnf alpha in 8 hours. EPA also regulates autoimmune markers in endometriosis
  4. L-5-methyltetrahydrofolate 5mg daily, vitamin B12 1000mcg qd and vitamin B6 75mg qd to improve homocysteine and folate metabolism. Screen for history of cancer before using high dose folate. Trimethylglycine 1000mg qd may also be used to lower homocysteine levels in selected patients.
  5. N-Acetyl Cysteine 600mg bid. Reduces inflammatory cytokines. Improves autoimmune thyroid disease NAC also enhances semen parameters and the oxidative status and quality of the endometrium . NAC also protects the integrity of ovaries subjected to physical and oxidative damage, and aids liver detoxifcation pathways.
  6. For patients with thyroid antibodies, l-selenomethionine 200mcg daily,,,. If hypothyroid, use of bio-identical hormone therapy may be indicated to prevent miscarriage. Trace minerals for thyroid function are also be beneficial.
  7. Thyroid protomorphogen may be useful for patients with antithyroid antibodies to act as a decoy. Increase dosage slowly to 1 tablet tid.
  8. Elimination of gluten should be implemented as required for patients with positive serology.
  9. Probiotics 20 billion CFUs daily. Rotate strains monthly to modulate immunity and repair gut lining. Treat candida if present.
  10. Support liver detoxification pathways.
  11. Bio-identical progesterone is a potent immunosuppressive agent capable of blocking both cytokine release and action . May be used in the luteal phase of the cycle to support early pregnancy.
  12. DHEA – can be useful in premature ovarian insufficiency and to improve pregnancy rate and reduce miscarriage in advanced maternal age. It has also been found to be beneficial in the treatment of autoimmune disease,, and to reduce NK cell activity. DHEA should only be used after serum DHEA-S and androgen evaluation. Dose adjusted according to patient need but is often 25mg tid or less.
  13. Addressing stress is very important in all patients suffering from the effects of reproductive challenges. Autoimmune diseases are aggravated by stress as it can increase humoral immunity and shift TH1:TH2 ratios. Adrenal therapies, sufficient sleep, yoga, meditation, movement therapy, and prayer can all positively effect patients in this journey


  1. Beer, A, Kantecki J, Reed J.  Is your Body Baby Friendly?  1st edition. AJR Publishing 2006.
  2. Nothnick, WB.  Treating endometriosis as an autoimmune disease. Fertility and sterility. 2001 Aug;76(2): 223-231.
  3. Antsiferova YS, Sotnikova NY, Posiseeva LV, Shor AL. Changes in the T-helper cytokine profile and in lymphocyte activation at the systemic and local levels in women with endometriosis. Fertil Steril. 2005;84(6):1705-11.
  4. Gitlits VM, Toh BH, Sentry JW. Disease association, origin, and clinical relevance of autoantibodies to the glycolytic enzyme enolase.J Investig Med. 2001. 49(2):138-45.
  5. Kim NY, Cho HJ, Kim HY, et al. Thyroid Autoimmunity and its Association with Cellular and Humoral Immunity in Women with Reproductive Failures. Am J Reprod Immunol. 2011;65(1):78-87
  6. Ott J,  Aust S,  Kurz  C et al. Elevated antithyroid peroxidase antibodies indicating Hashimoto’s thyroiditis are associated with the treatment response in infertile women with polycystic ovary syndrome. Fertility and sterility. 2010;94(7): 2895-2897.
  7. Guliter S, Yakaryilmaz F, Ozkurt Z, et al. Prevalence of coeliac disease in patients with autoimmune thyroiditis in a Turkish population. World J Gastroenterol 2007; 13(10): 1599-1601
  8. Geva E, Lerner-Geva L, Burke M, Vardinon N, Lessing JB, Amit A. Undiagnosed systemic lupus erythematosus in a cohort of infertile women. Am J Reprod Immunol. 2004;51(5):336-40.
  9. Kumar A, Meena M, Begum N, et al. Latent celiac disease in reproductive performance of women  Fertility and sterility 24 November 2010. Epub ahead of print
  10. Yamada H, Atsumi T, Kato EH, et al. Prevalence of diverse antiphospholipid antibodies in women with recurrent spontaneous abortion.Fertil Steril. 2003;80(5):1276-1278.
  11. Kwak-Kim JY, Chung-Bang HS, Ng SC, et al. Increased T helper 1 cytokine responses by circulating T cells are present in women with recurrent pregnancy losses and in infertile women with multiple implantation failures after IVF. Human Reproduction. 2003;18(4):767-73.
  12. Emmer P, Nelen W, Steegers, E et al.  Peripheral natural killer cytotoxicity and CD56posCD16pos cells increase during early pregnancy in women with a history of recurrent spontaneous abortion Hum. Reprod. (2000) 15(5): 1163-1169
  13. Dosiou C, and Giudice  LC. Natural Killer Cells in Pregnancy and Recurrent Pregnancy Loss: Endocrine and Immunologic Perspectives.  Endocr. Rev. 2005;26(1):44-62.
  14. Tamura T, Picciano MF. Folate and human reproduction. Am J Clin Nutr. 2006;83:993–1016
  15. Mao R, Fan Y, Zuo L, et al. Association study between methylenetetrahydrofolate reductase gene polymorphisms  and Graves’ disease. Cell Biochem Funct. 2010; 28(7): 585-90.
  16. Brustolin S, Giugliani R, Felix TM. Genetics of homocysteine metabolism and associated disorders. Braz J Medio Res, 2010; 43(1):1-7
  17. Klotz L, Farkas M, Bain N, et al.  The variant methylenetetrahydrofolate reductase c.1298A>C (p.E429A) is associated with multiple sclerosis in a German case-control study. Neurosci Lett. 2010; 468(3):183-5.
  18. Altmäe S, Stavreus-Evers A, Ruiz JR, et al. Variations in folate pathway genes are associated with unexplained female infertility.Fertil Steril. 2010;94(1):130-7.
  19. Klotz L, Farkas M, Bain N, et al. The variant methylenetetrahydrofolate reductase c.1298A>C (p.E429A) is associated with multiple sclerosis in a German case-control study. Neurosci Lett. 2010; 468(3):183-5.
  20. Safarinejad MR, Shafiei N, Safarinejad S. Relationship Between Genetic Polymorphisms of Methylenetetrahydrofolate Reductase (C677T, A1298C, and G1793A) as Risk Factors for Idiopathic Male Infertility. Reprod Sci. 2010 Oct 26 [Epub ahead of print]
  21. Cho KJ et al.  Inhibition mechanisms of bioflavonoids extracted from the bark of Pinus maritime on the expression of pro inflammatory cytokines. Ann NY Acad Sci. 2001;(928)141-56.
  22. Falchetti R, Fuggetta MP, Lanzilli G, Tricarico M, Ravagnan G. Effects of resveratrol on human immune cell function. Life Sci. 2001; 21;70(1):81-96.
  23. Tian J, Gao J, Chen J, et al. Effects of resveratrol on proliferation and apoptosis of TNF-alpha induced rheumatoid arthritis fibroblast-like synoviocytes. Zhongguo Zhong Yao Za Zhi. 2010;35(14):1878-82.
  24. Zvetkova E, Wirleitner B, Tram NT, Schennach H, Fuchs D. Aqueous extracts of Crinum latifolium (L.) and Camellia sinensis show immunomodulatory properties in  human peripheral blood mononuclear cells. Int Immunopharmacol. 2001;1(12):2143-50.
  25. Gillespie K, Kodani I, Dickinson DP, et al. Effects of oral consumption of the green tea polyphenol EGCG in a murine model for human Sjogren’s syndrome, an autoimmune disease. Life Sci. 2008 Oct 24;83(17-18):581-8.
  26. Araghi-Niknam M, Hosseini S, Larson D, Rohdewald P, Watson RR. Pine bark extract reduces platelet aggregation. Integr Med. 2000 Mar 21;2(2):73-77
  27. Belcaro G, Cesarone MR, Rohdewald P, et al. Prevention of venous thrombosis and thrombophlebitis in long-haul flights with pycnogenol. Clin Appl Thromb Hemost. 2004 Oct;10(4):373-7
  28. Olas B, Wachowicz B, Saluk-Juszczak J, Zielinski T. Effect of resveratrol, a natural polyphenolic compound, on platelet activation induced by endotoxin or thrombin. Thromb Res. 2002 Aug 15;107(3-4):141-5.
  29. Figueras M, Olivan M, Busquets S, López-Soriano FJ, Argilés JM. Effects of Eicosapentaenoic Acid (EPA). Treatment on Insulin Sensitivity in an Animal Model of Diabetes. Improvement of the Inflammatory Status. Obesity (Silver Spring). 2010 Sep 30. [Epub ahead of print]
  30. Vanschoonbeek K, Feijge MA, Paquay M, et al. Variable hypocoagulant effect of fish oil intake in humans: modulation of fibrinogen level and thrombin generation. Arterioscler Thromb Vasc Biol. 2004 Sep;24(9):1734-40.
  31. Dangardt F, Osika W, Chen Y, et al. Omega-3 fatty acid supplementation improves vascular function and reduces inflammation in obese adolescents. Atherosclerosis. 2010; 212(2):580-5.
  32. Bhattacharya A, Sun D, Rahman M, Fernandes G. Different ratios of eicosapentaenoic and docosahexaenoic omega-3 fatty acids in commercial fish oils  differentially alter pro-inflammatory cytokines in peritoneal macrophages from C57BL/6 female mice. J Nutr Biochem. 2007 Jan;18(1):23-30.
  33. Netsu S, Konno R, Odagiri K, Soma M, Fujiwara H, Suzuki M. Oral eicosapentaenoic acid supplementation as possible therapy for endometriosis. Fertility and sterility. 2008; (90)4: 1496-1502.
  34. Stanislaus R, Gilg AG, Singh AK, Singh I. N-acetyl-L-cysteine ameliorates the  inflammatory disease process in experimental autoimmune encephalomyelitis in Lewis rats. J Autoimmune Dis. 2005 May 3;2(1):4.
  35. Poncin S,  Colin IM, Decallonne B, et al. N-Acetylcysteine and 15 Deoxy-?12,14-Prostaglandin J2 Exert a Protective Effect Against Autoimmune Thyroid Destruction in Vivo but Not Against Interleukin-1a/Interferon ?-Induced Inhibitory Effects in Thyrocytes in Vitro.The American journal of pathology. 2010;177(1)219-228
  36. Ciftci H, Verit A, Savas M, Yeni E, Erel O. Effects of N-acetylcysteine on semen parameters and oxidative/antioxidant status.Urology. 2009;74(1):73-6.
  37. Estany S, Palacio JR, Barnadas R, Sabes M, Iborra A, Martínez P. Antioxidant activity of N-acetylcysteine, flavonoids and alpha-tocopherol on endometrial cells in culture. J Reprod Immunol. 2007; 75(1):1-10.
  38. Mishra DP, Dhali A. Endotoxin induces luteal cell apoptosis through the mitochondrial pathway. Prostaglandins Other Lipid Mediat. 2007;83(1-2):75-88.
  39. Usta U, Inan M, Erbas H, Aydogdu N, Oz Puyan F, Altaner S. Tissue damage in rat ovaries subjected to torsion and detorsion: effects of L-carnitine and N-acetyl cysteine. Pediatr Surg Int. 2008; 24(5):567-73
  40. Zagrodzki P, Ratajczak R. Selenium supplementation in autoimmune thyroiditis female patient–effects on thyroid and ovarian functions (case study). Biol Trace Elem Res. 2008; 126(1-3):76-82.
  41. Turker O, Kumanlioglu K, Karapolat I, Dogan I. Selenium treatment in autoimmune thyroiditis: 9-month follow-up with variable doses. J Endocrinol. 2006;190(1):151-6.
  42. Negro R, Greco G, Mangieri T, Pezzarossa A, Dazzi D, Hassan H. The influence of selenium supplementation on postpartum thyroid status in pregnant women with thyroid peroxidase autoantibodies. J Clin Endocrinol Metab. 2007;92(4):1263-8.
  43. Gärtner R, Gasnier BC, Dietrich JW, Krebs B, Angstwurm MW. Selenium supplementation in patients with autoimmune thyroiditis decreases thyroid peroxidase antibodies concentrations. J Clin Endocrinol Metab. 2002; 87(4):1687-91.
  44. Howard L. Weiner, MD. Oral tolerance for the treatement of autoimmune disease. Annual Review of Medicine. 1997; (48): 341-351.
  45. Raghupathy R, Al-Mutawa E, Al-Azemi M, Makhseed M, Azizieh F, Szekeres-Bartho  J. Progesterone-induced blocking factor (PIBF) modulates cytokine production by lymphocytes from women with recurrent miscarriage or preterm delivery. J Reprod Immunol. 2009 Jun;80(1-2):91-9
  46. Mamas L, Mamas E. Premature ovarian failure and dehydroepiandrosterone Fertil Steril.2009;91(2):644-646.
  47. Gleicher N, Ryan E, Weghofer A, Blanco-Mejia S, Barad DH. Miscarriage rates after dehydroepiandrosterone (DHEA) supplementation in women with diminished ovarian reserve: a case control study. Reprod Biol Endocrinol. 2009 Oct 7;7:108.
  48. Solerte SB, Precerutti S, Gazzaruso C, et al. Defect of a subpopulation of natural killer immune cells in Graves’ disease and Hashimoto’s thyroiditis: normalizing effect of dehydroepiandrosterone sulfate. Eur J Endocrinol. 2005;152(5):703-12.
  49. Crosbie D, Black C, McIntyre L, Royle PL, Thomas S. Dehydroepiandrosterone for systemic lupus erythematosus. Cochrane Database Syst Rev. 2007;(4):CD005114
  50. Hazeldine J, Arlt W, Lord JM. Dehydroepiandrosterone as a regulator of immune  cell function. J Steroid Biochem Mol Biol. 2010;120(2-3):127-36.
  51. Calcagni E, Elenkov I. Stress system activity, innate and T helper cytokines,  and susceptibility to immune-related diseases. Ann N Y Acad Sci.2006;1069:62-76


This post has not been tagged.

Share |
PermalinkComments (0)

Acupuncture Relieves Anxiety Before Surgery

Posted By Administration, Wednesday, April 20, 2011
Updated: Friday, April 18, 2014


by Nalini Chilkov, LAC, OMD

Who is calm and relaxed before surgery? I don’t know too many patients who are not anxious before surgery. Patients participating in a study in China who received acupuncture prior to surgery reported a greater than 50% decrease in their anxiety.

When patients have high levels of anxiety and stress hormones, lose sleep and cannot relax before an operation, the capacity to withstand the physiologic stress of surgery is decreased. This compromises the patient’s chances for a good outcome free of complications. Furthermore, having a good healing of surgical incisions, improved resistance to infection, normal digestion and elimination, restful sleep and decreased pain are all enhanced  when a patient is less anxious and is experiencing less stress.

While there are many ways to help patients deal with the stressors associated with surgery, acupuncture is a cost effective method that can be offered to pre-surgical patients.

Although the study participants were all adults, children who are facing surgery would also benefit from the calming effects of acupuncture.

Additionally, other studies have shown that acupuncture modulates immune function further improving resistance to infection which is important after surgery and  especially while in the hospital environment where risk of infection is much higher.

It is common to see patients in Chinese hospitals have the benefit of BOTH modern biomedicine as well as Traditional Chinese Medicine.

We live in a time with access to a wide array of healing and medical modalities. Whether that be the scalpel or the acupuncture needle, it is of great benefit to offer patients an Integrative and Collaborative approach to health care.


Tags:  acupuncture  anxiety  surgery 

Share |
PermalinkComments (0)

Five Foods to Keep you Healthy and Well

Posted By Administration, Wednesday, April 13, 2011
Updated: Friday, April 18, 2014

Dr. Magaziner was interviewed live by Pat Ciarrochi on CBS' "Talk Philly" on April 12th. During the segment, he served up valuable information about the five foods he deems fabulous for health and wellness.
These super foods include salmon, which is high in Omega-3 fatty acids and helps reduce inflammation, risk of heart disease and triglycerides, while helping combat depression, memory loss and arthritis; sweet potatoes, which are high in Vitamin A, antioxidants and calcium to help in maintaining bone density; celery, which can help lower blood pressure and stress; buckwheat, which stabilizes both blood sugar and blood pressure and cinnamon, which can help reduce blood sugar.

For more info on "meals that heal," please visit


Tags:  diet  food and drink 

Share |
PermalinkComments (0)

Bacteria to the Rescue

Posted By Administration, Monday, April 4, 2011
Updated: Friday, April 18, 2014


by Dr, Matt Angove, ND

Your intestinal tract is home to approximately 100,000,000,000,000 (100 trillion) microorganism.  Your gut actually has 10x more bacteria than all the cells that make you a human combined.  Perhaps they have some therapeutic function!

This massive array of bacteria is responsible for synthesizing B vitamins, vitamin K , producing digestive enzymes, metabolizing proteins and carbohydrates, breaking down bile salts, enhancing short term and long term immunity, and inhibiting pro inflammatory mediators.  They also breakdown nondigestable carbohydrates like fiber creating short-chain fatty acids, which lower the pH of the intestines creating an environment that is inhospitable to pathogenic bacteria such as E. coli and Salmonella.  Sounds delicious…

Symptoms and diseases associated with mutant gut flora:

Inflammatory bowel disease

Yeast infections

Skin problems (acne, eczema, psoriasis, fungal)



Malabsorption syndrome

Depression and anxiety

Autoimmune disease (SLE, scleroderma, RA, Sjogrens, etc.)


Intestinal cancers (treatment and prevention)

Immune deficient conditions

Build on the Bacteria

If you were going to add one foundational element to your dietary supplement regimen, I would add some living microbes.  Many people think of yogurt as a great way to increase their good bacteria.  It is true many yogurts have bacteria in them that are beneficial to your health.  However, the levels in yogurt or kefir are not enough to overcome disease and dysfunction.  You will need millions of little bacteria to enable the development of a healing environment.

Probiotics are best consumed with a moderate amount of food no warmer than room temperature.

If you are taking antibiotics, probiotics should be taken 1 hour before or 2 hours after the antibiotics.  It is vital if you are taking or have taken antibiotics that you make a concerted effort to reestablished optimal gut flora. 


Tags:  bacteria 

Share |
PermalinkComments (0)

Why 80% of Cancer Patients Use Integrative Medicine

Posted By Administration, Monday, March 28, 2011
Updated: Friday, April 18, 2014

by Nalini Chilkov, LAC, OMD

Approximately 83 percent of people with cancer use at least one complementary and alternative medicine (CAM) modality (11).

Using my experience as a health and wellness expert, I have compiled a list of what cancer patients say about the choices they make regarding cancer treatment:

  •  To be proactive, to take control, to  take charge of decisions that affect my care, my health, my experience, my results and outcomes.
  • To participate in my own care and my own decisions rather than giving power to make all decisions away to my care providers.
  • To feel a sense of empowerment rather than be disenfranchised and disempowered.
  • To decrease and manage my fear, stress and anxiety and to support, increase and improve my peace of mind.
  • To ask my care providers to work with me as a team and to show respect for my values, my feelings and my choices in all decisions.
  • I choose to reject an approach based solely on a 'war on cancer' that only targets my cancer tumor cells and neglects the whole person and the environment.
  • I choose a comprehensive care approach using a wide range of therapies, tools and resources from many traditions and many points of view.
  • I choose individualized and targeted care which views me and my cancer as unique and in which decisions and choices are based on a careful analysis of the traits and characteristics of my cancer cells and my unique physiology, genetics and risk factors rather than a generic one size fits all approach.
  • I choose humane, caring and compassionate whole person patient centered care for my body, mind and spirit.
  • I choose safe and non toxic therapies whenever possible.

  • To actively manage and reduce both short term and long term toxic side effects from conventional cancer treatments such as surgery, chemotherapy, radiation therapy, hormones and other drugs used by oncologists, radiologists and surgeons.
  • To manage and reduce my pain with safe and non-toxic therapies.
  • To enhance and improve the therapeutic benefit and effect of my treatments.
  • To enhance and improve my survival.
  • To use therapies that prevent further cancers and recurrences or that may increase and extend my disease free time to recurrence.
  • To enhance and improve the quality of my life during and after cancer treatment.
  • To support and strengthen my sense of well-being.
  • To feel a sense of hope over hopelessness and despair.
  • To include a plan and a goal for health and wellness in my cancer journey.
  • To clearly recognize that absence of disease is not the same as rebuilding, nourishing and sustaining health and healthy function.
  • To protect, support and stimulate all systems including my immune system, digestive system, heart, liver, kidneys, brain, skin and bone marrow affected by my treatments.
  • To protect my cells, tissues and organs from damage during my treatment.
  • To grow and develop effective coping strategies for myself.
  • To address the continuous small and large traumatic experiences that cancer patients undergo as part of every stage of my cancer journey.
  • To develop and cultivate positive, supportive healing relationships with my care providers, my team.
  • To utilize integrative cancer care and alternative treatments when the conventional oncology treatment offered to me is perceived as worse than the disease itself.
  • To utilize integrative cancer care when there are no conventional oncology treatments that offer me a therapeutic benefit.
  • To utilize integrative oncology care when the known risks of conventional oncology treatments are greater than the known benefits of those treatments.
  • To utilize integrative cancer and alternatives to conventional care and to use integrative cancer care without conventional oncology treatments when there are no effective  conventional cancer treatments recommended or available to me.
  • To meet the diagnosis and experience of cancer as an opportunity to find meaning, to grow, to develop and to transform emotionally, psychologically and spiritually.
  • I have fundamental confidence in the value and benefits of integrative cancer treatments that address the whole person and have my health, recovery, survival, quality of life and peace of mind (not just absence of disease) as both a short term and a long term goal.

Choosing an integrative cancer care approach makes a significant difference for each unique individual cancer patient.  In this model, the patient is a fully empowered participant in making decisions and choices related to their cancer treatment, cancer recovery and cancer survivorship in concert with their team of care providers.  

This is the goal of evidence based, compassionate person centered health care: combining the best of science and nature, modern knowledge and ancient healing wisdom, in order to transform disease, restore healthy function, wholeness and quality of life to each unique individual patient.  

Rather than a model focused primarily on disease management, this is a model which also includes health, healing and the whole person as well as the internal and external environments of each unique individual to form a matrix in which the continuum of health and disease can be more fully met and understood.  

When a health care model includes not only disease management, but also restored health and function, different choices are made by both patients and care providers.

Even if the disease is not eradicated and recovery is not possible, healing and wholeness may still unfold. Even in terminal illness, when compassionate care becomes the primary care, the patient can achieve integration of the experience and a capacity to face the end of life and make peace with what is so.


1. Block KI, Gyllenhaal C, Tripathy D, Freels S, Mead MN, Block PB, Steinmann WC, Newman RA, Shoham J. Survival Impact of Integrative Cancer Care in Advanced Metastatic Breast Cancer. Breast J. 2009 May 12. [Epub ahead of print] PubMed PMID: 19470134

2. Frattaroli J, Weidner G, Dnistrian AM, Kemp C, Daubenmier JJ, Marlin RO, Crutchfield L, Yglecias L, Carroll PR, Ornish D. Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology. 2008 Dec;72(6):1319-23. Epub 2008 Jul 7. PubMed PMID: 18602144.

3. Molassiotis A, Fernadez-Ortega P, Pud D, Ozden G, Scott JA, Panteli V, Margulies A, Browall M, Magri M, Selvekerova S, Madsen E, Milovics L, Bruyns I, Gudmundsdottir G, Hummerston S, Ahmad AM, Platin N, Kearney N, Patiraki E. Use of complementary and alternative medicine in cancer patients: a European survey. Ann Oncol. 2005 Apr;16(4):655-63. Epub 2005 Feb 2. PubMed PMID: 15699021.

4. Mulkins AL, Verhoef MJ. Supporting the transformative process: experiences of cancer patients receiving integrative care. Integr Cancer Ther. 2004 Sep;3(3):230-7. PubMed PMID: 15312264. 5. Nahleh Z, Tabbara IA. Complementary and alternative medicine in breast cancer patients. Palliat

5. Support Care. 2003 Sep;1(3):267-73. Review. PubMed PMID: 16594427.Support Care. 2003 Sep;1(3):267-73. Review. PubMed PMID: 16594427. 6. Ornish D, Lin J, Daubenmier J, Weidner G, Epel E, Kemp C, Magbanua MJ, Marlin R, Yglecias L,

6. Carroll PR, Blackburn EH. Increased telomerase activity and comprehensive lifestyle changes: a pilot study. Lancet Oncol. 2008 Nov;9(11):1048-57. Epub 2008 Sep 15. Erratum in: Lancet Oncol. 2008 Dec;9(12):1124. PubMed PMID: 18799354.

7. Ornish, D., M. J. Magbanua, G. Weidner, V. Weinberg, C. Kemp, C. Green, M.D. Mattie, R. Marlin, J. Simko, K. Shinohara, C. M. Haqq, and P. R. Carroll. 2008a. Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proc Natl Acad Sci U S A 105 (24):8369-74.

8. Pud D, Kaner E, Morag A, Ben-Ami S, Yaffe A. Use of complementary and alternative medicine among cancer patients in Israel. Eur J Oncol Nurs. 2005 Jun;9(2):124-30. PubMed PMID: 15944105.

9. Verhoef MJ, Balneaves LG, Boon HS, Vroegindewey A. Reasons for and characteristics associated with complementary and alternative medicine use among adult cancer patients: a systematic review. Integr Cancer Ther. 2005 Dec;4(4):274-86. Review. PubMed PMID: 16282504.

10. Verhoef MJ, Mulkins A, Boon H. Integrative health care: how can we determine whether patients benefit? J Altern Complement Med. 2005;11 Suppl 1:S57-65. PubMed PMID: 16332188.

11. Richardson MA, Mâsse LC, Nanny K, Sanders C. Discrepant views of oncologists and cancer patients on complementary/alternative medicine. Support Care Cancer. 2004 Nov;12(11):797-804.
PMID: 15378417

12. Ruth E. Patterson, Marian L. Neuhouser, Monique M. Hedderson, Stephen M. Schwartz, Leanna J. Standish, Deborah J. Bowen, Lynn M. Marshall. The Journal of Alternative and Complementary Medicine. August 2002, 8(4): 477-485. doi:10.1089/107555302760253676.


Tags:  cancer  integrative medicine 

Share |
PermalinkComments (0)
Page 10 of 15
 |<   <<   <  5  |  6  |  7  |  8  |  9  |  10  |  11  |  12  |  13  |  14  |  15
Community Search
Sign In
Sign In securely

9/14/2017 » 9/16/2017
ACAM 2017 Annual Meeting

Latest News