In the “About Us” tab, you will find information about our company history, our mission, and our distribution services.

The “Our Products” tab will guide you to the links of our distribution partners’ websites, so you never have to leave the Purity Life Professionals website in order to navigate through multiple quality leading brands and hundreds of products. The “Affiliations” tab will introduce you to the organizations in the natural health field that we fully support. In our “Account Resources” tab, you will find new account applications and incentives, our price list, monthly specials, the RxBalance order form, and the Purity Life Retail Products Catalogue (some options are password protected-please call us to set up your e-account 1-866-831-4035)

In order to help you serve your clients, we have developed a Home Health site; a place where practitioners and pharmacists can send their patients for product and ingredient information, helpful articles and videos about general health, and eventually webinars. You can also use this site as a reference site to research medical conditions, ingredients, and drug-nutrient depletion and interactions (found under health library).

We hope to develop and improve this site continuously with new and innovative resources, product information and educational material to better serve your every practice needs.

Sincerely,
The Purity Life Professionals Team

[Ed. Note: James LaValle is the founding Director of the LaValle Metabolic Institute, one of the largest integrative medicine practices in the country.  Dr. LaValle is the author of The Metabolic Code Diet: Unleashing the Power of Your Metabolism for Lasting Weight Loss and Vitality and the Executive Editor of THB’s The Healing Prescription.

Introduction
Gluten-sensitive enteropathy (celiac disease) is a heritable inflammatory process of the small intestine, resulting from a genetically based immunologic intolerance to gluten. The disease classically manifests with diarrhea/steatorrhea, weight loss, or failure to thrive. The disease is common among Caucasians, family members and is strongly associated with HLA phenotypes B8, BR3, DQw2. Siblings who share HLA type DQw2 have a 40% likelihood of concordance for celiac disease and monozygotic twins have a 70% concordance. These facts suggest that there are at least two genes that contribute to the risk of developing the disease [1]. Prevalence of the disease in many European countries has been estimated at 1:300[2]. The deleterious proteins causing celiac disease are gliadins, hordeins, and secalins which are derived from wheat, barley and rye [2]. Celiac disease may manifest clinically with an array of nongastrointestinal symptomsamong which are: dermatitis herpetiformis; dementia; depression; various neurological symptoms; osteoporosis; osteomalacia; dental enamel defects, and anemia of various types [1]. Celiac disease has also been associated with endocrine and other diseases including type I diabetes, hypothyroidism, Addison disease, and trisomy 21 [1–4]. Diagnosis is based upon duodenal biopsy demonstrating characteristic changes (loss of villous structures, crypt hyperplasia, lymphoplasmocytic predominance in the inflamed lamina propria, and increased density intraepithelial lymphocytes), accompanied by positive serology to anti-endomysial antibodies and clinical response to a gluten-free diet [1]. Although throughout the recent decades significant data have accumulated regarding the association between celiac disease, male and female fertility and pregnancy, many primary care obstetricians and gynecologists and perinatologists are not aware of these important relationships. The aim therefore of this review is to describe the possible effects of celiac disease and its treatment upon the reproductive cycle, fertility and pregnancy.
Fertility
Female
Among the various nongastrointestinal manifestations of celiac disease little attention has been paid to fertility. Infertility may be the first clinical symptom of subclinical celiac disease. In the early 1970s, Morris et al. [5] described 3 patients in whom active celiac disease was associated with infertility which abated when the disease was controlled with dietary gluten restriction. None of these patients were malnourished or severely anemic, all had normal serum B12 levels and only 1 had low serum folate levels. Spontaneous conception following correction of folate deficiency in a patient with celiac disease without a gluten-free diet was reported by Hirson [6] emphasizing the importance of folate deficiency. Subsequently, a number of large case-control studies regarding fertility in patients with celiac disease were conducted. Fergusson et al. [7] examined the effect of celiac disease on fertility in 74 patients, 54 of whom were on a normal diet, and 20 were on a gluten-free diet and reported that menarche was significantly delayed in untreated patients versus those on a gluten-free diet (15 B 2 vs. 13.5 B 1 years, respectively). In addition 16 of the 54 untreated patients had periods of amenorrhea of above 3 months’
duration compared to 2 of 20 patients on a gluten-free diet. Moreover, early menopause occurred in untreatedpatients compared to controls (45 B 5.5 vs. 53 B 1.2 years, respectively). Molteni et al. [8] compared the obstetrical and gynecological history of 64 patients with recently diagnosed celiac disease and 54 healthy controls matched for age, origin and sexual behavior. Significantly delayed menarche was confirmed among untreated patients with celiac disease (13.5 vs. 12.1 years). Thirty-nine percent of the patients had periods of amenorrhea compared with 9% of controls, and again menopause occurred earlier among patients compared with controls (45.5 vs. 49.5 years) [8]. Sher and Mayberry [9] conducted a questionnaire based case-control study (response rate of 68%) of 68 patients and matched controls. This study confirmed a significantly delayed menarche (13.6 B 1.9 vs. 12.7 B 1.4 years), significantly earlier age of menopause (47.6 B 4.4 vs. 50.1 B 3.5 years), and a significant decrease in the number of children (1.9 B 0.9 vs. 2.5 B 1.2 years), concluding that women with celiac disease are subfertile. Another questionnaire-based case-control study performed by Smecuol et al. [10] demonstrated again that patients with untreated celiac disease had significantly delayed menarche, earlier menopause, and an increased prevalence of secondary amenorrhea. In a reverse fashion, Collins et al. [11] investigated the occurrence of celiac disease among patients with infertility. One hundred and fifty women in the reproductive age group with infertility composed the study group and a similar number of controls consisted of women undergoing sterilization. Circulating IgA class antibodies against reticulin and gliadin were utilized for screening for celiac disease. Positive cases were confirmed by endoscopic small bowel biopsy. Four of 150 (2.7%) women in the infertility group versus none of the control patients were noted to have celiac disease. The incidence of celiac disease among the 98 patients with unexplained infertility was significantly higher (4.1%) [11]. None of the patients with celiac disease had folic acid or B12 deficiency and 2 of 4 had iron deficiency. The authors demonstrated that the observed frequency of positive serology to celiac disease among infertile women is over tenfold the expected in the general population, and concluded that this disease should be considered in the assessment of women with unexplained infertility [11]. Similarly, Meloni et al. [12] assessed the prevalence of celiac disease in 99 couples being evaluated for infertility in comparison with the known prevalence of celiac disease in Sardinia. Three of 99 women (3.03%) had evidence of celiac disease, a significantly higher prevalence than that found in the general population (1.06%). The prevalence was even higher among women with unexplained infertility, 2 of 25 (8%). Only 1 of the 99 males (1.01%) in this series had evidence of celiac disease, a prevalence similar to that of the general population. All celiac patients had normal serum B12 and folic acid levels [12]. Conversely, Kolho et al. [13] screened 47 women with unexplained infertility, 82 women with infertility of a known cause and 51 healthy controls, with anti-endomysium antibodies. They demonstrated a prevalence of 2.1% of celiac disease among patients with unexplained infertility compared to 2% among controls [13]. None of the women with infertility of a known cause had evidence of celiac disease [13]. The latter study notwithstanding, it appears that women with untreated celiac disease tend to have delayed menarche, earlier menopause, increased incidence of amenorrhea and infertility. These findings appear not to be related to the severity of celiac disease or the resulting nutritional status.

Male
In the early 1950s, Cooke et al. [14] noted that 11 of 33 (33%) married celiac patients had childless marriages. No correlation was apparent between infertility and disease stage [14]. With this in mind, male gonadal function was systematically investigated among patients with celiac disease. Green et al. [15] described a reversible androgen resistant, i.e., high plasma testosterone and free testosterone index and elevated plasma luteinizing hormone levels in patients with untreated celiac disease [15]. Farthing et al. [16] noted that 75% of men with untreated celiac disease had reduced sperm motility and 46% had abnormal sperm morphology. The abnormal morphology appeared to improve on a gluten-free diet [16]. Hypogonadism was noted in 7% of infertile men with celiac disease [16]. Baker and Read [17] reported reversal of infertility in 2 patients with oligospermia and low sperm motility on a gluten-free diet. Farthing et al. [16] subsequently reported on endocrine aspects of gonadal function in 41 fertile men with celiac disease in comparison with 19 patients with Crohn’s disease, 13 patients with rheumatoid arthritis, 18 patients with Hodgkin’s disease and 27 healthy controls. Among patients with untreated celiac disease, increased plasma testosterone and free testosterone index, reduced dehydrotestosterone and elevated serum luteinizing hormone were noted, all of which returned to normal as jejunal morphology improved with treatment. These findings were not noted in any of the patients with other diseases, or healthy controls Serum estradiol levels were modestly elevated in 10% of patients with celiac disease and 11% of patients
with Crohn’s disease, with no relation to jejunal morphology following treatment. These authors concluded that androgen resistance and associated hypothalamic-pituitary dysfunction appeared to be specific to the disease, could not be explained by malnutrition or chronic illness, and suggested that these abnormalities may be related to reproductive function in these patients.

Pregnancy
Celiac disease often affects women in their fertile years and malabsorption may interfere with embryogenesis, fetal nutrition and growth. The occurrence of subfecundity is well recognized in association with celiac disease [5, 7, 9–11]. The effects of untreated celiac disease on conception, recurrent miscarriage, fetal growth restriction, birth weight and perinatal outcome has been addressed by case reports [19–21] and cohort- or case-controlled studies. In the early 1970s, Ogborn [22] reviewed the outcomes of 60 pregnancies in 25 patients with celiac disease. Of these, 38 pregnancies occurred in mothers on normal diets and 22 on gluten-free diets [22]. Abortions and fetal growth restriction were the main problems associated with untreated disease occurring at rates of 21 and 16%, respectively, in comparison to 4 and 18%, respectively, among patients on gluten-free diets. Nevertheless, successful pregnancies occurred both before and after diagnosis and treatment. A cohort Danish study which included 211 newborns to 127 mothers with celiac disease and 1,260 control deliveries examined birth weight, low birth weight (! 2,500 g) and intrauterine growth retardation in relation to disease status and treatment. The mean birth weight of newborns to patients with untreated celiac disease was significantly lower (238 g) than that of control patients. Birth weight was 67 g higher among patients with treated celiac disease in comparison with controls [23]. The odds
ratio of increased risk of low birth weight among newborns of patients with untreated disease was 2.6 (95% CI 1.3–5.5), and the risk for fetal growth restriction was 3.4 (95% CI 1.6–7.2). No increased risk of low birth weight or fetal growth restriction was observed among newborns of treated patients, suggesting treatment is of importance in reducing the incidence of fetal growth restriction [23]. Ciacci et al. [24] conducted a case-control, before and after study regarding the effect of a gluten-free diet onpregnancy outcome and lactation in 125 patients. Three types of analysis were performed. The first examined pregnancy outcome in untreated versus treated patients with celiac disease. These authors noted that the individual/ abortion ratio was six times higher in nontreated versus treated patients, the prevalence of abortion being 17.8% among untreated patients versus 2.4% in treated patients, the relative risk being 8.9 times higher among untreated patients (95% CI 1.19–66.3). Also noted was a higher incidence of low birth weight/pregnancy ratio, with no difference in the rate of premature deliveries [24]. The second analysis assessed subclinical celiac disease and its effects on pregnancy outcome. No significant differences regarding abortion rate, threatened abortion, premature delivery, low birth weight and duration of breastfeeding was noted in patients with subclinical versus clinical disease. Finally, the intraindividual effect of a gluten-free diet on pregnancy outcome was assessed in 12 of the patients. The prevalence of abortion decreased from 43.3 to 7.7% when a gluten-free diet had been implemented, the relative
risk of abortion decreased by 9.18 (95% CI 1.05– 79.9), and the low birth weight from 29.4 to 0%. The duration of breastfeeding increased by 2.5 months among treated patients [24]. An increased incidence of miscarriage among patients with untreated celiac disease has been reported by a number of authors [7–10, 13]. Sher and Mayberry [9] reported a 15% spontaneous abortion rate among patients with untreated celiac disease, significantly increased in comparison with normal controls (6%). Following a glutenfree diet, the abortion rate among patients with celiac disease was similar to that of controls (7%). The stillbirth rate of patients with untreated celiac disease was 7 of 127 (5.52%), significantly higher than normal controls among whom the stillbirth rate was 1 of 162 (0.6%). These authors concluded that patients with untreated celiac disease have higher spontaneous abortion and stillbirth rates [9]. Molteni et al. [8] also noted a higher incidence of repeated abortions among patients with untreated celiac disease, 26 of 96 (27%) in comparison with 10 of 69 (6.9%) among controls. Furthermore, 5 of 38 patients with untreated celiac disease had repeated spontaneous abortions compared with none of the controls [8]. Fergusson et al. [7] reported a 17.8% abortion rate among 112 pregnancies of patients with untreated celiac disease, which decreased significantly when a gluten-free diet was implemented (9%). Six of 112 (5.4%) pregnancies ended in stillbirth, and 5 neonatal deaths occurred among patients with untreated celiac disease. Stillbirth was not recorded among patients with celiac disease on a glutenfreediet, and only 1 neonatal death occurred in this group of patients [7]. It should be emphasized that data regarding previous abortions may be affected by recall bias, as is noted by the wide range of reported rates of miscarriage in the control groups. Conversely, Kolho et al. [13] screened all patients seen because of recurrent miscarriage (63) for celiac disease utilizing IgA anti-endomysium antibodies [13]. Only 1 patient with recurrent abortions had celiac disease (1.6%), which was no different than observed among healthy controls [13].Periconceptual multivitamin supplementation (folic acid, B12) protects against neural tube defects. Dickey al. [25] investigated the possibility that celiac disease might be a maternal risk factor for neural tube defects as it may be associated with either folic acid or B12 deficiency. These authors screened 60 mothers of children with neural tube defects using IgA anti-endomysium antibodies and noted only 1 patient who had celiac disease (1.6%), and concluded that maternal celiac disease (and its dietary consequences) did not cause neural tube defects but rather folate deficiency [25]. Thus the literature supports the hypothesis that improvement of the disease associated with treatment may improve fetal nutritional support and overall perinatal outcome.

Effects of Pregnancy upon Celiac Disease
At times, reactivation of previously quiescent, deterioration of known, or unmasking of previously undiagnosed celiac disease has been reported during pregnancy or the puerperium [26–29]. Whitefield [29] reported in the early 1970s an incidence of 0.35% of malabsorption during pregnancy which subsequently led to the diagnosis of masked or exacerbated celiac disease. Malabsorption was present in 27 of 45 (60%) patients in whom megaloblastic anemia was diagnosed for the first time and in 7 of 9 (78%) pregnancies complicated by recurrent megaloblastosis [29]. Malnick et al. [27] described 3 patients in whom acute celiac disease presented in the puerperium and reviewed the literature which consists of 19 such patients. These authors postulate that an immune mechanism may explain the association of pregnancy and exacerbation of the disease. One of the speculated causes are the effects of pregnancy-related hormone on the immune system [27]. Smecuol et al. [10] found clinical deterioration in 22 of 130 (17%) pregnancies of patients with untreated celiac disease. Moreover, celiac disease was manifested for the first time during pregnancy (n = 7) or puerperium (n = 4) in 14% of patients [10]. Fergusson et al. [7] investigated the maternal health of patients with celiac disease during pregnancy and noted that the number of patients on a gluten-free diet in good general health was significantly higher than untreated patients (100 vs. 52%, respectively), with less diarrhea (3.3 vs. 37.3%, respectively), and free of abdominal pain (0 vs. 21%, respectively). These authors concluded that pregnancy did not cause serious health problems among mothers with celiac disease [7].

References
1 Murray JA: The widening spectrum of celiac disease. Am J Clin Nutr 1999;69:354–365.
2 Greco L, Di Donato F, Ansaldi N, et al: Analysis of incidence trends: An example from the Italian cohort; in Auricchio S, Visakorpi JK (eds): Common Food Intolerances. 1. Epidemiology of Coeliac Disease. Basel, Karger, 1992, pp 25–34.
3 Baker PG, Read AE: Oats and barley toxicity in coeliac patients. Postgrad Med J 1976;52:264–268.
4 Talal AH, Murray JA, Goeken JA, et al: Celiac in an adult population with insulin-dependent diabetes mellitus: Use of endomysial antibody testing. Am J Gastroenterol 1997;92:1280–1284.
5 Morris JS, Adjukiewicz AB, Read AE: Coeliac infertility: An indication for dietary gluten restriction. Lancet 1970;i:213.
6 Hirson C: Coeliac infertility – Folic acid therapy. Lancet 1970;i:412.
7 Ferguson R, Holmes GKT, Cooke WT: Coeliac disease, fertility and pregnancy. Scand J Gastroenterol 1982;17:65–68.
8 Molteni N, Bardella MT, Binchi PA: Obstetric and gynecological problems with untreated sprue. J Clin Gastroenterol 1990;12:37–39.
9 Sher KS, Mayberry JF: Female fertility, obstetric and gynaecological history in coeliac disease. Digestion 1994;55:243–246.
10 Smecuol E, Maurino E, Vasquez H, et al: Gynaecological and obstetric disorders in celiac disease: Frequent clinical onset during pregnancy or the pueperium. Eur J Gastroenterol Hepatol 1996;8:63–89.
11 Collins P, Vilska S, Heinonen PK, et al: Infertility and coeliac disease. Gut 1996;39:382– 384.
12 Meloni GF, Dessole S, Vargiu N, et al: The prevalence of coeliac disease in infertility. Hum Reprod 1999;14:2759–2761.
13 Kolho KL, Tiitinen A, Tulppala M, et al: Screening for coeliac disease in women with a history of recurrent miscarriage or infertility. Br J Obstet Gynaecol 1999;106:171–173.
14 Cooke WT, Peeney ALP, Hawkins CF: Symptoms, signs and diagnostic features of idiopathic steatorrhea. Q J Med 1953;12:59–77.
15 Green JRB, Goble HL, Edwards CRW, et al: Reversible insensitivity to androgens in men with untreated gluten enteropathy. Lancet 1977;i:280–282.
16 Farthing MJG, Edwards CRW, Rees LH, et al: Male gonadal function in coeliac disease. I. Sexual dysfunction, infertility and semen quality. Gut 1982;23:608–614.
17 Baker PG, Read AE: Reversible infertility in male coeliac disease. Br Med J 1975;ii:316– 317.
18 Farthing MJG, Rees LH, Edwards CRW, Dawson AM: Male gonadal function in coeliac disease.
II. Sex hormones. Gut 1983;24:127–135.
19 De Sandre G, Caramaschi P: Untreated celiac disease with bad outcome of three pregnancies
followed by a fourth normal pregnancy after two years of gluten-free diet. Am J Gastroenterol 1996;91:2653.
20 Dondorp AM, Degroot GH: Onset of coeliac disease after a spontaneous miscarriage during a holiday in Australia: Coincidence or causal relationship? Neth J Med 1998;52:147–149.
21 Joske RA, Martin JD: Coeliac disease presenting as recurrent abortion. J Obstet Gynaecol Br Comm 1971;78:754–758.
22 Ogborn ADR: Pregnancy in patients with coeliac disease. Br J Obstet Gynecol 1975;82:293–296.
23 Norgard S, Fonager K, Sorensen HT, Olsen J: Birth outcomes of women with celiac disease: A nationwide historical cohort study. Am J Gastroenterol 1999;94:2435–2440.
24 Ciacci C, Cirillo M, Auriemma G, et al: Celiac disease and pregnancy outcome. Am J Gastroenterol
1996;91:718–722.
25 Dickey W, Stewart F, Nelson J, et al: Screening for coeliac disease as a possible maternal risk
factor for neural tube defect. Clin Genet 1996; 49:106–108.
26 Erdozain JC, Martin de Argila C, Lizasoain J, et al: Adult celiac disease: Reactivation during
pregnancy. Am J Gastroenterol 1993;88:1139–1140.
27 Malnick SDH, Atali M, Lurie Y, et al: Celiac sprue presenting during the puerperium. J Clin
Gastroenterol 1998;26:164–166.
28 Myellot M: Anaemia in pregnancy and the small intestine. Br J Obstet Gynaecol 1976;83: 411–412.
29 Whitefield CR: Obstetric sprue. J Obstet Gynecol Br Comm 1970;77:577–586.

Toronto Congress Centre
650 Dixon Road
Toronto, ON  M9W 1J1
Map and Directions

This presentation by Dr. David Suzuki will mark the opening of the OAND annual convention, Revolutionizing Medicine: The Connection Between the Environment and Health. Dr. Suzuki will present his keynote address, “The Challenge of the 21st Century: Setting the Bottom Line”.

The OAND is thrilled to provide an opportunity for members, patients and the public at large to attend a live, in-person presentation with Dr. Suzuki. As part of his commitment to reducing his carbon footprint, the majority of his appearances are now via videoconference – so we are proud to present this exclusive event.

Please join the members of the OAND at our Naturopathic Doctor Marketplace before and after the presentation to find out how Naturopathic Doctors are getting at the root of it!

Type of Ticket                              Ticket Price
Regular Ticket                             $66.00
Student Ticket                             $40.00
Convetion Attendee Ticket   $30.00

* Regular Ticket price includes a $6.00 donation to support Evergreen in its efforts to improve the health of our cities—now and for the future. The OAND is proud to support Evergreen, a not-for-profit organization making cities more livable.

How to Purchase Tickets
Regular and Student Tickets: Tickets are available online or by phone at 1-800-838-3006.
Please note that anyone purchasing a Student Ticket will be asked to show valid Photo ID along with a valid Student ID (from a recognized Canadian or US high school, college or university) in order to gain entry to the event.

Convention Attendee Discounted Tickets: Are you an ND, student or other healthcare practitioner planning to attend the OAND Convention 2009 – Revolutionizing Medicine: The Connection Between the Environment and Health, taking place November 13-15, 2009 at the Toronto Congress Centre? If yes and if you register for the FULL convention, then you will be entitled to a reduced rate ticket of just $30 to attend Dr. David Suzuki’s presentation. A block of tickets has been reserved for convention attendees – please wait until registration opens for the convention (in July)… you will then have an opportunity to purchase a $30 ticket to see Dr. David Suzuki when you register for the full convention. Please note that you will be entitled to one (1) reduced-rate ticket as part of your convention registration; should you wish to purchase additional tickets for friends/family/colleagues to attend Dr. David Suzuki’s presentation, please use the above link to purchase Regular Tickets. All ticket sales are final and no refunds will be issued, so if you purchase a $66 ticket and then later register for the convention, we will be unable to offer a refund – if this happens, we recommend purchasing your $30 and bringing a friend with you to the event!

Cancellation Policy
All sales are final and tickets are non-refundable. However, should the event be postponed or cancelled, we offer refunds of the full face value of tickets. To receive a refund if this event is canceled or postponed, contact Brown Paper Tickets by telephone at 1-800-838-3006 or by e-mail at Support@BrownPaperTickets.com within three days of the event date. They will then provide you with instructions for receiving your refund. Please note that Brown Paper Tickets also offers a 12-hour grace period for refunds (you may request a refund within 12 hours of your purchase).

Take the Greener Way!
We encourage you to take public transit to this event. Travel to the Lawrence West Subway Station (on the Yonge-University-Spadina Subway Line) then transfer to the Malton #58 bus which will take you directly in front of the Toronto Congress Centre. For full transit maps and bus route details, please visit www3.ttc.ca/Routes/58/Map.jsp.

Enjoy a Green Facility!
The Toronto Congress Centre is one of the largest and most sustainable trade and convention facilities in North America and, in fact, the world. Interior finishes are low VOC (volatile organic compounds) and all cleaning products are eco-friendly; attractive tabletops for meetings and formal gatherings reduce the need for laundry and chemicals and high energy hand dryers in washrooms mean no paper towel disposal, resulting in linen-free, paper towel-free meetings; the venue’s Enviro-Friendly Purchasing Policy leads to the use of reusable, recyclable and returnable containers, ensuring a reduction in packaging; and during the TCC’s recent renovation, its Zero Waste Objectives have resulted in 75% of the materials from the demolished building having already been recycled. These are just a few highlights – to learn more, please read this Toronto Congress Centre Press Release (PDF, 64KB).

FAQs
1. What methods of payment are accepted?
You may pay online or by telephone using VISA, MasterCard or Discover.

2. How will my tickets be delivered to me?
USPS First Class Mail: This is the standard delivery method. It is available until 10 days prior to the event. This delivery method generally takes 4-7 business days. Priority delivery is available at an additional charge of $15.00 (delivery generally takes 3-4 business days). Express delivery is available at an additional charge of $30.00 (delivery generally takes 1-2 business days). Please note that delivery times are not guaranteed – these are just estimates. Occassionally, tickets get delayed crossing the border from the US, but generally, delivery times are as noted above.

3. Are e-tickets available for this event?
No. For this event, only real, paper tickets will be issued. See above for delivery methods.

4. Will my online transaction be secure?
Brown Paper Tickets uses the industry standard 256-bit Secure Sockets Layer (SSL) encryption for all transactions. You should also see a lock symbol somewhere on the edge of your browser window that will pull up our security certificate if you click on it. We currently use a third-party company called Thawte Communications to verify all transactions are secure. You can visit their website at http://www.thawte.com/ for more information.

5. What is “Brown Paper Tickets”?
Brown Paper Tickets is a fair-trade ticketing company and offers the smallest service charge in the industry. At least 5% of their profits are donated back to the communities they serve. They offer consistent pricing – ticket buyers pay the same fair fee whether they purchase online or by phone. There are no shipping charges to receive tickets by regular mail or to pick up your tickets at Will Call (on-site). Brown Paper Tickets is the official ticketing company being used by the OAND to handle the secure ticket sales for this event. Your online order will be placed using Brown Paper Tickets’ secure website and your telephone order will be handled directly by Brown Paper Tickets. Brown Paper Tickets will be responsible for mailing your tickets directly to you.

6. Who Should I Contact for Assistance?
For assistance with your order, please call Brown Paper Tickets at 1-800-838-3006 or email them at Support@BrownPaperTickets.ca. For questions related to the event itself (or about the convention, the venue, the association or naturopathic medicine in general), please contact the OAND at 416-233-2001 ext 29 or email tickets@oand.org.

According to researchers, the six-fold rise of Gastroesophageal reflux disease (GERD) in the United States in the last thirty years is associated with large-scale changes in the microbes that populate the esophagus. Until recently, scientists thought that no bacteria lived in the esophagus, but a diverse mix of microbes has been discovered there. People with esophagitis or Barrett’s esophagus, a complication of acid reflux, have higher levels of pathogenic microbes, such as Campylobacter. This new research emphasizes the importance of taking probiotics. Natren®, the leader in the probiotics industry, manufactures the highest-quality probiotics on the market today. One Natren HEALTHY TRINITY® capsule provides 30 billion colony forming units (cfu) of probiotic beneficial bacteria; GASTRO-pH®, specifically formulated for fast-acting relief of the burning sensation in your chest and throat, provides 1 billion cfu of Lactobacillus bulgaricus LB-51 per 2 chewable wafers.

Don’t Do Drugs

It is better to control GERD naturally rather than with prescription drugs. One recent study suggests the use of popular acidreducing heartburn drugs such as Prevacid, Zantac, Tagamet, Prilosec and Nexium may raise the risk of hip fractures. Another recent study shows that heart attack patients given the blood thinner Plavix plus a type of
heartburn medication called a proton pump inhibitor (PPI), such as Prilosec or Nexium, may be at increased risk of heart failure or a fatal heart attack. Natren probiotics are safe and natural. You can trust Natren.

You Can’t Ignore It

These recent studies showing the dangers of drugs for acid reflux might scare some people from trying to manage it at all, but ignoring the condition can be dangerous, too. Research shows that people with acid reflux, and especially people with Barrett’s esophagus, have altered cells in their esophagus that might allow the dominance of cancer-prone
cells. The type of cancer most associated with Barrett’s esophagus is the most rapidly rising cancer in the United States.

Natural Control with Natren Probiotics

Get good bacteria to once again reign supreme in your esophagus! Take Natren probiotics support your entire gastrointestinal tract with naturally protective bacteria. HEALTHY TRINITY will aid digestion (and boost immunity!). It provides Lactobacillus acidophilus, NAS for your upper gastrointestinal (GI) tract, Bifidobacterium bifidum, Malyoth, for your large intestine, and the ultra-important Lactobacillus bulgaricus, LB-51, for optimum protection against acid indigestion. Take at least one HEALTHY TRINITY capsule every day! For quick, on-the-spot relief from the burning sensation in your chest or throat, take GASTRO-pH. You can carry these delicious, L. bulgaricus wafers with you and chew a couple every time you have a flare-up. Enjoy the freedom to eat whatever foods you like. Since every body is different, you may need some guidance in customizing a probiotic regimen that is perfect for you. Call
Natren today and a Personal Probiotic Health Consultant will help you design a probiotic program perfect for your specific needs.

In my opinion, this AAP recommendation to prescribe statin drugs for children is off base for many reasons. We do have an obesity epidemic among children, and the problem of high cholesterol in children is increasing; however, the answer should not be to prescribe medications that have not been tested in children and could cause serious side effects.

Statins are a class of drugs that act by inhibiting an enzyme (HMG-CoA reductase) that is needed for the formation of cholesterol in the liver. In the process, statins also inhibit other substances that have important functions. For example, statins interfere with the production of coenzyme Q10 (CoQ10), a critical nutrient for cellular energy and muscle function.

The most common side effects of statins — most likely from a deficiency of CoQ10 –are muscle aches and wasting, slurred speech, and heart failure. Heart failure, because the heart relies on a plentiful supply of CoQ10 for proper functioning. Low levels of CoQ10 have even been reported to increase the risk of neurodegenerative diseases.

There are even more important reasons that cholesterol should not be artificially lowered in children.

It is essential for the developing brain and nervous system. That’s why it is advised that young children drink whole milk rather than low-fat. Adults on statin drugs have reported memory loss and brain fog. What would be the consequences of these side effects on a child’s ability to do well in school?

Sex hormones are made of cholesterol. Sex hormones are needed for the proper development of sex organs and the ability to conceive during the reproductive years. Cholesterol also is needed to make serotonin, the “feel good” hormone that helps us get a good night’s sleep and protects against depression.

Among its many other functions, cholesterol helps us digest the fats in our diet. It is also a precursor to vitamin D, which is formed when sunlight interacts with the cholesterol in our skin. Vitamin D makes bones strong and provides protection against several forms of cancer.

Statin drugs have been shown in a couple of studies to raise cancer risk.1-2 This may be due to its action of reducing the body’s production of cholesterol. The cancer studies were done in adults, but do we really need to recreate this experiment with children?

While there is a tendency in medicine to downplay the side effects of drugs, I have seen numerous patients with statin-induced health problems over the last decade. I would expect that children would be no different — and it could be worse because of the potential effects on their growth and development.

Recent studies are even questioning the efficacy of statins for their primary purpose (reducing calcification in coronary arteries) — and it is still to be proven that statin drugs really extend life.3-4

Let me be clear — giving children statin drugs is a disaster waiting to happen and we can’t have enough voices joining the protest against this recommendation. Fortunately, I have already seen a number of pediatricians questioning it.

We need to understand why more and more of our children are obese and at risk of future heart disease. In children as in adults, artery clogging high sugar diets and a lack of activity are the primary cause of heart disease insulin resistance. My experience has shown that in young people these factors are made worse by environmental pollutants, stress, and excessive prescription drug use.

But the good news is that the majority of kids can reduce weight and high cholesterol levels with exercise and a diet of whole, natural foods that are low in sugar and free of trans fatty acids. If children can learn these lifestyle habits at a young age, their risk of heart disease will be greatly reduced.

No statins needed!

References

1.http://www.medscape.com/viewarticle/578053.
2.Ravnskov U, The Cholesterol Myths, Washington, DC, New Trends, 2000; www.THINCS.org.
3.Ravnskov U, Quart J Med. 2003;96:927-934.
4.Jackson PR, et al. Br J Pharmacology 2001;52:439-446
[Ed. Note: James LaValle, R.Ph, ND, CCN, is the founding Director of the LaValle Metabolic Institute, one of the largest integrative medicine practices in the country.  He was named as one of the 50 most influential pharmacists in the US by American Druggist magazine.  Dr. LaValle is the author of more than a dozen books including the bestseller, Cracking the Metabolic Code: 9 Keys to Optimal Health.

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