Health Warnings-Lectins — A Little Known Trouble Maker

While most of the world seems to be touting the benefits of whole grains these days, a few people are insisting that grains are not as healthy as we think.
One of the reasons grains may be a problem in human nutrition is because they contain lectins, a class of molecules called glycoproteins (molecules that contain a protein and a sugar).
While dietary lectins are known in the scientific and nutritional communities, most lay people and even many medical professionals don’t know about them.
Lectins are involved in food allergies/sensitivities, inflammation and autoimmune disease, just to name a few.  For instance, lectins are linked to celiac disease. Even weight gain and low energy can be linked to lectins.
Whole grains, peanuts, kidney beans, and soybeans are high in lectins. Cow’s milk, nightshade vegetables (like potatoes and tomatoes) and some seafood also contain fairly high amounts of lectin.  In fact, estimates are that about 30% of our foods contain lectins, and about 5% of the lectins we eat will enter our circulation.
Lectins are problematic because they are sticky molecules that can bind to the linings of human tissue, especially intestinal cells.   In so doing, they disable cells in the GI tract, keeping them from repairing and rebuilding.1 Therefore, lectins can contribute to eroding your intestinal barrier (leaky gut).
Because the lectins also circulate throughout the bloodstream they can bind to any tissue in the body ¬— thyroid, pancreas, collagen in joints, etc.2 This binding can disrupt the function of that tissue and cause white blood cells to attack the lectin-bound tissue, destroying it. This is an autoimmune response.  The lectins in wheat for example, are specifically known to be involved in rheumatoid arthritis.
But why do only some people react to the lectins in foods while others can eat them with no apparent problems?   There are two answers to this question.  First, many people may be having problems but they just don’t realize it.  For example, autoimmune thyroiditis could be caused by dietary lectins.6
As another example, many of our patients who thought they had no food intolerance at all have experienced much improved energy and weight control when they eliminated wheat and dairy.  They didn’t realize until after they eliminated these foods that they were being affected by them.
But certainly many people tolerate these foods — why?
The answer lies in the balance of gut flora and a person’s immune system.  When you have adequate beneficial flora, it serves as a protective barrier against substances that travel through the intestines, including lectins.  But importantly, beneficial flora are needed to keep the production going in the intestines of two lectin-protective substances, mucin and secretory IgA.3,4
Mucin, like lectin, is a glycoprotein in the mucous lining of the intestines.  When lectins travel through the intestines, they should have mucin to bind to, rather than intestinal cells.  But if mucin is missing, lectins will bind to intestinal cells instead.  Secretory IgA also binds to lectins, preventing them from causing damage.5
If you have any lectin-related health issues like arthritis, allergies or autoimmune disease, our experience shows it is very helpful to reduce your intake of lectins, especially from wheat.  It’s also very important to balance immunity by working on stress management and gut health.
By taking a good quality probiotic you’ll help stimulate adequate mucin and secretory  IgA production.3,4 And controlling your stress response will help prevent the over production of IgA and maintain immune balance in the gut to improve your tolerance to lectins.
References
1. Pierini C. Vitamin Research News. Jan 2007. 21(1): 1-4.
2. http://www.sciencedaily.com/releases/2007/08/070801091240.htm.
3. Eur J Clin Nutr. 1993 Oct;47(10):691-9.
4. Deplancke B and  Rex-Gaskins H. AJCN. June 2001. 73(6):1131S-1141S.
5. Buts JP, et al. Digestive Disease and Sciences. Feb 1990. 35(2): 251-56.
6. Cordain L et al. British Journal of Nutrition (2000), 83, 207–217.

[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.

Celiac Disease: Fertility and Pregnancy

Abstract
Celiac disease (gluten-sensitive enteropathy) may manifest clinically with an array of nongastrointestinal symptoms among which are: dermatitis herpetiformis; dementia; depression; various neurological symptoms; osteoporosis; osteomalacia; dental enamel defects, and anemia of various types. Important data have accumulated in recent years regarding the association between celiac disease, fertility and pregnancy. Many primary care obstetricians and gynecologists and perinatologists are not aware of these important relationships. The aim of this review, utilizing a MEDLINE search from 1966 through March 2000 of the English language, is to describe the possible effects of celiac disease and its treatment upon the reproductive cycle, fertility, pregnancy, and menopause. Review of the literature reveals that patients with untreated celiac disease sustain a significantly delayed menarche, earlier menopause, and an increased prevalence of secondary amenorrhea. Patients with untreated celiac disease incur higher miscarriage rates, increased fetal growth restriction, and lower birth weights. It appears that improvement of celiac disease, as reflected by restoration of small bowel mucosa associated with implementation of a gluten-free diet, may decrease miscarriage rates, improve fetal nutritional support and overall perinatal outcome.

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.

Kidney Failure —The Unknown Epidemic

Most of us are aware of all the health problems that can result from insulin resistance like heart disease, diabetes, and hypertension,  But lost in the shuffle is another silent killer that is on the rise — chronic kidney disease. At LMI we’ve noticed a growing number of patients with kidney problems.
Our experience reflects both a national and international trend.  Kidney disease is increasing in young and old alike in the U.S. and around the world.1,2 And that’s why I feel compelled to warn you about it — and tell you how to keep your kidneys healthy.
Here’s some background. You have two kidneys, whose job is to remove wastes from the blood and to excrete them via urine; they then return cleaned blood to the body. The kidneys keep water and minerals at healthy levels and produce important hormones.
When the kidneys are diseased, they can’t efficiently filter out wastes and excess fluids. As the disease progresses, urine production decreases and eventually stops. At that point you need dialysis — a process in which the blood is filtered via either a machine or fluids that can be held in the abdominal cavity.
The primary causes of kidney disease are high blood pressure, diabetes or obesity. Indeed, obesity triples your risk,3 and the damage to kidneys from high blood sugar or blood pressure can occur even at the pre-disease stages.
So the first steps for protecting your kidneys are obvious: control your weight, blood sugar and blood pressure.  It is also important to keep yourself well hydrated. If you do that, you should have a very good chance of retaining good kidney function into your old age.
However, there are other factors that could be playing just as important a role in the health of your kidneys, and most people don’t know a thing about them.  Environmental chemicals and heavy metals damage kidney tissue and so can common over-the-counter (OTC) pain relievers.
For example, a study has found that a group of Central Americans who don’t have diabetes or high blood pressure is nevertheless experiencing high rates of kidney failure.5 The suspected cause: agricultural chemicals.
Heavy metals from the environment can also accumulate in the kidneys and can damage them.4 We are exposed to heavy metals like cadmium, mercury and lead everyday from mercury in our fish, cadmium in our air, and lead in our pipes for example.
Common OTC painkillers such as acetaminophen and aspirin have also been linked to kidney disease.5 One study looked at people with end-stage kidney failure and found that heavier acetaminophen use increases the risk of kidney failure, with the heaviest use of 5000 or more pills over several years more than doubling one’s risk.  In fact, about 10% of kidney failure is from acetaminophen use.6
Here are some ways to protect yourself.  First, be very careful not to overuse acetaminophen.  I see so many people making this big mistake, never realizing that it is compromising their kidneys.  If you have daily headaches, get to a practitioner who can help you get to their root cause, but don’t think for a minute that daily pain reliever is not seriously affecting you.
If you do need to use it, take some N-acetyl cysteine (NAC), a supplement that is given in cases of acetaminophen overdose. This is a powerful antioxidant derived from the amino acid cysteine, which is found in foods. NAC increases levels of the natural antioxidant glutathione, especially in the liver where glutathione also helps to detoxify the body of toxins like heavy metals and pesticides.
I highly recommend NAC for those who regularly take acetaminophen or ibuprofen, and usually recommend 600 to1200 mg per day.
To protect yourself against heavy metals, there are several other substance that have been shown to facilitate their removal from the body:
• Vitamin C.  Vitamin C also increases glutathione production, helping to detoxify and remove heavy metals including mercury and lead from the body. I recommend 1-2 g of vitamin C daily.
• Cilantro (Coriandrum sativum). Cilantro has been shown to help with detoxification of lead and mercury. Try to include cilantro as an herb in salads, soups, and pestos to help rid your body of mercury and other toxins. 
• Aged Garlic Extract (Allium sativum). Components found in aged garlic extract help balance the immune system and detoxify the body by activating the antioxidants glutathione and superoxide dismutase (SOD). Aged garlic activates Phase 2 enzymes in the liver which protect the body from potential carcinogens.  The typical dosage is 600 mg once or twice a day.
Chronic kidney failure comes on slowly and silently so I can’t stress enough how important it is for you to take good care of your kidneys.  Since kidney disease can be hard to stop once it is set into motion, this is one condition where prevention is vitally important.
References
1. “USRDS 2008 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States.” NIH 2008.
2. J Hypertens. 2005 Oct;23(10):1771-6.
3. Science Daily. Retrieved November 15, 2007, from
4. www.sciencedaily.com/releases/2006/05/060513122553.htm.
5. Nephron Physiology. 2005 99(4): 105-110.
6. N Engl J Med. 2001 Dec 20;345(25):1801-8.
7. Acta Biomed. 2005;76 Suppl 2:58-67.
8. NEJM. 1994. 331 (24):1675-79.
[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 E]

An evening with Dr. David Suzuki

Friday, November 13, 2009
Doors open: 5:30 pm
Dr. David Suzuki: 7:00-9:00 pm
Naturopathic Medicine Marketplace: 5:30-7:30 pm

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.

Statin Drugs and Children

On July 7, 2008, the American Academy of Pediatrics (AAP) issued a shocking new recommendation that stated children, starting at 2 years of age and no older than 10, should routinely get their cholesterol checked — and that some children as young as 8 should be started on statin drugs to lower their cholesterol and prevent future heart disease.

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.

totalhealthbreakthroughs.com/2008/08/statin-drugs-and-children

No Wheat, No Rye, No Barley — No Problem!

Receiving a disease diagnosis isn’t usually a good thing. But for people who learn they have celiac disease, the news often comes as a relief. Celiac disease is an autoimmune disorder in which the body overreacts to gluten, a protein found in wheat, rye and barley. When celiacs ingest gluten, their immune system attacks the hairlike villi lining their small intestines, hampering their ability to absorb nutrients to disperse to the bloodstream.
While diarrhea, bloating, constipation and vomiting are short-term hallmarks of celiac disease, the malabsorption of nutrients can lead to longer-term problems, including weakened bones, anemia and neurological problems. Celiacs are also at increased risk of gastrointestinal cancers, among other diseases.Left unchecked, celiac disease can even lead to death. Recent research suggests that the disease is far more common than had been believed, affecting as
many as one in 133 people.But once you get that diagnosis, the remedy is obvious: Eliminate gluten from your diet, and watch your symptoms vanish. Better yet, strict avoidance of gluten over time can reverse damage the disease has already done. Not only does diarrhea cease, intestines heal.
Vanessa Maltin was a 21-year-old junior studying journalism at George Washington University in 2004 when she learned she had celiac disease. Maltin had suffered chronic headaches all her life; nobody could figure out why. When at last a blood test pointed toward celiac disease, Maltin says she was “depressed for about six weeks. I lived in a college dorm, and it was hard not to eat the same things, like pizza and Chinese food, as my college friends.” Maltin’s depression was short-lived. She cut out gluten, and “within two months, I felt all better. The first day I woke up and didn’t have a headache, I was so blown away, I never missed eating gluten again.” Today Maltin is the food and lifestyle editor for Delight magazine, devoted to all things gluten-free. She’s also a member of the Washington Area Celiac Sprue Support Group, which has about 800 members (Sprue is another name for celiac).
Avoiding gluten was far trickier then than it is today. Whereas only a few small manufacturers produced gluten-free products just a few years back, gluten-free is big business now, with major companies such as General Mills, Betty Crocker and Wal-Mart offering no-gluten foods. That growth is fueled in part by consumers who, while not having received a diagnosis of celiac disease, find they don’t tolerate gluten well and would just as soon avoid it.
Gluten-free products are generally more expensive than their gluten-containing equivalents; some celiacs learn to rely heavily on meats, fruits and vegetables, and other foods that naturally contain no gluten. Dining out remains problematic. While Maltin says many restaurants, particularly in the Washington area, have begun offering gluten-free dishes, celiac diners have to remain vigilant, as gluten lurks not just in the obvious beer, bread and other baked goods but also in sauces, marinades, salad dressings and other places you might not expect to find grains. And one small mistake can lead to misery. “If I accidentally get some gluten,” she says, ” . . . it’s like having food poisoning. I have a four- or five-day reaction, and the headaches come back.” Maltin now calls restaurants ahead of her visit to discuss her dietary needs and makes it a habit to speak with the chef before ordering her meal. As Maltin is well aware, the improved digestion that comes with eliminating gluten often means the body takes in more calories. “All of a sudden, you’re absorbing everything,” she says. “After diagnosis, people typically gain 20 to 40 pounds.” Maltin gained weight herself after her diagnosis, moving from a size 2 to a size 4.(She’s currently planning an October 2010 wedding, with a gluten-free reception. The one exception: Her fiance, who Maltin says is extremely supportive of her gluten-free living, wants to drink Guinness at the event. Though gluten-free beers are available, Maltin’s fine with his choice).

Biopsy of the intestine’s lining via endoscopy remains the most definitive way to diagnose the disease. Blood tests can reveal whether a person’s body has developed antibodies to gluten proteins, a sign that celiac disease may be present. Genetic analyses, including a new saliva test developed by Prometheus Laboratories, can determine whether one has the genetic makeup associated with celiac; this at-home test has the advantage of being able to rule out celiac altogether. As with all autoimmune diseases, it’s believed that celiac occurs when a person who has a genetic predisposition encounters some environmental trigger that moves the faulty immune response into action. But celiac is the only autoimmune disease for which that environmental trigger — in this case, gluten — has been identified, according to Alessio Fasano, director of the University of Maryland Center for Celiac Research.That makes celiac disease an enticing research subject. As Fasano explains in a fascinating article in the current issue of Scientific American, celiac serves as a perfect model for studying the phenomenon of autoimmunity. Researchers can establish control groups for experiments, testing treatments on celiacs who continue to eat gluten and those who don’t and comparing the two groups’ responses. Fasano has discovered that people with autoimmune diseases tend to have abnormalities in their intestines that make them permeable — what he calls “leaky guts.” That permeability may be the factor that gives environmental triggers access to the immune systems of genetically susceptible people. Fasano has launched research of a drug called larazotide, which inhibits the action of zonulin, a protein that increases intestinal permeability.

Early results on people with celiac disease have been promising. Until the mysteries of their disease are solved, celiacs will have to continue watching what they eat. But as Maltin notes, the celiac life doesn’t have to be all that restrictive. “We travel all over the world and eat great food,” she says. In fact, “the hardest place is in the airport. I always bring my own food with me.”

Check out Tuesday’s Checkup blog post, in which Jennifer explores the world of gluten-free food. Subscribe to the Lean & Fit newsletter by going to washingtonpost.com/health

Cardiometabolic Disease-A Risk at Any Weight by James B. Lavalle

 

 

 

 

 

 

 

 

by James B. LaValle 08/26/2008

Just because you are not obese, doesn’t mean you’re off the hook when it comes to increased risk for heart disease and diabetes — known as cardiometabolic disease. If you’re just a little pudgy around the middle, you may pat your belly and chuckle about those few extra beers you had last night, but it is no laughing matter.

Two studies recently looked at the cardiometabolic health of three categories of white adults: normal weight, overweight, and obese. Researchers measured blood pressure, triglycerides, fasting plasma glucose, C-reactive protein (CRP), high-density lipoprotein (HDL), and assessed whether the study subjects were insulin resistant.

What they found was eye opening — 23.5% of “normal weight” adults were metabolically abnormal — and surprisingly, the research done by Wildman’s group found that approximately 30% of the “obese” group was actually metabolically pretty healthy.1 In the “overweight” group, it was split about 50-50 between those who were metabolically healthy and those who were at increased risk according to these measures.

So to summarize, the study found the risk for heart disease and diabetes in the three groups to be: normal body weight, 25% risk; overweight, 50% risk; obese, 70% risk.

Another study by Stefan et al. found that 25% of obese people did not have early signs of heart disease as determined by their blood vessel thickness and an oral glucose tolerance test used to measure insulin sensitivity.2 Nor were these people categorized at high risk according to their lipid profiles and blood pressure readings.

Both of these studies assessed whether central adiposity (belly fat) raised the risk of heart disease the most, as has been seen in other studies. According to the American Heart Association, if a man’s waistline is greater than 39 inches and a woman’s waistline is greater than 34 inches, it’s time to take action.

Interestingly, the Stefan study found that in already obese patients, the most “at risk” fat was not belly fat, but liver fat. However, in normal and overweight people, belly fat did increase risk the most. (This may be because it is very unusual to see liver fat accumulating in normal weight people.) The Wildman study also found that normal weight or slightly overweight patients are more at risk for heart disease if they have belly fat.

The blogs are now flying about this research. I have seen statements like, “These studies once again prove that just because you are obese doesn’t mean you are unhealthy.” And indeed these studies show that if you are obese, you have a 25 to 30% chance of being in the group that hasn’t yet developed heart disease or diabetes. But the overwhelming number of studies consistently shows that the vast majority of obese people do have heart disease and/or diabetes.

Even in the Wildman and Stefan studies, only 25 to 30% were escaping risk so far. The other 70% were at risk. In the normal weight category, 75% were metabolically healthy and 25% were at risk. I would take those odds any day.

I know some obese individuals will want to hang on to that 25% chance they may not be unhealthy just because they are severely overweight — but there are other health problems that can develop too. Certainly if you fall into the obese category, you should at least be thoroughly evaluated to find out.

What are the take home messages from this research? You can be at cardiometabolic risk even if you are at a normal body weight, especially if you have increased waist size. This is not news to me and most health practitioners, but it is a big wake up call for many people.

Increased belly fat/waist size puts you at increased risk for heart disease and diabetes — and the more overweight you become, the greater your risks. So, no matter who you are, you should take steps to prevent insulin resistance and control your weight to have the greatest chance of avoiding these two devastating diseases.

We also need to further study the 25% of the obese population to see what is keeping them from developing insulin resistance. For instance, the Wildman study found that increased physical activity reduced risk. Other studies have found that increased antioxidant intake from foods like green tea and turmeric may prevent damage to insulin receptors from the oxidative stress that can cause insulin resistance.

Perhaps these individuals have better sources of, or utilization of, the mineral chromium which helps regulate blood sugar. Or, they might have increased vitamin C intake from fruits, vegetables, and supplements which reduces the risk of insulin resistance and diabetes.3-4

Determining which factors can best lower risk of heart disease and diabetes, even in people who have not been able to lose weight, would be of tremendous value.

References

Stefan N, et al. Arch Intern Med. 2008;168:1609-1616.
Wildman RP, et al. Arch Intern Med. 2008;168:1617-1624.
nutritionandmetabolism.com/content/5/1/17
Arch Intern Med. 2008;168:1485-1499.
[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.

Melatonin: A Hormone that Protects Against Breast Cancer and Aging

Thursday, April 10, 2008 by: Barbara L. Minton

(NaturalNews) Melatonin is nature’s sleeping pill. It is secreted by the light sensitive pineal gland which regulates our biological clock and synchronizes our hormonal-immune network. Our level of melatonin rises with darkness and falls with light. According to Dr. Uzzi Reiss, in his book Natural Hormone Balance, a healthy pineal gland produces 2.5 milligrams of melatonin every twenty-four hours.

Melatonin plays a central role in the natural aging processes of the body. When pineal production begins to diminish, at around age 40, the decline sets off changes in the operation of the body’s cells. The physiology of the cell shifts from repair and rejuvenation to aging and degeneration.

Recent studies are now showing that as our levels of melatonin sink, our chances for breast cancer rise. Many women with breast cancer have lower levels of melatonin than those without the disease. Laboratory experiments indicate that lower levels of melatonin stimulate growth of breast cancer cells. Adding melatonin to these cells inhibits their growth.

Breast cancer and melatonin: studies and results

According to a study at the Department of Physiology, Faculty of Science, University of Extremadura, Badajoz, Spain, published in Molecular and Cellular Biochemistry, Oct. 2005, melatonin increases the survival time of animals with untreated mammary tumors.

The aim of the study was to evaluate the therapeutic effect of melatonin on rats with advanced and untreated mammary tumors. Mammary tumors were chemically induced in rats. Following appearance of the tumors, the effect of melatonin was evaluated based on the survival time, tumor multiplicity, and tumor volume up until the death of the animals. Additionally, the variations in prolactin, noradrenaline and adrenaline concentrations, and percentage of NK cells were evaluated after one month of the melatonin treatment.

Results indicate that daily administration of melatonin increased significantly the survival time of tumor bearing animals compared to the control non-melatonin receiving rats. However, the lengthened survival time did not correlate with changes in either tumor multiplicity or growth rates. Animals with mammary tumors exhibited increased levels of prolactin and catecholamine concentrations compared to the healthy animals. The administration of melatonin stabilized the hormone levels, returning them to the levels of the healthy animals. Rats with mammary tumors also presented lower percentages of NK cells, however these levels were not increased with the administration of melatonin. Researchers concluded that melatonin is beneficial during advanced breast cancer. It increases survival time, perhaps by improving the homeostatic and neuroendocrine equilibrium which is imbalanced during advanced breast cancer.

As published in the International Journal of Cancer, January, 2006, researchers at the Department of Physiology and Pharmacology, School of Medicine, University of Cantabria, Santander, Spain, found that melatonin inhibits the growth of induced mammary tumors by decreasing the local biosynthesis of estrogens through the modulation of aromatase activity. They note that melatonin inhibits the growth of breast cancer cells by interacting with estrogen-responsive pathways, effectively behaving as an anti-estrogenic hormone. They had previously described that melatonin reduces aromatase expression and activity in human breast cancer cells, thus modulating local estrogen biosynthesis.

To investigate the in vivo aromatase-inhibitory properties of melatonin in the current study, the indoleamine was administered to rats bearing induced mammary tumors ovariectomized and treated with testosterone. In these castrated animals, the growth of the estrogen-sensitive tumors depended on the local aromatization of testosterone to estrogens. Ovariectomy significantly reduced the size of the tumors while the administration of testosterone to ovariectomized animals stimulated tumor growth, an effect that was suppressed by administration of melatonin or the aromatase inhibitor aminoglutethimide. Uterine weight of the rats, which depended on the local synthesis of estrogens, was increased by testosterone, except in those animals that were also treated with melatonin or aminoglutethimide. The growth-stimulatory effects of testosterone on the uterus and tumors depended exclusively on locally formed estrogens, since no changes in serum estradiol were appreciated in testosterone treated rats.

Tumors from animals treated with melatonin had lower microsomal aromatase activity than tumors of animals from other groups, and incubation with melatonin decreased the aromatase activity of microsomal fractions of tumors. Animals treated with melatonin had the same survival probability as the castrated animals and significantly higher survival probability than those not castrated.

Researchers conclude that melatonin could exert its antitumoral effects on hormone dependent mammary tumors by inhibiting the aromatase activity of the tumoral tissue.

And in the April, 2007 edition of Oncology Report, this same research team at the University of Cantabria, Santander, Spain, reports the effects of MT1 melatonin receptor over-expression on the aromatase-suppressive effect of melatonin in human breast cancer cells. They note that a major mechanism through which melatonin reduces the development of breast cancer is based on its anti-estrogenic actions by interfering at different levels with the estrogen-signaling pathways.

Transfection of the MT1 melatonin receptor in the breast cancer cells significantly decreased aromatase activity, and MT1-transfected cells showed a level of aromatase activity that was 50% of vector-transfected cells. The proliferation of estrogen-sensitive cells in an estradiol-free media but in the presence of testosterone (an indirect measure of aromatase activity) was strongly inhibited by melatonin in those cells over-expressing the MT1 receptor. This inhibitory effect of melatonin on cell growth was higher on MT1 transfected cells than in vector transfected cells. In MT1-transfected cells, aromatase activity was inhibited by melatonin. The same concentrations of melatonin did not significantly influence the aromatase activity of the vector-transfected cells. MT1 melatonin receptor transfection induced a 55% inhibition of aromatase expression in comparison to vector-transfected cells. Additionally, in MT1-transfected cells, melatonin treatment inhibited aromatase expression and induced a higher down-regulation of aromatase expression than in vector-transfected cells.

The researchers concluded that their findings point to the importance of the MT1 melatonin receptor in mediating the oncostatic action of melatonin in human breast cancer cells, and confirm the MT1 melatonin receptor as a major mediator in the melatonin signaling pathway in breast cancer.

Supplementing with melatonin

Since production of melatonin by the pineal gland begins to decline at age 40, it follows that anyone over the age of 40 may be melatonin deficient and may benefit from supplementation as a preventative. Since melatonin is produced while you sleep, it also follows that if you do not get enough sleep, your levels of melatonin may be deficient. Enough sleep is 8 or more hours. Supplementing with melatonin may also be indicated for those who now have or once had breast cancer.

Your melatonin level can be measured with a simple blood test.

According to Dr. Reiss, you should not take melatonin if you have exhausted adrenal glands, symptomized by constant fatigue, low blood pressure, feeling faint when standing up, and low tolerance for physical and emotional stress. Melatonin can reduce the production of cortisol and would be contraindicated for this condition. When adrenal glands are again healthy, supplementation can be started. Women who are trying to conceive should not take melatonin as it could negatively impact the ovulation process.

Melatonin supplements are synthesized to be bio-identical with your own melatonin. They are available at health food stores in capsules, sublingual drops, pills, and as an oral spray.

For anti-aging, Dr. Reiss recommends starting with 0.25 to 0.5 milligrams and increasing the dose gradually until you notice a side effect. The optimal dose is usually 1 to 5 milligrams.

Side effects from excess melatonin are drowsiness upon waking, wild dreams that are not pleasant, waking up nervous, sweating, or with palpitations, and decreased estrogen and progesterone levels.

There is disagreement among authorities as to whether higher doses of melatonin should be recommended for cancer prevention. Dr. Reiss recommends 20 to 40 milligrams daily for prevention. He notes that participants in studies using these very high doses did not develop the side effects seen at lower doses.

Dr. John Lee, in his book What Your Doctor May Not Tell You About Breast Cancer, says that high melatonin levels reduce the ovarian production of estrogens and progesterone, and this is the feedback that is thought to be protective against breast cancer. However, he stresses that all the body’s hormones must be in balance, and more is not better when it comes to melatonin. He recommends supplementing with no more than 1 milligram of melatonin sublingually just before bedtime.

If you choose to rely on you own production of melatonin, be aware that production of melatonin rises from bedtime until the middle of the night, and then slowly declines throughout the rest of the night. This production is dependent on you sleeping in a dark room. If you get up during the night and turn on the light or open the refrigerator door, your melatonin production will abruptly stop.

About the author: Barbara is a school psychologist, a published author in the area of personal finance, a breast cancer survivor using “alternative” treatments, a born existentialist, and a student of nature and all things natural. Article from naturalnews.com

Natural Medicine for Women’s Health-an article from “The Doctor’s Research” by Dr. Michael A. Zeligs, M.D.

Women are becoming aware that nutritional intervention can help assure optimal health for their breasts. Anatomically, breasts are complex glandular structures which respond to the hormones estrogen and progesterone, and go through a monthly cycle of cellular growth and swelling. Pregnancy creates further growth, milk production, and lactation. During middle-age and later, breast tissue bears the burden of chronic estrogen-driven growth and inflammatory stimulation from environmental byproducts (1). Such frequent exposure to estrogen raises concerns regarding the risk of breast cancer. Recently, the importance of a healthy estrogen metabolism to support breast health has become known to the greater medical community (2). In addition to the benefits of a balanced diet and regular exercise, certain nutritional interventions are now known to promote breast health (3).

Breast Health Issues

Many pre-menopausal women experience painful, swollen breasts during the premenstrual phase of their menstrual cycle. This condition
is called “mastalgia.” Scientists have discovered that this recurrent breast pain reflects excess stimulation from estrogen (4). Women may develop
“fibrocystic changes” resulting innodular “lumpy” breasts which may be painful. Breast health issues range from these symptoms of painful breasts all the way to breast cancer.
Cancer risk in both pre- and postmenopausal women is now known to relate to unfavorable estrogen metabolism (5), exposure to environmental toxins including cigarette
smoke (6), and exposure to synthetic progesterones (7).

The Estrogen Connection to Breast Health

Healthy estrogen metabolism has been shown in multiple studies to be predictive of a lower risk of future breast cancer (8). A healthy estrogen metabolism is maintained by promoting increased 2-hydroxylation of estrogen (9), which elevates levels of the non-carcinogenic estrogen metabolite 2-hydroxyestrone. Nutritional factors, particularly the intake of cruciferous vegetables and Vitamin D, are associated with lower breast cancer risk. Cruciferous vegetables provide the indole phytonutrient Diindolylmethane (DIM). DIM is the most effective dietary substance to promote desirable estrogen metabolism. Absorbable DIM supplements have been shown to promote healthy estrogen metabolism in post-menopausal women (10), and help resolve recurrent breast pain in younger women (3). Similar but less activity is seen with other nutritional substances including lignans from sesame seeds, and isoflavones from soy.

Nutritional Supplement

Approaches to Breast Health In order to maintain breast health and hormonal balance, a healthy diet includes raw or lightly cooked cruciferous vegetables, frequent consumption of sesame and flax seeds, and supplemental VitaminD. Supplemental elemental iodine has been shown to be of benefit in women with fibrocystic changes
(12). In addition, the use of absorbable DIM supplements (75-300 mg) taken once or twice daily has been shown to promote breast comfort and healthy estrogen metabolism
in pre and post menopausal women (10, 3). Together, absorbable DIM, regular exercise, andthe suggested diet provides an effective avenue for hormonal
balance and maintaining healthy breasts.

Dr. Zeligs earned a Masters degree in stress-physiology from the University of California, Santa Barbara, completed a fellowship in Molecular Immunology, and
received his M.D. from the University of California, Irvine, College of Medicine. Dr. Zeligs is a leading authority on diindolylmethane (DIM). He was awarded a patent for his microencapsulated formulation of absorbable DIM and has numerous issued and pending patents for novel uses of DIM in preventive medicine. As a physician investigator,
he has sponsored clinical trials for HPV, cervical dysplasia, uterine and prostate health. These clinical trials are underway in collaboration with Cornell University, the NYU
School of Medicine, Cancer Research UK, Wayne State University, and New York Medical College. The National Cancer Institute, under a clinical
trials agreement with Dr. Zeligs, has sponsored additional clinical trials investigating microencapsulated DIM as a natural preventive and therapeutic candidate for cancer.

For more information on BioResponse DIM, please visit www.rxbalance.com or www.dimfaq.com

The Doctor’s Research Update Publications are available on the internet at: www.dimfaq.com

References:
1. Mukherjee S, Koner BC, Ray S, Ray A. Environmental contaminants in pathogenesis of breast cancer. Indian J Exp Biol. 2006
Aug;44(8):597-617.
2. Kabat GC, O’Leary ES, Gammon MD, Sepkovic DW, Teitelbaum SL, Britton JA, Terry MB, Neugut AI, Bradlow HL. Estrogen
metabolism and breast cancer. Epidemiology. 2006 Jan;17(1):80-8.
3. Zeligs, MA., Brownstone PK, Sharp, ME, Westerlind KC, Wilson, SM, and Johs SM. Managing Cyclical Mastalgia with Absorbable
Diindolymethane: A Randomized, Placebo-controlled Trial. JANA. 2005. 8(1): 5-15
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