Dr. Tori Hudson, N.D.

Researchers in Australia observed 1216 older women whose average age was 75, for close to 10 years and compared atherosclerotic vascular disease with chocolate intake, categorized as rare intake = < 1 25-50 gm serving per week and frequent intake = > 1servings per week.

Approximately half of the women rarely ate chocolate and 36% ate it weekly and 17% ate it daily. Women who consumed chocolate frequently were much less likely to be hospitalized for atherosclerotic vascular disease, or even die from it, than were women who consumed chocolate rarely. Women who ate chocolate frequently were also significantly less likely to develop ischemic heart disease, congestive heart failure and plaques in the carotid artery.

Other research results and higher intake of flavonoids, including chocolate, from prior studies have also shown an association between higher chocolate intake and improved cardiovascular outcomes. Cocoa is rich in flavonoids and is the principal ingredient in cocoa. While a high quality randomized double-blind trial could confirm these observational studies… it might indeed be difficult to find women who would be willing to be in the placebo group rather than the chocolate group. For now… I encourage women to eat 1-2 oz or greater than 70% dark chocolate at least once per week; I vote for 1 oz daily!!!

Reference

Lewis J, et al. Habitual chocolate intake and vascular disease: A prospective study of clinical outcomes in older women. Arch Intern Med 2010 Nov 8; 170:1857.

Breast cancer rates had been steadily climbing since the 1940s until about 2002 [1] but breast cancer rates decreased by about 2% between 1998 and 2007 in the U.S.[2] However, this decrease was only among women aged 50 and older. One of the more news worthy items has been a significant decline in breast cancer in US women in 2003. According to data from the National Cancer Institute (NCI) registries, the incidence fell by 6.7%. Data from 2004 showed a leveling off with no real additional decrease. The decrease, which started in mid-2003, was seen only in women 50 years of age or older and was 2 to 3 times more evident in estrogen-receptor-positive cancers. The decreases were similar for localized disease and more advanced disease, and were more evident in primary breast cancers but not in contralateral second primary or later breast cancers. [3]

A woman’s lifetime risk of breast cancer has nearly tripled during the past four decades. After lung cancer, breast cancer is the second leading cause of cancer deaths in U.S. women today. About 1.3 million women will be diagnosed with breast cancer annually, and throughout the world, about one half million will die each year from the disease. Deaths from breast cancer have decreased sine 1990, and it is suspected that this is largely due to earlier detection and advances in treatment.

One of the most well known risk factors for breast cancer is having a first degree relative with the disease, but, less than one out of every 10 cases of breast cancer occurs in women born with a genetic predisposition. At least half of all breast cancers occur in women with no known risk factor.

We have increased understanding that breast cancer arises from a mix of multiple factors— some inherited and some acquired, that lead to genetic mutations, alterations in gene expression or damage to genes. It is now thought that there is not any single exposure or event that is responsible for this affect on genes but rather the timing, duration and pattern of exposure, as well as the dose of a damaging agent. Even a small dose of a carcinogenic agent can have a devastating effect if it is during a critical window of a body system/organ development.

More than 100,000 synthetic chemicals are in use in the U.S. today with another 1,000 or so added each year, [4] and more than 90% of them have never been tested for their effects on human health. [5]

Evidence that environmental factors cause breast cancer runs from published studies showing a lack of evidence such as the Long Island Breast Cancer Study Report, [6] to multiple laboratory, animal and human studies covering a wide array of implications including ionizing radiation, xenoestrogens, hormone replacement therapy, oral contraceptives, polycyclic aromatic hydrocarbons, DDT, solvents, polyvinyl chloride, bisphenol-A, polychlorinated biphenyls, dioxin, flame retardants, ethylene oxide, insecticides, phthalates, food additives, methyl mercury, nicotine , hormones used in cattle feed and more items each year.[7]

Scientists, physicians, public health officials, politicians, activists and consumers of all walks of life have called for wide ranging changes in industry, the work place, our households and our personal habits in order to reduce the production of, use of and disposal of chemicals and exposures that are or may be associated with the increased risk of breast cancer. Unfortunately, there has been a large failure to act and change in all sectors–the personal, commercial and governmental. Too many individuals, for profit companies, politicians and government officials appear to base their decisions on the need for action based on absolute proof and a 95 percent certainty of cause and effect. While this may serve commercial interests and a short sighted view of the economy of a community, it is not the standard by which we should conduct ourselves when it comes to public health. It is time to make decisions based on possible harm rather than conclusive proof and follow the physician’s core principle of “do no harm”. Others might call this better safe than sorry or the precautionary principle. Whatever we call it, at the very least, we should require proof of the lack of negative health consequences before toxic chemicals are introduced into our bodies and our environment.

The “Breast Cancer Fund” and “Breast Cancer Action” have proposed a 10 point plan for reducing the risk of breast cancer:

1. Establish environmental health tracking programs at state and federal levels
2. Practice healthy purchasing by adopting precautionary purchasing laws at local, state and federal lands.
3. Protect workers from hazardous exposures
4. Educate the public about the health effects of radiation and how to reduce exposure to both ionizing and non-ionizing radiation
5. Hold corporations accountable for hazardous practices
6. Offer local, state and federal incentives for clean green practices
7. Strengthen right-to-know legislation and public participation in decisions about toxic exposures
8. Enforce existing environmental protection laws
9. Require greater transparency in funding of scientific and medical training, research and publications
10. Create a comprehensive chemicals policy based on the precautionary principle

Yes, there are known “environmental” lifestyle risk factors that we are easily in charge of— hi fiber/low saturated fat/high fruits and vegetables diets, low alcohol, increased regular exercise, stop smoking and optimal weight management.

We can each do more ourselves to reduce our risk from these environmental exposures and reduce the impact on ourselves, our family members, our friends, our community and Mother Nature that surrounds us. I recommend a personal action plan: use non-toxic cosmetics, health and body care items and home cleaning items. Do business with a “green” dry cleaner. Grow and/or purchase organic and pesticide free foods. Recycle more and use less— less plastic, wood, cardboard, metal, etc. It often comes down to awareness and then making simpler/safer choices for ourselves and regarding our impact on the environment around us.

References

[1] Parkin D, Bray F, Ferlay J, Pisani P. Global cancer statistics, 2002;CA: A Cancer Journal for Clinicians 1005;55:74-108.

[2] American Cancer Society Breast Cancer Facts and Figures 2008-2009

[3] Ravdin P, Cronin K, Howlander N, Chlebowski R, Berry D. A sharp decrease in breast ancer incidence in the United States in 2003. Breast Cancer Res Treat 2006; 100: Suppl: S2, a abstract.

[4] National Cancer Institute. Cancer and the Environment: What you need to know, what you can do. National Institutes of Health. 2003

[5] Bennett M, Davis B. The identification of mammary carcinogens in rodent bioassays. Environmental and Molectular Mutagenesis. 2002;39(2-3):150-157.

[6] Winn D. The Long Island Breast Cancer Study Project. Nature Reviews Cancer 2005 Dec;5(12):986-94.

[7] Gray, J. Breast Cancer Fund; State of the Evidence- The connection between the environment and breast cancer. 2010, 6^th edition.

A review of 25 trials that evaluated the risk of CHD related to the body’s omega-3 levels showed that there was an inverse relationship with major cardiovascular (CV) events and tissue levels of EPA and even more so, with DHA. [1] There have been three large randomized trials documenting omeg-3 polyunsaturated fatty acids (PUFA) in both primary and secondary prevention of CHD. In the Diet and Reinfarction Trial (DART),[2] men with recent MI (myocardial infarction) showed that omega-3 PUFA either in dietary oily fish or fish oil capsules, but far more in the fish oil capsules, reduced 20 year all-cause mortality by 29% and mostly all due to reduction in CHD mortality. The Gruppo Italiano per lo Studio della Sopravvivenza nell’ Infarto Miocardico (GISSI) [3] randomized 11,323 post MI patients with 1 capsules of 850 mg EPA/DHA in a 1.2:1 ratio versus customary care. After one year, patients taking the fish oil had a 21% reduction in total mortality and a 30% reduction in CV mortality. In addition, there was a highly significant 45% reduction in sudden cardiac death (SCD) after only 4 months.

The JELIS (Japan EPA Lipid Intervention Study) trial [4] included a total of 18,645 subjects (men aged 40-75 and postmenopausal women aged > 75 and a mean age of 61 years and 31% men). Those with a serum total cholesterol level of > 250 mg/dL were eligible. About 36% were hypertensive, 15% had diabetes and 20% had coronary artery disease. Subjects were randomized to pravastatin 10mg/day or simvastatin 5mg/day or the same statin doses with 1,800 mg/day of EPA. After 5 years, those in the EPA group had a 19% reduction in major cardiac events.

These three trials indicated that omega-3 PUFAs lowered the risk of CV disease in both primary and secondary prevention. While not all studies have shown favorable results, the numbers of patients treated, the doses used, and the results of the DART, GISSI and JELIS study are strong motivations to increase dietary fish intake and especially fish oil supplementation. In order to test and remove heavy metals, pesticides, other environmental contaminants and microbes, look for products that can produce independent third part testing for each lot of supplements.

Recommended doses for primary and secondary prevention:

1,000 mg/day of combined EPA/DHA

References:

[1] Harris W, Poston W, Hadock C. Tissue n-3 and n-6 fatty acids and risk for coronary heart disease events. Atherosclerosis 2007;193:1-10.

[2] Burr M, Fehily A, Gilbert J, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: Diet and Reinfarction Trial (DART). Lancet 1989;2:757-761.

[3] Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI. Lancet 2001; 357;642 and Lancet 2007;369:106 and Lancet 1999;354;447-455.

[4] Yokoyama M, Origasa H, Matsuzaki M, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. Lancet 2007;369:1090-1098.

The Childhood Autism Risks from Genetics and Environment (CHARGE) study is a population-based case-control study of Northern California families. Using standardized clinical assessments, enrolling 288 children aged 24–60, with autism and 144 with autism spectrum disorders, and compared them with 278 children who were developing normally. Researchers calculated the odds ratios for associations between autism and retrospectively collected data on maternal vitamin intake before and during pregnancy. They also explored interactions with functional genetic variants in select metabolic pathways carried by the mother or child.

During the three months before pregnancy or the first month of pregnancy, mothers of children with autism were less likely than those of typically developing children to report having taken prenatal vitamins. In addition, there were greater risks for autism observed in some of the metabolic genetic variants, in those mothers who did not take prenatal vitamins preconception and/or in the first month. In short, the use of prenatal vitamins, taken preconception, may reduce the risk of having children with autism, especially for genetically susceptible mothers and children.

Commentary: Attention is being increasingly given to the preconception time period and the health and nutritional status of the mother in particular. This is distinct from the use of vitamins/minerals/herbs to enhance fertility in men and women. I’m encouraged to see research in this area, and to see positive results, in something as simple and affordable as prenatal vitamins is especially reassuring, and in something as daunting as autism, with the incidence increasing and as yet with an unclear cause. According to “Autism Speaks”, a leading science and advocacy organization, it is estimated that 1 in 110 children in US are diagnosed with autism. Government statistics suggest the prevalence rate of autism is increasing 10 to 17 percent annually. We clearly need to become more aggressive in understanding the potential causes and influences on autism, and be assertive in any prevention strategies that can reduce the incidence.

Reference

Schmidt R, Hansen R, Hartiala J, et al. Prenatal Vitamins, One-carbon Metabolism Gene Variants, and Risk for Autism. Epidemiology; July 2011 – Volume 22 – Issue 4 – pp 476-485

Magnesium plays a role in more than 300 enzymatic reactions and is involved in energy metabolism, cellular metabolism, utilization of glucose, synthesis of protein and fatty acids, muscle contractions, all hormonal reactions, neurotransmitter production, and intracellular balance of sodium, potassium and calcium.[1]

The list is long for the consequences of a magnesium deficiency. Magnesium deficiencies can result in hypokalemia (low potassium), alkalosis, hypertension, congestive heart failure, arrhythmia, myocardial infarction, angina pectoris, clotting, atherosclerosis, type 2 diabetes, preeclampsia and other electrolyte deficiencies. [2]

Magnesium deficiency can be acquired many ways. A decrease in dietary consumption of magnesium has gone from 500mg/day in 1900 to 215-283 mg/day in 1990.[3]^{, [4]} It is estimated that the typical dietary intake of magnesium today in the U.S. provides only 35-75% of the recommended daily amount.[5]

Many over the counter and prescription drugs can influence magnesium nutrient levels and depletion. The list is long, but includes loop and thiazide diuretics, digoxin, carboplatin and cisplatin, corticosteroids, estrogen and oral contraceptives, insulin, proton pump inhibitors, tetracyclines, cyclosporine, laxatives and more.1 Advanced age is also associated with decreased serum and tissue magnesium levels.

Perhaps one of the more common problems with magnesium results in the relationship of calcium and magnesium. High calcium diets or calcium supplementation without attention to magnesium supplementation has been shown to decrease tissue magnesium levels, [6] increase magnesium requirements[7] and decrease magnesium absorption.[8] In individuals with low or suboptimal magnesium status, administration of calcium without concomitant magnesium may further compromise their magnesium status, further increasing their risk of the many of the health risks associated with magnesium insufficiency/deficiency that we have mentioned earlier.

Convenient serum testing for magnesium is usually inadequate because it does not reflect magnesium stores. Less convenient but more accurate testing would include a magnesium-loading test looking at 24-hour urinary magnesium excretion after an infusion of magnesium. Magnesium can also be measured in red blood cells, white blood cells, mononuclear blood cells, and muscle. An intracellular mineral electrolyte panel using cell scrapings under the tongue with electronic photon bombardment technology is available as well.

Supplementing the body’s magnesium stores through oral supplementation takes about six weeks but may be up to six months or more. [9]^,[10] Many different magnesium salts are available as supplements. Magnesium oxide contains the largest amount of elemental magnesium. Magnesium chloride has high bioavailability. Magnesium may also be bound to aspartate, malate, succinate, fumarate, citrate, gluconate, sulfate and chloride. Some manufacturers assert that magnesium chelated to malate, succinate, fumarate or citrate are better absorbed, utilized and tolerated, but this is variable and not definitive.

Given the prevalence of hypertension, congestive heart failure, arrhythmias, ischemic heart disease, heart attacks and type 2 diabetes in the U.S., magnesium has emerged as a very critical supplement for prevention and management of these conditions. Intervention doses vary from 250 mg/day to 1,000 mg/day depending on the condition, body weight, age, and tolerability. Individuals with kidney disease or heart blocks should not take magnesium unless under a physician’s supervision. Magnesium is generally well tolerated, although there is often a dose limiting amount above which causes loose stool.

Magnesium is an essential mineral for normal body physiology. Deficiencies and insufficiencies are more common than is easily detected, and may lead to numerous cardiovascular disorders, type 2 diabetes, preeclampsia and eclampsia.

In most cases, I recommend that calcium supplementation should also include magnesium supplementation and a ration of approximate 2 parts calcium: 1 part magnesium. Current reference guidelines for daily intake for your age and gender can be obtained from the Institute of Medicine or from www.nutrition.gov. It is important to keep in mind the dietary supplement dosages are in addition to the average daily amount you are getting in your diet, to achieve the recommended daily amount.

References

[1] Dacey M. Hypomagnesemic disorders. Crit Care Clin. 2001;17:155-173.

[2] Gums J. Magnesium in cardiovascular and other disorders. Am J Health-Syst Pharm 2004;61:1569—76.

[3] Kawano Y, Matsuoka H, Takishita S, et al. Effects of magnesium supplementation of hypertensive patients: assessment by office, home, and ambulatory blood pressures. Hypertension. 1998;32:260-5.

[4] Arsenian M. Magnesium and cardiovascular disease. Prog Cardiovasc Dis. 1993; 35:271-310.

[5] Altura B, Altura B. Magnesium and cardiovascular biology: an important link between cardiovascular risk factors and atherogenesis. Cell Mol Biol Res. 1995;41:347-59.

[6] Smith K, Luhrsen K. Trace mineral interactions during elevated calcium consumption. Fed Proc 1986;45:374.

[7] O’Dell BL, Morris ER, Regan WO. Magnesium requirement of guinea pigs and rats. Effect of calcium and phosphorus and symptoms of magnesium deficiency. J Nutr 1960;70:103-111.

[8] Clarkson E, Warren L, McDonald S, de Wardener H. The effect of a high intake of calcium on magnesium metabolism in normal subjects and patients with chronic renal failure. Clin Sci 1967;32:11-18.

[9] Hollifield J. Thiazide treatment of hypertension: effects of thiazide diuretics on serum potassium, magnesium, and ventricular ectopy. AmJ Med. 1986;80 (suppl 4A): 8-12.

[10] Whang R, Ham;pton E, Whang D. Magnesium homeostasis and clinical disorders of magnesium deficiency. Ann Pharmacother. 1994;28:220-6.

Premenopausal women appear to be more sensitive at detecting breast cancer when done during the first week of the menstrual cycle (day 1 of the menses to day 7) in women with a history of screening mammograms. Researchers analyzed 387,218 screening mammograms in premenopausal women that were associated with 1,283 breast cancers. Greater sensitivity was found in week 1 (79.5%) compared to week 2 (70.3%), week 3 (67.4%) or week 4 (73%). Oddly, in the small percentage of women who were getting a screening mammogram for the first time, the sensitivity was lower during week 1 (72.1%) than in week 2 (80.4%), week 3 (84.6%) and week 4 (93.8%).

Comments: Premenopausal women do tend to have denser breasts than postmenopausal women, due to more estrogen in their system. This is known to make it more difficult for mammography to detect small tumors. The results of this study, at least in the women with a history of screening mammograms, makes sense as the breast density may be less in the first part of the menstrual cycle when estrogen is the lowest.

Reference: Miglioretti D, Walker R, WEaber D, et al. Accuracy of screening mammography varies by week of menstrual cycle. Radiology 2011; 258(2):372-379.

In another study, from Spain, digital mammography results were compared with traditional screen film mammography and investigators found a lower false-positive rate in the digital mammography. After reviewing 242,838 mammograms (171,191 screen-film mammograms and 71,647 digital mammograms) from 103,613 women ages 45 to 69. The screen film mammograms had a 32% higher false-positive rate than the digital mammography. This was a false-positive rate of 7.6% in screen films and 5.7% in digital, although there was no significant difference in the overall cancer detection rate between the two groups.

Comments: The results of this study are not surprising. Digital mammography has been an important step in the evolution of mammography. It has been shown to be superior in contrast of normal vs. abnormal tissue with increased diagnostic quality of images, increased sensitivity particularly in dense breasts and a better ability to store images and transmit images electronically.

Reference : Sala M, Salas D, Belvis F, et al. Reduction in false-positive results after introduction of digital mammography analysis from four population-based breast cancer screening programs in Spain. Radiology. 2011;258(2):388-395.

The cause of premenstrual syndrome (PMS) is not convincingly known, and continued exploration into possible dietary associations goes on. Investigators conducted a study nested within the Nurses’ Health Study, a very large group of women who provide biennial reports on their diet and lifestyle and health status. The possible association of dietary B vitamin intake and PMS was evaluated over a 10 year period. PMS was diagnosed in 36% of the participants (1057 women) and 1,968 women did not have PMS.

Women who had the highest intake of thiamine were 25% less likely to develop PMS than those with the lowest intake. Women with the highest intake of riboflavin were 35% less likely to develop PMS. The intake of all B vitamins together in a B-complex supplement did not appear to lower the risk for PMS.

Comments: Vitamin B6 (pyridoxine) has shown benefits in treating PMS in most, but not all studies, and has shown a substantial and broad effect on the whole range of PMS symptoms in the positive studies. Doses have ranged from 50 gm to 500 mg per day. Given this body of research and information spanning since 1973, I’m not sure what compelled the investigators in this current study to track vitamins B1 and B2, rather than vitamin B6.

Reference: Chocano-Bedoya P, et al. Dietary B vitamin intake and incident premenstrual syndrome. Am J Clin Nutr 2011 May; 93:1080

Dear all,
I’m hoping to lead another group trip to the sacred holy land of the Navajo-Canyon de Chelly, September 2-5.
Our base camp is in the valley of the canyon, surrounded by beautiful canyon walls, with beautiful moon and sun rises and sets.  We do group cooking and eating in an outdoor kitchen.  We camp in our tents with an outhouse and primitive outdoor shower.  Our Navajo guides are Lupita and Jon McClanahan, who are local canyon residents, and very special people.  We will be camping on their ancestral land, in the remote regions of the canyon.

Our daily activities include incredible hikes.  Not too strenuous although for some people the heights can be a problem occasionally.  We hike up and down the canyon walls, hike to Anasazi ruins, and visit a traditional birthing Hogon.  One of my favorite parts is that we will hear incredibly wonderful stories-Navajo and Anasazi history, cultural insights, ceremonial healing ceremonies and some of the healing traditions of the Navajo.  We hear of the birthing traditions, Navajo spirituality, and "the beauty way".    At night, we sit around the fire and talk; Jon or Lupita also tell some stories= grandfather fire, stories from Lupita’s childhood living in the canyon in the traditional ways, and more. 

I have been to the canyon many times in the last 7 years.  Jon and Lupita have become close friends and deeply meaningful teachers.  They are beautiful in their ways of speaking and living.  Their spirituality, and their commitment to living their lives in keeping with their traditional spirituality, is evident in all that they do.  My life has changed in extraordinary and powerful ways as a result of knowing them. 

If you are interested in this fantastic trip, write Tori Hudson, N.D. at womanstime@aol.com or call, 503-222-2322. You can also learn a bit more about the canyon and Jon and Lupita, from their website, www.footpathjourneys.com

The cost of the trip is affected by the number of people on the trip but I anticipate 525.00. Most all of this money goes to Jon and Lupita except for the food supplies which I purchase and transport from Albuquerque. Your transportation costs to and from Chinle, Arizona are extra. I can work with you to arrange car pools/car rentals from Phoenix or Albuquerque.

Tori Hudson, N.D.

Maternal folate levels for the prevention of neural tube defects are considered a mainstay message for women of childbearing age. Side effects of synthetic folic acid supplementation have received some attention recently due to potential side effects. The most familiar is the potential to interfere with the diagnosis of a vitamin B12 deficiency related neurologic disease. This potential masking effect of folic acid supplementation occurs because megaloblastic anemia resulting from folate deficiency is not clinically distinguishable from megaloblastic anemia due to vitamin B12 deficiency. The megaloblastic anemia caused by a B12 deficiency responds to folic acid as does the megaloblastic anemia caused by folate deficiency. The problem is that the neurologic disease caused by a B12 deficiency does not respond to folic acid, only to Vitamin B12. As a result, a B12 deficient megaloblastic anemia and related neurologic problems will remain untreated and get worse if only folic acid is given. While this potentially harmful effect of masking is the primary reason that the Institute of Medicine (IOM) recommends that daily folic acid should not exceed 1,000 mcg per day,[i] synthetic L-5-methyl-THF, the bioavailable form of folate, does not have this masking effect.

In the last five years, some studies have suggested that high levels of unmetabolized folate may be associated with an increase in the risk for colorectal cancer. [ii]^{, [iii]}

In those individuals with premalignant colorectal lesions, excess folate, and in particular the thymidylate, a component of DNA that is synthesized from folate, could facilitate cell division of these premalignant lesions and lead to cancer. On the other hand, in those individuals without a premalignant lesion, folate may actually protect normal cells from becoming neoplastic. 3

Some evidence now exists for this “dual-modulator” effect of folate and colorectal neoplasia, whether dietary or supplemental. [iv],[v] This dual effect of folate, prevention vs. proliferative effect of premalignant lesions has been raised with prostate and breast cancer but recent studies have shown that appropriate folate intake does not significantly increase or decrease risks for breast[vi] and prostate cancer.[vii]

Adequate maternal intake of folic acid reduces the frequency of neural tube defects by up to 75%, and may also reduce the frequency of other birth defects such as ventricular septal defects, tetralogy of Fallot and transposition of the great vessels,[viii] urinary tract abnormalities [ix] and possibly even cleft lip and/or cleft palate.[x]

Currently, the average intake of folic acid from the diet of women of childbearing age is about 170mcg/day.[xi] A diet without folic acid fortified grains is typically 140 mcg/day. Clearly, too few women are achieving adequate serum folate levels through diet alone and do require supplementation. The RDA for folate in non-pregnant women is 400 mcg per day. [xii]The RDA for folate in pregnancy is 600 mcg per day[xiii] although the latest US Preventive Services Task Force recommendation is 400mcg-800 mcg per day for women of childbearing age.[xiv] The American College of Obstetricians and Gynecologists recommends that non pregnant women of childbearing aged consume 400 mcg/day. [xv] This variability reflects the uncertainty about the exact dose that is option for the prevention of neural tube defects. For women with a previous pregnancy resulting in a neural tube defect, 4,000 mcg is necessary to achieve these prevention benefits.15

While there is some concern about long term folic acid supplementation for a select number of individuals, the benefits for reproductive aged women, pre-pregnancy and pregnant, outweighs any concerns. A cautionary approach in terms of benefits and risks might be to meticulously track dietary intake to assure adequate levels, or to supplement with folic acid in combination with L-5-methyl-THF or L-5-methyl-THF alone.

[i] Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington, DC: National Academy Press; 1998.

[ii] Mason J, Dickstein A, Jacques P, et al. A temporal association between folic acid fortification and an increase in colorectal cancer rates myay be illuminating important biological principles : a hypothesis. Cancer Epidemiol Biomarkers Prev 2007;16(7):1325-1329

[iii] Sanjoaquin M, Allen N, Couto E, et al. Folate intake and colorectal cancer risk : a meta-analytical approach. Int J Cancer. 2005;113(5):825-828.

[iv] Mathers J. Folate intake and bowel cancer risk. Genes Nutr 2009;4(3)::173-178.

[v] Hubner R, Houlston R. Folate and colorectal cancer prevention. Br J Cancer. 2009;100(2):233-239.

[vi] Kim Y. Does a high folate intake increase rhe risk of breast cancer? Nutr Rev. 2006;64(10 pt 1):468-475

[vii] Figueiredo J, Grau M, Haile R, et al. Folic acid and risk of prostate cancer: results from a randomized clinical trial. J Natl Cancer Inst. 2009;101(6):432-435.

[viii] Botto L, Mulinare J, Erickson J. Do multivitamin or folic acid supplements reduce the risk for congenital heart defects? Evidence and gaps. Am J Med Genet. 2003;121A(2):95-101.

[ix] Czeizel A. Reduction of urinary tract and cardiovascular defects by periconceptional multivitamin supplementation. Am J Med Genet. 1996;62(2):179-183.

[x] Badovinac R, Werler M, Williams P, et al. Folic acid-containing supplement consumption during pregnancy and risk for oral clefts: a meta-analysis. Birth Defects Res A Clin Mol Teratol. 2007;79(1):8-15.

[xi] US Food and Drug Administration. Food standards: amendment of standards of identity for enriched grain products to require addition of folic acid. Final rule. 212 CFR Parts 136, 137, 139. Fed Regist. 1996;61(44):8781-8797

[xii] Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington DC: National Academy Press; 1998.

[xiii] Simpson J, Bailey L, Pietrzik K, Shane B, Holzgreve . Micronutrients and women of reproductive potential: required dietary intake and consdquences of dietary deficiency or escess. Part !-Folate, Vitamin B12, Vitamin B6. J Matern Fetal Neonatal Med 2010.

[xiv] US Preventive Services Task Force. Folic acid for the prevention of neural tube defects: US preventive services task force recommendation statement. Ann Intern Med 2009;150(9):626-631

[xv] Cheschier N. ACOG Committee on Practice Bulletins-Obstetrics. ACOG practice bulletin. Neural tube defects. November 44, July 2003. Int J Gynecol Obstet 2003;83(1):123-133.

The effect of Maitake extract was explored as to its ability to induce ovulation in women with polycystic ovarian syndrome (PCOS) in comparison with and in combination with clomiphene citrate (CC). An open trial was conducted in 80 women with PCOS at three different clinics in Japan. Seventy two patients were randomized and 36 received Maitake extract and 36 received CC for up to 12 weeks. Eighteen patients who did not respond to either the Maitake extract or the CC were then given a combination of Maitake extract and CC for up to 16 weeks. Eight patients with a history of failure to CC received the combination therapy from the beginning of the study.

The Maitake extract tablets contained 18 mg of an extract called “SX-fraction” (MSX), a water-soluble glycoprotein, and 250 mg of dried Maitake mushroom powder. Each patient was given 3 tablets, 3 times a day. For those who received the CC, they were given 50 mg/day from days 5 to 9 of menses and repeated up to 3 cycles. For patients who then took the combination, the same dosing regimen was used.

Twenty-six patients in the MSX group and 31 in the CC group were evaluated for ovulation with pelvic ultrasounds. The ovulation rate for MSX was 76.9% (20/26) and 93.5% (29/31) for CC. For the combination treatment, 7 of 7 patients who failed the MSX monotherapy and 6 of 8 patients who failed the CC monotherapy demonstrated ovulation.

Commentary: This study demonstrated the ability of a Maitake extract to induce ovulation in patients with PCOS and can be used as a monotherapy or as an adjunct to clomiphene citrate. The ovulation rate of 76.9% is quite impressive, even though the clomiphene citrate rate was much better at 93.5%.

Maitake extract is reported to modulate serum glucose levels, reduce blood pressure, optimize serum lipids and enhance insulin sensitivity in animal studies, all important core issues in women with PCOS.

Reference

Chen J, Tominaga K, Sato Y, et al. Maitake mushroom (Grifola frondosa) extract induces ovulation in patients with polycystic ovary syndrome: a possible monotherapy and a combination therapy after failure with first-line clomiphene citrate. J Alternative and Complementary Medicine 2010;12(12):1295-1299