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	<title>Dr. Tori Hudson, N.D. &#187; Prevention</title>
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	<link>http://drtorihudson.com</link>
	<description>Naturopathic Physician, Author, Educator and Researcher</description>
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		<copyright>Copyright &#xA9; Dr. Tori Hudson, N.D. 2010 </copyright>
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		<itunes:summary>Naturopathic Physician, Author, Educator and Researcher</itunes:summary>
		<itunes:author>Dr. Tori Hudson, N.D.</itunes:author>
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			<itunes:name>Dr. Tori Hudson, N.D.</itunes:name>
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		<title>The Habit of Exercise</title>
		<link>http://drtorihudson.com/general/the-habit-of-exercise/</link>
		<comments>http://drtorihudson.com/general/the-habit-of-exercise/#comments</comments>
		<pubDate>Tue, 29 Nov 2011 21:31:00 +0000</pubDate>
		<dc:creator>Tori Hudson, N.D.</dc:creator>
				<category><![CDATA[General]]></category>
		<category><![CDATA[Prevention]]></category>
		<category><![CDATA[Weight Management]]></category>

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		<description><![CDATA[I often say to my patients, “there is no medication, herb, vitamin, mineral or therapy that does as much for your health as does exercise”. Regular exercise is associated with so many health benefits… you wonder why we are so resistant to it. Exercise research is associated with reducing the risk of most of the [...]]]></description>
			<content:encoded><![CDATA[<p>I often say to my patients, “there is no medication, herb, vitamin, mineral or therapy that does as much for your health as does exercise”. Regular exercise is associated with so many health benefits… you wonder why we are so resistant to it. Exercise research is associated with reducing the risk of most of the significant/common American issues&#8212;cardiovascular disease, osteoporosis, type 2 diabetes, osteoarthritis, obesity and breast cancer. In addition, it is known to be an anti-depressant, reduces PMS symptoms, and improves the immune system. Of our many unhealthy habits that can lead to shorter life spans and chronic health problems, having a sedentary lifestyle is at the top of the list.</p>
<p>We often talk of exercise programs, gym memberships and exercise classes of all kinds, but it starts with… we just don’t move as much as we used to. Most of us are not living on farms and ranches, not hauling hay or planting, foraging and picking our food, not hauling and chopping our firewood, and not building our shelters. Most of us aren’t even playing outside anymore. Too many of us have acquired the thought that all our needs can be met by a flip of a switch or an indoor environment. Again, too many of us press the garage door opener, put our clothes in the washing machine and our dishes in the dishwasher, watch TV and play/work on the computer, take an elevator or escalator to our destination and park right in front of the store.</p>
<p>In addition to this lack of physical activity in our daily life, most individuals in modern America have sedentary jobs where we sit most of the work week&#8211; talking on the telephone, typing, writing, working on the computer, talking with clients or patients or working at the check out counter.</p>
<p>Our bodies are made to move and actually can do it quite well, but sadly, most us do not have any kind of routine exercise and have a bevy of excuses to support our choice&#8212;not enough time, too cold, too wet, too dark, too tired, too many aches and pains, and on and on. I’ve had them myself at times.</p>
<p><a href="http://drtorihudson.com/wp-content/uploads/2011/11/exercise.jpg"><img style="background-image: none; border-bottom: 0px; border-left: 0px; padding-left: 0px; padding-right: 0px; display: inline; float: left; border-top: 0px; border-right: 0px; padding-top: 0px" title="exercise" border="0" alt="exercise" align="left" src="http://drtorihudson.com/wp-content/uploads/2011/11/exercise_thumb.jpg" width="244" height="163" /></a>In working with patients, I take a gentle yet tough love approach full of support and empathy and education… it is useful to ask questions, find the limitations and obstacles, try to find out what they might like, try to strategize the practicalities, set goals, motivate and inspire and never give up on the potential for change. The tough love part is trying to find ways to make them realize that moving/exercising should be considered a mandatory part of their life. I even say some times… “You have got to get religion about exercise”. Some helpful keys to the process can be: 1) Focus on the fact that you can do it&#8211; you can become someone who regularly exercises. 2) Make a schedule for when it is going to happen. Each day… I plan for when I am going to get my 60 minutes of exercise in for that day and even the next. “Oh… on my lunch hour I can walk to the hardware store, shop for light bulbs, walk back to the office (that’s 30), and then I have another 30 minute walk after work&#8212; either to the grocery store after work, or on a forest trail next to my house once I get home. 3) Maybe find an exercise partner or a personal trainer or a class or a team of some kind&#8211; even for those who are not athletically inclined&#8212; paddling on a “dragon boat” team might be just the ticket. 4) Set goals and make them a priority&#8211; and set goals that are realistic. 5) Know your limits and don’t injure yourself or make a chronic health problem worse.</p>
<p>According to the American Heart Association and to reduce the risk of chronic disease we need to have 30 minutes of moderately intense physical activity per day most days of the week. For those women who need to lose significant weight… it will probably take more than that to overcome the physiological forces that are now in play&#8211; insulin resistance, slowed metabolism, loss of muscle mass and aging. In my women patients who desire weight loss… our goal is 60+ minutes per day of aerobic exercise (walking, treadmill, elliptical, bicycle, running) for 6-7 days per week and ideally, some kind of strength training (yoga, weight training) 2 days per week.</p>
<p>With education, desire, and a plan…. You can succeed!! You can make a change! You can improve the quality of your life!</p>
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		<title>Probiotic Therapy for Urinary Tract Infections</title>
		<link>http://drtorihudson.com/prevention/probiotic-therapy-for-urinary-tract-infections/</link>
		<comments>http://drtorihudson.com/prevention/probiotic-therapy-for-urinary-tract-infections/#comments</comments>
		<pubDate>Tue, 20 Sep 2011 22:32:00 +0000</pubDate>
		<dc:creator>Tori Hudson, N.D.</dc:creator>
				<category><![CDATA[Prevention]]></category>

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		<description><![CDATA[This trial involved 100 women with recurrent urinary tract infections (UTIs), who were seen at the University of Washington and an average age of 21. Lactobacillus crispatus or placebo was inserted vaginally for 5 days and then once weekly for 10 weeks, starting 7-10 days after they had received standard antibiotic therapy for their UTI. [...]]]></description>
			<content:encoded><![CDATA[<p>This trial involved 100 women with recurrent urinary tract infections (UTIs), who were seen at the University of Washington and an average age of 21. Lactobacillus crispatus or placebo was inserted vaginally for 5 days and then once weekly for 10 weeks, starting 7-10 days after they had received standard antibiotic therapy for their UTI. The lactobacillus crispatus suppositories contained 10 billion CFUs/mL.</p>
<p>The levels of L. crispatus colonization were evaluated with a vaginal swab and their UTI status was followed at 1 and 10 weeks. Women in both groups had depletion of Lactobacillus colonization. At week 10, at least one UTI had occurred in 15% of the L. crispatus individuals versus 27% in the placebo individuals. A high level of L. crispatus colonization was achieved in 93% of the crispatus subjects versus 68% of the placebo subjects. The risk for a recurrent UTI was lower in the women who received L. crispatus versus placebo, in those with high colonization.</p>
<p><b>Commentary:</b> UTIs are very common in women and more than half of women in the U.S. will experience at least one in their life. Ten to twenty percent of all women have a UTI at least once a year. The use of antibiotics for UTIs potentially adds to the problem, in that drug resistance occurs, and the antibiotic itself depletes the vaginal and bladder lactobacillus species that serve to prevent UTIs. Normal vaginal flora is dominated by hydrogen peroxide producing lactobacilli that competitively inhibit the infection causing bacteria of the urethra and bladder, particularly Escherichia coli. The question these researchers asked was, can a hydrogen peroxide producing vaginal probiotic prevent recurrent UTIs. The answer is, yes they can- and in this case, Lactobacillus crispatus was the test subject.</p>
<p><b>Reference</b></p>
<p>Stapleton A, et al. Randomized, placebo-controlled phase 2 trial of a Lactobacillus crispatus probiotic given intravaginally for prevention of recurrent urinary tract infection. Clin Infect Dis 2011; May 15; 52:1212</p>
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		<title>Good news for chocolate lovers</title>
		<link>http://drtorihudson.com/prevention/good-news-for-chocolate-lovers/</link>
		<comments>http://drtorihudson.com/prevention/good-news-for-chocolate-lovers/#comments</comments>
		<pubDate>Fri, 19 Aug 2011 20:28:00 +0000</pubDate>
		<dc:creator>Tori Hudson, N.D.</dc:creator>
				<category><![CDATA[Cardiovascular]]></category>
		<category><![CDATA[Prevention]]></category>

		<guid isPermaLink="false">http://drtorihudson.com/prevention/good-news-for-chocolate-lovers/</guid>
		<description><![CDATA[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 = &#60; 1 25-50 gm serving per week and frequent intake = &#62; 1servings per week. Approximately half of the women rarely ate chocolate and 36% [...]]]></description>
			<content:encoded><![CDATA[<p><a href="http://drtorihudson.com/wp-content/uploads/2011/08/clip_image002.jpg"><img style="background-image: none; border-bottom: 0px; border-left: 0px; padding-left: 0px; padding-right: 0px; display: inline; float: left; border-top: 0px; border-right: 0px; padding-top: 0px" title="clip_image002" border="0" hspace="12" alt="clip_image002" align="left" src="http://drtorihudson.com/wp-content/uploads/2011/08/clip_image002_thumb.jpg" width="202" height="134" /></a>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 = &lt; 1 25-50 gm serving per week and frequent intake = <u>&gt;</u> 1servings per week. </p>
<p>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. </p>
<p>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!!!</p>
<p><b>Reference</b></p>
<p><i>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.</i></p>
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		<title>Fish oils and Coronary Heart Disease (CHD)</title>
		<link>http://drtorihudson.com/prevention/fish-oils-and-coronary-heart-disease-chd/</link>
		<comments>http://drtorihudson.com/prevention/fish-oils-and-coronary-heart-disease-chd/#comments</comments>
		<pubDate>Fri, 22 Jul 2011 18:43:00 +0000</pubDate>
		<dc:creator>Tori Hudson, N.D.</dc:creator>
				<category><![CDATA[Cardiovascular]]></category>
		<category><![CDATA[Dietary Supplements]]></category>
		<category><![CDATA[Prevention]]></category>

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		<description><![CDATA[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 [...]]]></description>
			<content:encoded><![CDATA[<p>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. <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn1" name="_ednref1">[1]</a> 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),<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn2" name="_ednref2">[2]</a> 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) <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn3" name="_ednref3">[3]</a> 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. </p>
<p>The JELIS (Japan EPA Lipid Intervention Study) trial <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn4" name="_ednref4">[4]</a> included a total of 18,645 subjects (men <a href="http://drtorihudson.com/wp-content/uploads/2011/07/clip_image002.jpg"><img style="background-image: none; border-bottom: 0px; border-left: 0px; padding-left: 0px; padding-right: 0px; display: inline; float: left; border-top: 0px; border-right: 0px; padding-top: 0px" title="clip_image002" border="0" hspace="12" alt="clip_image002" align="left" src="http://drtorihudson.com/wp-content/uploads/2011/07/clip_image002_thumb.jpg" width="174" height="117" /></a>aged 40-75 and postmenopausal women aged <u>&gt;</u> 75 and a mean age of 61 years and 31% men). Those with a serum total cholesterol level of <u>&gt;</u> 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. </p>
<p>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. </p>
<p><i>Recommended doses for primary and secondary prevention: </i></p>
<p><i>1,000 mg/day of combined EPA/DHA</i></p>
<p><b>References:</b></p>
<hr align="left" size="1" width="33%" />
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref1" name="_edn1">[1]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref2" name="_edn2">[2]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref3" name="_edn3">[3]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref4" name="_edn4">[4]</a> 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.</p>
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		<title>Prenatal Vitamins and Autism</title>
		<link>http://drtorihudson.com/prevention/prenatal-vitamins-and-autism/</link>
		<comments>http://drtorihudson.com/prevention/prenatal-vitamins-and-autism/#comments</comments>
		<pubDate>Wed, 29 Jun 2011 23:15:00 +0000</pubDate>
		<dc:creator>Tori Hudson, N.D.</dc:creator>
				<category><![CDATA[Dietary Supplements]]></category>
		<category><![CDATA[Pregnancy]]></category>
		<category><![CDATA[Prevention]]></category>

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		<description><![CDATA[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 [...]]]></description>
			<content:encoded><![CDATA[<p>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.</p>
<p><a href="http://drtorihudson.com/wp-content/uploads/2011/06/clip_image002.jpg"><img style="background-image: none; border-bottom: 0px; border-left: 0px; padding-left: 0px; padding-right: 0px; display: inline; float: left; border-top: 0px; border-right: 0px; padding-top: 0px" title="clip_image002" border="0" hspace="12" alt="clip_image002" align="left" src="http://drtorihudson.com/wp-content/uploads/2011/06/clip_image002_thumb.jpg" width="133" height="190" /></a>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. </p>
<p><b>Commentary</b>: 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.</p>
<p><b>Reference</b></p>
<p>Schmidt R, Hansen R, Hartiala J, et al. Prenatal Vitamins, One-carbon Metabolism Gene Variants, and Risk for Autism. Epidemiology; July 2011 &#8211; Volume 22 &#8211; Issue 4 &#8211; pp 476-485</p>
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		<title>Magnesium- Risks of Deficiencies and Cardiovascular Disease, Problems in Absorption, and Improving Testing Methods</title>
		<link>http://drtorihudson.com/prevention/magnesium-risks-of-deficiencies-and-cardiovascular-disease-problems-in-absorption-and-improving-testing-methods/</link>
		<comments>http://drtorihudson.com/prevention/magnesium-risks-of-deficiencies-and-cardiovascular-disease-problems-in-absorption-and-improving-testing-methods/#comments</comments>
		<pubDate>Tue, 14 Jun 2011 23:47:00 +0000</pubDate>
		<dc:creator>Tori Hudson, N.D.</dc:creator>
				<category><![CDATA[Dietary Supplements]]></category>
		<category><![CDATA[Prevention]]></category>

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		<description><![CDATA[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 [...]]]></description>
			<content:encoded><![CDATA[<p>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.<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn1" name="_ednref1">[1]</a></p>
<p>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. <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn2" name="_ednref2">[2]</a></p>
<p><a href="http://drtorihudson.com/wp-content/uploads/2011/06/Periodic-table-Mg.jpg"><img style="background-image: none; border-bottom: 0px; border-left: 0px; padding-left: 0px; padding-right: 0px; display: inline; float: left; border-top: 0px; border-right: 0px; padding-top: 0px" title="Periodic table - Mg" border="0" alt="Periodic table - Mg" align="left" src="http://drtorihudson.com/wp-content/uploads/2011/06/Periodic-table-Mg_thumb.jpg" width="244" height="163" /></a>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.<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn3" name="_ednref3">[3]</a><sup>, <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn4" name="_ednref4">[4]</a></sup> It is estimated that the typical dietary intake of magnesium today in the U.S. provides only 35-75% of the recommended daily amount.<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn5" name="_ednref5">[5]</a></p>
<p>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.<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn6" name="_ednref6">1</a> Advanced age is also associated with decreased serum and tissue magnesium levels.</p>
<p>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, <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn7" name="_ednref7">[6]</a> increase magnesium requirements<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn8" name="_ednref8">[7]</a> and decrease magnesium absorption.<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn9" name="_ednref9">[8]</a> 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. </p>
<p>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.</p>
<p>Supplementing the body’s magnesium stores through oral supplementation takes about six weeks but may be up to six months or more. <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn10" name="_ednref10">[9]</a><sup>,<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn11" name="_ednref11">[10]</a></sup> 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.</p>
<p>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.</p>
<p>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.</p>
<p>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 <a href="http://www.nutrition.gov/">www.nutrition.gov</a>. 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.</p>
<p><b>References</b></p>
<hr align="left" size="1" width="33%" />
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref1" name="_edn1">[1]</a> Dacey M. Hypomagnesemic disorders. Crit Care Clin. 2001;17:155-173.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref2" name="_edn2">[2]</a> Gums J. Magnesium in cardiovascular and other disorders. Am J Health-Syst Pharm 2004;61:1569—76.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref3" name="_edn3">[3]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref4" name="_edn4">[4]</a> Arsenian M. Magnesium and cardiovascular disease. Prog Cardiovasc Dis. 1993; 35:271-310.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref5" name="_edn5">[5]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref6" name="_edn6"></a></p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref7" name="_edn7">[6]</a> Smith K, Luhrsen K. Trace mineral interactions during elevated calcium consumption. Fed Proc 1986;45:374.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref8" name="_edn8">[7]</a> O&#8217;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. </p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref9" name="_edn9">[8]</a> 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. </p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref10" name="_edn10">[9]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref11" name="_edn11">[10]</a> Whang R, Ham;pton E, Whang D. Magnesium homeostasis and clinical disorders of magnesium deficiency. Ann Pharmacother. 1994;28:220-6.</p>
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		<title>Mammogram timing and digital vs. screen film mammography</title>
		<link>http://drtorihudson.com/prevention/mammogram-timing-and-digital-vs-screen-film-mammography/</link>
		<comments>http://drtorihudson.com/prevention/mammogram-timing-and-digital-vs-screen-film-mammography/#comments</comments>
		<pubDate>Tue, 31 May 2011 19:39:00 +0000</pubDate>
		<dc:creator>Tori Hudson, N.D.</dc:creator>
				<category><![CDATA[Breast Cancer Prevention]]></category>
		<category><![CDATA[Prevention]]></category>

		<guid isPermaLink="false">http://drtorihudson.com/prevention/mammogram-timing-and-digital-vs-screen-film-mammography/</guid>
		<description><![CDATA[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 [...]]]></description>
			<content:encoded><![CDATA[<p><a href="http://drtorihudson.com/wp-content/uploads/2011/05/clip_image0021.jpg"><img style="background-image: none; border-bottom: 0px; border-left: 0px; padding-left: 0px; padding-right: 0px; display: inline; float: left; border-top: 0px; border-right: 0px; padding-top: 0px" title="clip_image002" border="0" hspace="12" alt="clip_image002" align="left" src="http://drtorihudson.com/wp-content/uploads/2011/05/clip_image002_thumb1.jpg" width="137" height="200" /></a>
<p>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%).</p>
<p><b>Comments</b>: 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.</p>
<p><b>Reference: </b><i>Miglioretti D, Walker R, WEaber D, et al. Accuracy of screening mammography varies by week of menstrual cycle. Radiology 2011; 258(2):372-379. </i></p>
<p>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.</p>
<p><b>Comments</b>: 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. </p>
<p><b>Reference : </b><i>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.</i></p>
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		<title>Benefits and Risks of Folic Acid Supplementation</title>
		<link>http://drtorihudson.com/general/benefits-and-risks-of-folic-acid-supplementation/</link>
		<comments>http://drtorihudson.com/general/benefits-and-risks-of-folic-acid-supplementation/#comments</comments>
		<pubDate>Fri, 15 Apr 2011 18:26:00 +0000</pubDate>
		<dc:creator>Tori Hudson, N.D.</dc:creator>
				<category><![CDATA[Dietary Supplements]]></category>
		<category><![CDATA[General]]></category>
		<category><![CDATA[Pregnancy]]></category>
		<category><![CDATA[Prevention]]></category>

		<guid isPermaLink="false">http://drtorihudson.com/general/benefits-and-risks-of-folic-acid-supplementation/</guid>
		<description><![CDATA[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 [...]]]></description>
			<content:encoded><![CDATA[<p>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,<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn1" name="_ednref1">[i]</a> synthetic L-5-methyl-THF, the bioavailable form of folate, does not have this masking effect. </p>
<p>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. <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn2" name="_ednref2">[ii]</a><sup>, <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn3" name="_ednref3">[iii]</a></sup></p>
<p><sup></sup></p>
<p>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. <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn4" name="_ednref4">3</a></p>
<p>Some evidence now exists for this “dual-modulator” effect of folate and colorectal neoplasia, whether dietary or supplemental. <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn5" name="_ednref5">[iv]</a>,<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn6" name="_ednref6">[v]</a> 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<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn7" name="_ednref7">[vi]</a> and prostate cancer.<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn8" name="_ednref8">[vii]</a></p>
<p>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,<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn9" name="_ednref9">[viii]</a> urinary tract abnormalities <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn10" name="_ednref10">[ix]</a> and possibly even cleft lip and/or cleft palate.<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn11" name="_ednref11">[x]</a></p>
<p>Currently, the average intake of folic acid from the diet of women of childbearing age is about 170mcg/day.<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn12" name="_ednref12">[xi]</a> 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. <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn13" name="_ednref13">[xii]</a>The RDA for folate in pregnancy is 600 mcg per day<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn14" name="_ednref14">[xiii]</a> although the latest US Preventive Services Task Force recommendation is 400mcg-800 mcg per day for women of childbearing age.<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn15" name="_ednref15">[xiv]</a> The American College of Obstetricians and Gynecologists recommends that non pregnant women of childbearing aged consume 400 mcg/day. <a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn16" name="_ednref16">[xv]</a> 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.<a href="file:///C:/Users/Estelle/Documents/Blog postings/#_edn17" name="_ednref17">15</a></p>
<p>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. </p>
<hr align="left" size="1" width="33%" />
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref1" name="_edn1">[i]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref2" name="_edn2">[ii]</a> 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</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref3" name="_edn3">[iii]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref4" name="_edn4"></a></p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref5" name="_edn5">[iv]</a> Mathers J. Folate intake and bowel cancer risk. Genes Nutr 2009;4(3)::173-178.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref6" name="_edn6">[v]</a> Hubner R, Houlston R. Folate and colorectal cancer prevention. Br J Cancer. 2009;100(2):233-239.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref7" name="_edn7">[vi]</a> Kim Y. Does a high folate intake increase rhe risk of breast cancer? Nutr Rev. 2006;64(10 pt 1):468-475</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref8" name="_edn8">[vii]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref9" name="_edn9">[viii]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref10" name="_edn10">[ix]</a> Czeizel A. Reduction of urinary tract and cardiovascular defects by periconceptional multivitamin supplementation. Am J Med Genet. 1996;62(2):179-183.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref11" name="_edn11">[x]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref12" name="_edn12">[xi]</a> 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</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref13" name="_edn13">[xii]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref14" name="_edn14">[xiii]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref15" name="_edn15">[xiv]</a> 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</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref16" name="_edn16">[xv]</a> 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.</p>
<p><a href="file:///C:/Users/Estelle/Documents/Blog postings/#_ednref17" name="_edn17"></a></p>
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		<title>Calcium/Vitamin D, IOM guidelines</title>
		<link>http://drtorihudson.com/prevention/calciumvitamin-d-iom-guidelines/</link>
		<comments>http://drtorihudson.com/prevention/calciumvitamin-d-iom-guidelines/#comments</comments>
		<pubDate>Mon, 10 Jan 2011 21:53:00 +0000</pubDate>
		<dc:creator>Tori Hudson, N.D.</dc:creator>
				<category><![CDATA[Bone Health]]></category>
		<category><![CDATA[Prevention]]></category>
		<category><![CDATA[Vitamin D]]></category>

		<guid isPermaLink="false">http://drtorihudson.com/prevention/calciumvitamin-d-iom-guidelines/</guid>
		<description><![CDATA[The Institute of Medicine (IOM) recently released their assessment of current data on health outcomes as they related to calcium and vitamin D after being commissioned by the U.S. and Canadian governments. The new reference values, expressed Dietary Reference Intakes (DRIs), are based on an abundance of information and higher quality published studies than were [...]]]></description>
			<content:encoded><![CDATA[<p>The Institute of Medicine (IOM) recently released their assessment of current data on health outcomes as they related to calcium and vitamin D after being commissioned by the U.S. and Canadian governments. The new reference values, expressed Dietary Reference Intakes (DRIs), are based on an abundance of information and higher quality published studies than were available for the 1997 government values. </p>
<p><a href="http://drtorihudson.com/wp-content/uploads/2011/01/vertebrae.jpg"><img style="background-image: none; border-right-width: 0px; padding-left: 0px; padding-right: 0px; display: inline; float: left; border-top-width: 0px; border-bottom-width: 0px; border-left-width: 0px; padding-top: 0px" title="vertebrae" border="0" alt="vertebrae" align="left" src="http://drtorihudson.com/wp-content/uploads/2011/01/vertebrae_thumb.jpg" width="138" height="194" /></a></p>
<p>A committee of experts evaluated more than one thousand studies and reports as well as listening to testimony from scientists and others. This committee considered that studies about the health benefits beyond bone health were most often from studies that provided mixed results, inconclusive results, or were not from randomized controlled trials. Thus, these were not considered reliable. Their focus then was on the bone growth and bone maintenance data. </p>
<p>&#160;</p>
<p>Their new Recommended Dietary Allowance (RDA) is now 600 IU per day for people ages 1 to 70 and 800 IU per day for those 71 and older. The old guidelines from 1997 were 200 IU per day through age 50, 400 IU per day for ages 51 to 70 and 600 IU per day for 71 and older. While I would consider these guidelines conservative to the extreme, (really a one year old and a 70 y.o. need the same amount????) they at least increased a new safe upper limit of 4,000 IU a day for those 9 years old and above, pregnant or not. The greatest concern I have with these guidelines is that they based their bone dosing guidelines on a target blood level of 20 ng/ml per day, rather than 30 ng/ml per day minimum published in most research about levels needed to suppress the parathyroid gland and avoid unnecessary bone loss. </p>
<p>Most practitioners and a studious group of consumers realize that there are scores of studies on other potential health benefits found in observational/epidemiological studies including colorectal cancer, breast cancer, select autoimmune disorders, cardiovascular disease and much more. It is too bad… that these were not considered, and once again, we may not have optimal prevention, risk reduction guidelines from our government agencies. </p>
<p>For a full list of the dosing guidelines by age group, gender, and pregnancy status, you can find these at <a href="http://www.iom.edu/vitamind">www.iom.edu/vitamind</a></p>
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		<title>Cranberry and Urinary Antimicrobial Effects</title>
		<link>http://drtorihudson.com/general/cranberry-and-urinary-antimicrobial-effects/</link>
		<comments>http://drtorihudson.com/general/cranberry-and-urinary-antimicrobial-effects/#comments</comments>
		<pubDate>Mon, 27 Dec 2010 22:56:00 +0000</pubDate>
		<dc:creator>Tori Hudson, N.D.</dc:creator>
				<category><![CDATA[General]]></category>
		<category><![CDATA[Prevention]]></category>

		<guid isPermaLink="false">http://drtorihudson.com/general/cranberry-and-urinary-antimicrobial-effects/</guid>
		<description><![CDATA[Here is another recent study on the urinary antimicrobial effects of cranberry. This study evaluated 20 adults who did not have an active urinary tract infection, and were not taking antibiotics. In phase 1 of the study, individuals collected first morning urine prior to ingesting 3 caps that contained 275 mg of a mixture of [...]]]></description>
			<content:encoded><![CDATA[<p><a href="http://drtorihudson.com/wp-content/uploads/2010/12/more-cranberries.jpg"><img style="background-image: none; border-right-width: 0px; padding-left: 0px; padding-right: 0px; display: inline; float: left; border-top-width: 0px; border-bottom-width: 0px; border-left-width: 0px; padding-top: 0px" title="Cranberry bog demonstration held at Rockafeller Center" border="0" alt="Cranberry bog demonstration held at Rockafeller Center" align="left" src="http://drtorihudson.com/wp-content/uploads/2010/12/more-cranberries_thumb.jpg" width="240" height="154" /></a>Here is another recent study on the urinary antimicrobial effects of cranberry. This study evaluated 20 adults who did not have an active urinary tract infection, and were not taking antibiotics. In phase 1 of the study, individuals collected first morning urine prior to ingesting 3 caps that contained 275 mg of a mixture of dried whole cranberry extract and 25 mg of a concentrate of cranberry extract. Urine was then collected at 2, 4 and 6 hours. In phase 2, individuals collected urine on 2 consecutive days with no cranberry on day 1 and 900 mg of cranberry preparation on day two. </p>
<p>Results: In phase 1, 7 of 20 (35%) individuals had anti-microbial activity against Escherichia coli, 13 of 20 (65%) had anti-microbial activity against Klebsiella pneumoniae and 9 of 20 (45%) against Candida albicans. In phase 2, 23% showed antimicrobial activity against E. coli, 33% against C. albicans and 67% against K. pneumoniae. </p>
<p><b>Commentary</b>: This study suggests that the anti-microbial activity of this cranberry extract was not significant for E. coli and that the most frequent anti-microbial activity occurred in both phases for only K. pneumoniae.</p>
<p>While not all studies of cranberry have shown significant antimicrobial effects, other studies of cranberry and urinary tract infections have been more positive. The current study did not study individuals with an active infection but their urine was inoculated with the three organisms and then the anti-microbial effects of the cranberry ingestion was measured as effective if there was a 50% or greater reduction in colony forming units.</p>
<p>It may be that a true anti-microbial effect and colony reduction of cranberry is not the main mechanism of action, but rather the ability of the cranberry to inhibit the adherence of the bacteria to the cells lining the bladder and the urethra and thus being flushed out of the urinary tract system. In addition, I would always recommend other key bladder infection ingredients in an acute treatment plan as well as a prevention of recurrence plan that would include Oregon grape root, pipsissewa, buchu, uva ursi, marshmallow root and Lactobacillus species that dominate the urogenital tract.</p>
<p><b>Reference:</b></p>
<p>Lee Y, Najm W, Owens J, et al. Anti-microbial activitiy of urine after ingestion of cranberry: a pilot study. Epublication prior to print publication: eCAM 2010;7(2):227-232 doi:10.1093/ecam/nem183</p>
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