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    <title>Articles</title>
    <link>http://www.lmreview.com/articles/</link>
    <description></description>
    <dc:language>en</dc:language>
    <dc:creator>lara@smart-publications.com</dc:creator>
    <dc:rights>Copyright 2010</dc:rights>
    <dc:date>2010-05-14T21:34:41+00:00</dc:date>
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    <item>
      <title>Getting off the Alzheimer&#8217;s Disease Interstate: Part II</title>
      <link>http://www.lmreview.com/articles/view/getting-off-the-alzheimers-disease-interstate-part-ii/</link>
      <guid>http://www.lmreview.com/articles/view/getting-off-the-alzheimers-disease-interstate-part-ii/#When:20:34:41Z</guid>
      <description>A clear association has been well documented in the peer&#45;reviewed medical literature between lifestyle habits&#8212;diet, intake of specific micronutrients, and exercise&#45;&#45;and the occurrence of Alzheimer&#8217;s disease . This review summarizes key, clinically relevant, findings.</description>
      <dc:subject>Latest Research</dc:subject>
      <dc:date>2010-05-14T20:34:41+00:00</dc:date>
    </item>

    <item>
      <title>Alzheimer&#8217;s and Atherosclerosis &#45; Siblings in a Dysfunctional Family: Part I</title>
      <link>http://www.lmreview.com/articles/view/alzheimers-and-atherosclerosis-siblings-in-a-dysfunctional-family-part-I/</link>
      <guid>http://www.lmreview.com/articles/view/alzheimers-and-atherosclerosis-siblings-in-a-dysfunctional-family-part-I/#When:18:30:28Z</guid>
      <description>Amyloid precursor protein (APP) is the transmembrane protein that, if cleaved by the enzyme beta&#45;secretase, produces amyloid beta (the histopathological hallmark of Alzheimer&#8217;s disease [AD]). If acted upon by the enzyme alpha&#45;secretase, however, APP cleavage produces neuroprotective compounds.  What determines which enzyme will gain access to APP? The answers to this question reveal connections among cardiovascular disease, neurological dysfunction and nutrient insufficiencies that provide the rationale for new therapeutic strategies to prevent AD.</description>
      <dc:subject>Latest Research</dc:subject>
      <dc:date>2010-04-21T18:30:28+00:00</dc:date>
    </item>

    <item>
      <title>Erectile Dysfunction as an Adverse Drug Reaction</title>
      <link>http://www.lmreview.com/articles/view/erectile-dysfunction-as-an-adverse-drug-reaction/</link>
      <guid>http://www.lmreview.com/articles/view/erectile-dysfunction-as-an-adverse-drug-reaction/#When:16:25:22Z</guid>
      <description>ED remains a greatly under&#45;reported adverse drug reaction (ADR) because male patients often are not forthcoming about, and doctors usually do not raise the issue of, sexual function. Research presented at the Second Princeton Consensus Conference on Sexual Dysfunction and Cardiac Risk indicates that ED affects more than half of men &gt;60 years.</description>
      <dc:subject>Latest Research</dc:subject>
      <dc:date>2010-03-05T16:25:22+00:00</dc:date>
    </item>

    <item>
      <title>Managing Erectile Dysfunction&#8212;When Viagra Doesn&#8217;t</title>
      <link>http://www.lmreview.com/articles/view/managing-erectile-dysfunction-when-viagra-doesnt/</link>
      <guid>http://www.lmreview.com/articles/view/managing-erectile-dysfunction-when-viagra-doesnt/#When:18:27:53Z</guid>
      <description>Phosphodiasterase&#45;5 (PDE&#45;5) inhibitors, e.g., sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis), are ineffective in 30&#45;40% of men diagnosed with erectile dysfunction (ED).  New studies show that erectile function can be restored in these men, without resorting to intracavernous injections or a penile prosthesis, by using natural agents (including NO&#45;producing substrates such as N&#45;hydroxyarginine [OH&#45;arginine]) in combination with the PDE&#45;5 inhibitors.</description>
      <dc:subject>Latest Research</dc:subject>
      <dc:date>2010-02-15T18:27:53+00:00</dc:date>
    </item>

    <item>
      <title>Common Genetic Variants and Other Host&#45;related Factors Greatly Increase Susceptibility to Vitamin A Deficiency</title>
      <link>http://www.lmreview.com/articles/view/common-genetic-variants-and-other-host-related-factors-greatly-increase-susceptibility-to-vitamin-a-deficiency/</link>
      <guid>http://www.lmreview.com/articles/view/common-genetic-variants-and-other-host-related-factors-greatly-increase-susceptibility-to-vitamin-a-deficiency/#When:23:28:53Z</guid>
      <description>In his presentation at the 2nd Hohenheim Nutrition Conference in Stuttgart, Germany, November 2009, Dr. Georg Lietz of England&#39;s Newcastle University reported that a high percentage of women in the UK are at risk of vitamin A deficiency.</description>
      <dc:subject>Latest Research</dc:subject>
      <dc:date>2010-02-04T23:28:53+00:00</dc:date>
    </item>

    <item>
      <title>Longevity Medicine Strategies for Cardiovascular Disease: Closing the Statin Gap in Endothelial Dysfunction and Insulin Resistance Naturally, with L&#45;Arginine and Citrulline: Part II</title>
      <link>http://www.lmreview.com/articles/view/longevity-medicine-strategies-for-cardiovascular-disease-closing-the-statin-gap-in-endothelial-dysfunction-and-insulin-resistance-naturally-with-l-arginine-and-citrulline-part-II/</link>
      <guid>http://www.lmreview.com/articles/view/longevity-medicine-strategies-for-cardiovascular-disease-closing-the-statin-gap-in-endothelial-dysfunction-and-insulin-resistance-naturally-with-l-arginine-and-citrulline-part-II/#When:20:24:52Z</guid>
      <description>Despite their efficacy in lowering cholesterol, statins remain ineffective for the primary or secondary prevention of myocardial infarction (MI) in two&#45;thirds of patients, and cardiovascular disease (CVD) remains the #1 cause of death in the U.S. A key reason for statins&#8217; failure to reduce MI incidence is that they ameliorate neither endothelial dysfunction, nor its corollary, hypertension. Additionally, statins do not impact insulin resistance, a major contributing factor to CVD as well as diabetes, which itself quadruples risk for CVD. Statins&#8217; lack of efficacy against these risk factors constitutes a treatment gap that results in high risk of morbidity notwithstanding low cholesterol levels&#8212;a gap that has now been connected to elevated levels of a recently identified CVD risk factor, asymmetric dimethylarginine, whose deleterious effects can be overcome by treatment with L&#45;arginine, which has been shown to significantly improve endothelial function both alone and when added to statin therapy, particularly if accompanied by necessary co&#45;factors, including tetrahydrobiopterin and the methylating factors, B6, B12 and folate. Part I of this review summarizes the latest research on L&#45;arginine&#8217;s beneficial effects on nitric oxide production, endothelial function and insulin resistance. Part II reviews the research on the co&#45;factors without which L&#45;arginine supplementation may not only lack efficacy, but could promote CVD; improvement in CVD outcomes from combined statin and L&#45;arginine therapy; and why L&#45;citrulline may offer an even better option.</description>
      <dc:subject>Latest Research</dc:subject>
      <dc:date>2009-12-18T20:24:52+00:00</dc:date>
    </item>

    <item>
      <title>Longevity Medicine Strategies for Cardiovascular Disease: Closing the Statin Gap in Endothelial Dysfunction and Insulin Resistance Naturally, with L&#45;Arginine and Citrulline: Part I</title>
      <link>http://www.lmreview.com/articles/view/longevity-medicine-strategies-for-cardiovascular-disease-closing-the-statin-gap-in-endothelial-dysfunction-and-insulin-resistance-naturally-with-l-arginine-and-citrulline-part-I/</link>
      <guid>http://www.lmreview.com/articles/view/longevity-medicine-strategies-for-cardiovascular-disease-closing-the-statin-gap-in-endothelial-dysfunction-and-insulin-resistance-naturally-with-l-arginine-and-citrulline-part-I/#When:20:17:55Z</guid>
      <description>Despite their efficacy in lowering cholesterol, statins remain ineffective for the primary or secondary prevention of myocardial infarction (MI) in two&#45;thirds of patients, and cardiovascular disease (CVD) remains the #1 cause of death in the U.S. A key reason for statins&#8217; failure to reduce MI incidence is that they ameliorate neither endothelial dysfunction, nor its corollary, hypertension. Additionally, statins do not impact insulin resistance, a major contributing factor to CVD as well as diabetes, which itself quadruples risk for CVD. Statins&#8217; lack of efficacy against these risk factors constitutes a treatment gap that results in high risk of morbidity notwithstanding low cholesterol levels&#8212;a gap that has now been connected to elevated levels of a recently identified CVD risk factor, asymmetric dimethylarginine, whose deleterious effects can be overcome by treatment with L&#45;arginine, which has been shown to significantly improve endothelial function both alone and when added to statin therapy, particularly if accompanied by necessary co&#45;factors, including tetrahydrobiopterin and the methylating factors, B6, B12 and folate. Part I of this review summarizes the latest research on L&#45;arginine&#8217;s beneficial effects on nitric oxide production, endothelial function and insulin resistance. Part II reviews the research on the co&#45;factors without which L&#45;arginine supplementation may not only lack efficacy, but could promote CVD; improvement in CVD outcomes from combined statin and L&#45;arginine therapy; and why L&#45;citrulline may offer an even better option.</description>
      <dc:subject>Latest Research</dc:subject>
      <dc:date>2009-12-01T20:17:55+00:00</dc:date>
    </item>

    <item>
      <title>Cardioprotective Strategies to Close the Statin Gap:&amp;nbsp; &#8220;News to Use&#8221; from the Latest Research</title>
      <link>http://www.lmreview.com/articles/view/cardioprotective-strategies-to-close-the-statin-gap-news-to-use-from-the-latest-research/</link>
      <guid>http://www.lmreview.com/articles/view/cardioprotective-strategies-to-close-the-statin-gap-news-to-use-from-the-latest-research/#When:16:39:16Z</guid>
      <description>Cardiovascular disease, which now afflicts more than 80 million Americans &#8211; 36.3% of the U.S. population, including 38,100,000 individuals &#8805; 60 &#8211; continues to be the No. 1 cause of death in the U.S., despite widespread use of statins, which, in 2002,  were being taken by &gt;30% of Medicare patients &#8805; 65. Statins, the most successful pharmacotherapy agents used to treat atherosclerosis, remain ineffective for the primary or secondary prevention of myocardial infarction in about two&#45;thirds of patients.</description>
      <dc:subject>Latest Research</dc:subject>
      <dc:date>2009-11-13T16:39:16+00:00</dc:date>
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    <item>
      <title>Beyond the Mitochondrial Tune Up: Part III</title>
      <link>http://www.lmreview.com/articles/view/beyond-the-mitochondrial-tune-up-part-III/</link>
      <guid>http://www.lmreview.com/articles/view/beyond-the-mitochondrial-tune-up-part-III/#When:20:42:16Z</guid>
      <description>Mitochondrial decay resulting from oxidative damage accumulates with age and is universally recognized as a major contributing factor to the whole range of functional decline and tissue deterioration associated with aging. Part I of this review discussed Bruce Ames&#8217; application of the Michaelis constant (KM) concept to the ramifications of age&#45;associated oxidative damage to proteins. Aging&#45;associated increases in oxidative damage to key enzymes results in their structural deformation and decreased binding affinity for the co&#45;enzyme, causing a decrease in enzyme funtion.8 Ames&#8217; research has demonstrated that increasing the availability of acetyl L&#45;carnitine and &#945;&#45;lipoic acid, two nutrients that serve as mitochondrial enzyme co&#45;factors, restores the velocity of the reactions (KM) in the related enzymes, and thus restores aging mitochondria&#8217;s ability to produce youthful levels of ATP. Part II focused on the inter&#45;relationships among the folate, methylation and transsulfuration pathways, whose dysfunction results in increased free radical production coupled with disruption of glutathione (GSH) synthesis, thus accelerating mitochondrial decay and aging.  Ensuring adequacy of all the nutrient co&#45;factors necessary to restore KM in these pathways, as well as in mitochondrial oxidative phosphorylation, is first line therapy for promoting healthy aging.</description>
      <dc:subject>Latest Research</dc:subject>
      <dc:date>2009-10-27T20:42:16+00:00</dc:date>
    </item>

    <item>
      <title>Beyond the Mitochondrial Tune Up: Part II</title>
      <link>http://www.lmreview.com/articles/view/beyond-the-mitochondrial-tune-up-part-II/</link>
      <guid>http://www.lmreview.com/articles/view/beyond-the-mitochondrial-tune-up-part-II/#When:20:11:56Z</guid>
      <description>Mitochondrial decay resulting from oxidative damage accumulates with age and is universally recognized as a major contributing factor to the whole range of functional decline and tissue deterioration associated with aging. Part I of this review discussed Bruce Ames&#8217; application of the Michaelis constant (KM) concept to the ramifications of age&#45;associated oxidative damage to proteins. Specifically, with age, increased oxidative damage to key enzymes produces deformation in their structure, resulting in an increased Michaelis constant (KM), i.e., a decreased binding affinity for the co&#45;enzyme (the nutrient co&#45;factor for the enzyme), thus causing a decrease in enzyme function. Ames&#8217; research has demonstrated that increasing the availability of acetyl L&#45;carnitine, the substrate for the enzyme acetyl&#45;L&#45;carnitine transferase, (which plays a key role in transporting long&#45;chain fatty acids into the mitochondria for &#946; oxidation and ATP production), along with &#945;&#45;lipoic acid, (a mitochondrial antioxidant that also serves as cofactor for two key enzymes in the Krebs cycle, pyruvate dehydrogenase and &#945;&#45;ketoglutarate dehydrogenase), restores the velocity of the reactions (KM) for these enzymes, and thus restores aging mitochondria&#8217;s ability to regain youthful levels of energy production.</description>
      <dc:subject>Latest Research</dc:subject>
      <dc:date>2009-09-26T20:11:56+00:00</dc:date>
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