Food About en Contributions to Nutrition <span property="schema:name" class="field field--name-title field--type-string field--label-hidden">Contributions to Nutrition</span> <span rel="schema:author" class="field field--name-uid field--type-entity-reference field--label-hidden"><span lang="" about="/about/team/alan-attridge" typeof="schema:Person" property="schema:name" datatype="">Alan</span></span> <span property="schema:dateCreated" content="2015-02-28T00:10:18+00:00" class="field field--name-created field--type-created field--label-hidden">Sat, 02/28/2015 - 00:10</span> <div property="schema:text" class="clearfix text-formatted field field--name-body field--type-text-with-summary field--label-hidden field__item"><p>Public health nutrition continues to be challenged by increasing expectations from the food supply on one hand, and fundamental gaps in nutrition knowledge on the other, which can constrain the development and implementation of nutrition and food policy (1). Current demands on the food supply are no longer limited to ensuring general safety and preventing micronutrient deficiences.  Increasingly, there is interest in engineering medicinal qualities into the food supply to enable diets that promote health and “nurture” a sense of well-being that transcends the mere absence of disease by improving biological functions and even increasing lifespans.  Unquestionably, nutrition is one of the primary environmental exposures that determines health. Common human chronic diseases, including type 2 diabetes, metabolic syndrome, cardiovascular and neurological disease, and many cancers are initiated and/or accelerated by nutrient/food exposures.  However, it is also recognized that chronic diseases are complex in their etiology and include a substantial genetic component; individuals respond differently to foods and even individual nutrients. Investigation in this new field of nutrition research, often referred to as nutritional genomics, focuses on deciphering the biological mechanisms that underlie both the acute and persistent genome-nutrient interactions that influences health.</p> <p>Nutritional genomics, while centered on the biology of individuals, distinguishes itself from other “omics” fields by its unique focus on disease prevention and healthy aging through the manipulation of gene–diet interactions.  Nutritional genomics promises to revolutionize both clinical and public health nutrition practice and facilitate the establishment of (a) genome-informed nutrient and food-based dietary guidelines for disease prevention and healthful aging, (b) individualized medical nutrition therapy for disease management, and (c) better targeted public health nutrition interventions, including micronutrient fortification and supplementation, that maximize benefit and minimize adverse outcomes within genetically diverse human populations.  Research dietitians are among the leading scientists pioneering this field, and food and nutrition professionals will be primarily responsible for its implementation.  In 2006, the Institute of Medicine convened a workshop to review the state of the various domains of nutritional genomics research and policy and to provide guidance for further development and translation of this knowledge into nutrition practice and policy (2).  Three scientific domains of nutritional genomics were discussed: (a) <em>nutritional</em> <em>genetics </em>or <em>nutrigenetics</em>, which involves the identification, classification, and characterization of human genetic variation that modifies nutrient metabolism/ utilization and food tolerances (Figure 1); (b) <em>nutritional</em> <em>epigenetics</em>, which refers to the effect of nutrients on deoxyribonucleic acid (DNA)/chromatin (and hence gene expression), which programs or reprograms biological networks with multigenerational consequences; and (c) <em>systems biology </em>and <em>nutritional engineering</em>, which is the application of nutrigenomics information to manipulate biological pathways and networks for benefit through nutrition, including the use of food-based diets, dietary restriction, or nutritional supplements to affect genome expression, stability, and/or direct dietary compensation for metabolic deficiencies (2).  This Institute of Medicine report provides background for this review, which is restricted in scope to highlighting the interactions of the B vitamin folate with the human genome and the current gaps in knowledge that must be overcome to achieve genomically driven nutrition practice and policies.  </p> <h3><strong>ORIGIN OF GENE–NUTRIENT INTERACTIONS</strong></h3> <p>The human genome, and the genetic variation present within human populations, is in part a product of adaptive evolution to an often scant and unpredictable food supply (3,4). Single nucleotide polymorphisms (SNPs), which are common, single base-pair differences in DNA sequence, represent a primary form of human genetic variation.  Of the approximately 10 million SNPs in the human genome, many are believed to have functional consequences (eg, alter the activity/function of the protein product) (5,6). SNPs arise through the sequential process of DNA mutation and subsequent expansion of the mutation within a population. Food and nutrient exposures affect both of these processes.  For example, B-vitamin deficiencies impair DNA synthesis/stability and increase DNA mutation rates (germ line and somatic DNA mutations) as do excesses of pro-oxidants, including iron.  Likewise, the nutritional environment can accelerate the expansion of fortuitous germ line DNA mutations within a population such that they accumulate and contribute to human genetic variation.</p> <p>Indeed, many SNPs that affect nutrient utilization display genomic “signatures” of such positive selection (3).  For example, a SNP located near the gene that encodes lactase enables carriers of this SNP to produce this enzyme throughout adulthood and thus continue to tolerate milk (7).  This SNP penetrated populations whose ancestors came from places where dairy herds could be raised safely and economically, such as in Europe (8,9). However, several gene variants that arose through positive selection are modern-day candidates for disease alleles; gene variants that permit adaptation to one environment can be deleterious when the environmental conditions change (eg, the nature and abundance of the food supply).  For example, the <em>HFE </em>gene variant that is associated with risk for hemochromatosis may have conferred advantage in iron-poor regions but confers risk for iron overload in iron-rich environments (10,11).  Expansion of a SNP also requires that the associated changes in biochemistry permit embryonic survival in the interuterine environment.  Both malnutrition and some gene variants that impair nutrient metabolism and/or utilization are risk factors for spontaneous abortion (12).  Nutrients and other bioactive food components can also regulate gene expression (Figure 1). All organisms have acquired the ability to sense and adapt to their nutrient environment by altering the expression of proteins that function in metabolic and signaling pathways. Salient examples include, but are not limited to, the regulation of gene transcription by vitamin A or vitamin D through interaction with their respective nuclear receptors. This ability of nutrients to communicate with the genome is an essential feature of organismal evolution.  Nutrients can elicit transient alterations in gene expression and/or influence more permanent whole genome reprogramming events that can be inherited (ie, passed onto offspring).  The term <em>epigenetics </em>refers to the inheritance of traits through mechanisms that are independent of DNA primary sequence and includes the inheritance of gene expression patterns and/or expression levels that contribute to phenotypic differences among individuals, including monozygotic twins (13).  The embryo seems to be especially susceptible to nutrient- induced adaptations in gene expression, a phenomenon referred to as <em>metabolic imprinting </em>or <em>metabolic programming</em> (14). These adaptations occur within critical windows during embryonic development and can persist into adulthood. The associated changes in metabolism resulting from these reprogramming events are believed to enable in utero survival in suboptimal nutrient environments, but predispose the individual to metabolic disease in adulthood (14).  This relationship among maternal nutrition, fetal epigenetic programming, and adult-onset chronic disease is the basis of the fetal origins of adult disease hypothesis, which proposes that nutrition acts very early in life to program risk for adverse outcomes in adult life (15).  This theory, which was originally supported only by epidemiological associations, has now been validated in whole-animal studies.  These studies demonstrate that early nutrition exposures increased risk in adulthood for obesity, hypertension, and insulin resistance, which are the antecedents of adult chronic disease including cardiovascular disease and diabetes (15).  The genome, in turn, can constrain diet (Figure 1).  Genetic variation and/or variations in epigenetic programming can affect nutrient absorption and utilization (eg, hemochromatosis) and thereby confer differences in food/nutrient tolerances (eg, iron) and may contribute to the variation in human nutrient requirements (3).</p> <p><strong>References</strong></p> <p><em>Excerpt from: Patrick J. Stover, PhD, Marie A. Caudill, PhD, RD. </em>"Genetic and Epigenetic Contributions to Human Nutrition and Health: Managing Genome–Diet Interactions."</p> <p>1. Garza C, Stover PJ. The role of science in identifying common ground in the GMO debate. <em>Trend Food Tech</em>. 2003;14:182-190.</p> <p>2. IOM. <em>Nutrigenomics and beyond: Informing the future</em>. Washington, DC: The National Academies Press; 2007.</p> <p>3. Stover PJ. Human nutrition and genetic variation. <em>Food Nutr Bull</em>. 2007;28(Suppl International 1):S101-S115.</p> <p>4. Tishkoff SA, Verrelli BC. Role of evolutionary history on haplotype block structure in the human genome: Implications for disease mapping. <em>Curr Opin Genet Dev</em>. 2003;13:569-575.</p> <p>5. Cargill M, Altshuler D, Ireland J, Sklar P, Ardlie K, Patil N, Shaw N, Lane CR, Lim EP, Kalyanaraman N, Nemesh J, Ziaugra L, Friedland L, Rolfe A, Warrington J, Lipshutz R, Daley GQ, Lander ES. Characterization of single-nucleotide polymorphisms in coding regions of human genes. <em>Nat Genet</em>. 1999;22:231-238.</p> <p>6. Tishkoff SA, Kidd KK. Implications of biogeography of human populations for ’race’ and medicine. <em>Nat Genet</em>. 2004;36(Suppl 11):S21-S27.</p> <p>7. Enattah NS, Sahi T, Savilahti E, Terwilliger JD, Peltonen L, Jarvela I. Identification of a variant associated with adult-type hypolactasia. <em>Nat Genet</em>. 2002;30:233-237.</p> <p>8. Bersaglieri T, Sabeti PC, Patterson N, Vanderploeg T, Schaffner SF, Drake JA, Rhodes M, Reich DE, Hirschhorn JN. Genetic signatures of strong recent positive selection at the lactase gene. <em>Am J Hum Genet</em>. 2004;74:1111-1120.</p> <p>9. Bloom G, Sherman PW. Dairying barriers and the distribution of lactose malabsorption. <em>Evolution and Human Behavior</em>. 2005;26:301- 312.</p> <p>10. Toomajian C, Ajioka RS, Jorde LB, Kushner JP, Kreitman M. A method for detecting recent selection in the human genome from allele age estimates. <em>Genetics</em>. 2003;165:287-297.</p> <p>11. Toomajian C, Kreitman M. Sequence variation and haplotype structure at the human HFE locus. <em>Genetics</em>. 2002;161:1609-1623.</p> <p>12. Stover PJ, Garza C. Bringing individuality to public health recommendations. <em>J Nutr</em>. 2002;132(8 Suppl):S2476-S2480.</p> <p>13. Dennis C. Epigenetics and disease: Altered states. <em>Nature</em>. 2003;421: 686-688.</p> <p>14. Waterland RA, Garza C. Potential mechanisms of metabolic imprinting that lead to chronic disease. <em>Am J Clin Nutr</em>. 1999;69:179-197.</p> <p>15. Barker DJ. Intrauterine programming of coronary heart disease and stroke. <em>Acta Paediatr Suppl</em>. 1997;423:178-182; discussion 183.</p> <p>16. Stover PJ. Physiology of folate and vitamin B12 in health and disease. <em>Nutr Rev</em>. 2004;62(6 Pt 2):S3-S12; discussion S13.</p> <p>17. Henikoff S, McKittrick E, Ahmad K. Epigenetics, histone H3 variants, and the inheritance of chromatin states. <em>Cold Spring Harb Symp</em> <em>Quant Biol</em>. 2004;69:235-243.</p></div> Sat, 28 Feb 2015 00:10:18 +0000 Alan 19 at Health <span property="schema:name" class="field field--name-title field--type-string field--label-hidden">Health</span> <span rel="schema:author" class="field field--name-uid field--type-entity-reference field--label-hidden"><span lang="" about="/about/team/alan-attridge" typeof="schema:Person" property="schema:name" datatype="">Alan</span></span> <span property="schema:dateCreated" content="2015-02-26T00:15:38+00:00" class="field field--name-created field--type-created field--label-hidden">Thu, 02/26/2015 - 00:15</span> <div property="schema:text" class="clearfix text-formatted field field--name-body field--type-text-with-summary field--label-hidden field__item"><ul> <li>The condition of being well or free from disease</li> <li>The overall condition of someone's body or mind</li> <li>The condition or state of something</li> </ul> <p> </p> <p>Journal of the Academy of Nutrition and Dietetics: <a href=""></a></p></div> Thu, 26 Feb 2015 00:15:38 +0000 Alan 20 at Human Microbiome <span property="schema:name" class="field field--name-title field--type-string field--label-hidden">Human Microbiome</span> <span rel="schema:author" class="field field--name-uid field--type-entity-reference field--label-hidden"><span lang="" about="/about/team/alan-attridge" typeof="schema:Person" property="schema:name" datatype="">Alan</span></span> <span property="schema:dateCreated" content="2014-12-29T00:44:12+00:00" class="field field--name-created field--type-created field--label-hidden">Mon, 12/29/2014 - 00:44</span> Mon, 29 Dec 2014 00:44:12 +0000 Alan 21 at Genetics & Epigenetics <span property="schema:name" class="field field--name-title field--type-string field--label-hidden">Genetics &amp; Epigenetics</span> <span rel="schema:author" class="field field--name-uid field--type-entity-reference field--label-hidden"><span lang="" about="/about/team/alan-attridge" typeof="schema:Person" property="schema:name" datatype="">Alan</span></span> <span property="schema:dateCreated" content="2014-12-25T00:57:08+00:00" class="field field--name-created field--type-created field--label-hidden">Thu, 12/25/2014 - 00:57</span> <div property="schema:text" class="clearfix text-formatted field field--name-body field--type-text-with-summary field--label-hidden field__item"><p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>The Institute of Medicine convened a workshop in 2009 </span></span></span></span><span><span><span><span>to review the state of the various domains of nutritional </span></span></span></span><span><span><span><span>genomics research and policy and to provide guidance for </span></span></span></span><span><span><span><span>further development and translation of this knowledge </span></span></span></span><span><span><span><span>into nutrition practice and policy. Nutritional genomics </span></span></span></span><span><span><span><span>holds the promise to revolutionize both clinical and public </span></span></span></span><span><span><span><span>health nutrition practice and facilitate the establishment </span></span></span></span><span><span><span><span>of</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>(a) genome-informed nutrient and food-based dietary </span></span></span></span><span><span><span><span>guidelines for disease prevention and healthful aging,</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>(b) individualized medical nutrition therapy for disease man­</span></span></span></span><span><span><span><span>agement, and</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>(c) better targeted public health nutrition </span></span></span></span><span><span><span><span>interventions (including micro-nutrient fortification and </span></span></span></span><span><span><span><span>supplementation) that maximize benefit and minimize </span></span></span></span><span><span><span><span>adverse outcomes within genetically diverse human</span></span></span></span><span><span><span><span> pop­</span></span></span></span><span><span><span><span>ulations.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>As the field of nutritional genomics matures, </span></span></span></span><span><span><span><span>which will include filling fundamental gaps in knowledge </span></span></span></span><span><span><span><span>of nutrient–genome interactions in health and disease </span></span></span></span><span><span><span><span>and demonstrating the potential benefits of customizing nutrition prescriptions based on genetics, registered die­titians will be faced with the opportunity of making ge­</span></span></span></span><span><span><span><span>netically driven dietary recommendations aimed at im­</span></span></span></span><span><span><span><span>proving human health.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><em><span><span><span><span>J Am Diet Assoc. 2008;108:1480-1487.</span></span></span></span></em></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p></div> Thu, 25 Dec 2014 00:57:08 +0000 Alan 22 at Newsletters and Documents <span property="schema:name" class="field field--name-title field--type-string field--label-hidden">Newsletters and Documents</span> <span rel="schema:author" class="field field--name-uid field--type-entity-reference field--label-hidden"><span lang="" about="/about/team/alan-attridge" typeof="schema:Person" property="schema:name" datatype="">Alan</span></span> <span property="schema:dateCreated" content="2014-03-06T00:47:03+00:00" class="field field--name-created field--type-created field--label-hidden">Thu, 03/06/2014 - 00:47</span> Thu, 06 Mar 2014 00:47:03 +0000 Alan 23 at NEWS - Staph, MSRA, Sweeteners, Food Access <span property="schema:name" class="field field--name-title field--type-string field--label-hidden">NEWS - Staph, MSRA, Sweeteners, Food Access</span> <span rel="schema:author" class="field field--name-uid field--type-entity-reference field--label-hidden"><span lang="" about="/about/team/alan-attridge" typeof="schema:Person" property="schema:name" datatype="">Alan</span></span> <span property="schema:dateCreated" content="2014-01-06T00:56:44+00:00" class="field field--name-created field--type-created field--label-hidden">Mon, 01/06/2014 - 00:56</span> <div property="schema:text" class="clearfix text-formatted field field--name-body field--type-text-with-summary field--label-hidden field__item"><p>A great article on Ebola in this months September 29, 2014 issue of Bloomberg Businessweek. “Ebola Rising.”  It explains the story behind a drug development.  A recommended reading for all.</p> <p><strong>Sweeteners:</strong><br /><br /> <br /></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><strong>Agricultural Economic Report No</strong>. (AER-741) 93 pp, August 1996</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>Microbial pathogens in food cause an estimated 6.5-33 million cases of human illness and up to 9,000 deaths in the United States each year. Over 40 different foodborne microbial pathogens, including fungi, viruses, parasites, and bacteria, are believed to cause human illnesses. For six bacterial pathogens, the costs of human illness are estimated to be $9.3-$12.9 billion annually. Of these costs, $2.9-$6.7 billion are attributed to foodborne bacteria. These estimates were developed to provide analytical support for USDA’s Hazard Analysis and Critical Control Point (HACCP) systems rule for meat and poultry. (Note that the parasite Toxoplasma gondii is not included in this report.) To estimate medical costs and productivity losses, ERS uses four severity categories for acute illnesses: those who did not visit a physician, visited a physician, were hospitalized, or died prematurely. The lifetime consequences of chronic disease are included in the cost estimates for E. coli O157:H7 and fetal listeriosis.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>The cost estimate for <em>E. coli</em> O157:H7 (now termed STEC O157) was subsequently updated in collaboration with FoodNet in 2005, using FoodNet surveillance data and a case-control study of STEC O157 patients.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>In 2003, ERS introduced the Foodborne Illness Cost Calculator, an interactive online version of the updated ERS cost estimates for selected foodborne pathogens. The Cost Calculator initially included the <em>Salmonella</em> cost estimate, and later added the STEC O157 estimate. The Cost Calculator provides detailed information about the assumptions underlying each estimate, and allows users to make alternative assumptions and re-estimate the costs. An updated version with additional pathogens of the Cost Calculator is in development.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><strong>Access to Food</strong></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>Efforts to encourage Americans to improve their diets and to eat more nutritious foods presume that a wide variety of these foods are accessible to everyone. But for some Americans and in some communities, access to healthy foods may be limited. Using population data from the 2010 Census, income and vehicle availability data from the 2006-2010 American Community Survey, and a 2010 directory of supermarkets, this report estimates that 9.7 percent of the U.S. population, or 29.7 million people, live in low-income areas more than 1 mile from a supermarket. However, only 1.8 percent of all households live more than 1 mile from a supermarket and do not have a vehicle. Estimated distance to the nearest three supermarkets is an indicator of the choices available to consumers and the level of competition among stores. Estimates show that half of the U.S. population lives within 2 miles of 3 supermarkets</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><strong><span>What Is a Staph Infection?</span></strong></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><em><span>Staphylococcus </span></em><span>is a group of bacteria </span><span>that can cause a number of diseases as a result of infection of various tissues of the body. <em>Staphylococcus</em> is more familiarly known as Staph (pronounced "staff"). Staph-related illness can range from mild and requiring no treatment to severe and potentially fatal.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>Over 30 different types of Staphylococci can infect humans, but most infections are caused by <em>Staphylococcus aureus</em>. Staphylococci can be found normally in the nose and on the skin (and less commonly in other locations) of around 25%-30% of healthy adults and in 25% of hospital workers. In the majority of cases, the bacteria do not cause disease. However, damage to the skin or other injury may allow the bacteria to overcome the natural protective mechanisms of the body, leading to infection.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>A</span><span> staph infection is caused by a <em>Staphylococcus</em> (or "staph") bacteria. Actually, about 25% of people normally carry staph in the nose, mouth, genitals, or anal area. The foot is</span><span> also very prone to picking up bacteria from the floor. The infection often begins with a little cut, which gets infected with bacteria.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>These staph infections range from a simple boil to antibiotic-resistant infections to flesh-eating infections. The difference between all these is the strength of the infection, how deep it goes, how fast it spreads, and how treatable it is with antibiotics. The antibiotic-resistant infections are more common in North America, because of our overuse of antibiotics.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>One type of staph infection that involves skin is called cellulitis and affects the skin's deeper layers. It is treatable with antibiotics.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>This type of infection is very common in the general population -- and more common and more severe in people with weak immune systems. People who have diabetes weakened immunity are particularly prone to developing cellulitis.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <h3><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><strong>What is MRSA</strong>?</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></h3> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>This tiny cluster of bacteria is methicillin-resistant Staphylococcus aureus (MRSA), seen under a microscope. This strain of the common "staph" bacteria causes infections in different parts of the body -- including the skin, lungs, and other areas. MRSA is sometimes called a "superbug" because it is resistant to many antibiotics. Though most MRSA infections aren't serious, some can be life-threatening.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><strong><span>What Are the Symptoms of a Staph Infection?</span></strong></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>Staph cellulitis usually begins as a small area of tenderness, swelling, and redness. Sometimes it begins with an open sore. Other times, there is no break in the skin at all -- and it's anyone's guess where the bacteria came from.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span>The signs of cellulitis are those of any inflammation -- redness, warmth, swelling, and pain. Any skin sore or ulcer that has these signs may be developing cellulitis.</span></span></p></div> Mon, 06 Jan 2014 00:56:44 +0000 Alan 25 at Fungi <span property="schema:name" class="field field--name-title field--type-string field--label-hidden">Fungi</span> <span rel="schema:author" class="field field--name-uid field--type-entity-reference field--label-hidden"><span lang="" about="/about/team/alan-attridge" typeof="schema:Person" property="schema:name" datatype="">Alan</span></span> <span property="schema:dateCreated" content="2014-01-06T00:51:09+00:00" class="field field--name-created field--type-created field--label-hidden">Mon, 01/06/2014 - 00:51</span> <div property="schema:text" class="clearfix text-formatted field field--name-body field--type-text-with-summary field--label-hidden field__item"><div> <div> <h3><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>WHAT ARE MEDICINAL MUSHROOMS?</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></h3> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>By the term mushrooms, we generally mean the definition of Chang and Miles (1992): a macro fungus with a distinctive fruiting body which can be hypogeous or epigeous, large enough to be seen with the naked eye and to be picked by hand. Numerous studies have demonstrated that certain components present in medicinal mushrooms have been responsible for the modulation of cellular and physiological changes in the host.  It is for this reason that mushrooms are often used as cancer therapeutic agents.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>Many medicinal mushrooms species contain valuable constituents including  <a href="">polysaccharides</a>, <a href="">lectins</a>, <a href="">lipids</a>, <a href=";bq=hericenone">hericenone</a>, <a href=";term=C497667">erinacol</a>,  <a href=";bq=erinacine">erinacine</a>, and <a href=";term=D013729">terpenoids</a>.  </span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>The number of mushroom species on Earth is estimated at 140,000, yet maybe only 10% (approximately 14,000 named species) are known.  Mushrooms comprise a vast and yet largely untapped source of powerful new chemical and pharmaceutical products. They represent an unlimited source of polysaccharides with antitumor and immuno-stimulating properties.  Data on mushroom polysaccharides have been collected from 651 species and 7 infraspecific taxa from 182 genera if higher Hetero and Homobasidiomycetes.  Mushroom polysaccharides prevent oncogenesis, show direct antitumor activity against various allogeneic and syngenetic tumors, and prevent tumor metastasis.  Polysaccharides from mushrooms do not attack cancer cells directly, but produce antitumor effects by activating different immune responses in the host. </span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>These substances are regarded as biological response modifiers.  This basically means that: (1) they cause no harm and place no additional stress on the body; (2) they help the body adapt to various environmental and biological stresses; and (3) they exert a non-specific action on the body, supporting some or all of the major systems, including nervous, hormonal, and immune systems, as well as regulatory functions.<br /> <br /> <span><span>Fungi working in a synergistic way, which have direct biological activity on mammals. These fungi live via an extra cellular process of digesting the food environment around it. The organic chemicals of fungal food are broken down by the mushroom’s catalysts, (enzymes), and these smaller molecules are absorbed and used within the mushroom’s cells. Fungal food sources are broken down, by a large contingent of special and diverse enzymes. Consumption of these mushrooms then makes these enzymes available to the user.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>In the process of the fungal cell growth, its cell structure is built from simple sugars, assembled into large macro molecules called beta-glucans. These large sugars have unique special characteristics. These stereo specific structures are produced by the fungi, and their shapes are regulated by the way the sugars attach to each other through linkages. These specialized sugar shaped molecules (Beta-glucans), attach to the surface of the cells within our bodies, just as a key fits a lock. The human cell receptors, then through a multi-step process perform chemistry within the cell. Some beta-glucans cause the cells to send communication signals, which adjust the internal chemistry of the cell, like the regulation of calcium and sodium concentrations. Some cell signaling (transductance) causes RNA to be transcribed through ribosomes into functioning proteins, and critical enzymes, regulating these newly formed proteins.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>Beyond Beta-glucans are glycoproteins. Complex sugar structures are attached to a protein stem. These structures look like a bristle brush, and act by attachment to human cell surfaces to express a large amount of functional chemistry. Through this process of cell transductance, receptors can open the cell walls to increase the flow of glucose, adrenaline, and insulin across the membrane. In these types of processes, blood glucose may be balanced, cholesterol and blood lipids may be lowered, nitric oxide may be produced, causing the dilation of blood vessels, macrophage cells may be activated, the efficiency of the ATP cycle may be enhanced, or enzymes may be created which quench free radical cascades.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>Enzymes, within the medicinal mushrooms are specific to breaking apart large cellular molecules of foods. When the Medicinal Mushrooms are consumed by the host, these enzymes act within the digestive track to break bonds of food complexes containing phosphorus, transition metals, vitamins, and other valuable organic chemistry. Now, these previously unavailable chemicals may be better absorbed through the animal’s digestive system, enabling previous cellular deficiencies to be fulfilled.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>The body processes chemistry and information through a cascade of protein to protein interactions.  These cycles rely on the cells possessing chemistry to complete the cycle.  When an intermediate chemical is non existent, the cycle stops, and the biological function cannot be accomplished.  The medicinal Mushrooms are composed of three to four thousand specific biological acting chemicals.  These chemicals are provided in a ratio which is beneficial to the host’s body. Because there are no large amounts of detrimental chemicals (as seen with drugs), the body’s natural processes use what they need and dispose of the rest. Therefore medicinal mushrooms can be consumed in large quantities as a whole food with no adverse effects.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> </div> <br /> <span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>The mushrooms contain all the essential amino acids and nucleosides, which are needed for protein synthesis. They contain transition metals which are incorporated within proteins to make up specific catalysts.  These metals, are bound up in an organic matrix, which allows transport across the digestion membrane, making them bioavailable.  The mushroom contains specialized catalysts, vitamins like B12, C, D, selenomethioneine, Lergothioneine.  Also contained, are very specialized small organic molecules like dilinoleoyl-phosphatedylethamine, cordycepin, hericium, triterpenes and other unique chemicals which cause specialized host response.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></div> <p><span><span><span><span>Disease states originate from excess or deficiency within metabolic cycle process of the body. When downstream protein to protein transductance from an insulin receptor are inhibited by deficiency of essential proteins, or organic chemistry, blood sugar levels may become hyper or hypo. Because of a lack of blood glucose the Crebs cycle produces less chemical energy which is ultimately stored in ATP. As cellular energy is decreased, the gene expression of RNA is diminished. The essential catalysts and proteins which should be produced now are not. As cells realize they are not functioning properly, the cell may signal programmed cell death, apoptosis. The build up of b-amylate, (plaques), on nerve tissue leads to diseases like Parkinson’s, Alzheimer’s, and dementia. High blood sugar levels leads to diabetes, and kidney failure. Excess free radical cascade reactions lead to athlesclerosis, high blood pressure, and heart disease. With deficiencies the Liver now has problems with the 157 separate chemical production cycles, leading to liver cirrhosis. People with serious deficiencies and chronic illness,  usually find fast and significant improvement with their symptoms upon consuming the medicinal mushroom blends. The medicinal mushroom blends called myshroom ( originates from living fungal life forms, which, because of their structure and life process being very  similar to ours, has within its biological matrix, the correct ratio of essential chemistry, for our cells daily needs.</span></span><br /> <br /> A medicinal mushroom blend product made from hybrid strains of medicinal mushrooms is available.  The strains are grow on a proprietary substrate in a clean room environment and are certified organic. This whole food product is unadulterated, organically grown, whole medicinal mushroom dried powder blends that come from rare strains of rare species of mushrooms. You get all of the beneficial chemistry from the whole mushroom. <strong> </strong>The mushroom product supports oxygen utilization and cellular protein synthesis and supports the body’s natural production of ATP.  This blend of mushrooms also supports the essential enzyme transport system shuttling anti-oxidants to points of oxidative stress.  By improving the body’s anti-oxidant cycle, fewer of the body’s cells are destroyed through oxidation. Then the body’s innate immune system spends less energy cleaning up dead cell debris, and is ready to defend against future invaders, thus improving your body’s overall health.</span></span></p> <p><span><span><span>The blends contain seven novel hybrid strains not available in the wild, including Almond mushroom or Royal Sun Agaricus (Agaricus blazei), Cordyceps senensis, and Turkey Tail (Coriolus versicolor).  The proprietary formulation and novel growing medium is produced in a GMP certified, sterile clean room environment facility.</span></span></span></p> <p>Most mushroom products on the market are different in that they are grown to generate quantity as opposed to quality. Many of these end-products are merely extracts, not whole foods. Why settle for anything less?</p> <p>You get all of the valuable culinary benefits of whole mushrooms in a simple, flavor enhancing powder. This makes it simple to boost the taste of many of your favorite foods (including desserts) and beverages. Many folks start with mixing 2 teaspoons per day into their food and/or beverages. And much more may be safely consumed daily (up to 16 teaspoons daily) – it’s just a food!</p> <p>See our recipe suggestions below…</p> <h3>BEVERAGE RECIPE:</h3> <p>1/3<sup>rd</sup> cup of hot water or your favorite herbal tea</p> <p>Stir 2 or more teaspoons of the powder</p> <p>Add in organic honey, Lo Han or stevia to taste.</p> <p>Cocoa may be added to taste.</p> <h3>FOOD SEASONING:</h3> <p>You may also sprinkle the mushroom powder on your food or snack, or add it to a salad dressing, poultry, steak, salsa or fish sauce, soup or baking mix. It can be added to a bread, pancake mix or an omelet. Standard cooking temperatures do not negatively impact the product.</p> <p><a href="">Buy medicinal mushrooms here.</a></p></div> Mon, 06 Jan 2014 00:51:09 +0000 Alan 24 at Energy Field <span property="schema:name" class="field field--name-title field--type-string field--label-hidden">Energy Field</span> <span rel="schema:author" class="field field--name-uid field--type-entity-reference field--label-hidden"><span lang="" about="/about/team/alan-attridge" typeof="schema:Person" property="schema:name" datatype="">Alan</span></span> <span property="schema:dateCreated" content="2014-01-04T00:58:58+00:00" class="field field--name-created field--type-created field--label-hidden">Sat, 01/04/2014 - 00:58</span> <div property="schema:text" class="clearfix text-formatted field field--name-body field--type-text-with-summary field--label-hidden field__item"><p>Science Measures the Human Energy Field Energy is a theme that permeates many areas of complementary health care, including Reiki. For historic and emotional reasons, two key words have not been mentionable in polite academic research society: "energy" and "touch." Hence it is not surprising that Reiki therapy has been neglected by mainstream biomedical science. This picture is changing rapidly because of exciting research from around the world.<br /> <br /> The tale of how concepts of "healing energy" have swung from suspicion and ridicule to respectability is one of the most fascinating and clinically significant stories that can be told.<br /> <br /> As in many other areas of investigation, what we were absolutely certain about 20 years ago has changed dramatically. For example, in a few decades scientists have gone from a conviction that there is no such thing as an energy field around the human body, to an absolute certainty that it exists. Moreover, we have begun to understand the roles of energy fields in health and disease.<br /> <br /> Most people are simply not aware of this research, and persist in the attitude that there is no logical basis for energy healing. The main reason for the change in outlook is that sensitive instruments have been developed that can detect the minute energy fields around the human body. Of particular importance is the SQUID magnetometer (1) which is capable of detecting tiny biomagnetic fields associated with physiological activities in the body. (Figure 1) This is the same field that sensitive individuals have been describing for thousands of years, but that scientists have ignored because there was no objective way to measure it. To summarize the discoveries that have been made, the editors of a new international journal commissioned a review of the concept of "healing energy" (2). While we have been researching this topic for some 15 years, the preparation of an in-depth review led to a thorough reexamination of the subject, with some unexpected conclusions. For the most part, key discoveries are not being made by scientists studying methods such as Reiki, TT and HT. Instead, traditional scientists, following customary logic and scientific methods, have begun to clarify the roles of various kinds of energy in the healing process. Hence the picture that is emerging has the same scientific foundations that underlie modern clinical medicine. For details, see our published articles (3). The human energy field. It has long been known that activities of cells and tissues generate electrical fields that can be detected on the skin surface. But the laws of physics demand that any electrical current generates a corresponding magnetic field in the surrounding space. Since these fields were too tiny to detect, biologists assumed they could have no physiological significance. This picture began to change in 1963. Gerhard Baule and Richard McFee of the Department of Electrical Engineering, Syracuse University, Syracuse, NY detected the biomagnetic field projected from the human heart. They used two coils, each with 2 million turns of wire, connected to a sensitive amplifier. In 1970, David Cohen of MIT, using a SQUID magnetometer, confirmed the heart measurements. By 1972, Cohen had improved the sensitivity of his instrument, enabling him to measure magnetic fields around the head produced by brain activities. Subsequently, it has been discovered that all tissues and organs produce specific magnetic pulsations, which have come to be known as biomagnetic fields. The traditional electrical recordings, such as the electrocardiogram and electroencephalogram, are now being complemented by biomagnetic recordings, called magnetocardiograms and magnetoencephalograms. For various reasons, mapping the magnetic fields in the space around the body often provides a more accurate indication of physiology and pathology than traditional electrical measurements. Pathology alters the biomagnetic field. In the 1920’s and 1930’s, a distinguished researcher at Yale University School of Medicine, Harold Saxon Burr, suggested that diseases could be detected in the energy field of the body before physical symptoms appear. Moreover, Burr was convinced that diseases could be prevented by altering the energy field. These concepts were ahead of their time, but are now being confirmed in medical research laboratories around the world. Scientists are using SQUID instruments to map the ways diseases alter biomagnetic fields around the body. Others are applying pulsating magnetic fields to stimulate healing. Again, sensitive individuals have been describing these phenomena for a long time, but there was no logical explanation of how it could happen. Projection of energy from the hands of healers. In the early 1980’s, Dr. John Zimmerman began a series of important studies on therapeutic touch, using a SQUID magnetometer at the University of Colorado School of Medicine in Denver. Zimmerman discovered that a huge pulsating biomagnetic field emanated from the hands of a TT practitioner. The frequency of the pulsations is not steady, but "sweeps" up and down, from 0.3 to 30 Hz (cycles per second), with most of the activity in the range of 7-8 Hz (Figure 2). The biomagnetic pulsations from the hands are in the same frequency range as brain waves and scientific studies of the frequencies necessary for healing indicate that they naturally sweep back and forth through the full range of therapeutic frequencies, thus being able to stimulate healing in any part of the body. Confirmation of Zimmerman’s findings came in 1992, when Seto and colleagues, in Japan, studied practitioners of various martial arts and other healing methods. The "Qi emission" from the hands is so strong that they can be detected with a simple magnetometer consisting of two coils, of 80,000 turns of wire. Since then, a number of studies of QiGong practitioners have extended these investigations to the sound, light, and thermal fields emitted by healers. What is particularly interesting is that the pulsation frequency varies from moment to moment. Moreover, medical researchers developing pulsating magnetic field therapies are finding that these same frequencies are effective for ‘ jump starting’ healing in a variety of soft and hard tissues, even in patients unhealed for as long as 40 years. Specific frequencies stimulate the growth of nerves, bones, skin, capillaries, and ligaments. Of course Reiki practitioners and their patients have daily experiences of the healing process being "jump started," and academic medicine is now beginning to accept this therapy as logical and beneficial because of these new scientific findings. In Figure 2 we have bracketed portions of the signal that correspond to the frequencies used in medical devices that stimulate the healing of particular tissues. Individual differences in energy projection and detection. To study the projection of energy from the hands of therapists, scientists must first recognize that there are huge individual differences between people. Repeated practice of various techniques can enhance the effect. There are logical neurophysiological and biophysical explanations for the roles of practice and intention. [Editors note: It would be interesting to use these detection techniques to measure the effect of a Reiki attunement on the strength and frequency of biomagnetic energies coming from the hands and also to measure how therapeutic frequencies may change when treating various conditions in the body.] It is not widely understood that "brain waves" are not confined to the brain, but actually spread throughout the body via the perineural system, the connective tissue sheathes surrounding all of the nerves. Dr. Robert O. Becker has described how this system, more than any other, regulates injury repair processes throughout the body. Hence the entire nervous system acts as an "antenna" for projecting the biomagnetic pulsations that begin in the brain, specifically in the thalamus. Moreover, waves that begin as relatively weak pulsations in the brain appear to gather strength as they flow along the peripheral nerves and into the hands. The mechanism of this amplification probably involves the perineural system and the other connective tissue systems, such as the fascia that are intimately associated with it. Conclusion In this brief summary, it shows how some of the experiences of energy therapists have a basis in biology and physics. After centuries of neglect, energetic therapies can take their appropriate place in clinical medicine. The great discoveries of biologists and of sensitive bodyworkers are being integrated to give us a deeper understanding of life, disease, and healing. Science cannot take away the ultimate mystery of life, nor can it detract from the spiritual component of healing. We believe that research on the energy therapies can lead to much a more complete understanding of life, disease, and healing. Jim Oschman. References: (1) SQUID is an acronym for Superconducting Quantum Interference Device. (2) Journal of Bodywork and Movement Therapies, Harcourt Brace &amp; Co., Ltd., Edinburgh.</p></div> Sat, 04 Jan 2014 00:58:58 +0000 Alan 26 at Vitamin D <span property="schema:name" class="field field--name-title field--type-string field--label-hidden">Vitamin D</span> <span rel="schema:author" class="field field--name-uid field--type-entity-reference field--label-hidden"><span lang="" about="/about/team/alan-attridge" typeof="schema:Person" property="schema:name" datatype="">Alan</span></span> <span property="schema:dateCreated" content="2014-01-01T01:12:45+00:00" class="field field--name-created field--type-created field--label-hidden">Wed, 01/01/2014 - 01:12</span> <div property="schema:text" class="clearfix text-formatted field field--name-body field--type-text-with-summary field--label-hidden field__item"><p>Known as the sunshine vitamin, vitamin D is produced by the body in response to skin being exposed to sunlight.  It also occurs naturally in a few foods,  including some mushrooms, green vegetables, fish, fish oils, and egg yolks --- and in fortified dairy and food products. <br /> <br /> Vitamin D is essential for strong bones, muscles and the immune system.<br /> <br /> Low blood levels of the vitamin have been associated with the following:</p> <ul> <li>Increased risk of death from Cardiovascular disease</li> <li>Cognitive impairment in older adults</li> <li>Sever asthma in children</li> <li>Cancer</li> </ul> <p>To get the most out of your bone boosting diet, you'll want to do regular weight bearing exercise. This includes any activity that uses the weight of your body or outside weights to stress the bones and muscles. The result is that body  lays down more bone material, and your bones become more denser. Brisks walks, dancing, tennis, and yoga are good have all been shown to benefit your bones.<br /> <br /> In 2009, German scientists investigated the effect of vitamin D (calcitrol-the active form of vitamin D) levels on mortality in a cohort of 510 patients with serious, life-threatening illnesses: 67% with heart failure (two-thirds in end stage), 64.3% with hypertension, 33.7% with coronary heart disease, 20.2% with diabetes, and 17.3 % with renal failure.<br /> <br /> Many of these patients had multiple co-morbidities (diseases or conditions that coexist with a primary disease but they also stand on their own as specific diseases).  The scientists assessed vitamin D (Calcitrol) status at the beginning of the study, and assigned the patients to the following quintiles: &lt;16.7 ng/L, 16.7-25.2 ng/L, 25.3-33.2 ng/L, 33.3-43.4 ng/L, and &gt;43.4 ng/L.<br /> <br /> No supplementation was provided, although the patients were administered standard medications, and were followed for one year.<br /> <br /> Broken down by quintiles, the probability of survival was: 66.7% in the lowest quintile, 82.5% in the second quintile, 86.7 % in the third quintile, 88.8% in the fourth quintile, and 96.1% in the highest quintile.<br /> <br /> These survival improvement percent with calcitrol concentrations &gt;58.8 ng/L died during follow-up.<br /> <br /> More recently, in 2013, scientists from John Hopkins University, Baltimore, MD, examined 10,170 participants using National Health and Nutrition Examination Survey data to estimate hazard ratios (HRs) for all-cause and cardiovascular disease mortality for each 10-unit increase in serum 250HD. The authors concluded that there is "an inverse association between 250HD and all-cause and cardiovascular disease mortality in healthy adults with serum 250HD levels of &lt;21 ng/ml." Said differently, 25-hydroxyvitamin D blood levels below 21 ng/ml in this study increased the risk of dropping dead!<br /> <br /> 1. Zitterman A, Schleithoff SS, Frisch S, et al. Circulating calcitrol concentrations and total mortality. Clin Chem. 2009 Jun; 55(6): 1163-70.<br /> <br /> Published reports over the past 10 years indicate that higher vitamin D levels may help protect against virtually all degenerative diseases.<br /> <br /> A study published by PLOS medicine identified single nucleotide polymorphisms that were strongly associated with lower 25-hydroxyvitamin D levels.<br /> <br /> The researchers studied the odds of MS on those with genetically lower vitamin D levels from the International Multiple Sclerosis Consortium study.  Considered the largest genetic association study to date for MS, it included 14,498 subjects with MS and 24,091 healthy controls. The authors concluded that genetically lowered vitamin D levels were strongly associated with an increase risk for MS. 2<br /> <br /> 2. Mokry LE, Ross S, Admad OS, et al. Vitamin D and risk of multiple sclerosis: a mendelian randomization study. PLoS Med. 2015;12 (8):e1001866.<br /> <br /> The new data on Vitamin D heavily reinforces the statistics and research on vitamin D for MS.  Trials show that more than 90% of people with MS have deficient vitamin D. Deficient is defined at a level below 20 ng/L.<br /> <br /> Dr. Hui Wang, MD, PhD, Professor of the Institute for Nutritional Sciences at the Shanghai Institutes for Biological Sciences at the Chinese Academy of Sciences in Shanghai reviewed studies on Vitamin D Levels in 17,332 cancer patients.  His teams analysis demonstrated that vitamin D levels are linked to better outcomes in cancer. The risks of dying decreased from between 37% to 52%. (JCEM. 2014 April 29.)<br /> <br /> References: Pub Med, Web MD, MedlinePlus.<br /> <br />  </p></div> Wed, 01 Jan 2014 01:12:45 +0000 Alan 27 at Opinion of Scientific Peer Reviewed in Crisis <span property="schema:name" class="field field--name-title field--type-string field--label-hidden">Opinion of Scientific Peer Reviewed in Crisis</span> <span rel="schema:author" class="field field--name-uid field--type-entity-reference field--label-hidden"><span lang="" about="/about/team/alan-attridge" typeof="schema:Person" property="schema:name" datatype="">Alan</span></span> <span property="schema:dateCreated" content="2013-11-06T16:52:35+00:00" class="field field--name-created field--type-created field--label-hidden">Wed, 11/06/2013 - 16:52</span> <div property="schema:text" class="clearfix text-formatted field field--name-body field--type-text-with-summary field--label-hidden field__item"><p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>The publication of a scientific study in a peer-reviewed journal is commonly recognized as a kind of “nobilitation” of the study that confirms its worth.  The peer-review process was designed to assure the validity and quality of science that seeks publication. This is not always the case.  If and when peer review fails, sloppy science gets published.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p>According to a recent analysis published in <em><a href="">Proceedings of the National Academy of Sciences</a></em>, about 67 percent of 2047 studies retracted from biomedical and life-science journals (as of May 3, 2012) resulted from scientific misconduct.  However, the same <em>PNAS</em> study indicated that about 21 percent of the retractions were attributed to a scientific error.  This indicates that failures in peer-review led to the publication of studies that shouldn’t have passed muster.  This relatively low number of studies published in error (ca. 436) might be the tip of a larger iceberg, caused by the unwillingness of the editors to take an action.</p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>Peer review is clearly an imperfect process, to say the least.  Shoddy reviewing or reviewers have allowed subpar science into the literature.  We hear about some of these oversights when studies are retracted due to “scientific error.”  Really, the error in these cases lies with reviewers, who should have caught such mistakes or deceptions in their initial review of the research.  But journal editors are also to blame for not sufficiently using their powers to retract scientifically erroneous studies.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>Case in point: In May 2011, the International Agency for Research on Cancer (IARC) <a href="">classified</a> cell phone radiation as a possible human carcinogen based predominantly on epidemiological evidence.  In December 2011, the update of the largest recent epidemiological study, the so-called Danish Cohort, failed to find any causal link between brain cancer and cell phone radiation. It was published in the <em><a href="">British Medical Journal</a></em>.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>However, as pointed out by a number of scientists, <a href="">including myself</a>, peer-review of the Danish Cohort study failed to recognize a number of flaws, which invalidate the study’s conclusions.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>The only information collected pertaining to a person’s exposure to cell phone radiation was the length of their cell phone subscription.  Hence, two persons using cell phones—one many hours and another only a few minutes per week—were classified and analyzed in the same exposure group if their subscriptions were of equal length.  This meant that in the Danish Cohort study highly exposed people and nearly unexposed people were actually mixed up in the same exposure groups.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>From the initial size of the cohort of 723,421 cell phone subscribers, more than 420,000 private subscribers were included in the study but more than 200,000 corporate subscribers were excluded.  The exclusion of the corporate cell phone users meant that, most probably, the heaviest users were excluded (unless they had also a private subscription).  In addition to being excluded from user categories in the study, corporate users were also classified as unexposed. This means that the control group was contaminated. As the <em>BMJ</em> study admitted: “<em>…</em>Because we excluded corporate subscriptions, mobile phone users who do not have a subscription in their own name will have been misclassified as unexposed…”</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>Another flaw of the study was a 12-year gap between data collected on cell phone subscriptions and information culled from a cancer registry.  The study considered people with cell phone subscriptions as of 1995, while cancer registry data from 2007 was used in the follow-up study. That means that any person who started a cell phone subscription after 1995 was classified as unexposed. So the study’s authors considered a person who was diagnosed with brain cancer in 2007, but who had started a cell phone plan in 1996 as unexposed.  In reality, that person with brain cancer had been exposed to cell phone radiation for 11 years.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>It is clear to me that these flaws invalidate the conclusions of the Danish Cohort study. Peer-review failed, and a study that should never have got published due to its unfounded conclusions remains as a valid peer-reviewed article in the <em>British Medical Journal</em>.  As long as the flawed study is not withdrawn it will be used by scientists and by decision makers to justify their actions—e.g. a reference to the Danish Cohort study was recently used as supporting evidence in failing to indicate a causal link between cell phone radiation and brain cancer by the <a href="">US Government Accountability Office</a>.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>How is it possible that the <em>British Medical Journal</em> allowed such a poor quality peer review? Were the peer reviewers incompetent or did they have conflicts of interest?  What was the involvement of the <em>BMJ</em>’s editors? Why, once alerted to serious design flaws by readers, have <em>BMJ</em> editors not taken any action?</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>In my opinion the Danish Cohort study should be retracted because no revision or rewriting can rescue it.  The study is missing crucial data on exposure to cell phone radiation. Furthermore, an investigation should be launched to determine why such a flawed study was published.  Was it peer reviewer and <em>BMJ</em> editor incompetence alone or was a conflict of interest among reviewers involved?  (The authors of the study declared no conflicts of interest, but the original cohort was <a href="">reportedly established</a> with funding from a Danish phone company.) Answering these questions is important because it might help to avoid similar mistakes in the future.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><em><strong>DISCLAIMER</strong>: All opinions presented are author’s own and should not be considered as opinions of any of his employers.</em></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><em><strong>Dariusz Leszczynski is a research professor at the Radiation and Nuclear Safety Authority in Finland and a visiting professor at Swinburne University of Technology in Australia.</strong></em></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p> <p><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span><span>The review by the American Society for Microbiology stated that they find about 70% of the studies published in journals are flawed.</span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></span></p></div> Wed, 06 Nov 2013 16:52:35 +0000 Alan 28 at