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Metabolic Syndrome Metabolic Syndrome Anejo Health Communications // Pocket Guide to Metabolic Syndrome Metabolic Syndrome Peter Steinberg Anejo Health Communications Anejo Health Communications Address: Lavalle 715 5th floor. (1047) Bs. As. - ArgentinaPhone: (011) 4322-1110 / 1199 / 0109E-mail: [email protected] First edition June 2012All rights reservedPrinted in June 2012 Although the information about medication given in this book hasbeen carefully checked, the author and publisher accept no liability forthe accuracy of this information. In every individual case the user must check such information by consultingthe relevant literature.
This work is subject to copyright. All rights are reserved, whether thewhole or part of the material is concerned, specifically the rights oftranslation, reprinting, reuse of illustrations, recitation, broadcasting,reproduction on microfilm or in any other way, and storage in data banks.
ISBN 978-950-9647-85-5 // Pocket Guide to Metabolic Syndrome Table of Contents History of Metabolic Syndrome
. Type 1 Diabetes, Type 2 Diabetes, and Insulin Resistance. A Precursor to Cardiovascular Disease and Diabetes Developing - and reconciling a formal definition
Population differences in prevalence
Diagnosis Metabolic Syndrome
. Medical History . Waist Circumference . Measuring Waist Circumference . Measuring Blood Pressure Laboratory Test
. Assessing Insulin Resistance
. Assessing Dyslipidemia Two possible accompanyng diagnosis
. Cushing's Syndrome Causes of Metabolic Syndrome
. Intra-Abdominal Obesity . Insulin Resistence . Urinary Symptoms in Men The health consequences
. Coronary heart disease . Type 2 diabetes Treatment of Metabolic Syndrome
. Goals of Treatment . Healthy Lifestyle Changes . Psychological Counseling Prevention of Metabolic Syndrome
. Physical Activity . Routine Health Maintenance // Pocket Guide to Metabolic Syndrome Introduction Metabolic syndrome is a term used to describe a particular clusterof health problems that were first identified in 1988 by Gerald Rea-ven, an endocrinologist at Stanford University.1 He originally calledit syndrome X, and at various times the syndrome has also been re-ferred to as dysmetabolic syndrome, insulin resistance syndrome, andobesity dyslipidemia syndrome. The term metabolic syndrome is nowwidely accepted, whereas syndrome X fell into disfavor due to con-fusion with a similarly named cardiac syndrome. In essence, metabolic syndrome is characterized by abdominal obe-sity and insulin resistance (reduced responsiveness of the body tis-sues to insulin). Metabolic syndrome is often accompanied byhypertension and two lipid disorders: high blood levels of triglyce-rides and low blood levels of high-density lipoprotein (HDL) cho-lesterol. Compared to someone without the syndrome, a person withmetabolic syndrome has a fivefold greater risk of developing type 2diabetes, and is three times as likely to have – and twice as likely todie from – a heart attack or stroke.2 A major public health problem, metabolic syndrome affects one-quarter of the world's adults.2 A 2009 study found that individualswith metabolic syndrome incur almost 1.6 times the medical costsof those without the syndrome ($5,732 vs. $3,581 annually). Addi- tionally, annual medical costs were nearly double among individualswith diabetes who had risk factors for metabolic syndrome, compa-red to nondiabetics who had such risk factors ($8,067 vs. $4,638).3 // Pocket Guide to Metabolic Syndrome History of MetabolicSyndrome Type 1 Diabetes, Type 2 Diabetes, and Insulin Resistance In the early 1920s, the Canadian surgeon Frederick Banting and hisassistant Charles Best, a medical student, extracted a compound theynamed insulin from the islets of Langerhans in the pancreas. Wheninjected into diabetic dogs, the compound decreased the levels of sugarin the dogs' blood and urine.4 The discovery, coupled with the purifi-cation of insulin, helped transform childhood diabetes from a fataldisease to a chronic illness.
By the 1930s, it had become common to classify people with diabetesaccording to how they reacted to an injection of insulin. Those whowere "insulin-sensitive" or "insulin-dependent" were found to easilyprocess an oral dose of glucose when also given a subcutaneous insulininjection. On the other hand, "insulin-insensitive" or "non-insulin-dependent" diabetics did not experience a significant reduction inblood glucose after receiving the same amount of insulin.
Today, most people use the term type 1 diabetes to refer to what used
to be known as "insulin-sensitive" or "insulin-dependent" diabetes.
Type 1 diabetes results from an autoimmune reaction whereby the
body's defense system attacks insulin-producing cel s, although the rea-
son for this is not entirely understood. Individuals with type 1 diabetesproduce little or no insulin. Although the disease can strike at any age,it occurs more often in children and young adults, and is sometimescalled juvenile-onset diabetes. People with type 1 diabetes require dailyinjections of insulin in order to control their blood glucose levels.5 Type 2 diabetes has largely replaced the terms "insulin-insensitive"
and "non-insulin-dependent" diabetes. Type 2 accounts for at least
90% of all cases of diabetes, and is sometimes referred to as adult-
onset diabetes because it usually arises in adults over the age of 40, al-
though it can occur at any age, especially in populations with high
diabetes prevalence. This type of diabetes is characterized by insulin
resistance, a phenomenon by which an individual's body tissues have
a diminished response to insulin, causing the body to produce larger
quantities of insulin to maintain normal blood glucose levels.5,6
By the late 1980s insulin resistance had become an important field of
research, as physicians began to understand it not only as a precondi-
tion of type 2 diabetes, but as also associated with conditions such as
obesity, pre-diabetes (a condition marked by elevated blood glucose
levels after fasting or after a 2-hour glucose tolerance test), heart dis-
ease, and polycystic ovarian syndrome (PCOS), an endocrine disor-
der that affects 3-10% of premenopausal women as a result of the
formation of cysts in the ovaries, leading to irregular menstrual peri-
ods, infertility, hirsutism (excess body hair), or other indications of
high blood levels of androgens (male sex hormones).6
With the emergence of insulin resistance as a public health and clinicalproblem, researchers increasingly recognized that it frequently pre-sented as part of a particular cluster of metabolic disorders that alsoincluded intra-abdominal obesity, high blood levels of triglycerides,low blood levels of HDL cholesterol, and high blood pressure. Thiscluster appeared to meet the criteria of a syndrome: "a clustering offactors that occur together more often than by chance alone and forwhich the cause is often uncertain."7 // Pocket Guide to Metabolic Syndrome A Precursor to Cardiovascular Disease and Diabetes Although there is general agreement within the medical community thatmetabolic syndrome deserves greater attention, there has been widespreaddisagreement with regard to the terminology and diagnostic criteria relatedto the syndrome. Nevertheless, there appears to be a consensus amongphysicians that the term metabolic syndrome is an acceptable way to de-scribe the presence of multiple risk factors for cardiovascular disease(CVD) and diabetes. On the other hand, several clinical definitions ofmetabolic syndrome have been proposed (as discussed below), causingsome confusion among clinicians in terms of how to identify patients whohave the syndrome.7 Some of the confusion may reflect the complexity and interrelatedness
of the factors that contribute to metabolic syndrome. The syndrome is
not an indicator of absolute risk because it does not include many of the
factors that determine absolute risk of disease, such as age, sex, cigarette
smoking, and low-density lipoprotein (LDL) cholesterol levels. Neverthe-
less, it is wel known that metabolic syndrome increases the risk of CVD
and type 2 diabetes.7,8 Moreover, the most widely recognized metabolic
risk factors – dyslipidemia, high blood pressure, and elevated plasma glu-
cose – often manifest as a prothrombotic and proinflammatory state. Most
persons with metabolic syndrome have abdominal obesity and insulin re-
sistance, both of which appear to contribute to the development of meta-
bolic risk factors, although the mechanisms for these contributions are
not completely understood.7
The most common clinical definition of metabolic syndrome uses a smalset of direct measurements: waist circumference, elevated triglycerides, re-duced HDL cholesterol, elevated blood pressure, and elevated fasting glu-cose.7 These measurements can facilitate an objective diagnosis of thesyndrome, while also providing actionable targets for basic research, drugdevelopment, and therapeutic advances. As currently defined, metabolic syndrome is a useful but imperfect pre-dictor of a person's chance of developing serious health problems. As thesyndrome continues to draw researchers' attention, its definition wil likelyevolve.

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Betydningen af svampemidlernes formulering samt fysiologiske effekter

Physiological Effects of Fungicides Course for Advisers Koldkaergaard / Aarhus, September 6th 2012 Physiological Effects of Fungicides Physiological Effects of Fungicides: Guidelines for presentation Life can only be understood backwards; but it must be lived forwards Motto for advise in plant protection: As little as possible but as much as neccessary

GUIDELINE WATCH (OCTOBER 2014): PRACTICE GUIDELINE FOR THE TREATMENT OF PATIENTS WITH ALZHEIMER'S DISEASE AND OTHER DEMENTIAS Peter V. Rabins, M.D., M.P.H.Barry W. Rovner, M.D.Teresa Rummans, M.D.Lon S. Schneider, M.D.Pierre N. Tariot, M.D. During development and approval of this guideline watch, from July 2012 to September 2014, Dr. Rabins reports providing legaltestimony for Janssen Pharmaceutica, Dr. Rovner reports serving as a consultant to GE Healthcare, and Dr. Rummans reports thatshe has nothing to disclose. From 3 years before development was initiated in July 2012 through September 2014, Dr. Schneider andthe University of Southern California received research or other grants from Abbott Laboratories, AstraZeneca, Baxter, Forest Phar-maceuticals, Inc., Forum, Genentech, Johnson & Johnson, Eli Lilly and Company, Lundbeck, Merck, Myriad, Novartis, Pfizer,Roche, and TauRx, Ltd. and from NIH (USC ADRC, ADCS, ADNI, Banner Alzheimer's Initiative, CitAD, phytoSERMs, Alzheim-er's disease trial simulations, allopregnanolone, P50 AG05142, R01 AG033288, R01 AG037561, UF1 AG046148), and the state ofCalifornia (California Alzheimer's Disease Program, California Institute for Regenerative Medicine). During that same time period,Dr. Schneider served as a consultant or on advisory panels for Abbott Laboratories, Abbvie, AC Immune, Accera, Allon, AstraZeneca,Avraham Pharmaceuticals, Ltd., Biogen Idec, Cerespir, Forest Pharmaceuticals, Inc., Forum, GSK, Johnson & Johnson, Eli Lilly andCompany, Lundbeck, Merck, Novartis, Orion, Roche, Servier, Stemedica, Ltd., Takeda, Targacept, TauRx, Toyama/FujiFilm, andZinfandel. In addition, Dr. Schneider serves on the editorial boards of Alzheimer's and Dementia: Translational Research and ClinicalIntervention (editor-in-chief), The Lancet Neurology (editorial board), Cochrane Collaboration (editor base), BMC Psychiatry (section ed-itor), Alzheimer's & Dementia (senior associate editor), Current Alzheimer Research (associate editor), Clinical Neuropharmacology (edi-torial board) and on the guidelines committee for the World Federation of Societies of Biological Psychiatry; served as an expert wit-ness or consultant on federal and state cases for plaintiffs against Lilly, Johnson & Johnson, and Pfizer and for defendants AstraZenecaand Pfizer; and has consulted with the state of California Department of Justice. During development and approval of this guidelinewatch, Dr. Tariot reports receiving consulting fees from Abbott Laboratories, AbbVie, AC Immune, Adamas, Avanir, Avid, Boehringer-Ingelheim, Bristol Myers Squibb, California Pacific Medical Center, Chase Pharmaceuticals, Chiesi, CME, Inc., Cognoptix, Elan,Eli Lilly, GlaxoSmithKline, Janssen, Medavante, Medivation, Merck and Company, Merz, Otsuka, Roche, and Sanofi-Aventis. Dr.Tariot reports receiving research support from AstraZeneca, Avanir, Avid, Baxter Healthcare Corp., Bristol Myers Squibb, Cognop-tix, Eli Lilly, Functional Neuromodulation (f(nm)), GE, Genentech, GlaxoSmithKline, Janssen, Medivation, Merck and Company,Pfizer, Roche, Targacept, and Toyama as well as the National Institute on Aging and the Arizona Department of Health Services. Dr.Tariot also reports stock options in Adamas and that he is listed as a contributor to a patent owned by the University of Rochester,"Biomarkers of Alzheimer's Disease."