2014 szeptember 1-én lépett volna életbe a menzákon felszolgált ételek sótartalmát csökkentő rendelet, amely az óvodákban, bölcsödékben már most változást tett volna kötelezővé, az iskoláknak viszont türelmi időt adott egészen 2020-ig. Csak az a sok volna ne lenne, a menzákon ugyanis ma még ne keressenek semmiféle változást.
Szeptember helyett jövő év január 1-jén lép hatályba a közétkeztetésről szóló rendelet, amely szabályozza az iskolai menzákon, kórházakban adandó ételek elkészítését, tápanyagtartalmát, és mérföldkő a sófogyasztás csökkentésében - jelentette be Novák Katalin, az Emberi Erőforrások Minisztériuma család- és ifjúságügyért felelős államtitkára még augusztusban. Így a sokat beharangozott eseményt ne várják, ne keressék. A menzareform hátteréről a közétkeztetők szempontjából mi is írtunk, amit itt olvashat:
( http://www.origo.hu/tafelspicc/kozelet/20140516-palotaforradalom-eloszele-a-menzakon.html )
Mi volt a régi dátum?
A rendelet 2014. szeptember elsejétől hatályos, a bölcsődei (napi 1,5 g só) és óvodai (napi 2 g) étkezésben már akkortól az új rendeletben meghatározott mennyiségeket kell használni, az iskolai napi sóadag 3,5 grammra csökkentésére 6 évet kaptak a közétkeztetők.
Mi az új dátum?
Az államtitkár elmondta: a sótartalomra vonatkozó intézkedések az ötévesnél fiatalabb gyerekek számára január 1-jén lépnek hatályba, az idősebbeknél fokozatosan, 2021-ig kell elérni a kívánatosnak tartott öt gramm/nap adagot.
“We’ve got smarter and smarter in the 20th century, but now there are signs that IQs have begun to fall in countries such as the UK and Australia”
Komment 2014.08.26., még várakozik a jóváhagyásra
tetrakomment megosztva 2014.08.26
comments várakoznak jóváhagyásra
The long-term rise in IQ scores might be coming to a halt, but we should focus on improving social conditions rather than worrying about idiocracy.
We started and speeds our devolution.
In a new study published in Nature Communications, research scientists from Uppsala University present for the first time a large-scale study of the significance of genetic, clinical and lifestyle factors for protein levels in the bloodstream. The results of the study show that genetics and lifestyle are determining factors for protein levels, a discovery which greatly influences the possibilities for using more biomarkers to identify disease.
Biomarkers used for diagnosing disease should preferably indicate variations in protein levels only for those individuals who are suffering from a particular disease. Nor should they vary for reasons which have nothing to do with the disease. By analysing 92 protein biomarkers for cancer and inflammation in a clinical study of 1,000 healthy individuals, researchers at Uppsala University have for the first time surveyed the significance of genetic, clinical and lifestyle factors for protein levels in the bloodstream. The results of the study show that hereditary factors play a significant role for more than 75 per cent of the proteins, and a detailed genetic analysis demonstrates 16 genes with a strong effect on protein levels.
“These results are important, as they show which variables are significant for variations in the measurable values. If these factors are known, we have a greater possibility of seeing variations and we get clearer breakpoints between elevated values and normal values. By extension this may lead to the possibility of using more biomarkers clinically,” explains Stefan Enroth, researcher at the Department of Immunology, Genetics and Pathology at Uppsala University.
According to the study, genetics and lifestyle together account in some cases for more than 50 per cent of variations in protein levels among healthy individuals. This means that information about both genetic and lifestyle factors must be taken into account in order for protein biomarkers to be used effectively.
Entropy is growing = devolution.
Calcium buildup in the coronary arteries of chronic kidney disease patients may be a strong indicator of heart disease risk, according to a new study in the Journal of the American Society of Nephrology (JASN). Researchers at the Johns Hopkins Bloomberg School of Public Health assert that coronary calcium outperforms two other commonly used measures of subclinical atherosclerosis in predicting the risk of heart disease among individuals with kidney disease.
Approximately 50 percent of all patients with chronic kidney disease (CKD) die from cardiovascular disease, but some previous studies concluded that conventional risk factors for predicting heart disease — such as blood pressure and lipid levels — were not as useful in CKD patients.
Kunihiro Matsushita, MD, PhD, an assistant scientist in the Bloomberg School’s Department of Epidemiology, and his colleagues, decided to investigate whether other tests might be more helpful in predicting cardiovascular disease in those with CKD. They compared three measures of atherosclerosis — calcium levels within blood vessel walls, the thickness of the carotid artery walls, and narrowing of arteries in the legs.
Although the amount of coronary calcium is a potent predictor of heart disease in the general population, Matsushita says it wasn’t clear whether it would be as useful in people with CKD. The kidneys help regulate the body’s calcium levels, and individuals with CKD often have an altered calcium metabolism, which researchers were concerned could influence the usefulness of calcium in the coronary artery walls as a predictor of heart disease. Coronary calcium levels are determined by computer tomography (CT).
The study included 6,553 adults in the Multi-Ethnic Study of Atherosclerosis between the ages of 45 and 84 years who did not have prior cardiovascular disease; 1,284 of them had CKD. After eight years, 650 cardiovascular events (coronary heart disease, stroke, heart failure, and peripheral artery disease) occurred, with 236 of the events occurring in those with CKD. Looking back, the researchers determined that calcium buildup was more accurate in correctly determining CKD patients’ risk of cardiovascular disease (especially coronary heart disease and heart failure), than measures of thickening of the carotid artery walls or narrowing of arteries in the legs.
“Our research is important since it assures the usefulness of coronary artery calcium for better cardiovascular disease prediction in persons with CKD, a population at high risk for cardiovascular disease but with potential caveats for the use of traditional risk factors,” Matsushita says.
Washington, DC (August 21, 2014) — Calcium buildup in the coronary arteries may be a better indicator of kidney disease patients’ risk of heart disease than traditional risk factors used in the general population, according to a study appearing in an upcoming issue of the Journal of the American Society of Nephrology (JASN). The findings provide valuable new information that could help safeguard the heart health of patients with kidney disease.
Heart disease is the leading cause of death in individuals with chronic kidney disease (CKD). Some studies have found that conventional risk factors for predicting an individual’s likelihood of developing heart disease aren’t as useful in CKD patients as they are in the general population.
Kunihiro Matsushita, MD, PhD (Johns Hopkins Bloomberg School of Public Health) and his colleagues looked to see if calcium measurements within blood vessel walls might be helpful. Because the kidney helps regulate the body’s calcium levels, individuals with chronic kidney disease often have altered calcium metabolism, which may influence the usefulness of calcium in the coronary artery walls as an indicator of heart disease.
The researchers studied 6553 adults aged 45 to 84 years who did not have prior cardiovascular disease and who were participating in the Multi-Ethnic Study of Atherosclerosis. Among the participants, 1284 had CKD.
During a median follow-up of 8.4 years, 650 cardiovascular events (coronary heart disease, stroke, heart failure, and peripheral artery disease) occurred, with 236 of the events occurring in participants with CKD. The investigators found that calcium build-up in the coronary artery walls was more useful for correctly determining CKD patients’ risk of cardiovascular disease (particularly coronary heart disease and heart failure) than other measures of atherosclerosis such as thickness of the carotid artery walls and narrowing of the arteries in the legs.
“Our research is important since it assures the usefulness of coronary artery calcium for better cardiovascular disease prediction in persons with CKD, a population at high risk for cardiovascular disease but with potential caveats for the use of traditional risk factors,” said Dr. Matsushita.
Magyarországon nem lehet egészséges kenyeret vásárolni.
20 év alatt majdnem megkétszereződött azoknak az újszülötteknek a száma, akik hipospadiázissal, húgycsőhasadékkal jönnek világra Svédországban. Svéd kutatók szerint környezetszennyezés állhat a háttérben.
Egyre több kisfiú születik rendellenes nemi szervvel. A hipospadiázissal világra jött kisfiúk aránya az elmúlt 20 évben majdnem megkétszereződött Svédországban – derült ki a svéd Dagens Medicin orvosi lap által közzétett tanulmányból. A stockholmi Astrid Lindgren Kórház kutatói feltételezik, hogy a növekedés a környezeti hatások okozta hormonális zavar számlájára írható.
Míg 1990-ben ezerből 4,5 baba született a rendellenességgel, 2009-ben már nyolc. A számok a hipospadiázis enyhébb és súlyosabb eseteit is magukban foglalják: a húgycső kivezető nyílásának rossz elhelyezkedésétől olyan komoly zavarokig terjedhet a skála, amikor gyakran a csecsemő neme sem állapítható meg.
Az előfordulási arány megduplázódása a szakértők szerint nem magyarázható csupán a klasszikus kockázati tényezőkkel, többek közt a mesterséges megtermékenyítéssel, bár ezek aránya is emelkedett a svédek körében. A környezetbe kerülő hormonmérgeknek szintén lehet szerepük a rendellenesség terjedésében.
A condition which causes baby boys to be born with deformed penises is becoming more common in Sweden, for reasons unknown to scientists.
Researchers in Sweden assessed data collected on Hypospadias between 1973 and 2009. They found that before 1990, only 4.5 per cent of boys out of every thousand had the condition known as hypospadias. But after 1990, the figure had risen to 8 per cent per 1000 boys. In an attempt to explain the rise, the experts from Stockholm’s Karolinksa Institute considered factors known to cause the defect, including low-birth weight, being born a twin, and parents who used IVF treatment to conceive.
However, scientists could not link the rise to any previously known causes, and instead concluded that an unknown factor was behind the trend, The Local reported.Hypospadias can cause a combination of three separate problems: the meatus, the hole through which urine passes, is not being at the tip of the penis; the foreskin becoming gathered at the back of the penis with none at the front; and the penis being bent when stiff, according to the NHS.
While hypospadias is not life threatening, it can make it difficult to urinate standing up, and can make having sex difficult. The issues are usually fixed by an operation to move the meatus, and a circumcision to remove the foreskin.
Speaking with the Dagens Medicin newspaper, Anna Skarin Nordenvall from the institute did not reject the idea that chemicals that interfere with the hormones of mammals, known as endocrine disruptors, could be linked to the rise of hypospadias.
According to the WHO, endocrine disruptors are mostly man-made and are found in various materials such as pesticides, metals, additives or contaminants in food, and personal care products.
The chemicals have suspected associations with altered reproductive function in males and females, increased incidence of breast cancer, and abnormal growth patterns.
Swedish docs puzzled by deformed penis trend
Hypospadias, a birth defect where the urethral opening is abnormally placed, is becoming a more common case among Sweden’s new-born boys.
Researchers at Stockholm’s Karolinksa Institute have published results from a 40-year study in which they collected data from all males born between 1973 and 2009.
They found that before 1990, cases of hypospadias were recorded in 4.5 boys out of every thousand. After 1990, the figure increased to 8 per 1,000 boys.
The study looked into factors that are known to cause the defect, such as low-birth weight, being born a twin, or parents who used in vitro fertilization (IVF) to conceive, but researchers stated that the increase did not correlate with these factors.
Researchers concluded that the increase could not be put down to previously known factors, but rather that an unknown factor was behind the deformations.Speaking with the Dagens Medicin newspaper, Anna Skarin Nordenvall from the institute refused to rule out the possibility that environmental agents known as endocrine disruptors could be interfering with human hormonal systems, and therefore behind the increase in statistics.
Endocrine disruptors are chemicals that can disrupt the hormone system, and have been linked to cancer, birth defects, and brain development problems. They can be found in food, plastics, and various household products.
We studied the incidence of hypospadias in Sweden during a 40-year period to determine if changes were associated with known risk factors.
Materials and Methods
We analyzed prospective data from nationwide health care and demographic registers collected for all males (1,948,591 total) born in Sweden between 1973 and 2009. The incidence of hypospadias per 1,000 live-born boys was calculated as number of cases divided by total number of births yearly. The association between hypospadias and risk factors was estimated using logistic regression, expressed as odds ratios.
The nationwide incidence of boys diagnosed with hypospadias was approximately 4.5 per 1,000 live-born boys until 1990, increasing to 8 per 1,000 boys during the following decade. Mild and severe phenotypes comprised the increase. Boys born small for gestational age (OR 4.34), as a twin (OR 1.8), as a result of in vitro fertilization (OR 1.15), or with parents from Asia (OR 1.45) or continental Europe (OR 1.41) were at increased risk for hypospadias. Multivariate analyses revealed that changes in risk factors did not explain the increased incidence. However, a systematic change in the classification of the diagnosis in registers could not be ruled out.
This nationwide study demonstrates an increased incidence of hypospadias diagnoses in Sweden from 1990 to 1999 that is not attributable to previously known risk factors. The increase includes mild and severe phenotypes, suggesting that shifts in the diagnostic criteria are not the underlying cause.
3 komment 2014.08.27.
(érdekes lehet: http://www.ncl.ac.uk/magres/research/diabetes/reversal.htm = junk)
“Work by scientists at the Universities of Manchester and Auckland suggest that both major forms of diabetes are the result of the same mechanism.
The findings, published today in the FASEB Journal (20 August), provide compelling evidence that juvenile-onset or type-1 diabetes and type-2 diabetes are both caused by the formation of toxic clumps of a hormone called amylin.
The results, based on 20 years’ work in New Zealand, suggest that type-1 and type-2 diabetes could both be slowed down and potentially reversed by medicines that stop amylin forming these toxic clumps.
Professor Garth Cooper, from The University of Manchester working with his University of Auckland-based research team, led the study.
As well as producing insulin, cells in the pancreas also produce another hormone called amylin. Insulin and amylin normally work together to regulate the body’s response to food intake. If they are no longer produced, then levels of sugar in the blood rise resulting in diabetes and causing damage to organs such as the heart, kidneys, eyes and nerves if blood sugar levels aren’t properly controlled.
However, some of the amylin that is produced can get deposited around cells in the pancreas as toxic clumps, which then, in turn, destroy those cells that produce insulin and amylin. The consequence of this cell death is diabetes.
Research published previously by Professor Cooper suggested that this is the causative mechanism in type-2 diabetes. This new research provides strong evidence that type-1 diabetes results from the same mechanism.
The difference is that the disease starts at an earlier age and progresses more rapidly in type-1 compared to type-2 diabetes because there is more rapid deposition of toxic amylin clumps in the pancreas.
Professor Cooper’s group expects to have potential medicines ready to go into clinical trials in the next two years and it is anticipated that these will be tested in both type-1 and type-2 diabetic patients. These clinical trials are being planned with research groups in England and Scotland.”
“According to the American Heart Association , the prevalence of diabetes for all age groups worldwide was estimated to be 2.8% in 2000 and is projected to be 4.4% in 2030. The total number of people with diabetes is projected to rise from 171 million in 2000 to 366 million in 2030. Similar figures have been produced by other groups such as the International Diabetes Federation.”
Sodium-Induced Disorder and devolution.