domingo, 10 de junio de 2012

carbodratos o azucares

A Lesson in Basic Nutrition

by John McDougall MD on Tuesday, July 21, 2009 at 6:21pm ·
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Nutrients are substances which are essential for the maintenance, repair, growth, and reproduction of all our body tissues. Our foods contain the following basic nutrients: carbohydrates, fats, proteins, and water.

Carbohydrates, our body's most efficient source of energy and an essential component in the production of many structural and functional materials, are produced by plants in the process of photosynthesis. They are made of compounds of carbon, hydrogen, and oxygen called sugars or saccharides. Molecules of these simple sugars attach together to make long branching chains that are called complex carbohydrates. These large carbohydrate molecules are also commonly referred to as starch.

Once you eat them, digestion by intestinal enzymes disassembles these chains back into the simple sugars, which then pass easily through the intestinal wall into the bloodstream, where they journey to the body's tissues. Metabolic processes change these simple sugars into energy, which provides fuel for the body's activity.

Dietary fibers are even longer chains of complex carbohydrates. Unlike starch molecules, these fibers resist digestion because of their chemical configurations. Therefore, most fibers eventually end up in the colon and form the bulk of your stool. Most people think that fibers are only the husks of grains and the long stringy components in fruits and vegetables, but actually, dietary fibers are present in all plant tissues. For example, after a potato is peeled, the white matter we eat has plenty of relatively indigestible fibers in it.

Fats too are complex molecules made up of carbon, oxygen, and hydrogen. Although they are not as easily digested as sugars are, fats are sources of energy and they provide important structural materials for building different components of the human body. Fats are divided into two categories: saturated fats (solid at room temperature), found mostly in animal tissues, and unsaturated fats (liquid), found mostly in plant tissues. Most fats can be synthesized by our own bodies from carbohydrates as they are needed. The fats that we can synthesize are said to be nonessential because they are not necessary ingredients in our diet. The only fats we cannot synthesize for ourselves are a few unsaturated fats. They must be provided to us, ready-made, in our foods and therefore are called essential fats.

Proteins provide the raw materials for a large part of the functional and structural components of our bodies. Only as a last resort are they used as a source of energy. The building blocks that make up all proteins are called amino acids. Various combinations of the same twenty two- amino acids, put together as are the letters of the alphabet that can form a whole dictionary of words with different meanings, make all of the proteins in nature. Proteins are found in all foods derived from animals and plants, unless they have been removed or altered by refining processes. Only eight of the twenty-two amino acids are essential to us, because they cannot be made in human metabolism. These eight essential amino acids must be present in sufficient quantities in our food for us to enjoy good health.

Water makes up a large part of our foods. Although it yields no energy, for many reasons water is an essential element for life. It is not just a passive solvent in which salts, compounds and gasses interact; water participates actively in forming building blocks of cells and is the environment in which cells live. Approximately 60 percent of body weight is water.

Because the four nutrients discussed above - carbohydrates, fats, proteins, and water make up the largest portion of any foodstuff by weight, they are often referred to as macronutrients. Our foods also contain two micronutrients--vitamins and minerals--which make up only a tiny percentage of our food by weight.

Vitamins are organic compounds that are synthesized for the most part only by plants and bacteria. Humans and most large animals can synthesize vitamin D (with the help of sunlight), and some animal species can make vitamin C (ascorbic acid). Thus, our supply of vitamins must come from plant foods and our own bowel bacteria. Vita means life, and, as the name indicates, vitamins are essential for our existence. Without adequate amounts, disease can develop.

Minerals are also micronutrients, but they come from inorganic matter, primarily the earth. Their presence in adequate amounts in our foods is also essential for our good health. They participate in thousands of metabolic reactions that must take place throughout the body. For instance, iron in the enzyme hemoglobin transports oxygen in our red blood cells. Some minerals are important elements in our structural material. Calcium, for example, is a large part of bones and teeth.

Our foods also contain various non-nutrients, substances that are not necessary for life or good health. Many of these substances, such as cholesterol, pesticides, herbicides, and additives, present real threats to our health. Even though these non-nutrients make up a small amount by weight of our foods, their health significance can be great, causing problems such as heart disease, cancer and allergies.

Carbohydrates are made by plants and stored in their leaves, stems, roots, and fruits. Plant foods contain both simple and complex carbohydrates in various amounts. Fruits are often more than 90 percent carbohydrate, but most of their carbohydrates are the sweet-tasting simple forms of carbohydrate, such as glucose and fructose. Green and yellow vegetables store most of their calories as complex carbohydrates, but since they contain very few total calories the amount of complex carbohydrate they provide in the diet is small. Whole grains (rice, corn) and the whole grain flours (wheat, rye) and whole grain pastas (wheat, soba) made from them, tubers (potatoes, yams), legumes (beans, peas), and winter squashes (acorn, hubbard) contain large quantities of complex carbohydrates and thus are known as starches. Rice, corn, and other grains, and potatoes typically store about 80 percent of their calories in the form of complex carbohydrates. Beans, peas, and lentils are approximately 70 percent complex carbohydrates.

Starches contain sufficient calories to easily meet the energy requirements of the active person, and they are abundant in proteins (with all their essential amino acids), essential fats, fibers, and minerals required to meet our daily dietary needs, Many starches, such as the maligned potato, have a full complement of vitamins as well. (Grains and legumes need the help of fruits or green and yellow vegetables in order to provide adequate vitamin A and C.)

You have probably heard that marathon runners and other endurance athletes "load up" on carbohydrates before an event, devouring large meals of spaghetti, rice, and potatoes in order to store energy-providing carbohydrates for the long race. Carbohydrate-loading several times a day will give you too the energy to race through your busy life.

The only food from animals in which a carbohydrate is found in significant amounts is milk, which contains a simple sugar called lactose. However, lactose cannot be digested by most adults,* and consequently, when they drink milk, they suffer assorted evidences of indigestion, such as diarrhea, stomach cramps, and hurtful amounts of gas. In the sense of total amount of carbohydrates in their diet, Americans eat far too few calories from this source--only about 40% of their diet is carbohydrate. To make things worse the kinds of carbohydrates eaten are mostly "empty calories" in the form of white sugar, corn syrup, and fructose. A healthy diet, like the McDougall diet, is more 80% carbohydrate from nutritious foods--starches, vegetables and fruits.

When we hear or read the word sugar most of us think of granular white table sugar. Unlike the simple sugars found in ripe fruit, this kind of sugar should be eaten only in limited quantities. After the refining process, it contains no fibers, proteins, essential fats, vitamins, or minerals. It is purely concentrated sugar. Nothing could better deserve the descriptive term "empty calories," because calories is all it provides. Although refined sugar can provide energy, too much refined sugar in the diet can lead to tooth decay, contribute to obesity, and raise triglycerides. A nutritional imbalance, weakening the body's defense and repair system making us susceptible to disease processes from infection to cancer, may result when "empty calories" make up a substantial part of the diet.

Fibers are made only by plants and FOUND ONLY IN VEGETABLE FOODS. There is no fiber in beef, pork, chicken, lobster, cheese, egg, or other animal-derived foods.

domingo, 27 de mayo de 2012

como el sistema inmune reconoce a los virus

Doherty and Zinkernagel inoculated mice with a virus causing meningitis. They isolated the immune T killer cells and found that these had to recognize two things on the surface of the infected cells in order to kill them: virus antigen, as expected, but also an MHC molecule of the infected mouse strain. MHC molecules are normal components of healthy cells. They were known to differ among individuals and to cause rejection of organ transplants and they are therefore sometimes called transplantation antigens. It came as a surprise that they were also involved in recognition of infected cells.

Doherty and Zinkernagel presented two main theoretical models to explain their observations. These models have inspired immunologists and set the stage for research on cell-mediated immunity for at least two decades.

Wrong combination: the right virus antigen (x) but the wrong MHC molecule (b).
Wrong combination again: the right MHC molecule (a) but the wrong virus antigen (y).
The correct combination or virus antigen (x) and MHC molecule (a) leads to killer cell attack.
 A T killer cell (upper right) attaching to and sensing the antigens on a target cell. If the target cell carries the correct antigens fitting the receptor of this particular T cell, the "kiss of death" will follow: the target cell will be destroyed.  

 

The "dual recognition" model assumed that two receptors on the T cell recognized virus antigen and the MHC molecule separately (best illustrated by the previous figure of the "correct combination").

The "altered self" model was based on one T-cell receptor recognizing an MHC molecule modified by virus antigen - or "a little bit of transplantation antigen, a little bit of virus," as Doherty and Zinkernagel have phrased it. (This is illustrated in the "zoom" above, like the previous model based on figures in the original reports.) Through important discoveries made later by other scientists, we are now getting a clearer picture of the scenario. The T-cell receptor, not yet identified at the time of the discovery, recognizes a small part of a virus protein, attached in a cleft formed by the transplantation antigen.





Copyright © Nobel Media AB 2012

martes, 1 de noviembre de 2011

drugs son seguras para ADHD

Original Article

ADHD Drugs and Serious Cardiovascular Events in Children and Young Adults

William O. Cooper, M.D., M.P.H., Laurel A. Habel, Ph.D., Colin M. Sox, M.D., K. Arnold Chan, M.D., Sc.D., Patrick G. Arbogast, Ph.D., T. Craig Cheetham, Pharm.D., Katherine T. Murray, M.D., Virginia P. Quinn, Ph.D., M.P.H., C. Michael Stein, M.B., Ch.B., S. Todd Callahan, M.D., M.P.H., Bruce H. Fireman, M.A., Frank A. Fish, M.D., Howard S. Kirshner, M.D., Anne O'Duffy, M.D., Frederick A. Connell, M.D., M.P.H., and Wayne A. Ray, Ph.D.

November 1, 2011 (10.1056/NEJMoa1110212)

Comments open through November 8, 2011

Abstract
Article
References
Comments

Medications that are used to treat attention deficit–hyperactivity disorder (ADHD) are prescribed for more than 2.7 million children in the United States each year1 and have been considered to be relatively safe.2-5 However, reports of adverse events from Canada and the United States that have included cases of sudden death, myocardial infarction, and stroke in conjunction with the use of these drugs have raised concern about their safety.6,7 Although case reports from adverse-event reporting systems can be an important source for identifying medication safety signals, they cannot reliably quantify risk. Thus, there is a compelling need to obtain better safety data for these drugs. We used data from four large, geographically and demographically diverse U.S. health plans to conduct a retrospective cohort study of the use of ADHD drugs and the risk of serious cardiovascular events in children and young adults, with review of medical records to validate study end points. The study was conducted in parallel with a study of ADHD drug use and serious cardiovascular events in adults between the ages of 25 and 64 years.

Methods

Data Sources

We obtained study data from computerized health records of four health plans that together annually covered 22.4 million persons during the study period: Tennessee Medicaid, Washington State Medicaid, Kaiser Permanente California (Northern and Southern regions), and OptumInsight Epidemiology (national private insurance health-plan data). We augmented health-plan data with linkage to state death certificates and the National Death Index. Health-plan data included enrollment records, outpatient and inpatient claims, and records of filled prescriptions (including the dispensing date, drug name, dose, quantity, and duration of supply), which have been shown to be good measures of medication use.8-11 The initiation of the study differed according to site on the basis of the earliest availability of the site's computerized data (ranging from 1986 to 2002). Follow-up concluded for all sites at the end of 2005. Each site prepared standardized files from health-plan data and used computer programs from the lead site (Vanderbilt University) to define study variables and create files in which identifiers of patients had been removed. These files were sent to the lead site for analyses.

Study Population

To assemble the cohort, we identified patients who met the following criteria: use of an ADHD drug (methylphenidate, dexmethylphenidate, dextroamphetamines, amphetamine salts, atomoxetine, or pemoline) during the study period; an age of 2 to 24 years on the first day of qualifying use; continuous enrollment with drug benefits for 365 days preceding the first day of qualifying use (allowing for short administrative gaps in enrollment); and the absence of possibly life-threatening serious illness (Section 1 in the Supplementary Appendix, available with the full text of this article at NEJM.org). Because patients with congenital heart disease may be vulnerable to the effects of ADHD medications, such patients were included in the study. Exclusion criteria included a hospital discharge during the preceding 365 days with a primary diagnosis of acute myocardial infarction or stroke. The last day of study follow-up was the last day of the study or the date on which the patient no longer met study criteria. A given patient was allowed to reenter the cohort as long as all the cohort eligibility requirements were met.

For each patient receiving an ADHD medication, we randomly selected up to two nonuser control subjects from health-plan members at the same site who were enrolled on the first day of qualifying use at the age of 2 to 24 years, who met continuous-enrollment requirements, and who did not have a serious illness. Nonusers were matched with users on the basis of calendar year, age, and sex and were allowed to have previous nonqualifying use of ADHD drugs before the first day of qualifying use. Follow-up for nonusers began on the first day of qualifying use for the matched users of ADHD drugs and ended on the nonuser's last day of study follow-up (Section 2 in the Supplementary Appendix). Follow-up time did not include the time during hospitalization and the 30 days after discharge because in-hospital deaths were not considered to be study end points and health-plan files did not include drugs dispensed in the hospital.

Use of Study Drugs

Every person-day during study follow-up was classified according to use of ADHD drugs (Section 2 in the Supplementary Appendix). Current use was defined as use during the period between the prescription start date and the end of the days of supply (including up to a 7-day carryover from previous prescriptions). Former use was defined as use during the period after current use through the end of study follow-up. Nonuse was defined as no prescribed use of ADHD drugs on the day being classified or any preceding days. Former users and nonusers could become current users of ADHD drugs during follow-up, and when this occurred, their user person-time was classified as described above.

Study End Points

The primary study end point was a serious cardiovascular event, which was defined as sudden cardiac death, myocardial infarction, or stroke. Sudden cardiac death was defined as a sudden, pulseless condition or collapse consistent with a ventricular tachyarrhythmia occurring in a community setting and including both fatal and resuscitated cardiac arrest (cases in which an arrest occurred in the community but the patient was successfully resuscitated).12-16 The diagnosis of acute myocardial infarction required hospitalization and met the international diagnostic criteria for myocardial infarction.17-19 Stroke was defined as an acute neurologic deficit of sudden onset that persisted for more than 24 hours, corresponded to a vascular territory, and was not explained by other causes (e.g., trauma, infection, vasculitis, or profound systemic hypotension).17,20,21

Potential end points were identified from claims and vital records and adjudicated through review of all pertinent medical records, including hospitalizations, reports of emergency medical services, autopsies, and death certificates (Section 3 in the Supplementary Appendix). Criteria for potential cases were intentionally broad to increase sensitivity because we anticipated that study end points would be rare and planned to review medical records for all potential cases. All events were adjudicated by two cardiologists (for sudden cardiac death and acute myocardial infarction) or two neurologists (for stroke). These adjudicators reviewed cases from all sites and were unaware of exposure status (Section 4 in the Supplementary Appendix). Disagreements among adjudicators (<5% of cases) were resolved by consensus with the study principal investigator.

Cases were excluded if the documentation suggested a cause other than a cardiovascular cause (e.g., motor-vehicle accident or drug overdose) or for sudden cardiac death, if clinically severe heart disease was present and sudden cardiac death was not unexpected (e.g., end-stage congestive heart failure). Congenital heart defects that had not been diagnosed until autopsy were noted but did not result in the exclusion of the potential case. In cases in which we were unable to obtain pertinent medical records or had insufficient information for adjudication (21% of cases), we determined the case status using a computer case definition, derived from cases with completed adjudication. The positive predictive value of the computerized case definition for serious cardiovascular events was 91% (Section 5 in the Supplementary Appendix).

Study Oversight

The study was approved by the institutional review board at each of the participating institutions and by the Food and Drug Administration (FDA) Research in Human Subjects Committee. In addition, permission was obtained from the data sources for each site. In all cases the need for informed consent was waived. The study was planned by the authors. Data were gathered from each site and analyzed by the study biostatistician, who vouches for the data and the analysis along with the first author.

Statistical Analysis

We calculated the hazard ratio for users of ADHD drugs, as compared with nonusers, using Cox regression models with robust sandwich variance estimators to account for the matched study design and for persons entering the cohort multiple times.22 The hazard ratio was adjusted for both baseline characteristics and changes in characteristics that occurred during follow-up. We calculated the adjusted incidence of end points by multiplying the incidence rate in the nonusers by the hazard ratio.

Because the number of covariates that reflected baseline cohort characteristics was large in comparison to the number of end points, we adjusted for these covariates by including a site-specific propensity score in the regression models. The propensity score was defined as the probability that the patient was currently receiving an ADHD drug on the first day of study follow-up, estimated for each site by means of logistic regression.23 The baseline variables in the propensity score included sociodemographic characteristics as well as information on medical care encounters consistent with psychiatric disorders, asthma and other respiratory illnesses, seizure and other neurologic disorders, unintentional injuries, cardiovascular diseases, and other diseases. For each site, we tested the adequacy of the propensity-score models by calculating the propensity-score adjusted means of baseline variables for users and nonusers of ADHD drugs; these values were similar (Section 6 in the Supplementary Appendix).

In our primary analysis, we adjusted for study site, propensity-score decile, and several time-dependent covariates (medical and psychiatric conditions, health care utilization, age, and calendar year) (Section 7 in the Supplementary Appendix). In order to test key study assumptions, we performed additional analyses that were stratified according to age group (2 to 17 years and 18 to 24 years) and that used alternative exposure groups, cohort inclusion criteria, and end-point exclusions. We performed all statistical analyses using SAS software, version 9.1 (SAS Institute).

Results

Study Population

The study cohort included 1,200,438 children and young adults. The mean age of cohort members at baseline was 11.1 years (mean range at the study sites, 8.7 to 12.0) (Table 1Table 1Study Cohorts, According to Site.). The mean length of follow-up for the cohort was 2.1 years (mean range at the study sites, 1.5 to 3.9) for a total follow-up of 2,579,104 person-years. The characteristics of current users and nonusers at baseline are shown in Table 2Table 2Characteristics of Cohort Members, According to the Use of ADHD Drugs at Baseline.. Generally, current users had more evidence of health care utilization of all types. In addition, they had greater prevalence of psychiatric illnesses and greater use of psychotropic medications. Current users were also more likely to have asthma, seizures, and congenital heart defects. For both current users and nonusers, alcohol and drug use, as determined from records of medical care encounters, were uncommon.

Study End Points

A total of 81 cohort members had a serious cardiovascular event, or 3.1 per 100,000 person-years, including 33 sudden cardiac deaths (1.3 per 100,000 person-years), 9 acute myocardial infarctions (0.3 per 100,000 person-years), and 39 strokes (1.5 per 100,000 person-years). Characteristics of the confirmed cases according to exposure to an ADHD drug are shown in Section 8 in the Supplementary Appendix. In the multivariate model, an older age, current use of an antipsychotic drug, a major psychiatric illness, a serious cardiovascular condition, and chronic illness were associated with an increased risk of serious cardiovascular events (Section 7 in the Supplementary Appendix).

There were 7 confirmed events among 373,667 person-years of follow-up for current users, 25 confirmed events among 607,475 person-years of follow-up for former users, and 49 confirmed events among 1,597,962 person-years of follow-up for nonusers. As compared with the nonusers, the adjusted rate of serious cardiovascular events did not differ significantly among current users of ADHD drugs (hazard ratio, 0.75; 95% confidence interval [CI], 0.31 to 1.85) or among former users (hazard ratio, 1.03; 95% CI, 0.57 to 1.89) (Figure 1Figure 1Adjusted Rates of Serious Cardiovascular Events, According to the Use of ADHD Drugs.). When former users served as the reference group (in which the possible effect of unmeasured confounding was assessed), there was no increased risk of serious cardiovascular events among current users (hazard ratio, 0.70; 95% CI, 0.29 to 1.72) (Section 9 in the Supplementary Appendix). There was also no evidence of increased risk for the individual end points of sudden cardiac death, acute myocardial infarction, or stroke (Table 3Table 3Adjusted Hazard Ratios for Individual Cardiovascular End Points, According to the Use of ADHD Drugs.). We found no evidence of increased risk for methylphenidate (hazard ratio, 0.96; 95% CI, 0.31 to 2.97), the most frequently used ADHD drug (Section 10 in the Supplementary Appendix). Data were too sparse for other individual drugs to fit regression models.

Alternative Analyses

We performed several alternative analyses to test the robustness of study findings (Table 4Table 4Alternative Analyses with Adjusted Hazard Ratios for Serious Cardiovascular Events, According to the Use of ADHD Drugs., and Section 11 in the Supplementary Appendix). To assess for possible bias from the inclusion of persons who used ADHD drugs before the beginning of follow-up,10 we restricted current users of ADHD drugs only to new users (which was defined as no use of ADHD drugs during the 365 days preceding the first day of qualifying use). Findings were essentially identical to those of the primary analysis (hazard ratio, 0.73; 95% CI, 0.24 to 2.10). When we included seven patients who had been excluded from the primary analysis because they had evidence of severe underlying cardiac disease for which sudden cardiac death would not be unexpected, we found no increased risk for current users (hazard ratio, 0.71; 95% CI, 0.29 to 1.72). In analyses that included only children 2 to 17 years of age, we found no association between the use of ADHD drugs and serious cardiovascular events (hazard ratio, 0.98; 95% CI, 0.41 to 2.36). When children with evidence of serious psychiatric disease were excluded, we also found no significant association (hazard ratio, 0.66; 95% CI, 0.20 to 2.16).

We also performed analyses to test other key study assumptions. A site-specific analysis suggested a potential difference between Medicaid and non-Medicaid sites, although numbers were very small and we saw no evidence of significant heterogeneity in pooled analyses of rate differences between users and nonusers (Section 12 in the Supplementary Appendix). Another analysis expanded the definition of current use to include the 89 days after the end of current use to account for a possible misclassification in exposure related to the clinical use of ADHD drugs or for drugs that were discontinued after prodromal symptoms of an end point (e.g., headache preceding stroke). Finally, we performed an analysis in which time-dependent variables were fixed at baseline. The findings of these analyses were essentially identical to those reported here.

Discussion

Several regulatory and policy decisions resulted from the review of adverse-event reports of serious cardiovascular events associated with the use of ADHD drugs in Canada and the United States. In Canada, Health Canada removed and then reinstated marketing of extended-release mixed amphetamine salts.6,7 In the United States, three different FDA advisory committees considered the issue and recommended a black-box warning for stimulants, as well as a medication guide for patients.24 In a controversial policy statement, the American Heart Association stated that obtaining electrocardiograms in children who were initiating ADHD stimulant therapy was "reasonable,"25 a recommendation that was subsequently revised on the basis of input from several pediatric organizations.24 This led to concern and confusion among health care providers, patients, and families about the risks of these drugs.26 In this context, we studied the cardiovascular safety of ADHD drugs in more than 1.2 million children and young adults from four geographically diverse health plans with more than 2.5 million person-years of follow-up. The point estimate of the relative risk provided no evidence that the use of ADHD drugs increased the risk of serious cardiovascular events, although the upper limit of the 95% confidence interval was consistent with up to a doubling in the risk.

In the study population, which excluded children with possibly life-threatening illness, the incidence of serious cardiovascular events was 3.1 per 100,000 person-years, a finding that was consistent with other studies.27-30 The low number of events limited the statistical power of the study, particularly for individual end points and individual drugs, as well as for subgroups that might be particularly vulnerable to the effects of ADHD drugs. We also had limited information for longer durations of use.

Could the study findings be the result of confounding? The comparison between current users and nonusers at baseline indicated a greater incidence of medical and psychiatric coexisting conditions among current users. The analyses were adjusted for an extensive set of cardiovascular disease variables, which were included in site-specific propensity scores. Using this method, we could account for many important risk factors for cardiovascular disease. However, differences in factors that we were unable to measure, such as adherence to a drug regimen, differential prescribing of ADHD drugs to children at lower risk for a study outcome, or illicit use of medications resulting in misclassification, may have affected the results.31,32

We performed several alternative analyses to test the robustness of our findings. We used former users as the reference group, which could address many of the issues related to comparability between current users and nonusers. We performed an analysis restricted to new users to address bias that would be introduced from the inclusion of prevalent users in the cohort.10 Another analysis included patients who had been excluded from the primary analysis because of preexisting severe cardiac disease for which sudden cardiac death would not be unexpected. We also performed analyses stratified according to age. The findings from these additional analyses were essentially identical to our primary analysis.

Our findings that the use of ADHD drugs was not associated with an increased risk of serious cardiovascular events in children and young adults are consistent with the results of several reports33-36 that have appeared since the FDA safety review of adverse-event data for ADHD drugs,6,7 although our results differed from the findings of another report.37 Our study included nearly twice the person-time of the combined person-time in four recent cohort studies and included several provisions to ensure accurate case ascertainment, including a review of medical records and autopsies.

In conclusion, in our study involving children and young adults with 2.5 million person-years of follow-up, there were 3.1 serious cardiovascular events per 100,000 person-years. Although the point estimates of the relative risks for ADHD drugs did not indicate increased risk, the upper limit of the 95% confidence interval suggested that a doubling in the risk could not be ruled out. However, the absolute magnitude of any increased risk would be low.

Supported by contracts (HHSA290-2005-0042, to Vanderbilt University; and HHSA290-2005-0033, to Harvard Pilgrim Health Care Institute) from the Agency for Healthcare Research and Quality, Department of Health and Human Services, as part of the Developing Evidence to Inform Decisions about Effectiveness program; and by contracts (223-2005-10100C, to Vanderbilt University; 223-2005-10012, to Kaiser Permanente Northern California; 223-2005-10006C, to OptumInsight Epidemiology; and 223-2005-10012C, to Harvard Pilgrim Health Care Institute) from the FDA.

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.

This article (10.1056/NEJMoa1110212) was published on November 1, 2011, at NEJM.org.

We thank the TennCare Bureau, Tennessee Department of Health, Washington State Health and Recovery Services Administration, Kaiser Permanente California (Northern and Southern regions), and OptumInsight Epidemiology for providing data needed to conduct the study; Patricia A. Gideon, Michelle DeRanieri, Leanne Balmer, Shannon D. Stratton, James R. Daugherty, Judith A. Dudley, Lynne Caples, Tracy Crowley, Ning Chen, and Eli Poe of Vanderbilt University School of Medicine; Sherry Quinn, Eva Ng, and Clorinda Hoffman of OptumInsight Epidemiology; Connie Uratsu and Ninah Achacoso of Kaiser Permanente Northern California; Chantal Avila and Yan Luo of Kaiser Permanente Southern California; and Li Zheng of the University of Washington.

Source Information

From the Divisions of General Pediatrics (W.O.C.), Adolescent Medicine (S.T.C.), and Pediatric Cardiology (F.A.F.), Department of Pediatrics; the Department of Biostatistics (P.G.A.); the Division of Pharmacoepidemiology, Department of Preventive Medicine (W.O.C., W.A.R.); the Divisions of Cardiology (K.T.M.), Rheumatology (C.M. Stein), and Clinical Pharmacology (K.T.M., C.M. Stein), Department of Medicine; and the Stroke Division, Department of Neurology (H.S.K., A.O.) — all at Vanderbilt University, Nashville; the Division of Research, Kaiser Permanente Northern California, Oakland (L.A.H., B.H.F.); the Department of Population Medicine, Harvard Pilgrim Health Care, Harvard Medical School, and the Department of Pediatrics, Boston University School of Medicine — all in Boston (C.M. Sox); OptumInsight Epidemiology, Waltham, MA (K.A.C.); Pharmacy Analytical Service (T.C.C.) and the Research and Evaluation Department (V.P.Q.), Kaiser Permanente Southern California, Pasadena; and the School of Public Health, University of Washington, Seattle (F.A.C.).

Address reprint requests to Dr. Cooper at Suite 313, Oxford House, 1313 21st Ave. S., Nashville, TN 37232-4313, or at .

soya y patas de gallo

Un suplemento de soja reduciría las patas de gallo


Un suplemento experimental derivado de la soja ayudaría a las mujeres posmenopáusicas a reducir un poco las "patas de gallo".

cerebro lucido y sueno

El cerebro de un soñador lúcido se activa igual durmiendo que estando despierto


Los soñadores lúcidos mientras duermen, son conscientes de que están soñando y pueden controlar sus acciones. Foto: Tim Snell
Un estudio realizado con soñadores conscientes, que pueden controlar sus propios sueños, muestra que las zonas del cerebro relacionadas con planear y ordenar acciones se activan igual mientras duermen que durante la vigilia. Los autores creen que en el futuro, la habilidad de estas personas, combinada con la neuroimagen y los patrones de la actividad cerebral, permitirá predecir el contenido de los sueños.

SINC | 28.10.2011 10:55 Más adelante se podrían estudiar experiencias en sueños que difícilmente evaluables durante la vigilia, como volar

Hay personas que, mientras duermen, son conscientes de que están soñando y pueden controlar sus acciones. Este estado tan complejo se conoce como 'sueño lúcido' o 'consciente'. Las personas con esta habilidad, que se puede aprender y entrenar, incluso tienen acceso a su memoria mientras se desarrolla el sueño.

Las últimas investigaciones del Instituto Max Planck de Psiquiatría en Múnich (Alemania) han revelado la primera prueba, gracias a estos 'soñadores', de que "se puede acceder al contenido del sueño utilizando técnicas de neuroimagen y que las áreas del cerebro se activan igual en los sueños que cuando se ejecutan esas tareas reales durante la vigilia", explica a SINC Michael Czisch, investigador del Instituto Max Planck y coautor del trabajo, que se publicará en noviembre en la revista Current Biology.

"Soñar no es simplemente ver la película de un sueño", declara Martin Dresler, del Instituto Max Planck y autor principal del estudio. "Las regiones del cerebro que están relacionadas con los movimientos del cuerpo se activan al soñar", añade el experto.

Este descubrimiento puede suponer una oportunidad para estudiar las reacciones neuronales que provocan los sueños y "para investigar cómo cambia la actividad cerebral en el momento que alguien se convierte en un soñador lúcido", afirma Dresler.

Cobayas ideales para la ciencia del sueño

Más adelante "se podrían estudiar experiencias en sueños que son difícilmente evaluables durante la vigilia, como por ejemplo, volar", opina Czisch, quien también cree será posible conocer más sobre las diferencias entre la conciencia durante el sueño normal y el sueño lúcido.

"El principal obstáculo hasta ahora al estudiar los contenidos de un sueño era que la actividad espontánea en el sueño no se puede controlar experimentalmente porque las personas, por lo general, no pueden realizar acciones mentales predefinidas mientras duermen", reconoce Czisch. En cambio, "utilizando la habilidad de quienes tienen sueños lúcidos se pueden superar estos obstáculos", añade el investigador.

Los responsables del trabajo opinan que utilizando esta cualidad, combinada con la neuroimagen y analizando patrones de la actividad cerebral, en el futuro podría ser posible predecir el contenido de los sueños.

"Para realizar las pruebas, nos centramos en un contenido del sueño muy simple como es el movimiento de las manos", explica Czisch. Utilizando las señales de los ojos como marcadores, durante los experimentos se midió la actividad neuronal mediante resonancia magnética funcional (fMRI, por sus siglas en inglés) y Espectroscopía de Infrarrojo Cercano (NIR).

Toda la información obtenida se relacionó con los movimientos de la mano durante el sueño lúcido. Los participantes debían mover la mano dentro de su sueño y avisar a los investigadores cuando esto ocurría reproduciendo esos movimientos con los ojos a modo de señal.

Los datos del estudio se obtuvieron escaneando los cerebros de seis hombres de 21 a 38 años, tres o cuatro horas durante la segunda mitad de la noche cuando la incidencia del sueño es más alta. Estos sujetos fueron previamente entrenados durante varios años hasta que consiguieron tener sueños lúcidos.


Referencia Bibliográfica

Martin Dresler, Stefan P. Koch, Renate Wehrle, Victor I. Spoormaker, Florian Holsboer, Axel Steiger, Philipp G. Sämann, Hellmuth Obrig, Michael Czisch; "Dreamed Movement Elicits Activation in the Sensorimotor Cortex", Current Biology, 21, (1-5) November 8, 2011, DOI:10.1016/j.cub.2011.09.029
Localización: Europa

sábado, 15 de octubre de 2011

Pueraria 2

Pueraria mirifica

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Kwao Krua
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Clasificación científica
Reino: Plantae
Subreino: Tracheobionta
División: Magnoliophyta
Clase: Magnoliopsida
Subclase: Rosidae
Orden: Fabales
Familia: Fabaceae
Subfamilia: Faboideae
Tribu: Phaseoleae
Subtribu: Glycininae
Género: Pueraria
Especie: P. mirifica
Nombre binomial
Pueraria mirifica
Airy Shaw & Suvatab.
Sinonimia
  • Pueraria candollei var. mirifica
  • [1]

Pueraria mirifica (Kwao Krua, o Butea Superba) es una especie botánica de Tailandia y Birmania.

Sus tubérculos contienen fitoestrógenos como miroestrol, deoximiroestrol, coumestanes, y se usa para mejora de mamas, en cremas como MiroHealth, Mirifem, St. Herb, Maxi Breast.

La variedad farmaceuticamente usada es Kwao Krua blanca; las otras son Kwao Krua roja y la negra.

Los miroestrol u deoximiroestrol son descubiertos solo en Pueraria mirifica. Son mucho más fuertes que las isoflavonas de soja o de trébol rojo

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