<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_437"
                     title="Autism Risk Linked to Maternal Age (CME/CE)"
                     score="0.014"
                     href="http://www.medpagetoday.com/Pediatrics/Autism/tb/18341?impressionId=1265721085100"
                     
      Older women are more likely to give birth to a child who develops autism than younger women, but the father&apos;s age is a factor only when moms are younger, a large case-control study showed.&lt;br&gt;
&lt;br&gt;In an analysis of nearly five million births and more than 12,000 autism cases, every five-year increase in maternal age at delivery was associated with an 18% greater risk of the child later being diagnosed with autism, according to Janie Shelton, MPH, a doctoral student at the University of California Davis, and colleagues.&lt;br&gt;
&lt;br&gt;Mothers who gave birth when they were 40 or older had a 51% increased risk of having a child with autism compared with those who were 25 to 29, the largest age group (OR 1.51, 95% CI 1.35 to 1.70), the researchers reported in the February issue of &lt;em&gt;Autism Research&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;The effect of the biological father&apos;s age appeared to depend on the mother&apos;s. When the mothers were 30 and older, paternal age did not significantly increase the risk of having a child develop autism. In mothers younger than 30, paternal age did contribute to the autism risk.&lt;p&gt;&lt;/p&gt;
&lt;p&gt;&quot;This study builds upon earlier work that has demonstrated associations between parental age and autism risk,&quot; commented Bryan King, MD, program director of the Seattle Children&apos;s Autism Center, in an e-mail.&lt;/p&gt;
&lt;p&gt;But previous studies have yielded mixed results on the relative contributions of the mothers&apos; and fathers&apos; ages.&lt;/p&gt;
&lt;p&gt;&quot;I think the size of the sample used in the present study (close to five million births) has resulted in a clear signal that both maternal and paternal age are involved,&quot; said King, who was not involved in the study.&lt;/p&gt;
&lt;p&gt;He noted, however, that parental age &quot;does not account for the big increase in autism prevalence, although it may be contributing somewhat.&quot;&lt;/p&gt;
&lt;p&gt;Shelton and her colleagues calculated that the rising average maternal age during their study  --  covering 1990 to 1999  --  contributed to a 4.6% increase in autism incidence. That compares with about a six-fold increase in autism rates in that decade, Shelton said in an interview.&lt;/p&gt;
&lt;p&gt;&quot;I worry a little bit that in the media attention on this issue that mothers who had children at ages 37, 38, 39 might think that, &apos;Okay, well that&apos;s why my child had autism,&apos;&quot; she said. &quot;And so, I think it&apos;s important to stress that the increased number of cases that we&apos;ve observed can&apos;t be attributable towards women having children later.&quot;&lt;/p&gt;
&lt;p&gt;The researchers looked at data from 4,935,776 singleton births in California in the 1990&apos;s using records from the state Department of Development Services. Records identified 12,159 cases of &quot;Full Syndrome Autism&quot; diagnosed before age 6.&lt;/p&gt;
&lt;p&gt;That diagnosis may include autistic disorder, as well as Asperger&apos;s disorder and pervasive developmental disorder not otherwise specified. However, the breakdown of specific diagnoses could not be determined from this data set, Shelton said.&lt;/p&gt;
&lt;p&gt;Even after controlling for parental education, the year of the child&apos;s birth, the race/ethnicity of the parents, the mother&apos;s parity, and insurance payment type, older maternal age was associated with an increased risk of autism in the child.&lt;/p&gt;
&lt;p&gt;Nancy Minshew, MD, director of the Center of Excellence in Autism Research at the University of Pittsburgh, said in an e-mail that the results were not surprising because genetic errors are more common with older parents.&lt;/p&gt;
&lt;p&gt;King said genetics were one possible mechanism underlying the relationship.&lt;/p&gt;
&lt;p&gt;&quot;The mechanisms by which risk goes up might include a greater likelihood of chromosomal changes, a greater likelihood of problems at birth like prematurity, and many other factors,&quot; he said. &quot;The possibility of environmental exposures would also be expected to increase with age, and so this finding does not necessarily help narrow our focus on causes.&quot;&lt;/p&gt;
&lt;p&gt;Sheldon and her colleagues wrote, &quot;It is plausible that multiple exposure types may increase the risk of autism through a common pathway or pathways (i.e., mitochondrial function, thyroid function, epigenetics, hormonal alterations) and be represented as a generalized increased risk with age.&quot;&lt;/p&gt;
&lt;p&gt;&quot;In this case,&quot; they continued, &quot;maternal or paternal age would serve as an index of lifetime exposure status and be a proxy for the true underlying etiologic agent.&quot;&lt;/p&gt;
&lt;p&gt;Shelton said further research is needed to determine why biological age is serving as a risk factor for autism.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by grants from the National Institute of Environmental Health Sciences and the Environmental Protection Agency and by the University of California Davis School of Medicine and Office of Graduate Studies.&lt;/p&gt;&lt;p&gt;The researchers did not report any conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;&lt;p&gt;&lt;em&gt;This article was developed in collaboration with ABC News. &lt;/em&gt;&lt;img src=&quot;http://www.medpagetoday.com/upload/2009/10/1/14357_1.jpg&quot; mce_src=&quot;http://www.medpagetoday.com/upload/2009/10/1/14357_1.jpg&quot; alt=&quot;&quot;&gt;&lt;/p&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_368"
                     title="Lancet Retracts 1998 MMR-Autism Paper"
                     score="0.011"
                     href="http://www.medpagetoday.com/Pediatrics/Vaccines/tb/18255?impressionId=1265721085100"
                     
      &lt;p&gt;Editors of &lt;em&gt;The Lancet&lt;/em&gt; have retracted the 1998 study that first suggested autism might be caused by the MMR vaccine, less than a week after an official rebuke to the paper&apos;s lead author, Andrew Wakefield, MBBS, and two co-authors.&lt;/p&gt;
&lt;p&gt;In a brief note posted on the journal&apos;s Web site, &lt;em&gt;Lancet&lt;/em&gt; editors wrote, &quot;It has become clear that several elements of the 1998 paper by Wakefield et al. are incorrect, contrary to the findings of an earlier investigation.... Therefore, we fully retract this paper from the published record.&quot;&lt;/p&gt;
&lt;p&gt;Evidence presented in a Jan. 28 hearing before the U.K. General Medical Council&apos;s Fitness to Practise Panel persuaded the journal that the paper had misrepresented how the study was conducted.&lt;/p&gt;
&lt;p&gt;&lt;span class=&quot;msgBody&quot;&gt;The council, which has no direct American equivalent, is an independent, nationwide regulatory body that registers doctors and enforces standards of medical practice in the U.K.&lt;/span&gt;&lt;/p&gt;
&lt;p&gt;Hospital records and other sources contradicted findings of a 2004 investigation by Wakefield&apos;s institution, the Royal Free and University College, that the study had been properly vetted by an institutional review board.&lt;/p&gt;
&lt;p&gt;&quot;The claims in the original paper that children were &apos;consecutively referred&apos; and that investigations were &apos;approved&apos; by the local ethics committee have been proven to be false,&quot; according to the &lt;em&gt;Lancet&lt;/em&gt; editors.&lt;/p&gt;
&lt;p&gt;The editor of Britain&apos;s other leading medical journal, &lt;em&gt;BMJ&lt;/em&gt;, congratulated &lt;em&gt;The Lancet&lt;/em&gt; for its action.&lt;/p&gt;
&lt;p&gt;&quot;This will help to restore faith in this globally important vaccine and in the integrity of the scientific literature,&quot; according to a statement from Fiona Godlee, MB, BChir, BSc.&lt;/p&gt;
&lt;p&gt;In the 1998 paper, Wakefield and colleagues reported on findings in 12 children who, they said, had developed intestinal inflammation and autistic symptoms following MMR vaccination. They suggested that the inflammation released gut proteins into the circulation that eventually migrated to the brain, causing permanent damage reflected in autism symptoms.&lt;/p&gt;
&lt;p&gt;The report and the ensuing mass-media publicity sparked consternation among parents and the medical community. Vaccination rates in Britain and the U.S. dropped sharply, and measles rates spiked in consequence.&lt;/p&gt;
&lt;p&gt;Although subsequent population-based research and other studies have failed to confirm a causal link between MMR vaccines and autism, a vocal group of parents of autistic children continues to insist that it is real. They call Wakefield a hero.&lt;/p&gt;
&lt;p&gt;However, a nearly decade-long investigation by a British journalist, Brian Deer, uncovered discrepancies between the &lt;em&gt;Lancet&lt;/em&gt; paper and hospital records and other sources. (See &lt;a href=&quot;http://www.medpagetoday.com/Pediatrics/Autism/12850&quot; mce_href=&quot;http://www.medpagetoday.com/Pediatrics/Autism/12850&quot; target=&quot;_blank&quot;&gt;Father of Vaccine-Autism Link Said to Have Fudged Data&lt;/a&gt;)&lt;/p&gt;
&lt;p&gt;Whereas the &lt;em&gt;Lancet&lt;/em&gt; paper indicated that, in most cases, symptoms developed within days of vaccination, the records indicated that this was true only for one child, according to Deer&apos;s account in the &lt;em&gt;Times of London&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The patients&apos; records also indicated that five of the children had psychosocial problems before vaccination, said the &lt;em&gt;Times&lt;/em&gt;, but the &lt;em&gt;Lancet&lt;/em&gt; paper described them as &quot;developmentally normal.&quot;&lt;/p&gt;
&lt;p&gt;In addition, the &lt;em&gt;Lancet&lt;/em&gt; paper described abnormal intestinal pathology results in the children, but the hospital pathology reports showed no findings of inflammation, the &lt;em&gt;Times&lt;/em&gt; report said.&lt;/p&gt;
&lt;p&gt;At last week&apos;s hearing, the U.K.&apos;s General Medical Council panel heard evidence that Wakefield had taken blood samples from children attending his son&apos;s birthday party and performed spinal taps on other children in a hospital without due regard for their safety.&lt;/p&gt;
&lt;p&gt;The panel found Wakefield guilty of more than 30 charges that he had acted unethically in conducting the study. He could be stripped of his license to practice in Britain, but no ruling has been made yet.&lt;/p&gt;
&lt;p&gt;Two of Wakefield&apos;s 12 co-authors on the 1998 paper, John Walker-Smith, MD, and Simon Murch, PhD, were also found to have committed ethical violations. The other 10 co-authors had previously repudiated the paper&apos;s findings and were not charged.&lt;/p&gt;
&lt;p&gt;Wakefield was in London while the hearing took place but did not attend. Afterward, he told reporters he was innocent of wrongdoing and would continue his research.&lt;/p&gt;
&lt;p&gt;Wakefield is now based at Thoughtful House, a private autism research and treatment facility in Austin, Texas. After the panel&apos;s ruling, it issued a statement expressing disappointment and calling the charges &quot;unfounded and unfair.&quot;&lt;/p&gt;

    </recommendedItem>
    <recommendedItem id="20100101_19_395"
                     title="Evidence-Based Care Cuts ADHD Symptoms, Not Impairment (CME/CE)"
                     score="0.01"
                     href="http://www.medpagetoday.com/Pediatrics/ADHD-ADD/tb/18292?impressionId=1265721085100"
                     
      Adhering to guidelines when treating children with attention deficit hyperactivity disorder (ADHD) relieved symptoms but had no effect on kids&apos; performance in school or in their relationships with others, researchers found.&lt;br&gt;
&lt;br&gt;Although parents and teachers noted significant improvements in symptoms among ADHD kids (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) in a special treatment program, there weren&apos;t similar outcomes for functional impairment, Jeffery N. Epstein, PhD, of the Center for ADHD at Cincinnati Children&apos;s Hospital in Ohio, reported in the February &lt;em&gt;Archives of Pediatrics and Adolescent Medicine&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;&quot;This finding highlights the need for physicians to work with or refer patients to educational and mental healthcare specialists who can work with children to develop skills to address targeted areas of deficit,&quot; the researchers wrote.&lt;/p&gt;
&lt;p&gt;University-associated trials have shown stimulants are effective against ADHD, but these findings may not be translated into community practices  --  a potential public health concern, the researchers suggested.&lt;/p&gt;
&lt;p&gt;Guidelines for proper treatment exist, but they can be difficult to put into practice because of time, effort, and reimbursement concerns.&lt;/p&gt;
&lt;p&gt;So the researchers decided to test the efficacy of a quality improvement intervention called ADHD Collaborative, designed to enhance physician adherence to evidence-based, ADHD treatment guidelines.&lt;/p&gt;
&lt;p&gt;They conducted a case series involving 785 children ages 7 to 11, who were treated by 158 physicians at rural, suburban, and urban practices.&lt;/p&gt;
&lt;p&gt;The researchers found that, based on teacher and parent ratings, children showed vast improvements in ADHD symptoms (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;&quot;Improvement of ADHD symptoms occurred mainly in the first three months of treatment and remained improved and relatively stable thereafter,&quot; the researchers wrote. &quot;These results suggest that community-based physicians can achieve gains in ADHD symptom improvement comparable with carefully controlled, university-based clinical trials.&quot;&lt;/p&gt;
&lt;p&gt;However, there were no significant improvements in functional impairment as measured by parents and teachers.&lt;/p&gt;
&lt;p&gt;The proportion of functionally impaired children didn&apos;t change after treatment for any outcomes except teachers&apos; ratings of writing and assignment completion (&lt;em&gt;P&lt;/em&gt;=0.03 and &lt;em&gt;P&lt;/em&gt;=0.04, respectively).&lt;/p&gt;
&lt;p&gt;&quot;Effective treatment likely requires a multimodal strategy that includes a focus on teaching children [organizational and learning] skills,&quot; they wrote, adding that collaboration with other mental health or educational services &quot;appears to be warranted.&quot;&lt;/p&gt;
&lt;p&gt;Researchers said the study was limited because it didn&apos;t have a control group. Thus, it couldn&apos;t determine whether a similar pattern of treatment response would have been observed without physician training.&lt;/p&gt;
&lt;p&gt;The lack of a control group also made it impossible to account for any potential placebo effects.&lt;/p&gt;
&lt;p&gt;Finally, the authors didn&apos;t collect data on medication adherence.&lt;/p&gt;
&lt;p&gt;Still, they concluded that &quot;large improvements in symptoms can be achieved in primary care settings when physicians provide evidence-based ADHD care using medication.&quot;&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by the Cincinnati Children&apos;s Hospital Medical Center Patient Innovation Fund.&lt;/p&gt;&lt;p&gt;The researchers reported no conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_372"
                     title="Low Serotonin Eyed as Mechanism for SIDS (CME/CE)"
                     score="0.009"
                     href="http://www.medpagetoday.com/Neurology/GeneralNeurology/tb/18262?impressionId=1265721085100"
                     
      Low brainstem levels of serotonin and the enzyme that makes it could underlie sudden infant death syndrome (SIDS), researchers suggested.&lt;br&gt;
&lt;br&gt;In an autopsy study, SIDS cases showed 26% lower serotonin levels in two major components of the medulla&apos;s serotonin system  --  the raph&amp;#233; obscurus (&lt;em&gt;P&lt;/em&gt;=0.05) and paragigantocellularis lateralis (&lt;em&gt;P&lt;/em&gt;=0.04)  --  compared with age-adjusted controls who died from known causes.&lt;br&gt;
&lt;br&gt;These brainstem circuits control breathing, blood pressure, and heart rate during sleep, Hannah C. Kinney, MD, of Children&apos;s Hospital Boston, and colleagues reported in the Feb. 3 issue of the &lt;em&gt;Journal of the American Medical Association&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;A baby with an abnormality in control of these systems might not be able to respond to a life-threatening challenge like asphyxia by rousing from sleep or turning its head the researchers explained.&lt;p&gt;&lt;/p&gt;
&lt;p&gt;SIDS occurs in the &quot;critical first year of life, when homeostatic systems are still maturing,&quot; they noted.&lt;/p&gt;
&lt;p&gt;Mary McClain, RN, MS, of Boston University Medical Center, who counsels families that have lost a baby to SIDS, commented that these findings help establish the biological basis for urging parents to place their babies on their backs to sleep.&lt;/p&gt;
&lt;p&gt;The researchers obtained tissue samples from autopsies of 41 children who died from SIDS, seven who died acutely from known causes (including a car accident, drowning, pneumonia, and unsuspected congenital heart disease), and five who died in the hospital with chronic conditions causing hypoxia-ischemia.&lt;/p&gt;
&lt;p&gt;SIDS cases had mean serotonin levels of 31.4 pmol/mg of protein in the paragigantocellularis lateralis, compared with 40.0 pmol/mg among the controls who died acutely (&lt;em&gt;P&lt;/em&gt;=0.04).&lt;/p&gt;
&lt;p&gt;Levels averaged 55.4 versus 75.5 pmol/mg of protein, respectively, in the raph&amp;#233; obscurus (&lt;em&gt;P&lt;/em&gt;=0.05).&lt;/p&gt;
&lt;p&gt;These abnormalities in the medulla did not appear to involve the catecholamine system. Catecholamine levels were similar between SIDS cases and controls.&lt;/p&gt;
&lt;p&gt;Nor was there evidence for excessive degradation of dopamine or neurotransmitter turnover in SIDS cases, supporting the idea that the key abnormality is reduced synthesis of serotonin, the researchers said.&lt;/p&gt;
&lt;p&gt;Another marker of serotonin function  --  tryptophan hydroxylase (TPH2), the key enzyme involved in synthesis of serotonin  --  also supported this conclusion, with 22% lower levels in the raph&amp;#233; obscurus in SIDS than in controls (&lt;em&gt;P&lt;/em&gt;=0.03).&lt;/p&gt;
&lt;p&gt;Serotonin receptor binding was 29% to 55% lower in three medullary nuclei that receive serotonin projections, notable for a decrease in binding with older age in SIDS cases, but not controls, the researchers noted.&lt;/p&gt;
&lt;p&gt;Given similar findings in three previous investigations, this &quot;may reflect a progressive decrease with age in those infants with the &apos;SIDS abnormality,&apos;&quot; they wrote. Or it&apos;s possible that those with a &quot;stronger abnormality take longer to outgrow the risk period for SIDS and continue to die at older ages,&quot; Kinney&apos;s group wrote.&lt;/p&gt;
&lt;p&gt;Likewise, serotonin receptor binding in infants who died from SIDS was significantly lower in those without known risk factors for SIDS, such as &lt;a href=&quot;http://www.medpagetoday.com/Pediatrics/GeneralPediatrics/17365&quot; mce_href=&quot;http://www.medpagetoday.com/Pediatrics/GeneralPediatrics/17365&quot; target=&quot;_blank&quot;&gt;sleeping face down&lt;/a&gt;, &quot;suggesting that additional risk factors are necessary to precipitate death when the medullary serotonin system is less compromised,&quot; they added.&lt;/p&gt;
&lt;p&gt;Although repetitive apnea and agonal &lt;a href=&quot;http://www.medpagetoday.com/Pulmonology/SleepDisorders/2817&quot; mce_href=&quot;http://www.medpagetoday.com/Pulmonology/SleepDisorders/2817&quot; target=&quot;_blank&quot;&gt;impaired gasping&lt;/a&gt; before death have been reported in some SIDS cases, chronic impaired oxygenation in the hospitalized children in the study produced a very different serotonin pattern than that seen in SIDS.&lt;/p&gt;
&lt;p&gt;Children who died with chronic hypoxia conditions had 55% higher serotonin levels in the raph&amp;#233; obscurus (&lt;em&gt;P&lt;/em&gt;=0.02) and 126% higher levels in the paragigantocellularis lateralis (&lt;em&gt;P&lt;/em&gt;=0.002) than the SIDS cases.&lt;/p&gt;
&lt;p&gt;They also had 640% higher dopamine levels in the raph&amp;#233; obscurus than the SIDS cases (&lt;em&gt;P&lt;/em&gt;=0.006).&lt;/p&gt;
&lt;p&gt;This suggested &quot;that the primary mechanisms underlying serotonin abnormalities in SIDS are not mediated by chronic hypoxia-ischemia,&quot; Kinney&apos;s group wrote.&lt;/p&gt;
&lt;p&gt;The researchers cautioned that their neurotransmitter measurements may have been off somewhat due to prolonged postmortem intervals.&lt;/p&gt;
&lt;p&gt;They also warned that the study was limited by inability to perform these measurements at the synapse in postmortem tissues and by the small sample of controls.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by the First Candle/SIDS Alliance, CJ Martin Overseas Fellowship (National Health and Medical Research Council of Australia), CJ Murphy Foundation for Solving the Puzzle of SIDS, CJ Foundation for SIDS, National Institute of Child Health and Development, and the Developmental Disabilities Research Center at Children&apos;s Hospital Boston.&lt;/p&gt;&lt;p&gt;The researchers reported no conflicts of interest.&lt;/p&gt;&lt;p&gt;McClain provided no information on conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_346"
                     title="Daytime Sleepiness More Common in Young (CME/CE)"
                     score="0.008"
                     href="http://www.medpagetoday.com/PrimaryCare/SleepDisorders/tb/18221?impressionId=1265721085100"
                     
      &lt;p&gt;Compared with 20-somethings and seniors, middle-age adults are less likely to suffer daytime sleepiness when they don&apos;t get a good night&apos;s sleep, according to a small study.&lt;/p&gt;
&lt;p&gt;When three groups of healthy adults  --  young (20 to 30 years old), middle-age (40 to 55) and older (66 to 83)  --  were studied over four nights, slow wave sleep decreased and the number of nocturnal awakenings progressively increased with age, wrote Derk-Jan Dijk, PhD, of the Surrey Sleep Center at the University of Surrey in Guildford, England, and colleagues in the Feb. 1 issue of &lt;em&gt;Sleep.&lt;/em&gt;&lt;/p&gt;

&lt;p&gt;As the likelihood for eight hours of uninterrupted deep sleep decreased with age, there was no increase in the likelihood of daytime sleepiness, which led Dijk and colleagues to conclude that as people age there may be a change in the &quot;sleep (duration and depth) required to maintain alertness.&quot;&lt;/p&gt;
&lt;p&gt;Based on that observation, the authors wrote that it could be argued that &quot;an eight-hour episode rich in [slow wave sleep] is insufficient for young adults but that an eight-hour sleep episode with less [slow wave sleep] is sufficient for older adults.&quot;&lt;/p&gt;
&lt;p&gt;As a result, middle-age and older adults are less likely to build up &quot;sleep debt&quot; during the daylight hours, so they manage with less time in deep sleep at night, less homeostatic sleep pressure.&lt;/p&gt;
&lt;p&gt;The authors hypothesized that this apparent need for less sleep may be a factor in age-related insomnia.&lt;/p&gt;
&lt;p&gt;If older adults are unaware of the need for less sleep, &quot;their self-selected time in bed, which provides an input to the sleep homeostat, may become maladaptive and lead to reduced sleep consolidation and associated complaints.&quot;&lt;/p&gt;
&lt;p&gt;Dijk and colleagues recruited 44 young adults, 35 middle-age adults, and 31 older adults for their study. All were healthy at baseline and all were initially assessed for an eight-hour nocturnal sleep episode.&lt;/p&gt;
&lt;p&gt;They were then randomized to two nights of either selective short wave sleep interruption by acoustic stimuli or sleep without disruption, followed by one night of recovery sleep.&lt;/p&gt;
&lt;p&gt;Two standardized measurement tools, the Multiple Sleep Latency Test (MSLT) and the Karolinska Sleepiness Scale (KSS), were used to assess objective and subjective sleep propensity.&lt;/p&gt;
&lt;p&gt;&quot;Total sleep time per eight hour time in bed decreased significantly and progressively across the age groups such that older adults slept approximately 20 minutes less than middle-aged, who slept 23 minutes less than young adults,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;The reduction in total sleep time &quot;was primarily related to an increase in the number of awakenings and the duration of wakefulness after sleep onset, rather than an increase in latency to sleep onset.&quot;&lt;/p&gt;
&lt;p&gt;As a result, sleep efficiency decreased significantly from 92.1% for the youngest group, to 82% for the older group (effect of age, &lt;em&gt;P&amp;lt;&lt;/em&gt;0.0001).&lt;/p&gt;
&lt;p&gt;The subjective sleep propensity tests revealed that &quot;young people were significantly sleepier than the middle-age people, who were the least sleepy of the three groups.&quot; Daytime sleepiness for the oldest group &quot;fell in between the other two groups [and] was not significantly different from either.&quot;&lt;/p&gt;
&lt;p&gt;All three groups, regardless of age, demonstrated increased daytime sleepiness following a night of experimental disruption of slow wave sleep, but when the participants had an uninterrupted eight hours of deep sleep, it was only the youngest group that was drowsy during the daytime hours.&lt;/p&gt;
&lt;p&gt;The authors noted that although there was less daytime sleepiness among middle-age and older adults in this study, sleep propensity was not measured during the evening hours, so it was possible that the age-related difference might diminish at twilight.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was sponsored by H. Lundbeck A/S.&lt;/p&gt;&lt;p&gt;Dijk reported receiving research support from the Air Force Office of Scientific Research, the Biotechnology and Biological Sciences Research Council, GlaxoSmithKline, H. Lundbeck A/S, Merck, Pfizer, Philips Lighting, sanofi-aventis, and Takeda.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
</recommendedContent>