<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_3302"
                     title="Cigarette Smoke May Affect Fertility (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/PrimaryCare/Smoking/tb/22069?impressionId=1284026491248"
                     
      &lt;p&gt;Smoking may provide an explanation for reduced fertility, results of two studies suggested.&lt;/p&gt;
&lt;p&gt;The first, by Claus Yding Andersen, MD, of the University of Copenhagen, and colleagues, found significant reductions in germ and somatic cells in the testes of male embryos from mothers who smoked during pregnancy, possibly related to the polycyclic aromatic hydrocarbons found in cigarette smoke.&lt;/p&gt;
&lt;p&gt;&quot;This effect may have long-term consequences on the future fertility of exposed offspring,&quot; the authors wrote online in &lt;em&gt;Human Reproduction&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The second study, by Mohamed Hammadeh, DVM, of Saarland University in Saarbr&amp;#252;cken, Germany, and colleagues, found that adult males who smoked had reduced levels of one of the proteins important in sperm formation. The findings were also published in &lt;em&gt;Human Reproduction&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;Smoking male partners of couples facing infertility should be counseled to stop smoking,&quot; Hammadeh and his colleagues wrote.&lt;/p&gt;
&lt;p&gt;Andersen&apos;s group assessed the numbers of germ and somatic cells in the testes of 24 male embryos obtained following abortion during the first trimester (mean ages 37 to 68 days post-conception).&lt;/p&gt;
&lt;p&gt;According to self-report and confirmed by cotinine testing, fifteen of the mothers smoked during pregnancy. Median intake was 11 to 15 cigarettes a day.&lt;/p&gt;
&lt;p&gt;The smoking and nonsmoking mothers were similar in age, height, and body mass index.&lt;/p&gt;
&lt;p&gt;Compared with embryos from nonsmoking mothers, those from smoking mothers had significant reductions in germ cells (by 55%) and somatic cells (by 37%; &lt;em&gt;P&lt;/em&gt;&amp;lt;0.05 for both). The relationship was dose-dependent, with greater reductions associated with heavier smoking.&lt;/p&gt;
&lt;p&gt;The researchers combined the data from the current study with data on 28 female embryos from a previous study.&lt;/p&gt;
&lt;p&gt;Regardless of gender, there were still reductions in germ cells (by 41%) and somatic cells (by 29%) in embryonic gonads exposed to smoking in utero (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.05 for both).&lt;/p&gt;
&lt;p&gt;The findings remained consistent after controlling for alcohol use and coffee consumption.&lt;/p&gt;
&lt;p&gt;The authors noted that the study could not determine whether the declines were permanent or a reflection of a growth delay that would be compensated for later in life.&lt;/p&gt;
&lt;p&gt;The study by Hammadeh and his colleagues evaluated the relationship between smoking and the formation of sperm  --  specifically the protamination process  --  among 53 heavy smokers (more than 20 cigarettes a day) and 63 nonsmokers. All were partners of a couple seeking treatment for infertility.&lt;/p&gt;
&lt;p&gt;Although smoking was not associated with semen volume or sperm concentration, smokers had significantly lower sperm vitality, motility, membrane integrity, and morphology (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.05 for all).&lt;/p&gt;
&lt;p&gt;The researchers also looked at levels of protamines 1 and 2, which are integral in sperm formation.&lt;/p&gt;
&lt;p&gt;Concentrations of protamine 2  --  but not protamine 1  --  were significantly lower in smokers (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.05). Consequently, the P1/P2 ratio was greater in smokers (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01).&lt;/p&gt;
&lt;p&gt;Cotinine levels and three oxidative stress biomarkers  --  reactive oxygen species, malondialdehyde, 8-hydroxyguanosine  --  were higher in smokers and correlated with P1/P2 ratios (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01 for all).&lt;/p&gt;
&lt;p&gt;The findings suggest that oxidative stress  --  which has been shown to be a major cause of male infertility  --  is greater in smokers, according to the researchers.&lt;/p&gt;
&lt;p&gt;The study provided support for the link between oxidative stress and infertility by showing that the oxidative stress biomarkers were significantly related to the percentages of sperm that had noncondensed chromatin and DNA fragmentation.&lt;/p&gt;
&lt;p&gt;&quot;Taken together, the results of the present study suggest a negative biological effect of smoking on spermatozoa DNA integrity and protamine distribution,&quot; the authors wrote.&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 by Andersen and colleagues was funded by the Danish Medical Research Council. The authors reported no conflicts of interest.&lt;/p&gt;&lt;p&gt;Hammadeh and his colleagues did not report any funding sources or 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_3258"
                     title="Bisphosphonates Tied to Esophageal Cancer (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/Endocrinology/Osteoporosis/tb/22017?impressionId=1284026491248"
                     
      &lt;p&gt;A second look at British registry data indicates that esophageal cancer may be more common after all in patients taking oral bisphosphonate drugs for long periods.&lt;/p&gt;
&lt;p&gt;In a nested case-control analysis involving some 80,000 patients tracked for more than seven years on average, individuals diagnosed with esophageal cancer of were 1.93 times as likely (95% CI 1.37 to 2.70) to have received at least 10 prescriptions for oral bisphosphonates, compared with controls not having cancer, reported Jane Green, MD, DPhil, of the University of Oxford in England, and colleagues online in &lt;em&gt;BMJ&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The likelihood of receiving at least one bisphosphonate prescription among esophageal cancer patients was 1.30 (95% CI 1.02 to 1.66) relative to controls, the researchers found.&lt;/p&gt;
&lt;p&gt;The findings were especially remarkable because another research group conducting a case-control study of the same registry  --  Great Britain&apos;s General Practice Research Database, containing records on some six million patients  --  &lt;a href=&quot;http://www.medpagetoday.com/Oncology/OtherCancers/21629&quot; mce_href=&quot;http://www.medpagetoday.com/Oncology/OtherCancers/21629&quot; target=&quot;_blank&quot;&gt;recently reported no increase&lt;/a&gt; in esophageal cancer rates in patients treated with bisphosphonates.&lt;/p&gt;
&lt;p&gt;Green and colleagues explained the discrepancy by noting that mean observation time prior to diagnosis in the other analysis was substantially shorter, 4.5 versus 7.7 years.&lt;/p&gt;
&lt;p&gt;Also, they noted, their study used five matched controls for each case, whereas the earlier study had equal numbers of cases and controls.&lt;/p&gt;
&lt;p&gt;&quot;Our study thus had the potential to include people with longer durations of bisphosphonate use and also had greater statistical power,&quot; Green and colleagues asserted.&lt;/p&gt;
&lt;p&gt;An accompanying editorial by an FDA epidemiologist, Diane Wysowski, PhD, noted that links between bisphosphonates and esophageal cancer have been proposed for more than 15 years. (The editorial carried a disclaimer that it did not necessarily express the agency&apos;s official view.)&lt;/p&gt;
&lt;p&gt;The FDA has collected a total of 68 case reports of esophageal cancer in patients taking bisphosphonates, half in the U.S. and the rest in Europe and Japan, but has not ordered label warnings. Prescribing information for oral bisphosphonates does include information on risks of other esophageal effects such as erosions and strictures, and dosing instructions are geared toward speeding the drugs through the esophagus.&lt;/p&gt;
&lt;p&gt;The suggestion of a connection between these agents and esophageal cancer have prompted efforts at systematic research, including the new study.&lt;/p&gt;
&lt;p&gt;Green and colleagues examined records of 2,954 patients with esophageal cancer, 2,018 patients with stomach cancer, and 10,641 with colon cancer, along with five controls for each of these cases matched for age, sex, observation time prior to diagnosis, and practice location.&lt;/p&gt;
&lt;p&gt;About 3.1% of the esophageal cancer patients had received at least one bisphosphonate prescription before diagnosis, compared with 2.4% of the controls over a similar period (relative risk 1.30 after adjusting for smoking status, alcohol intake, and body mass index).&lt;/p&gt;
&lt;p&gt;Rates of bisphosphonate use were similar in the stomach and colon cancer patients relative to controls, the researchers found.&lt;/p&gt;
&lt;p&gt;In the esophageal cancer patients, the relationship with bisphosphonate use appeared to strengthen with the number of prescriptions and with the estimated duration of use.&lt;/p&gt;
&lt;p&gt;Green and colleagues calculated a relative risk of 1.93 for receiving at least 10 prescriptions in cases versus controls, whereas esophageal cancer patients had virtually the same likelihood of receiving one to nine prescriptions as controls (RR 0.93, 95% CI 0.66 to 1.31).&lt;/p&gt;
&lt;p&gt;Similarly, estimated duration of use (based on the distribution of prescriptions over time) of at least three years was linked to esophageal cancer with a relative risk of 2.24 (95% CI 1.47 to 3.42), but shorter duration was seen in about equal numbers of cases and controls.&lt;/p&gt;
&lt;p&gt;These patterns were also not seen in the stomach or colorectal cancer patients.&lt;/p&gt;
&lt;p&gt;&quot;The association [in esophageal cancer patients] did not vary materially within subgroups defined by age, sex, smoking status, alcohol drinking, or body mass index; diagnosis of osteoporosis, previous fracture, or previous upper gastrointestinal disease; or prescription of nonsteroidal anti-inflammatory drugs, corticosteroids, or acid suppressant drugs,&quot; Green and colleagues added.&lt;/p&gt;
&lt;p&gt;But the researchers stopped short of concluding that bisphosphonate treatment contributes to esophageal cancer, noting that they could not &quot;rule out the possibility that the associations observed reflect other, unknown, factors that are linked to prolonged use of bisphosphonates and that also increase the risk of esophageal cancer.&quot;&lt;/p&gt;
&lt;p&gt;Other limitations included the lack of data on the extent to which patients used drugs prescribed to them or on prescriptions received before entry into the database.&lt;/p&gt;
&lt;p&gt;in the editorial, Wysowski didn&apos;t take a position on whether there is a causal link, noting that the evidence remains divided and weak. Even if there is such a connection, she wrote, &quot;the incidence in the population would be expected to remain relatively low.&quot;&lt;/p&gt;
&lt;p&gt;Still, she suggested that physicians consider the possibility of risk when prescribing the drugs and, when talking to patients, reiterate the importance of following the label directions for taking these drugs, which minimize the drugs&apos; direct contact with the esophageal tract.&lt;/p&gt;
&lt;p&gt;Wysowski also recommended that doctors urge patients to report difficulty swallowing or other gastrointestinal symptoms promptly.&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 UK Medical Research Council and Cancer Research UK provided funding for the database project and the current analysis.&lt;/p&gt;&lt;p&gt;Study authors and the editorialist declared they had no competing financial interests.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_3278"
                     title="Investigation Reveals More Woes for Rosiglitazone"
                     score="0.012"
                     href="http://www.medpagetoday.com/Cardiology/Diabetes/tb/22050?impressionId=1284026491248"
                     
      &lt;p&gt;On July 15 -- a day after the FDA completed &lt;a href=&quot;http://www.medpagetoday.com/ProductAlert/Prescriptions/21161&quot; mce_href=&quot;http://www.medpagetoday.com/ProductAlert/Prescriptions/21161&quot; target=&quot;_blank&quot;&gt;two days of hearings&lt;/a&gt; on rosiglitazone (Avandia) -- a British advisory commission on drugs concluded that the product should be withdrawn from the market, according to an investigation conducted by &lt;em&gt;BMJ.&lt;/em&gt;&lt;/p&gt;
&lt;p&gt;The Commission on Human Medicines&apos; opinion was passed on to the U.K.&apos;s regulatory authority, the Medicines and Healthcare Products Regulatory Agency (MHRA), which has now told &lt;em&gt;BMJ &lt;/em&gt; that rosiglitazone &quot;no longer has a place on the U.K. market.&quot; The evidence for increased risk of cardiovascular events outweighs any potential benefit, according to an MHRA statement given to &lt;em&gt;BMJ&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Yet six weeks after the commission submitted its recommendations on rosiglitazone, the drug is still on the market in Britain. The MHRA has yet to share its negative assessment of the drug with either physicians or patients.&lt;/p&gt;
&lt;p&gt;Instead, on July 26 it sent providers a &quot;dear doctor&quot; letter suggesting merely that it would be wise to consider alternatives to rosiglitazone, wrote Deborah Cohen, features editor at &lt;em&gt;BMJ. &lt;/em&gt;&lt;/p&gt;
&lt;p&gt;The &lt;em&gt;BMJ &lt;/em&gt;investigation was detailed in a feature article published online today and also the subject of a BBC news report. The report appears to be the first confirmation that U.K. regulators are ready to withdraw the drug from the market.&lt;/p&gt;
&lt;p&gt;The lengthy article reveals no new information about the FDA&apos;s handling of rosiglitazone from its approval through two subsequent safety reviews, but it does give insight into the machinations of the approval process in Europe.&lt;/p&gt;
&lt;p&gt;For example, the European Medicines Agency initially rejected rosiglitazone, only to come back a year later in 2000 to approve the drug. As a condition of that approval, the EMA ordered a post-marketing study to verify the safety of the drug. That study, called RECORD, was an open-label trial that has been roundly criticized on both sides of the Atlantic for its poor design.&lt;/p&gt;
&lt;p&gt;Cohen quoted numerous sources who all pointed to the influence of the drug maker, GlaxoSmithKline (SmithKlineBeecham during the initial approval process), as the reason that the EMA reversed itself on rosiglitazone.&lt;/p&gt;
&lt;p&gt;&quot;According to Edwin Gale, a diabetologist and adviser to European regulators, in the years before rosiglitazone&apos;s approval diabetologists were also putting pressure on the regulators and clamouring to use this new class of drug. Some of this clamour was fuelled by pharmaceutical analysts touting its blockbuster potential, which at the time they said was crucial to Smithkline Beecham&apos;s future growth,&quot; Cohen wrote.&lt;/p&gt;
&lt;p&gt;Cohen also pointed out that the EMA does not publicly release names of members of advisory panels who review drugs for the EMA. By comparison, she wrote, the FDA process, often the subject of criticism in the U.S., is open and transparent.&lt;/p&gt;
&lt;p&gt;In a editorial that accompanied Cohen&apos;s article, Richard Lehman, PhD, of the University of Oxford, John S. Yudkin, MD, of University College in London, and Harlan Krumholz, MD, of Yale University, said there is plenty of blame to pass around in the rosiglitazone saga.&lt;/p&gt;
&lt;p&gt;Back in 1999, clinicians were &quot;strongly disposed to welcome a new drug for type 2 diabetes, and it was vigorously promoted to a receptive market,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;&quot;Our mistake then -- and we have yet to put it right -- was that we did not demand better proof before we embarked on mass medication of a large group of patients who looked to us for advice and treatment.&quot;&lt;/p&gt;
&lt;p&gt;In a commentary, which was also published with the Cohen article, Nick Freemantle, PhD, of the University of Birmingham in England, argued that much of the controversy surrounding the thiazolidinediones can be laid at the feet of poor trial design -- so poor that critical questions were not answered.&lt;/p&gt;
&lt;p&gt;For example, regulators have been willing to permit high rates of loss to follow-up, especially in trials that rely on surrogate endpoints, a position that he contended &quot;makes no sense.&quot;&lt;/p&gt;
&lt;p&gt;And &quot;even when trials examine serious morbidity and mortality, loss to follow-up remains a problem. The RECORD trial, conducted to examine the safety of rosiglitazone and sponsored by GlaxoSmithKline in the UK, failed to follow-up survival in 127 participants (2.9%),&quot; he wrote. The loss to follow-up in RECORD meant that one could conclude that rosiglitazone &quot;was associated with either an increase or a decrease in mortality given different assumptions on the fate of those lost to follow-up.&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;Cohen declared no competing interests.&lt;/p&gt;&lt;p&gt;Lehman, Yudkin and Krumholz all declared they had received no support for the submitted work; no financial relationships with any organization that might have an interest in the submitted work in the previous three years; and no other relationships or activities that could appear to have influenced the submitted work.&lt;/p&gt;&lt;p&gt;Freemantle declared no support for the submitted work, but he disclosed that he has received funding for research and travel and consulting fees from Novo Nordisk, Sanofi-Aventis, Johnson &amp;amp; Johnson, and Eli Lilly.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_3250"
                     title="Attitudes More than Growth Response Drive Growth Hormone Therapy (CME/CE)"
                     score="0.01"
                     href="http://www.medpagetoday.com/Endocrinology/GeneralEndocrinology/tb/22010?impressionId=1284026491248"
                     
      &lt;p&gt;While a physician&apos;s decision to start a child on growth hormone is usually consistent with evidence-based guidelines, continuation or intensification of therapy is strongly influenced by factors other than treatment response, according to a new survey.&lt;/p&gt;
&lt;p&gt;Doctors&apos; attitudes and other factors, such as parent preference, exerted more influence on continuation decisions than did the growth response to therapy, Leona Cuttler, MD, of Case Western Reserve University, in Cleveland, and colleagues reported in &lt;em&gt;Pediatrics&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;At minimum, the results underscore the need for more emphasis and guidance on criteria for discontinuing growth hormone and perhaps other similar medications,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;Growth hormone is one of the fastest-growing classes of pharmaceuticals: biologicals, many with &quot;controversial indications and unclear endpoints for treating chronic conditions,&quot; Cuttler and colleagues wrote.&lt;/p&gt;
&lt;p&gt;Initiation and continuation of treatment is decided solely by the physician, but the determinants of those decisions are unclear.&lt;/p&gt;
&lt;p&gt;So to examine how physicians decided to begin growth hormone therapy among patients with idiopathic short stature, as well as how they decided to continue, the researchers assessed data from a survey questionnaire of 727 pediatric endocrinologists. The structured survey included different case scenarios;&lt;strong&gt; &lt;/strong&gt;the response rate was 90%.&lt;/p&gt;
&lt;p&gt;The researchers found that in previously untreated children, recommendations to initiate growth hormone were largely consistent with guidelines and were also influenced by family preferences and physician attitudes &lt;em&gt;(P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;For instance, 93% of endocrinologists said they would likely initiate growth hormone for a very short child with very low predicted adult height (PAH), very slow growth velocity, and a family wishing treatment.&lt;/p&gt;
&lt;p&gt;On the other end of the spectrum, 74% said they wouldn&apos;t initiate treatment for the child when growth parameters were less impaired and the family was neutral about treatment.&lt;/p&gt;
&lt;p&gt;Physicians ranked PAH as the most important parameter for initiating treatment, followed by baseline height and growth velocity.&lt;/p&gt;
&lt;p&gt;Family preference had almost as strong an influence as growth velocity, the researchers said.&lt;/p&gt;
&lt;p&gt;Compared with decisions on initiating therapy, decisions about continuation or intensification of treatment were more divergent.&lt;/p&gt;
&lt;p&gt;Overall, physicians demonstrated a preference for continuation (47.3%) and intensification (36.7%) versus discontinuation (16%).&lt;/p&gt;
&lt;p&gt;Those decisions were driven by nonphysiologic and contextual factors including physician attitude, family preference, and initiation recommendations (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001 for all).&lt;/p&gt;
&lt;p&gt;The combination of family preference and low response to treatment was particularly powerful in increasing dose, the researchers said (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;Also, factors present at initiation significantly influenced continuation decisions independent of the child&apos;s response to treatment. Doctors were likely to increase the dose of growth hormone if baseline PAH was very short, and decisions were also influenced by baseline height, growth velocity, and family preference.&lt;/p&gt;
&lt;p&gt;&quot;This is particularly striking because their influence persisted even after new evidence on growth response and family preference was known,&quot; the researchers wrote. &quot;This suggests that physicians may continue to be influenced by perceived disability associated with short stature, rather than guided primarily by evidence of the child&apos;s response to treatment.&quot;&lt;/p&gt;
&lt;p&gt;Physicians&apos; personal beliefs were also powerful influences on continuation of treatment. Concerns about emotional well-being and belief in the use of individualized growth hormone trials increased the likelihood of intensifying treatment and reduced the&lt;strong&gt; &lt;/strong&gt;likelihood of discontinuation (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;Those who believed that drug companies provide useful information were less likely to discontinue growth hormone (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;Together, attitudinal and contextual factors exerted more influence on continuation decisions than did the growth response to therapy, the researchers said.&lt;/p&gt;
&lt;p&gt;The study was limited by the use of scenarios and potential response bias although 96% of respondents said the questionnaire resembled cases in their practice, and the scenarios were vetted in advance.&lt;/p&gt;
&lt;p&gt;Still, the researchers concluded that the results may hold insights into medication management for chronic conditions treated with drugs that have unclear endpoints.&lt;/p&gt;
&lt;p&gt;The findings also underscore need for more evidence-based guidance for discontinuing growth hormone therapy, the researchers wrote.&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 National Institutes of Health.&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_3317"
                     title="Healthcare Reform Covers More and Costs More"
                     score="0.01"
                     href="http://www.medpagetoday.com/Washington-Watch/Reform/tb/22089?impressionId=1284026491248"
                     
      &lt;p&gt;WASHINGTON  --  The healthcare reform law will not slow the growth of healthcare spending in the next decade  --  in fact, it will accelerate healthcare spending slightly  --  but it will also significantly expand healthcare coverage, a new government report found.&lt;/p&gt;
&lt;p&gt;The report, issued by Centers for Medicare and Medicaid Services (CMS) Office of the Actuary, casts doubt on predictions from the Obama administration and congressional Democrats that healthcare reform would slow the trajectory of healthcare spending.&lt;/p&gt;
&lt;p&gt;The CMS analysis pegs healthcare spending growth at an average rate of 6.3% over the next decade, or 0.2 percentage points faster than healthcare spending would have grown had the Affordable Care Act (ACA) not become law.&lt;/p&gt;
&lt;p&gt;Put another way, nearly 20% of the U.S. gross domestic product (GDP)  --  or one in five U.S. dollars spent  --  will be devoted to healthcare costs in 2019. (That projection is 0.3 percentage points higher than pre-reform projections).&lt;/p&gt;
&lt;p&gt;However, the projection  --  which was published Thursday in the policy journal &lt;em&gt;Health Affairs&lt;/em&gt;  --  does support another promise of reform  --  to expand coverage to 32 million people.&lt;/p&gt;
&lt;p&gt;The CMS actuaries who wrote the report estimate that nearly 93% of the U.S population will have health insurance in 2019, which is an additional 32.5 million above the current number of insured people.&lt;/p&gt;
&lt;p&gt;This is the second 10-year health spending projection released by CMS this year. The first, which was released in &lt;a href=&quot;http://www.medpagetoday.com/Washington-Watch/Washington-Watch/18302&quot; mce_href=&quot;http://www.medpagetoday.com/Washington-Watch/Washington-Watch/18302&quot; target=&quot;_blank&quot; title=&quot;In&amp;#8200;Bad&amp;#8200;Economy,&amp;#8200;Record&amp;#8200;Growth&amp;#8200;in&amp;#8200;Health&amp;#8200;Spending&quot;&gt;February&lt;/a&gt;, did not account for the impact of the &lt;a href=&quot;http://www.medpagetoday.com/Washington-Watch/Reform/19351&quot; mce_href=&quot;http://www.medpagetoday.com/Washington-Watch/Reform/19351&quot; target=&quot;_blank&quot; title=&quot;What&apos;s&amp;#8200;in&amp;#8200;the&amp;#8200;Healthcare&amp;#8200;Reform&amp;#8200;Law&quot;&gt;Affordable Care Act &lt;/a&gt;(ACA), which was signed into law in March.&lt;/p&gt;
&lt;p&gt;The main driver of increased spending according to this latest report is the estimated $38 billion cost for establishing the new health insurance exchanges. Close behind is the expected $31 billion increase in the cost of Medicaid. Under ACA, any person under the age of 65 who has an income under 138% of the federal poverty level will be eligible for Medicaid.&lt;/p&gt;
&lt;p&gt;Taken together, the insurance exchanges and the Medicaid expansion, provide the new structure that will provide care to the uninsured.&lt;/p&gt;
&lt;p&gt;Healthcare reform could bring down costs after 2019, but the CMS researchers didn&apos;t look beyond the next decade.&lt;/p&gt;
&lt;p&gt;The projection outlines some healthcare spending patterns that will likely emerge over the upcoming years as a result of the ACA.&lt;/p&gt;
&lt;p&gt;For example, in 2010, healthcare spending is estimated to grow at a rate of 5.8%, but it&apos;s scheduled to slow in 2011 to 4.2%.&lt;/p&gt;
&lt;p&gt;But there are problems with that projection since spending slow-down hinges on a planned 23% pay cut for physicians who treat Medicare patients going into effect. In June, Congress passed a &lt;a href=&quot;http://www.medpagetoday.com/Washington-Watch/Washington-Watch/20889&quot; mce_href=&quot;http://www.medpagetoday.com/Washington-Watch/Washington-Watch/20889&quot; target=&quot;_blank&quot; title=&quot;&amp;#8200;Log&amp;#8200;in&amp;#8200;or&amp;#8200;create&amp;#8200;a&amp;#8200;free&amp;#8200;account&amp;#8200;for&amp;#8200;complete&amp;#8200;access&amp;#8200;to&amp;#8200;everything&amp;#8200;MedPage&amp;#8200;Today&amp;#8200;has&amp;#8200;to&amp;#8200;offer!&amp;#8200;House&amp;#8200;Passes&amp;#8200;Six-Month&amp;#8200;SGR&amp;#8200;Delay&quot;&gt;law &lt;/a&gt;to update physician Medicare rates by 2.2%, but that temporary fix runs out on Dec. 1. Come Jan. 1, 2011, physicians would also be slapped with an additional 3% cut in Medicare reimbursement.&lt;/p&gt;
&lt;p&gt;If history is any indication, Congress will likely vote again to override the cut, likely making the projection that healthcare spending will slow in 2011 no longer applicable.&lt;/p&gt;
&lt;p&gt;Some immediate changes brought by the law will cause a near-term spike in total national health expenditures to occur, the researchers found. For example, implementing the &lt;a href=&quot;http://www.medpagetoday.com/Washington-Watch/Reform/20991&quot; mce_href=&quot;http://www.medpagetoday.com/Washington-Watch/Reform/20991&quot; target=&quot;_blank&quot; title=&quot;Enrollment&amp;#8200;in&amp;#8200;Temporary&amp;#8200;High-Risk&amp;#8200;Pools&amp;#8200;Begins&amp;#8200;Today&quot;&gt;temporary high-risk insurance pool&lt;/a&gt;, and providing coverage to dependents under the age of 26 will add more than $10 billion to national health spending through 2013.&lt;/p&gt;
&lt;p&gt;  &lt;/p&gt;
&lt;p&gt;CMS researchers said that while reform won&apos;t tamp down healthcare spending in the next decade, that&apos;s far from the complete picture.&lt;/p&gt;
&lt;p&gt;&quot;While the impacts are relatively moderate on net spending, the underlying effects on coverage and financing are more pronounced,&quot; Andrea Sisko, an economist with CMS&apos; Office of the Actuary and lead author of the study, told reporters Wednesday.&lt;/p&gt;
&lt;p&gt;&quot;When you peel back the onion, and you look past the surface, you start to see much more pronounced impacts,&quot; said John Poisal, deputy director of the National Health Statistics Group at CMS&apos; Office of the Actuary, and one of the authors of the study.&lt;/p&gt;
&lt;p&gt;One of those layers, he said, is the high projected rate of insured people likely by 2019.&lt;/p&gt;
&lt;p&gt;Of the newly insured, about eight million will be enrolled in their state&apos;s Children&apos;s Health Insurance Plan (CHIP), and nearly 31 million will be enrolled in the new insurance exchanges that the ACA will establish beginning in 2014.&lt;/p&gt;
&lt;p&gt;Enrollment in Medicaid and CHIP will increase by one-third over the next decade, and enrollment in private insurance will increase from 15.8 million in 2014 to 30.6 million in 2019, the researchers wrote.&lt;/p&gt;
&lt;p&gt;The researchers also determined that when federally-mandated COBRA subsidies expire in 2011, the unemployed will be stuck paying for a large share of their insurance coverage, which will lead to slightly higher out-of-pocket health costs starting that year. But by 2014, when many people who did not have insurance will be insured, out-of-pocket spending will drop by 1.1%, instead of rising by 6.4% percent, which was the pre-reform projection.&lt;/p&gt;
&lt;p&gt;However, the reduction in out-of-pocket spending won&apos;t last, and, by 2018, employee spending will actually grow faster than had reform not passed. The CMS actuaries told reporters the projected increase would be caused by the tax on high-benefit, expensive plans. The actuaries predicted that employers would do an end-run to avoid the financial penalty for offering the so-called &quot;Cadillac&quot; plans by passing the extra costs onto all employees.&lt;/p&gt;
&lt;p&gt;Finally, crystal balls are notoriously inaccurate so the researchers cautioned that as the provisions of the ACA are implemented, the &quot;actual impacts may well differ considerably form these estimates.&quot;&lt;/p&gt;


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