Robert Finn

Major Finding: Seven of eight athletes who had a concussion had significantly increased length of reaction times with the device.

Data Source: Screening of 209 Division I athletes.

Disclosures: A provisional patent application has been filed on an updated version of the device. The study was supported by the Foundation for Physical Medicine and Rehabilitation and the University of Michigan.

An extremely simple device that tests an athlete's reaction time is showing promise in diagnosing concussions, according to a study announced in advance of its scheduled presentation at the annual meeting of the American Academy of Neurology.

Seven of eight Division I athletes who had suffered a concussion showed significantly slowedincaction times with the device, Dr. James T. Eckner said in an interview.

“It's actually very similar to an experiment that's done commonly in physics classrooms in high schools,” said Dr. Eckner, of the department of physical medicine and rehabilitation at the University of Michigan, Ann Arbor. In that experiment, reaction times are judged by the speed with whichhpeople can catch a ruler dropped between their fingers.

The device “is a fancier ruler, essentially,” Dr. Eckner said. “It's basically a dowel rod that we've coated in friction tape, and we've marked it in centimeter increments. And then at the base of it there's a little rubber disc, which is actually a hockey puck that it's embedded in.”

The device is so simple that it has the potential of being used on the sidelines of a football game. The person being tested sits with his or her forearm resting on a table. The person administering the test holds the device so that the subject's hand is encircling, but not touching, the hockey puck. At a random moment the investigator drops the device, and the subject catches it as soon as he or she can.

“We measure then how many centimeters it fell before they caught it, and then we use a simple physics equation for a body falling under the influence of gravity to convert that into how many milliseconds it fell for,” Dr. Eckner said.

Dr. Eckner and his colleagues recruited 209 members of Division I football, wrestling, and soccer teams. Before the start of the season the investigators measured each athlete's normal baseline reaction time. During the course of the season, eight of the athletes suffered concussions diagnosed by a physician. The investigators tested those eight8 athletes within 72 hours of their injury.

Seven of the eight athletes showed significant slowing of reaction

“I think that our results are still a little bit preliminary,” Dr. Eckner said. “They're all very encouraging, but the study we've got so far is fairly small. We've done some preliminary reliability data showing the inter-tester reliability and the test-retest reliability. But we do want to do that in a bigger sample to firm up the numbers that we have so far.

Seven of eight athletes with a concussion had increased reaction times measured with the ruler-like device, which could be used on the athletic field, said Dr. James T. Eckner shown demonstrating the device.

Source Courtesy Dr. James T. Eckner

Major Finding: Seven of eight athletes who had a concussion had significantly increased length of reaction times with the device.

Data Source: Screening of 209 Division I athletes.

Disclosures: A provisional patent application has been filed on an updated version of the device. The study was supported by the Foundation for Physical Medicine and Rehabilitation and the University of Michigan.

An extremely simple device that tests an athlete's reaction time is showing promise in diagnosing concussions, according to a study announced in advance of its scheduled presentation at the annual meeting of the American Academy of Neurology.

Seven of eight Division I athletes who had suffered a concussion showed significantly slowedincaction times with the device, Dr. James T. Eckner said in an interview.

“It's actually very similar to an experiment that's done commonly in physics classrooms in high schools,” said Dr. Eckner, of the department of physical medicine and rehabilitation at the University of Michigan, Ann Arbor. In that experiment, reaction times are judged by the speed with whichhpeople can catch a ruler dropped between their fingers.

The device “is a fancier ruler, essentially,” Dr. Eckner said. “It's basically a dowel rod that we've coated in friction tape, and we've marked it in centimeter increments. And then at the base of it there's a little rubber disc, which is actually a hockey puck that it's embedded in.”

The device is so simple that it has the potential of being used on the sidelines of a football game. The person being tested sits with his or her forearm resting on a table. The person administering the test holds the device so that the subject's hand is encircling, but not touching, the hockey puck. At a random moment the investigator drops the device, and the subject catches it as soon as he or she can.

“We measure then how many centimeters it fell before they caught it, and then we use a simple physics equation for a body falling under the influence of gravity to convert that into how many milliseconds it fell for,” Dr. Eckner said.

Dr. Eckner and his colleagues recruited 209 members of Division I football, wrestling, and soccer teams. Before the start of the season the investigators measured each athlete's normal baseline reaction time. During the course of the season, eight of the athletes suffered concussions diagnosed by a physician. The investigators tested those eight8 athletes within 72 hours of their injury.

Seven of the eight athletes showed significant slowing of reaction

“I think that our results are still a little bit preliminary,” Dr. Eckner said. “They're all very encouraging, but the study we've got so far is fairly small. We've done some preliminary reliability data showing the inter-tester reliability and the test-retest reliability. But we do want to do that in a bigger sample to firm up the numbers that we have so far.

Seven of eight athletes with a concussion had increased reaction times measured with the ruler-like device, which could be used on the athletic field, said Dr. James T. Eckner shown demonstrating the device.

Source Courtesy Dr. James T. Eckner

Major Finding: Seven of eight athletes who had a concussion had significantly increased length of reaction times with the device.

Data Source: Screening of 209 Division I athletes.

Disclosures: A provisional patent application has been filed on an updated version of the device. The study was supported by the Foundation for Physical Medicine and Rehabilitation and the University of Michigan.

An extremely simple device that tests an athlete's reaction time is showing promise in diagnosing concussions, according to a study announced in advance of its scheduled presentation at the annual meeting of the American Academy of Neurology.

Seven of eight Division I athletes who had suffered a concussion showed significantly slowedincaction times with the device, Dr. James T. Eckner said in an interview.

“It's actually very similar to an experiment that's done commonly in physics classrooms in high schools,” said Dr. Eckner, of the department of physical medicine and rehabilitation at the University of Michigan, Ann Arbor. In that experiment, reaction times are judged by the speed with whichhpeople can catch a ruler dropped between their fingers.

The device “is a fancier ruler, essentially,” Dr. Eckner said. “It's basically a dowel rod that we've coated in friction tape, and we've marked it in centimeter increments. And then at the base of it there's a little rubber disc, which is actually a hockey puck that it's embedded in.”

The device is so simple that it has the potential of being used on the sidelines of a football game. The person being tested sits with his or her forearm resting on a table. The person administering the test holds the device so that the subject's hand is encircling, but not touching, the hockey puck. At a random moment the investigator drops the device, and the subject catches it as soon as he or she can.

“We measure then how many centimeters it fell before they caught it, and then we use a simple physics equation for a body falling under the influence of gravity to convert that into how many milliseconds it fell for,” Dr. Eckner said.

Dr. Eckner and his colleagues recruited 209 members of Division I football, wrestling, and soccer teams. Before the start of the season the investigators measured each athlete's normal baseline reaction time. During the course of the season, eight of the athletes suffered concussions diagnosed by a physician. The investigators tested those eight8 athletes within 72 hours of their injury.

Seven of the eight athletes showed significant slowing of reaction

“I think that our results are still a little bit preliminary,” Dr. Eckner said. “They're all very encouraging, but the study we've got so far is fairly small. We've done some preliminary reliability data showing the inter-tester reliability and the test-retest reliability. But we do want to do that in a bigger sample to firm up the numbers that we have so far.

Seven of eight athletes with a concussion had increased reaction times measured with the ruler-like device, which could be used on the athletic field, said Dr. James T. Eckner shown demonstrating the device.

Source Courtesy Dr. James T. Eckner

Major Finding: Among AIDS-defining cancers, the cancer-attributable mortality rose from 69% to 88%. Among non–AIDS-defining cancers, the cancer-attributable mortality rose from 72% to 87%.

Data Source: Records of 372,364 people with AIDS along with links to corresponding cancer registry records.

Disclosures: Dr. Simard had no conflicts to report.

SAN FRANCISCO — AIDS-related mortality has declined since highly active antiretroviral therapy became widely available in the mid-1990s, but there has been a corresponding increase in the incidence of cancer among people with AIDS, according to a study of more than 300,000 individuals.

The rates of the AIDS-defining cancers—Kaposi's sarcoma, non-Hodgkin's lymphoma, and cervical cancer—remain high in people with AIDS compared with the general population, but people with AIDS are also at high risk of several types of non–AIDS-defining cancers.

“Among those who die with AIDS and cancer, cancer now accounts for the vast majority of all deaths,” said Edgar P. Simard, Ph.D., of the National Cancer Institute in Rockville, Md. “And in the entire population, non–AIDS-defining cancers represent an increasing fraction of all deaths.”

Dr. Simard and his colleagues used data from 372,364 people diagnosed with AIDS in the United States between 1980 and 2006 and linked those with corresponding cancer registry records. The investigators divided their analyses into three eras: 1980–1989, when there was little in the way of effective AIDS treatment; 1990–1995, when one- and two-drug regimens were typical; and 1996–2006, when highly active antiretroviral therapy (HAART) became widely used.

Since numerous studies have already been done on cancer in the 2 years following AIDS diagnosis, the investigators focused on cancer risk 3–5 years after AIDS onset, Dr. Simard said at the Conference on Retroviruses and Opportunistic Infections.

As expected, the incidence of AIDS-defining cancers was very high during years 3–5 after diagnosis. Compared with the general population, people with AIDS had 5,321 times the risk of developing Kaposi's sarcoma, 32 times the risk of non-Hodgkin's lymphoma, and 5.6 times the risk of cervical cancer, he reported.

People with AIDS also had significant increases in the risk of developing four different non–AIDS-defining cancers. They had a 27-fold increase in the risk of anal cancer, a 9.1-fold increase in the risk of Hodgkin's lymphoma, a 3.7-fold increase in the risk of liver cancer, and a 3.0-fold increase in the risk of lung cancer. Overall, people with AIDS had a statistically significant 70% increase in the risk of developing any non–AIDS-defining cancer.

The cumulative incidence of AIDS-defining cancers declined significantly. At 60 months following diagnosis the cumulative incidence was 8.7% for the 1980–1989 era, 6.4% for 1990–1995, and 2.1% for 1996–2006, Dr. Simard said.

On the other hand, the cumulative incidence of the four non–AIDS-defining cancers increased significantly. The 60-month cumulative incidence of lung cancer rose from 0.14% in 1980–1989 to 0.28% in 1990–1995 and to 0.37% in 1996–2006. Similarly, the cumulative incidence of Hodgkin's lymphoma rose from 0.04% in 1980–1989 to 0.10% in 1990–1995 to 0.17% in the 1996–2006 era, he said.

Among AIDS-defining cancers, the cancer-attributable mortality rose from 69% to 88% from the earliest to the latest treatment eras, and among non–AIDS-defining cancers, the cancer-attributable mortality rose from 72% to 87%.

Major Finding: Among AIDS-defining cancers, the cancer-attributable mortality rose from 69% to 88%. Among non–AIDS-defining cancers, the cancer-attributable mortality rose from 72% to 87%.

Data Source: Records of 372,364 people with AIDS along with links to corresponding cancer registry records.

Disclosures: Dr. Simard had no conflicts to report.

SAN FRANCISCO — AIDS-related mortality has declined since highly active antiretroviral therapy became widely available in the mid-1990s, but there has been a corresponding increase in the incidence of cancer among people with AIDS, according to a study of more than 300,000 individuals.

The rates of the AIDS-defining cancers—Kaposi's sarcoma, non-Hodgkin's lymphoma, and cervical cancer—remain high in people with AIDS compared with the general population, but people with AIDS are also at high risk of several types of non–AIDS-defining cancers.

“Among those who die with AIDS and cancer, cancer now accounts for the vast majority of all deaths,” said Edgar P. Simard, Ph.D., of the National Cancer Institute in Rockville, Md. “And in the entire population, non–AIDS-defining cancers represent an increasing fraction of all deaths.”

Dr. Simard and his colleagues used data from 372,364 people diagnosed with AIDS in the United States between 1980 and 2006 and linked those with corresponding cancer registry records. The investigators divided their analyses into three eras: 1980–1989, when there was little in the way of effective AIDS treatment; 1990–1995, when one- and two-drug regimens were typical; and 1996–2006, when highly active antiretroviral therapy (HAART) became widely used.

Since numerous studies have already been done on cancer in the 2 years following AIDS diagnosis, the investigators focused on cancer risk 3–5 years after AIDS onset, Dr. Simard said at the Conference on Retroviruses and Opportunistic Infections.

As expected, the incidence of AIDS-defining cancers was very high during years 3–5 after diagnosis. Compared with the general population, people with AIDS had 5,321 times the risk of developing Kaposi's sarcoma, 32 times the risk of non-Hodgkin's lymphoma, and 5.6 times the risk of cervical cancer, he reported.

People with AIDS also had significant increases in the risk of developing four different non–AIDS-defining cancers. They had a 27-fold increase in the risk of anal cancer, a 9.1-fold increase in the risk of Hodgkin's lymphoma, a 3.7-fold increase in the risk of liver cancer, and a 3.0-fold increase in the risk of lung cancer. Overall, people with AIDS had a statistically significant 70% increase in the risk of developing any non–AIDS-defining cancer.

The cumulative incidence of AIDS-defining cancers declined significantly. At 60 months following diagnosis the cumulative incidence was 8.7% for the 1980–1989 era, 6.4% for 1990–1995, and 2.1% for 1996–2006, Dr. Simard said.

On the other hand, the cumulative incidence of the four non–AIDS-defining cancers increased significantly. The 60-month cumulative incidence of lung cancer rose from 0.14% in 1980–1989 to 0.28% in 1990–1995 and to 0.37% in 1996–2006. Similarly, the cumulative incidence of Hodgkin's lymphoma rose from 0.04% in 1980–1989 to 0.10% in 1990–1995 to 0.17% in the 1996–2006 era, he said.

Among AIDS-defining cancers, the cancer-attributable mortality rose from 69% to 88% from the earliest to the latest treatment eras, and among non–AIDS-defining cancers, the cancer-attributable mortality rose from 72% to 87%.

Major Finding: Among AIDS-defining cancers, the cancer-attributable mortality rose from 69% to 88%. Among non–AIDS-defining cancers, the cancer-attributable mortality rose from 72% to 87%.

Data Source: Records of 372,364 people with AIDS along with links to corresponding cancer registry records.

Disclosures: Dr. Simard had no conflicts to report.

SAN FRANCISCO — AIDS-related mortality has declined since highly active antiretroviral therapy became widely available in the mid-1990s, but there has been a corresponding increase in the incidence of cancer among people with AIDS, according to a study of more than 300,000 individuals.

The rates of the AIDS-defining cancers—Kaposi's sarcoma, non-Hodgkin's lymphoma, and cervical cancer—remain high in people with AIDS compared with the general population, but people with AIDS are also at high risk of several types of non–AIDS-defining cancers.

“Among those who die with AIDS and cancer, cancer now accounts for the vast majority of all deaths,” said Edgar P. Simard, Ph.D., of the National Cancer Institute in Rockville, Md. “And in the entire population, non–AIDS-defining cancers represent an increasing fraction of all deaths.”

Dr. Simard and his colleagues used data from 372,364 people diagnosed with AIDS in the United States between 1980 and 2006 and linked those with corresponding cancer registry records. The investigators divided their analyses into three eras: 1980–1989, when there was little in the way of effective AIDS treatment; 1990–1995, when one- and two-drug regimens were typical; and 1996–2006, when highly active antiretroviral therapy (HAART) became widely used.

Since numerous studies have already been done on cancer in the 2 years following AIDS diagnosis, the investigators focused on cancer risk 3–5 years after AIDS onset, Dr. Simard said at the Conference on Retroviruses and Opportunistic Infections.

As expected, the incidence of AIDS-defining cancers was very high during years 3–5 after diagnosis. Compared with the general population, people with AIDS had 5,321 times the risk of developing Kaposi's sarcoma, 32 times the risk of non-Hodgkin's lymphoma, and 5.6 times the risk of cervical cancer, he reported.

People with AIDS also had significant increases in the risk of developing four different non–AIDS-defining cancers. They had a 27-fold increase in the risk of anal cancer, a 9.1-fold increase in the risk of Hodgkin's lymphoma, a 3.7-fold increase in the risk of liver cancer, and a 3.0-fold increase in the risk of lung cancer. Overall, people with AIDS had a statistically significant 70% increase in the risk of developing any non–AIDS-defining cancer.

The cumulative incidence of AIDS-defining cancers declined significantly. At 60 months following diagnosis the cumulative incidence was 8.7% for the 1980–1989 era, 6.4% for 1990–1995, and 2.1% for 1996–2006, Dr. Simard said.

On the other hand, the cumulative incidence of the four non–AIDS-defining cancers increased significantly. The 60-month cumulative incidence of lung cancer rose from 0.14% in 1980–1989 to 0.28% in 1990–1995 and to 0.37% in 1996–2006. Similarly, the cumulative incidence of Hodgkin's lymphoma rose from 0.04% in 1980–1989 to 0.10% in 1990–1995 to 0.17% in the 1996–2006 era, he said.

Among AIDS-defining cancers, the cancer-attributable mortality rose from 69% to 88% from the earliest to the latest treatment eras, and among non–AIDS-defining cancers, the cancer-attributable mortality rose from 72% to 87%.

Major Finding: There was no significant difference between pregnant women who received treatment for periodontal disease and those who did not in terms of spontaneous preterm birth, gestational age at birth, or major neonatal adverse outcomes.

Data Source: Randomized, controlled trial of 756 pregnant women with periodontal disease.

Disclosures: None reported.

Treating periodontal disease in pregnant women does not decrease the chances of preterm birth, according to a study of 756 women.

Previous studies have found that pregnant women with periodontal disease have an increased likelihood of giving birth prematurely, but this was the first study to use a randomized controlled trial to test the idea that treating periodontal disease may improve pregnancy outcomes.

Periodontal disease is very common, affecting more than 30% of individuals in some populations. The investigators, led by Dr. George A. Macones of Washington University in St. Louis found that 50% of the 3,563 pregnant women they screened had either gingivitis or periodontitis (Am. J. Obstet. Gynecol. 2010;202:147.e1–8).

Women were included in the study if they had periodontal disease and were 6–20 weeks pregnant. They were excluded if they had already received periodontal treatment during their pregnancy, if they had used antibiotics or antibiotic mouthwash within 2 weeks, if they had a multiple pregnancy, or if they had known mitral valve prolapse.

The 376 women in the active treatment group received thorough periodontal treatment, in which trained dental hygienists removed stains, plaque, and calculus above and below the gum line, leaving the root surfaces smooth and clean. The 380 women in the control group received only a superficial cleaning and stain removal above the gum line.

The primary outcome was spontaneous preterm birth, which the investigators defined as births occurring before 35 weeks' gestation. Secondary outcomes included the type of preterm birth (either spontaneous or indicated), delivery before 37 weeks' gestation, gestational age at delivery, birth weight, and major neonatal adverse outcomes, such as death, sepsis, and chronic lung disease.

There were no significant differences between active treatment and control groups on any of these measures. Investigators did, however, find one significant difference within the planned subgroup analyses: Among women with a history of previous preterm birth, those in the active treatment arm had a greater risk of preterm birth than those in the control treatment arm. The investigators suggested that this one statistically significant result among many results that were not significant may have arisen by chance.

In an editorial, Dr. Kim A. Boggess of the University of North Carolina at Chapel Hill offered another possibility. Dr. Boggess suggested that scaling and root planing may have disseminated oral pathogens or their toxins to the rest of the body, accounting for the apparently increased risk of active treatment in this one subgroup of women (Am. J. Obstet. Gynecol. 2010;202:101–2).

Major Finding: There was no significant difference between pregnant women who received treatment for periodontal disease and those who did not in terms of spontaneous preterm birth, gestational age at birth, or major neonatal adverse outcomes.

Data Source: Randomized, controlled trial of 756 pregnant women with periodontal disease.

Disclosures: None reported.

Treating periodontal disease in pregnant women does not decrease the chances of preterm birth, according to a study of 756 women.

Previous studies have found that pregnant women with periodontal disease have an increased likelihood of giving birth prematurely, but this was the first study to use a randomized controlled trial to test the idea that treating periodontal disease may improve pregnancy outcomes.

Periodontal disease is very common, affecting more than 30% of individuals in some populations. The investigators, led by Dr. George A. Macones of Washington University in St. Louis found that 50% of the 3,563 pregnant women they screened had either gingivitis or periodontitis (Am. J. Obstet. Gynecol. 2010;202:147.e1–8).

Women were included in the study if they had periodontal disease and were 6–20 weeks pregnant. They were excluded if they had already received periodontal treatment during their pregnancy, if they had used antibiotics or antibiotic mouthwash within 2 weeks, if they had a multiple pregnancy, or if they had known mitral valve prolapse.

The 376 women in the active treatment group received thorough periodontal treatment, in which trained dental hygienists removed stains, plaque, and calculus above and below the gum line, leaving the root surfaces smooth and clean. The 380 women in the control group received only a superficial cleaning and stain removal above the gum line.

The primary outcome was spontaneous preterm birth, which the investigators defined as births occurring before 35 weeks' gestation. Secondary outcomes included the type of preterm birth (either spontaneous or indicated), delivery before 37 weeks' gestation, gestational age at delivery, birth weight, and major neonatal adverse outcomes, such as death, sepsis, and chronic lung disease.

There were no significant differences between active treatment and control groups on any of these measures. Investigators did, however, find one significant difference within the planned subgroup analyses: Among women with a history of previous preterm birth, those in the active treatment arm had a greater risk of preterm birth than those in the control treatment arm. The investigators suggested that this one statistically significant result among many results that were not significant may have arisen by chance.

In an editorial, Dr. Kim A. Boggess of the University of North Carolina at Chapel Hill offered another possibility. Dr. Boggess suggested that scaling and root planing may have disseminated oral pathogens or their toxins to the rest of the body, accounting for the apparently increased risk of active treatment in this one subgroup of women (Am. J. Obstet. Gynecol. 2010;202:101–2).

Major Finding: There was no significant difference between pregnant women who received treatment for periodontal disease and those who did not in terms of spontaneous preterm birth, gestational age at birth, or major neonatal adverse outcomes.

Data Source: Randomized, controlled trial of 756 pregnant women with periodontal disease.

Disclosures: None reported.

Treating periodontal disease in pregnant women does not decrease the chances of preterm birth, according to a study of 756 women.

Previous studies have found that pregnant women with periodontal disease have an increased likelihood of giving birth prematurely, but this was the first study to use a randomized controlled trial to test the idea that treating periodontal disease may improve pregnancy outcomes.

Periodontal disease is very common, affecting more than 30% of individuals in some populations. The investigators, led by Dr. George A. Macones of Washington University in St. Louis found that 50% of the 3,563 pregnant women they screened had either gingivitis or periodontitis (Am. J. Obstet. Gynecol. 2010;202:147.e1–8).

Women were included in the study if they had periodontal disease and were 6–20 weeks pregnant. They were excluded if they had already received periodontal treatment during their pregnancy, if they had used antibiotics or antibiotic mouthwash within 2 weeks, if they had a multiple pregnancy, or if they had known mitral valve prolapse.

The 376 women in the active treatment group received thorough periodontal treatment, in which trained dental hygienists removed stains, plaque, and calculus above and below the gum line, leaving the root surfaces smooth and clean. The 380 women in the control group received only a superficial cleaning and stain removal above the gum line.

The primary outcome was spontaneous preterm birth, which the investigators defined as births occurring before 35 weeks' gestation. Secondary outcomes included the type of preterm birth (either spontaneous or indicated), delivery before 37 weeks' gestation, gestational age at delivery, birth weight, and major neonatal adverse outcomes, such as death, sepsis, and chronic lung disease.

There were no significant differences between active treatment and control groups on any of these measures. Investigators did, however, find one significant difference within the planned subgroup analyses: Among women with a history of previous preterm birth, those in the active treatment arm had a greater risk of preterm birth than those in the control treatment arm. The investigators suggested that this one statistically significant result among many results that were not significant may have arisen by chance.

In an editorial, Dr. Kim A. Boggess of the University of North Carolina at Chapel Hill offered another possibility. Dr. Boggess suggested that scaling and root planing may have disseminated oral pathogens or their toxins to the rest of the body, accounting for the apparently increased risk of active treatment in this one subgroup of women (Am. J. Obstet. Gynecol. 2010;202:101–2).

Major Finding: Consumption of sugar-sweetened beverages contributed to an estimated 130,000 new cases of diabetes and 14,000 new cases of coronary heart disease between 2000 and 2010.

Data Source: Computer simulation based on the Coronary Heart Disease Policy Model.

Disclosures: Supported by a grant from the American Heart Association Western States Affiliate.

SAN FRANCISCO — The increase in the consumption of sugar-sweetened beverages between 1990 and 2000 contributed to 130,000 new cases of diabetes and 14,000 new cases of coronary heart disease between 2000 and 2010, according to estimates from a computer model of the U.S. population.

In addition, the rising consumption of sugar-sweetened beverages, which include soda, sports drinks, and fruit drinks, led to an estimated 1.4 million additional life-years burdened by diabetes and 50,000 additional life-years burdened by coronary heart disease in the first decade of the 21st century.

To derive those estimates, Dr. Litsa K. Lambrakos of the University of California, San Francisco, and her colleagues used data from the 1990–2000 National Health and Nutrition Examination Survey (NHANES) on consumption of sugar-sweetened beverages. She combined that with the Coronary Heart Disease Policy Model, a computer simulation of heart disease in U.S. adults aged 35–84 years.

According to that model, the relative risk of incident diabetes related to the daily consumption of sugar-sweetened beverages was 1.32 after adjusting for body mass index. Dr. Lambrakos presented the findings during a poster session at a conference sponsored by the American Heart Association.

The estimated increase in coronary heart disease related to the increased consumption of sugar-sweetened beverages would have generated an additional $300-$500 million in health care costs between 2000 and 2010.

“Those numbers about excess health care costs are very conservative, because they only account for health care costs attributed to coronary heart disease,” Dr. Lambrakos said in an interview.

“We know we have an increase in diabetes as well that we can attribute to soft drink consumption,” she continued.

The investigators also analyzed how a 1-cent per ounce tax on sugar-sweetened beverages might have limited coronary heart disease costs, had it been implemented in the year 2000. Based on economic studies, the computer model assumed that such a tax would decrease consumption by 10%. This would translate to a savings of $170 million in health care costs over 10 years.

In a statement, the American Heart Association said that it “acknowledges the importance of limiting intake of added sugars, including sugar-sweetened beverages. The association is still evaluating the research to determine which strategies accomplish this best, comparing more punitive strategies like taxation with more positive incentives like subsidies or lowering prices for healthy foods. The AHA will continue to monitor the best available research to more fully understand the connection between taxation policy and consumption trends, and ensure that our public policy positions reflect the best available science.”

Asked what message primary care physicians should take from the findings, Dr. Lambrakos said that “what we're talking about here is primary prevention …. It's important for the general public and physicians to understand that these drinks may lead to adverse health outcomes over time, and that they really shouldn't be considered a staple of the American diet.”

A 1-cent tax on soda would have saved $170 million in health care costs over 10 years.

Source ©Lori Martin/Fotolia.com

Major Finding: Consumption of sugar-sweetened beverages contributed to an estimated 130,000 new cases of diabetes and 14,000 new cases of coronary heart disease between 2000 and 2010.

Data Source: Computer simulation based on the Coronary Heart Disease Policy Model.

Disclosures: Supported by a grant from the American Heart Association Western States Affiliate.

SAN FRANCISCO — The increase in the consumption of sugar-sweetened beverages between 1990 and 2000 contributed to 130,000 new cases of diabetes and 14,000 new cases of coronary heart disease between 2000 and 2010, according to estimates from a computer model of the U.S. population.

In addition, the rising consumption of sugar-sweetened beverages, which include soda, sports drinks, and fruit drinks, led to an estimated 1.4 million additional life-years burdened by diabetes and 50,000 additional life-years burdened by coronary heart disease in the first decade of the 21st century.

To derive those estimates, Dr. Litsa K. Lambrakos of the University of California, San Francisco, and her colleagues used data from the 1990–2000 National Health and Nutrition Examination Survey (NHANES) on consumption of sugar-sweetened beverages. She combined that with the Coronary Heart Disease Policy Model, a computer simulation of heart disease in U.S. adults aged 35–84 years.

According to that model, the relative risk of incident diabetes related to the daily consumption of sugar-sweetened beverages was 1.32 after adjusting for body mass index. Dr. Lambrakos presented the findings during a poster session at a conference sponsored by the American Heart Association.

The estimated increase in coronary heart disease related to the increased consumption of sugar-sweetened beverages would have generated an additional $300-$500 million in health care costs between 2000 and 2010.

“Those numbers about excess health care costs are very conservative, because they only account for health care costs attributed to coronary heart disease,” Dr. Lambrakos said in an interview.

“We know we have an increase in diabetes as well that we can attribute to soft drink consumption,” she continued.

The investigators also analyzed how a 1-cent per ounce tax on sugar-sweetened beverages might have limited coronary heart disease costs, had it been implemented in the year 2000. Based on economic studies, the computer model assumed that such a tax would decrease consumption by 10%. This would translate to a savings of $170 million in health care costs over 10 years.

In a statement, the American Heart Association said that it “acknowledges the importance of limiting intake of added sugars, including sugar-sweetened beverages. The association is still evaluating the research to determine which strategies accomplish this best, comparing more punitive strategies like taxation with more positive incentives like subsidies or lowering prices for healthy foods. The AHA will continue to monitor the best available research to more fully understand the connection between taxation policy and consumption trends, and ensure that our public policy positions reflect the best available science.”

Asked what message primary care physicians should take from the findings, Dr. Lambrakos said that “what we're talking about here is primary prevention …. It's important for the general public and physicians to understand that these drinks may lead to adverse health outcomes over time, and that they really shouldn't be considered a staple of the American diet.”

A 1-cent tax on soda would have saved $170 million in health care costs over 10 years.

Source ©Lori Martin/Fotolia.com

Major Finding: Consumption of sugar-sweetened beverages contributed to an estimated 130,000 new cases of diabetes and 14,000 new cases of coronary heart disease between 2000 and 2010.

Data Source: Computer simulation based on the Coronary Heart Disease Policy Model.

Disclosures: Supported by a grant from the American Heart Association Western States Affiliate.

SAN FRANCISCO — The increase in the consumption of sugar-sweetened beverages between 1990 and 2000 contributed to 130,000 new cases of diabetes and 14,000 new cases of coronary heart disease between 2000 and 2010, according to estimates from a computer model of the U.S. population.

In addition, the rising consumption of sugar-sweetened beverages, which include soda, sports drinks, and fruit drinks, led to an estimated 1.4 million additional life-years burdened by diabetes and 50,000 additional life-years burdened by coronary heart disease in the first decade of the 21st century.

To derive those estimates, Dr. Litsa K. Lambrakos of the University of California, San Francisco, and her colleagues used data from the 1990–2000 National Health and Nutrition Examination Survey (NHANES) on consumption of sugar-sweetened beverages. She combined that with the Coronary Heart Disease Policy Model, a computer simulation of heart disease in U.S. adults aged 35–84 years.

According to that model, the relative risk of incident diabetes related to the daily consumption of sugar-sweetened beverages was 1.32 after adjusting for body mass index. Dr. Lambrakos presented the findings during a poster session at a conference sponsored by the American Heart Association.

The estimated increase in coronary heart disease related to the increased consumption of sugar-sweetened beverages would have generated an additional $300-$500 million in health care costs between 2000 and 2010.

“Those numbers about excess health care costs are very conservative, because they only account for health care costs attributed to coronary heart disease,” Dr. Lambrakos said in an interview.

“We know we have an increase in diabetes as well that we can attribute to soft drink consumption,” she continued.

The investigators also analyzed how a 1-cent per ounce tax on sugar-sweetened beverages might have limited coronary heart disease costs, had it been implemented in the year 2000. Based on economic studies, the computer model assumed that such a tax would decrease consumption by 10%. This would translate to a savings of $170 million in health care costs over 10 years.

In a statement, the American Heart Association said that it “acknowledges the importance of limiting intake of added sugars, including sugar-sweetened beverages. The association is still evaluating the research to determine which strategies accomplish this best, comparing more punitive strategies like taxation with more positive incentives like subsidies or lowering prices for healthy foods. The AHA will continue to monitor the best available research to more fully understand the connection between taxation policy and consumption trends, and ensure that our public policy positions reflect the best available science.”

Asked what message primary care physicians should take from the findings, Dr. Lambrakos said that “what we're talking about here is primary prevention …. It's important for the general public and physicians to understand that these drinks may lead to adverse health outcomes over time, and that they really shouldn't be considered a staple of the American diet.”

A 1-cent tax on soda would have saved $170 million in health care costs over 10 years.

Source ©Lori Martin/Fotolia.com

HONOLULU — High-dose OROS methylphenidate was associated with small but statistically significant increases in systolic blood pressure and heart rate in a 6-month, open-label study in adolescents.

The study found no significant long-term increases in diastolic blood pressure or in electrocardiographic measures, Dr. Paul Hammerness said at the annual meeting of the American Academy of Child and Adolescent Psychiatry.

The findings are consistent with studies involving younger children and lower doses, said Dr. Hammerness of Massachusetts General Hospital and Harvard Medical School, Boston.

Because of concerns about possible associations between stimulant medications for ADHD and cardiovascular complications—including sudden cardiac death—the Food and Drug Administration in June 2009 recommended that physicians pay special attention to a child's cardiovascular system when prescribing stimulants.

The study involved 114 adolescents with a mean age of 14 years at baseline (range 12-18 years). All were healthy, and all had a diagnosis of ADHD based on full DSM-IV criteria. The researchers analyzed data taken from an ongoing trial of OROS methylphenidate for the prevention of cigarette smoking in adolescents with ADHD (J. Pediatr. 2009;155:84-9).

Participants were excluded if they had a history of cardiovascular disease or had untreated mood or anxiety disorders, eating disorders, psychosis, or substance use disorders.

The beginning dose of OROS methylphenidate was 0.5-0.75 mg/kg per day, and that was titrated upward to a maximum of 1.5 mg/kg per day by week 3. At week 6, the mean total daily dose was 63 mg, and 50% of the participants were taking 72 mg or more.

As expected, OROS methylphenidate was highly effective in treating the participants' ADHD. Their Rating Scale scores declined from a mean of 26.9 at baseline to 9.7 at week 6.

Of the 114 participants who entered the study, 73% were male. Mean systolic blood pressure at baseline was 113 mm Hg, and that increased to 117 mm Hg at 6 months, a significant increase. Mean diastolic blood pressure began at 63 mm Hg, increased significantly to 65 mm Hg at week 6, but then returned to 64 mm Hg at 6 months. Mean heart rate began at 82 beats per minute, increased significantly to 86 beats per minute at week 6, and remained at about that rate at 6 months.

The investigators found no statistically significant or clinically meaningful changes in ECG variables, including PR, QRS, or QTC.

Reasoning that any adverse cardiovascular effects of OROS methylphenidate might be restricted to certain subsets of adolescents, the investigators separately analyzed those 16 participants who met criteria for prehypertension or hypertension at baseline, based on at least one blood pressure reading above the 90th or 95th percentile. The investigators found no impact of abnormal premedication blood pressure readings on blood pressure changes during treatment.

Participants experienced no serious adverse events or serious cardiovascular adverse events during the study. Ten of the 114 subjects reported one or more subjective cardiovascular complaints, including palpitations, chest pain, and fast or racing heartbeat. Of those, six had a lifetime diagnosis of comorbid anxiety disorder.

One participant discontinued treatment because of recurrent palpitations. She had a lifetime history of comorbid generalized anxiety disorder and migraines. But she showed no change from baseline in any cardiovascular measurement, and her primary care physician did not find her complaints to be consistent with cardiac disease. She later used a different stimulant medication with no subsequent cardiovascular symptoms.

“The FDA continues to review and still concludes that the overall risk-benefit ratio supports the use of stimulant medications for ADHD,” Dr. Hammerness said. But he did recommend that clinicians carefully evaluate an adolescent's cardiovascular symptoms and family history before prescribing stimulants.

In particular, clinicians should be alert for a family history of cardiovascular disease at a young age, such as QT syndrome, cardiomyopathy, or perhaps a cousin who died suddenly during exercise.

Electrocardiograms are not mandatory, although Dr. Hammerness said clinicians may consider them as part of a general premedication evaluation or during treatment.

Disclosures: Dr. Hammerness acknowledged serving as a speaker for, receiving research funds from, or participating in CME activities and research studies funded by several pharmaceutical companies, including McNeil, which sponsored this study and which markets OROS methylphenidate under the brand name Concerta.

HONOLULU — High-dose OROS methylphenidate was associated with small but statistically significant increases in systolic blood pressure and heart rate in a 6-month, open-label study in adolescents.

The study found no significant long-term increases in diastolic blood pressure or in electrocardiographic measures, Dr. Paul Hammerness said at the annual meeting of the American Academy of Child and Adolescent Psychiatry.

The findings are consistent with studies involving younger children and lower doses, said Dr. Hammerness of Massachusetts General Hospital and Harvard Medical School, Boston.

Because of concerns about possible associations between stimulant medications for ADHD and cardiovascular complications—including sudden cardiac death—the Food and Drug Administration in June 2009 recommended that physicians pay special attention to a child's cardiovascular system when prescribing stimulants.

The study involved 114 adolescents with a mean age of 14 years at baseline (range 12-18 years). All were healthy, and all had a diagnosis of ADHD based on full DSM-IV criteria. The researchers analyzed data taken from an ongoing trial of OROS methylphenidate for the prevention of cigarette smoking in adolescents with ADHD (J. Pediatr. 2009;155:84-9).

Participants were excluded if they had a history of cardiovascular disease or had untreated mood or anxiety disorders, eating disorders, psychosis, or substance use disorders.

The beginning dose of OROS methylphenidate was 0.5-0.75 mg/kg per day, and that was titrated upward to a maximum of 1.5 mg/kg per day by week 3. At week 6, the mean total daily dose was 63 mg, and 50% of the participants were taking 72 mg or more.

As expected, OROS methylphenidate was highly effective in treating the participants' ADHD. Their Rating Scale scores declined from a mean of 26.9 at baseline to 9.7 at week 6.

Of the 114 participants who entered the study, 73% were male. Mean systolic blood pressure at baseline was 113 mm Hg, and that increased to 117 mm Hg at 6 months, a significant increase. Mean diastolic blood pressure began at 63 mm Hg, increased significantly to 65 mm Hg at week 6, but then returned to 64 mm Hg at 6 months. Mean heart rate began at 82 beats per minute, increased significantly to 86 beats per minute at week 6, and remained at about that rate at 6 months.

The investigators found no statistically significant or clinically meaningful changes in ECG variables, including PR, QRS, or QTC.

Reasoning that any adverse cardiovascular effects of OROS methylphenidate might be restricted to certain subsets of adolescents, the investigators separately analyzed those 16 participants who met criteria for prehypertension or hypertension at baseline, based on at least one blood pressure reading above the 90th or 95th percentile. The investigators found no impact of abnormal premedication blood pressure readings on blood pressure changes during treatment.

Participants experienced no serious adverse events or serious cardiovascular adverse events during the study. Ten of the 114 subjects reported one or more subjective cardiovascular complaints, including palpitations, chest pain, and fast or racing heartbeat. Of those, six had a lifetime diagnosis of comorbid anxiety disorder.

One participant discontinued treatment because of recurrent palpitations. She had a lifetime history of comorbid generalized anxiety disorder and migraines. But she showed no change from baseline in any cardiovascular measurement, and her primary care physician did not find her complaints to be consistent with cardiac disease. She later used a different stimulant medication with no subsequent cardiovascular symptoms.

“The FDA continues to review and still concludes that the overall risk-benefit ratio supports the use of stimulant medications for ADHD,” Dr. Hammerness said. But he did recommend that clinicians carefully evaluate an adolescent's cardiovascular symptoms and family history before prescribing stimulants.

In particular, clinicians should be alert for a family history of cardiovascular disease at a young age, such as QT syndrome, cardiomyopathy, or perhaps a cousin who died suddenly during exercise.

Electrocardiograms are not mandatory, although Dr. Hammerness said clinicians may consider them as part of a general premedication evaluation or during treatment.

Disclosures: Dr. Hammerness acknowledged serving as a speaker for, receiving research funds from, or participating in CME activities and research studies funded by several pharmaceutical companies, including McNeil, which sponsored this study and which markets OROS methylphenidate under the brand name Concerta.

HONOLULU — High-dose OROS methylphenidate was associated with small but statistically significant increases in systolic blood pressure and heart rate in a 6-month, open-label study in adolescents.

The study found no significant long-term increases in diastolic blood pressure or in electrocardiographic measures, Dr. Paul Hammerness said at the annual meeting of the American Academy of Child and Adolescent Psychiatry.

The findings are consistent with studies involving younger children and lower doses, said Dr. Hammerness of Massachusetts General Hospital and Harvard Medical School, Boston.

Because of concerns about possible associations between stimulant medications for ADHD and cardiovascular complications—including sudden cardiac death—the Food and Drug Administration in June 2009 recommended that physicians pay special attention to a child's cardiovascular system when prescribing stimulants.

The study involved 114 adolescents with a mean age of 14 years at baseline (range 12-18 years). All were healthy, and all had a diagnosis of ADHD based on full DSM-IV criteria. The researchers analyzed data taken from an ongoing trial of OROS methylphenidate for the prevention of cigarette smoking in adolescents with ADHD (J. Pediatr. 2009;155:84-9).

Participants were excluded if they had a history of cardiovascular disease or had untreated mood or anxiety disorders, eating disorders, psychosis, or substance use disorders.

The beginning dose of OROS methylphenidate was 0.5-0.75 mg/kg per day, and that was titrated upward to a maximum of 1.5 mg/kg per day by week 3. At week 6, the mean total daily dose was 63 mg, and 50% of the participants were taking 72 mg or more.

As expected, OROS methylphenidate was highly effective in treating the participants' ADHD. Their Rating Scale scores declined from a mean of 26.9 at baseline to 9.7 at week 6.

Of the 114 participants who entered the study, 73% were male. Mean systolic blood pressure at baseline was 113 mm Hg, and that increased to 117 mm Hg at 6 months, a significant increase. Mean diastolic blood pressure began at 63 mm Hg, increased significantly to 65 mm Hg at week 6, but then returned to 64 mm Hg at 6 months. Mean heart rate began at 82 beats per minute, increased significantly to 86 beats per minute at week 6, and remained at about that rate at 6 months.

The investigators found no statistically significant or clinically meaningful changes in ECG variables, including PR, QRS, or QTC.

Reasoning that any adverse cardiovascular effects of OROS methylphenidate might be restricted to certain subsets of adolescents, the investigators separately analyzed those 16 participants who met criteria for prehypertension or hypertension at baseline, based on at least one blood pressure reading above the 90th or 95th percentile. The investigators found no impact of abnormal premedication blood pressure readings on blood pressure changes during treatment.

Participants experienced no serious adverse events or serious cardiovascular adverse events during the study. Ten of the 114 subjects reported one or more subjective cardiovascular complaints, including palpitations, chest pain, and fast or racing heartbeat. Of those, six had a lifetime diagnosis of comorbid anxiety disorder.

One participant discontinued treatment because of recurrent palpitations. She had a lifetime history of comorbid generalized anxiety disorder and migraines. But she showed no change from baseline in any cardiovascular measurement, and her primary care physician did not find her complaints to be consistent with cardiac disease. She later used a different stimulant medication with no subsequent cardiovascular symptoms.

“The FDA continues to review and still concludes that the overall risk-benefit ratio supports the use of stimulant medications for ADHD,” Dr. Hammerness said. But he did recommend that clinicians carefully evaluate an adolescent's cardiovascular symptoms and family history before prescribing stimulants.

In particular, clinicians should be alert for a family history of cardiovascular disease at a young age, such as QT syndrome, cardiomyopathy, or perhaps a cousin who died suddenly during exercise.

Electrocardiograms are not mandatory, although Dr. Hammerness said clinicians may consider them as part of a general premedication evaluation or during treatment.

Disclosures: Dr. Hammerness acknowledged serving as a speaker for, receiving research funds from, or participating in CME activities and research studies funded by several pharmaceutical companies, including McNeil, which sponsored this study and which markets OROS methylphenidate under the brand name Concerta.

An extremely simple device that tests an athlete's reaction time is showing promise in diagnosing concussions, according to a study announced in advance of its scheduled presentation at the annual meeting of the American Academy of Neurology.

Seven of eight Division I athletes who had suffered a concussion showed significantly slowed reaction times when tested with the device, Dr. James T. Eckner said in an interview.

“It's actually very similar to an experiment that's done commonly in physics classrooms in high schools,” said Dr. Eckner, of the department of physical medicine and rehabilitation at the University of Michigan, Ann Arbor. In that experiment, reaction times are judged by the speed with which people can catch a ruler dropped between their fingers.

The device “is a fancier ruler, essentially,” he said. “It's basically a dowel rod that we've coated in friction tape, and we've marked it in centimeter increments. And then at the base of it there's a little rubber disc, which is actually a hockey puck that it's embedded in.”

The device is so simple that it has the potential of being used on the sidelines of a football game. The person being tested sits with his or her forearm resting on a table. The person administering the test holds the device so that the subject's hand is encircling, but not touching, the hockey puck. At a random moment the tester drops the device, and the subject catches it as soon as he or she can.

“We measure then how many centimeters it fell before they caught it, and then we use a simple physics equation for a body falling under the influence of gravity to convert that into how many milliseconds it fell for,” Dr. Eckner said.

For the study, he and his colleagues recruited 209 members of Division I football, wrestling, and soccer teams. Before the start of the season the researchers measured each athlete's normal baseline reaction time. The eight athletes who suffered physician-diagnosed concussions during the season were tested with the device within 72 hours of their injury.

Seven of the eight athletes showed significant slowing of reaction. Their average reaction time increased from 193 milliseconds at the start of the season to 222 milliseconds after their injuries, a statistically significant difference. In practice, a 10%–15% increase in the length of reaction time might clinically significant, Dr. Eckley said.

“Our results are still a little bit preliminary,” he added. “We've done some preliminary reliability data showing the inter-tester reliability and the test-retest reliability. But we do want to do that in a bigger sample to firm up the numbers that we have so far…. Once we've done that I think that it would be reasonable to begin using it in a clinical setting.”

Meanwhile, the investigators have developed a fancier version of the device, and they're applying for a patent.

Disclosures: The Foundation for Physical Medicine and Rehabilitation and the University of Michigan supported the study.

Dr. James T. Eckner (standing) demonstrates how a simple ruler-like device is dropped to measure reaction times in athletes who are suspected of having a concussion.

Source Courtesy Dr. James T. Eckner

An extremely simple device that tests an athlete's reaction time is showing promise in diagnosing concussions, according to a study announced in advance of its scheduled presentation at the annual meeting of the American Academy of Neurology.

Seven of eight Division I athletes who had suffered a concussion showed significantly slowed reaction times when tested with the device, Dr. James T. Eckner said in an interview.

“It's actually very similar to an experiment that's done commonly in physics classrooms in high schools,” said Dr. Eckner, of the department of physical medicine and rehabilitation at the University of Michigan, Ann Arbor. In that experiment, reaction times are judged by the speed with which people can catch a ruler dropped between their fingers.

The device “is a fancier ruler, essentially,” he said. “It's basically a dowel rod that we've coated in friction tape, and we've marked it in centimeter increments. And then at the base of it there's a little rubber disc, which is actually a hockey puck that it's embedded in.”

The device is so simple that it has the potential of being used on the sidelines of a football game. The person being tested sits with his or her forearm resting on a table. The person administering the test holds the device so that the subject's hand is encircling, but not touching, the hockey puck. At a random moment the tester drops the device, and the subject catches it as soon as he or she can.

“We measure then how many centimeters it fell before they caught it, and then we use a simple physics equation for a body falling under the influence of gravity to convert that into how many milliseconds it fell for,” Dr. Eckner said.

For the study, he and his colleagues recruited 209 members of Division I football, wrestling, and soccer teams. Before the start of the season the researchers measured each athlete's normal baseline reaction time. The eight athletes who suffered physician-diagnosed concussions during the season were tested with the device within 72 hours of their injury.

Seven of the eight athletes showed significant slowing of reaction. Their average reaction time increased from 193 milliseconds at the start of the season to 222 milliseconds after their injuries, a statistically significant difference. In practice, a 10%–15% increase in the length of reaction time might clinically significant, Dr. Eckley said.

“Our results are still a little bit preliminary,” he added. “We've done some preliminary reliability data showing the inter-tester reliability and the test-retest reliability. But we do want to do that in a bigger sample to firm up the numbers that we have so far…. Once we've done that I think that it would be reasonable to begin using it in a clinical setting.”

Meanwhile, the investigators have developed a fancier version of the device, and they're applying for a patent.

Disclosures: The Foundation for Physical Medicine and Rehabilitation and the University of Michigan supported the study.

Dr. James T. Eckner (standing) demonstrates how a simple ruler-like device is dropped to measure reaction times in athletes who are suspected of having a concussion.

Source Courtesy Dr. James T. Eckner

An extremely simple device that tests an athlete's reaction time is showing promise in diagnosing concussions, according to a study announced in advance of its scheduled presentation at the annual meeting of the American Academy of Neurology.

Seven of eight Division I athletes who had suffered a concussion showed significantly slowed reaction times when tested with the device, Dr. James T. Eckner said in an interview.

“It's actually very similar to an experiment that's done commonly in physics classrooms in high schools,” said Dr. Eckner, of the department of physical medicine and rehabilitation at the University of Michigan, Ann Arbor. In that experiment, reaction times are judged by the speed with which people can catch a ruler dropped between their fingers.

The device “is a fancier ruler, essentially,” he said. “It's basically a dowel rod that we've coated in friction tape, and we've marked it in centimeter increments. And then at the base of it there's a little rubber disc, which is actually a hockey puck that it's embedded in.”

The device is so simple that it has the potential of being used on the sidelines of a football game. The person being tested sits with his or her forearm resting on a table. The person administering the test holds the device so that the subject's hand is encircling, but not touching, the hockey puck. At a random moment the tester drops the device, and the subject catches it as soon as he or she can.

“We measure then how many centimeters it fell before they caught it, and then we use a simple physics equation for a body falling under the influence of gravity to convert that into how many milliseconds it fell for,” Dr. Eckner said.

For the study, he and his colleagues recruited 209 members of Division I football, wrestling, and soccer teams. Before the start of the season the researchers measured each athlete's normal baseline reaction time. The eight athletes who suffered physician-diagnosed concussions during the season were tested with the device within 72 hours of their injury.

Seven of the eight athletes showed significant slowing of reaction. Their average reaction time increased from 193 milliseconds at the start of the season to 222 milliseconds after their injuries, a statistically significant difference. In practice, a 10%–15% increase in the length of reaction time might clinically significant, Dr. Eckley said.

“Our results are still a little bit preliminary,” he added. “We've done some preliminary reliability data showing the inter-tester reliability and the test-retest reliability. But we do want to do that in a bigger sample to firm up the numbers that we have so far…. Once we've done that I think that it would be reasonable to begin using it in a clinical setting.”

Meanwhile, the investigators have developed a fancier version of the device, and they're applying for a patent.

Disclosures: The Foundation for Physical Medicine and Rehabilitation and the University of Michigan supported the study.

Dr. James T. Eckner (standing) demonstrates how a simple ruler-like device is dropped to measure reaction times in athletes who are suspected of having a concussion.

Source Courtesy Dr. James T. Eckner

SAN FRANCISCO — The increase in the consumption of sugar-sweetened beverages between 1990 and 2000 contributed to 130,000 new cases of diabetes and 14,000 new cases of coronary heart disease between 2000 and 2010, according to estimates from a computer model of the U.S. population.

In addition, the rising consumption of sugar-sweetened beverages, which include soda, sports drinks, and fruit drinks, led to an estimated 1.4 million additional life-years burdened by diabetes and 50,000 additional life-years burdened by coronary heart disease in the first decade of the 21st century.

To derive those estimates, Dr. Litsa K. Lambrakos of the University of California, San Francisco, and her colleagues used data from the 1990-2000 National Health and Nutrition Examination Survey (NHANES) on consumption of sugar-sweetened beverages. She combined that with the Coronary Heart Disease Policy Model, a computer simulation of heart disease in U.S. adults aged 35-84 years.

According to that model, the relative risk of incident diabetes related to the daily consumption of sugar-sweetened beverages was 1.32 after adjusting for body mass index. Dr. Lambrakos presented the findings during a poster session at a conference sponsored by the American Heart Association.

The estimated increase in coronary heart disease related to the increased consumption of sugar-sweetened beverages would have generated an additional $300-$500 million in health care costs between 2000 and 2010.

“Those numbers about excess health care costs are very conservative, because they only account for health care costs attributed to coronary heart disease,” Dr. Lambrakos said in an interview. “We know we have an increase in diabetes as well that we can attribute to soft drink consumption. And those costs—the cost of caring for and treating patients with diabetes—is a very large number as well.”

The investigators also analyzed how a 1 cent per ounce tax on sugar-sweetened beverages might have limited coronary heart disease costs, had it been implemented in the year 2000. Based on economic studies, the computer model assumed that such a tax would decrease consumption by 10%. This would translate to a savings of $170 million in health care costs over 10 years.

Commenting on the findings, the American Heart Association issued a statement that it “acknowledges the importance of limiting intake of added sugars, including sugar-sweetened beverages. The association is still evaluating the research to determine which strategies accomplish this best, comparing more punitive strategies like taxation with more positive incentives like subsidies or lowering prices for healthy foods…. Robust evaluation should be part of any tax measures that are passed and advocates for broader nutrition policy efforts that make healthy foods more affordable and accessible to all consumers and bring food pricing and subsidies in line with federal dietary guidelines and AHA nutrition recommendations.”

Asked what message primary care physicians should take from the findings, Dr. Lambrakos said that “what we're talking about here is primary prevention…. It's important for the general public and physicians to understand that these drinks may lead to adverse health outcomes over time, and that they really shouldn't be considered a staple of the American diet.”

SAN FRANCISCO — The increase in the consumption of sugar-sweetened beverages between 1990 and 2000 contributed to 130,000 new cases of diabetes and 14,000 new cases of coronary heart disease between 2000 and 2010, according to estimates from a computer model of the U.S. population.

In addition, the rising consumption of sugar-sweetened beverages, which include soda, sports drinks, and fruit drinks, led to an estimated 1.4 million additional life-years burdened by diabetes and 50,000 additional life-years burdened by coronary heart disease in the first decade of the 21st century.

To derive those estimates, Dr. Litsa K. Lambrakos of the University of California, San Francisco, and her colleagues used data from the 1990-2000 National Health and Nutrition Examination Survey (NHANES) on consumption of sugar-sweetened beverages. She combined that with the Coronary Heart Disease Policy Model, a computer simulation of heart disease in U.S. adults aged 35-84 years.

According to that model, the relative risk of incident diabetes related to the daily consumption of sugar-sweetened beverages was 1.32 after adjusting for body mass index. Dr. Lambrakos presented the findings during a poster session at a conference sponsored by the American Heart Association.

The estimated increase in coronary heart disease related to the increased consumption of sugar-sweetened beverages would have generated an additional $300-$500 million in health care costs between 2000 and 2010.

“Those numbers about excess health care costs are very conservative, because they only account for health care costs attributed to coronary heart disease,” Dr. Lambrakos said in an interview. “We know we have an increase in diabetes as well that we can attribute to soft drink consumption. And those costs—the cost of caring for and treating patients with diabetes—is a very large number as well.”

The investigators also analyzed how a 1 cent per ounce tax on sugar-sweetened beverages might have limited coronary heart disease costs, had it been implemented in the year 2000. Based on economic studies, the computer model assumed that such a tax would decrease consumption by 10%. This would translate to a savings of $170 million in health care costs over 10 years.

Commenting on the findings, the American Heart Association issued a statement that it “acknowledges the importance of limiting intake of added sugars, including sugar-sweetened beverages. The association is still evaluating the research to determine which strategies accomplish this best, comparing more punitive strategies like taxation with more positive incentives like subsidies or lowering prices for healthy foods…. Robust evaluation should be part of any tax measures that are passed and advocates for broader nutrition policy efforts that make healthy foods more affordable and accessible to all consumers and bring food pricing and subsidies in line with federal dietary guidelines and AHA nutrition recommendations.”

Asked what message primary care physicians should take from the findings, Dr. Lambrakos said that “what we're talking about here is primary prevention…. It's important for the general public and physicians to understand that these drinks may lead to adverse health outcomes over time, and that they really shouldn't be considered a staple of the American diet.”

SAN FRANCISCO — The increase in the consumption of sugar-sweetened beverages between 1990 and 2000 contributed to 130,000 new cases of diabetes and 14,000 new cases of coronary heart disease between 2000 and 2010, according to estimates from a computer model of the U.S. population.

In addition, the rising consumption of sugar-sweetened beverages, which include soda, sports drinks, and fruit drinks, led to an estimated 1.4 million additional life-years burdened by diabetes and 50,000 additional life-years burdened by coronary heart disease in the first decade of the 21st century.

To derive those estimates, Dr. Litsa K. Lambrakos of the University of California, San Francisco, and her colleagues used data from the 1990-2000 National Health and Nutrition Examination Survey (NHANES) on consumption of sugar-sweetened beverages. She combined that with the Coronary Heart Disease Policy Model, a computer simulation of heart disease in U.S. adults aged 35-84 years.

According to that model, the relative risk of incident diabetes related to the daily consumption of sugar-sweetened beverages was 1.32 after adjusting for body mass index. Dr. Lambrakos presented the findings during a poster session at a conference sponsored by the American Heart Association.

The estimated increase in coronary heart disease related to the increased consumption of sugar-sweetened beverages would have generated an additional $300-$500 million in health care costs between 2000 and 2010.

“Those numbers about excess health care costs are very conservative, because they only account for health care costs attributed to coronary heart disease,” Dr. Lambrakos said in an interview. “We know we have an increase in diabetes as well that we can attribute to soft drink consumption. And those costs—the cost of caring for and treating patients with diabetes—is a very large number as well.”

The investigators also analyzed how a 1 cent per ounce tax on sugar-sweetened beverages might have limited coronary heart disease costs, had it been implemented in the year 2000. Based on economic studies, the computer model assumed that such a tax would decrease consumption by 10%. This would translate to a savings of $170 million in health care costs over 10 years.

Commenting on the findings, the American Heart Association issued a statement that it “acknowledges the importance of limiting intake of added sugars, including sugar-sweetened beverages. The association is still evaluating the research to determine which strategies accomplish this best, comparing more punitive strategies like taxation with more positive incentives like subsidies or lowering prices for healthy foods…. Robust evaluation should be part of any tax measures that are passed and advocates for broader nutrition policy efforts that make healthy foods more affordable and accessible to all consumers and bring food pricing and subsidies in line with federal dietary guidelines and AHA nutrition recommendations.”

Asked what message primary care physicians should take from the findings, Dr. Lambrakos said that “what we're talking about here is primary prevention…. It's important for the general public and physicians to understand that these drinks may lead to adverse health outcomes over time, and that they really shouldn't be considered a staple of the American diet.”

Major Finding: There was no significant difference between pregnant women who received treatment for periodontal disease and those who did not in terms of spontaneous preterm birth, gestational age at birth, or major neonatal adverse outcomes.

Data Source: Randomized, controlled trial of 756 pregnant women with periodontal disease.

Disclosures: The study was supported by the Pennsylvania Department of Health, the National Center for Research Resources, and the National Center on Minority and Health Disparities. No conflicts of interest were reported.

Treating periodontal disease in pregnant women does not decrease their chances of preterm birth, according to a study of 756 women.

Several previous studies have found that pregnant women with periodontal disease have an increased likelihood of giving birth prematurely.

But this was the first study to use a randomized controlled trial to test the idea that treating periodontal disease may improve a woman's chances of carrying her pregnancy to term.

Periodontal disease is very common, affecting more than 30% of individuals in some populations. The investigators, led by Dr. George A. Macones of Washington University in St. Louis found that 50% of the 3,563 pregnant women they screened had either gingivitis or periodontitis (Am. J. Obstet. Gynecol. 2010;202:147.e1-8).

Women were included in the study if they had periodontal disease and were 6–20 weeks pregnant. They were excluded if they had already received periodontal treatment during their pregnancy, if they had used antibiotics or antibiotic mouthwash within 2 weeks, if they had a multiple pregnancy, or if they had known mitral valve prolapse.

The 376 women in the active treatment group received thorough periodontal treatment, in which trained dental hygienists removed stains, plaque, and calculus above and below the gum line, leaving the root surfaces smooth and clean. The 380 women in the control group received only a superficial cleaning and stain removal above the gum line.

The primary outcome was spontaneous preterm birth, which the investigators defined as births occurring before 35 weeks' gestation.

Secondary outcomes included the type of preterm birth (either spontaneous or indicated), delivery before 37 weeks' gestation, gestational age at delivery, birth weight, and major neonatal adverse outcomes, such as death, sepsis, and chronic lung disease.

There were no significant differences between active treatment and control groups on any of these measures. Investigators did, however, find one significant difference within the planned subgroup analyses: Among women with a history of previous preterm birth, those in the active treatment arm had a greater risk of preterm birth than those in the control treatment arm.

The investigators suggested that this one statistically significant result among many results that were not significant may have arisen by chance.

In an accompanying editorial, Dr. Kim A. Boggess of the University of North Carolina at Chapel Hill offered another possibility. Dr. Boggess suggested that scaling and root planing may have disseminated oral pathogens or their toxins to the rest of the body, accounting for the apparently increased risk of active treatment in this one subgroup of women (Am. J. Obstet. Gynecol. 2010;202:101-2).

Regarding the idea of treating pregnant women for periodontal disease, Dr. Boggess wrote: “Although promising, the current data do not support periodontal treatment during pregnancy to reduce the preterm birth risk.”

However, she also said that the trial “confirmed that periodontal treatment improves the oral health of pregnant women, and oral health for the sake of oral health cannot be disputed.”

Major Finding: There was no significant difference between pregnant women who received treatment for periodontal disease and those who did not in terms of spontaneous preterm birth, gestational age at birth, or major neonatal adverse outcomes.

Data Source: Randomized, controlled trial of 756 pregnant women with periodontal disease.

Disclosures: The study was supported by the Pennsylvania Department of Health, the National Center for Research Resources, and the National Center on Minority and Health Disparities. No conflicts of interest were reported.

Treating periodontal disease in pregnant women does not decrease their chances of preterm birth, according to a study of 756 women.

Several previous studies have found that pregnant women with periodontal disease have an increased likelihood of giving birth prematurely.

But this was the first study to use a randomized controlled trial to test the idea that treating periodontal disease may improve a woman's chances of carrying her pregnancy to term.

Periodontal disease is very common, affecting more than 30% of individuals in some populations. The investigators, led by Dr. George A. Macones of Washington University in St. Louis found that 50% of the 3,563 pregnant women they screened had either gingivitis or periodontitis (Am. J. Obstet. Gynecol. 2010;202:147.e1-8).

Women were included in the study if they had periodontal disease and were 6–20 weeks pregnant. They were excluded if they had already received periodontal treatment during their pregnancy, if they had used antibiotics or antibiotic mouthwash within 2 weeks, if they had a multiple pregnancy, or if they had known mitral valve prolapse.

The 376 women in the active treatment group received thorough periodontal treatment, in which trained dental hygienists removed stains, plaque, and calculus above and below the gum line, leaving the root surfaces smooth and clean. The 380 women in the control group received only a superficial cleaning and stain removal above the gum line.

The primary outcome was spontaneous preterm birth, which the investigators defined as births occurring before 35 weeks' gestation.

Secondary outcomes included the type of preterm birth (either spontaneous or indicated), delivery before 37 weeks' gestation, gestational age at delivery, birth weight, and major neonatal adverse outcomes, such as death, sepsis, and chronic lung disease.

There were no significant differences between active treatment and control groups on any of these measures. Investigators did, however, find one significant difference within the planned subgroup analyses: Among women with a history of previous preterm birth, those in the active treatment arm had a greater risk of preterm birth than those in the control treatment arm.

The investigators suggested that this one statistically significant result among many results that were not significant may have arisen by chance.

In an accompanying editorial, Dr. Kim A. Boggess of the University of North Carolina at Chapel Hill offered another possibility. Dr. Boggess suggested that scaling and root planing may have disseminated oral pathogens or their toxins to the rest of the body, accounting for the apparently increased risk of active treatment in this one subgroup of women (Am. J. Obstet. Gynecol. 2010;202:101-2).

Regarding the idea of treating pregnant women for periodontal disease, Dr. Boggess wrote: “Although promising, the current data do not support periodontal treatment during pregnancy to reduce the preterm birth risk.”

However, she also said that the trial “confirmed that periodontal treatment improves the oral health of pregnant women, and oral health for the sake of oral health cannot be disputed.”

Major Finding: There was no significant difference between pregnant women who received treatment for periodontal disease and those who did not in terms of spontaneous preterm birth, gestational age at birth, or major neonatal adverse outcomes.

Data Source: Randomized, controlled trial of 756 pregnant women with periodontal disease.

Disclosures: The study was supported by the Pennsylvania Department of Health, the National Center for Research Resources, and the National Center on Minority and Health Disparities. No conflicts of interest were reported.

Treating periodontal disease in pregnant women does not decrease their chances of preterm birth, according to a study of 756 women.

Several previous studies have found that pregnant women with periodontal disease have an increased likelihood of giving birth prematurely.

But this was the first study to use a randomized controlled trial to test the idea that treating periodontal disease may improve a woman's chances of carrying her pregnancy to term.

Periodontal disease is very common, affecting more than 30% of individuals in some populations. The investigators, led by Dr. George A. Macones of Washington University in St. Louis found that 50% of the 3,563 pregnant women they screened had either gingivitis or periodontitis (Am. J. Obstet. Gynecol. 2010;202:147.e1-8).

Women were included in the study if they had periodontal disease and were 6–20 weeks pregnant. They were excluded if they had already received periodontal treatment during their pregnancy, if they had used antibiotics or antibiotic mouthwash within 2 weeks, if they had a multiple pregnancy, or if they had known mitral valve prolapse.

The 376 women in the active treatment group received thorough periodontal treatment, in which trained dental hygienists removed stains, plaque, and calculus above and below the gum line, leaving the root surfaces smooth and clean. The 380 women in the control group received only a superficial cleaning and stain removal above the gum line.

The primary outcome was spontaneous preterm birth, which the investigators defined as births occurring before 35 weeks' gestation.

Secondary outcomes included the type of preterm birth (either spontaneous or indicated), delivery before 37 weeks' gestation, gestational age at delivery, birth weight, and major neonatal adverse outcomes, such as death, sepsis, and chronic lung disease.

There were no significant differences between active treatment and control groups on any of these measures. Investigators did, however, find one significant difference within the planned subgroup analyses: Among women with a history of previous preterm birth, those in the active treatment arm had a greater risk of preterm birth than those in the control treatment arm.

The investigators suggested that this one statistically significant result among many results that were not significant may have arisen by chance.

In an accompanying editorial, Dr. Kim A. Boggess of the University of North Carolina at Chapel Hill offered another possibility. Dr. Boggess suggested that scaling and root planing may have disseminated oral pathogens or their toxins to the rest of the body, accounting for the apparently increased risk of active treatment in this one subgroup of women (Am. J. Obstet. Gynecol. 2010;202:101-2).

Regarding the idea of treating pregnant women for periodontal disease, Dr. Boggess wrote: “Although promising, the current data do not support periodontal treatment during pregnancy to reduce the preterm birth risk.”

However, she also said that the trial “confirmed that periodontal treatment improves the oral health of pregnant women, and oral health for the sake of oral health cannot be disputed.”

Major Finding: The rates of teen pregnancy, birth, and abortion increased in 2006 after declining every year since 1990.

Data Source: Data compiled from national-level and state-level sources.

Disclosures: Preparation of the report was funded by the Brush Foundation, the California Wellness Foundation, and the Annie E. Casey Foundation.

Teen pregnancy rates increased 3% in the United States in 2006 after declining every year since 1990, according to a report from the Guttmacher Institute.

In addition, teen births rose 4% and teen abortions rose 1% between 2005 and 2006, according to the report, which the institute compiled from a variety of national and state-level sources.

The teen pregnancy rate hit its peak in 1990, with 117 pregnancies per 1,000 women aged 15–19 years. By 2005 it had declined 40%, to 70/1,000. But in 2006, the rate increased to 72/1,000.

“After more than a decade of progress, this reversal is deeply troubling,” Heather Boonstra, a senior public policy associate at the Guttmacher Institute, said in a prepared statement. “It coincides with an increase in rigid abstinence-only-until-marriage programs, which received major funding boosts under the Bush administration. A strong body of research shows that these programs do not work. Fortunately, the heyday of this failed experiment has come to an end with the enactment of a new teen pregnancy prevention initiative that ensures that programs will be age appropriate, medically accurate, and, most importantly, based on research demonstrating their effectiveness.”

Two experts interviewed by this news organization weren't so sure that the increase in pregnancy rates could be attributed to abstinence-only sex education. “The temporal association between the increase in abstinence-only programs and the increase in the pregnancy rate definitely deserves closer attention,” said Dr. Lee Savio Beers, a pediatrician who is director of the healthy generations clinic at Children's National Medical Center, Washington, D.C. “I don't know that anyone knows for sure whether it's directly related, but the two kind of came together. It's such a multifactorial issue that we may never have an answer on that.”

Dr. Melissa Kottke, who is with the department of ob.gyn. at Emory University and is director of the Jane Fonda Center for Adolescent Reproductive Health, both in Atlanta, said, “I think there's going to be a lot of things contributing to [increases in teen pregnancy rates], and I don't think we're going to know what all of those are.”

Dr. Kottke listed some of the other possibilities: teenage sexual activity, poverty, the media, parenting, funding for care, and funding for family planning services. “All of those things are going to contribute,” she said, “and I don't think we're going to be able to point our finger at one thing or the other.”

About the Guttmacher Institute, Dr. Beers said, “They're a well-respected organization. Their policy views tend to be on the liberal side. But I think everyone pretty much agrees that their facts are good, and their numbers are good, and for pregnancy numbers, they're better than pretty much anyone.”

Although the long decline and recent uptick in teen pregnancy rates were seen in blacks, Hispanics, and non-Hispanic whites, there were some substantial racial and ethic differences (see box). Among black teens, the pregnancy rate declined by 45%, from 224/1,000 in 1990 to 123/1,000 in 2005, and then increased 2.4%, to 126/1,000 in 2006.

Among Hispanic teens, the pregnancy rate declined by 26%, from 170/1,000 in 1992 to 125/1,000 in 2005, and then increased 1% to 127/1,000 in 2006.

And among non-Hispanic whites, the rate declined by 51%, from 87/1,000 in 1990 to 43/1,000 in 2005, and then increased 2% to 44/1,000 in 2006.

State-level data were not available for 2006, but in 2005 the highest teen pregnancy rates were in New Mexico (93/1,000), Nevada (90/1,000), and Arizona (89/1,000). The lowest rates were in New Hampshire (33/1,000), Vermont (49/1,000), and Maine (48/1,000).

Although there has been a long decline in the teen pregnancy rate in the United States, even at their low point in 2005, the U.S teen pregnancy, birth, and abortion rates were still way above those for all other developed nations, Dr. Beers said.

And Dr. Kottke said that there's already evidence that the 1-year uptick is not a statistical fluke. She's seen preliminary data for 2007 indicating that the increase in teen pregnancy, birth, and abortion rates increased for a second year.

Physicians have a unique opportunity to help turn these numbers around, she said. “What we know is that young people still trust their physicians, and they look to their physicians for important education. Physicians who are serving young teens need to make sure they are an avenue for education, for care, and for confidentiality.”

The full report is available at www.guttmacher.org/pubs/USTPtrends.pdf

Vitals

Source Elsevier Global Medical News

Major Finding: The rates of teen pregnancy, birth, and abortion increased in 2006 after declining every year since 1990.

Data Source: Data compiled from national-level and state-level sources.

Disclosures: Preparation of the report was funded by the Brush Foundation, the California Wellness Foundation, and the Annie E. Casey Foundation.

Teen pregnancy rates increased 3% in the United States in 2006 after declining every year since 1990, according to a report from the Guttmacher Institute.

In addition, teen births rose 4% and teen abortions rose 1% between 2005 and 2006, according to the report, which the institute compiled from a variety of national and state-level sources.

The teen pregnancy rate hit its peak in 1990, with 117 pregnancies per 1,000 women aged 15–19 years. By 2005 it had declined 40%, to 70/1,000. But in 2006, the rate increased to 72/1,000.

“After more than a decade of progress, this reversal is deeply troubling,” Heather Boonstra, a senior public policy associate at the Guttmacher Institute, said in a prepared statement. “It coincides with an increase in rigid abstinence-only-until-marriage programs, which received major funding boosts under the Bush administration. A strong body of research shows that these programs do not work. Fortunately, the heyday of this failed experiment has come to an end with the enactment of a new teen pregnancy prevention initiative that ensures that programs will be age appropriate, medically accurate, and, most importantly, based on research demonstrating their effectiveness.”

Two experts interviewed by this news organization weren't so sure that the increase in pregnancy rates could be attributed to abstinence-only sex education. “The temporal association between the increase in abstinence-only programs and the increase in the pregnancy rate definitely deserves closer attention,” said Dr. Lee Savio Beers, a pediatrician who is director of the healthy generations clinic at Children's National Medical Center, Washington, D.C. “I don't know that anyone knows for sure whether it's directly related, but the two kind of came together. It's such a multifactorial issue that we may never have an answer on that.”

Dr. Melissa Kottke, who is with the department of ob.gyn. at Emory University and is director of the Jane Fonda Center for Adolescent Reproductive Health, both in Atlanta, said, “I think there's going to be a lot of things contributing to [increases in teen pregnancy rates], and I don't think we're going to know what all of those are.”

Dr. Kottke listed some of the other possibilities: teenage sexual activity, poverty, the media, parenting, funding for care, and funding for family planning services. “All of those things are going to contribute,” she said, “and I don't think we're going to be able to point our finger at one thing or the other.”

About the Guttmacher Institute, Dr. Beers said, “They're a well-respected organization. Their policy views tend to be on the liberal side. But I think everyone pretty much agrees that their facts are good, and their numbers are good, and for pregnancy numbers, they're better than pretty much anyone.”

Although the long decline and recent uptick in teen pregnancy rates were seen in blacks, Hispanics, and non-Hispanic whites, there were some substantial racial and ethic differences (see box). Among black teens, the pregnancy rate declined by 45%, from 224/1,000 in 1990 to 123/1,000 in 2005, and then increased 2.4%, to 126/1,000 in 2006.

Among Hispanic teens, the pregnancy rate declined by 26%, from 170/1,000 in 1992 to 125/1,000 in 2005, and then increased 1% to 127/1,000 in 2006.

And among non-Hispanic whites, the rate declined by 51%, from 87/1,000 in 1990 to 43/1,000 in 2005, and then increased 2% to 44/1,000 in 2006.

State-level data were not available for 2006, but in 2005 the highest teen pregnancy rates were in New Mexico (93/1,000), Nevada (90/1,000), and Arizona (89/1,000). The lowest rates were in New Hampshire (33/1,000), Vermont (49/1,000), and Maine (48/1,000).

Although there has been a long decline in the teen pregnancy rate in the United States, even at their low point in 2005, the U.S teen pregnancy, birth, and abortion rates were still way above those for all other developed nations, Dr. Beers said.

And Dr. Kottke said that there's already evidence that the 1-year uptick is not a statistical fluke. She's seen preliminary data for 2007 indicating that the increase in teen pregnancy, birth, and abortion rates increased for a second year.

Physicians have a unique opportunity to help turn these numbers around, she said. “What we know is that young people still trust their physicians, and they look to their physicians for important education. Physicians who are serving young teens need to make sure they are an avenue for education, for care, and for confidentiality.”

The full report is available at www.guttmacher.org/pubs/USTPtrends.pdf

Vitals

Source Elsevier Global Medical News

Major Finding: The rates of teen pregnancy, birth, and abortion increased in 2006 after declining every year since 1990.

Data Source: Data compiled from national-level and state-level sources.

Disclosures: Preparation of the report was funded by the Brush Foundation, the California Wellness Foundation, and the Annie E. Casey Foundation.

Teen pregnancy rates increased 3% in the United States in 2006 after declining every year since 1990, according to a report from the Guttmacher Institute.

In addition, teen births rose 4% and teen abortions rose 1% between 2005 and 2006, according to the report, which the institute compiled from a variety of national and state-level sources.

The teen pregnancy rate hit its peak in 1990, with 117 pregnancies per 1,000 women aged 15–19 years. By 2005 it had declined 40%, to 70/1,000. But in 2006, the rate increased to 72/1,000.

“After more than a decade of progress, this reversal is deeply troubling,” Heather Boonstra, a senior public policy associate at the Guttmacher Institute, said in a prepared statement. “It coincides with an increase in rigid abstinence-only-until-marriage programs, which received major funding boosts under the Bush administration. A strong body of research shows that these programs do not work. Fortunately, the heyday of this failed experiment has come to an end with the enactment of a new teen pregnancy prevention initiative that ensures that programs will be age appropriate, medically accurate, and, most importantly, based on research demonstrating their effectiveness.”

Two experts interviewed by this news organization weren't so sure that the increase in pregnancy rates could be attributed to abstinence-only sex education. “The temporal association between the increase in abstinence-only programs and the increase in the pregnancy rate definitely deserves closer attention,” said Dr. Lee Savio Beers, a pediatrician who is director of the healthy generations clinic at Children's National Medical Center, Washington, D.C. “I don't know that anyone knows for sure whether it's directly related, but the two kind of came together. It's such a multifactorial issue that we may never have an answer on that.”

Dr. Melissa Kottke, who is with the department of ob.gyn. at Emory University and is director of the Jane Fonda Center for Adolescent Reproductive Health, both in Atlanta, said, “I think there's going to be a lot of things contributing to [increases in teen pregnancy rates], and I don't think we're going to know what all of those are.”

Dr. Kottke listed some of the other possibilities: teenage sexual activity, poverty, the media, parenting, funding for care, and funding for family planning services. “All of those things are going to contribute,” she said, “and I don't think we're going to be able to point our finger at one thing or the other.”

About the Guttmacher Institute, Dr. Beers said, “They're a well-respected organization. Their policy views tend to be on the liberal side. But I think everyone pretty much agrees that their facts are good, and their numbers are good, and for pregnancy numbers, they're better than pretty much anyone.”

Although the long decline and recent uptick in teen pregnancy rates were seen in blacks, Hispanics, and non-Hispanic whites, there were some substantial racial and ethic differences (see box). Among black teens, the pregnancy rate declined by 45%, from 224/1,000 in 1990 to 123/1,000 in 2005, and then increased 2.4%, to 126/1,000 in 2006.

Among Hispanic teens, the pregnancy rate declined by 26%, from 170/1,000 in 1992 to 125/1,000 in 2005, and then increased 1% to 127/1,000 in 2006.

And among non-Hispanic whites, the rate declined by 51%, from 87/1,000 in 1990 to 43/1,000 in 2005, and then increased 2% to 44/1,000 in 2006.

State-level data were not available for 2006, but in 2005 the highest teen pregnancy rates were in New Mexico (93/1,000), Nevada (90/1,000), and Arizona (89/1,000). The lowest rates were in New Hampshire (33/1,000), Vermont (49/1,000), and Maine (48/1,000).

Although there has been a long decline in the teen pregnancy rate in the United States, even at their low point in 2005, the U.S teen pregnancy, birth, and abortion rates were still way above those for all other developed nations, Dr. Beers said.

And Dr. Kottke said that there's already evidence that the 1-year uptick is not a statistical fluke. She's seen preliminary data for 2007 indicating that the increase in teen pregnancy, birth, and abortion rates increased for a second year.

Physicians have a unique opportunity to help turn these numbers around, she said. “What we know is that young people still trust their physicians, and they look to their physicians for important education. Physicians who are serving young teens need to make sure they are an avenue for education, for care, and for confidentiality.”

The full report is available at www.guttmacher.org/pubs/USTPtrends.pdf

Vitals

Source Elsevier Global Medical News

Algorithms based on common laboratory values outperformed expensive metabolite testing in determining which patients with inflammatory bowel disease are likely to respond to thiopurine therapy, Dr. Akbar K. Waljee and his colleagues reported.

Thiopurines are known to be effective immunomodulators in patients with inflammatory bowel disease (IBD) who have failed 5-aminosalicylic acid therapy. The problem is that thiopurines have a narrow therapeutic index, and individuals vary widely in how they metabolize these agents.

Experienced clinicians can use inexpensive complete blood count and standard blood chemistry values to balance efficacy and risk in individual patients, but this takes expert judgment, and there are no established algorithms.

A more reproducible approach is to measure the metabolites 6-thioguanine (6-TGN) and 6 methylmercaptopurine (6-MMP). Unfortunately, monitoring these metabolites is expensive, and the sensitivity and specificity of this approach are only 62% and 72%, respectively.

In an effort to resolve this dilemma, Dr. Waljee and his colleagues from the University of Michigan, Ann Arbor, used a machine learning technique to tease out the most accurate algorithms based on CBC and blood chemistries (Clin. Gastroenterol. Hepatol. 2010 [doi:10.1016/j.cgh.2009.09.031]).

The investigators used data collected in 774 cases from 346 individuals who were seen at the University of Michigan between May 2004 and August 2006. To be included in the study, the patients had to have had thiopurine metabolite analysis, CBC, and a comprehensive chemistry panel within the same 24-hour period.

Using a randomly selected 70% of the cases, investigators used a statistical technique called the “random forest” method to derive the most accurate algorithms based on data from the CBC and chemistry panels. They then tested that algorithm on the remaining 30% of the cases, comparing the accuracy to that of thiopurine metabolite analysis.

Their primary outcome measure was the area under the receiver operating characteristic curve (AuROC), a standard measure of accuracy.

The random forest algorithm differentiated clinical response from nonresponse with an AuROC of 0.856, compared with 0.594, for 6-TGN levels, a difference that was highly statistically significant.

The most important independent variables in differentiating responders from nonresponders were neutrophil count, alkaline phosphatase, red-cell distribution width, age, and white blood cell count.

The investigators also derived a random forest algorithm that would predict patient nonadherence, and another that would predict which patients were likely to have unfavorable pharmacodynamic responses to thiopurine therapy. Both of those algorithms proved to be significantly better than thiopurine metabolite analysis.

They also developed a simple prediction rule that was reasonably accurate at differentiating responders from nonresponders. Patients with a ratio of mean corpuscular volume (MCV) to white blood cell count (WBC) of 12 or more had a 67% likelihood of having a clinical response, while those with a ratio less than 12 had a 35% likelihood of having a clinical response. This simplified algorithm was significantly worse than the more complex algorithm, but it was still significantly better than metabolite analysis.

The investigators disclosed that the Regents of the University of Michigan, along with several of the study's coauthors, have applied for a patent on the application of machine learning to the prediction of clinical response to thiopurines.

Algorithms based on common laboratory values outperformed expensive metabolite testing in determining which patients with inflammatory bowel disease are likely to respond to thiopurine therapy, Dr. Akbar K. Waljee and his colleagues reported.

Thiopurines are known to be effective immunomodulators in patients with inflammatory bowel disease (IBD) who have failed 5-aminosalicylic acid therapy. The problem is that thiopurines have a narrow therapeutic index, and individuals vary widely in how they metabolize these agents.

Experienced clinicians can use inexpensive complete blood count and standard blood chemistry values to balance efficacy and risk in individual patients, but this takes expert judgment, and there are no established algorithms.

A more reproducible approach is to measure the metabolites 6-thioguanine (6-TGN) and 6 methylmercaptopurine (6-MMP). Unfortunately, monitoring these metabolites is expensive, and the sensitivity and specificity of this approach are only 62% and 72%, respectively.

In an effort to resolve this dilemma, Dr. Waljee and his colleagues from the University of Michigan, Ann Arbor, used a machine learning technique to tease out the most accurate algorithms based on CBC and blood chemistries (Clin. Gastroenterol. Hepatol. 2010 [doi:10.1016/j.cgh.2009.09.031]).

The investigators used data collected in 774 cases from 346 individuals who were seen at the University of Michigan between May 2004 and August 2006. To be included in the study, the patients had to have had thiopurine metabolite analysis, CBC, and a comprehensive chemistry panel within the same 24-hour period.

Using a randomly selected 70% of the cases, investigators used a statistical technique called the “random forest” method to derive the most accurate algorithms based on data from the CBC and chemistry panels. They then tested that algorithm on the remaining 30% of the cases, comparing the accuracy to that of thiopurine metabolite analysis.

Their primary outcome measure was the area under the receiver operating characteristic curve (AuROC), a standard measure of accuracy.

The random forest algorithm differentiated clinical response from nonresponse with an AuROC of 0.856, compared with 0.594, for 6-TGN levels, a difference that was highly statistically significant.

The most important independent variables in differentiating responders from nonresponders were neutrophil count, alkaline phosphatase, red-cell distribution width, age, and white blood cell count.

The investigators also derived a random forest algorithm that would predict patient nonadherence, and another that would predict which patients were likely to have unfavorable pharmacodynamic responses to thiopurine therapy. Both of those algorithms proved to be significantly better than thiopurine metabolite analysis.

They also developed a simple prediction rule that was reasonably accurate at differentiating responders from nonresponders. Patients with a ratio of mean corpuscular volume (MCV) to white blood cell count (WBC) of 12 or more had a 67% likelihood of having a clinical response, while those with a ratio less than 12 had a 35% likelihood of having a clinical response. This simplified algorithm was significantly worse than the more complex algorithm, but it was still significantly better than metabolite analysis.

The investigators disclosed that the Regents of the University of Michigan, along with several of the study's coauthors, have applied for a patent on the application of machine learning to the prediction of clinical response to thiopurines.

Algorithms based on common laboratory values outperformed expensive metabolite testing in determining which patients with inflammatory bowel disease are likely to respond to thiopurine therapy, Dr. Akbar K. Waljee and his colleagues reported.

Thiopurines are known to be effective immunomodulators in patients with inflammatory bowel disease (IBD) who have failed 5-aminosalicylic acid therapy. The problem is that thiopurines have a narrow therapeutic index, and individuals vary widely in how they metabolize these agents.

Experienced clinicians can use inexpensive complete blood count and standard blood chemistry values to balance efficacy and risk in individual patients, but this takes expert judgment, and there are no established algorithms.

A more reproducible approach is to measure the metabolites 6-thioguanine (6-TGN) and 6 methylmercaptopurine (6-MMP). Unfortunately, monitoring these metabolites is expensive, and the sensitivity and specificity of this approach are only 62% and 72%, respectively.

In an effort to resolve this dilemma, Dr. Waljee and his colleagues from the University of Michigan, Ann Arbor, used a machine learning technique to tease out the most accurate algorithms based on CBC and blood chemistries (Clin. Gastroenterol. Hepatol. 2010 [doi:10.1016/j.cgh.2009.09.031]).

The investigators used data collected in 774 cases from 346 individuals who were seen at the University of Michigan between May 2004 and August 2006. To be included in the study, the patients had to have had thiopurine metabolite analysis, CBC, and a comprehensive chemistry panel within the same 24-hour period.

Using a randomly selected 70% of the cases, investigators used a statistical technique called the “random forest” method to derive the most accurate algorithms based on data from the CBC and chemistry panels. They then tested that algorithm on the remaining 30% of the cases, comparing the accuracy to that of thiopurine metabolite analysis.

Their primary outcome measure was the area under the receiver operating characteristic curve (AuROC), a standard measure of accuracy.

The random forest algorithm differentiated clinical response from nonresponse with an AuROC of 0.856, compared with 0.594, for 6-TGN levels, a difference that was highly statistically significant.

The most important independent variables in differentiating responders from nonresponders were neutrophil count, alkaline phosphatase, red-cell distribution width, age, and white blood cell count.

The investigators also derived a random forest algorithm that would predict patient nonadherence, and another that would predict which patients were likely to have unfavorable pharmacodynamic responses to thiopurine therapy. Both of those algorithms proved to be significantly better than thiopurine metabolite analysis.

They also developed a simple prediction rule that was reasonably accurate at differentiating responders from nonresponders. Patients with a ratio of mean corpuscular volume (MCV) to white blood cell count (WBC) of 12 or more had a 67% likelihood of having a clinical response, while those with a ratio less than 12 had a 35% likelihood of having a clinical response. This simplified algorithm was significantly worse than the more complex algorithm, but it was still significantly better than metabolite analysis.

The investigators disclosed that the Regents of the University of Michigan, along with several of the study's coauthors, have applied for a patent on the application of machine learning to the prediction of clinical response to thiopurines.