The American Heart Association has released its recommendations regarding the sale and usage of e-cigarettes, cautioning that the devices should be regulated to avoid enticing children to smoke while also saying that e-cigarettes could be used as a way to help some current smokers quit.

The guidelines, published online Aug. 24 in Circulation, state that clinicians "should not discourage" their patients from resorting to e-cigarettes if other approved forms of smoking cessation, such as the nicotine patch, have been exhausted. The AHA warned, however, that further studies are needed to fully understand the effects of e-cigarette usage, stressing that e-cigarettes have not been approved by the Food and Drug Administration as an acceptable smoking cessation device and could contain low amounts of toxic chemicals that would prove more harmful than helpful to patients in the long run.

©goldy/Thinkstockphotos.com

"E-cigarettes have caused a major shift in the tobacco-control landscape," Aruni Bhatnagar, Ph.D., lead author of the guidelines and chair of cardiovascular medicine at the University of Louisville, Ky., said in a statement. "It’s critical that we rigorously examine the long-term impact of this new technology on public health, cardiovascular disease, and stroke, and pay careful attention to the effect of e-cigarettes on adolescents."

For now, the AHA says that clinicians should tell their patients who use e-cigarettes to set a firm quit date, warning that any device that delivers nicotine into the body is harmful and likely lethal.

"Nicotine is a dangerous and highly addictive chemical no matter what form it takes – conventional cigarettes or some other tobacco product," Dr. Elliott Antman, AHA president, said in the statement. "Every life that has been lost to tobacco addiction" could have been saved, he noted.

To that end, the AHA also called for strong regulations regarding the potential marketability of e-cigarettes to youngsters. The group recommended a federal ban on the sale of e-cigarettes to minors, warning that the devices could become a gateway to actual cigarettes for young people who see e-cigarettes as "high-tech, accessible, and convenient," according to a JAMA Pediatrics study of 40,000 middle and high school students. The AHA also recommended that all existing rules and regulations in place for tobacco-related products should apply to e-cigarettes.

"We must protect future generations from any potential smokescreens in the tobacco product landscape that will cause us to lose precious ground in the fight to make our nation 100% tobacco-free," Dr. Antman said.

According to the AHA, 20 million Americans have lost their lives to tobacco over the last 50 years.

[email protected]

The American Heart Association has released its recommendations regarding the sale and usage of e-cigarettes, cautioning that the devices should be regulated to avoid enticing children to smoke while also saying that e-cigarettes could be used as a way to help some current smokers quit.

The guidelines, published online Aug. 24 in Circulation, state that clinicians "should not discourage" their patients from resorting to e-cigarettes if other approved forms of smoking cessation, such as the nicotine patch, have been exhausted. The AHA warned, however, that further studies are needed to fully understand the effects of e-cigarette usage, stressing that e-cigarettes have not been approved by the Food and Drug Administration as an acceptable smoking cessation device and could contain low amounts of toxic chemicals that would prove more harmful than helpful to patients in the long run.

©goldy/Thinkstockphotos.com

"E-cigarettes have caused a major shift in the tobacco-control landscape," Aruni Bhatnagar, Ph.D., lead author of the guidelines and chair of cardiovascular medicine at the University of Louisville, Ky., said in a statement. "It’s critical that we rigorously examine the long-term impact of this new technology on public health, cardiovascular disease, and stroke, and pay careful attention to the effect of e-cigarettes on adolescents."

For now, the AHA says that clinicians should tell their patients who use e-cigarettes to set a firm quit date, warning that any device that delivers nicotine into the body is harmful and likely lethal.

"Nicotine is a dangerous and highly addictive chemical no matter what form it takes – conventional cigarettes or some other tobacco product," Dr. Elliott Antman, AHA president, said in the statement. "Every life that has been lost to tobacco addiction" could have been saved, he noted.

To that end, the AHA also called for strong regulations regarding the potential marketability of e-cigarettes to youngsters. The group recommended a federal ban on the sale of e-cigarettes to minors, warning that the devices could become a gateway to actual cigarettes for young people who see e-cigarettes as "high-tech, accessible, and convenient," according to a JAMA Pediatrics study of 40,000 middle and high school students. The AHA also recommended that all existing rules and regulations in place for tobacco-related products should apply to e-cigarettes.

"We must protect future generations from any potential smokescreens in the tobacco product landscape that will cause us to lose precious ground in the fight to make our nation 100% tobacco-free," Dr. Antman said.

According to the AHA, 20 million Americans have lost their lives to tobacco over the last 50 years.

[email protected]

The American Heart Association has released its recommendations regarding the sale and usage of e-cigarettes, cautioning that the devices should be regulated to avoid enticing children to smoke while also saying that e-cigarettes could be used as a way to help some current smokers quit.

The guidelines, published online Aug. 24 in Circulation, state that clinicians "should not discourage" their patients from resorting to e-cigarettes if other approved forms of smoking cessation, such as the nicotine patch, have been exhausted. The AHA warned, however, that further studies are needed to fully understand the effects of e-cigarette usage, stressing that e-cigarettes have not been approved by the Food and Drug Administration as an acceptable smoking cessation device and could contain low amounts of toxic chemicals that would prove more harmful than helpful to patients in the long run.

©goldy/Thinkstockphotos.com

"E-cigarettes have caused a major shift in the tobacco-control landscape," Aruni Bhatnagar, Ph.D., lead author of the guidelines and chair of cardiovascular medicine at the University of Louisville, Ky., said in a statement. "It’s critical that we rigorously examine the long-term impact of this new technology on public health, cardiovascular disease, and stroke, and pay careful attention to the effect of e-cigarettes on adolescents."

For now, the AHA says that clinicians should tell their patients who use e-cigarettes to set a firm quit date, warning that any device that delivers nicotine into the body is harmful and likely lethal.

"Nicotine is a dangerous and highly addictive chemical no matter what form it takes – conventional cigarettes or some other tobacco product," Dr. Elliott Antman, AHA president, said in the statement. "Every life that has been lost to tobacco addiction" could have been saved, he noted.

To that end, the AHA also called for strong regulations regarding the potential marketability of e-cigarettes to youngsters. The group recommended a federal ban on the sale of e-cigarettes to minors, warning that the devices could become a gateway to actual cigarettes for young people who see e-cigarettes as "high-tech, accessible, and convenient," according to a JAMA Pediatrics study of 40,000 middle and high school students. The AHA also recommended that all existing rules and regulations in place for tobacco-related products should apply to e-cigarettes.

"We must protect future generations from any potential smokescreens in the tobacco product landscape that will cause us to lose precious ground in the fight to make our nation 100% tobacco-free," Dr. Antman said.

According to the AHA, 20 million Americans have lost their lives to tobacco over the last 50 years.

[email protected]

Although there are some glimmers of hope that U.S. birthweights may be declining, the average infant birthweight has remained significantly tilted toward obesity. Moreover, and alarming number of infants, children, and adolescents are obese.

In 2007-2008, 9.5% of infants and toddlers were at or above the 95th percentile of the weight-for-recumbent-length growth charts. Among children and adolescents aged 2-19 years, 11.9% were at or above the 97th percentile of the body-mass-index-for-age growth charts; 16.9% were at or above the 95th percentile; and 31.7% were at or above the 85th percentile of BMI for age (JAMA 2010;303:242-9).

While more recent reports of obesity in children indicate a modest decline in obesity among 2- to 5-year-olds (JAMA 2014;311:806-14), an alarming number of infants and children have excess adiposity (roughly twice what is expected). In addition, cardiovascular mortality later in life continues to rise.

The question arises, have childhood and adult obesity rates remained high because mothers are feeding their children the wrong foods or because these children were born obese? One also wonders, with respect to cardiovascular mortality in adulthood, is the in utero environment playing a role?

 

Old lessons, growing relevance

More than 3 decades ago, the late British physician Dr. David Barker got us thinking about how a challenging life in the womb can set us up for downstream ill health. He studied births from 1910 to 1945 and found that the cardiovascular mortality of individuals born during that time was inversely related to birthweight. Smaller babies, he found, could have cardiovascular mortality risks that were double or even quadruple the risks of larger babies.

Dr. Barker theorized that, when faced with undernutrition, the fetus adapts by sending more blood to the brain and sacrificing blood flow to less essential tissues. His theory about how growth and nutrition before birth may affect the heart became known as the "Barker Hypothesis." It was initially controversial, but it led to an explosion of research – especially since 2000 – on various downstream effects of the intrauterine environment.

Investigators have learned that it is not only cardiovascular mortality that is affected by low birthweight, but also the risk of developing diabetes and being overweight. This is because the fetus makes less essential systems insulin resistant. Insulin resistance persists in the womb and after birth as well, predisposing individuals to insulin resistance and obesity, both of which are closely linked to the risk of metabolic syndrome – a group of risk factors that raises the likelihood of developing heart disease, stroke, and diabetes.

In fact, further research on cohorts of Barker children – individuals who had low birthweights – has shown that not only have they had higher rates of cardiovascular disease, but they have had higher blood sugars and higher rates of insulin resistance as well.

Today, we appreciate a fuller picture of the Barker data, one that shows a reversal of this trend when birthweights reach 4,000-4,500 grams. At this point, what was a progressively downward slope of cardiovascular mortality rates with increasing birthweight suddenly shoots upward again when birthweight exceeds 4,000 g.

It is this end of the curve that is most relevant – and most concerning – for ob.gyns. today. Our problem in the United States is not so much one of starving or growth-restricted newborns, as these babies account for 5% or less of all births. It is one of overweight and obese newborns who now represent as many as 1 in 7 births. Just like the Barker babies who were growth restricted, these newborns have high insulin levels and increased risk of cardiovascular disease as adults.

 

Changing the trajectory

Both maternal obesity and gestational diabetes get at the heart of the Barker Hypothesis, albeit a twist, in that excessive maternal adiposity and associated insulin resistance results in high maternal blood glucose, transferring excessive nutrients to the fetus. This causes accumulation of fat in the fetus and programs the fetus for an increased and persistent risk of adiposity after birth, early-onset metabolic syndrome, and downstream cardiovascular disease in adulthood.

Dr. Dana Dabelea’s sibling study of almost 15 years ago demonstrated the long-term impact of the adverse intrauterine environment associated with maternal diabetes. Matched siblings who were born after their mothers had developed diabetes had almost double the rate of obesity as adolescents, compared with the siblings born before their mothers were diagnosed with diabetes. In childhood, these siblings ate at the same table and came from the same gene pools (with the same fathers), but they experienced dramatically different health outcomes (Diabetes 2000:49:2208-11).

This landmark study has been reproduced by other investigators who have compared children of mothers who had gestational diabetes and/or were overweight, with children whose mothers did not have gestational diabetes mellitus (GDM) or were of normal weight. Such studies have consistently shown that, faced with either or both maternal obesity and diabetes in utero, offspring were significantly more likely to become overweight children and adults with insulin resistance and other components of the metabolic syndrome.

Importantly, we have evidence from randomized trials that interventions to treat GDM can effectively reduce rates of newborn obesity. While differences in birthweight between treatment and no-treatment arms have been modest, reductions in neonatal body fat, as measured by skin-fold thickness, the ponderal index, and birthweight percentile, have been highly significant.

The offspring of mothers who were treated in these trials, the Australian Carbohydrate Intolerance Study in Pregnant Women (N. Engl. J. Med. 2005;352:2477-86), and a study by Dr. Mark B. Landon and his colleagues (N. Engl. J. Med. 2009;361:1339-48), had approximately half of the newborn adiposity than did offspring of mothers who were not treated. In the latter study, maternal dietary measures alone were successful in reducing neonatal adiposity in over 80% of infants.

While published follow-up data of the offspring in these cohorts have covered only 5-8 years (showing persistently less adiposity in the treated groups), the offspring in the Australian cohort are still being monitored. Based on the cohort and case-control studies summarized above, it seems fair to expect that the children of mothers who were treated for GDM will have significantly better health profiles into and through adulthood.

 

We know from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study that what were formerly considered mild and inconsequential maternal blood glucose levels are instead potentially quite harmful. The study showed a clear linear relationship between maternal fasting blood glucose levels, fetal cord blood insulin concentrations (a reflection of fetal glucose levels), and newborn body fat percentage (N. Engl. J. Med. 2008;358:1991-2002).

Interestingly, Dr. Patrick Catalano’s analysis of data from the HAPO study (Diabetes Care 2012;35:780-6) shows us more: Maternal obesity is almost as strong a driver of newborn obesity as is GDM. Compared with GDM (which increased the percentage of infant birthweights to greater than the 90th percentile by a factor of 2.19), maternal obesity alone increased the frequency of LGA by a factor of 1.73, and maternal obesity and GDM together increased LGA newborns by 3.62-fold.

In light of these recent findings, it is critical that we not only treat our patients who have GDM, but that we attempt to interrupt the chain of obesity that passes from mother to fetus, and from obese newborns onto their subsequent offspring.

A growing proportion of women across all race and ethnicity groups gain more than 40 pounds during pregnancy for singleton births, and many of them do not lose the weight between pregnancies. Increasingly, we have patients whose first child may not have been exposed to obesity in utero, but whose second child is exposed to overweight or obesity and higher levels of insulin resistance and glycemia.

The Institute of Medicine documented these issues in its 2009 report, "Weight Gain During Pregnancy: Reexamining the Guidelines." Data on maternal postpartum weights are not widely available, but data that have been collected suggest that gaining above recommended ranges is associated with excess maternal weight retention post partum, regardless of prepregnancy BMI. Women who gained above the range recommended by the IOM in 1990 had postpartum weight retention of 15-20 pounds. Among women who gained excessive amounts of weight, moreover, more than 40% retained more than 20 pounds, according to the report.

We must break the intergenerational transfer of obesity and insulin resistance by liberally treating GDM and optimizing glucose control during pregnancy. More importantly, we must emphasize to women the importance of having healthy weights at the time of conception. Recent research affirms that moderately simple interventions, such as dietary improvements and exercise can go a long way to achieving these goals. If we don’t – in keeping with the knowledge spurred on by Dr. Barker – we will be programming more newborns for life with insulin resistance, obesity, and disease.

Dr. Moore is a perinatologist who is chair of the department of reproductive medicine at the University of California, San Diego. He said he had no relevant financial disclosures.

Although there are some glimmers of hope that U.S. birthweights may be declining, the average infant birthweight has remained significantly tilted toward obesity. Moreover, and alarming number of infants, children, and adolescents are obese.

In 2007-2008, 9.5% of infants and toddlers were at or above the 95th percentile of the weight-for-recumbent-length growth charts. Among children and adolescents aged 2-19 years, 11.9% were at or above the 97th percentile of the body-mass-index-for-age growth charts; 16.9% were at or above the 95th percentile; and 31.7% were at or above the 85th percentile of BMI for age (JAMA 2010;303:242-9).

While more recent reports of obesity in children indicate a modest decline in obesity among 2- to 5-year-olds (JAMA 2014;311:806-14), an alarming number of infants and children have excess adiposity (roughly twice what is expected). In addition, cardiovascular mortality later in life continues to rise.

The question arises, have childhood and adult obesity rates remained high because mothers are feeding their children the wrong foods or because these children were born obese? One also wonders, with respect to cardiovascular mortality in adulthood, is the in utero environment playing a role?

 

Old lessons, growing relevance

More than 3 decades ago, the late British physician Dr. David Barker got us thinking about how a challenging life in the womb can set us up for downstream ill health. He studied births from 1910 to 1945 and found that the cardiovascular mortality of individuals born during that time was inversely related to birthweight. Smaller babies, he found, could have cardiovascular mortality risks that were double or even quadruple the risks of larger babies.

Dr. Barker theorized that, when faced with undernutrition, the fetus adapts by sending more blood to the brain and sacrificing blood flow to less essential tissues. His theory about how growth and nutrition before birth may affect the heart became known as the "Barker Hypothesis." It was initially controversial, but it led to an explosion of research – especially since 2000 – on various downstream effects of the intrauterine environment.

Investigators have learned that it is not only cardiovascular mortality that is affected by low birthweight, but also the risk of developing diabetes and being overweight. This is because the fetus makes less essential systems insulin resistant. Insulin resistance persists in the womb and after birth as well, predisposing individuals to insulin resistance and obesity, both of which are closely linked to the risk of metabolic syndrome – a group of risk factors that raises the likelihood of developing heart disease, stroke, and diabetes.

In fact, further research on cohorts of Barker children – individuals who had low birthweights – has shown that not only have they had higher rates of cardiovascular disease, but they have had higher blood sugars and higher rates of insulin resistance as well.

Today, we appreciate a fuller picture of the Barker data, one that shows a reversal of this trend when birthweights reach 4,000-4,500 grams. At this point, what was a progressively downward slope of cardiovascular mortality rates with increasing birthweight suddenly shoots upward again when birthweight exceeds 4,000 g.

It is this end of the curve that is most relevant – and most concerning – for ob.gyns. today. Our problem in the United States is not so much one of starving or growth-restricted newborns, as these babies account for 5% or less of all births. It is one of overweight and obese newborns who now represent as many as 1 in 7 births. Just like the Barker babies who were growth restricted, these newborns have high insulin levels and increased risk of cardiovascular disease as adults.

 

Changing the trajectory

Both maternal obesity and gestational diabetes get at the heart of the Barker Hypothesis, albeit a twist, in that excessive maternal adiposity and associated insulin resistance results in high maternal blood glucose, transferring excessive nutrients to the fetus. This causes accumulation of fat in the fetus and programs the fetus for an increased and persistent risk of adiposity after birth, early-onset metabolic syndrome, and downstream cardiovascular disease in adulthood.

Dr. Dana Dabelea’s sibling study of almost 15 years ago demonstrated the long-term impact of the adverse intrauterine environment associated with maternal diabetes. Matched siblings who were born after their mothers had developed diabetes had almost double the rate of obesity as adolescents, compared with the siblings born before their mothers were diagnosed with diabetes. In childhood, these siblings ate at the same table and came from the same gene pools (with the same fathers), but they experienced dramatically different health outcomes (Diabetes 2000:49:2208-11).

This landmark study has been reproduced by other investigators who have compared children of mothers who had gestational diabetes and/or were overweight, with children whose mothers did not have gestational diabetes mellitus (GDM) or were of normal weight. Such studies have consistently shown that, faced with either or both maternal obesity and diabetes in utero, offspring were significantly more likely to become overweight children and adults with insulin resistance and other components of the metabolic syndrome.

Importantly, we have evidence from randomized trials that interventions to treat GDM can effectively reduce rates of newborn obesity. While differences in birthweight between treatment and no-treatment arms have been modest, reductions in neonatal body fat, as measured by skin-fold thickness, the ponderal index, and birthweight percentile, have been highly significant.

The offspring of mothers who were treated in these trials, the Australian Carbohydrate Intolerance Study in Pregnant Women (N. Engl. J. Med. 2005;352:2477-86), and a study by Dr. Mark B. Landon and his colleagues (N. Engl. J. Med. 2009;361:1339-48), had approximately half of the newborn adiposity than did offspring of mothers who were not treated. In the latter study, maternal dietary measures alone were successful in reducing neonatal adiposity in over 80% of infants.

While published follow-up data of the offspring in these cohorts have covered only 5-8 years (showing persistently less adiposity in the treated groups), the offspring in the Australian cohort are still being monitored. Based on the cohort and case-control studies summarized above, it seems fair to expect that the children of mothers who were treated for GDM will have significantly better health profiles into and through adulthood.

 

We know from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study that what were formerly considered mild and inconsequential maternal blood glucose levels are instead potentially quite harmful. The study showed a clear linear relationship between maternal fasting blood glucose levels, fetal cord blood insulin concentrations (a reflection of fetal glucose levels), and newborn body fat percentage (N. Engl. J. Med. 2008;358:1991-2002).

Interestingly, Dr. Patrick Catalano’s analysis of data from the HAPO study (Diabetes Care 2012;35:780-6) shows us more: Maternal obesity is almost as strong a driver of newborn obesity as is GDM. Compared with GDM (which increased the percentage of infant birthweights to greater than the 90th percentile by a factor of 2.19), maternal obesity alone increased the frequency of LGA by a factor of 1.73, and maternal obesity and GDM together increased LGA newborns by 3.62-fold.

In light of these recent findings, it is critical that we not only treat our patients who have GDM, but that we attempt to interrupt the chain of obesity that passes from mother to fetus, and from obese newborns onto their subsequent offspring.

A growing proportion of women across all race and ethnicity groups gain more than 40 pounds during pregnancy for singleton births, and many of them do not lose the weight between pregnancies. Increasingly, we have patients whose first child may not have been exposed to obesity in utero, but whose second child is exposed to overweight or obesity and higher levels of insulin resistance and glycemia.

The Institute of Medicine documented these issues in its 2009 report, "Weight Gain During Pregnancy: Reexamining the Guidelines." Data on maternal postpartum weights are not widely available, but data that have been collected suggest that gaining above recommended ranges is associated with excess maternal weight retention post partum, regardless of prepregnancy BMI. Women who gained above the range recommended by the IOM in 1990 had postpartum weight retention of 15-20 pounds. Among women who gained excessive amounts of weight, moreover, more than 40% retained more than 20 pounds, according to the report.

We must break the intergenerational transfer of obesity and insulin resistance by liberally treating GDM and optimizing glucose control during pregnancy. More importantly, we must emphasize to women the importance of having healthy weights at the time of conception. Recent research affirms that moderately simple interventions, such as dietary improvements and exercise can go a long way to achieving these goals. If we don’t – in keeping with the knowledge spurred on by Dr. Barker – we will be programming more newborns for life with insulin resistance, obesity, and disease.

Dr. Moore is a perinatologist who is chair of the department of reproductive medicine at the University of California, San Diego. He said he had no relevant financial disclosures.

Although there are some glimmers of hope that U.S. birthweights may be declining, the average infant birthweight has remained significantly tilted toward obesity. Moreover, and alarming number of infants, children, and adolescents are obese.

In 2007-2008, 9.5% of infants and toddlers were at or above the 95th percentile of the weight-for-recumbent-length growth charts. Among children and adolescents aged 2-19 years, 11.9% were at or above the 97th percentile of the body-mass-index-for-age growth charts; 16.9% were at or above the 95th percentile; and 31.7% were at or above the 85th percentile of BMI for age (JAMA 2010;303:242-9).

While more recent reports of obesity in children indicate a modest decline in obesity among 2- to 5-year-olds (JAMA 2014;311:806-14), an alarming number of infants and children have excess adiposity (roughly twice what is expected). In addition, cardiovascular mortality later in life continues to rise.

The question arises, have childhood and adult obesity rates remained high because mothers are feeding their children the wrong foods or because these children were born obese? One also wonders, with respect to cardiovascular mortality in adulthood, is the in utero environment playing a role?

 

Old lessons, growing relevance

More than 3 decades ago, the late British physician Dr. David Barker got us thinking about how a challenging life in the womb can set us up for downstream ill health. He studied births from 1910 to 1945 and found that the cardiovascular mortality of individuals born during that time was inversely related to birthweight. Smaller babies, he found, could have cardiovascular mortality risks that were double or even quadruple the risks of larger babies.

Dr. Barker theorized that, when faced with undernutrition, the fetus adapts by sending more blood to the brain and sacrificing blood flow to less essential tissues. His theory about how growth and nutrition before birth may affect the heart became known as the "Barker Hypothesis." It was initially controversial, but it led to an explosion of research – especially since 2000 – on various downstream effects of the intrauterine environment.

Investigators have learned that it is not only cardiovascular mortality that is affected by low birthweight, but also the risk of developing diabetes and being overweight. This is because the fetus makes less essential systems insulin resistant. Insulin resistance persists in the womb and after birth as well, predisposing individuals to insulin resistance and obesity, both of which are closely linked to the risk of metabolic syndrome – a group of risk factors that raises the likelihood of developing heart disease, stroke, and diabetes.

In fact, further research on cohorts of Barker children – individuals who had low birthweights – has shown that not only have they had higher rates of cardiovascular disease, but they have had higher blood sugars and higher rates of insulin resistance as well.

Today, we appreciate a fuller picture of the Barker data, one that shows a reversal of this trend when birthweights reach 4,000-4,500 grams. At this point, what was a progressively downward slope of cardiovascular mortality rates with increasing birthweight suddenly shoots upward again when birthweight exceeds 4,000 g.

It is this end of the curve that is most relevant – and most concerning – for ob.gyns. today. Our problem in the United States is not so much one of starving or growth-restricted newborns, as these babies account for 5% or less of all births. It is one of overweight and obese newborns who now represent as many as 1 in 7 births. Just like the Barker babies who were growth restricted, these newborns have high insulin levels and increased risk of cardiovascular disease as adults.

 

Changing the trajectory

Both maternal obesity and gestational diabetes get at the heart of the Barker Hypothesis, albeit a twist, in that excessive maternal adiposity and associated insulin resistance results in high maternal blood glucose, transferring excessive nutrients to the fetus. This causes accumulation of fat in the fetus and programs the fetus for an increased and persistent risk of adiposity after birth, early-onset metabolic syndrome, and downstream cardiovascular disease in adulthood.

Dr. Dana Dabelea’s sibling study of almost 15 years ago demonstrated the long-term impact of the adverse intrauterine environment associated with maternal diabetes. Matched siblings who were born after their mothers had developed diabetes had almost double the rate of obesity as adolescents, compared with the siblings born before their mothers were diagnosed with diabetes. In childhood, these siblings ate at the same table and came from the same gene pools (with the same fathers), but they experienced dramatically different health outcomes (Diabetes 2000:49:2208-11).

This landmark study has been reproduced by other investigators who have compared children of mothers who had gestational diabetes and/or were overweight, with children whose mothers did not have gestational diabetes mellitus (GDM) or were of normal weight. Such studies have consistently shown that, faced with either or both maternal obesity and diabetes in utero, offspring were significantly more likely to become overweight children and adults with insulin resistance and other components of the metabolic syndrome.

Importantly, we have evidence from randomized trials that interventions to treat GDM can effectively reduce rates of newborn obesity. While differences in birthweight between treatment and no-treatment arms have been modest, reductions in neonatal body fat, as measured by skin-fold thickness, the ponderal index, and birthweight percentile, have been highly significant.

The offspring of mothers who were treated in these trials, the Australian Carbohydrate Intolerance Study in Pregnant Women (N. Engl. J. Med. 2005;352:2477-86), and a study by Dr. Mark B. Landon and his colleagues (N. Engl. J. Med. 2009;361:1339-48), had approximately half of the newborn adiposity than did offspring of mothers who were not treated. In the latter study, maternal dietary measures alone were successful in reducing neonatal adiposity in over 80% of infants.

While published follow-up data of the offspring in these cohorts have covered only 5-8 years (showing persistently less adiposity in the treated groups), the offspring in the Australian cohort are still being monitored. Based on the cohort and case-control studies summarized above, it seems fair to expect that the children of mothers who were treated for GDM will have significantly better health profiles into and through adulthood.

 

We know from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study that what were formerly considered mild and inconsequential maternal blood glucose levels are instead potentially quite harmful. The study showed a clear linear relationship between maternal fasting blood glucose levels, fetal cord blood insulin concentrations (a reflection of fetal glucose levels), and newborn body fat percentage (N. Engl. J. Med. 2008;358:1991-2002).

Interestingly, Dr. Patrick Catalano’s analysis of data from the HAPO study (Diabetes Care 2012;35:780-6) shows us more: Maternal obesity is almost as strong a driver of newborn obesity as is GDM. Compared with GDM (which increased the percentage of infant birthweights to greater than the 90th percentile by a factor of 2.19), maternal obesity alone increased the frequency of LGA by a factor of 1.73, and maternal obesity and GDM together increased LGA newborns by 3.62-fold.

In light of these recent findings, it is critical that we not only treat our patients who have GDM, but that we attempt to interrupt the chain of obesity that passes from mother to fetus, and from obese newborns onto their subsequent offspring.

A growing proportion of women across all race and ethnicity groups gain more than 40 pounds during pregnancy for singleton births, and many of them do not lose the weight between pregnancies. Increasingly, we have patients whose first child may not have been exposed to obesity in utero, but whose second child is exposed to overweight or obesity and higher levels of insulin resistance and glycemia.

The Institute of Medicine documented these issues in its 2009 report, "Weight Gain During Pregnancy: Reexamining the Guidelines." Data on maternal postpartum weights are not widely available, but data that have been collected suggest that gaining above recommended ranges is associated with excess maternal weight retention post partum, regardless of prepregnancy BMI. Women who gained above the range recommended by the IOM in 1990 had postpartum weight retention of 15-20 pounds. Among women who gained excessive amounts of weight, moreover, more than 40% retained more than 20 pounds, according to the report.

We must break the intergenerational transfer of obesity and insulin resistance by liberally treating GDM and optimizing glucose control during pregnancy. More importantly, we must emphasize to women the importance of having healthy weights at the time of conception. Recent research affirms that moderately simple interventions, such as dietary improvements and exercise can go a long way to achieving these goals. If we don’t – in keeping with the knowledge spurred on by Dr. Barker – we will be programming more newborns for life with insulin resistance, obesity, and disease.

Dr. Moore is a perinatologist who is chair of the department of reproductive medicine at the University of California, San Diego. He said he had no relevant financial disclosures.

On Aug. 27, 2013, the field of obstetrics and gynecology suffered a great loss: the passing of Dr. David J.P. Barker. Dr. Barker was a visionary and leader whose hypothesis about the links between a mother’s health and the long-term health of her children was controversial when he first posed it in the late 1980s. However, after subsequent decades of maternal-fetal practice and research, his idea that preventing chronic disease starts with a healthy mother and baby, is embraced by the medical and science communities today.

I was just starting my career when Dr. Barker’s hypothesis, known then as the "fetal origins hypothesis" but subsequently referred to as the "Barker Hypothesis," was published. During my fellowship in maternal-fetal medicine at Yale University, I had the privilege of attending one of Dr. Barker’s lectures and meeting him. While my colleagues and I thought him an eloquent and impassioned speaker, Dr. Barker’s theory – that there was a relationship between a person’s birth weight and his or her lifetime risk for chronic disease – was highly contentious. He had based his hypothesis on large epidemiological studies conducted in Finland, India, the Netherlands, the United Kingdom, and the United States – all of which revealed that the lower a person’s birth weight, the higher his or her risk for developing coronary heart disease. In addition, he concluded that the lower a person’s birth weight, but the faster the weight gain after age 2 years, the higher a person’s risk for hypertension, stroke, and type 2 diabetes.

At that time, we did not fully realize the significance, gravity, and enormity of Dr. Barker’s contribution to the ob.gyn. field. I could not imagine the impact that his work would have on my professional path. Dr. Barker’s early papers often concluded with a section looking to the future, and in one of them he stated that "we now need to progress beyond epidemiologic associations [between in utero conditions and health later in life] to greater understanding of the cellular and molecular processes that underlie them"(Am. J. Clin. Nutr. 2000;71:1344s-52s). From my work as a physician with diabetic pregnant women to my scientific research devoted to understanding how, at the molecular level, maternal diabetes affects the developing fetus, I have a great appreciation and respect for Dr. Barker’s work.

Therefore, I am very pleased that this month’s Master Class is devoted to a discussion of how the Barker Hypothesis applies today. We have invited Dr. Thomas R. Moore, a perinatologist who is chair of the department of reproductive medicine at the University of California, San Diego, to give his reflection on how Dr. Barker’s once radical ideas revolutionized our field.

Dr. Reece, who specializes in maternal-fetal medicine, is vice president for medical affairs at the University of Maryland, Baltimore, as well as the John Z. and Akiko K. Bowers Distinguished Professor and dean of the school of medicine. Dr. Reece said he had no relevant financial disclosures. He is the medical editor of the Master Class column. Contact him at [email protected].

On Aug. 27, 2013, the field of obstetrics and gynecology suffered a great loss: the passing of Dr. David J.P. Barker. Dr. Barker was a visionary and leader whose hypothesis about the links between a mother’s health and the long-term health of her children was controversial when he first posed it in the late 1980s. However, after subsequent decades of maternal-fetal practice and research, his idea that preventing chronic disease starts with a healthy mother and baby, is embraced by the medical and science communities today.

I was just starting my career when Dr. Barker’s hypothesis, known then as the "fetal origins hypothesis" but subsequently referred to as the "Barker Hypothesis," was published. During my fellowship in maternal-fetal medicine at Yale University, I had the privilege of attending one of Dr. Barker’s lectures and meeting him. While my colleagues and I thought him an eloquent and impassioned speaker, Dr. Barker’s theory – that there was a relationship between a person’s birth weight and his or her lifetime risk for chronic disease – was highly contentious. He had based his hypothesis on large epidemiological studies conducted in Finland, India, the Netherlands, the United Kingdom, and the United States – all of which revealed that the lower a person’s birth weight, the higher his or her risk for developing coronary heart disease. In addition, he concluded that the lower a person’s birth weight, but the faster the weight gain after age 2 years, the higher a person’s risk for hypertension, stroke, and type 2 diabetes.

At that time, we did not fully realize the significance, gravity, and enormity of Dr. Barker’s contribution to the ob.gyn. field. I could not imagine the impact that his work would have on my professional path. Dr. Barker’s early papers often concluded with a section looking to the future, and in one of them he stated that "we now need to progress beyond epidemiologic associations [between in utero conditions and health later in life] to greater understanding of the cellular and molecular processes that underlie them"(Am. J. Clin. Nutr. 2000;71:1344s-52s). From my work as a physician with diabetic pregnant women to my scientific research devoted to understanding how, at the molecular level, maternal diabetes affects the developing fetus, I have a great appreciation and respect for Dr. Barker’s work.

Therefore, I am very pleased that this month’s Master Class is devoted to a discussion of how the Barker Hypothesis applies today. We have invited Dr. Thomas R. Moore, a perinatologist who is chair of the department of reproductive medicine at the University of California, San Diego, to give his reflection on how Dr. Barker’s once radical ideas revolutionized our field.

Dr. Reece, who specializes in maternal-fetal medicine, is vice president for medical affairs at the University of Maryland, Baltimore, as well as the John Z. and Akiko K. Bowers Distinguished Professor and dean of the school of medicine. Dr. Reece said he had no relevant financial disclosures. He is the medical editor of the Master Class column. Contact him at [email protected].

On Aug. 27, 2013, the field of obstetrics and gynecology suffered a great loss: the passing of Dr. David J.P. Barker. Dr. Barker was a visionary and leader whose hypothesis about the links between a mother’s health and the long-term health of her children was controversial when he first posed it in the late 1980s. However, after subsequent decades of maternal-fetal practice and research, his idea that preventing chronic disease starts with a healthy mother and baby, is embraced by the medical and science communities today.

I was just starting my career when Dr. Barker’s hypothesis, known then as the "fetal origins hypothesis" but subsequently referred to as the "Barker Hypothesis," was published. During my fellowship in maternal-fetal medicine at Yale University, I had the privilege of attending one of Dr. Barker’s lectures and meeting him. While my colleagues and I thought him an eloquent and impassioned speaker, Dr. Barker’s theory – that there was a relationship between a person’s birth weight and his or her lifetime risk for chronic disease – was highly contentious. He had based his hypothesis on large epidemiological studies conducted in Finland, India, the Netherlands, the United Kingdom, and the United States – all of which revealed that the lower a person’s birth weight, the higher his or her risk for developing coronary heart disease. In addition, he concluded that the lower a person’s birth weight, but the faster the weight gain after age 2 years, the higher a person’s risk for hypertension, stroke, and type 2 diabetes.

At that time, we did not fully realize the significance, gravity, and enormity of Dr. Barker’s contribution to the ob.gyn. field. I could not imagine the impact that his work would have on my professional path. Dr. Barker’s early papers often concluded with a section looking to the future, and in one of them he stated that "we now need to progress beyond epidemiologic associations [between in utero conditions and health later in life] to greater understanding of the cellular and molecular processes that underlie them"(Am. J. Clin. Nutr. 2000;71:1344s-52s). From my work as a physician with diabetic pregnant women to my scientific research devoted to understanding how, at the molecular level, maternal diabetes affects the developing fetus, I have a great appreciation and respect for Dr. Barker’s work.

Therefore, I am very pleased that this month’s Master Class is devoted to a discussion of how the Barker Hypothesis applies today. We have invited Dr. Thomas R. Moore, a perinatologist who is chair of the department of reproductive medicine at the University of California, San Diego, to give his reflection on how Dr. Barker’s once radical ideas revolutionized our field.

Dr. Reece, who specializes in maternal-fetal medicine, is vice president for medical affairs at the University of Maryland, Baltimore, as well as the John Z. and Akiko K. Bowers Distinguished Professor and dean of the school of medicine. Dr. Reece said he had no relevant financial disclosures. He is the medical editor of the Master Class column. Contact him at [email protected].

Rheumatoid arthritis patients who tested positive for both rheumatoid factor and anticitrullinated protein antibodies showed a greater prevalence and size of bone erosions than did patients who came up negative for both in a prospective cohort study.

High-resolution peripheral quantitative CT revealed a prevalence of around 5.35 bone erosions per patient among 112 who were positive for both rheumatoid factor (RF) and anticitrullinated protein antibodies (ACPAs), compared with 2.49 in 69 who were negative for both of the autoantibodies. Another 29 patients who were ACPA positive and RH negative had 2.41 erosions, while 28 patients who were ACPA negative and RH positive had 2.00 erosions. The size of the bone erosion had a similar pattern, with the greatest volume observed in patients positive for both autoantibodies (7.66 mm³), followed by ACPA-positive patients (6.20 mm³), patients negative for both autoantibodies (3.32 mm³), and RH-positive patients (2.76 mm³).

The size of erosions was also associated with the presence and titer of rheumatoid factor in ACPA-positive but not ACPA-negative patients (Ann. Rheum. Dis. 2014 Aug. 12 [doi:10.1136/annrheumdis-2014-205428]).

"These observations suggest that RF may act as an enhancer of bone loss in patients with RA, and acts as an additive to ACPAs," wrote Dr. Carolin Hecht of the University of Erlangen-Nuremberg (Germany) and colleagues.

The study was supported by the Deutsche Forschungsgemeinschaft, the Bundesministerium fu¨r Bildung und Forschung, the Marie Curie project OSTEOIMMUNE, the TEAM and MASTERSWITCH projects of the European Union, and the IMI-funded project BTCure. There were no other conflicts of interest declared.

Rheumatoid arthritis patients who tested positive for both rheumatoid factor and anticitrullinated protein antibodies showed a greater prevalence and size of bone erosions than did patients who came up negative for both in a prospective cohort study.

High-resolution peripheral quantitative CT revealed a prevalence of around 5.35 bone erosions per patient among 112 who were positive for both rheumatoid factor (RF) and anticitrullinated protein antibodies (ACPAs), compared with 2.49 in 69 who were negative for both of the autoantibodies. Another 29 patients who were ACPA positive and RH negative had 2.41 erosions, while 28 patients who were ACPA negative and RH positive had 2.00 erosions. The size of the bone erosion had a similar pattern, with the greatest volume observed in patients positive for both autoantibodies (7.66 mm³), followed by ACPA-positive patients (6.20 mm³), patients negative for both autoantibodies (3.32 mm³), and RH-positive patients (2.76 mm³).

The size of erosions was also associated with the presence and titer of rheumatoid factor in ACPA-positive but not ACPA-negative patients (Ann. Rheum. Dis. 2014 Aug. 12 [doi:10.1136/annrheumdis-2014-205428]).

"These observations suggest that RF may act as an enhancer of bone loss in patients with RA, and acts as an additive to ACPAs," wrote Dr. Carolin Hecht of the University of Erlangen-Nuremberg (Germany) and colleagues.

The study was supported by the Deutsche Forschungsgemeinschaft, the Bundesministerium fu¨r Bildung und Forschung, the Marie Curie project OSTEOIMMUNE, the TEAM and MASTERSWITCH projects of the European Union, and the IMI-funded project BTCure. There were no other conflicts of interest declared.

Rheumatoid arthritis patients who tested positive for both rheumatoid factor and anticitrullinated protein antibodies showed a greater prevalence and size of bone erosions than did patients who came up negative for both in a prospective cohort study.

High-resolution peripheral quantitative CT revealed a prevalence of around 5.35 bone erosions per patient among 112 who were positive for both rheumatoid factor (RF) and anticitrullinated protein antibodies (ACPAs), compared with 2.49 in 69 who were negative for both of the autoantibodies. Another 29 patients who were ACPA positive and RH negative had 2.41 erosions, while 28 patients who were ACPA negative and RH positive had 2.00 erosions. The size of the bone erosion had a similar pattern, with the greatest volume observed in patients positive for both autoantibodies (7.66 mm³), followed by ACPA-positive patients (6.20 mm³), patients negative for both autoantibodies (3.32 mm³), and RH-positive patients (2.76 mm³).

The size of erosions was also associated with the presence and titer of rheumatoid factor in ACPA-positive but not ACPA-negative patients (Ann. Rheum. Dis. 2014 Aug. 12 [doi:10.1136/annrheumdis-2014-205428]).

"These observations suggest that RF may act as an enhancer of bone loss in patients with RA, and acts as an additive to ACPAs," wrote Dr. Carolin Hecht of the University of Erlangen-Nuremberg (Germany) and colleagues.

The study was supported by the Deutsche Forschungsgemeinschaft, the Bundesministerium fu¨r Bildung und Forschung, the Marie Curie project OSTEOIMMUNE, the TEAM and MASTERSWITCH projects of the European Union, and the IMI-funded project BTCure. There were no other conflicts of interest declared.

 

 

 

“Health care professionals know that they need to take care of themselves and tend to know what to do to fight stress—they just don’t take the time to do it.”  That is according to the National Center for Telehealth and Technology (T2), which brings to health care providers a mobile app designed to guide users on a daily path toward resilience. It is a reality check, like a call from a loved one, reminding the user to take a break and care for him- or herself before returning to work.

Part of self-care is avoiding compassion fatigue, which means avoiding negative feelings toward the ability to complete a job effectively or handle work-related stress. Compassion fatigue has 2 components, according to T2: burnout and secondary traumatic stress. To avoid or combat compassion fatigue, the app gives frontline providers tools to keep themselves productive and emotionally healthy as they help our nation’s service members, veterans, and their families.

DASHBOARD

The app’s home screen is a dashboard, which tracks wellbeing across 4 parameters, all based on self-assessments: vacation time, burnout scale, builders and killers checklist, and professional quality-of-life (ProQOL) measures. Each of these 4 assessments calculates the user’s resilience rating, displayed by a colored meter measuring from 0 (low) to 100 (high).

Beneath the resilience rating meter is a prominent vacation clock, running time down to the minute since the user’s last recorded vacation day. To measure burnout, the app offers a survey for 10 measures that should be updated by the user at least once a week. The question asked of users is, “How would you describe yourself as you approach your workday today?” All measures, including happy, trapped, satisfied, and preoccupied, can be rated from “Not at All” to “Very Much So.”  

Builders and Killers is a daily check-in on the user’s work-life balance. Selecting from a quick 10-item checklist across 2 pages is all it takes to update this section. Items from the list include “Did you take a short walk” and “Did you come to work sick today?” There are even 2 editable items where the user may enter his or her own “Personal Killer.”

The professional quality-of-life (ProQOL) quiz is the longest of all—30 questions—but the resilience rating relies on an update only every 30 days. This quiz measures 3 critical components of ProQOL: compassion satisfaction, burnout, and secondary traumatic stress. Average scores provide the following output for each section:

1. Compassion Satisfaction: “You’ve scored in the average range of Compassion Satisfaction. … This suggests that you don’t find your work to be consistently satisfying, but that you do derive some degree of satisfaction from your daily work activities."

2. Burnout: “Your Burnout score is in the average range. … This may indicate that you are currently experiencing frustration in your work and may be feeling discouraged or ineffective. It may be worth reviewing your answers to see if you can pin down the source of these feelings and determine how you might improve your experience at work.”

3. Secondary Traumatic Stress: “If you are working with clients or patients who are describing highly traumatic experiences, be sure to focus on self-care, which includes maintaining physical, emotional, social, and spiritual supports.”

The dashboard also tracks how many days until the user needs to update each section, and daily reminders (push notifications) to do so may be modified in Settings.

TOOLS

There are 7 videos currently loaded into the app. Two informational videos (both running under 10 minutes) cover burnout and secondary traumatic stress so that users can gain a richer understanding either of what they are experiencing or what they are trying to avoid. The remaining 5 videos are shorter and  can be found in the “Remind Me Why I Do This” menu. These videos cover important patient characteristics that have been found to lead to compassion fatigue, including alcohol, anger, depression, depression support, and stigma.

Scrolling flashcards can be found in “Physical Exercise” and include an assortment of stretching exercises the user can perform at his or her work desk. And if stretching doesn’t release enough endorphins, the user can raise his or her spirit browsing the cartoons found in “I Need A Laugh.” All of the cartoons are office-related, updated daily, and archived for the user’s pleasure.

VALUE CARDS

Nearly 100 inspirational flashcards are loaded onto the app, each one defining a valuable character trait, associated quote, and affirmations. To scroll through the cards, which are listed alphabetically from “Acceptance” through “Unity,” simply swipe left or right. To flip the card over, swipe up or down on the screen.

 

FINAL THOUGHTS

Certain luxuries we have grown accustomed to, such as rotating a device to change display orientation, don’t perform on this app, a feature missed greatly when viewing videos and a good reason to use the app on a tablet, not a phone.

And although everyone needs the occasional short break or multiday vacation, tolerance levels differ from person to person. Hence, it is important to use the app over a period of time so that the user can learn what his or her “normal” is and track readings not necessarily against the general population, but against him- or herself on the plotted ProQOL and burnout graphs.

“Health care professionals know that they need to take care of themselves and tend to know what to do to fight stress—they just don’t take the time to do it.”  That is according to the National Center for Telehealth and Technology (T2), which brings to health care providers a mobile app designed to guide users on a daily path toward resilience. It is a reality check, like a call from a loved one, reminding the user to take a break and care for him- or herself before returning to work.

Part of self-care is avoiding compassion fatigue, which means avoiding negative feelings toward the ability to complete a job effectively or handle work-related stress. Compassion fatigue has 2 components, according to T2: burnout and secondary traumatic stress. To avoid or combat compassion fatigue, the app gives frontline providers tools to keep themselves productive and emotionally healthy as they help our nation’s service members, veterans, and their families.

DASHBOARD

The app’s home screen is a dashboard, which tracks wellbeing across 4 parameters, all based on self-assessments: vacation time, burnout scale, builders and killers checklist, and professional quality-of-life (ProQOL) measures. Each of these 4 assessments calculates the user’s resilience rating, displayed by a colored meter measuring from 0 (low) to 100 (high).

Beneath the resilience rating meter is a prominent vacation clock, running time down to the minute since the user’s last recorded vacation day. To measure burnout, the app offers a survey for 10 measures that should be updated by the user at least once a week. The question asked of users is, “How would you describe yourself as you approach your workday today?” All measures, including happy, trapped, satisfied, and preoccupied, can be rated from “Not at All” to “Very Much So.”  

Builders and Killers is a daily check-in on the user’s work-life balance. Selecting from a quick 10-item checklist across 2 pages is all it takes to update this section. Items from the list include “Did you take a short walk” and “Did you come to work sick today?” There are even 2 editable items where the user may enter his or her own “Personal Killer.”

The professional quality-of-life (ProQOL) quiz is the longest of all—30 questions—but the resilience rating relies on an update only every 30 days. This quiz measures 3 critical components of ProQOL: compassion satisfaction, burnout, and secondary traumatic stress. Average scores provide the following output for each section:

1. Compassion Satisfaction: “You’ve scored in the average range of Compassion Satisfaction. … This suggests that you don’t find your work to be consistently satisfying, but that you do derive some degree of satisfaction from your daily work activities."

2. Burnout: “Your Burnout score is in the average range. … This may indicate that you are currently experiencing frustration in your work and may be feeling discouraged or ineffective. It may be worth reviewing your answers to see if you can pin down the source of these feelings and determine how you might improve your experience at work.”

3. Secondary Traumatic Stress: “If you are working with clients or patients who are describing highly traumatic experiences, be sure to focus on self-care, which includes maintaining physical, emotional, social, and spiritual supports.”

The dashboard also tracks how many days until the user needs to update each section, and daily reminders (push notifications) to do so may be modified in Settings.

TOOLS

There are 7 videos currently loaded into the app. Two informational videos (both running under 10 minutes) cover burnout and secondary traumatic stress so that users can gain a richer understanding either of what they are experiencing or what they are trying to avoid. The remaining 5 videos are shorter and  can be found in the “Remind Me Why I Do This” menu. These videos cover important patient characteristics that have been found to lead to compassion fatigue, including alcohol, anger, depression, depression support, and stigma.

Scrolling flashcards can be found in “Physical Exercise” and include an assortment of stretching exercises the user can perform at his or her work desk. And if stretching doesn’t release enough endorphins, the user can raise his or her spirit browsing the cartoons found in “I Need A Laugh.” All of the cartoons are office-related, updated daily, and archived for the user’s pleasure.

VALUE CARDS

Nearly 100 inspirational flashcards are loaded onto the app, each one defining a valuable character trait, associated quote, and affirmations. To scroll through the cards, which are listed alphabetically from “Acceptance” through “Unity,” simply swipe left or right. To flip the card over, swipe up or down on the screen.

 

FINAL THOUGHTS

Certain luxuries we have grown accustomed to, such as rotating a device to change display orientation, don’t perform on this app, a feature missed greatly when viewing videos and a good reason to use the app on a tablet, not a phone.

And although everyone needs the occasional short break or multiday vacation, tolerance levels differ from person to person. Hence, it is important to use the app over a period of time so that the user can learn what his or her “normal” is and track readings not necessarily against the general population, but against him- or herself on the plotted ProQOL and burnout graphs.

“Health care professionals know that they need to take care of themselves and tend to know what to do to fight stress—they just don’t take the time to do it.”  That is according to the National Center for Telehealth and Technology (T2), which brings to health care providers a mobile app designed to guide users on a daily path toward resilience. It is a reality check, like a call from a loved one, reminding the user to take a break and care for him- or herself before returning to work.

Part of self-care is avoiding compassion fatigue, which means avoiding negative feelings toward the ability to complete a job effectively or handle work-related stress. Compassion fatigue has 2 components, according to T2: burnout and secondary traumatic stress. To avoid or combat compassion fatigue, the app gives frontline providers tools to keep themselves productive and emotionally healthy as they help our nation’s service members, veterans, and their families.

DASHBOARD

The app’s home screen is a dashboard, which tracks wellbeing across 4 parameters, all based on self-assessments: vacation time, burnout scale, builders and killers checklist, and professional quality-of-life (ProQOL) measures. Each of these 4 assessments calculates the user’s resilience rating, displayed by a colored meter measuring from 0 (low) to 100 (high).

Beneath the resilience rating meter is a prominent vacation clock, running time down to the minute since the user’s last recorded vacation day. To measure burnout, the app offers a survey for 10 measures that should be updated by the user at least once a week. The question asked of users is, “How would you describe yourself as you approach your workday today?” All measures, including happy, trapped, satisfied, and preoccupied, can be rated from “Not at All” to “Very Much So.”  

Builders and Killers is a daily check-in on the user’s work-life balance. Selecting from a quick 10-item checklist across 2 pages is all it takes to update this section. Items from the list include “Did you take a short walk” and “Did you come to work sick today?” There are even 2 editable items where the user may enter his or her own “Personal Killer.”

The professional quality-of-life (ProQOL) quiz is the longest of all—30 questions—but the resilience rating relies on an update only every 30 days. This quiz measures 3 critical components of ProQOL: compassion satisfaction, burnout, and secondary traumatic stress. Average scores provide the following output for each section:

1. Compassion Satisfaction: “You’ve scored in the average range of Compassion Satisfaction. … This suggests that you don’t find your work to be consistently satisfying, but that you do derive some degree of satisfaction from your daily work activities."

2. Burnout: “Your Burnout score is in the average range. … This may indicate that you are currently experiencing frustration in your work and may be feeling discouraged or ineffective. It may be worth reviewing your answers to see if you can pin down the source of these feelings and determine how you might improve your experience at work.”

3. Secondary Traumatic Stress: “If you are working with clients or patients who are describing highly traumatic experiences, be sure to focus on self-care, which includes maintaining physical, emotional, social, and spiritual supports.”

The dashboard also tracks how many days until the user needs to update each section, and daily reminders (push notifications) to do so may be modified in Settings.

TOOLS

There are 7 videos currently loaded into the app. Two informational videos (both running under 10 minutes) cover burnout and secondary traumatic stress so that users can gain a richer understanding either of what they are experiencing or what they are trying to avoid. The remaining 5 videos are shorter and  can be found in the “Remind Me Why I Do This” menu. These videos cover important patient characteristics that have been found to lead to compassion fatigue, including alcohol, anger, depression, depression support, and stigma.

Scrolling flashcards can be found in “Physical Exercise” and include an assortment of stretching exercises the user can perform at his or her work desk. And if stretching doesn’t release enough endorphins, the user can raise his or her spirit browsing the cartoons found in “I Need A Laugh.” All of the cartoons are office-related, updated daily, and archived for the user’s pleasure.

VALUE CARDS

Nearly 100 inspirational flashcards are loaded onto the app, each one defining a valuable character trait, associated quote, and affirmations. To scroll through the cards, which are listed alphabetically from “Acceptance” through “Unity,” simply swipe left or right. To flip the card over, swipe up or down on the screen.

 

FINAL THOUGHTS

Certain luxuries we have grown accustomed to, such as rotating a device to change display orientation, don’t perform on this app, a feature missed greatly when viewing videos and a good reason to use the app on a tablet, not a phone.

And although everyone needs the occasional short break or multiday vacation, tolerance levels differ from person to person. Hence, it is important to use the app over a period of time so that the user can learn what his or her “normal” is and track readings not necessarily against the general population, but against him- or herself on the plotted ProQOL and burnout graphs.

The risk of premature menopause among survivors of Hodgkin lymphoma (HL) may vary greatly, according to a study of more than 2000 women.

The results suggest that ovarian radiotherapy and certain chemotherapeutic regimens increase a woman’s risk of premature menopause.

And the radiation dose, number of treatment cycles, and patient age at treatment all influence that risk.

The findings appear in the Journal of the National Cancer Institute.

Previous research suggested that women with HL who receive certain types of chemotherapy or radiotherapy are at an increased risk of early menopause, but there was insufficient information to provide patients with detailed advice.

To gain more insight, Anthony Swerdlow, DSc, of The Institute of Cancer Research in London, UK, and his colleagues studied 2127 women who were treated for HL in England or Wales between 1960 and 2004.

All of the women were younger than 36 at the time of treatment, and all had received chest radiotherapy, sometimes alongside other treatments.

Some 605 of the women underwent non-surgical menopause before the age of 40. The researchers said this was a large enough number for them to estimate accurate risks of menopause, depending on the type and dose of treatments patients received and the age they received them.

The team found that several treatments caused a sharp increase in premature menopause risk, and menopause was more like among women treated at older ages.

The risk of premature menopause increased more than 20-fold after ovarian radiotherapy, alkylating chemotherapy other than dacarbazine, or BEAM (bis-chloroethylnitrosourea, etoposide, cytarabine, melphalan) chemotherapy given prior to stem cell transplant.

However, there was no significant increase in risk after receiving adriamycin, bleomycin, vinblastine, dacarbazine (ABVD).

Within 5 years of treatment, menopause had occurred in 62.5% of patients who received ≥5 Gy of ovarian radiotherapy, 50.9% of patients who received BEAM, and 24.2% of patients who received ≥6 cycles of alkylating chemotherapy.

The cumulative risk of menopause by age 40 was 81.3% after ≥ 5 Gy of ovarian radiotherapy, 75.3% after BEAM, 49.1% after ≥ 6 cycles of alkylating chemotherapy, 3.0% after solely supradiaphragmatic radiotherapy, and 1.4% after ABVD.

“We hope our study will help women to understand better, in consultation with their doctors, their risks of future infertility following treatment for this malignancy,” Dr Swerdlow said.

“By looking in a much larger group of women than previous studies of this type, we were able to produce age- and treatment-specific risk estimates that we hope will be of practical use to individual women.”

The risk of premature menopause among survivors of Hodgkin lymphoma (HL) may vary greatly, according to a study of more than 2000 women.

The results suggest that ovarian radiotherapy and certain chemotherapeutic regimens increase a woman’s risk of premature menopause.

And the radiation dose, number of treatment cycles, and patient age at treatment all influence that risk.

The findings appear in the Journal of the National Cancer Institute.

Previous research suggested that women with HL who receive certain types of chemotherapy or radiotherapy are at an increased risk of early menopause, but there was insufficient information to provide patients with detailed advice.

To gain more insight, Anthony Swerdlow, DSc, of The Institute of Cancer Research in London, UK, and his colleagues studied 2127 women who were treated for HL in England or Wales between 1960 and 2004.

All of the women were younger than 36 at the time of treatment, and all had received chest radiotherapy, sometimes alongside other treatments.

Some 605 of the women underwent non-surgical menopause before the age of 40. The researchers said this was a large enough number for them to estimate accurate risks of menopause, depending on the type and dose of treatments patients received and the age they received them.

The team found that several treatments caused a sharp increase in premature menopause risk, and menopause was more like among women treated at older ages.

The risk of premature menopause increased more than 20-fold after ovarian radiotherapy, alkylating chemotherapy other than dacarbazine, or BEAM (bis-chloroethylnitrosourea, etoposide, cytarabine, melphalan) chemotherapy given prior to stem cell transplant.

However, there was no significant increase in risk after receiving adriamycin, bleomycin, vinblastine, dacarbazine (ABVD).

Within 5 years of treatment, menopause had occurred in 62.5% of patients who received ≥5 Gy of ovarian radiotherapy, 50.9% of patients who received BEAM, and 24.2% of patients who received ≥6 cycles of alkylating chemotherapy.

The cumulative risk of menopause by age 40 was 81.3% after ≥ 5 Gy of ovarian radiotherapy, 75.3% after BEAM, 49.1% after ≥ 6 cycles of alkylating chemotherapy, 3.0% after solely supradiaphragmatic radiotherapy, and 1.4% after ABVD.

“We hope our study will help women to understand better, in consultation with their doctors, their risks of future infertility following treatment for this malignancy,” Dr Swerdlow said.

“By looking in a much larger group of women than previous studies of this type, we were able to produce age- and treatment-specific risk estimates that we hope will be of practical use to individual women.”

The risk of premature menopause among survivors of Hodgkin lymphoma (HL) may vary greatly, according to a study of more than 2000 women.

The results suggest that ovarian radiotherapy and certain chemotherapeutic regimens increase a woman’s risk of premature menopause.

And the radiation dose, number of treatment cycles, and patient age at treatment all influence that risk.

The findings appear in the Journal of the National Cancer Institute.

Previous research suggested that women with HL who receive certain types of chemotherapy or radiotherapy are at an increased risk of early menopause, but there was insufficient information to provide patients with detailed advice.

To gain more insight, Anthony Swerdlow, DSc, of The Institute of Cancer Research in London, UK, and his colleagues studied 2127 women who were treated for HL in England or Wales between 1960 and 2004.

All of the women were younger than 36 at the time of treatment, and all had received chest radiotherapy, sometimes alongside other treatments.

Some 605 of the women underwent non-surgical menopause before the age of 40. The researchers said this was a large enough number for them to estimate accurate risks of menopause, depending on the type and dose of treatments patients received and the age they received them.

The team found that several treatments caused a sharp increase in premature menopause risk, and menopause was more like among women treated at older ages.

The risk of premature menopause increased more than 20-fold after ovarian radiotherapy, alkylating chemotherapy other than dacarbazine, or BEAM (bis-chloroethylnitrosourea, etoposide, cytarabine, melphalan) chemotherapy given prior to stem cell transplant.

However, there was no significant increase in risk after receiving adriamycin, bleomycin, vinblastine, dacarbazine (ABVD).

Within 5 years of treatment, menopause had occurred in 62.5% of patients who received ≥5 Gy of ovarian radiotherapy, 50.9% of patients who received BEAM, and 24.2% of patients who received ≥6 cycles of alkylating chemotherapy.

The cumulative risk of menopause by age 40 was 81.3% after ≥ 5 Gy of ovarian radiotherapy, 75.3% after BEAM, 49.1% after ≥ 6 cycles of alkylating chemotherapy, 3.0% after solely supradiaphragmatic radiotherapy, and 1.4% after ABVD.

“We hope our study will help women to understand better, in consultation with their doctors, their risks of future infertility following treatment for this malignancy,” Dr Swerdlow said.

“By looking in a much larger group of women than previous studies of this type, we were able to produce age- and treatment-specific risk estimates that we hope will be of practical use to individual women.”

A semi-automated system may allow healthcare professionals to diagnose malaria infection with more than 90% accuracy.

With this system, a computer algorithm analyzes red blood cells from a digitized slide, ranks them according to the likelihood of infection, and presents the user with more than 100 images from which to make a diagnosis.

Johan Lundin, MD, PhD, of the Institute for Molecular Medicine Finland, and his colleagues described the system in PLOS ONE.

The researchers noted that high-quality microscopy is still the most accurate method for detecting malaria infection. However, as microscopy can be time-consuming, the team wanted to streamline the process by developing a semi-automated system.

“We are not suggesting that the whole malaria diagnostic process could or should be automated,” Dr Lundin said. “Rather, our aim is to develop methods that are significantly less labor-intensive than the traditional ones and have a potential to considerably increase the throughput in malaria diagnostics.”

The group’s method is based on computer vision algorithms similar to those used in facial recognition software. First, a thin layer of blood smeared on a microscope slide is digitized. Then, a computer algorithm analyzes more than 50,000 red blood cells per sample and ranks them according to the probability of malaria infection.

Next, the program creates a panel containing images of more than a hundred cells that are the most likely to be infected and presents that panel to the user. The final diagnosis is made by a healthcare professional based on the images.

To test this system, Dr Lundin and his colleagues used a set of samples from 19 patients already diagnosed with malaria and 12 control subjects. From each sample, the researchers created a digitized slide, and the system generated 128 images of the most probable parasite candidate regions.

Two expert microscopists viewed the images on a tablet computer to determine whether a subject was infected with Plasmodium falciparum.

The diagnostic sensitivity was 90% with one viewer and 95% for the other. The specificity was 100% for both viewers.

Based on these results, the researchers said this system has the potential to increase the throughput in malaria diagnostics. However, it does require some tweaking, and the team would like to expand its capabilities.

“The equipment needed for digitization of the samples is a challenge in developed countries,” said study author Nina Linder, MD, PhD, also of the Institute for Molecular Medicine Finland. “In the next phase of our project, we will test the system in combination with inexpensive mobile microscopy devices that our group has also developed.”

“There is also a strong need for fast and accurate methods for measuring the malaria parasite load in a sample,” she added. “Various malaria drug screening programs are underway, and the parasite load in a large number of samples needs to be quantified for determining the efficacy of potential drugs. We are further developing the computer algorithms used in this study to meet this need as well.”

Lastly, the researchers said this system could be applied in various other fields of medicine. In addition to other infectious diseases such as tuberculosis, the group is planning to test the system’s utility in cancer diagnosis.

A semi-automated system may allow healthcare professionals to diagnose malaria infection with more than 90% accuracy.

With this system, a computer algorithm analyzes red blood cells from a digitized slide, ranks them according to the likelihood of infection, and presents the user with more than 100 images from which to make a diagnosis.

Johan Lundin, MD, PhD, of the Institute for Molecular Medicine Finland, and his colleagues described the system in PLOS ONE.

The researchers noted that high-quality microscopy is still the most accurate method for detecting malaria infection. However, as microscopy can be time-consuming, the team wanted to streamline the process by developing a semi-automated system.

“We are not suggesting that the whole malaria diagnostic process could or should be automated,” Dr Lundin said. “Rather, our aim is to develop methods that are significantly less labor-intensive than the traditional ones and have a potential to considerably increase the throughput in malaria diagnostics.”

The group’s method is based on computer vision algorithms similar to those used in facial recognition software. First, a thin layer of blood smeared on a microscope slide is digitized. Then, a computer algorithm analyzes more than 50,000 red blood cells per sample and ranks them according to the probability of malaria infection.

Next, the program creates a panel containing images of more than a hundred cells that are the most likely to be infected and presents that panel to the user. The final diagnosis is made by a healthcare professional based on the images.

To test this system, Dr Lundin and his colleagues used a set of samples from 19 patients already diagnosed with malaria and 12 control subjects. From each sample, the researchers created a digitized slide, and the system generated 128 images of the most probable parasite candidate regions.

Two expert microscopists viewed the images on a tablet computer to determine whether a subject was infected with Plasmodium falciparum.

The diagnostic sensitivity was 90% with one viewer and 95% for the other. The specificity was 100% for both viewers.

Based on these results, the researchers said this system has the potential to increase the throughput in malaria diagnostics. However, it does require some tweaking, and the team would like to expand its capabilities.

“The equipment needed for digitization of the samples is a challenge in developed countries,” said study author Nina Linder, MD, PhD, also of the Institute for Molecular Medicine Finland. “In the next phase of our project, we will test the system in combination with inexpensive mobile microscopy devices that our group has also developed.”

“There is also a strong need for fast and accurate methods for measuring the malaria parasite load in a sample,” she added. “Various malaria drug screening programs are underway, and the parasite load in a large number of samples needs to be quantified for determining the efficacy of potential drugs. We are further developing the computer algorithms used in this study to meet this need as well.”

Lastly, the researchers said this system could be applied in various other fields of medicine. In addition to other infectious diseases such as tuberculosis, the group is planning to test the system’s utility in cancer diagnosis.

A semi-automated system may allow healthcare professionals to diagnose malaria infection with more than 90% accuracy.

With this system, a computer algorithm analyzes red blood cells from a digitized slide, ranks them according to the likelihood of infection, and presents the user with more than 100 images from which to make a diagnosis.

Johan Lundin, MD, PhD, of the Institute for Molecular Medicine Finland, and his colleagues described the system in PLOS ONE.

The researchers noted that high-quality microscopy is still the most accurate method for detecting malaria infection. However, as microscopy can be time-consuming, the team wanted to streamline the process by developing a semi-automated system.

“We are not suggesting that the whole malaria diagnostic process could or should be automated,” Dr Lundin said. “Rather, our aim is to develop methods that are significantly less labor-intensive than the traditional ones and have a potential to considerably increase the throughput in malaria diagnostics.”

The group’s method is based on computer vision algorithms similar to those used in facial recognition software. First, a thin layer of blood smeared on a microscope slide is digitized. Then, a computer algorithm analyzes more than 50,000 red blood cells per sample and ranks them according to the probability of malaria infection.

Next, the program creates a panel containing images of more than a hundred cells that are the most likely to be infected and presents that panel to the user. The final diagnosis is made by a healthcare professional based on the images.

To test this system, Dr Lundin and his colleagues used a set of samples from 19 patients already diagnosed with malaria and 12 control subjects. From each sample, the researchers created a digitized slide, and the system generated 128 images of the most probable parasite candidate regions.

Two expert microscopists viewed the images on a tablet computer to determine whether a subject was infected with Plasmodium falciparum.

The diagnostic sensitivity was 90% with one viewer and 95% for the other. The specificity was 100% for both viewers.

Based on these results, the researchers said this system has the potential to increase the throughput in malaria diagnostics. However, it does require some tweaking, and the team would like to expand its capabilities.

“The equipment needed for digitization of the samples is a challenge in developed countries,” said study author Nina Linder, MD, PhD, also of the Institute for Molecular Medicine Finland. “In the next phase of our project, we will test the system in combination with inexpensive mobile microscopy devices that our group has also developed.”

“There is also a strong need for fast and accurate methods for measuring the malaria parasite load in a sample,” she added. “Various malaria drug screening programs are underway, and the parasite load in a large number of samples needs to be quantified for determining the efficacy of potential drugs. We are further developing the computer algorithms used in this study to meet this need as well.”

Lastly, the researchers said this system could be applied in various other fields of medicine. In addition to other infectious diseases such as tuberculosis, the group is planning to test the system’s utility in cancer diagnosis.

A recombinant factor VIII (rFVIII) product known as BAX 855 can prevent bleeding in hemophilia A patients, according to Baxter International, the company developing the product.

BAX 855 is a pegylated version of ADVATE, a full-length rFVIII product already approved to treat hemophilia A.

In a phase 3 study, BAX 855 met the primary endpoint of reducing annualized bleed rates (ABRs) among hemophilia A patients when used as prophylaxis rather than on-demand treatment.

The trial included 138 patients age 12 and older with previously treated hemophilia A. The patients received BAX 855 either twice weekly (45 IU/kg) or on-demand and were followed for 6 months.

The primary objective was to show that BAX 855 prophylaxis can reduce ABRs compared to on-demand treatment. The researchers’ other objectives were to evaluate the safety and immunogenicity of the compound when administered as prophylaxis or on-demand.

BAX 855 met its primary endpoint in the control and prevention of bleeding, routine prophylaxis, and perioperative management.

Patients in the twice-weekly prophylaxis arm experienced a 95% reduction in median ABR compared to those in the on-demand arm (1.9% vs 41.5%, respectively). BAX 855 was also effective in treating bleeding episodes, 96% of which were controlled with 1 or 2 infusions.

The half-life of BAX 855 was 1.4 to 1.5 times that of ADVATE, which is consistent with the findings from a phase 1 study.

No patients developed inhibitors to BAX 855 and no treatment-related serious adverse events, including hypersensitivity, were reported. The most common treatment-related adverse event was headache, which occurred in 3 patients.

Baxter said it expects to submit a biologics license application for BAX 855 to the US Food and Drug Administration before the end of 2014 and to present additional trial data in the coming months.

In addition to an ongoing continuation study for patients who have completed the pivotal trial, the company is starting a phase 3 study to evaluate the safety and efficacy of BAX 855 among 60 previously treated hemophilia A patients younger than 12 years of age.

Consistent with guidelines published by the European Medicines Agency that require a study in children less than 12 years of age prior to filing, Baxter expects to file a marketing authorization application with the agency upon the completing the pediatric study.

A recombinant factor VIII (rFVIII) product known as BAX 855 can prevent bleeding in hemophilia A patients, according to Baxter International, the company developing the product.

BAX 855 is a pegylated version of ADVATE, a full-length rFVIII product already approved to treat hemophilia A.

In a phase 3 study, BAX 855 met the primary endpoint of reducing annualized bleed rates (ABRs) among hemophilia A patients when used as prophylaxis rather than on-demand treatment.

The trial included 138 patients age 12 and older with previously treated hemophilia A. The patients received BAX 855 either twice weekly (45 IU/kg) or on-demand and were followed for 6 months.

The primary objective was to show that BAX 855 prophylaxis can reduce ABRs compared to on-demand treatment. The researchers’ other objectives were to evaluate the safety and immunogenicity of the compound when administered as prophylaxis or on-demand.

BAX 855 met its primary endpoint in the control and prevention of bleeding, routine prophylaxis, and perioperative management.

Patients in the twice-weekly prophylaxis arm experienced a 95% reduction in median ABR compared to those in the on-demand arm (1.9% vs 41.5%, respectively). BAX 855 was also effective in treating bleeding episodes, 96% of which were controlled with 1 or 2 infusions.

The half-life of BAX 855 was 1.4 to 1.5 times that of ADVATE, which is consistent with the findings from a phase 1 study.

No patients developed inhibitors to BAX 855 and no treatment-related serious adverse events, including hypersensitivity, were reported. The most common treatment-related adverse event was headache, which occurred in 3 patients.

Baxter said it expects to submit a biologics license application for BAX 855 to the US Food and Drug Administration before the end of 2014 and to present additional trial data in the coming months.

In addition to an ongoing continuation study for patients who have completed the pivotal trial, the company is starting a phase 3 study to evaluate the safety and efficacy of BAX 855 among 60 previously treated hemophilia A patients younger than 12 years of age.

Consistent with guidelines published by the European Medicines Agency that require a study in children less than 12 years of age prior to filing, Baxter expects to file a marketing authorization application with the agency upon the completing the pediatric study.

A recombinant factor VIII (rFVIII) product known as BAX 855 can prevent bleeding in hemophilia A patients, according to Baxter International, the company developing the product.

BAX 855 is a pegylated version of ADVATE, a full-length rFVIII product already approved to treat hemophilia A.

In a phase 3 study, BAX 855 met the primary endpoint of reducing annualized bleed rates (ABRs) among hemophilia A patients when used as prophylaxis rather than on-demand treatment.

The trial included 138 patients age 12 and older with previously treated hemophilia A. The patients received BAX 855 either twice weekly (45 IU/kg) or on-demand and were followed for 6 months.

The primary objective was to show that BAX 855 prophylaxis can reduce ABRs compared to on-demand treatment. The researchers’ other objectives were to evaluate the safety and immunogenicity of the compound when administered as prophylaxis or on-demand.

BAX 855 met its primary endpoint in the control and prevention of bleeding, routine prophylaxis, and perioperative management.

Patients in the twice-weekly prophylaxis arm experienced a 95% reduction in median ABR compared to those in the on-demand arm (1.9% vs 41.5%, respectively). BAX 855 was also effective in treating bleeding episodes, 96% of which were controlled with 1 or 2 infusions.

The half-life of BAX 855 was 1.4 to 1.5 times that of ADVATE, which is consistent with the findings from a phase 1 study.

No patients developed inhibitors to BAX 855 and no treatment-related serious adverse events, including hypersensitivity, were reported. The most common treatment-related adverse event was headache, which occurred in 3 patients.

Baxter said it expects to submit a biologics license application for BAX 855 to the US Food and Drug Administration before the end of 2014 and to present additional trial data in the coming months.

In addition to an ongoing continuation study for patients who have completed the pivotal trial, the company is starting a phase 3 study to evaluate the safety and efficacy of BAX 855 among 60 previously treated hemophilia A patients younger than 12 years of age.

Consistent with guidelines published by the European Medicines Agency that require a study in children less than 12 years of age prior to filing, Baxter expects to file a marketing authorization application with the agency upon the completing the pediatric study.

Researchers say they’ve developed a new computational method to predict the function of disease-causing genes and proteins, and this has enabled an important discovery.

The team used the method to study EXP1, a protein known to be essential to the malaria parasite Plasmodium falciparum, although its exact mechanism has been unclear.

The research revealed that EXP1 enables the parasite to detoxify the main metabolic byproducts it creates in red blood cells.

The researchers also found that EXP1 has a direct role in drug action and susceptibility to artesunate, an important member of the artemisinin drug family.

“Through this multiyear collaborative effort, we now have an improved understanding of the protective molecular mechanisms of the malaria parasite and its drug susceptibility to artesunate,” said study author Olivier Lichtarge, MD, PhD, of the Baylor College of Medicine in Houston, Texas.

“As we are witnessing a rise of resistance to artemisinins, these results may help [us in] finding new pathways to successor drugs.”

Dr Lichtarge and his colleagues described this research in Cell.

The team devised a computational method that allows biological information to flow from gene to gene across the supergenomic network.

“The network connects millions of genes from hundreds of species based on their interactions within the organism or based on their ancestral relations between different species,” said study author Andreas Martin Lisewski, PhD, also of the Baylor College of Medicine.

“Normally, computing the flow of functional information would be costly and slow, but we developed a compression method that reduces this gigantic network into one that is much smaller and now computationally tractable. The surprise is that these biological networks are compressible, much like digital data in today’s computers.”

To test their method, the researchers looked at functional predictions of P falciparum. It’s been more than 10 years since this parasite’s genome was fully sequenced, but little is known about the function for most of its genes.

“To better understand this disease, we need to identify more functions of the parasite’s genes,” Dr Lisewski said. “This understanding may eventually help us to stem the rise of drug-resistant malaria, such as the emerging resistance to artemisinins.”

With that in mind, the researchers used their computational method to study EXP1. And they discovered the protein is a membrane glutathione S-transferase that degrades cytotoxic hematin but is inhibited by artesunate.

Researchers say they’ve developed a new computational method to predict the function of disease-causing genes and proteins, and this has enabled an important discovery.

The team used the method to study EXP1, a protein known to be essential to the malaria parasite Plasmodium falciparum, although its exact mechanism has been unclear.

The research revealed that EXP1 enables the parasite to detoxify the main metabolic byproducts it creates in red blood cells.

The researchers also found that EXP1 has a direct role in drug action and susceptibility to artesunate, an important member of the artemisinin drug family.

“Through this multiyear collaborative effort, we now have an improved understanding of the protective molecular mechanisms of the malaria parasite and its drug susceptibility to artesunate,” said study author Olivier Lichtarge, MD, PhD, of the Baylor College of Medicine in Houston, Texas.

“As we are witnessing a rise of resistance to artemisinins, these results may help [us in] finding new pathways to successor drugs.”

Dr Lichtarge and his colleagues described this research in Cell.

The team devised a computational method that allows biological information to flow from gene to gene across the supergenomic network.

“The network connects millions of genes from hundreds of species based on their interactions within the organism or based on their ancestral relations between different species,” said study author Andreas Martin Lisewski, PhD, also of the Baylor College of Medicine.

“Normally, computing the flow of functional information would be costly and slow, but we developed a compression method that reduces this gigantic network into one that is much smaller and now computationally tractable. The surprise is that these biological networks are compressible, much like digital data in today’s computers.”

To test their method, the researchers looked at functional predictions of P falciparum. It’s been more than 10 years since this parasite’s genome was fully sequenced, but little is known about the function for most of its genes.

“To better understand this disease, we need to identify more functions of the parasite’s genes,” Dr Lisewski said. “This understanding may eventually help us to stem the rise of drug-resistant malaria, such as the emerging resistance to artemisinins.”

With that in mind, the researchers used their computational method to study EXP1. And they discovered the protein is a membrane glutathione S-transferase that degrades cytotoxic hematin but is inhibited by artesunate.

Researchers say they’ve developed a new computational method to predict the function of disease-causing genes and proteins, and this has enabled an important discovery.

The team used the method to study EXP1, a protein known to be essential to the malaria parasite Plasmodium falciparum, although its exact mechanism has been unclear.

The research revealed that EXP1 enables the parasite to detoxify the main metabolic byproducts it creates in red blood cells.

The researchers also found that EXP1 has a direct role in drug action and susceptibility to artesunate, an important member of the artemisinin drug family.

“Through this multiyear collaborative effort, we now have an improved understanding of the protective molecular mechanisms of the malaria parasite and its drug susceptibility to artesunate,” said study author Olivier Lichtarge, MD, PhD, of the Baylor College of Medicine in Houston, Texas.

“As we are witnessing a rise of resistance to artemisinins, these results may help [us in] finding new pathways to successor drugs.”

Dr Lichtarge and his colleagues described this research in Cell.

The team devised a computational method that allows biological information to flow from gene to gene across the supergenomic network.

“The network connects millions of genes from hundreds of species based on their interactions within the organism or based on their ancestral relations between different species,” said study author Andreas Martin Lisewski, PhD, also of the Baylor College of Medicine.

“Normally, computing the flow of functional information would be costly and slow, but we developed a compression method that reduces this gigantic network into one that is much smaller and now computationally tractable. The surprise is that these biological networks are compressible, much like digital data in today’s computers.”

To test their method, the researchers looked at functional predictions of P falciparum. It’s been more than 10 years since this parasite’s genome was fully sequenced, but little is known about the function for most of its genes.

“To better understand this disease, we need to identify more functions of the parasite’s genes,” Dr Lisewski said. “This understanding may eventually help us to stem the rise of drug-resistant malaria, such as the emerging resistance to artemisinins.”

With that in mind, the researchers used their computational method to study EXP1. And they discovered the protein is a membrane glutathione S-transferase that degrades cytotoxic hematin but is inhibited by artesunate.