From MedscapeCME Clinical Briefs
News Author: Pauline Anderson
CME Author: Charles P. Vega, MD
Headache. Published online June 7, 2010.
Clinical Context
Somatic complaints are common among adolescent girls, according to a study by Ghandour and colleagues, which appeared in the August 2004 issue of Archives of Pediatric & Adolescent Medicine. In a survey of 8250 adolescent girls across the United States, researchers found that the prevalence rates of stomach ache and back pain occurring more than once a week each exceeded 20%. A total of 30.6% of girls reported regular symptoms of morning fatigue, and 29.1% experienced headaches more than once a week. Multiple somatic symptoms also tended to cluster in the same individual.
Lifestyle factors have been linked to a higher risk for headaches among adults, but there is less information on this potential relationship among children and adolescents. The current study addresses this issue.
Study Highlights
The study was completed at 11 public schools in Germany. Researchers focused on students in the 10th and 11th grades (aged between 14 and 20 years).
Study participants completed a questionnaire regarding headache and lifestyle factors. Adolescents who reported headache in the last 6 months were asked to provide more data about the headache, which were then used to give them a provisional headache diagnosis.
The main study outcome was the relationship between lifestyle factors and the prevalence of headache. Lifestyle factors included diet, exercise, smoking, and alcohol consumption. The study analysis was adjusted to account for age, sex, and socioeconomic status.
1260 adolescents provided study data. Many participants had a poor diet: 28.4% never had breakfast, and only 13.3% ate 3 to 5 servings of fruit and vegetables per day.
Nearly one quarter of the study cohort smoked cigarettes, and 56.6% of respondents drank coffee. Alcohol use was also widespread.
83.1% of participants reported headache in the last 6 months. 48.7% of participants had TTH, and 10.2% had migraine headache. The remainder of the headaches was mixed type or not classified.
Drinking cocktails at least once a week, drinking at least 1 cup of coffee per day, and low levels of physical activity were all associated with an adjusted OR of 2.0 for headache.
The OR for migraine among adolescents who reported drinking at least 1 cup of coffee per day was 3.4, and the respective OR among students who were less physically active was 4.2.
TTH was most associated with being less physically active (OR, 1.7).
Smoking was less associated with the risk for headache, and skipping breakfast had no correlation with headache. Consuming beer and fruit and vegetable consumption were also not significantly associated with the prevalence of headache.
Clinical Implications
A previous survey of adolescent girls in the United States found high rates of stomachache, back pain, morning fatigue, and headache. Symptoms tended to cluster in individual adolescents.
The current study demonstrates a correlation between headaches among adolescents and drinking cocktails, low levels of physical activity, and coffee consumption. Low levels of fruit and vegetable consumption, skipping breakfast, and drinking beer were not significantly associated with the prevalence of headache.
Tuesday, July 6, 2010
Friday, July 2, 2010
Caffeine May Ward Off Exercise-Related Hypoglycemia in Type 1 Diabetes
From Medscape Medical News
Fran Lowry
July 1, 2010 (Orlando, Florida) — A small proof-of-concept study in adult athletes with type 1 diabetes suggests that ingesting caffeine before exercise may reduce or prevent hypoglycemia. Results were presented here at the American Diabetes Association (ADA) 70th Scientific Sessions.
Currently, adult athletes with type 1 diabetes have very few tools they can use, said Ian W. Gallen, MD, consultant physician at Buckinghamshire Hospitals Trust, High Wycombe, United Kingdom, in a poster presentation.
"All they can do is reduce their shots of insulin or take extra food," said Dr. Gallen, who tries to help young athletes with type 1 diabetes perform better in their sports because of difficulties with hypoglycemia and poor performance."
Dr. Gallen studied 4 men and 1 woman (mean age, 38 years; mean body mass index, 27 kg/m2) who were on a multiple daily injection regimen with glargine-aspart. On study day 1, he measured their maximum oxygen consumption (VO2 max) to assess workload. On day 2, the subjects ingested caffeine, 5 mg/kg, or placebo tablets mixed with a drink, in random order, 2 hours after a meal and insulin injection. They then rested for 30 minutes.
After their rest, the subjects exercised on a stationary bicycle for 10 minutes at 50% VO2 max, and then for another 30 minutes at 70% VO2 max. Work output was measured by gas exchange to ensure that work output was fixed and arterialized blood samples were analyzed throughout the study.
The subjects then were crossed over to placebo or caffeine and the study was repeated.
On the day that the subjects received caffeine, their blood glucose levels stayed up and they did not need glucose, but when they received placebo, their blood glucose levels fell and they needed glucose, Dr. Gallen said.
When receiving placebo, subjects' blood glucose when they began to exercise was 10.3 ± 1.4 mmol/L and decreased to 8.0 ± 1.7 mmol/L during exercise. Two subjects required 20 g of oral glucose to avoid hypoglycemia.
When on caffeine, subjects' blood glucose level when they began to exercise was 13.1 ± 2.1 mmol/L and increased to 15.3 + 3.4 mmol/L during exercise. Glucose was not required for any subject when they were in the caffeine group.
Asked how caffeine augments blood glucose in this setting, Dr. Gallen explained that there is evidence that the counter-regulatory hormone response to exercise is reduced in type 1 diabetes, and caffeine could amplify this poor response, thus making it more normal.
He cautioned that this is a proof-of-concept study, and that larger trials need to be done. Also, the dose of caffeine used in this study was equivalent to twice the daily average for UK caffeine consumption and would not be a practical dose in the real world. Another study is planned with a lower dose of caffeine.
"This method would work very well for unplanned exercise late in the postprandial period when you can't change your shots," Dr. Gallen said. "It would save you having to take extra food and avoid unnecessary weight control."
M. Sue Kirkman, MD, of the American Diabetes Association in Alexandria, Virginia, agreed.
"Hypoglycemia is a big problem, especially with exercise. People can try to prevent it by eating a snack before they exercise or letting their blood sugar run a little higher before they exercise, but those aren't necessarily the healthiest things to do if you have trouble with your weight. If you are having to eat more, this defeats the purpose of exercising," she commented during an interview with Medscape Medical News.
"I think this study is intriguing because it shows that caffeine, which is readily available, can prevent the exercise-induced hypoglycemia in type 1 diabetes. However, it was a small study, just 5 people, and it would need further study, but it is interesting, and it does suggest that something as simple as drinking some coffee might help prevent what really can sometimes be a barrier to people exercising."
Dr. Gallen and Dr. Kirkman have disclosed no relevant financial interests.
American Diabetes Association 70th Scientific Session: Abstract 1184-P. Presented June 26, 2010.
Fran Lowry
July 1, 2010 (Orlando, Florida) — A small proof-of-concept study in adult athletes with type 1 diabetes suggests that ingesting caffeine before exercise may reduce or prevent hypoglycemia. Results were presented here at the American Diabetes Association (ADA) 70th Scientific Sessions.
Currently, adult athletes with type 1 diabetes have very few tools they can use, said Ian W. Gallen, MD, consultant physician at Buckinghamshire Hospitals Trust, High Wycombe, United Kingdom, in a poster presentation.
"All they can do is reduce their shots of insulin or take extra food," said Dr. Gallen, who tries to help young athletes with type 1 diabetes perform better in their sports because of difficulties with hypoglycemia and poor performance."
Dr. Gallen studied 4 men and 1 woman (mean age, 38 years; mean body mass index, 27 kg/m2) who were on a multiple daily injection regimen with glargine-aspart. On study day 1, he measured their maximum oxygen consumption (VO2 max) to assess workload. On day 2, the subjects ingested caffeine, 5 mg/kg, or placebo tablets mixed with a drink, in random order, 2 hours after a meal and insulin injection. They then rested for 30 minutes.
After their rest, the subjects exercised on a stationary bicycle for 10 minutes at 50% VO2 max, and then for another 30 minutes at 70% VO2 max. Work output was measured by gas exchange to ensure that work output was fixed and arterialized blood samples were analyzed throughout the study.
The subjects then were crossed over to placebo or caffeine and the study was repeated.
On the day that the subjects received caffeine, their blood glucose levels stayed up and they did not need glucose, but when they received placebo, their blood glucose levels fell and they needed glucose, Dr. Gallen said.
When receiving placebo, subjects' blood glucose when they began to exercise was 10.3 ± 1.4 mmol/L and decreased to 8.0 ± 1.7 mmol/L during exercise. Two subjects required 20 g of oral glucose to avoid hypoglycemia.
When on caffeine, subjects' blood glucose level when they began to exercise was 13.1 ± 2.1 mmol/L and increased to 15.3 + 3.4 mmol/L during exercise. Glucose was not required for any subject when they were in the caffeine group.
Asked how caffeine augments blood glucose in this setting, Dr. Gallen explained that there is evidence that the counter-regulatory hormone response to exercise is reduced in type 1 diabetes, and caffeine could amplify this poor response, thus making it more normal.
He cautioned that this is a proof-of-concept study, and that larger trials need to be done. Also, the dose of caffeine used in this study was equivalent to twice the daily average for UK caffeine consumption and would not be a practical dose in the real world. Another study is planned with a lower dose of caffeine.
"This method would work very well for unplanned exercise late in the postprandial period when you can't change your shots," Dr. Gallen said. "It would save you having to take extra food and avoid unnecessary weight control."
M. Sue Kirkman, MD, of the American Diabetes Association in Alexandria, Virginia, agreed.
"Hypoglycemia is a big problem, especially with exercise. People can try to prevent it by eating a snack before they exercise or letting their blood sugar run a little higher before they exercise, but those aren't necessarily the healthiest things to do if you have trouble with your weight. If you are having to eat more, this defeats the purpose of exercising," she commented during an interview with Medscape Medical News.
"I think this study is intriguing because it shows that caffeine, which is readily available, can prevent the exercise-induced hypoglycemia in type 1 diabetes. However, it was a small study, just 5 people, and it would need further study, but it is interesting, and it does suggest that something as simple as drinking some coffee might help prevent what really can sometimes be a barrier to people exercising."
Dr. Gallen and Dr. Kirkman have disclosed no relevant financial interests.
American Diabetes Association 70th Scientific Session: Abstract 1184-P. Presented June 26, 2010.
Friday, June 25, 2010
Tics, Tic Disorders, and TS
http://www.medscape.com/viewarticle/442029_2
TS is a neurobiological condition characterized by vocal and motor tics that change over time and wax and wane in severity. TS is part of a spectrum of tic disorders, including transient tic disorder and chronic tic disorder ( Table 1 ).
Diagnosis is based on history and observation, with no specific diagnostic tests available (Bagheri, Kergeshian & Burd, 1999; Kiessling, 2001).
In reviewing family-genetic and epidemiological studies, some researchers suggest that there is little evidence to support the diagnostic distinction between, for example, chronic tics and TS (Peterson, Pine, Cohen & Brook, 2001).
Tics can be defined as "sudden, repetitive, stereotyped motor movements or phonic productions that involve discrete muscle groups" (Leckman, King, & Cohen, 1999, p. 24).
In contrast to other movement disorders, such as chorea or dystonia, tics are exaggerations and repetitions of normal movements (Bagheri et al., 1999; Leckman, Peterson, King, Scahill, & Cohen, 2001).
Primary tics such as TS have no identifiable cause or may be genetic in origin (Jankovic, 2001).
Conditions that could cause secondary tics include head trauma, encephalitis, and some medications.
There is an increased incidence of tics in children with pervasive developmental disorder (Kiessling, 2001).
Tics are commonly classified as simple or complex. Shoulder shrugging, neck twitching, and facial movements are examples of simple motor tics. Touching objects, skipping, and squatting in a rhythmic sequence (such as every four steps) are examples of complex motor tics. Simple vocal tics include sniffing, barking, coughing, yelling, and hiccupping. Complex vocal tics include repeating parts of words or phrases, talking to oneself, assuming different intonations, and uttering obscenities (Bagheri et al., 1999; Leckman et al., 1999).
There is a growing body of literature suggesting that tics are intentional responses to unwanted sensations or urges (Coffey & Park, 1997; Jankovic, 1997).
Up to 90% of older children and adults with TS report some premonitory sensations related to their tics, while children under 10 are more likely to view their tics as completely involuntary (Leckman et al., 1999).
Although many children are able to suppress their tics for some period of time, the urge to tic remains, and the tics must eventually be "released." Some children are able to remain relatively tic-free during school hours, only to engage in bouts of tics for several hours at home (Leckman et al.; Packer, 1997). Others report that tics are quiescent while they are engaged in an absorbing mental or physical task (Jankovic, 1997). Stress can exacerbate tics, but they can also increase when a child is in a relaxed state, such as watching television, and can be present during sleep (Jankovic, 1997). While this cycle of relative suppressibility and release is characteristic of tics in TS, it can lead to confusion and misguided attempts on the part of parents and teachers to use discipline or conditioning to stop the tics (Packer, 1997).
Presentation and Classification of Tic Disorders
As many as 10-20% of all school-age children have transient motor and, less commonly, vocal tics lasting less than 1 year (Bagheri et al., 1999; Zohar et al., 1999).
The majority of these children present with tics in the head, neck, or upper extremities (Leckman et al., 2001).
In children who are eventually diagnosed with TS, almost half report that eye blinking was their initial tic, followed by other head and facial tics. Others report vocal tics such as throat clearing and sniffing to be an early symptom of TS (Jankovic, 1997) and less commonly of transient tic disorder (Leckman et al., 2001). In many children with transient tic disorder, symptoms resolve before the family seeks medical attention (Leckman et al., 2001).
In 3-4% of school age children, symptoms of either motor or vocal tics, but not both, persist for more than 1 year (Leckman et al., 2001).
These children would be considered to have a chronic tic disorder, and they may or may not have associated behavioral and developmental conditions discussed below (Leckman et al., 2001). Children with both vocal and motor tics that persist for more than 1 year generally fulfill the criteria for TS.
The diagnostic criteria for TS have changed over time (Leckman et al., 2001). The DSM IV (APA, 1994, p. 103) criteria for TS are:
Both multiple motor and one or more vocal tics have been present at some time during the illness, although not necessarily concurrently.
The tics occur many times a day (usually in bouts), nearly every day or intermittently throughout a period of more than 1 year, and during this period there was never a tic-free period of more than 3 consecutive months.
The disturbance causes marked distress or significant impairment in social, occupational, or other important areas of functioning.
Onset is before age 18 years.
The disturbance is not due to the direct physiological effects of a substance (e.g., stimulants) or a general medical condition (e.g., Huntington's disease or post-viral encephalitis).
There is some controversy about this definition, which has significant changes from the DSM-III-R (APA, 1987) and from the TS Classification Study Group (1993). The primary concern is that the DSM-IV definition relies on an undefined and subjective criterion of "distress," rather than a more objective measure of symptom severity (Erenberg & Fahn, 1996; Leckman et al., 2001).
Many researchers and clinicians in the field continue to use DSM III-R criteria in order to maintain a more uniform definition of TS (Bawden, Stokes, Camfield, Camfield & Salisbury, 1998; Carter et al., 2000; Coffey et al., 2000; Sherman, Shepard, Joschko & Freeman, 1998; Spencer et al., 1998). For a child who fulfills all criteria except psychological dysfunction or distress, an ICD-9 code can be used instead of a DSM diagnosis (Leckman et al., 2001).
Etiology, Course, and Prognosis of TS
First documented in the 19th century and named after a French neurologist, Gilles de la Tourette, TS was thought for a long time to have psychiatric origins (Coffey & Park, 1997). Contemporary research on dopamine receptors and the limbic system evolved after it was noticed that empiric treatment with neuroleptics such as haloperidol reduced tic severity (Coffey & Park, 1997). It is currently felt that there is an underlying defect of either excess dopamine or hypersensitivity of postsynaptic dopamine receptors (Bagheri et al., 1999).
Recent studies suggest that basal ganglia dysfunction may be involved in TS (Sherman et al., 1998). According to Leckman and Cohen (1999), some of the circuits that convey information from the cortex throughout the basal ganglia are selectively disinhibited in both TS and OCD, making them unusually sensitive to alterations in the environment. In this conceptual model, TS is seen as a disorder in which individuals are unable to inhibit premonitory sensory urges, leading to the emergence of motor and phonic behavior. In OCD, individuals are unable to inhibit specific innate worries, leading to the emergence of intense obsessions and compulsions.
In a cross-sectional study of 36 children with TS who were contacted 7 years after diagnosis, Leckman et al. (1998) found that the mean onset of tics at 5.6 years of age was followed by progressive worsening of tics, peaking at age 10.
While 22% of the sample had tics that were severe enough to jeopardize or prevent their functioning in school at the peak of tic symptoms, the tics steadily declined during adolescence, with 50% of the individuals virtually tic-free by age 18.
Most of the remaining 18-year-olds experienced minimal to mild symptoms, while only 10% reported moderate or marked tics.
TS and Genetics
Several studies have reported a risk for TS of 11.5% in brothers and 4.8% in sisters of children with TS (Tourette Syndrome Association International Consortium for Genetics, 1999). Based on extended family studies, most researchers associate TS, chronic tics, OCD, and OCS as part of a spectrum of expression of the same underlying genetic disorder (Alsobrook & Pauls, 1997). They suggest an autosomal dominant model with sex-specific penetrance, accounting for the higher incidence of TS among boys, but cannot rule out a multifactorial or intermediate mode of inheritance (Alsobrook & Pauls, 1997; Haasstedt, Leppert, Filloux, van de Wetering, & McMahon, 1995). While some researchers have suggested possible locations for the "TS gene," their findings have not been replicated (Alsobrook & Pauls, 1997).
Pediatric Autoimmune Neuropsychiatric Disorders Associated With Streptococcus (PANDAS)
There has been some research into the association of TS and OCD with streptococcal infections, noting that Sydenham's chorea, which involves abnormal movements, OCD-like symptoms, and emotional lability, is felt to be caused by a reaction between antibodies to Group A Beta hemolytic streptococcus and neuronal tissue (Müller et al., 2001; Perlmutter et al., 1999). In some children, infection with streptococcus, borrelia burgdorfi (Lyme's disease), and mycoplasma appear to exacerbate TS symptoms (Müller et al., 2001). These researchers hypothesize that a subset of children with TS belong to a category known as PANDAS (Müller et al., 2001). Criteria that would suggest PANDAS include abrupt onset of symptoms associated with a streptococcal infection, periods of remission, and exacerbations after additional streptococcal infections (Perlmutter et al., 1999). Müller et al. (2001) noted that adults with TS have higher levels of specific antibodies to streptococcus than controls without TS. Perlmutter et al. (1999) found that children with TS who fit the PANDAS criteria had their TS and OCD symptoms significantly reduced after being treated with either intravenous immune globulin or plasma exchange. At the moment, identification and treatment of PANDAS remains experimental, with many questions left unanswered (Hollenbeck, 2000).
TS is a neurobiological condition characterized by vocal and motor tics that change over time and wax and wane in severity. TS is part of a spectrum of tic disorders, including transient tic disorder and chronic tic disorder ( Table 1 ).
Diagnosis is based on history and observation, with no specific diagnostic tests available (Bagheri, Kergeshian & Burd, 1999; Kiessling, 2001).
In reviewing family-genetic and epidemiological studies, some researchers suggest that there is little evidence to support the diagnostic distinction between, for example, chronic tics and TS (Peterson, Pine, Cohen & Brook, 2001).
Tics can be defined as "sudden, repetitive, stereotyped motor movements or phonic productions that involve discrete muscle groups" (Leckman, King, & Cohen, 1999, p. 24).
In contrast to other movement disorders, such as chorea or dystonia, tics are exaggerations and repetitions of normal movements (Bagheri et al., 1999; Leckman, Peterson, King, Scahill, & Cohen, 2001).
Primary tics such as TS have no identifiable cause or may be genetic in origin (Jankovic, 2001).
Conditions that could cause secondary tics include head trauma, encephalitis, and some medications.
There is an increased incidence of tics in children with pervasive developmental disorder (Kiessling, 2001).
Tics are commonly classified as simple or complex. Shoulder shrugging, neck twitching, and facial movements are examples of simple motor tics. Touching objects, skipping, and squatting in a rhythmic sequence (such as every four steps) are examples of complex motor tics. Simple vocal tics include sniffing, barking, coughing, yelling, and hiccupping. Complex vocal tics include repeating parts of words or phrases, talking to oneself, assuming different intonations, and uttering obscenities (Bagheri et al., 1999; Leckman et al., 1999).
There is a growing body of literature suggesting that tics are intentional responses to unwanted sensations or urges (Coffey & Park, 1997; Jankovic, 1997).
Up to 90% of older children and adults with TS report some premonitory sensations related to their tics, while children under 10 are more likely to view their tics as completely involuntary (Leckman et al., 1999).
Although many children are able to suppress their tics for some period of time, the urge to tic remains, and the tics must eventually be "released." Some children are able to remain relatively tic-free during school hours, only to engage in bouts of tics for several hours at home (Leckman et al.; Packer, 1997). Others report that tics are quiescent while they are engaged in an absorbing mental or physical task (Jankovic, 1997). Stress can exacerbate tics, but they can also increase when a child is in a relaxed state, such as watching television, and can be present during sleep (Jankovic, 1997). While this cycle of relative suppressibility and release is characteristic of tics in TS, it can lead to confusion and misguided attempts on the part of parents and teachers to use discipline or conditioning to stop the tics (Packer, 1997).
Presentation and Classification of Tic Disorders
As many as 10-20% of all school-age children have transient motor and, less commonly, vocal tics lasting less than 1 year (Bagheri et al., 1999; Zohar et al., 1999).
The majority of these children present with tics in the head, neck, or upper extremities (Leckman et al., 2001).
In children who are eventually diagnosed with TS, almost half report that eye blinking was their initial tic, followed by other head and facial tics. Others report vocal tics such as throat clearing and sniffing to be an early symptom of TS (Jankovic, 1997) and less commonly of transient tic disorder (Leckman et al., 2001). In many children with transient tic disorder, symptoms resolve before the family seeks medical attention (Leckman et al., 2001).
In 3-4% of school age children, symptoms of either motor or vocal tics, but not both, persist for more than 1 year (Leckman et al., 2001).
These children would be considered to have a chronic tic disorder, and they may or may not have associated behavioral and developmental conditions discussed below (Leckman et al., 2001). Children with both vocal and motor tics that persist for more than 1 year generally fulfill the criteria for TS.
The diagnostic criteria for TS have changed over time (Leckman et al., 2001). The DSM IV (APA, 1994, p. 103) criteria for TS are:
Both multiple motor and one or more vocal tics have been present at some time during the illness, although not necessarily concurrently.
The tics occur many times a day (usually in bouts), nearly every day or intermittently throughout a period of more than 1 year, and during this period there was never a tic-free period of more than 3 consecutive months.
The disturbance causes marked distress or significant impairment in social, occupational, or other important areas of functioning.
Onset is before age 18 years.
The disturbance is not due to the direct physiological effects of a substance (e.g., stimulants) or a general medical condition (e.g., Huntington's disease or post-viral encephalitis).
There is some controversy about this definition, which has significant changes from the DSM-III-R (APA, 1987) and from the TS Classification Study Group (1993). The primary concern is that the DSM-IV definition relies on an undefined and subjective criterion of "distress," rather than a more objective measure of symptom severity (Erenberg & Fahn, 1996; Leckman et al., 2001).
Many researchers and clinicians in the field continue to use DSM III-R criteria in order to maintain a more uniform definition of TS (Bawden, Stokes, Camfield, Camfield & Salisbury, 1998; Carter et al., 2000; Coffey et al., 2000; Sherman, Shepard, Joschko & Freeman, 1998; Spencer et al., 1998). For a child who fulfills all criteria except psychological dysfunction or distress, an ICD-9 code can be used instead of a DSM diagnosis (Leckman et al., 2001).
Etiology, Course, and Prognosis of TS
First documented in the 19th century and named after a French neurologist, Gilles de la Tourette, TS was thought for a long time to have psychiatric origins (Coffey & Park, 1997). Contemporary research on dopamine receptors and the limbic system evolved after it was noticed that empiric treatment with neuroleptics such as haloperidol reduced tic severity (Coffey & Park, 1997). It is currently felt that there is an underlying defect of either excess dopamine or hypersensitivity of postsynaptic dopamine receptors (Bagheri et al., 1999).
Recent studies suggest that basal ganglia dysfunction may be involved in TS (Sherman et al., 1998). According to Leckman and Cohen (1999), some of the circuits that convey information from the cortex throughout the basal ganglia are selectively disinhibited in both TS and OCD, making them unusually sensitive to alterations in the environment. In this conceptual model, TS is seen as a disorder in which individuals are unable to inhibit premonitory sensory urges, leading to the emergence of motor and phonic behavior. In OCD, individuals are unable to inhibit specific innate worries, leading to the emergence of intense obsessions and compulsions.
In a cross-sectional study of 36 children with TS who were contacted 7 years after diagnosis, Leckman et al. (1998) found that the mean onset of tics at 5.6 years of age was followed by progressive worsening of tics, peaking at age 10.
While 22% of the sample had tics that were severe enough to jeopardize or prevent their functioning in school at the peak of tic symptoms, the tics steadily declined during adolescence, with 50% of the individuals virtually tic-free by age 18.
Most of the remaining 18-year-olds experienced minimal to mild symptoms, while only 10% reported moderate or marked tics.
TS and Genetics
Several studies have reported a risk for TS of 11.5% in brothers and 4.8% in sisters of children with TS (Tourette Syndrome Association International Consortium for Genetics, 1999). Based on extended family studies, most researchers associate TS, chronic tics, OCD, and OCS as part of a spectrum of expression of the same underlying genetic disorder (Alsobrook & Pauls, 1997). They suggest an autosomal dominant model with sex-specific penetrance, accounting for the higher incidence of TS among boys, but cannot rule out a multifactorial or intermediate mode of inheritance (Alsobrook & Pauls, 1997; Haasstedt, Leppert, Filloux, van de Wetering, & McMahon, 1995). While some researchers have suggested possible locations for the "TS gene," their findings have not been replicated (Alsobrook & Pauls, 1997).
Pediatric Autoimmune Neuropsychiatric Disorders Associated With Streptococcus (PANDAS)
There has been some research into the association of TS and OCD with streptococcal infections, noting that Sydenham's chorea, which involves abnormal movements, OCD-like symptoms, and emotional lability, is felt to be caused by a reaction between antibodies to Group A Beta hemolytic streptococcus and neuronal tissue (Müller et al., 2001; Perlmutter et al., 1999). In some children, infection with streptococcus, borrelia burgdorfi (Lyme's disease), and mycoplasma appear to exacerbate TS symptoms (Müller et al., 2001). These researchers hypothesize that a subset of children with TS belong to a category known as PANDAS (Müller et al., 2001). Criteria that would suggest PANDAS include abrupt onset of symptoms associated with a streptococcal infection, periods of remission, and exacerbations after additional streptococcal infections (Perlmutter et al., 1999). Müller et al. (2001) noted that adults with TS have higher levels of specific antibodies to streptococcus than controls without TS. Perlmutter et al. (1999) found that children with TS who fit the PANDAS criteria had their TS and OCD symptoms significantly reduced after being treated with either intravenous immune globulin or plasma exchange. At the moment, identification and treatment of PANDAS remains experimental, with many questions left unanswered (Hollenbeck, 2000).
Thursday, June 24, 2010
HPV Vaccine - Questions & Answers
http://www.cdc.gov/vaccines/vpd-vac/hpv/vac-faqs.htm
Why are HPV vaccines needed?
HPV vaccines prevent serious health problems, such as cervical cancer and other, less common cancers, which are caused by HPV (human papillomavirus). In addition to cancer, HPV can also cause other health problems, such as genital warts. HPV is a common virus that is easily spread by skin-to-skin contact during sexual activity with another person. It is possible to have HPV without knowing it, so it is possible to unknowingly spread HPV to another person. Safe, effective vaccines are available to protect females and males against some of the most common types of HPV and the health problems that the virus can cause.
How common are the health problems caused by HPV?
HPV is the main cause of cervical cancer in women. There are about 11,000 new cervical cancer cases each year in the United States. Cervical cancer causes about 4,000 deaths in women each year in the United States.
About 1 in 100 sexually active adults in the United States have genital warts at any one time.
What HPV vaccines are available in the United States?
Two HPV vaccines are licensed by the FDA and recommended by CDC. These vaccines are Cervarix (made by GlaxoSmithKline) and Gardasil (made by Merck).
How are the two HPV vaccines similar?
Both vaccines are very effective against HPV types 16 and 18, which cause most cervical cancers.
So both vaccines prevent cervical cancer and precancer in women.
Both vaccines are very safe.
Both vaccines are made with very small parts of the human papillomavirus (HPV) that cannot cause infection with HPV, so neither of the vaccines can cause HPV infection.
Both vaccines are given as shots and require 3 doses.
How are the two HPV vaccines different?
Only one of the vaccines (Gardasil) also protects against HPV types 6 and 11. These HPV types cause most genital warts in females and males.
The vaccines have different adjuvants—a vaccine adjuvant is a substance that is added to the vaccine to increase the body's immune response.
Who should get HPV vaccine?
Cervarix and Gardasil are licensed, safe, and effective for females ages 9 through 26 years.
CDC recommends that all girls who are 11 or 12 years old get the 3 doses (shots) of either brand of HPV vaccine to protect against cervical cancer and precancer. Gardasil also protects against most genital warts.
Girls and young women ages 13 through 26 should get all 3 doses of an HPV vaccine if they have not received all doses yet.
Gardasil is also licensed, safe, and effective for males ages 9 through 26 years. Boys and young men may choose to get this vaccine to prevent genital warts.
People who have already had sexual contact before getting all 3 doses of an HPV vaccine might still benefit if they were not infected before vaccination with the HPV types included in the vaccine they received.
The best way to be sure that a person gets the most benefit from HPV vaccination is to complete all three doses before sexual activity begins.
Why is Gardasil not on the immunization schedule for boys and men?
CDC did not add this vaccine to the recommended immunization schedules for males in these age groups because studies suggest that the best way to prevent the most disease due to HPV is to vaccinate as many girls and women as possible.
Parents of boys can decide if Gardasil is right for their sons by talking with their sons’ health care providers. Young men can also discuss this vaccine with their doctors.
Why is HPV vaccine recommended at ages 11 or 12 years?
For the HPV vaccine to work best, it is very important to get all 3 doses (shots) before being exposed to HPV.
Someone can be infected with HPV the very first time they have sexual contact with another person.
It is also possible to get HPV even if sexual contact only happens one time.
How does getting HPV vaccine at ages 11 or 12 fit with other health recommendations?
Doctors recommend health check-ups for preteens.
The first dose of an HPV vaccine should be given to girls aged 11 or 12 years during a pre-teen health check-up. The first dose of Gardasil can also be given to boys during their pre-teen check-ups. Two other vaccines are recommended for pre-teens. During one visit, either HPV vaccine can be given safely with these other pre-teen vaccines. A check-up in the pre-teen years is also a time when pre-teens and their parents can talk to their providers about other ways to stay healthy and safe.
What is the recommended schedule (or timing) of the 3 HPV doses (shots)?
For both females and males, 3 doses (shots) are needed. CDC recommends that the second dose be given one to two months after the first, and the third dose be given six months after the first dose.
Will someone be protected against HPV-related diseases if they do not get all 3 doses?
No studies so far have shown whether or not 1 or 2 doses protect as well as getting 3 doses, so it is very important to get all 3 doses.
Are the HPV vaccines safe and effective?
FDA has licensed the vaccines as safe and effective. Both vaccines were tested in thousands of people around the world. These studies showed no serious side effects. Common, mild side effects included pain where the shot was given, fever, headache, and nausea. As with all vaccines, CDC and FDA continue to monitor the safety of these vaccines very carefully.
Do people faint after getting HPV vaccines?
People faint for many reasons. Some people may faint after getting any vaccine, including HPV vaccines. Falls and injuries can occur after fainting. Sitting or lying down for about 15 minutes after a vaccination can help prevent fainting and injuries.
Can HPV vaccines treat HPV infections, cancers, or warts?
HPV vaccines will not treat or get rid of existing HPV infections. Also, HPV vaccines do not treat or cure health problems (like cancer or warts) caused by an HPV infection that occurred before vaccination.
Are there other HPV diseases that the two vaccines may prevent?
Studies have shown that Gardasil prevents cancers of the vagina and vulva, which like cervical cancer, can be caused by HPV types 16 and 18. Studies of Cervarix have not specifically looked at protection against vaginal and vulvar cancers.
Published studies have not looked at other health problems that might be prevented by HPV vaccines. It is possible that HPV vaccines will also prevent cancers of the head and neck, penis, and anus due to HPV 16 or 18. Gardasil might prevent recurrent respiratory papillomatosis (RRP), a rare condition caused by HPV 6 or 11 in which warts grow in the throat.
Are kids getting too many vaccines?
Vaccines strengthen the body’s immune system—they do not overload it. No reputable science shows that getting recommended vaccines hurts the immune systems of healthy kids. The HPV vaccines are important tools to prevent cervical cancer and genital warts. As with all vaccines, the benefits outweigh potential risks.
Why aren’t HPV vaccines recommended for people older than 26?
Both vaccines were studied in thousands of people from 9 through 26 years old and found to be safe and effective for these ages. The FDA will consider licensing HPV vaccines for other ages if new studies show that this would also be safe and effective.
Should pregnant women be vaccinated?
Pregnant women are not included in the recommendations for HPV vaccines. Studies show neither vaccine caused problems for babies born to women who got the HPV vaccine while they were pregnant. Getting the HPV vaccine when pregnant is not a reason to consider ending a pregnancy. But, to be on the safe side until even more is known, a pregnant woman should not get any doses of either HPV vaccine until her pregnancy is completed.
What should a woman do if she realizes she received HPV vaccination while pregnant?
If a woman realizes that she got any shots of an HPV vaccine while pregnant, she should do two things:
Wait until after her pregnancy to finish the remaining HPV vaccine doses.
Report the vaccination to the appropriate pregnancy registry. There are pregnancy registries to help us learn more about how pregnant women respond to each of the vaccines. So, if a woman realizes that she got any shots of either HPV vaccine while pregnant, she should work with her health care provider to report it to the appropriate pregnancy registry:
The toll-free number for Gardasil is 800-986-8999
The toll-free number for Cervarix is 888-452-9622
Will HPV vaccination be covered by health insurance?
Most health insurance plans cover recommended vaccines. But there may be a lag time after a vaccine is recommended before it gets added to insurance plans. Some insurance plans may not cover any or all vaccines. Check with your insurance provider to see if the cost of the vaccine is covered before going to the doctor.
How can my child get an HPV vaccine if I don’t have insurance?
The Vaccines for Children (VFC) program helps families of eligible children who might not otherwise have access to vaccines. The program provides vaccines at no cost to doctors who serve eligible children. Children younger than 19 years of age are eligible for VFC vaccines if they are Medicaid-eligible, American Indian, or Alaska Native or have no health insurance. "Underinsured" children who have health insurance that does not cover vaccination can receive VFC vaccines through Federally Qualified Health Centers or Rural Health Centers. Parents of uninsured or underinsured children who receive vaccines at no cost through the VFC Program should check with their health care providers about possible administration fees that might apply. These fees help providers cover the costs that result from important services like storing the vaccines and paying staff members to give vaccines to patients. For more information about the VFC program, visit www.cdc.gov/vaccines/programs/vfc/.
Why are HPV vaccines needed?
HPV vaccines prevent serious health problems, such as cervical cancer and other, less common cancers, which are caused by HPV (human papillomavirus). In addition to cancer, HPV can also cause other health problems, such as genital warts. HPV is a common virus that is easily spread by skin-to-skin contact during sexual activity with another person. It is possible to have HPV without knowing it, so it is possible to unknowingly spread HPV to another person. Safe, effective vaccines are available to protect females and males against some of the most common types of HPV and the health problems that the virus can cause.
How common are the health problems caused by HPV?
HPV is the main cause of cervical cancer in women. There are about 11,000 new cervical cancer cases each year in the United States. Cervical cancer causes about 4,000 deaths in women each year in the United States.
About 1 in 100 sexually active adults in the United States have genital warts at any one time.
What HPV vaccines are available in the United States?
Two HPV vaccines are licensed by the FDA and recommended by CDC. These vaccines are Cervarix (made by GlaxoSmithKline) and Gardasil (made by Merck).
How are the two HPV vaccines similar?
Both vaccines are very effective against HPV types 16 and 18, which cause most cervical cancers.
So both vaccines prevent cervical cancer and precancer in women.
Both vaccines are very safe.
Both vaccines are made with very small parts of the human papillomavirus (HPV) that cannot cause infection with HPV, so neither of the vaccines can cause HPV infection.
Both vaccines are given as shots and require 3 doses.
How are the two HPV vaccines different?
Only one of the vaccines (Gardasil) also protects against HPV types 6 and 11. These HPV types cause most genital warts in females and males.
The vaccines have different adjuvants—a vaccine adjuvant is a substance that is added to the vaccine to increase the body's immune response.
Who should get HPV vaccine?
Cervarix and Gardasil are licensed, safe, and effective for females ages 9 through 26 years.
CDC recommends that all girls who are 11 or 12 years old get the 3 doses (shots) of either brand of HPV vaccine to protect against cervical cancer and precancer. Gardasil also protects against most genital warts.
Girls and young women ages 13 through 26 should get all 3 doses of an HPV vaccine if they have not received all doses yet.
Gardasil is also licensed, safe, and effective for males ages 9 through 26 years. Boys and young men may choose to get this vaccine to prevent genital warts.
People who have already had sexual contact before getting all 3 doses of an HPV vaccine might still benefit if they were not infected before vaccination with the HPV types included in the vaccine they received.
The best way to be sure that a person gets the most benefit from HPV vaccination is to complete all three doses before sexual activity begins.
Why is Gardasil not on the immunization schedule for boys and men?
CDC did not add this vaccine to the recommended immunization schedules for males in these age groups because studies suggest that the best way to prevent the most disease due to HPV is to vaccinate as many girls and women as possible.
Parents of boys can decide if Gardasil is right for their sons by talking with their sons’ health care providers. Young men can also discuss this vaccine with their doctors.
Why is HPV vaccine recommended at ages 11 or 12 years?
For the HPV vaccine to work best, it is very important to get all 3 doses (shots) before being exposed to HPV.
Someone can be infected with HPV the very first time they have sexual contact with another person.
It is also possible to get HPV even if sexual contact only happens one time.
How does getting HPV vaccine at ages 11 or 12 fit with other health recommendations?
Doctors recommend health check-ups for preteens.
The first dose of an HPV vaccine should be given to girls aged 11 or 12 years during a pre-teen health check-up. The first dose of Gardasil can also be given to boys during their pre-teen check-ups. Two other vaccines are recommended for pre-teens. During one visit, either HPV vaccine can be given safely with these other pre-teen vaccines. A check-up in the pre-teen years is also a time when pre-teens and their parents can talk to their providers about other ways to stay healthy and safe.
What is the recommended schedule (or timing) of the 3 HPV doses (shots)?
For both females and males, 3 doses (shots) are needed. CDC recommends that the second dose be given one to two months after the first, and the third dose be given six months after the first dose.
Will someone be protected against HPV-related diseases if they do not get all 3 doses?
No studies so far have shown whether or not 1 or 2 doses protect as well as getting 3 doses, so it is very important to get all 3 doses.
Are the HPV vaccines safe and effective?
FDA has licensed the vaccines as safe and effective. Both vaccines were tested in thousands of people around the world. These studies showed no serious side effects. Common, mild side effects included pain where the shot was given, fever, headache, and nausea. As with all vaccines, CDC and FDA continue to monitor the safety of these vaccines very carefully.
Do people faint after getting HPV vaccines?
People faint for many reasons. Some people may faint after getting any vaccine, including HPV vaccines. Falls and injuries can occur after fainting. Sitting or lying down for about 15 minutes after a vaccination can help prevent fainting and injuries.
Can HPV vaccines treat HPV infections, cancers, or warts?
HPV vaccines will not treat or get rid of existing HPV infections. Also, HPV vaccines do not treat or cure health problems (like cancer or warts) caused by an HPV infection that occurred before vaccination.
Are there other HPV diseases that the two vaccines may prevent?
Studies have shown that Gardasil prevents cancers of the vagina and vulva, which like cervical cancer, can be caused by HPV types 16 and 18. Studies of Cervarix have not specifically looked at protection against vaginal and vulvar cancers.
Published studies have not looked at other health problems that might be prevented by HPV vaccines. It is possible that HPV vaccines will also prevent cancers of the head and neck, penis, and anus due to HPV 16 or 18. Gardasil might prevent recurrent respiratory papillomatosis (RRP), a rare condition caused by HPV 6 or 11 in which warts grow in the throat.
Are kids getting too many vaccines?
Vaccines strengthen the body’s immune system—they do not overload it. No reputable science shows that getting recommended vaccines hurts the immune systems of healthy kids. The HPV vaccines are important tools to prevent cervical cancer and genital warts. As with all vaccines, the benefits outweigh potential risks.
Why aren’t HPV vaccines recommended for people older than 26?
Both vaccines were studied in thousands of people from 9 through 26 years old and found to be safe and effective for these ages. The FDA will consider licensing HPV vaccines for other ages if new studies show that this would also be safe and effective.
Should pregnant women be vaccinated?
Pregnant women are not included in the recommendations for HPV vaccines. Studies show neither vaccine caused problems for babies born to women who got the HPV vaccine while they were pregnant. Getting the HPV vaccine when pregnant is not a reason to consider ending a pregnancy. But, to be on the safe side until even more is known, a pregnant woman should not get any doses of either HPV vaccine until her pregnancy is completed.
What should a woman do if she realizes she received HPV vaccination while pregnant?
If a woman realizes that she got any shots of an HPV vaccine while pregnant, she should do two things:
Wait until after her pregnancy to finish the remaining HPV vaccine doses.
Report the vaccination to the appropriate pregnancy registry. There are pregnancy registries to help us learn more about how pregnant women respond to each of the vaccines. So, if a woman realizes that she got any shots of either HPV vaccine while pregnant, she should work with her health care provider to report it to the appropriate pregnancy registry:
The toll-free number for Gardasil is 800-986-8999
The toll-free number for Cervarix is 888-452-9622
Will HPV vaccination be covered by health insurance?
Most health insurance plans cover recommended vaccines. But there may be a lag time after a vaccine is recommended before it gets added to insurance plans. Some insurance plans may not cover any or all vaccines. Check with your insurance provider to see if the cost of the vaccine is covered before going to the doctor.
How can my child get an HPV vaccine if I don’t have insurance?
The Vaccines for Children (VFC) program helps families of eligible children who might not otherwise have access to vaccines. The program provides vaccines at no cost to doctors who serve eligible children. Children younger than 19 years of age are eligible for VFC vaccines if they are Medicaid-eligible, American Indian, or Alaska Native or have no health insurance. "Underinsured" children who have health insurance that does not cover vaccination can receive VFC vaccines through Federally Qualified Health Centers or Rural Health Centers. Parents of uninsured or underinsured children who receive vaccines at no cost through the VFC Program should check with their health care providers about possible administration fees that might apply. These fees help providers cover the costs that result from important services like storing the vaccines and paying staff members to give vaccines to patients. For more information about the VFC program, visit www.cdc.gov/vaccines/programs/vfc/.
Brain Tumour Risk in Relation to Mobile Telephone Use: Results of the INTERPHONE
From International Journal of Epidemiology
International Case–Control Study
The INTERPHONE Study Group
Posted: 06/17/2010; International Journal of Epidemiology. 2010;39(3):675-694. © 2010 Oxford University Press
Abstract
Background The rapid increase in mobile telephone use has generated concern about possible health risks related to radiofrequency electromagnetic fields from this technology.
Methods An interview-based case–control study with 2708 glioma and 2409 meningioma cases and matched controls was conducted in 13 countries using a common protocol.
Results A reduced odds ratio (OR) related to ever having been a regular mobile phone user was seen for glioma [OR 0.81; 95% confidence interval (CI) 0.70–0.94] and meningioma (OR 0.79; 95% CI 0.68–0.91), possibly reflecting participation bias or other methodological limitations. No elevated OR was observed ≥10 years after first phone use (glioma: OR 0.98; 95% CI 0.76–1.26; meningioma: OR 0.83; 95% CI 0.61–1.14). ORs were <1.0 for all deciles of lifetime number of phone calls and nine deciles of cumulative call time. In the 10th decile of recalled cumulative call time, ≥1640 h, the OR was 1.40 (95% CI 1.03–1.89) for glioma, and 1.15 (95% CI 0.81–1.62) for meningioma; but there are implausible values of reported use in this group. ORs for glioma tended to be greater in the temporal lobe than in other lobes of the brain, but the CIs around the lobe-specific estimates were wide. ORs for glioma tended to be greater in subjects who reported usual phone use on the same side of the head as their tumour than on the opposite side.
Conclusions Overall, no increase in risk of glioma or meningioma was observed with use of mobile phones. There were suggestions of an increased risk of glioma at the highest exposure levels, but biases and error prevent a causal interpretation. The possible effects of long-term heavy use of mobile phones require further investigation.
Introduction
Mobile phone use has increased dramatically in many countries since its introduction in the early-to-mid 1980s. The expanding use of this technology has been accompanied by concerns about health and safety. In the late 1990s, several expert groups critically reviewed the evidence on health effects of low-level exposure to radiofrequency (RF) electromagnetic fields, and recommended research into the possible adverse health effects of mobile telephony.[1–4] As a result, the International Agency for Research on Cancer (IARC) coordinated a feasibility study in 1998 and 1999, which concluded that an international study of the relationship between mobile phone use and brain tumour risk would be feasible and informative.[5,6]
INTERPHONE was therefore initiated as an international set of case–control studies focussing on four types of tumours in tissues that most absorb RF energy emitted by mobile phones: tumours of the brain (glioma and meningioma), acoustic nerve (schwannoma) and parotid gland. The objective was to determine whether mobile phone use increases the risk of these tumours and, specifically, whether RF energy emitted by mobile phones is tumourigenic.
This article presents the results of analyses of brain tumour risk in relation to mobile phone use in all INTERPHONE study centres combined. Analyses of brain tumours in relation to mobile phone use have been reported from a number of cohort[7–9] and case–control studies, including several of the national components of INTERPHONE.[10–25] No studies, however, have included as many exposed cases, particularly long-term and heavy users of mobile phones, as this study.
http://www.medscape.com/viewarticle/723258?src=mp&spon=9&uac=71630FV
International Case–Control Study
The INTERPHONE Study Group
Posted: 06/17/2010; International Journal of Epidemiology. 2010;39(3):675-694. © 2010 Oxford University Press
Abstract
Background The rapid increase in mobile telephone use has generated concern about possible health risks related to radiofrequency electromagnetic fields from this technology.
Methods An interview-based case–control study with 2708 glioma and 2409 meningioma cases and matched controls was conducted in 13 countries using a common protocol.
Results A reduced odds ratio (OR) related to ever having been a regular mobile phone user was seen for glioma [OR 0.81; 95% confidence interval (CI) 0.70–0.94] and meningioma (OR 0.79; 95% CI 0.68–0.91), possibly reflecting participation bias or other methodological limitations. No elevated OR was observed ≥10 years after first phone use (glioma: OR 0.98; 95% CI 0.76–1.26; meningioma: OR 0.83; 95% CI 0.61–1.14). ORs were <1.0 for all deciles of lifetime number of phone calls and nine deciles of cumulative call time. In the 10th decile of recalled cumulative call time, ≥1640 h, the OR was 1.40 (95% CI 1.03–1.89) for glioma, and 1.15 (95% CI 0.81–1.62) for meningioma; but there are implausible values of reported use in this group. ORs for glioma tended to be greater in the temporal lobe than in other lobes of the brain, but the CIs around the lobe-specific estimates were wide. ORs for glioma tended to be greater in subjects who reported usual phone use on the same side of the head as their tumour than on the opposite side.
Conclusions Overall, no increase in risk of glioma or meningioma was observed with use of mobile phones. There were suggestions of an increased risk of glioma at the highest exposure levels, but biases and error prevent a causal interpretation. The possible effects of long-term heavy use of mobile phones require further investigation.
Introduction
Mobile phone use has increased dramatically in many countries since its introduction in the early-to-mid 1980s. The expanding use of this technology has been accompanied by concerns about health and safety. In the late 1990s, several expert groups critically reviewed the evidence on health effects of low-level exposure to radiofrequency (RF) electromagnetic fields, and recommended research into the possible adverse health effects of mobile telephony.[1–4] As a result, the International Agency for Research on Cancer (IARC) coordinated a feasibility study in 1998 and 1999, which concluded that an international study of the relationship between mobile phone use and brain tumour risk would be feasible and informative.[5,6]
INTERPHONE was therefore initiated as an international set of case–control studies focussing on four types of tumours in tissues that most absorb RF energy emitted by mobile phones: tumours of the brain (glioma and meningioma), acoustic nerve (schwannoma) and parotid gland. The objective was to determine whether mobile phone use increases the risk of these tumours and, specifically, whether RF energy emitted by mobile phones is tumourigenic.
This article presents the results of analyses of brain tumour risk in relation to mobile phone use in all INTERPHONE study centres combined. Analyses of brain tumours in relation to mobile phone use have been reported from a number of cohort[7–9] and case–control studies, including several of the national components of INTERPHONE.[10–25] No studies, however, have included as many exposed cases, particularly long-term and heavy users of mobile phones, as this study.
http://www.medscape.com/viewarticle/723258?src=mp&spon=9&uac=71630FV
Wednesday, June 23, 2010
Breast-Feeding Until 4 Months May Protect Infants From Respiratory, GI Infections
From Medscape Medical News
Laurie Barclay, MD
June 21, 2010 — Breast-feeding until age 4 months is linked to lower rates of respiratory and gastrointestinal (GI) infection morbidity, according to the results of a population-based, prospective, cohort study reported online June 21 in Pediatrics.
"Exclusive breastfeeding seems to decrease the risk of infectious diseases in infancy," Liesbeth Duijts, MD, PhD, from Erasmus Medical Center in Rotterdam, the Netherlands. "However, the World Health Organization has called for more research regarding the benefits for 6 months instead of 4 months of exclusive breastfeeding."
The goal of this study, which was embedded in the Generation R Study, a study from fetal life onward in the Netherlands, was to evaluate the associations of duration of exclusive breast-feeding with upper respiratory tract infections (URTI), lower respiratory tract infections (LRTI), and GI tract infections in infancy.
There were 4164 subjects who completed questionnaires on rates of breast-feeding during the first 6 months (never; partial for < 4 months, not thereafter; partial for 4 - 6 months; exclusive for 4 months, not thereafter; exclusive for 4 months, partial thereafter; and exclusive for 6 months) and doctor-attended URTI, LRTI, and GI infections until age 12 months.
Risks for URTI, LRTI, and GI tract infection until age 6 months were lower in infants who were breast-fed exclusively until age 4 months and partially thereafter vs infants who were never breast-fed. Adjusted odds ratios (ORs) were 0.65 (95% confidence interval [CI], 0.51 - 0.83) for URTI, 0.50 (95% CI, 0.32 - 0.79) for LRTI, and 0.41 (95% CI, 0.26 -0.64) for GI tract infection. The adjusted OR for LRTIs in infants between the ages of 7 and 12 months was 0.46 (95% CI, 0.31 - 0.69).
For infants who were exclusively breast-fed for at least 6 months, trends were similar. However, partial breast-feeding, even for 6 months, was not associated with significantly lower risks for these infections.
"Exclusive breastfeeding until the age of 4 months and partially thereafter was associated with a significant reduction of respiratory and gastrointestinal morbidity in infants," the study authors write. "Our findings support health policy strategies to promote exclusive breastfeeding for at least 4 months, but preferably 6 months, in industrialized countries."
Limitations of this study include questionnaires with breast-feeding data available for only 65% of eligible participants of the Generation R Study and possible misclassification related to questionnaire use.
"Biological, cultural, and social constraints related to breastfeeding habits need to be studied more extensively," the study authors write. "The effects of prolonged and exclusive breastfeeding on infectious diseases at older ages in industrialized countries remain to be studied."
Exclusive breast-feeding until age 4 months and partially thereafter was associated with a significant reduction of respiratory and GI morbidity rates in infants.
The first phase of the Generation R Study was funded by Erasmus Medical Center, Erasmus University Rotterdam, and Netherlands Organization for Health Research and Development (Zon Mw). The present study was supported by an additional grant from Stichting W. H. Kröger (00–048) and AGS Kinderstichting. The study authors have disclosed no relevant financial relationships.
Pediatrics. Published online June 21, 2010.
Laurie Barclay, MD
June 21, 2010 — Breast-feeding until age 4 months is linked to lower rates of respiratory and gastrointestinal (GI) infection morbidity, according to the results of a population-based, prospective, cohort study reported online June 21 in Pediatrics.
"Exclusive breastfeeding seems to decrease the risk of infectious diseases in infancy," Liesbeth Duijts, MD, PhD, from Erasmus Medical Center in Rotterdam, the Netherlands. "However, the World Health Organization has called for more research regarding the benefits for 6 months instead of 4 months of exclusive breastfeeding."
The goal of this study, which was embedded in the Generation R Study, a study from fetal life onward in the Netherlands, was to evaluate the associations of duration of exclusive breast-feeding with upper respiratory tract infections (URTI), lower respiratory tract infections (LRTI), and GI tract infections in infancy.
There were 4164 subjects who completed questionnaires on rates of breast-feeding during the first 6 months (never; partial for < 4 months, not thereafter; partial for 4 - 6 months; exclusive for 4 months, not thereafter; exclusive for 4 months, partial thereafter; and exclusive for 6 months) and doctor-attended URTI, LRTI, and GI infections until age 12 months.
Risks for URTI, LRTI, and GI tract infection until age 6 months were lower in infants who were breast-fed exclusively until age 4 months and partially thereafter vs infants who were never breast-fed. Adjusted odds ratios (ORs) were 0.65 (95% confidence interval [CI], 0.51 - 0.83) for URTI, 0.50 (95% CI, 0.32 - 0.79) for LRTI, and 0.41 (95% CI, 0.26 -0.64) for GI tract infection. The adjusted OR for LRTIs in infants between the ages of 7 and 12 months was 0.46 (95% CI, 0.31 - 0.69).
For infants who were exclusively breast-fed for at least 6 months, trends were similar. However, partial breast-feeding, even for 6 months, was not associated with significantly lower risks for these infections.
"Exclusive breastfeeding until the age of 4 months and partially thereafter was associated with a significant reduction of respiratory and gastrointestinal morbidity in infants," the study authors write. "Our findings support health policy strategies to promote exclusive breastfeeding for at least 4 months, but preferably 6 months, in industrialized countries."
Limitations of this study include questionnaires with breast-feeding data available for only 65% of eligible participants of the Generation R Study and possible misclassification related to questionnaire use.
"Biological, cultural, and social constraints related to breastfeeding habits need to be studied more extensively," the study authors write. "The effects of prolonged and exclusive breastfeeding on infectious diseases at older ages in industrialized countries remain to be studied."
Exclusive breast-feeding until age 4 months and partially thereafter was associated with a significant reduction of respiratory and GI morbidity rates in infants.
The first phase of the Generation R Study was funded by Erasmus Medical Center, Erasmus University Rotterdam, and Netherlands Organization for Health Research and Development (Zon Mw). The present study was supported by an additional grant from Stichting W. H. Kröger (00–048) and AGS Kinderstichting. The study authors have disclosed no relevant financial relationships.
Pediatrics. Published online June 21, 2010.
Monday, June 14, 2010
Conflicts of interest and pandemic flu
Published 3 June 2010, doi:10.1136/bmj.c2947
Cite this as: BMJ 2010;340:c2947
Editorials
WHO must act now to restore its credibility, and Europe should legislate
The world should of course be thankful that the 2009 influenza A/H1N1 pandemic proved such a damp squib. With so many fewer lives lost than had been predicted, it almost seems ungrateful to carp about the cost. But carp we must because the cost has been huge. Some countries—notably Poland—declined to join the panic buying of vaccines and antivirals triggered when the World Health Organization declared the pandemic a year ago this week. However, countries like France and the United Kingdom who have stockpiled drugs and vaccines are now busy unpicking vaccine contracts, selling unused vaccine to other countries, and sitting on huge piles of unused oseltamivir.Meanwhile drug companies have banked vast profits—$7bn (£4.8bn; 5.7bn) to $10bn from vaccines alone according to investment bank JP Morgan.1 Given the scale of public cost and private profit, it would seem important to know that WHO’s key decisions were free from commercial influence.
An investigation by the BMJ and the Bureau of Investigative Journalism, published this week (doi:10.1136/bmj.c2912 ), finds that this was far from the case.2 As reported by Deborah Cohen and Philip Carter, some of the experts advising WHO on the pandemic had declarable financial ties with drug companies that were producing antivirals and influenza vaccines. As an example, WHO’s guidance on the use of antivirals in a pandemic was authored by an influenza expert who at the same time was receiving payments from Roche, the manufacturer of oseltamivir (Tamiflu), for consultancy work and lecturing. Although most of the experts consulted by WHO made no secret of their industry ties in other settings, WHO itself has so far declined to explainto what extent it knew about these conflicts of interest or how it managed them.
This lack of transparency is compounded by the existence of a secret "emergency committee," which advised the director general Margaret Chan on when to declare the pandemic—a decision that triggered costly pre-established vaccine contracts around the world. Curiously, the names of the 16 committee members are known only to people within WHO.
Cohen and Carter’s findings resonate with those of other investigations, most notably an inquiry by the Council of Europe, which reports this week and is extremely critical of WHO.1 It concludes that decision making around the influenza A/H1N1 crisis has been lacking in transparency.
One of its chief protagonists is Paul Flynn, a UK member of parliament and a member of the council’s Parliamentary Assembly. He and others raised concerns last year about the lack of evidence to justify the scale of the international response to H1N1 (as also covered in the BMJ in December3 ), and the lack of transparency around the decision making process for declaringthe pandemic.1
WHO’s response to these concerns has been disappointing. Although Margaret Chan has ordered an inquiry and WHO has stressed its commitment to transparency, her office has turned down requests to clear up concerns about potential conflicts of interest.2 And at a hearing of the Council of Europe’s Parliamentary Assembly in January, WHO denied any industry influence on the scientific advice it received.1 Such a knee jerk defence beforethe facts were known may come to haunt the organisation.
This response is also disappointing given WHO’s track record of standing up to industry. In the late 1970s WHO sparked two iconic clashes with multinational companies over the marketing of breast milk substitutes in the developing world and the setting up of the Essential Drugs Programme.4 Both issues set WHO at loggerheads with the United States where these industries had major holdings. Partly in response to WHO’s position, America withdrew contributions to WHO’s budget.
More recently, in 1999, when the forced disclosure of confidential tobacco industry documents alerted WHO to possible interference in its anti-tobacco activities, its then director general Gro Harlem Brundtland quickly set up an independent inquiry. She then published and press released its shocking findings—of an elaborate industry funded campaign to undermine WHO—without any attempt at interference or spin.5 The report recommended that all staff, consultants, temporary advisers, and members of expert committees should be required to declare their conflicts of interest, with well enforced penalties for those who failed to do so.6
As Cohen and Carter report, WHO subsequently published in 2003 new rules on managing conflicts of interest. These recommended that people with a conflict of interest should not be involved in the part of the discussion or the piece of work affected by that interest or, in certain circumstances, that they should not participate in the relevant discussion or work at all.7 WHO seems not to have followed its own rules for the decision making around the pandemic.
WHO will not be the only body to come under scrutiny for its handling of the pandemic. The coming months will see a spate of reports, from the European Commission, the European Parliament, and from national bodies including the French Senate, and the UK’s Cabinet Office. This soul searching takes place against a backdrop of hardening attitudes to conflicts of interest aroundthe world. Last year’s report from the Institute of Medicine8 has been followed by new guidance from groups such as the World Association of Medical Editors9 and the American College of Chest Physicians,10 which stress that declaration alone is no longer enough. To quote the Institute of Medicine report, "Disclosure is the essential though limited first step in identifying and responding to conflicts of interest." The big question is what to do about the conflicts.
On the basis of our own investigation and those of others, the answer is now inescapable. As Barbara Mintzes says in Cohen and Carter’s report, "No one should be on a committee developing guidelines if they have links to companies that either produce a product—vaccine or drug—or a medical device or test for a disease." The same, and more, must apply to committeesmaking major decisions on public health. Where entirely independent experts are hard to find, experts who are involved with industry could be consulted but should be excluded from decision making. The United States has made important progress with its Sunshine Act and other legislation. European legislation on managing conflicts of interest is long overdue.
As for WHO, its credibility has been badly damaged. Recovery will be fastest if it publishes its own report without delay or defensive comment; makes public the membership and conflicts of interest of its emergency committee; and develops, commits to, and monitors stricter rules of engagement with industrythat keep commercial influence away from its decision making.
In a briefing at the end of last year, a spokesperson for WHO said, "Given the discrepancy between what was expected [from the pandemic] and what has happened, a search for ulterior motives on the part of WHO and its scientific advisors is understandable, though without justification."11 The implication is that, had there been a huge death toll, the process behind WHO’s decision making would not have been subject to such scrutiny. This is almost certainly true. But it does not mean that we are wrong to ask hard questions. Neither does it make the answers we have found any less troubling. And nor does it remove from WHO the urgent need to restore its credibility and public trustbefore the next pandemic comes along.
Cite this as: BMJ 2010;340:c2947
Fiona Godlee, editor in chief
1 BMJ, London WC1H 9JP
fgodlee@bmj.com
Feature, doi:10.1136/bmj.c2912
Competing interests: The author has completed the Unified CompetingInterest form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declares: (1) No financial support for the submitted work from anyone other than her employer; (2) No financial relationships with commercial entities that might have an interest in the submitted work; (3) No spouse, partner, or children with relationships withcommercial entities that might have an interest in the submitted work; (4) FG has written articles on the challenges faced by WHO, and on the influence of the drugs industry. She is in favour of a more assertive approach to conflict of interest and supports efforts to control the influence of the drugs industry on medical research, medical education, and health policy.
Provenance and peer review: Commissioned; not externally peer reviewed.
Cite this as: BMJ 2010;340:c2947
Editorials
WHO must act now to restore its credibility, and Europe should legislate
The world should of course be thankful that the 2009 influenza A/H1N1 pandemic proved such a damp squib. With so many fewer lives lost than had been predicted, it almost seems ungrateful to carp about the cost. But carp we must because the cost has been huge. Some countries—notably Poland—declined to join the panic buying of vaccines and antivirals triggered when the World Health Organization declared the pandemic a year ago this week. However, countries like France and the United Kingdom who have stockpiled drugs and vaccines are now busy unpicking vaccine contracts, selling unused vaccine to other countries, and sitting on huge piles of unused oseltamivir.Meanwhile drug companies have banked vast profits—$7bn (£4.8bn; 5.7bn) to $10bn from vaccines alone according to investment bank JP Morgan.1
An investigation by the BMJ and the Bureau of Investigative Journalism, published this week (doi:10.1136/bmj.c2912
This lack of transparency is compounded by the existence of a secret "emergency committee," which advised the director general Margaret Chan on when to declare the pandemic—a decision that triggered costly pre-established vaccine contracts around the world. Curiously, the names of the 16 committee members are known only to people within WHO.
Cohen and Carter’s findings resonate with those of other investigations, most notably an inquiry by the Council of Europe, which reports this week and is extremely critical of WHO.1
One of its chief protagonists is Paul Flynn, a UK member of parliament and a member of the council’s Parliamentary Assembly. He and others raised concerns last year about the lack of evidence to justify the scale of the international response to H1N1 (as also covered in the BMJ in December3
WHO’s response to these concerns has been disappointing. Although Margaret Chan has ordered an inquiry and WHO has stressed its commitment to transparency, her office has turned down requests to clear up concerns about potential conflicts of interest.2
This response is also disappointing given WHO’s track record of standing up to industry. In the late 1970s WHO sparked two iconic clashes with multinational companies over the marketing of breast milk substitutes in the developing world and the setting up of the Essential Drugs Programme.4
More recently, in 1999, when the forced disclosure of confidential tobacco industry documents alerted WHO to possible interference in its anti-tobacco activities, its then director general Gro Harlem Brundtland quickly set up an independent inquiry. She then published and press released its shocking findings—of an elaborate industry funded campaign to undermine WHO—without any attempt at interference or spin.5
As Cohen and Carter report, WHO subsequently published in 2003 new rules on managing conflicts of interest. These recommended that people with a conflict of interest should not be involved in the part of the discussion or the piece of work affected by that interest or, in certain circumstances, that they should not participate in the relevant discussion or work at all.7
WHO will not be the only body to come under scrutiny for its handling of the pandemic. The coming months will see a spate of reports, from the European Commission, the European Parliament, and from national bodies including the French Senate, and the UK’s Cabinet Office. This soul searching takes place against a backdrop of hardening attitudes to conflicts of interest aroundthe world. Last year’s report from the Institute of Medicine8
On the basis of our own investigation and those of others, the answer is now inescapable. As Barbara Mintzes says in Cohen and Carter’s report, "No one should be on a committee developing guidelines if they have links to companies that either produce a product—vaccine or drug—or a medical device or test for a disease." The same, and more, must apply to committeesmaking major decisions on public health. Where entirely independent experts are hard to find, experts who are involved with industry could be consulted but should be excluded from decision making. The United States has made important progress with its Sunshine Act and other legislation. European legislation on managing conflicts of interest is long overdue.
As for WHO, its credibility has been badly damaged. Recovery will be fastest if it publishes its own report without delay or defensive comment; makes public the membership and conflicts of interest of its emergency committee; and develops, commits to, and monitors stricter rules of engagement with industrythat keep commercial influence away from its decision making.
In a briefing at the end of last year, a spokesperson for WHO said, "Given the discrepancy between what was expected [from the pandemic] and what has happened, a search for ulterior motives on the part of WHO and its scientific advisors is understandable, though without justification."11
Cite this as: BMJ 2010;340:c2947
Fiona Godlee, editor in chief
1 BMJ, London WC1H 9JP
fgodlee@bmj.com
Feature, doi:10.1136/bmj.c2912
Competing interests: The author has completed the Unified CompetingInterest form at www.icmje.org/coi_disclosure.pdf
Provenance and peer review: Commissioned; not externally peer reviewed.
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