Tuesday, December 22, 2009

on depression, Depressed People Can't Hold Onto Happiness; it would be interesting to see if dysthymics look different in terms of the their functional mri

Depressed People Can't Hold Onto Happiness
Novel study found they could feel good, just couldn't sustain positive feelings

MONDAY, Dec. 21 (HealthDay News) -- It's not that depressed people can't feel good, it's that they can't hang on to that feeling, a new study claims.

The novel notion upends previous beliefs that depressed people don't even start out with positive emotions, and that they have no or little response in the areas of the brain related to good feelings.

"This tells us that a consideration of positive emotion is as important, if not more important, in understanding depression," said Richard Davidson, senior author of a study appearing online Dec. 21 in the Proceedings of the National Academy of Sciences.

"It further suggests that we may be able to develop cognitive strategies that aren't so much focused on minimizing negative emotion but rather enhancing and sustaining positive emotion," continued Davidson, who is director of the Waisman Laboratory for Brain Imaging and Behavior at the University of Wisconsin-Madison.

"Previous knowledge agreed that patients who have anhedonia [inability to experience pleasure, a component of depression] have a decreased ability to experience positive emotions," added Eva E. Redei, the David Lawrence Stein professor of psychiatry at the Feinberg School of Medicine at Northwestern University in Chicago. "The novelty of this finding is that it's not that they cannot experience positive emotions, but that they can't hang on to it."

The findings may also affect which medications are used for different cases of depression, namely that medications that affect the dopamine or reward system of the brain may be effective in this type of disorder.

"Although depression is considered a mood disorder, we really don't know how mood is disordered in depression," said Davidson. "One of the ignored areas in depression is the possibility that one of the major abnormalities in depression is not so much a disorder of negative emotion but rather a disorder of positive emotion. The idea here is that patients with depression or at least a subgroup of them have a problem in sustaining or maintaining positive emotion."

The study was designed to investigate whether people with depression have trouble maintaining positive emotions over time.

Twenty-seven depressed adults and 19 non-depressed controls were asked to look at images meant to elicit positive or negative emotions, such as a nature scene or a mother hugging her baby for the positive side.

"We asked people to feel whatever emotion was elicited by the picture and then enhance the emotion to the best of their ability using mental or cognitive strategies," Davidson explained.

As an example, participants viewing the mother and baby picture could imagine the love the mother was conveying to her baby.

Participants were then asked to sustain the positive emotion for 45 minutes while undergoing functional MRI.

"What we found is that normal controls are able to do this and show activation in areas of brain that we know are important for positive emotion, especially the nucleus accumbens, which is critical for reward and positive emotion," Davidson said. "The depressed patients showed activation in this area comparable to healthy controls in the beginning but were unable to sustain this activation over time."

The research was funded by the National Institute of Mental Health, Wyeth-Ayerst Pharmaceuticals and different foundations.

More information

The National Institute of Mental Health has more on depression.


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zpeds texting driving adding to the cumulative evidence.

Texting While Driving Raises Crash Risk Sixfold
While drivers message, distance between cars shrinks and reaction times grow, study finds

MONDAY, Dec. 21 (HealthDay News) -- Drivers who text-message are putting themselves and others in danger as they switch their attention between two complex tasks, a new study confirms.

Researchers who placed young adults in a virtual driving simulator found that the gap between the driver's car and the car ahead shrank when texting came into the mix, but the driver's reaction times slowed.

The result: Drivers who were texting were six times more likely to be involved in a virtual 'crash' than those who were concentrating just on driving.

Texting seemed to raise the danger factor for drivers more than talking on a cell phone, the researchers noted.

While talking on a cell phone, "drivers apparently attempt to divide attention between a phone conversation and driving, adjusting the processing priority of the two activities, depending on task demands," wrote the research team, led by Frank Drews, an associate professor of psychology at the University of Utah.

Texting, on the other hand, requires drivers to switch their attention completely to that task, and away from driving, they found, and this made for slower reaction and braking times.

In addition, they found that reading text messages proved more distracting than composing messages.

In the study, reported in the journal Human Factors, Drew and his colleagues had 20 male and female drivers, 19 to 23 years old, engage in either driving or driving while texting in a "high-fidelity [driving] simulator." All of the participants were experienced texters.

The team found that drivers' median reaction time increased by 9 percent while they were on a cell phone, vs. 30 percent while texting, compared with the driving-only condition. At the same time, the "minimum following distance" between themselves and the virtual car ahead shrank.

Numerous U.S. cities have banned texting while driving after accidents linked to the practice began to rise.

More information

The U.S. National Highway Traffic Safety Administration has more on cell phone use while driving.


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John C Kim MD
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zpeds Behavioral approach is best, but hard to do to treat insomnia; and insomnia related to headache and reflux symptoms, ? what is causal and what is correlation?

Link Between Insomnia Symptoms And Medical Complaints In Young School-Aged Children

Main Category: Sleep / Sleep Disorders / Insomnia
Also Included In: Pediatrics / Children's Health;  GastroIntestinal / Gastroenterology;  Headache / Migraine
Article Date: 15 Dec 2009 - 3:00 PST

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A study in the Dec. 15 issue of the Journal of Clinical Sleep Medicineindicates that significant associations exist between parent-reported insomniasymptoms and medical complaints of gastrointestinal regurgitation andheadaches in young school-aged children. 

Results of multivariate regression analysis show that parent-reported insomnia was 3.3 times more likely in children with gastrointestinal regurgitation and 2.3 times more likely in children with headaches. Nineteen percent of children met the criteria for insomnia, which was defined as often having trouble falling asleep and/or waking up often in the night. Gastrointestinal regurgitation was reported in 7.5 percent of children with insomnia and two percent of children who did not have sleep disturbances. Headaches were reported in 24.4 percent of children with insomnia and 13.2 percent of children without disturbed sleep. 

Lead author Ravi Singareddy, MD, assistant professor in the department of psychiatry at Penn State College of Medicine in Hershey, Pa., said that children who have insomnia symptoms should be screened by their physician for underlying medical conditions. 

"The first and most important step in children with medical complaints and sleep disturbances would be an evaluation for underlying medical disorders and providing treatment," said Singareddy. "If the associated sleep disturbances do not improve despite improvement in medical complaints the disturbances should be further assessed and treated." 

Data from 700 children between the ages of five and 12 years (mean 8.8 years) were collected from the Penn State Children's Cohort for this cross-sectional study. All children underwent a medical and psychiatric history, physical examination, overnight polysomnography and neuropsychological testing. Comprehensive sleep and development questionnaires were completed by a parent. To assess gastrointestinal regurgitation the parent was asked, "Does food or liquid come back up into your child's mouth or does your child complain of tasting food or liquid back up in his mouth?" 

Children with sleep disturbances had significantly more parent-reported complaints of gastrointestinal symptoms (heartburn, pain/colic and regurgitation), headaches and bedwetting. After controlling for demographic variables; apnea-hypopnea index; learning, psychiatric and behavioral disorders; and socioeconomic and minority status, only gastrointestinal regurgitation and headaches remained significantly associated with insomnia symptoms. 

According to the authors, the cross-sectional nature of the study did not allow for the assessment of a cause-and-effect relationship, which could be bidirectional in nature. The insomnia symptoms may have resulted in medical complaints since it is known that the respiratory, cardiovascular and gastrointestinal systems undergo significant physiological changes during sleep. Activation of the stress response system in association with hyperarousal also could have been responsible for both the sleep disturbances and the comorbid medical complaints in these children. 

The authors suggest that future studies should explore the possible underlying pathophysiological causes of such comorbidity between insomnia symptoms and medical complaints in children. These studies should explore whether treatment of sleep complaints improves the associated medical complaints and vice versa. 

The AASM published "Practice parameters for behavioral treatment of bedtime problems and night wakings in infants and young children" in the journal SLEEP in 2006. About 94 percent of the studies that were reviewed reported that behavioral interventions as a whole produced clinically significant improvements in bedtime resistance and night waking. 

In 2003 an AASM task force of sleep experts examined the use of medications to treat insomnia in children. A consensus meeting summary was published in 2005 in the Journal of Clinical Sleep Medicine. The task force emphasized that behavioral treatment approaches to bedtime struggles and night waking in children have a well-documented empirical basis and are the mainstay of treatment, and that pharmacologic approaches should be largely considered adjuncts in the treatment of pediatric insomnia. 

Source: Kelly Wagner 
American Academy of Sleep Medicine 


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John C Kim MD
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Thursday, December 10, 2009

The 'Sex Talk' Often Comes Too Late; parent(s) are invariably surp that their kids are having sex; and the denial represents to the kids that their parent(s) shoud not be in the loop in their decision making

The 'Sex Talk' Often Comes Too Late - American Academy Of Pediatrics

The American Academy of Pediatrics recommends that parents educate
their children about sexuality beginning early in life. According to
the study, "Timing of Parent and Child Communication About Sexuality
Relative to Children's Sexual Behaviors," published in the January
issue of Pediatrics, many of these discussions are occurring after
adolescents have already passed key sexual milestones.

In a series of surveys with 141 parents and their teen-aged children,
researchers found more than 40 percent of children had sexual
intercourse before any discussion with their parents about sexually
transmitted disease symptoms, condom use, choosing birth control, or
what to do if a partner refuses a condom.

Researchers suggest pediatricians encourage parents to have more
timely communication with their children about important sex-related
topics. Suggestions for specific topics that should be covered and
advice on how to discuss them would help guide parents who don't know
what to say. Pediatricians also can address these issues in one-on-one
conversations with adolescents in their office.

Source
American Academy of Pediatrics

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John C Kim MD
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Introduction Of Solid Foods And Allergic Reactions; kind of opposite of what we had been telling people, confusing because new data comes along, and we try to adapt

ntroduction Of Solid Foods And Allergic Reactions - American Academy
Of Pediatrics

09 Dec 2009

Late introduction of solid foods may increase the risk of allergic
sensitization to food and inhalant allergens. In the study, "Age at
the Introduction of Solid Foods During the First Year and Allergic
Sensitization at Age 5 Years," published in the January issue of
Pediatrics, researchers examined the diets and allergic sensitivities
of 994 children with susceptibility to type 1 diabetes. Results
indicate that late introduction of solid foods was associated with
increased allergic sensitization to food and inhalant allergens.

Eggs, wheat and oats were most commonly related to food sensitization,
while potatoes and fish were strongly associated with inhalant
sensitization. The American Academy of Pediatrics recommends the
introduction of solid foods between the ages of 4 and 6 months. Study
authors conclude that neither extended, exclusive breastfeeding, nor
delaying the introduction of solid foods, may prevent allergic
diseases in children.

Source
American Academy of Pediatrics
Article URL: http://www.medicalnewstoday.com/articles/173462.php

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John C Kim MD
719 439 3730 NEW MOBILE PHONE

Wednesday, December 9, 2009

Pistachios May Reduce Lung Cancer Risk ; Yum


Pistachios May Reduce Lung Cancer Risk

ScienceDaily (Dec. 9, 2009) — A diet that incorporates a daily dose of pistachios may help reduce the risk of lung and other cancers, according to data presented at the American Association for Cancer Research Frontiers in Cancer Prevention Research Conference, held Dec. 6-9.

"It is known that vitamin E provides a degree of protection against certain forms of cancer. Higher intakes of gamma-tocopherol, which is a form of vitamin E, may reduce the risk of lung cancer," said Ladia M. Hernandez, M.S., R.D., L.D., senior research dietitian in the Department of Epidemiology at the University of Texas M. D. Anderson Cancer Center, and doctoral candidate at Texas Woman's University -- Houston Center.

"Pistachios are a good source of gamma-tocopherol. Eating them increases intake of gamma-tocopherol so pistachios may help to decrease lung cancer risk," she said.

Pistachios are known to provide a heart-healthy benefit by producing a cholesterol-lowering effect and providing the antioxidants that are typically found in food products of plant origin. Hernandez and colleagues conducted a six-week, controlled clinical trial to evaluate if the consumption of pistachios would increase dietary intake and serum levels of gamma-tocopherol. A pistachio-rich diet could potentially help reduce the risk of other cancers from developing as well, according to Hernandez.

"Because epidemiologic studies suggest gamma-tocopherol is protective against prostate cancer, pistachio intake may help," she said. "Other food sources that are a rich source of gamma-tocopherol include nuts such as peanuts, pecans, walnuts, soybean and corn oils."

The study, conducted at Texas Woman's University -- Houston Center, included 36 healthy participants who were randomized into either a control group or the intervention group consisting of a pistachio diet. There were 18 participants in the control group and 18 in the intervention group. There was a two-week baseline period, followed by a four-week intervention period in which the intervention group was provided with 68 grams (about 2 ounces or 117 kernels) of pistachios per day; the control group continued with their normal diet.

The effect on the intake and serum cholesterol-adjusted gamma-tocopherol was investigated. Intake was calculated using the Nutrition Data System for Research Version 2007, and consumption was monitored using diet diaries and by measuring the weights of the returned pistachios.

Hernandez and colleagues found a significant increase in energy-adjusted dietary intake of gamma-tocopherol at weeks three and four in those on the pistachio diet compared with those on the control diet. The similar effect was seen at weeks five and six among those on the pistachio diet compared with those on the control diet. For those on the pistachio diet, cholesterol-adjusted serum gamma-tocopherol was significantly higher at the end of the intervention period compared to baseline.

"Pistachios are one of those 'good-for-you' nuts, and 2 ounces per day could be incorporated into dietary strategies designed to reduce the risk of lung cancer without significant changes in body mass index," said Hernandez.

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John C Kim MD
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Dirty in childhood protective?

Everyday Germs in Childhood May Prevent Diseases in Adulthood

ScienceDaily (Dec. 9, 2009) — A new Northwestern University study suggests that American parents should ease up on antibacterial soap and perhaps allow their little ones a romp or two in the mud --- or at least a much better acquaintance with everyday germs.

The study is the first to look at how microbial exposures early in life affect inflammatory processes related to diseases associated with aging in adulthood.

Most provocatively, the Northwestern study suggests that exposure to infectious microbes early in life may actually protect individuals from cardiovascular diseases that can lead to death as an adult.

"Contrary to assumptions related to earlier studies, our research suggests that ultra-clean, ultra-hygienic environments early in life may contribute to higher levels of inflammation as an adult, which in turn increases risks for a wide range of diseases," said Thomas McDade, lead author of the study, associate professor of anthropology in Northwestern's Weinberg College of Arts and Sciences and a faculty fellow at the Institute for Policy Research.

Relatively speaking, humans only recently have lived in such hyper-hygienic environments, he stressed.

The research suggests that inflammatory systems may need a higher level of exposure to common everyday bacteria and microbes to guide their development. "In other words, inflammatory networks may need the same type of microbial exposures early in life that have been part of the human environment for all of our evolutionary history to function optimally in adulthood," said McDade, also a member of Northwestern's Cells to Society (C2S).

The Northwestern study is the first research on microbial effects on inflammatory systems in infancy that relate in later life to diseases associated with aging. Advancing the scientific literature on the developmental origins of disease, the study arguably is the most significant research on long-term effects of early environments on human physiological function and health in adulthood.

The research took advantage of a longitudinal study of Filipinos, following participants in utero through 22 years of age, to get a better understanding of how environments early in life affect production of C-reactive protein (CRP) production in adulthood.

Levels of the protein rise in the blood due to inflammation, an integral part of the immune system's fight against infection. CRP research mostly has centered on the protein as a predictor of heart disease, independent of lipids, cholesterol and blood pressure, though researchers still dispute that association. Researchers have been looking at excess body fat as a primary source of pro-inflammatory cytokines that produce CRP and behavioral factors related to diet, exercise and smoking. And the CRP research largely has been conducted in relatively affluent settings, such as in the United States, with low levels of infectious diseases.

The Northwestern researchers were interested in what CRP production looks like in the Philippines, a population with a high level of infectious diseases in early childhood compared to Western countries. Relative to Western countries, the Philippines also has relatively low rates of obesity and cardiovascular diseases, consistent with the Northwestern research findings.

Blood tests showed that C-reactive protein was at least 80 percent lower for study participants in the Philippines when they reached young adulthood, relative to their American counterparts, though the Filipinos suffered from many more infectious diseases as infants and toddlers. Filipino participants in their early 20s had average CRP concentrations of .2 milligrams per liter -- five to seven times lower than average CRP levels for Americans. CRP concentrations for Americans in their early 20s were on average around 1 to 1.5 milligram per liter.

"Early Origins of Inflammation: Microbial Exposures in Infancy Predict Lower Levels of C-reactive Protein in Adulthood," will be published online December 9 in the journal Proceedings of the Royal Society B: Biological Sciences. Besides Northwestern's McDade, the co-authors are Julienne Rutherford, University of Illinois at Chicago; Linda Adair, University of North Carolina, Chapel Hill; and Christopher Kuzawa, associate professor of anthropology in Weinberg at Northwestern.

The Northwestern study drew its data from a longitudinal study that began in the early 1980s with 3,327 Filipino mothers in the third trimester of pregnancy. The mothers were interviewed for behaviors related to care giving, and breast feedings were recorded. The household environment was assessed in terms of socioeconomic resources, hygiene (whether domestic animals, such as pigs and dogs, roamed freely) and density of inhabitants.

Researchers visited with the mothers at the delivery of their infants and subsequently every two months for the first two years of the children's lives. Thereafter, the researchers followed up with the children every four or five years until they reached their early 20s. The records they kept on the children include data on infectious diseases, growth in height and weight.

"In the U.S we have this idea that we need to protect infants and children from microbes and pathogens at all possible costs," McDade concluded.

"But we may be depriving developing immune networks of important environmental input needed to guide their function throughout childhood and into adulthood. Without this input, our research suggests, inflammation may be more likely to be poorly regulated and result in inflammatory responses that are overblown or more difficult to turn off once things get started."

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John C Kim MD
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Maternal infection during pregnancy and schizophrenia; Nice summary of literature.

J Psychiatry Neurosci. 2008 May; 33(3): 183–185.
PMCID: PMC2441883
Maternal infection during pregnancy and schizophrenia
Patricia Boksa
Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montréal, Que.
Medical subject headings: infection, influenza, human, pregnancy, schizophrenia
For the 2007–2008 season, the Canadian National Advisory Committee on Immunization has for the first time recommended that all pregnant women be vaccinated against influenza. In the United States, the Centers for Disease Control and Prevention have recommended influenza vaccination for pregnant women in the second and third trimester of pregnancy since 1997; in 2004, this recommendation was revised to include pregnant women in all trimesters (see Mak and colleagues1 for further discussion of current policies on influenza vaccination during pregnancy in other countries). Although the decision to vaccinate is based mainly on the increased risk in pregnant women for acute cardiopulmonary complications due to influenza, increased influenza vaccination during pregnancy could have implications for the development of schizophrenia.
For a few decades now, maternal infection during pregnancy has been considered a plausible risk factor for schizophrenia. The story essentially began in Finland with the publication in 1988 of a paper by Mednick and colleagues2 reporting an increased risk for schizophrenia in people who were fetuses during the 1957 influenza epidemic. The story has continued up to the publication in December 2007 of a study coming again from Scandinavia, this time from Denmark. Using a much more sophisticated database (i.e., a national longitudinal registry of health records), this study again showed an increased risk for schizophrenia associated with maternal influenza during pregnancy.3 During the intervening 20 years, more than 25 epidemiologic studies have examined this issue, using various sources for information on the infection, ranging from simple correlation with known dates of epidemics to maternal recall, hospital records and national registry records on documented influenza occurrence. About one-half have replicated the finding, and about one-half have not. These failures to replicate could be due to inaccurate information on infection or other factors, or they may represent true findings of no association between maternal influenza and schizophrenia in some populations. Interestingly, increased rates of diagnosis for major affective disorder have also been reported following exposure to an influenza epidemic during the second trimester,4 indicating that effects may not be specific for schizophrenia.
In addition to influenza, a wide variety of other maternal infections during pregnancy have been reported to be associated with increased risk for schizophrenia. These include maternal infections with other viruses (measles, rubella, varicella-zoster, polio) as well as maternal bronchopneumonia (which is largely bacterial), maternal infection with the parasite causing toxoplasmosis and infections of the maternal genital and reproductive systems. The rubella study is particularly striking in that up to 20% of subjects exposed to rubella (serologically confirmed) in the first trimester developed adult schizophrenia.5 Thus it appears that maternal infection with a wide variety of agents might potentially increase risk for schizophrenia, suggesting that factors common to many infections may be mechanistically responsible.
More recently, some laboratories have attempted to confirm maternal infection more precisely by analyzing antibodies for viral infection in maternal serum that had been stored from 30 to 40 years until offspring had grown and developed schizophrenia. As can be appreciated, these are very challenging studies with limits in the sample size due to limited availability of stored serum, questions about storage and stability of samples, etc. Studies by Brown and colleagues6 found an association between schizophrenia spectrum disorders and maternal influenza during the first trimester of pregnancy that just missed statistical significance (p = 0.08) and during the first half of pregnancy that also barely missed significance (p = 0.052). Interestingly, while earlier epidemiologic studies had quite consistently implicated influenza in the second trimester of pregnancy, Brown and colleagues' studies with archived maternal serum have implicated the first third to half of pregnancy. It has been pointed out that, if the association between maternal influenza and schizophrenia holds, then maternal influenza could account for an appreciable amount of the population-associable risk for schizophrenia because influenza is so prevalent. Clearly, these important studies require replication and confirmation.
Other studies examining serologically confirmed maternal infection are those published by Buka and colleagues from the US National Collaborative Perinatal Project.7 Assaying maternal serum taken at the end of pregnancy, these studies have reported that elevated titres of maternal antibodies to herpes simplex virus type 2 (HSV-2) are associated with increased incidence of psychosis (both schizophrenic and affective combined, and schizophrenic alone) in offspring. It was noted that the effect sizes for these associations were comparable in magnitude to those reported for some genetic polymorphisms linked to schizophrenia. However, by contrast, Brown and colleagues found no significant association between seropositivity for HSV-2 in late pregnancy maternal serum and risk for schizophrenia spectrum disorders in offspring in their sample population.8
Overall, it is noteworthy that, with the exception of studies of influenza, most of the epidemiologic studies implicating prenatal infection with various agents as risk factors for schizophrenia have been reported only by single groups and await replication by others. As an interesting twist, controlling for a series of confounders, Sørensen and colleagues9 have reported that maternal exposure to analgesics (ASA and other anti-inflammatory agents, codeine and, rarely, morphine) in the second trimester of pregnancy is also associated with an increased risk for schizophrenia. If maternal infection is a risk factor for schizophrenia, it is also evident that the epidemiologic studies have not yet clearly defined which stage of pregnancy might be the main vulnerability period. Both the first and second trimesters have been implicated.
Of course, maternal infection during pregnancy is not thought to be the sole cause of schizophrenia but is speculated to act in interaction with other etiologic factors. For example, the effects of prenatal infection on fetal neurodevelopment may be exaggerated in those with a particular genetic vulnerability. As another example, patients with schizophrenia who were exposed to second trimester influenza have been reported to be more likely to have experienced a subsequent obstetric complication and to have had a lower birth weight, compared with patients who did not have second trimester exposure.10
Since 2000, there has been a veritable explosion of animal studies designed to ask whether it is plausible that maternal infection during pregnancy could cause changes in brain development relevant to schizophrenia. These studies have modelled maternal infection either using live influenza viruses or using viral RNA mimics or bacterial endotoxin to produce more controlled infections. Overall, a large number of studies have now demonstrated that, in rodents, maternal infection during pregnancy can indeed produce changes in central nervous system (CNS) structure, function and behaviour in offspring. These changes include many relevant to schizophrenia, such as deficits in prepulse inhibition of startle, latent inhibition, memory and social interaction; increases in amphetamine-and MK-801–induced locomotion; alterations in CNS levels of dopamine and tyrosine hydroxylase; and cell death, cell atrophy or reduced volume in the hippocampus. Although the overall conclusion from these studies supports the idea that maternal infection can alter brain development, as in many fields, each laboratory works with its own particular model, precluding across-laboratory replication of specific findings. Thus each laboratory works with its own species (rat, mouse), dose and type of infectious agent (virus, viral mimic, bacterial endotoxin) given at different times of gestation, and each laboratory tends to measure different end points in offspring.
Work in the area of animal modelling is now also attempting to approach the question of the mechanism by which a maternal infection might affect fetal brain development. Several possibilities are being considered:
1. Live virus may directly reach and affect the fetal brain. This has been supported by one study employing intranasal administration of influenza virus to pregnant mice,11 although not by another.12
2. Chemical mediators of infection may mediate changes in brain development. During a maternal infection, chemical mediators of inflammation, most prominently the cytokines, interleukin-1β (IL-1β), IL-6 and tumour necrosis factor-α, are increased in the mother's blood and in the placenta. It is still unclear whether these are routinely increased in the fetal brain after maternal infection. Such cytokines could affect fetal brain development by direct effects on fetal brain, by compromising placental function or by effects mediated through the mother.
3. Fever itself, as a consequence of increased maternal cytokine release, may affect fetal neurodevelopment. Research in the field of exercise physiology undertaken owing to concerns about increases in maternal body temperature during exercise in pregnancy have shown that quite brief exposure of pregnant rodents to temperatures from 40°C to 43°C can result in fetal resorption and CNS anomalies. For example, Khan and Brown13have shown that maintaining pregnant rats at 42°C for 45 minutes on gestation day 17 is sufficient to increase apoptosis in the cerebral cortex of fetuses. (One wonders about such effects in the face of global warming and record summer temperatures in several countries.)
4. It has been suggested that antibodies against infectious agents may cross react with and injure fetal brain structures. There is not yet evidence that such an autoimmune mechanism occurs in schizophrenia. However the notion is not without precedent. For example, there is some experimental support for the idea that antibodies against Group A β-hemolytic streptococci may cross-react with basal ganglia, leading to cases of Tourette syndrome or obsessive–compulsive disorder following strep throat infections.14
5. Medications such as analgesics and anti-inflammatory drugs taken during an infection in pregnancy could affect fetal development.
If maternal infection is a clear risk factor for schizophrenia, this raises several clinical questions for prevention. Should maternal influenza vaccination be more aggressively promoted? What about prevention of other infections? Do anti-inflamatory/antipyretic drugs have positive or negative effects? Is reduction of fever sufficient, or should inhibition of specific cytokines be targeted? Etc.
Footnotes
Competing interests: None declared.
Correspondence to: Dr. P. Boksa, Douglas Institute — Research, Pavilion Perry, Rm. E-2110, 6875 LaSalle Blvd., Verdun, Montréal QC H4H 1R3; fax 514 762-3034;patricia.boksa@mcgill.ca
1. Mak TK, Mangtani P, Leese J, et al. Influenza vaccination in pregnancy: current evidence and selected national policies. Lancet Infect Dis 2008;8:44-52. [PubMed]
2. Mednick SA, Machon RA, Huttunen MO, et al. Adult schizophrenia following prenatal exposure to an influenza epidemic. Arch Gen Psychiatry 1988;45:189-92. [PubMed]
3. Byrne M, Agerbo E, Bennedsen B, et al. Obstetric conditions and risk of first admission with schizophrenia: a Danish national register based study. Schizophr Res2007;97:51-9. [PubMed]
4. Machón RA, Mednick SA, Huttunen MO. Adult major affective disorder after prenatal exposure to an influenza epidemic. Arch Gen Psychiatry 1997;54:322-8. [PubMed]
5. Brown AS, Cohen P, Harkavy-Friedman J, et al. Prenatal rubella, premorbid abnormalities, and adult schizophrenia. Biol Psychiatry 2001; 49:473-86. [PubMed]
6. Brown AS, Begg MD, Gravenstein S, et al. Serologic evidence of prenatal influenza in the etiology of schizophrenia. Arch Gen Psychiatry 2004;61:774-80. [PubMed]
7. Buka SL, Cannon TD, Torrey EF, et al; Collaborative Study Group on the Perinatal Origins of Severe Psychiatric Disorders. Maternal exposure to herpes simplex virus and risk of psychosis among adult affspring. Biol Psychiatry 2008;63:809-15. [PubMed]
8. Brown AS, Schaefer CA, Quesenberry CP Jr, et al. No evidence of relation between maternal exposure to herpes simplex virus type 2 and risk of schizophrenia? Am J Psychiatry 2006;163:2178-80. [PubMed]
9. Sørensen HJ, Mortensen EL, Reinisch JM, et al. Association between prenatal exposure to analgesics and risk of schizophrenia. Br J Psychiatry 2004;185:366-71.[PubMed]
10. Wright P, Takei N, Rifkin L, et al. Maternal influenza, obstetric complications, and schizophrenia. Am J Psychiatry 1995;152:1714-20. [PubMed]
11. Aronsson F, Lannebo C, Paucar M, et al. Persistence of viral RNA in the brain of offspring to mice infected with influenza A/WSN/33 virus during pregnancy. J Neurovirol2002;8:353-7. [PubMed]
12. Shi L, Tu N, Patterson PH. Maternal influenza infection is likely to alter fetal brain development indirectly: the virus is not detected in the fetus. Int J Dev Neurosci2005;23:299-305. [PubMed]
13. Khan VR, Brown IR. The effect of hyperthermia on the induction of cell death in brain, testis, and thymus of the adult and developing rat. Cell Stress Chaperones2002;7:73-90. [PubMed]
14. Hoekstra PJ, Anderson GM, Limburg PC, et al. Neurobiology and neuroimmunology of Tourette's syndrome: an update. Cell Mol Life Sci 2004;61:886-98. [PubMed]


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John C Kim MD
719 439 3730 NEW MOBILE PHONE

The Long-Term Evidence for Vaccines . Newsweek article ,backlash to the backlash

 


PRINT THIS

The Long-Term Evidence for Vaccines

Vaccination does more than protect against flu. Study after study shows that keeping children safe from viruses has long-lasting, positive health benefits.

By Laurie Garrett and Dana March | Newsweek Web Exclusive 

Dec 7, 2009

With some reports saying that the worst of the H1N1 outbreak may have already come and gone this flu season in North America but not worldwide, parents who decided to sit out vaccinations for their children may feel validated. But not only is that strategy risky, it's uninformed, and ignores a larger truth about the benefit of vaccines. Throughout North America and Europe, an anti-vaccination movement has steadily grown over the past two decades, and was recently jet-propelled amid anxiety over immunizing pregnant women and children against the H1N1 "swine flu." The greatest fall-off in child vaccination, and the strongest proponents of various theoretical dangers associated with vaccines, are all rooted in wealthy, mostly Caucasian communities, located in the rich world. At a time when billions of people living in poorer countries are clamoring for equitable access to life-sparing drugs and vaccines for their families, the college-educated classes of the United States and other rich countries are saying "no thanks," even accusing their governments of "forcing" them to give "poison" to their children.

Will the children of these naysaying parents of the rich world turn to Mom and Dad 30 years from now and say, "Thanks for not getting me immunized. Thanks especially for saying no to the flu vaccine?"

Probably not.

If a woman is exposed to influenza while pregnant, or if an unvaccinated child gets the flu in his or her first year of life, the baby's developing brain may be severely damaged by the virus. Analysis of medical records of Americans who were born in the late '50s and early '60s shows that having the mother catch the flu while pregnant increased the chance her child would later develop schizophrenia. It's not a trivial difference: the children of moms who had flu midway during their pregnancies were as much as eight times more likely to become schizophrenic.

Overall, prenatal and infant exposure to influenza is strongly associated with cognitive failures. Babies are born with brains and immune systems that are still developing, and will not be hard-wired and strong until their second year of life. Scientists are increasingly discovering links between viral infections during those precious times, and psychiatric problems ranging from lifelong depression to acute learning deficits. In utero or infancy infection with chickenpox doubles the risk of cerebral palsy, according to Australian researchers. Having rubella during pregnancy increases by 80 percent the chances of severe birth defects in that mother's child, including small brains and hearts, blindness, deafness, and severe learning deficits.

Children who contract measles, chickenpox, or whooping cough can develop encephalitis or meningitis—infections of the central nervous system—which can cause epilepsy, brain damage, and death. Parents cannot protect their children's brains against everything, but the basic battery of vaccines can block the bulk of these viral insults. And the good news is that the still-developing immune system of babies and infants is ripe for the vaccine-induced programming that can confer decades—in some cases, lifelong—protection.

Other vaccine-preventable diseases—measles, rubella, mumps, chickenpox, and whooping cough—can damage the optic nerves and hearing of fetuses and newborns. The effect in these cases is immediate and obvious. In the pre-vaccine era in the United States, a thousand kids lost their hearing every year due to measles infection, five out of every 10,000 children who contracted mumps suffered permanent deafness, and 10 percent of child deafness was due to rubella (a.k.a. German measles).

And today, in countries with spotty child-immunization achievements—including the United Kingdom—viral infection in utero or in infancy accounts for 10 to 25 percent of child deafness.

Influenza in utero or in the first year of a child's life is a major cause of adult cardiovascular disease—heart attacks and strokes. People who suffered influenza during the Great Pandemic of 1918–19 were 20 percent more likely to develop heart disease as adults. To put that in perspective, having a "bad cholesterol count" of more than 240mg confers a 20 percent elevated risk of heart attacks, according to the American Heart Association.

Dr. Marietta Vázquez studied 350 mothers and infants from birth to 12 months of age who were hospitalized at Yale-New Haven Hospital over nine flu seasons (2000–2009). The babies of flu-vaccinated moms were larger, healthier, and, 85 percent of the time, fully protected against influenza. Similar findings have recently been reported out of Bangladesh, where the babies of vaccinated moms averaged a half pound larger than their unprotected peers and were less likely to be born prematurely.

The good news is that five decades of global child-vaccination programs have dramatically reduced infant and child mortality rates, and improved life expectancies in most of the world. In September, UNICEF reported that for the first time since WWII the number of children dying in the world annually fell below 10 million in 2008, largely due to child immunization. Vaccines, UNICEF says, are saving 2.5 million kids from dying every single year.

But outbreaks of vaccine-preventable diseases are surfacing wherever clusters of people either decline immunization, or are denied it by virtue of population poverty. The unimmunized few are a threat to all, as they may harbor viruses and pass them onto others whose vaccine-induced immunity is waning due to HIV, cancer, or simply the passing of time. Conversely, failing to be immunized in childhood renders young adults vulnerable to infectious diseases that they may not encounter until they go off to college or travel outside of their home regions.

A cursory search of outbreak reports over the last 13 months demonstrates that measles, mumps, diphtheria, whooping cough, polio, and typhoid fever are surfacing now in all sorts of settings, from jet planes to college dormitories, from Dutch religious sects to villages of Caribbean islands. Some of these outbreaks are tiny, involving no more than a cluster of individuals. But over the last year, several outbreaks have reached epidemic levels.

The United Kingdom has more such outbreaks than any other wealthy country, and that comes as no surprise as Dr. Andrew Wakefield—a key proponent of the theory that additives in vaccines cause autism—started his anti-immunization career in the U.K., in 1998 publishing now thoroughly refuted "evidence" of an autism link. Wakefield is now the subject of a hearing conducted by the U.K.'s General Medical Council for alleged medical misconduct. The discovery that he was secretly funded by personal-injury lawyers that sued vaccine makers has further fueled inquiries. Still, Wakefield's ideas continue to resonate in the UK, to the dismay of the country's pediatricians. Today, 20 percent of U.K. children enter primary school without having completed their full schedule of basic vaccinations— 40 percent, in some parts of the country—according to the Department of Health.

For those fighting disease on the global stage, the H1N1 pandemic has brought into stark relief a puzzling, difficult dichotomy. In the wealthy world, where individuals have the luxury of demanding 100 percent safety, the balance between individual and population rights has shifted so far toward individualism that it is nearly impossible for public-health authorities to persuade people to accept even one in 1 billion risks on behalf of society as a whole. (The exception is the U.S. armed forces, where duty to country includes an obligation to accept full vaccination.) But the very tools of protection that many individuals in the rich world are rejecting—especially the H1N1 vaccine—are completely unavailable to more than half the population of the world. Some 24 million children last year had no access to basic vaccines, says UNICEF, and at least 4 billion people cannot get flu vaccines right now.

For the poor and emerging-market countries, this inequity in access to life-sparing public-health tools is viewed as not only grossly unfair, but as a sign of the arrogant hypocrisy of the wealthy world. The rich countries demand that the planet's poor make sacrifices to slow down epidemics—such as slaying their chickens to stop bird flu, or losing tourist dollars by publicly acknowledging outbreaks within their borders—but offer little in return, including access to precious vaccines.

Yes, the proper adjective is "precious": miracles of science that, combined with smallpox immunization, saved more lives during the 20th century than were lost in all the wars, all the genocides, and all the epidemics of that hundred years. When a baby in an African village dies of measles, or a schoolchild in China succumbs to typhoid fever, none can question how precious that lost life was, or how vital a difference a vaccine could have made.

GARRETT is a Pulitzer Prizewinning writer and senior fellow for global health at the Council on Foreign Relations. MARCH is a doctoral candidate at the Mailman School of Public Health at Columbia University, specializing in life course, social, and psychiatric epidemiology.

Find this article athttp://www.newsweek.com/id/226097

 

Tuesday, December 8, 2009

NOt much documented in literature, but interesting notion, ie childbirth is stressful for both parents though obviously in different ways, and cumulative stress may be depressogenic

Postpartum Depression Strikes Fathers, Too

Published: December 7, 2009

The pregnancy was easy, the delivery a breeze. This was the couple's first baby, and they were thrilled. But within two months, the bliss of new parenthood was shattered by postpartum depression.

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Health Guide: Post-Partum Depression

A sad, familiar story. But this one had a twist: The patient who came to me for treatment was not the mother but her husband.

A few weeks after the baby arrived, he had become uncharacteristically anxious, sad and withdrawn. He had trouble sleeping, even though his wife was the one up at night breast-feeding their new son. What scared her enough to bring him to my office was that he had become suicidal.

Up to 80 percent of women experience minor sadness — the so-called baby blues — after giving birth, and about 10 percent plummet into severe postpartum depression. But it turns out that men can also have postpartum depression, and its effects can be every bit as disruptive — not just on the father but on mother and child.

We don't know the exact prevalence of male postpartum depression; studies have used different methods and diagnostic criteria. Dr. Paul G. Ramchandani, a psychiatrist at the University of Oxford in England who dida study based on 26,000 parents, reported in The Lancet in 2005 that 4 percent of fathers had clinically significant depressive symptoms within eight weeks of the birth of their children. But one thing is clear: It isn't something most people, including physicians, have ever heard of.

At first, my patient insisted that everything was just fine. He and his wife had been trying to conceive for more than a year. He was ecstatic at the prospect of fatherhood, and he did not acknowledge feeling depressed or suicidal.

Suspicious of his rosy appraisal, I pushed a little.

It turned out that he had just taken a new high-pressure job in finance six months before the birth of his son. Though he was reluctant to admit it, he clearly had more than a little concern about his family's financial future.

And he was anxious about his marriage and his new life. "We go out a lot with friends to dinner and theater," he said wistfully, as I recall. "Now I guess that's all going to end."

He had spent the nine months of pregnancy in a state of excitement about being a father without really registering what a life-transforming event it was going to be.

Unlike women, men are not generally brought up to express their emotions or ask for help. This can be especially problematic for new fathers, since the prospect of parenthood carries all kinds of insecurities: What kind of father will I be? Can I support my family? Is this the end of my freedom?

And there is probably more to male postpartum depression than just social or psychological stress; like motherhood, fatherhood has its own biology, and it may actually change the brain.

A 2006 study on marmoset monkeys, published in the journal Nature Neuroscience, reported that new fathers experienced a rapid increase in receptors for the hormonevasopressin in the brain's prefrontal cortex. Along with other hormones, vasopressin is involved in parental behavior in animals, and it is known that the same brain area in humans is activated when parents are shown pictures of their children.

There is also some evidence that testosterone levels tend to drop in men during their partner's pregnancy, perhaps to make expectant fathers less aggressive and more likely to bond with their newborns. Given the known association between depression and low testosterone in middle-aged men, it is possible that this might also put some men at risk of postpartum depression.

By far the strongest predictor of paternal postpartum depression is having a depressed partner. In one study, fathers whose partners were also depressed were at nearly two and a half times the normal risk for depression. That was a critical finding, for clinicians tend to assume that men can easily step up to the plate and help fill in for a depressed mother. In fact, they too may be stressed and vulnerable to depression.

And there is the child to think about. Research has clearly shown that maternal postpartum depression can impair the emotional and cognitive development of infants. A father could well buffer the infant from some of the adverse effects of maternal depression — but that is a tall order if he too is depressed.

Dr. Ramchandani, who also followed children for three and a half years after birth, reported that they were affected differently depending on which parent was depressed. Maternal postpartum depression was associated with adverse emotional and behavioral effects in children regardless of sex; depression in fathers was linked only with behavioral problems in boys. (The study did not report on possible effects when both parents were depressed.)

As for my patient, he recovered within two months with the help of psychotherapy and an antidepressant. Afterward, he summed up the situation in just 10 words: "And I thought only women get this kind of thing."

All too many doctors think so too.

Richard A. Friedman is a professor of psychiatry at Weill Cornell Medical College.

The Mind column on Tuesday, about postpartum depression in men, misidentified the journal that published a 2006 finding that among marmoset monkeys, new fathers experienced a rapid increase in receptors for vasopressin, a brain hormone involved in parental behavior. The study appeared in Nature Neuroscience , not Nature Reviews Neuroscience.


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John C Kim MD
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