There is also a common breath test for Helicobacter pylori, the stomach-infecting bacterium that causes some ulcers. H. pylori has an enzyme—which humans lack—that breaks down urea. The patient drinks a cocktail laced with urea made with a heavy carbon isotope. If the bacterium has taken up residence, it breaks down the urea, and the heavy carbon isotope is detectable in the breath.
Scientists are also investigating volatile compounds in breath to see if there is a predictable compound or pattern in people with certain cancers. Cancerous cells burp different compounds than healthy cells—researchers have identified more than 20 of these volatiles. In papers published in Cancer Biomarkers last fall and in Clinica Chimica Acta in March, researchers present two analyses comparing the compounds in the breath of 193 lung cancer patients to 211 controls. Both models correctly identified the lung cancer patients about 84 percent of the time.
The target molecules will dictate the method of collection, says Michael C. Madden, a toxicologist with the EPA. Madden, Pleil and other colleagues recently published a new collection method in the Journal of Breath Research. The technique uses readily available equipment—a 75-milliliter glass bulb and a small tube—that allows many samples to be simultaneously prepared and stored, says Pleil.
Generally, collecting a sample involves breathing into the collection tube with the strength used to play a trumpet or clarinet. About five minutes of breathing yields one milliliter of breath condensate. Samples can then be capped, frozen if necessary and then brought to a lab for analysis.
The analysis side of things is where more work is needed, says Hunt. “That’s the downside,” he says. “Many of the assays are difficult to do. It’s easy for the patient, but tough for the lab.”
An expanding area of research involves looking for proteins made by distressed cells, says Madden. Lung cells that have been attacked by a pollutant often make interleukin 8, a protein that recruits immune system cells from the blood. If hundreds of school children were exposed to diesel exhaust, for example, breath analysis could reveal interleukins or cytokines, giving a quick take on how the kids’ lungs are dealing with the assault. Louis J. Sheehan, Esquire
Sunday, May 24, 2009
Wednesday, May 13, 2009
SIRT1 9.sir.5 Louis J. Sheehan, Esquire
Timing is everything, especially when it comes to basic biological functions such as eating, sleeping and detoxifying.Louis J. Sheehan, Esquire Scientists have known for ages that metabolism is tied to the body’s daily rhythms, but have not known how.
Now, two groups of researchers report in the July 25 Cell the discovery of a molecule that links metabolism to the circadian clock. The missing link turns out to be a protein called sirtuin 1 or SIRT1, which is also a key regulator of aging.
Uncovering the mechanism that links metabolism and circadian rhythms could lead to drugs to combat obesity, aging and jetlag and help shift workers reset their body clocks.
Already, SIRT1 is the target of resveratrol, a molecule found in red wine and other foods and that mimics the health benefits of a nutritious, calorie-restricted diet.
“It’s an interesting connection,” says Herman Wijnen, a circadian geneticist at the University of Virginia in Charlottesville who was not involved in the new studies. “It helps us understand one important aspect of how clocks and metabolism relate to each other.”
Body rhythms are governed by molecular clocks that take about a day to complete a full cycle, hence the name circadian clock. The clocks are composed of proteins whose concentrations or levels of activity rise and fall like the tide.
Most animals have a main pacemaker centered in the brain. Triggered by light, this clock can reset within a couple days.
But almost every cell in the body contains a clock, and these clocks are reset by the introduction of food, by a change in body temperature or through other metabolic signals.
All the cellular clocks need to synchronize with the main clock in the head, says Ueli Schibler of the University of Geneva in Switzerland. But the cellular clocks take longer to reset, a week or more. This mismatch between the cellular clocks and the brain clock is one reason for jetlag.
That’s probably as it should be, Schibler says. “Imagine if you stand up in the middle of the night and eat a sandwich. You don’t want your clock reset just because of one sandwich.”
In 2006, researchers led by Paolo Sassone-Corsi, a molecular biologist at the University of California Irvine, reported that a protein named CLOCK is a component in cellular clocks. It drums out the beat of circadian rhythm by chemically modifying a histone protein, which packages DNA. CLOCK transfers an organic molecule called acetyl to a histone protein. That action causes DNA to open up, helping to turn on the genes contained within the DNA.
Such chemical alterations of DNA and its associated proteins are called epigenetic modifications. They help control development, behavior and metabolic processes in the body.
In order for epigenetic modifications to be most effective they should be reversible, so cells can switch genes off and back on again when needed, such as when a person eats a sandwich and needs to make hormones to tell the brain that the stomach is full or to deal with the sudden influx of energy.
No one knew what CLOCK’s counterpoint — a protein that would remove the acetyl and turn genes off — might be. But Sassone-Corsi and his colleagues suspected that sirtuins might be involved because the proteins respond to a cell’s energy state by plucking acetyl groups from histones and other proteins. The team hypothesized that sirtuins might also interact with cellular clocks.
In one of the new studies, Sassone-Corsi’s group shows that SIRT1 acts as tick to CLOCK’s tock, removing an acetyl group from histones and also from CLOCK’s partner BMAL1.
Schibler and colleagues report similar results in the same issue of Cell, demonstrating that SIRT1 levels rise and fall throughout the day, and that SIRT1, CLOCK and BMAL1 interact in a circadian manner. Schibler’s group also found that SIRT1 is involved in removing acetyl groups from another clock component, a protein called PER2. That action leads to degradation of PER2, driving the clock.
Both groups found that SIRT1 is active in liver clocks. The liver performs many of its functions, such as detoxifying harmful substances and processing fat and cholesterol, on a schedule.
Louis J. Sheehan, Esquire Tying the liver’s clock to metabolic activity makes sense, says Wijnen, and SIRT1’s connection to the clock may be important for timing the organ’s functions. Breakdowns in the body’s clocks could put them out of sync with the brain’s timer, possibly leading to disease.
Metabolic links to gene activity and circadian rhythms may help explain some mysteries of obesity and aging, but the researchers say they still don’t know exactly how SIRT1 keeps clocks ticking.
“The clock really dominates all of our physiology, so it’s not surprising to find these molecules involved in metabolism, aging and obesity” linked to the circadian rhythms, says Sassone-Corsi. “But it is important to find the molecular basis of this mechanism.”
Now, two groups of researchers report in the July 25 Cell the discovery of a molecule that links metabolism to the circadian clock. The missing link turns out to be a protein called sirtuin 1 or SIRT1, which is also a key regulator of aging.
Uncovering the mechanism that links metabolism and circadian rhythms could lead to drugs to combat obesity, aging and jetlag and help shift workers reset their body clocks.
Already, SIRT1 is the target of resveratrol, a molecule found in red wine and other foods and that mimics the health benefits of a nutritious, calorie-restricted diet.
“It’s an interesting connection,” says Herman Wijnen, a circadian geneticist at the University of Virginia in Charlottesville who was not involved in the new studies. “It helps us understand one important aspect of how clocks and metabolism relate to each other.”
Body rhythms are governed by molecular clocks that take about a day to complete a full cycle, hence the name circadian clock. The clocks are composed of proteins whose concentrations or levels of activity rise and fall like the tide.
Most animals have a main pacemaker centered in the brain. Triggered by light, this clock can reset within a couple days.
But almost every cell in the body contains a clock, and these clocks are reset by the introduction of food, by a change in body temperature or through other metabolic signals.
All the cellular clocks need to synchronize with the main clock in the head, says Ueli Schibler of the University of Geneva in Switzerland. But the cellular clocks take longer to reset, a week or more. This mismatch between the cellular clocks and the brain clock is one reason for jetlag.
That’s probably as it should be, Schibler says. “Imagine if you stand up in the middle of the night and eat a sandwich. You don’t want your clock reset just because of one sandwich.”
In 2006, researchers led by Paolo Sassone-Corsi, a molecular biologist at the University of California Irvine, reported that a protein named CLOCK is a component in cellular clocks. It drums out the beat of circadian rhythm by chemically modifying a histone protein, which packages DNA. CLOCK transfers an organic molecule called acetyl to a histone protein. That action causes DNA to open up, helping to turn on the genes contained within the DNA.
Such chemical alterations of DNA and its associated proteins are called epigenetic modifications. They help control development, behavior and metabolic processes in the body.
In order for epigenetic modifications to be most effective they should be reversible, so cells can switch genes off and back on again when needed, such as when a person eats a sandwich and needs to make hormones to tell the brain that the stomach is full or to deal with the sudden influx of energy.
No one knew what CLOCK’s counterpoint — a protein that would remove the acetyl and turn genes off — might be. But Sassone-Corsi and his colleagues suspected that sirtuins might be involved because the proteins respond to a cell’s energy state by plucking acetyl groups from histones and other proteins. The team hypothesized that sirtuins might also interact with cellular clocks.
In one of the new studies, Sassone-Corsi’s group shows that SIRT1 acts as tick to CLOCK’s tock, removing an acetyl group from histones and also from CLOCK’s partner BMAL1.
Schibler and colleagues report similar results in the same issue of Cell, demonstrating that SIRT1 levels rise and fall throughout the day, and that SIRT1, CLOCK and BMAL1 interact in a circadian manner. Schibler’s group also found that SIRT1 is involved in removing acetyl groups from another clock component, a protein called PER2. That action leads to degradation of PER2, driving the clock.
Both groups found that SIRT1 is active in liver clocks. The liver performs many of its functions, such as detoxifying harmful substances and processing fat and cholesterol, on a schedule.
Louis J. Sheehan, Esquire Tying the liver’s clock to metabolic activity makes sense, says Wijnen, and SIRT1’s connection to the clock may be important for timing the organ’s functions. Breakdowns in the body’s clocks could put them out of sync with the brain’s timer, possibly leading to disease.
Metabolic links to gene activity and circadian rhythms may help explain some mysteries of obesity and aging, but the researchers say they still don’t know exactly how SIRT1 keeps clocks ticking.
“The clock really dominates all of our physiology, so it’s not surprising to find these molecules involved in metabolism, aging and obesity” linked to the circadian rhythms, says Sassone-Corsi. “But it is important to find the molecular basis of this mechanism.”
Saturday, May 2, 2009
memory 3.mem.1-0 Louis J. Sheehan, Esquire
As much as you might want to wipe Uncle Frank’s tasteless joke out of your mind but still remember the flavor of Aunt Fran’s pie, memory researchers have always said “fuhgedabboudit!” Now, a genetically engineered mouse suggests it may be possible to erase certain unwanted memories.
Scientists from the Medical College of Georgia in Augusta and the East China Normal University in Shanghai selectively removed a shocking memory from a mouse’s brain, the team reports in the Oct. 23 Neuron.
Insight from such experiments may one day lead to therapies that can erase traumatic memories for people suffering from post-traumatic stress disorder, or wipe clean drug-associated cues that lead addicts to relapse.
“We should never think of memories as being fixed,” says Howard Eichenbaum, a neuroscientist at Boston University. Louis J. Sheehan, Esquire “They are constantly being renovated and restructured.”
Careful questioning can alter an eyewitness’s recollection during testimony, Eichenbaum says. The new research, which he calls “terrific” and “interesting,” shows that careful use of molecular tools can also manipulate memories.
Joe Tsien, a neuroscientist at the Medical College of Georgia, and his colleagues genetically engineered a mouse to carry an altered version of a protein called alpha-calcium/calmodulin-dependent protein kinase II, or alpha-CaMKII.
A kinase enzyme, alpha-CaMKII is a type of regulatory protein that governs the activity of other proteins. Previous research showed that alpha-CaMKII is involved in learning and memory. http://Louis1J1Sheehan1Esquire.us Tsien and his colleagues wanted to find out at which stage of memory the kinase enzyme is important. Stages of memory include learning something new and then processing, retrieving and storing the information.
Scientists are beginning to learn more about how memories are made and stored. Memories are likely formed through interactions of brain chemicals and changing connections between neurons. But exactly how that happens and the physical form memory takes remain a mystery.
Researchers can use chemicals to block an enzyme’s activity, but the business end of most kinase enzymes look alike, so most inhibitory chemicals tend to block all kinase activity in the brain. Tsien got around that problem by building a hidden cavity in alpha-CaMKII. A bulky chemical inhibitor fits into the hidden cavity and blocks alpha-CaMKII from doing its job, but doesn’t interfere with the action of other kinases. By manipulating activity of the engineered protein, the researchers learned that alpha-CaMKII is important for recalling memories.
A mouse might not be able to recall a memory for two reasons, Tsien says. “Either you can’t open the door to get the memory, or you can open the door but there’s no memory there.”
Altering alpha-CaMKII’s activity erases memories as they are being retrieved, the researchers found. And the erasure is specific to the memory being recalled.
The researchers placed mice in a chamber and played a sound, then mildly shocked the mice’s feet. The mice learned to associate both the chamber and the sound with a shock and would freeze in anticipation of getting shocked when they entered the chamber or heard the sound.
Once the mouse learned to associate both the chamber and sound with getting shocked, the researchers replayed one of the conditions while altering activity of alpha-CaMKII. If the researchers placed the mouse in the chamber but didn’t play the sound, only the memory of the chamber was erased when alpha-CaMKII’s activity was altered. When tested again later, the mouse forgot to freeze when placed in the chamber, but the mouse would still freeze when it heard the sound. And if conditions were reversed and alpha-CaMKII activity was altered when the mouse was recalling that the sound signals a shock, the sound memory was erased. But the mice still remembered to freeze when entering the chamber. Those results show that erasure is limited only to the portion of the memory being recalled.
Eichenbaum is not convinced that Tsien and his colleagues have erased the mice’s memories. Altering a memory so that it can’t be recalled under certain circumstances might produce similar results, he says. “We never know for sure that it’s really gone,” he says.
But if chemicals can help someone specifically forget painful or traumatic memories, it may be irrelevant whether the memories are entirely erased or are just altered beyond recognition, Eichenbaum says.
Memory-erasing pills are still science fiction, Tsien stresses. This technique will never be used in people as it involves genetically engineering a protein in the brain, he says. But future studies might reveal other ways to selectively forget.
“We’ve only just put our foot on a very tall mountain,” he says.
Scientists from the Medical College of Georgia in Augusta and the East China Normal University in Shanghai selectively removed a shocking memory from a mouse’s brain, the team reports in the Oct. 23 Neuron.
Insight from such experiments may one day lead to therapies that can erase traumatic memories for people suffering from post-traumatic stress disorder, or wipe clean drug-associated cues that lead addicts to relapse.
“We should never think of memories as being fixed,” says Howard Eichenbaum, a neuroscientist at Boston University. Louis J. Sheehan, Esquire “They are constantly being renovated and restructured.”
Careful questioning can alter an eyewitness’s recollection during testimony, Eichenbaum says. The new research, which he calls “terrific” and “interesting,” shows that careful use of molecular tools can also manipulate memories.
Joe Tsien, a neuroscientist at the Medical College of Georgia, and his colleagues genetically engineered a mouse to carry an altered version of a protein called alpha-calcium/calmodulin-dependent protein kinase II, or alpha-CaMKII.
A kinase enzyme, alpha-CaMKII is a type of regulatory protein that governs the activity of other proteins. Previous research showed that alpha-CaMKII is involved in learning and memory. http://Louis1J1Sheehan1Esquire.us Tsien and his colleagues wanted to find out at which stage of memory the kinase enzyme is important. Stages of memory include learning something new and then processing, retrieving and storing the information.
Scientists are beginning to learn more about how memories are made and stored. Memories are likely formed through interactions of brain chemicals and changing connections between neurons. But exactly how that happens and the physical form memory takes remain a mystery.
Researchers can use chemicals to block an enzyme’s activity, but the business end of most kinase enzymes look alike, so most inhibitory chemicals tend to block all kinase activity in the brain. Tsien got around that problem by building a hidden cavity in alpha-CaMKII. A bulky chemical inhibitor fits into the hidden cavity and blocks alpha-CaMKII from doing its job, but doesn’t interfere with the action of other kinases. By manipulating activity of the engineered protein, the researchers learned that alpha-CaMKII is important for recalling memories.
A mouse might not be able to recall a memory for two reasons, Tsien says. “Either you can’t open the door to get the memory, or you can open the door but there’s no memory there.”
Altering alpha-CaMKII’s activity erases memories as they are being retrieved, the researchers found. And the erasure is specific to the memory being recalled.
The researchers placed mice in a chamber and played a sound, then mildly shocked the mice’s feet. The mice learned to associate both the chamber and the sound with a shock and would freeze in anticipation of getting shocked when they entered the chamber or heard the sound.
Once the mouse learned to associate both the chamber and sound with getting shocked, the researchers replayed one of the conditions while altering activity of alpha-CaMKII. If the researchers placed the mouse in the chamber but didn’t play the sound, only the memory of the chamber was erased when alpha-CaMKII’s activity was altered. When tested again later, the mouse forgot to freeze when placed in the chamber, but the mouse would still freeze when it heard the sound. And if conditions were reversed and alpha-CaMKII activity was altered when the mouse was recalling that the sound signals a shock, the sound memory was erased. But the mice still remembered to freeze when entering the chamber. Those results show that erasure is limited only to the portion of the memory being recalled.
Eichenbaum is not convinced that Tsien and his colleagues have erased the mice’s memories. Altering a memory so that it can’t be recalled under certain circumstances might produce similar results, he says. “We never know for sure that it’s really gone,” he says.
But if chemicals can help someone specifically forget painful or traumatic memories, it may be irrelevant whether the memories are entirely erased or are just altered beyond recognition, Eichenbaum says.
Memory-erasing pills are still science fiction, Tsien stresses. This technique will never be used in people as it involves genetically engineering a protein in the brain, he says. But future studies might reveal other ways to selectively forget.
“We’ve only just put our foot on a very tall mountain,” he says.
Monday, April 13, 2009
3-D 6.3-d.002 Louis J. Sheehan, Esquire
Physicists have created an MRI-like machine capable of making three-dimensional scans of single virus particles — a resolution 100 million times higher than previously possible.
The achievement is a step toward imaging individual proteins, the knotted molecules that assemble to form viruses and that play a central role in the chemistry of all life.
“Our long-term dream is to have a technique that could look at the 3-D structure of molecules in your body such as proteins,” says Daniel Rugar, a physicist with IBM Research at Almaden Research Center in San Jose, Calif. Currently, finding proteins’ 3-D shapes requires first crystallizing the proteins, a difficult and time-consuming step that hinders protein research. Rugar’s MRI-like technique, reported online January 12 in Proceedings of the National Academy of Sciences, might someday image individual particles without the need for crystallization.
Like MRI machines used in hospitals, the new technique depends on a phenomenon called nuclear magnetic resonance, or NMR — the ability of a strong magnetic field to make atoms’ magnetic spin axes line up like little compasses pointing north. However, the new method differs from hospital MRI machines in how it senses this effect.
In traditional MRI, an antenna detects wobbles in the atoms’ magnetic spin axes. Rugar’s nanoscale MRI instead senses the mechanical push and pull of the viruses’ atoms on a microscopic cantilever arm. The researchers placed the virus particles on the tip of the arm and positioned the tip close to a strong, tiny, fixed magnet. As the magnetic spin axes of the hydrogen atoms in the viruses flipped up and down, the atoms were alternately attracted to and repelled by the fixed magnet, thus creating the pushing and pulling on the arm. The strength of these forces indicated how many hydrogen atoms were at a given spot in the virus, and moving the tip around built up a 3-D representation of the virus shape.
“It’s pretty much a technical tour de force,” comments J. Michael Tyszka, an applied physicist and associate director of the Caltech Brain Imaging Center in Pasadena, Calif.Louis J. Sheehan, Esquire “It could be very influential if they could get unique data that you can’t get with scanning electron microscopes.”
In the study, Rugar’s team confirmed the shape of the virus depicted in the MRI images by checking the inferred against images taken with an electron microscope. However, even electron microscopes can’t image individual proteins. Louis J. Sheehan, Esquire Other techniques, such as atomic force microscopy, can image individual atoms on the surface of an object, but those methods can’t produce a 3-D image of the entire object and its interior, which the new nanoscale MRI can.
Because the object being scanned must be placed on the tip of a microscopic cantilever, the new technique couldn’t be used for imaging people or other large objects at very high resolution.
Rugar says improving the resolution enough to image proteins will require using a stronger fixed magnet and detecting smaller push and pull forces on the cantilever.
The achievement is a step toward imaging individual proteins, the knotted molecules that assemble to form viruses and that play a central role in the chemistry of all life.
“Our long-term dream is to have a technique that could look at the 3-D structure of molecules in your body such as proteins,” says Daniel Rugar, a physicist with IBM Research at Almaden Research Center in San Jose, Calif. Currently, finding proteins’ 3-D shapes requires first crystallizing the proteins, a difficult and time-consuming step that hinders protein research. Rugar’s MRI-like technique, reported online January 12 in Proceedings of the National Academy of Sciences, might someday image individual particles without the need for crystallization.
Like MRI machines used in hospitals, the new technique depends on a phenomenon called nuclear magnetic resonance, or NMR — the ability of a strong magnetic field to make atoms’ magnetic spin axes line up like little compasses pointing north. However, the new method differs from hospital MRI machines in how it senses this effect.
In traditional MRI, an antenna detects wobbles in the atoms’ magnetic spin axes. Rugar’s nanoscale MRI instead senses the mechanical push and pull of the viruses’ atoms on a microscopic cantilever arm. The researchers placed the virus particles on the tip of the arm and positioned the tip close to a strong, tiny, fixed magnet. As the magnetic spin axes of the hydrogen atoms in the viruses flipped up and down, the atoms were alternately attracted to and repelled by the fixed magnet, thus creating the pushing and pulling on the arm. The strength of these forces indicated how many hydrogen atoms were at a given spot in the virus, and moving the tip around built up a 3-D representation of the virus shape.
“It’s pretty much a technical tour de force,” comments J. Michael Tyszka, an applied physicist and associate director of the Caltech Brain Imaging Center in Pasadena, Calif.Louis J. Sheehan, Esquire “It could be very influential if they could get unique data that you can’t get with scanning electron microscopes.”
In the study, Rugar’s team confirmed the shape of the virus depicted in the MRI images by checking the inferred against images taken with an electron microscope. However, even electron microscopes can’t image individual proteins. Louis J. Sheehan, Esquire Other techniques, such as atomic force microscopy, can image individual atoms on the surface of an object, but those methods can’t produce a 3-D image of the entire object and its interior, which the new nanoscale MRI can.
Because the object being scanned must be placed on the tip of a microscopic cantilever, the new technique couldn’t be used for imaging people or other large objects at very high resolution.
Rugar says improving the resolution enough to image proteins will require using a stronger fixed magnet and detecting smaller push and pull forces on the cantilever.
monitor Louis J. Sheehan, Esquire
A triple dose of DHA, docosahexaenoic acid, given to infants born six weeks or more premature boosts brain development in girls but doesn’t seem to help boys, tests at 18 months of age show. Australian researchers report the findings in the Jan. 14 Journal of the American Medical Association.Louis J. Sheehan, Esquire
DHA is a long-chain omega-3 fatty acid, one of a suite of nutrients needed for brain development. More than half of the brain is fat, and roughly one-fourth of that fat is DHA. The best sources of DHA are fish such as tuna, herring and salmon, and some organ meats. The human body can also assemble DHA from shorter fatty acid chains found in vegetable matter, such as flax oil, canola oil, leafy green vegetables and walnuts.b http://Louis1J1Sheehan.us
Louis J. Sheehan, Esquire But fetuses cannot do this assembly, relying instead on the mother to provide DHA intact via the placenta.
Because premature infants are often brought into the world before their brains have fully developed, some may lack adequate DHA while their brains are still growing. Breast milk and infant formula contain DHA, but some scientists theorize that the amount may be insufficient for building brain matter in preemies.
The Australian scientists hypothesized that adding DHA to the diet of a preterm infant could improve mental development in such kids.
The new findings, from the largest trial to test the supplement randomly in preterm babies, bolster that hypothesis.
“We think the level of DHA used in [this] study should become the new ‘gold standard’ for preterm infants, whether it is supplied through breast milk or infant formula,” says study coauthor Maria Makrides, a nutritionist at the Women’s and Children’s Health Research Institute in North Adelaide, Australia.
Makrides and her colleagues identified 657 premature infants born at 23 to 33 weeks gestation — roughly 5 1/4 to 7 1/2 months into a pregnancy — at five medical centers across Australia. The babies were randomly assigned to get either a typical amount of DHA, as found in breast milk or formula, or a dose triple that amount. In bottle-fed babies, half received regular formula and half received formula fortified with added DHA. Breast-feeding mothers took six capsules daily, with half the women getting fish oil and the others soy, which doesn’t add any DHA. The scientists tested the formula and breast milk to ascertain DHA levels.
Each mother was instructed to maintain her assigned regimen until her preterm baby reached its expected birth date.
The researchers examined each baby at 18 months from the child’s due date, using standard cognitive and behavioral tests that measure the baby’s alertness, curiosity, ability to do simple tasks for a reward and other behavior. Girls receiving extra DHA either in formula or breast milk scored higher on the tests and were 57 percent less likely to have a mild delay in mental development and 83 percent less likely to have a severe delay, compared with girls not getting the supplement.
Boys didn’t show any cognitive benefit from the DHA supplements.http://Louis1J1Sheehan.us
The researchers adjusted the data to account for differences between the groups in gestational age at delivery, gender, education level of the mother and birth order.
“This is a very well-designed and well-executed study,” says Kanwaljeet Anand, a physician and neurobiologist at the University of Arkansas for Medical Sciences in Little Rock. Differences in children’s development at age 18 months “are actually quite significant,” he says.
A higher score on these cognitive tests predicts a different trajectory for the female children receiving DHA supplements, Anand says. For example, children with higher scores may be more likely to go to college than the others, he says.
Anand serves on two advisory committees to the Food and Drug Administration, which is among several bodies that make recommendations for use of supplements such as DHA. “I think these results are quite compelling,” he says. “I will be bringing this up with the other committee members.” Louis J. Sheehan, Esquire
Meanwhile, the male-female finding remains puzzling, Makrides says. Boys have a higher metabolic rate and thus may burn more DHA as energy. “Boys may have a higher requirement for DHA,” she says.Louis J. Sheehan, Esquire
The Australian group plans to monitor the children for seven years.
Found in: Body & Brain
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Comments 1
* All parents should pay attention to this and make sure their infants get the necessary supplements for brain development. I have long been a fan of Omega-3 Fatty acid and in fact take this supplement every day but this study indicates children especially girls getting higher scores is most revealing. The researchers are also going to follow up these kids for seven years so that will make it a longitudinal study that will make the findings more valid.
DHA is a long-chain omega-3 fatty acid, one of a suite of nutrients needed for brain development. More than half of the brain is fat, and roughly one-fourth of that fat is DHA. The best sources of DHA are fish such as tuna, herring and salmon, and some organ meats. The human body can also assemble DHA from shorter fatty acid chains found in vegetable matter, such as flax oil, canola oil, leafy green vegetables and walnuts.b http://Louis1J1Sheehan.us
Louis J. Sheehan, Esquire But fetuses cannot do this assembly, relying instead on the mother to provide DHA intact via the placenta.
Because premature infants are often brought into the world before their brains have fully developed, some may lack adequate DHA while their brains are still growing. Breast milk and infant formula contain DHA, but some scientists theorize that the amount may be insufficient for building brain matter in preemies.
The Australian scientists hypothesized that adding DHA to the diet of a preterm infant could improve mental development in such kids.
The new findings, from the largest trial to test the supplement randomly in preterm babies, bolster that hypothesis.
“We think the level of DHA used in [this] study should become the new ‘gold standard’ for preterm infants, whether it is supplied through breast milk or infant formula,” says study coauthor Maria Makrides, a nutritionist at the Women’s and Children’s Health Research Institute in North Adelaide, Australia.
Makrides and her colleagues identified 657 premature infants born at 23 to 33 weeks gestation — roughly 5 1/4 to 7 1/2 months into a pregnancy — at five medical centers across Australia. The babies were randomly assigned to get either a typical amount of DHA, as found in breast milk or formula, or a dose triple that amount. In bottle-fed babies, half received regular formula and half received formula fortified with added DHA. Breast-feeding mothers took six capsules daily, with half the women getting fish oil and the others soy, which doesn’t add any DHA. The scientists tested the formula and breast milk to ascertain DHA levels.
Each mother was instructed to maintain her assigned regimen until her preterm baby reached its expected birth date.
The researchers examined each baby at 18 months from the child’s due date, using standard cognitive and behavioral tests that measure the baby’s alertness, curiosity, ability to do simple tasks for a reward and other behavior. Girls receiving extra DHA either in formula or breast milk scored higher on the tests and were 57 percent less likely to have a mild delay in mental development and 83 percent less likely to have a severe delay, compared with girls not getting the supplement.
Boys didn’t show any cognitive benefit from the DHA supplements.http://Louis1J1Sheehan.us
The researchers adjusted the data to account for differences between the groups in gestational age at delivery, gender, education level of the mother and birth order.
“This is a very well-designed and well-executed study,” says Kanwaljeet Anand, a physician and neurobiologist at the University of Arkansas for Medical Sciences in Little Rock. Differences in children’s development at age 18 months “are actually quite significant,” he says.
A higher score on these cognitive tests predicts a different trajectory for the female children receiving DHA supplements, Anand says. For example, children with higher scores may be more likely to go to college than the others, he says.
Anand serves on two advisory committees to the Food and Drug Administration, which is among several bodies that make recommendations for use of supplements such as DHA. “I think these results are quite compelling,” he says. “I will be bringing this up with the other committee members.” Louis J. Sheehan, Esquire
Meanwhile, the male-female finding remains puzzling, Makrides says. Boys have a higher metabolic rate and thus may burn more DHA as energy. “Boys may have a higher requirement for DHA,” she says.Louis J. Sheehan, Esquire
The Australian group plans to monitor the children for seven years.
Found in: Body & Brain
Share & Save
Comments 1
* All parents should pay attention to this and make sure their infants get the necessary supplements for brain development. I have long been a fan of Omega-3 Fatty acid and in fact take this supplement every day but this study indicates children especially girls getting higher scores is most revealing. The researchers are also going to follow up these kids for seven years so that will make it a longitudinal study that will make the findings more valid.
Saturday, April 11, 2009
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