New Nanoparticle Technique Captures Chemical Reactions In Single Living Cell With Amazing Clarity

Source:

http://www.sciencedaily.com/releases/2007/11/071119170147.htm

ScienceDaily (Nov. 19, 2007) — Bioengineers at the University of California, Berkeley, have discovered a technique that for the first time enables the detection of biomolecules' dynamic reactions in a single living cell.

By taking advantage of the signature frequency by which organic and inorganic molecules absorb light, the team of researchers, led by Luke Lee, professor of bioengineering and director of UC Berkeley's Biomolecular Nanotechnology Center, can determine in real time whether specific enzymes are activated or particular genes are expressed, all with unprecedented resolution within a single living cell.
The technique could lead to a new era in molecular imaging with implications for cell-based drug discovery and biomedical diagnostics.
The researchers point out that other techniques, such as nuclear magnetic resonance, can at best provide information about a cluster of cells. But to determine the earliest signs of disease progression or of stem cell proliferation, it's necessary to drill down deeper to the molecular dynamics within a single cell.
To study the biochemical processes of a cell, scientists currently cut through its outer membrane to separate and analyze the cellular components. That method can never provide a real-time view of how components function together because the cell is killed in the process of extracting its components.
"Until now, there has been no non-invasive method that exists that can capture the chemical fingerprints of molecules with nanoscale spatial resolution within a single living cell," said Lee, who is also a faculty affiliate of the California Institute for Quantitative Biosciences and the co-director of the Berkeley Sensor and Actuator Center. "There is great hope that stem cells can one day be used to treat diseases, but one of the biggest challenges in this field is understanding exactly how individual cells differentiate. What is happening inside a stem cell as it develops into a heart muscle instead of a tooth or a strand of hair? To find out, we need to look at the telltale chemical signals involved as proteins and genes function together within a cell."
The researchers tackled this challenge by improving upon conventional optical absorption spectroscopy, a technique by which light is passed through a solution of molecules to determine which wavelengths are absorbed. Cytochrome c, for instance, is a protein involved in cell metabolism and cell death that has several optical absorption peaks of around 550 nanometers.
The absorption spectra of a molecule can change based upon the chemical changes that occur as it interacts with other molecules, such as oxygen.
"For conventional optical absorption spectroscopy to work, a relatively high concentration of biomolecules and a large volume of solution is needed in order to detect these subtle changes in frequencies and absorption peaks," said Lee. "That's because optical absorption signals from a single biomolecule are very weak, so you need to kill hundreds to millions of cells to fish out enough of the target molecule for detection."
The researchers came up with a novel solution to this problem by coupling biomolecules, the protein cytochrome c in this study, with tiny particles of gold measuring 20-30 nanometers long. The electrons on the surface of metal particles such as gold and silver are known to oscillate at specific frequencies in response to light, a phenomenon known as plasmon resonance. The resonant frequencies of the gold nanoparticles are much easier to detect than the weak optical signals of cytochrome c, giving the researchers an easier target.
Gold nanoparticles were chosen because they have a plasmon resonance wavelength ranging from 530 to 580 nanometers, corresponding to the absorption peak of cytochrome c.
"When the absorption peak of the biomolecule overlaps with the plasmon resonance frequency of the gold particle, you can see whether they are exchanging energy," said study co-lead author Gang Logan Liu, who conducted the research as a UC Berkeley Ph.D. student in bioengineering. "This energy transfer shows up as small dips, something we call 'quenching,' in the characteristic absorption peak of the gold particle."
A relatively small concentration of the molecule is needed to create these quenching dips, so instead of a concentration of millions of molecules, researchers can get by with hundreds or even dozens of molecules. The sensitivity and selectivity of the quenching dips will improve the molecular diagnosis of diseases and be instrumental in the development of personalized medicine, the researchers said.
The researchers repeated the experiment matching the protein hemoglobin with silver nanoparticles and achieved similar results.
"Our technique kills two birds with one stone," Lee said. "We're reducing the spatial resolution required to detect the molecule at the same time we're able to obtain chemical information about molecules while they are in a living cell. In a way, these gold particles are like 'nano-stars' because they illuminate the inner life of a cellular galaxy."
Other researchers on the UC Berkeley team are Yi-Tao Long, co-lead author and postdoctoral scholar in bioengineering; Yeonho Choi, a Ph.D. student in mechanical engineering; and Taewook Kang, a postdoctoral scholar in bioengineering.
This research is described in the Nov. 18 issue of the journal Nature Methods. The Ministry of Science and Technology in Korea helped support this research.
Adapted from materials provided by University of California - Berkeley.

Fausto Intilla

www.oloscience.com

Evolution Is Deterministic, Not Random, Biologists Conclude From Multi-species Study

Source:

http://www.sciencedaily.com/releases/2007/11/071119123929.htm

ScienceDaily (Nov. 19, 2007) — A multi-national team of biologists has concluded that developmental evolution is deterministic and orderly, rather than random, based on a study of different species of roundworms.

The researchers were interested in how development evolves in organs which themselves do not change. To do so, they examined the vulva -- the female's copulatory and egg-laying organ -- in nearly 50 species of roundworms. Because the vulva does not significantly change across species, one might predict that there would be little variation in vulva development. However, the researchers found an astonishing amount of developmental variation. They then reasoned that this variation, since it did not affect the final adult vulva, should have evolved in a stochastic, or random, fashion.
In executing the study, the research team analyzed more than 40 characteristics of vulva development, including cell death, cell division patterns, and related aspects of gonad development. They plotted the evolution of these traits on a new phylogenetic tree, which illustrates how species are related to one another and provides a map as to how evolutionary changes are occurring.
Their results showed an even greater number of evolutionary changes in vulva development than the researchers had expected. In addition, they found that evolutionary changes among these species were unidirectional in nearly all instances.
For example, they concluded that the number of cell divisions needed in vulva development declined over time -- instead of randomly increasing and decreasing. In addition, the team noted that the number of rings used to form the vulva consistently declined during the evolutionary process. These results demonstrate that, even where we might expect evolution to be random, it is not.
The leading author is Karin Kiontke, a post-doctoral fellow in New York University's Department of Biology. The research team included NYU Biology Professor David Fitch as well as researchers from the University of Paris, the Israel Institute of Technology, and the Max-Planck Institute for Developmental Biology in Germany.
The findings are reported in the latest issue of the journal Current Biology.
The study was supported, in part, by a grant from the National Science Foundation.
Adapted from materials provided by New York University.

Fausto Intilla

www.oloscience.com

Hormone Of Darkness: Melatonin Could Hurt Memory Formation At Night

Source:

http://www.sciencedaily.com/releases/2007/11/071115164438.htm

ScienceDaily (Nov. 17, 2007) — What do you do when a naturally occurring hormone in your body turns against you? What do you do when that same hormone – melatonin – is a popular supplement you take to help you sleep? A University of Houston professor and his team of researchers may have some answers.

Gregg W. Roman, assistant professor in the department of biology and biochemistry at UH, describes his team’s findings in Science.
Frequently called “the hormone of darkness,” melatonin is a hormone the body produces that may regulate patterns of sleeping and awakening in humans. In almost all organisms tested, this antioxidant’s natural levels are high during the night and low during the day. In addition to what the body produces naturally, many people also take melatonin supplements to fight jet lag, balance out seasonal affect disorder and regulate nighttime dementia.
Roman says, however, that melatonin could actually be hurting you at night, finding in a study with zebrafish (Danio rerio) that melatonin directly inhibits memory formation.
“This work is about the mechanism by which the biological clock controls the formation of new memories,” Roman said. “We were interested in the circadian control – the day-night cycle control – of learning and memory formation. We found zebrafish are capable of learning very well during their active phase during the day, but learn very poorly at night during their sleep or quiet phase.”
The experiments were performed using zebrafish for several reasons. They’re small and breed in large numbers (thereby being less expensive to use), and they are diurnal, having the same activity rhythms as people. Zebrafish are most active during the day and less active at night, whereas many other vertebrate model systems, such as rodents, are nocturnal. Roman reasons that if you are interested in how the biological clock regulates cognitive function in humans, you should use a model system that reacts to the clock the same way people do.
More than two years worth of work, including the discovery that the ability to learn and remember was controlled by an endogenous (or internal) clock originating within the zebrafish, led Roman and his colleagues to hypothesize that melatonin may be responsible for poor learning and memory formation during the night. In order to test whether melatonin was involved in inhibiting nighttime learning and memory formation, they treated the zebrafish during the day with this hormone to see how the fish performed. Interestingly, melatonin failed to affect learning, but dramatically inhibited the formation of new memories, with the melatonin-treated fish resembling fish trained during the night in a test for 24-hour memory.
“The next step was to inhibit melatonin signaling during the night with a melatonin receptor antagonist and test for effects on memory formation,” Roman said. “It was tremendous – the results were, excuse the expression, like night and day. We saw dramatic improvements in nighttime memory formation by inhibiting melatonin signaling, indicating that the reason the zebrafish did not form memories at night was because of the melatonin hormone.”
Next, with the pineal gland being the primary source of melatonin in fish and in people, Roman’s student Oliver Rawashdeh removed this gland from the fish and found they could now form memories at high levels even during the night. Removing this melatonin-producing gland allowed the researchers to alleviate the hormone’s negative side effects, further demonstrating that melatonin inhibits the formation of new memories during the night.
With these findings, Roman hopes to be able to retain the beneficial effects of melatonin’s antioxidant properties. Such benefits include fighting free radical damage to slow some forms of neurodegeneration, such as in Parkinson’s and Alzheimer’s diseases, and stopping DNA damage, which has potential to act as a preventative against cancer. And, since the positive antioxidant effect is direct and independent of receptor signaling, there is hope that removing the melatonin receptor signaling will combat only this hormone’s negative effects on cognitive function.
Additionally, Roman said that inhibiting melatonin signaling with receptor antagonists may help with a large number of nighttime cognitive tasks, helping such people as students studying for finals, airplane pilots, ER physicians and night-shift workers. Roman also thinks that a natural role of melatonin may be to facilitate the storage of memories made during the day and that more studies are required to understand the ultimate role melatonin has in memory formation.
“The value of melatonin as a supplement is largely due to its antioxidant properties,” Roman said. “The use of melatonin receptor antagonists will not affect this attribute, but may alleviate an important side effect on nighttime cognitive function.”
In other words, a ‘best of both worlds’ scenario could result, taking advantage of melatonin’s antioxidant benefits while improving nighttime memory formation that is now inhibited by it.
Roman’s team at UH for this breakthrough study includes Gregory M. Cahill, associate professor of biology and biochemistry, and two of their students and research assistants, Oliver Rawashdeh and Nancy Hernandez de Borsetti.
The Science article is entitled “Melatonin Suppresses Nighttime Memory Formation in Zebrafish,” and will be published Nov. 16.
Adapted from materials provided by University of Houston.

Fausto Intilla

www.oloscience.com

Imaging Neural Progenitor Cells In The Living Human Brain

Source:

http://www.sciencedaily.com/releases/2007/11/071108141511.htm

ScienceDaily (Nov. 17, 2007) — For the first time, investigators have identified a way to detect neural progenitor cells (NPCs), which can develop into neurons and other nervous system cells, in the living human brain using a type of imaging called magnetic resonance spectroscopy (MRS). The finding may lead to improved diagnosis and treatment for depression, Parkinson's disease, brain tumors, and a host of other disorders.

Research has shown that, in select brain regions, NPCs persist into adulthood and may give rise to new neurons. Studies have suggested that the development of new neurons from NPCs, called neurogenesis, is disrupted in disorders ranging from depression and schizophrenia to Parkinson's disease, epilepsy, and cancer. Until now, however, there has been no way to monitor neurogenesis in the living human brain.
"The recent finding that neural progenitor cells exist in adult human brain has opened a whole new field in neuroscience. The ability to track these cells in living people would be a major breakthrough in understanding brain development in children and continued maturation of the adult brain. It could also be a very useful tool for research aimed at influencing NPCs to restore or maintain brain health," says Walter J. Koroshetz, M.D., deputy director of the NIH's National Institute of Neurological Disorders and Stroke (NINDS), which helped fund the work. The study was also funded by the NIH's National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).
"This is the first noninvasive approach to identify neural progenitor cells in the human brain," says Grigori Enikolopov, Ph.D., of Cold Spring Harbor Laboratory in New York, who conducted the new study along with co-corresponding author Mirjana Maletic-Savatic, M.D., Ph.D., of the State University of New York, Stony Brook and their colleagues at SUNY Stony Brook and Brookhaven National Laboratory. MRS is an imaging technique that can be used to detect proteins and other compounds normally present in body fluids or tissues. The study results are published in the November 9, 2007, issue of Science.*
Previously developed techniques using positron emission tomography and other types of brain imaging allow investigators to identify NPCs in animals. However, those techniques require pre-labeling the cells with radioactive agents or magnetic nanoparticles -- strategies that are not practical in people. In the new study, the researchers identified an innate property of NPCs that can be detected by MRS. This enables them to image NPCs without introducing drugs or other agents.
The researchers used a technique related to MRS to compare the signals of NPCs from embryonic mice to those of neurons, astrocytes, and oligodendrocytes. Astrocytes and oligodendrocytes are non-neuronal cells that are very common in the brain. The investigators found that NPCs showed a specific signal, or marker, that was not as common in other cell types.
Next, the researchers studied NPCs at various points as they differentiated into other cell types in the laboratory. The level of the NPC signal decreased over time, while the levels of other markers common in neurons and astrocytes rose. The newly identified marker was more common in brain cells from embryonic mice than in those from adult mice. It also was more common in cells from the mouse hippocampus, a region where neurogenesis occurs constantly, than in cells from the brain's cortex, where new neurons are not normally formed.
Dr. Maletic-Savatic, Dr. Enikolopov and their colleagues then gave adult mice a form of electrical stimulation that increases the amount of neurogenesis in the brain. They found that the marker they had identified increased significantly after the stimulation. Additional results indicated that the marker is probably a mixture of lipids (fatty acids), although the exact identity of the lipids, and how they function in NPCs, is still undetermined.
The researchers then developed a signal processing method that allowed them to separate the marker from other signals in the living brain. They transplanted NPCs into the cortex of the adult rat brain and found that they could clearly detect the marker in the area where the NPCs were injected. They also found that it increased after stimulation.
Finally, the investigators tested their MRS imaging technique in healthy people. They found major differences in the concentration of the marker between the hippocampus and the cortex. They also imaged the brains of pre-adolescents, adolescents, and adults and found that the marker decreased with age.
The findings suggest that the marker identified in these experiments can be used to detect NPCs and neurogenesis in the live human brain using MRS. They also show that NPCs decrease during brain development. Previous research had shown that neurogenesis decreases with age in animals, but this is the first study to demonstrate that it also decreases in the living human brain.
"This study identifies a novel biomarker and shows that we can use it to see progenitor cells in the live brain," Dr. Enikolopov says. "This protocol can now be used to study a variety of problems." For example, researchers might study people with depression to see if neurogenesis correlates with alterations in depression or schizophrenia. The technique might also be used to study changes that occur in neurological diseases such as traumatic brain injury, stroke, epilepsy, and Parkinson's disease. It might even be useful for detecting cancer, because researchers believe some brain tumors are associated with aberrant proliferation of NPCs, Dr. Enikolopov adds.
The researchers are now planning studies that will test the usefulness of the new imaging technique in people with disease. They also hope to improve their understanding of how the lipids they detected function in NPCs and to refine the sensitivity of their technique.
This research was supported by the National Institutes of Health (NIH).
*Manganas LN, Zhang X, Li Y, Hazel RD, Smith SD, Wagshul ME, Henn F, Benveniste H, Djuric PM, Enikolopov G, Maletic-Savatic M. "Magnetic Resonance Spectroscopy Identifies Neural Progenitor Cells in the Live Human Brain." Science, November 9, 2007, Vol. 318, No. 5852, p. 980.
Adapted from materials provided by NIH/National Institute of Neurological Disorders and Stroke.

Fausto Intilla

www.oloscience.com

Are There Rearrangement Hot Spots In The Human Genome?

Source:

http://www.sciencedaily.com/releases/2007/11/071109100207.htm

ScienceDaily (Nov. 13, 2007) — The debate over the validity of genomic rearrangement “hotspots” has its most recent addition in a new theory put forth by researchers at the University of California San Diego. The study, published on November 9 in PLoS Computational Biology, holds that there are indeed rearrangement hotspots in the human genome.
Doctors Max Alekseyev and Pavel Pevzner developed a theory for analyzing complex rearrangements (including transpositions) which demonstrates that even if transpositions were a dominant evolutionary force, there are still rearrangement hotspots in mammalian genomes.
In 1970 the random breakage model (RBM) was proposed by Susumo Ohno, and later formalized by Nadeau and Taylor in 1984. This model postulates that rearrangements are “random,” and thus there are no rearrangement hotspots in mammalian genomes. Biologists largely embraced the model as it held such predictive powers.
However, in 2003 the model was refuted by Pevzner and Tesler, who suggested an alternative fragile breakage model (FBM) of chromosome evolution. FBM implies that the human genome is a mosaic of solid regions with low propensity for rearrangements and fragile regions where rearrangement hotspots reside. The rebuttal of RBM resulted in a rebuttal of the rebuttal, and a scientific divide was begun.
Most recent studies support the existence of rearrangement hotspots, but some researchers still uphold the RBM model. This study represents a major advance in the debate.
CITATION: Alekseyev MA, Pevzner PA (2007) Are there rearrangement hotspots in the human genome? PLoS Comput Biol 3(11): e209. doi:10.1371/journal.pcbi.0030209 (http://dx.doi.org/10.1371/journal.pcbi.0030209)
Adapted from materials provided by Public Library of Science.

Fausto Intilla
www.oloscience.com

In DNA Era, New Worries About Prejudice

Source:

http://www.nytimes.com/2007/11/11/us/11dna.html?_r=1&ref=science&oref=slogin

By AMY HARMON
Published: November 11, 2007

When scientists first decoded the human genome in 2000, they were quick to portray it as proof of humankind’s remarkable similarity. The DNA of any two people, they emphasized, is at least 99 percent identical.
But new research is exploring the remaining fraction to explain differences between people of different continental origins.
Scientists, for instance, have recently identified small changes in DNA that account for the pale skin of Europeans, the tendency of Asians to sweat less and West Africans’ resistance to certain diseases.
At the same time, genetic information is slipping out of the laboratory and into everyday life, carrying with it the inescapable message that people of different races have different DNA. Ancestry tests tell customers what percentage of their genes are from Asia, Europe, Africa and the Americas. The heart-disease drug BiDil is marketed exclusively to African-Americans, who seem genetically predisposed to respond to it. Jews are offered prenatal tests for genetic disorders rarely found in other ethnic groups.
Such developments are providing some of the first tangible benefits of the genetic revolution. Yet some social critics fear they may also be giving long-discredited racial prejudices a new potency. The notion that race is more than skin deep, they fear, could undermine principles of equal treatment and opportunity that have relied on the presumption that we are all fundamentally equal.
“We are living through an era of the ascendance of biology, and we have to be very careful,” said Henry Louis Gates Jr., director of the W. E. B. Du Bois Institute for African and African American Research at Harvard University. “We will all be walking a fine line between using biology and allowing it to be abused.”
Certain superficial traits like skin pigmentation have long been presumed to be genetic. But the ability to pinpoint their DNA source makes the link between genes and race more palpable. And on mainstream blogs, in college classrooms and among the growing community of ancestry test-takers, it is prompting the question of whether more profound differences may also be attributed to DNA.
Nonscientists are already beginning to stitch together highly speculative conclusions about the historically charged subject of race and intelligence from the new biological data. Last month, a blogger in Manhattan described a recently published study that linked several snippets of DNA to high I.Q. An online genetic database used by medical researchers, he told readers, showed that two of the snippets were found more often in Europeans and Asians than in Africans.
No matter that the link between I.Q. and those particular bits of DNA was unconfirmed, or that other high I.Q. snippets are more common in Africans, or that hundreds or thousands of others may also affect intelligence, or that their combined influence might be dwarfed by environmental factors. Just the existence of such genetic differences between races, proclaimed the author of the Half Sigma blog, a 40-year-old software developer, means “the egalitarian theory,” that all races are equal, “is proven false.”
Though few of the bits of human genetic code that vary between individuals have yet to be tied to physical or behavioral traits, scientists have found that roughly 10 percent of them are more common in certain continental groups and can be used to distinguish people of different races. They say that studying the differences, which arose during the tens of thousands of years that human populations evolved on separate continents after their ancestors dispersed from humanity’s birthplace in East Africa, is crucial to mapping the genetic basis for disease.
But many geneticists, wary of fueling discrimination and worried that speaking openly about race could endanger support for their research, are loath to discuss the social implications of their findings. Still, some acknowledge that as their data and methods are extended to nonmedical traits, the field is at what one leading researcher recently called “a very delicate time, and a dangerous time.”
“There are clear differences between people of different continental ancestries,” said Marcus W. Feldman, a professor of biological sciences at Stanford University. “It’s not there yet for things like I.Q., but I can see it coming. And it has the potential to spark a new era of racism if we do not start explaining it better.”
Dr. Feldman said any finding on intelligence was likely to be exceedingly hard to pin down. But given that some may emerge, he said he wanted to create “ready response teams” of geneticists to put such socially fraught discoveries in perspective.
The authority that DNA has earned through its use in freeing falsely convicted inmates, preventing disease and reconstructing family ties leads people to wrongly elevate genetics over other explanations for differences between groups.
“I’ve spent the last 10 years of my life researching how much genetic variability there is between populations,” said Dr. David Altshuler, director of the Program in Medical and Population Genetics at the Broad Institute in Cambridge, Mass. “But living in America, it is so clear that the economic and social and educational differences have so much more influence than genes. People just somehow fixate on genetics, even if the influence is very small.”
But on the Half Sigma blog and elsewhere, the conversation is already flashing forward to what might happen if genetically encoded racial differences in socially desirable — or undesirable — traits are identified.
“If I were to believe the ‘facts’ in this post, what should I do?” one reader responded on Half Sigma. “Should I advocate discrimination against blacks because they are less smart? Should I not hire them to my company because odds are I could find a smarter white person? Stop trying to prove that one group of people are genetically inferior to your group. Just stop.”
Renata McGriff, 52, a health care consultant who had been encouraging black clients to volunteer genetic information to scientists, said she and other African-Americans have lately been discussing “opting out of genetic research until it’s clear we’re not going to use science to validate prejudices.”
“I don’t want the children in my family to be born thinking they are less than someone else based on their DNA,” added Ms. McGriff, of Manhattan.
Such discussions are among thousands that followed the geneticist James D. Watson’s assertion last month that Africans are innately less intelligent than other races. Dr. Watson, a Nobel Prize winner, subsequently apologized and quit his post at the Cold Spring Harbor Laboratory on Long Island.
But the incident has added to uneasiness about whether society is prepared to handle the consequences of science that may eventually reveal appreciable differences between races in the genes that influence socially important traits.
New genetic information, some liberal critics say, could become the latest rallying point for a conservative political camp that objects to social policies like affirmative action, as happened with “The Bell Curve,” the controversial 1994 book that examined the relationship between race and I.Q.
Yet even some self-described liberals argue that accepting that there may be genetic differences between races is important in preparing to address them politically.
“Let’s say the genetic data says we’ll have to spend two times as much for every black child to close the achievement gap,” said Jason Malloy, 28, an artist in Madison, Wis., who wrote a defense of Dr. Watson for the widely read science blog Gene Expression. Society, he said, would need to consider how individuals “can be given educational and occupational opportunities that work best for their unique talents and limitations.”
Others hope that the genetic data may overturn preconceived notions of racial superiority by, for example, showing that Africans are innately more intelligent than other groups. But either way, the increased outpouring of conversation on the normally taboo subject of race and genetics has prompted some to suggest that innate differences should be accepted but, at some level, ignored.
“Regardless of any such genetic variation, it is our moral duty to treat all as equal before God and before the law,” Perry Clark, 44, wrote on a New York Times blog. It is not necessary, argued Dr. Clark, a retired neonatologist in Leawood, Kan., who is white, to maintain the pretense that inborn racial differences do not exist.
“When was the last time a nonblack sprinter won the Olympic 100 meters?” he asked.
“To say that such differences aren’t real,” Dr. Clark later said in an interview, “is to stick your head in the sand and go blah blah blah blah blah until the band marches by.”
Race, many sociologists and anthropologists have argued for decades, is a social invention historically used to justify prejudice and persecution. But when Samuel M. Richards gave his students at Pennsylvania State University genetic ancestry tests to establish the imprecision of socially constructed racial categories, he found the exercise reinforced them instead.
One white-skinned student, told she was 9 percent West African, went to a Kwanzaa celebration, for instance, but would not dream of going to an Asian cultural event because her DNA did not match, Dr. Richards said. Preconceived notions of race seemed all the more authentic when quantified by DNA.
“Before, it was, ‘I’m white because I have white skin and grew up in white culture,’ ” Dr. Richards said. “Now it’s, ‘I really know I’m white, so white is this big neon sign hanging over my head.’ It’s like, oh, no, come on. That wasn’t the point.”

Fausto Intilla
www.oloscience.com

Breastfeeding Boosts IQ In Infants With 'Helpful' Genetic Variant

Source:

http://www.sciencedaily.com/releases/2007/11/071105171949.htm

ScienceDaily (Nov. 6, 2007) — The known association between breast feeding and slightly higher IQ in children has been shown to relate to a particular gene in the babies, according to a report in the Proceedings of the National Academy of Sciences.

In two studies of breast-fed infants involving more than 3,000 children in Britain and New Zealand, breastfeeding was found to raise intelligence an average of nearly 7 IQ points if the children had a particular version of a gene called FADS2.
"It is this genetic variant in FADS2, a gene involved in the control of fatty acid pathways, that may help the children make better use of the breast milk and promote the brain development that is associated with a higher IQ score," said Julia Kim-Cohen, assistant professor of psychology at Yale and a member of the research team.
"Children who do not carry the 'helpful' genetic variant have normal average IQ scores," Kim-Cohen said. "Being breastfed for them is not associated with an IQ advantage."
"There has been some criticism of earlier studies about breastfeeding and IQ that they didn't control for socioeconomic status, or the mother's IQ or other factors, but our findings take an end-run around those arguments by showing the physiological mechanism that accounts for the difference," said Terrie Moffitt, a professor of psychological and brain sciences in Duke University's Institute for Genome Sciences and Policy.
The intelligence quotient (IQ) has long been at the heart of debates about nature versus nurture. Twin studies document both strong genetic influences and nongenetic environmental influences on IQ, particularly for young children.
Moffitt, who performed the research with her husband and co-author Avshalom Caspi at King's College in London, found that the baby's intellectual development is influenced by both genes and environment or, more specifically, by the interaction of its genes with its environment.
"The argument about intelligence has been about nature versus nurture for at least a century," Moffitt said. "We're finding that nature and nurture work together."
Ninety percent of the children in the two study groups had at least one copy of the "C" version of FADS2, which yielded higher IQ if they were breast-fed. The other 10 percent, with only the "G" versions of the gene, showed no IQ advantage or disadvantage from breastfeeding.
The gene was singled out for the researchers' attention because it produces an enzyme that helps convert dietary fatty acids into the polyunsaturated fatty acids DHA (docosahexaenoic acid) and AA (arachidonic acid) that have been shown to accumulate in the human brain during the first months after birth.
Since the first findings about breastfeeding and IQ appeared a decade ago, many formula makers have added DHA and AA fatty acids to their products. The children in these studies however were born in 1972-73 in New Zealand and 1994-95 in England, before fatty acid supplementation in formula began.
Though the jury is still out on whether such supplementation has made a difference in humans, laboratory studies in which rodents and primates were fed supplemental fatty acids have shown increased brain DHA concentrations and enhanced abilities in tests of learning, memory and problem-solving.
"Our findings support the idea that the nutritional content of breast milk accounts for the differences seen in human IQ," Moffitt said. "But it's not a simple all-or-none connection: it depends to some extent on the genetic makeup of each infant."
Moffitt and Caspi joined the Duke faculty in August, but are finishing up their research in London before moving to Durham in December.
Moffitt noted that the researchers aren't particularly interested in IQ or breastfeeding, per se. Rather, this study fits into a body of work they have done on gene-environment interactions and the brain.
"We're more interested in proving to the psychiatric community that genes usually have a physiological effect," Moffitt said. "When looking at depression or intelligence, the key bit that's often left out here is the environmental effects."
Journal reference: PNAS Early Edition: doi/10.1073/pnas.0704292104
The research was supported by the National Institute of Mental Health (US), the Medical Research Council (UK), and the Health Research Council (New Zealand).
Adapted from materials provided by Duke University.

Fausto Intilla

www.oloscience.com