Antigravics

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>> Published online today in the February issue of the journal Autism Research, the study, "Independent and Dependent Contributions of Advanced Maternal and Paternal Ages to Autism Risk," is one of the largest population-based studies to quantify how each parent's age — separately and together — affects the risk of having a child with autism.

The study found that the incremental risk of having a child with autism increased by 18 percent — nearly one fifth — for every five-year increase in the mother's age. A 40-year-old woman's risk of having a child later diagnosed with autism was 50 percent greater than that of a woman between 25 and 29 years old.

Advanced parental age is a known risk factor for having a child with autism. However, previous research has shown contradictory results regarding whether it is the mother, the father or both who contribute most to the increased risk of autism. For example, one study reported that fathers over 40 were six times more likely than fathers under 30 to have a child with autism.

"This study challenges a current theory in autism epidemiology that identifies the father's age as a key factor in increasing the risk of having a child with autism," said Janie Shelton, the study's lead author and a doctoral student in the UC Davis Department of Public Health Sciences. "It shows that while maternal age consistently increases the risk of autism, the father's age only contributes an increased risk when the father is older and the mother is under 30 years old. Among mothers over 30, increases in the father's age do not appear to further increase the risk of autism."

Autism is a pervasive developmental disorder of deficits in social skills and communication, as well as repetitive and restricted behaviors, with onset occurring prior to age 3. Abnormal brain development, probably beginning in the womb, is known to be fundamental to the behaviors that characterize autism. Current estimates place the incidence of autism at between 1 in 100 and 1 in 110 children in the United States.

During the 1990s, the number of California women over 40 giving birth increased by more than 300 percent. But only about 5 percent of the 600-percent increase in the number of autism cases in the state can be attributed to women waiting longer to have children, the study suggests.

To conduct their investigation, the researchers obtained the electronic records for all births in California between Jan. 1, 1990 and Dec. 31, 1999. The records incorporated detailed demographic information, including the ages of both parents. To identify which children would develop autism, the researchers obtained electronic records identifying children born during the study period who later received an autism diagnosis from state Department of Developmental Services. In this study autism was defined as a diagnosis of full-syndrome autism at a California Regional Center.

The researchers also excluded a small number of births where demographic information about parents, such as their ages and levels of education, was not available. Instances of multiple births were analyzed separately. The exclusions brought the total size of the study sample to approximately 4.9 million births and 12,159 cases of autism.

For older mothers, the step-wise progression in the risk of having a child who later would be diagnosed with autism was apparent among every age group of fathers. When the father was older and the mother was younger — under 30 — the child's risk for developing autism also was elevated. For example, among births to mothers under 25, children fathered by a man over 40 were twice as likely to develop autism as those whose father was between 25 and 29. Among mothers over 30, the increased risk associated with older fathers dissipated, the study found.

Because of the large study size, the researchers were able to show how risk for autism was affected by each parent's age by holding one parent's age constant and then comparing autism incidence across the age of the other parent across five-year increments. The subtle interaction of how each parent's age affects the risk of autism then became quantifiable even when it was reliant on the other parent's age. This methodology is more efficacious and requires fewer assumptions than the mathematical modeling used by earlier studies, the researchers said.

The researchers note that understanding the relationship between increased parental age and autism risk is critical to understanding its biological causes. Earlier studies have observed that advanced maternal age is a risk factor for a variety of other birth-related conditions, including infertility, early fetal loss, low birth-weight, chromosomal aberrations and congenital anomalies.

Irva Hertz-Picciotto, professor of public health sciences, a researcher at the UC Davis MIND Institute and the study's senior author, said the reason that having an older parent places a child at risk for autism is not known.

"We still need to figure out what it is about older parents that puts their children at greater risk for autism and other adverse outcomes, so that we can begin to design interventions," Hertz-Picciotto said.

One possible clue comes from a 2008 UC Davis study that found some mothers of children with autism had antibodies to fetal brain protein, while none of the mothers of typical children did. Advancing age has been associated with an increase in autoantibody production. Further work investigating advancing age in such findings may be useful, the study authors said. They added that some persistent environmental chemicals accumulate in the body and also may have a role to play in autism, possibly contributing to the apparent effect of parental age.

The study also suggests that epigenetic changes over time "may enable an older parent to transfer a multitude of molecular functional alterations to a child ... thus epigenetics may be involved in the risks contributed by advancing parental age as a result of changes induced by stresses from environmental chemicals, co-morbidity or assistive reproductive therapy." >>>

http://www.physorg.com/news184860933.html

>> Researchers reported that CP (Cerebral Palsy) is associated with inflammation of the connective tissue in the umbilical cord. This inflammation is more common in premature births from preterm labor and premature rupturing of the amniotic sac versus early deliveries due to preeclampsia. Premature births from preterm labor and rupturing of the amniotic sac also are often associated with infections while preeclampsia is not.

“These findings are valuable, as we continue to study the link between premature births and cerebral palsy,” said John Gianopolous, MD, chair, Mary Isabella Caestecker professor and chair, Department of Obstetrics & Gynecology, LUHS. “While further investigation is needed, managing inflammation may reduce the risk of certain complications in these infants.”

CP is a disorder that impairs movement due to brain damage. This condition typically develops by age 2 or 3. More than 500,000 Americans have CP, and it is one of the most common causes of chronic childhood disability.

Researchers evaluated 222 preterm placentas for this study. Reasons for premature births were categorized into four groups: premature rupture of the amniotic sac or preterm labor; preterm preeclampsia; maternal disease related to heart complications; and uncomplicated births of multiples. Of those patients who went into preterm labor or had their amniotic sac rupture early, 30 percent had an inflamed umbilical cord compared with only 3 percent of patients with preeclampsia.

LUHS maternal-fetal medicine specialists conducted this study. These physicians work in conjunction with neonatologists, geneticists and obstetrical anesthesiologists to provide care for patients with medical or surgical complications during pregnancy. >>>>

http://www.physorg.com/news185043019.html

>> A study by University of Michigan researchers offers new insight into what happens to mercury deposited onto Arctic snow from the atmosphere.

The work also provides a new approach to tracking mercury's movement through Arctic ecosystems.

Mercury is a naturally occurring element, but some 2000 tons of it enter the global environment each year from human-generated sources such as coal-burning power plants, incinerators and chlorine-producing plants.

"When released into the atmosphere in its reduced form, mercury is not very reactive. It can float around in the atmosphere as a gas for a year or more, and it's not really an environmental problem at the concentrations at which it occurs," said Joel Blum, the John D. MacArthur Professor of Geological Sciences.

But once mercury is oxidized, through a process that involves sunlight and often the element bromine, it becomes very reactive. Deposited onto land or into water, the mercury is picked up by microorganisms, which convert some of it to methylmercury, a highly toxic form that builds up in fish and the animals that eat them.

As bigger animals eat smaller ones, the methylmercury is concentrated. In wildlife, exposure to methylmercury can interfere with reproduction, growth, development and behavior and may even cause death. Effects on humans include damage to the central nervous system, heart and immune system. The developing brains of young and unborn children are especially vulnerable.

The research is described in a paper published online Feb. 7 in the journal Nature Geoscience.

In the Arctic, mercury remains in its benign gaseous form through the dark winter, because there's no sunlight to drive oxidation and little bromine to catalyze the process. But in polar springtime, that all changes.

As sea ice breaks up, water vapor rises in great clouds through the openings in the ice, bringing with it bromine from the sea water. The bromine enters the atmosphere, where it conspires with sunlight to convert mercury gas into the reactive form. The activated mercury sticks to snowflakes and ice crystals in the air and travels with them onto the surface of the snow.

This leads to what's known as a mercury depletion event. The normally steady levels of mercury in the atmosphere quickly drop to near zero, as concentrations of mercury on the surface of the snow rise to extremely high levels.

"When we first started observing these events, we didn't know how much of that mercury returned back to the atmosphere, so the high level of mercury in snow was a great concern," Blum said. "But the more we learned, the more we realized that the sunlight shining on the snow typically will cause much of the oxidized mercury to become reduced and return to the atmosphere as a gas. And it turns out that its re-release to the atmosphere has a striking "fingerprint' that we can use to study the progress of this reaction through time."

The fingerprint is the result of a natural phenomenon called isotopic fractionation, in which different isotopes (atoms with different numbers of neutrons) of mercury react to form new compounds at slightly different rates. In one type of isotopic fractionation, mass-dependent fractionation (MDF), the differing rates depend on the masses of the isotopes. In mass-independent fractionation (MIF), the behavior of the isotopes depends not on their absolute masses but on whether their masses are odd or even.

In the work described in the Nature Geoscience paper, the researchers confirmed, through sample collection and experiments, that MIF occurs during the sunlight-driven reactions in snow, resulting in a characteristic MIF fingerprint that is absent in atmospheric mercury.

"This finding allowed us to use the MIF fingerprint to estimate how much mercury was lost from the snowpack and how much remained behind, with the potential to enter Arctic ecosystems," said U-M graduate student Laura Sherman, the paper's first author. "Our experiments showed that a significant portion of mercury deposited to snow was re-emitted. Any mercury that is not re-emitted is likely to retain the unique fingerprint, so we hope future researchers will be able to use our discovery to track mercury through Arctic ecosystems." >>>

http://www.guardian.co.uk/world/2010/fe ... -proposals

>> Childhood temper tantrums, teenage irritability and binge eating may soon rate as psychiatric disorders in the US, according to proposed changes to the Diagnostic and Statistical Manual, the bible of the psychiatric profession.

The proposals are the product of a 10-year effort to update the handbook, which influences the vast network of American healthcare providers, insurance companies, courts, prisons and universities. At stake are billions of dollars in insurance payments, pharmaceutical sales and medical fees. The proposed revisions, published online today , will be subject to public comment until late April.

"It not only determines how mental disorders are diagnosed, it can impact how people see themselves and how we see each other," Alan Schatzberg, president of the American Psychiatric Association, which publishes the guide, told reporters. "It influences how research is conducted as well as what is researched. It affects legal matters, industry and government programmes."

The DSM is in its fourth edition. It has been criticised for formalising character traits and emotions into mental conditions and for encouraging their medical treatment, often with drugs that have powerful side effects.

Christopher Lane, a professor at Northwestern University and author of 2007 DSM critique Shyness:

How Normal Behavior Became a Sickness, said:

"The organisation is clearly opening another Pandora's box here, as well as paving the way for the medication of even-greater numbers of children and teenagers cycling through emotional stages as part of normal development."

In an email, Lane said that categorising binge eating as a psychiatric disorder risks classifying millions of Americans as mentally ill at a time when the country is trying to rein in health care costs.

Among the proposals is a new condition, "temper dysregulation with dysphoria", characterised by "severe, recurrent outbursts of temper" several times a week, that are "grossly out of proportion to the situation or provocation and that interfere significantly with functioning". To be considered, the "symptoms" must have been "diagnosed" before age 10.

The proposed revisions would also recognise binge eating as a disorder. The condition is "characterised by recurring episodes of the consumption of unusually large amounts of food, accompanied by a sense of loss of control and strong feelings of embarrassment and guilt". These episodes would need to occur at least once a week over the last three months, and the writers were keen to distinguish it from mere overeating.

"While overeating is a challenge for many Americans, recurrent binge eating is much less common and far more severe and is associated with significant physical and psychological problems," wrote Dr B Timothy Walsh.

The panels proposed a new category of condition called "risk syndromes", in which a patient is at risk for a mental disorder that is not yet present.

For example, a moody teenager who displays "excessive suspicion, delusions and disorganised speech or behaviour" may be labelled as having psychosis risk syndrome. The panel estimated that a quarter to a third of people who suffer from those "symptoms" go on to develop a psychotic disorder, and the writers acknowledged the new category could lead to inaccurate diagnosis of some who are not at risk.

"Given the severity of psychotic disorders, and evidence that early treatment may mitigate its long-term consequences, we believed that it was important to begin to recognise these conditions as early as possible," wrote Dr William Carpenter of the American Psychiatric Association's psychotic disorders work group.

The panels who proposed the revisions also took into account how race, ethnicity and gender affect the incidence of psychiatric disorders, and studied how those categories affect the expression of symptoms. For example, researchers noted differing ways of experiencing and describing symptoms of panic among some Asian and Hispanic patients.

The panel also recommended discarding the term "mental retardation" in diagnoses, replacing it with "intellectual disability". >>>>

http://www.physorg.com/news186226998.html

>> University of California researchers found that the incidence rate for all causes of dementia in people age 90 and older is 18.2% annually and significantly increases with age in both men and women. This research, called "The 90+ Study," is one of only a few to examine dementia in this age group, and the first to have sufficient participation of centenarians. Findings of the study appear in the February issue of Annals of Neurology, a journal published by Wiley-Blackwell on behalf of the American Neurological Association.

Dementia (senility) is a progressive, degenerative disorder that affects memory, language, attention, emotions, and problem solving capabilities. A variety of diseases cause dementia including Alzheimer's disease, stroke, and other neurodegenerative disorders. According to a 2000 report from the World Health Organization (WHO), approximately 6%-10% of the population 65 years and older in North America have dementia, with Alzheimer's disease accounting for two-thirds of those cases.

For their population-based, longitudinal study of aging and dementia, Maria Corrada, Sc.D., and colleagues invited members who were originally part of The Leisure World Cohort Study and 90 years of age or older as of January 1, 2003. As of December 31, 2007 there were 950 participants in The 90+ Study and 539 who had completed a full evaluation that included neurological testing, functional ability assessments and a questionnaire covering demographics, past medical history, and medication use. Evaluations were repeated every 6-12 months with a final dementia questionnaire completed shortly after death.

Analysis was completed on 330 participants who were primarily women (69.7%) between the ages of 90 to 102, and who showed no signs of dementia at baseline. Researchers identified 140 new cases of dementia during follow-up with 60% of those cases attributed to Alzheimer's disease (AD), 22% vascular dementia, 9% mixed AD and vascular dementia and 9% with other or unknown cause.

Dr. Corrada explained, "Our findings show dementia incidence rates almost double every five years in those 90 and older." Researchers found the overall incidence rate based on 770 person-years of follow-up was 18.2% per year. Rates increased with age from 12.7% per year in the 90-94 age group, to 21.2% per year in the 95-99 age group, to 40.7% per year in the 100+ age group. Incidence rates were very similar for men and women. Previous results from The 90+ Study found higher estimates of dementia prevalence in women (45%) compared to men (28%), a result also seen in other similar studies.

Prior reports estimate there were 2 million Americans aged 90 and older in 2007 and the number is expected to reach 8.7 million by 2050, making the oldest-old the fastest growing segment of the U.S. population. "In contrast to other studies, we found that the incidence of dementia increases exponentially with age in both men and women past age 90," said Dr. Corrada. "Given the population projections for this age group along with our findings, dementia in the oldest-old threatens to become an epidemic with enormous public health impact." >>>

http://www.physorg.com/news186318007.html

>> "Exposure to BPA may be harmful during pregnancy; this exposure may permanently affect the fetus," said Hugh S. Taylor, Ph.D., co-author of the study from Yale University School of Medicine in New Haven, Connecticut.

"We need to better identify the effects of environmental contaminants on not just crude measures such as birth defects, but also their effect in causing more subtle developmental errors."

Taylor and colleagues made this discovery by exposing fetal mice to BPA during pregnancy and examining gene expression and DNA in the uteruses of female fetuses. Results showed that BPA exposure permanently affected the uterus by decreasing regulation of gene expression.

These epigenetic changes caused the mice to over-respond to estrogen throughout adulthood, long after the BPA exposure.

This suggests that early exposure to BPA genetically "programmed" the uterus to be hyper-responsive to estrogen. Extreme estrogen sensitivity can lead to fertility problems, advanced puberty, altered mammary development and reproductive function, as well as a variety of hormone-related cancers. BPA has been widely used in plastics and other materials.

Examples include use in water bottles, baby bottles, epoxy resins used to coat food cans, and dental sealants.

"The BPA baby bottle scare may be only the tip of the iceberg." said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal.

"Remember how diethylstilbestrol (DES) caused birth defects and cancers in young women whose mothers were given such hormones during pregnancy. We'd better watch out for BPA, which seems to carry similar epigenetic risks across the generations. " >>>

http://www.physorg.com/news186668504.html

>> Atrazine, one of the world's most widely used pesticides, wreaks havoc with the sex lives of adult male frogs, emasculating three-quarters of them and turning one in 10 into females, according to a new study by University of California, Berkeley, biologists.

The 75 percent that are chemically castrated are essentially "dead" because of their inability to reproduce in the wild, reports UC Berkeley's Tyrone B. Hayes, professor of integrative biology.

"These male frogs are missing testosterone and all the things that testosterone controls, including sperm. So their fertility is as low as 10 percent in some cases, and that is only if we isolate those animals and pair them with females," he said. "In an environment where they are competing with unexposed animals, they have zero chance of reproducing."

The 10 percent or more that turn from males into females ‑ something not known to occur under natural conditions in amphibians ‑ can successfully mate with male frogs but, because they are genetically male, all their offspring are male.

"When we grow these guys up, depending on the family, we will get anywhere from 10 to 50 percent females," Hayes said. "In a population, the genetically male females can decrease or wipe out a population just because they skew sex ratios so badly."

Though the experiments were performed on a common laboratory frog, the African clawed frog (Xenopus laevis), field studies indicate that atrazine, a potent endocrine disruptor, similarly affects frogs in the wild, and could possibly be one of the causes of amphibian declines around the globe, Hayes said.

"These kinds of problems, like sex-reversing animals skewing sex ratios, are much more dangerous than any chemical that would kill off a population of frogs," he said. "In exposed populations, it looks like there are frogs breeding but, in fact, the population is being very slowly degraded by the introduction of these altered animals."

Some 80 million pounds of the herbicide atrazine are applied annually in the United States on corn and sorghum to control weeds and increase crop yield, but such widespread use also makes atrazine the most common pesticide contaminant of ground and surface water, according to various studies.

More and more research, however, is showing that atrazine interferes with endocrine hormones, such as estrogen and testosterone - in fish, amphibians, birds, reptiles, laboratory rodents and even human cell lines at levels of parts per billion. Recent studies also found a possible link between human birth defects and low birth weight and atrazine exposure in the womb.

As a result of these studies, the Environmental Protection Agency (EPA) is reviewing its regulations on use of the pesticide. Several states are considering banning atrazine, and six class action lawsuits have been filed seeking to eliminate its use.

The European Union already bars the use of atrazine.

Hayes's studies in the early 2000s were the first to show that the hormonal effects of atrazine disrupt sexual development in amphibians. Working with the African clawed frog, Hayes and his colleagues showed in 2002 that tadpoles raised in atrazine-contaminated water become hermaphrodites - they develop both female (ovaries) and male (testes) gonads.

This occurred at atrazine levels as low as 0.1 parts per billion (ppb), 30 times lower than levels allowed in drinking water by the EPA (3 ppb).

Subsequent studies showed that native leopard frogs (Rana pipiens) collected from atrazine-contaminated streams in the Midwest, including from areas up to 1,000 miles from where atrazine is applied, often had eggs in their testes. And many males had lower testosterone levels than normal females and smaller than normal voice boxes, presumably limiting their ability to call mates.

Hayes' research also established that many frogs in Midwestern streams contaminated by atrazine and other pesticides have compromised immune systems, leading to increased mortality from bacterial disease.

Those early studies were hampered by the inability to easily distinguish genetically male from genetically female frogs. Male frogs have two identical sex chromosomes (ZZ) while females have both a Z and a W - the opposite of XX female and XY male humans. But because all frog chromosomes look the same under a light microscope, it's not simple to distinguish male from female.

To overcome this, Hayes' colleague Roger Liu developed a line of all-male frogs so that the genetics would be unequivocal.

"Before, we knew we got fewer males than we should have, and we got hermaphrodites. Now, we have clearly shown that many of these animals are sex-reversed males," Hayes said. "We have animals that are females, in the sense that they behave like females: They have estrogen, lay eggs, they mate with other males.

Atrazine has caused a hormonal imbalance that has made them develop into the wrong sex, in terms of their genetic constitution."

Coincidentally, another lab in 2008 discovered a sex-linked genetic marker in Xenopus, which has allowed Hayes to confirm the genetic sex of his frogs.

In Hayes' study, where 40 frogs lived for about three years after hatching in water with 2.5 ppb atrazine, about 10 percent of the frogs appeared to be resistant to the effects of the pesticide. In ongoing studies, Hayes is investigating whether this apparent resistance is inherited, as well as whether the sex-reversed males have more susceptible offspring.

Syngenta, which manufactures atrazine, disputes many of these studies, including Hayes', that show adverse effects of the presticide. But Hayes said that "when you have studies all over the world showing problems with atrazine in every vertebrate that has been looked at - fish, frogs, reptiles, birds, mammals - all of them can't be wrong."

"What people have to realize is that, just as with taking pharmaceuticals, they have to decide whether the benefits outweigh the costs," he said.

"Not every frog or every human will be affected by atrazine, but do you want to take a chance, what with all the other things that we know atrazine does, not just to humans but to rodents and frogs and fish?" >>>

http://www.physorg.com/news186759049.html

>> Tested on fathead minnows ╨ an organism often used to test the effects of toxicity on aquatic life -- nanosilver suspended in solution proved toxic and even lethal to the minnows. When the nanosilver was allowed to settle, the solution became several times less toxic but still caused malformations in the minnows.

"Silver nitrate is a lot more toxic than nanosilver, but when nanosilver was sonicated, or suspended, its toxicity increased tenfold," said Maria Sepulveda, an assistant professor of forestry and natural resources whose findings were published in the journal Ecotoxicology. "There is reason to be concerned."

Sepulveda and doctoral student Geoff Laban exposed fathead minnows to nanosilver at several stages of their development, from embryo to the point where they swim up from the bottom of their habitats to eat for the first time. Even without sonication, nanosilver caused malformations that included head hemorrhages and edema, and ultimately proved lethal.

Using electron microscopy, Sepulveda was able to detect nanosilver particles measuring 30 nanometers or less inside the minnow embryos. Thirty nanometers is more than 3,000 times smaller than the diameter of a human hair.

"These nanosilver particles are so small they are able to cross the egg membranes and move into the fish embryos in less than a day," Sepulveda said. "They had a potentially high dose of silver in them."

Nanosilver is growing in popularity as a component of many products. It is used to kill bacteria in goods such as odor-control clothing, countertops, cutting boards and detergents. Currently, there are few regulations for nanosilver's applications in products, but Ron Turco, professor of agronomy and the paper's co-author, said the Environmental Protection Agency is reviewing the situation.

Turco also indicated there has been little work done to estimate the current level of nanosilver being released into the environment.

"Silver has been used in the past as an antimicrobial agent. It's a known toxicant to microorganisms," he said. "Nanosilver is being considered by the EPA for environmental exposure profiling, much like a pesticide."

Turco said it's unclear how nanosilver exposure might affect human health; however, he said that silver solutions have been considered by some to be a probiotic, and low dosages are sometimes consumed for intestinal health.

"The use of nanosilver could provide a number of sanitary benefits if used properly," Turco said. "However, the indiscriminate inclusion of nanosilver into products to simply allow them to say they are antimicrobial is creating a cautionary issue."

Sepulveda said she plans to develop tests to understand the effect different nanoparticles have on fish and other organisms. She also wants to develop testing to determine nanosilver concentrations in the environment.

"How are we going to know the risk unless we know the concentration of these particles?" Sepulveda said. >>>>

http://www.physorg.com/news186746178.html

>> With concern over mercury contamination of tuna on the rise and growing information about the health effects of eating contaminated fish, scientists would like to know exactly where the pollutant is coming from and how it's getting into open-ocean fish species.

Mercury is a naturally occurring element, but some 2,000 tons of it enter the global environment each year from human-generated sources such as coal-burning power plants, incinerators and chlorine-producing plants. Deposited onto land or into water, mercury is picked up by microorganisms, which convert some of it to methylmercury, a highly toxic form that builds up in fish and the animals---and people---that eat them.

The primary way people in the United States are exposed to methylmercury is by eating fish and shellfish. Health effects include damage to the central nervous system, heart and immune system, and the developing brains of young and unborn children are especially vulnerable.

In the current study, the researchers wanted to know if tuna and other open-ocean fish pick up methylmercury by eating contaminated fish that live closer to shore or by some other means. They studied 11 species of fish, including red snapper, speckled trout, Spanish mackerel and two species of tuna. Seven of the species studied live in the shallow, coastal waters of the Gulf of Mexico; the two tuna species live far out in the ocean and are highly migratory; the remaining two species spend parts of their lives in both habitats.

It's no mystery how the coastal fish acquire methylmercury, said Joel Blum, who is the John D. MacArthur Professor of Geological Sciences at U-M. "We know that there's a lot of mercury pollution in the coastal zone. A large amount of mercury comes down the Mississippi River, and there's also air pollution and deposition of mercury from the highly industrialized coastal Gulf region." In this environment, methylation occurs in the low-oxygen conditions of the lower water column and sediments, and the methylmercury wends its way up the food web, becoming more concentrated at each step along the way.

"It's much less clear how methylmercury gets into open-ocean fish species, some of which don't come anywhere close to shore but can still have very high levels," said the study's lead author, David Senn, formerly of the Harvard School of Public Health, and now a senior researcher at the Swiss Federal Institute of Aquatic Science and Technology. Scientists have proposed three possibilities.

One is that open-ocean fish visit coastal areas to feed, picking up methylmercury from the coastal food web. Another possibility is that small organisms that acquire methylmercury in coastal regions are washed out to sea, where they enter the open-ocean food web. In the third scenario, mercury is directly deposited into the open ocean, where it undergoes methylation.

By looking at three chemical signatures in the fish---nitrogen isotopes, carbon isotopes and mercury isotopes--- Senn, Blum and colleagues learned that coastal fish and open-ocean fish are feeding from two separate food webs.

"That rules out the first explanation, that these tuna were getting their methylmercury by feeding off coastal fish," Senn said.

"We think it's unlikely that the mercury is being methylated in coastal sediments and then washed out to the open ocean, so the most likely alternative is that there is deposition and methylation of mercury in the open ocean," Blum said. The finding runs counter to the long-held view that the open ocean is too oxygen-rich to support methylation, but it is consistent with recent studies suggesting more methylation may be occurring in that environment than was previously thought.

"It turns out there are probably low-oxygen microenvironments on tiny particles of organic matter, where methylation may be able to occur," Blum said.

One of the biggest differences the researchers found between coastal and open-ocean fish was in their mercury "fingerprint." The fingerprint is the result of a natural phenomenon called isotopic fractionation, in which different isotopes of mercury react to form new compounds at slightly different rates. In one type of isotopic fractionation, mass-dependent fractionation (MDF), the differing rates depend on the masses of the isotopes. In mass-independent fractionation (MIF), the behavior of the isotopes depends not on their absolute masses but on whether their masses are odd or even.

The researchers found that open-ocean fish have a much stronger MIF fingerprint than do coastal fish, a discovery that opens the door to new ways of analyzing human exposure to mercury.

"We can do an isotopic analysis of the mercury in your hair, and by looking at this mass-independent signal, tell you how much of the mercury is coming from inorganic sources, such as exposure to mercury gas or amalgams in your dental fillings, versus how much is coming from the fish that you eat," Blum said. "We think this could become a widespread technique for identifying sources of mercury contamination." >>>

http://www.physorg.com/news186746465.html

>> In 2009, the Centers for Disease Control and Prevention recommended an end to universal testing for children on Medicaid as long as state and local health departments are pursuing other methods of assessing the risk of elevated blood lead levels. The existing strategy relies primarily on Medicaid status and classifying ZIP codes as high or low risk.

"The key benefit of our method is that it identifies even more of those children who need testing and will lead to fewer unnecessary tests," said Kaplowitz, principal investigator on the project. "Hence it will improve the health of children and families at less cost to the taxpayers."

The researchers created risk scores for more than 500,000 children in Michigan who were tested for lead poisoning from 1998 to 2005. The scores are based on race, Medicaid eligibility and statistics about the socio-demographic characteristics and age of the housing in the child's neighborhood. The researchers found that their scores would have been better predictors of whether a child should be tested than the criteria used by the universal testing method.

If Michigan health officials had used the researchers' risk assessment, the method would have saved about $153,000 between 2002 and 2005 by not administering thousands of tests that came up negative, the researchers say. At the same time, the new method would have suggested testing even more of those who had elevated blood lead levels than did the old method.

To implement the method, parents or medical providers in Michigan use a specialized Web site. They input a child's address, Medicaid eligibility and race, and immediately are provided with a highly reliable assessment of whether the child's lead-poisoning risk is high enough to merit a blood test. The Web site was developed in cooperation with the Michigan Department of Community Health and funded by the CDC. The site currently is being updated and should be operational again this summer, Kaplowitz said.

Some 250,000 U.S. children under the age of 6 have blood lead levels greater than 10 micrograms of lead per deciliter of blood, the level at which CDC recommends public health actions be initiated. If undetected, lead poisoning can cause permanent developmental disabilities, brain damage and even death.

Children in the United States absorb lead primarily by ingesting chips or dust from lead paint. This occurs either when the paint deteriorates or from household remodeling projects. Another source is lead contamination found in water and soil. >>>

http://www.physorg.com/news186773867.html

>> This study is one of the first to provide two valuable lessons, said Sherry. The first, already noted, is that soluble fiber has direct anti-inflammatory effects and builds up the immune system. The second is that the amount of soluble fiber necessary to achieve these health benefits is a reasonable, not a pharmacological, amount.

The recommended daily dietary recommendation is 28 to 35 grams of total fiber, but most of the FDA's health claims are for insoluble fiber, and that's where things get a bit complicated, she said.

"Not all fiber is created equal, although you wouldn't know that by reading nutrition labels," said Sherry. "Most manufacturers don't tell you how much of each type of fiber a food contains, and we think it's important that this information be included on a product's packaging."

Good sources of soluble fiber are oat bran, barley, nuts, seeds, lentils, citrus fruits, apples, strawberries, and carrots.

"We used a citrus-based pectin in our study," Sherry said.

Insoluble fiber, found in whole wheat and whole-grain products, wheat bran, and green, leafy vegetables, is also valuable for providing bulk and helping food move through the digestive system, but it doesn't provide the boost to the immune system that soluble fiber provides. >>>

a mental illness crisis in Australia....He said someone takes their life in Australia every four hours.

http://www.physorg.com/news187277637.html

>> The collection of symptoms that is the metabolic syndrome -- insulin resistance, high cholesterol, fatty liver, and a greater risk for diabetes, heart disease, and stroke -- are all related to obesity

In fact, says Roger Unger of the University of Texas Southwestern at Dallas, obesity is the body's way of storing lipids where they belong, in fat tissue, in an effort to protect our other organs from lipids' toxic effects. It's when the surplus of calories coming in gets to be too much for our fat tissue to handle that those lipids wind up in other places they shouldn't be, and the cascade of symptoms known as metabolic syndrome sets in.

It comes down to simple facts that all of us know on some level or another: Americans since the 1950s eat too much high-calorie food loaded with carbs and fat (what Unger calls "potent adipogenic nutrient mixtures") and, thanks to modern technology, we move far too little. Until that changes, Unger doesn't see any end to the growing epidemic of metabolic syndrome. Still, our metabolisms aren't broken; the pathways that squirrel fat away as an energy source for use in lean times are just completely overwhelmed.

"We are pushing our homeostatic capability to the maximum," says Unger, who coined the term "lipotoxicity" in 1994. "Overnutrition used to be rare—reserved for those in the castle. Today, it's just the opposite. Bad calories are so cheap that anyone can afford to get overweight."

Unger cites plenty of evidence in support of a protective role for obesity. Genetic manipulations in mice that increase or decrease fat formation have provided evidence that adipogenesis, meaning the generation of fat cells, delays other metabolic consequences of overeating. The reverse is also true, he writes. Obesity-resistant mice have in some cases been found to develop severe diabetes upon eating too much, as a result of lipid accumulation in tissues other than fat.

There is some disagreement in the field about whether insulin resistance is a primary cause of metabolic syndrome or just one of its features, Unger notes. But on this, too, he has a clear view. Insulin resistance is not the cause of metabolic syndrome, he says, it is a "passive byproduct" of fat deposition in the liver and muscle once storage in fat cells begins to fail.

It also makes sense in Unger's estimation that cells that have already taken on too much fat would begin to exclude glucose, causing its levels in blood and urine to rise. Once in cells, glucose becomes a substrate for the production of more fat. "The body is doing what we should have done—keep excess calories out—and it may be protective," Unger says.

At the center of the transition from protective obesity to metabolic syndrome is resistance to the fat hormone leptin, well known for its appetite-suppressing effects, Unger says. The hormone is also responsible for partitioning fat in the body. The rise of leptin as fat stores grow is therefore an adaptive response, but that can only go so far before resistance sets in.

Based on the genes they carry, some people will be better able to sustain lipid storage in fat and can get away with being overweight, even obese, without the other symptoms. Eventually, though, the need to cut calories is something all of us will face.

"Once you reach a certain age, almost everybody is leptin resistant," he says. "Nature stops protecting you once you pass the reproductive years," requiring all of us to watch our diets and do exercise.

Unger's perspective comes from the research he does at UT Southwestern's Touchstone Center for Diabetes Research and a thorough understanding of the scientific literature, but it also stems from his own memories in childhood when one only saw fat ladies at the circus. "That's how unusual it was," he says. "The younger you are, the more skewed your perception is of an epidemic that surrounds you."

Unger concludes his review article this way: "Based on evidence reviewed here, it seems that prevalent forms of metabolic syndrome and T2DM [type 2 diabetes mellitus] result from unremitting caloric surplus complicated by failure of adipocytes to maintain protection against lipotoxicity.

If one imagines the USA population to be unwitting volunteers in the largest (300 million subjects) and longest (50 years) clinical research project in history, the specific aim of which was to determine if the deleterious effects of sustained caloric surplus in rodents also can occur in humans, the outcome of the project becomes clear—after 50 years of exposure to an inexpensive calorie-dense diet high in fat and carbohydrates, 200 million subjects are overweight and >50 million have metabolic syndrome.

The failure of healthcare providers and pharmaceutical industries to contain the pandemic suggests that elimination of 'bargain basement' calories will be required to 'price obesity out of the market.' Unfortunately, this would have profound socioeconomic implications: How do we tax excessive calories while at the same time guaranteeing sufficient access to high-quality foods for the underprivileged?" >>>

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Metal ions are stored in fat....

http://www.physorg.com/news187960970.html

>> Researchers from the Miguel Hernández University have identified cloves (Syzygium aromaticum) as the best antioxidant spice, due to the fact they contain high levels of phenolic compounds, as well as having other properties.

"Out of the five antioxidant properties tested, cloves had the highest capacity to give off hydrogen, reduced lipid peroxidation well, and was the best iron reducer", Juana Fernández-López, one of the authors of the study and a researcher at the UMH, tells SINC.

"The results show that use of the natural oxidants occurring in spices used in the Mediterranean diet, or their extracts, is a viable option for the food industry, as long as the organoleptic characteristics of the food product are not affected", adds the researcher.

"These substances exhibit high antioxidant capacity, and could have beneficial effects for health", says the researcher

The team also evaluated the antioxidant effect of the essential oils from other spices used in the Mediterranean diet - oregano (Origanum vulgare), thyme (Thymus vulgaris), rosemary, (Rosmarinus funcionarios cinalis) and sage (Salvia funcionarios cinalis).

The objective of the study is to enable these spices to be incorporated into food products (above all meat products) as natural antioxidants.

"Lipid oxidation is one of the main reasons for foods deteriorating, and causes a significant reduction in their nutritional value, as well as loss of taste", says Fernández-López.

These alterations lead to a reduction in the useful lifespan of the food product. To avoid such deterioration, the food industry uses synthetic antioxidants in its products. However, as these are chemical compounds, questions have been raised about their potential toxicity and side-effects.

As a result, there is a growing interest in using plant-based products (spices, aromatic and medicinal plants) with potential antioxidant activity, in order to replace the synthetic antioxidants with "natural" substances. >>>

http://www.physorg.com/news188051661.html

>> The Inner Harbour on the Cataraqui River in Kingston, Ont., has mercury levels in sediment more than two times the Canadian government's most severe effect limits, according to a Queen's University study.

"Mercury levels in this part of the river have never been studied before," says biology professor Linda Campbell. "Now we know the sources of the problem and just how widespread it is."

Most of the western shore of the Cataraqui River south of Belle Park and above the LaSalle Causeway Bridge had levels of contamination, with the worst area around the Cataraqui Canoe Club, just south of the former Davis Tannery.

Over the past century, the area has been home to many industries, such as a coal gasification plant, tannery and lead smelter, municipal dump, textile mill and fuel depot. The report found rain is washing contaminated shoreline soil near the canoe club into the river, adding to the sediment already contaminated by decades of industry.

The mercury comes in two forms, mercury and its organic and more toxic form, methylmercury. Right now, most of the mercury around the rowing club seems to be associated with the sediment in its inorganic form, with very little if any actually being mobile in the river water.

Rower and canoeists don't have to be too concerned about the high mercury levels because they don't drink the water or spend a long periods of time swimming there. But more studies will be needed to determine the impact on marine life.

Allison Rutter, Director of Analytical Services Unit in the Environmental Studies department worked on the study with Dr. Campbell, along with geography PhD student Nathan Manion.

"People have always been worried about lead, chromium and PCBs in the Cataraqui River," says Professor Rutter. "This study looked at mercury. We need to know what and where the major sources of contamination are before we can make a decision on how to solve the problem." >>>