Clues To Reversing Aging Of Human Muscle Discovered.

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ScienceDaily (Sep. 30, 2009) — A study led by researchers at the University of California, Berkeley, has identified critical biochemical pathways linked to the aging of human muscle. By manipulating these pathways, the researchers were able to turn back the clock on old human muscle, restoring its ability to repair and rebuild itself.

The findings will be reported in the Sept. 30 issue of the journal EMBO Molecular Medicine, a peer-reviewed, scientific publication of the European Molecular Biology Organization.
"Our study shows that the ability of old human muscle to be maintained and repaired by muscle stem cells can be restored to youthful vigor given the right mix of biochemical signals," said Professor Irina Conboy, a faculty member in the graduate bioengineering program that is run jointly by UC Berkeley and UC San Francisco, and head of the research team conducting the study. "This provides promising new targets for forestalling the debilitating muscle atrophy that accompanies aging, and perhaps other tissue degenerative disorders as well."
Previous research in animal models led by Conboy, who is also an investigator at the Berkeley Stem Cell Center and at the California Institute for Quantitative Biosciences (QB3), revealed that the ability of adult stem cells to do their job of repairing and replacing damaged tissue is governed by the molecular signals they get from surrounding muscle tissue, and that those signals change with age in ways that preclude productive tissue repair.
Those studies have also shown that the regenerative function in old stem cells can be revived given the appropriate biochemical signals. What was not clear until this new study was whether similar rules applied for humans. Unlike humans, laboratory animals are bred to have identical genes and are raised in similar environments, noted Conboy, who received a New Faculty Award from the California Institute of Regenerative Medicine (CIRM) that helped fund this research. Moreover, the typical human lifespan lasts seven to eight decades, while lab mice are reaching the end of their lives by age 2.
Working in collaboration with Dr. Michael Kjaer and his research group at the Institute of Sports Medicine and Centre of Healthy Aging at the University of Copenhagen in Denmark, the UC Berkeley researchers compared samples of muscle tissue from nearly 30 healthy men who participated in an exercise physiology study. The young subjects ranged from age 21 to 24 and averaged 22.6 years of age, while the old study participants averaged 71.3 years, with a span of 68 to 74 years of age.
In experiments conducted by Dr. Charlotte Suetta, a post-doctoral researcher in Kjaer's lab, muscle biopsies were taken from the quadriceps of all the subjects at the beginning of the study. The men then had the leg from which the muscle tissue was taken immobilized in a cast for two weeks to simulate muscle atrophy. After the cast was removed, the study participants exercised with weights to regain muscle mass in their newly freed legs. Additional samples of muscle tissue for each subject were taken at three days and again at four weeks after cast removal, and then sent to UC Berkeley for analysis.
Morgan Carlson and Michael Conboy, researchers at UC Berkeley, found that before the legs were immobilized, the adult stem cells responsible for muscle repair and regeneration were only half as numerous in the old muscle as they were in young tissue. That difference increased even more during the exercise phase, with younger tissue having four times more regenerative cells that were actively repairing worn tissue compared with the old muscle, in which muscle stem cells remained inactive. The researchers also observed that old muscle showed signs of inflammatory response and scar formation during immobility and again four weeks after the cast was removed.
"Two weeks of immobilization only mildly affected young muscle, in terms of tissue maintenance and functionality, whereas old muscle began to atrophy and manifest signs of rapid tissue deterioration," said Carlson, the study's first author and a UC Berkeley post-doctoral scholar funded in part by CIRM. "The old muscle also didn't recover as well with exercise. This emphasizes the importance of older populations staying active because the evidence is that for their muscle, long periods of disuse may irrevocably worsen the stem cells' regenerative environment."
At the same time, the researchers warned that in the elderly, too rigorous an exercise program after immobility may also cause replacement of functional muscle by scarring and inflammation. "It's like a Catch-22," said Conboy.
The researchers further examined the response of the human muscle to biochemical signals. They learned from previous studies that adult muscle stem cells have a receptor called Notch, which triggers growth when activated. Those stem cells also have a receptor for the protein TGF-beta that, when excessively activated, sets off a chain reaction that ultimately inhibits a cell's ability to divide.
The researchers said that aging in mice is associated in part with the progressive decline of Notch and increased levels of TGF-beta, ultimately blocking the stem cells' capacity to effectively rebuild the body.
This study revealed that the same pathways are at play in human muscle, but also showed for the first time that mitogen-activated protein (MAP) kinase was an important positive regulator of Notch activity essential for human muscle repair, and that it was rendered inactive in old tissue. MAP kinase (MAPK) is familiar to developmental biologists since it is an important enzyme for organ formation in such diverse species as nematodes, fruit flies and mice.
For old human muscle, MAPK levels are low, so the Notch pathway is not activated and the stem cells no longer perform their muscle regeneration jobs properly, the researchers said.
When levels of MAPK were experimentally inhibited, young human muscle was no longer able to regenerate. The reverse was true when the researchers cultured old human muscle in a solution where activation of MAPK had been forced. In that case, the regenerative ability of the old muscle was significantly enhanced.
"The fact that this MAPK pathway has been conserved throughout evolution, from worms to flies to humans, shows that it is important," said Conboy. "Now we know that it plays a key role in regulation and aging of human tissue regeneration. In practical terms, we now know that to enhance regeneration of old human muscle and restore tissue health, we can either target the MAPK or the Notch pathways. The ultimate goal, of course, is to move this research toward clinical trials."
Other co-authors of the EMBO Molecular Medicine paper include Abigail Mackey at the University of Copenhagen in Denmark, and Per Aagaard at the University of Southern Denmark.
The National Institutes of Health, the California Institute of Regenerative Medicine, the Danish Medical Research Council and the Glenn Foundation for Medical Research helped support this research.
Journal reference:
Morgan E. Carlson, Charlotte Suetta, Michael J. Conboy, Per Aagaard, Abigail Mackey, Michael Kjaer, Irina Conboy. Molecular aging and rejuvenation of human muscle stem cells. EMBO Molecular Medicine, 2009; DOI: 10.1002/emmm.200900045
Adapted from materials provided by University of California - Berkeley, via EurekAlert!, a service of AAAS.

Scientists Present First Genetic Evidence For Why Placebos Work

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ScienceDaily (July 22, 2009) — Placebos are a sham — usually mere sugar pills designed to represent "no treatment" in a clinical treatment study. The effectiveness of the actual medication is compared with the placebo to determine if the medication works.

And yet, for some people, the placebo works nearly as well as the medication. How well placebos work varies widely among individuals. Why that is so, and why they work at all, remains a mystery, thought to be based on some combination of biological and psychological factors.
Now, researchers at UCLA have found a new explanation: genetics. Dr. Andrew Leuchter, a professor of psychiatry at the UCLA Semel Institute for Neuroscience and Human Behavior, and colleagues report that in people suffering from major depressive disorder, or MDD, genes that influence the brain's reward pathways may modulate the response to placebos. The research appears in the August edition of the Journal of Clinical Psychopharmacology.
Placebos are thought to act by stimulating the brain's central reward pathways by releasing a class of neurotransmitters called monoamines, specifically dopamine and norepinephrine. These are the brain chemicals that make us "feel good." Because the chemical signaling done by monoamines is under strong genetic control, the scientists reasoned that common genetic variations between individuals — called genetic polymorphisms — could influence the placebo response.
Researchers took blood samples from 84 people diagnosed with MDD; 32 were given medication and 52 a placebo. The researchers looked at the polymorphisms in genes that coded for two enzymes that regulate monoamine levels: catechol-O-methyltransferase (COMT) and monoamine oxidase A (MAO-A). Subjects with the highest enzyme activity within the MAO-A polymorphism had a significantly lower placebo response than those with other genotypes. With respect to COMT, those with lower enzyme activity within this polymorphism had a lower placebo response.
"Our findings suggest that patients with MDD who have specific MAO-A and COMT genotypes may be biologically advantaged or disadvantaged in mounting a placebo response, because of the activity of these two enzymes," said Leuchter, who directs the Laboratory of Brain, Behavior and Pharmacology at the UCLA Semel Institute.
"To our knowledge, this is the first study to examine the association between MAO-A and COMT polymorphisms and a response to placebo in people who suffer from major depressive disorder," he said.
Leuchter noted that this is not the sole explanation for a response to a placebo, which is likely to be caused by many factors, both biological and psychosocial. "But the data suggests that individual differences in response to placebo are significantly influenced by individual genotypes," he said.
Including the influence of genotype in the design of clinical trials could facilitate more powerful testing of future treatments, Leuchter said.
Funding for the study was provided by the National Center for Complementary and Alternative Medicine of the National Institutes of Health, Eli Lilly and Co., and Pfizer Inc.
Other authors included James McCracken, Aimee Hunter and Ian Cook, all of UCLA, and Jonathan Alpert of Massachusetts General Hospital and Harvard University.
Dr. Andrew Leuchter has provided scientific consultation or served on advisory boards of a number of companies, including Eli Lilly and Co., where he has also served in the speakers bureau. He has received research/grant support from the National Center for Complementary and Alternative Medicine, Eli Lilly and Co., and Pfizer Inc., among others.
Dr. James T. McCracken has served as an adviser and consultant for Eli Lilly and Co. and other companies and receives research support from, among others, Eli Lilly and Co.
Dr. Ian A. Cook has served in the speakers bureau for Pfizer Pharmaceuticals Inc. and other companies and has received research support from, among others, Eli Lilly and Co. and Pfizer Inc.
Dr. Jonathan E. Alpert has served as an adviser and consultant for Eli Lilly and Co. and other companies and has served in the speakers bureau for Eli Lilly and Co. He receives research support from, among others, Eli Lilly and Co. and Pfizer Inc.
Adapted from materials provided by University of California - Los Angeles.

Better Than A Hearing Aid? Better Hearing With Bone Conducted Sound

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ScienceDaily (July 9, 2009) — New technology to hear vibrations through the skull bone has been developed at Chalmers University of Technology. Besides investigating the function of a new implantable bone conduction hearing aid, Sabine Reinfeldt has studied the sensitivity for bone conducted sound and also examined the possibilities for a two-way communication system that is utilizing bone conduction in noisy environments.

A new Bone Conduction Implant (BCI) hearing system was investigated by Sabine Reinfeldt. "This hearing aid does not require a permanent skin penetration, in contrast to the Bone-Anchored Hearing Aids (BAHAs) used today," she said.
Measurements showed that the new BCI hearing system can be a realistic alternative to the BAHA.
Sound is normally perceived through Air Conduction (AC), which means that the sound waves in the air enter the ear-canal and are transmitted to the cochlea in the inner ear. However, sound can also be perceived via Bone Conduction (BC). Vibrations are then transmitted to the cochleae through the skull bone from either one's own voice, the surrounding sound field, or a BC transducer.
In two-way communication systems, BC is believed to improve the sound quality when used in extremely noisy environments which require hearing protection devices in the ear-canals.
Several studies were performed to investigate the possibilities for a BC communication system and to increase the general knowledge of BC sound perception.
The low-frequency increase in perceived BC sound when wearing ear-plugs and/or ear-muffs is called the occlusion effect. This effect was studied by different methods and it was found that it is lower for deeper insertion of ear-plugs and for larger ear-muffs, and that it varies for different stimulations.
The difference in sensitivity of the BC and AC parts of one's own voice was estimated, showing that the BC component dominated for most sounds between 1 and 2 kHz. To be able to measure the BC component of a person's own voice, a large ear-muff was developed to attenuate the AC sound and to minimize the occlusion effect.
The study also showed that the sensitivity difference between the BC and AC parts of one's own voice were different for different kinds of sounds, depending on where in the mouth the sound is produced and on the influence from the vocal cords.
Also estimated was the difference in sensitivity between BC and AC sound from a surrounding sound field, demonstrating that the BC part was 40 to 60 dB lower than the AC part. This measure gives the maximum attenuation achievable with ordinary hearing protection devices, like ear-plugs and ear-muffs. It also shows the possible noise reduction from the surrounding noise by using a BC microphone, instead of an ordinary AC microphone in front of the mouth, to record one's own voice in a noisy environment.
Moreover, the amount of BC sound reaching the cochleae from different positions of the skull bone was examined with the conclusion that relative BC hearing can be estimated from ear-canal sound pressure and cochlear vibrations.
Adapted from materials provided by The Swedish Research Council, via AlphaGalileo.

Chemical In Common Consumer Products (Phthalates) May Play A Role In Pre-term Births

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ScienceDaily (July 7, 2009) — A new study of expectant mothers suggests that a group of common environmental contaminants called phthalates, which are present in many industrial and consumer products including everyday personal care items, may contribute to the country's alarming rise in premature births.

Researchers at the University of Michigan School of Public Health found that women who deliver prematurely have, on average, up to three times the phthalate level in their urine compared to women who carry to term.
Professors John Meeker, Rita Loch-Caruso and Howard Hu of the SPH Department of Environmental Health Sciences and collaborators from the National Institute of Public Health in Mexico and the U.S. Centers for Disease Control and Prevention analyzed data from a larger study directed by Hu, which follows a cohort of Mexican women recruited during pre-natal visits at one of four clinics of the Mexican Institute of Social Security in Mexico City.
Meeker and colleagues looked at data from 60 women: 30 who carried to term and 30 who delivered prematurely (defined as less than 37 weeks gestation). They analyzed urine samples collected during the third trimester and compared them to the control group who carried to term. They found significantly higher phthalate metabolite levels in the women who delivered prematurely.
Premature birth is a significant risk factor for many health problems in childhood that can persist into adulthood, Meeker says. In the United States, premature births have increased by more than 30 percent since 1981 and by 18 percent since 1990. In 2004, premature births accounted for 12.8 percent of live births nationwide.
Premature births, he says, account for one-third of infant deaths in the United States, making it the leading cause of neonatal mortality. Being born too early can also lead to chronic health problems such as blindness, deafness, cerebral palsy, low IQ and more.
Phthalates are commonly used compounds in plastics, personal care products, home furnishings (vinyl flooring, carpeting, paints, etc.) and many other consumer and industrial products. The toxicity varies by specific phthalates or their breakdown products, but past studies show that several phthalates cause reproductive and developmental toxicity in animals.
A couple of human studies have reported associations between phthalates and gestational age, but this is the first known study to look at the relationship between phthalates and premature births, Meeker says.
"We looked at these commonly used compounds found in consumer products based on the growing amount of animal toxicity data and since national human data show that a large proportion of the population are unknowingly exposed," Meeker said. "One of the problems for consumers is that you don't know exactly which products contain phthalates because the products do not have to be labeled accordingly."
Meeker says the U-M study is a stepping stone to larger and more detailed studies examining the role of phthalates and premature births. The researchers hope to examine a larger population of pregnant women to corroborate these initial study findings, and conduct experimental lab studies to further explore the biological mechanisms of how phthalates work in the body.
Journal reference:
Meeker et al. Urinary phthalate metabolites in relation to preterm birth in Mexico City. Environmental Health Perspectives, 2009; DOI: 10.1289/ehp.0800522
Adapted from materials provided by University of Michigan.

Physics Research With Atomic Force Microscope Could Lead To Better Health Care

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ScienceDaily (July 6, 2009) — Where biology, chemistry and physics intersect, a Kansas State University professor expects to find applications to improve human health.

Robert Szoszkiewicz, an assistant professor of physics at K-State, is continuing research on molecules both singularly and as a group. His study of proteins as a single molecule shows promise to help scientists understand the causes of diseases like some cancers. Meanwhile, his research on bunched molecules could lead to a more efficient way to identify antibodies in blood.
Szoszkiewicz's research on proteins began at Columbia University and some of it was published in June in Nature Chemistry. He and his former colleagues looked at the unexpected complexity in the dynamics of stretching and breaking of a single chemical bond between two atoms embedded in a protein. A cleavage of that particular bond has been precisely signaled by unfolding and elongation of a part of a protein.
"There is lots of potential for this research to really address issues of major importance in biology because this will be related to particular pathways through which some kinds of diseases, cancers and biological processes develop," he said. "And, we can study that on the very molecular level by studying the single proteins involved and stretching them and seeing how this contributes to the overall picture."
The research uses an atomic force microscope, a tool involving a cantilever with a sharp tip that under certain circumstances becomes attached to the protein molecule. The researchers stretch the molecules and measure precisely their tiny displacements.
"Any work that we do on the ground level of stretching any kind of chemical bonds is fundamentally important because it's the kind of knowledge no one has ever measured on this scale," he said. "Proteins constantly fold and unfold. A folded protein is the one that's biologically active and performing a function. So any problems during its folding and unfolding translate to some potential diseases like cancers."
Szoszkiewicz received a grant from K-State's Terry C. Johnson Center for Basic Cancer Research to use these techniques to stretch some proteins that are significant in breast cancer. He is collaborating with Anna Zolkiewska and Michal Zolkiewski, both K-State associate professors of biochemistry.
Another area of Szoszkiewicz's research began while at the Georgia Institute of Technology. It involves changing the properties of a surface at the very local scale by using an atomic force microscope in which the sharp cantilever tip can be heated up to between 500 degrees and 600 degrees Celsius.
When this heated tip is scraped across a surface, Szoszkiewicz said, the heat can -- under certain circumstances -- initiate a chemical reaction on that very surface. He and his colleagues have created patches of chemically changed surface only 10 to 15 nanometers across, but Szoszkiewicz thinks he will be able to change the surface just bunch of molecules at a time. This ability to pattern the surface, he said, could improve personalized medicine by allowing scientists to create tiny chips on which many tests can be run simultaneously.
"You could take a small sample of blood and screen it for any possible drug that could work for you," he said. "Ordinarily to do such a screening would require a humongous amount of testing material and antibodies. If you could prepare a surface that will selectively bind only one or two molecules of a kind and then see if you have bound or not, then you would need only a few milliliters of blood, and you could test it against millions of molecules. Of course, there are other factors involved and the particular interactions between single blood molecules and their antibodies might not be that simple. But this still remains to be seen."
Szoszkiewicz said that if scientists can pattern the surface in the way they like, another application might be tiny electric circuits and lenses that guide, respectively, electrons and photons. Also, using an atomic force microscope in this way, he said, physicists can not only change the chemical properties of the surface but they also can change the topography of a surface -- in other words, how the surface looks.
For example, Szoszkiewicz and colleagues have created and investigated the nature of nanoscale ripples created on polymers, or the "polymer dunes" at a nanoscale level. Using custom-made polymers, the researchers scratched them with the hot tip while using enough heat to indent within the polymer during scratching but not to destroy the polymer sample. Such research investigated how these tiny dunes created on polymers change with the application of heat. In this case, heat functions like wind would on real sand dunes. The researchers investigated under which conditions the dune gets pushed in the way they wanted it and forms a desired shape.
"This way you can prepare structures that can serve to sort materials at the nanoscale," he said. "Later on you virtually throw some other molecules on the surface, and maybe some of it will go into the grooves, depending on the chemistry."
The researchers were able to prepare several types of nanoscopic ripples -- these so-called tiny dunes -- with the most common type being the one in which the ripples organize in a roughly linear fashion. However, they also explored circular geometry. Their work has been published in the June issue of the journal Physical Review B.
"What we have proven in this paper is that, under certain conditions, by scanning continuously along these circles, you can make the ripples along your circular scanning path, and under certain circumstances to move them collectively and continuously," Szoszkiewicz said. "Measuring the collective velocities, we found that they would approach the velocities of shifting a big sand dune, just scaled down."
Szoszkiewicz's continuation of these projects in his lab at K-State include several other researchers: Heidi Martin, sophomore in physics from Junction City; Ashim Dey, doctoral student in physics, Manhattan; Neelam Khan, May 2009 doctoral graduate in physics; and Vera Okuneva, research assistant in biology.
Adapted from materials provided by Kansas State University.

Nitrates May Be Environmental Trigger For Alzheimer’s, Diabetes And Parkinson's Disease

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ScienceDaily (July 6, 2009) — A new study by researchers at Rhode Island Hospital have found a substantial link between increased levels of nitrates in our environment and food with increased deaths from diseases, including Alzheimer's, diabetes mellitus and Parkinson's. The study was published in the Journal of Alzheimer's Disease.

Led by Suzanne de la Monte, MD, MPH, of Rhode Island Hospital, researchers studied the trends in mortality rates due to diseases that are associated with aging, such as diabetes, Alzheimer's, Parkinson's, diabetes and cerebrovascular disease, as well as HIV. They found strong parallels between age adjusted increases in death rate from Alzheimer's, Parkinson's, and diabetes and the progressive increases in human exposure to nitrates, nitrites and nitrosamines through processed and preserved foods as well as fertilizers. Other diseases including HIV-AIDS, cerebrovascular disease, and leukemia did not exhibit those trends. De la Monte and the authors propose that the increase in exposure plays a critical role in the cause, development and effects of the pandemic of these insulin-resistant diseases.
De la Monte, who is also a professor of pathology and lab medicine at The Warren Alpert Medical School of Brown University, says, "We have become a 'nitrosamine generation.' In essence, we have moved to a diet that is rich in amines and nitrates, which lead to increased nitrosamine production. We receive increased exposure through the abundant use of nitrate-containing fertilizers for agriculture." She continues, "Not only do we consume them in processed foods, but they get into our food supply by leeching from the soil and contaminating water supplies used for crop irrigation, food processing and drinking."
Nitrites and nitrates belong to a class of chemical compounds that have been found to be harmful to humans and animals. More than 90 percent of these compounds that have been tested have been determined to be carcinogenic in various organs. They are found in many food products, including fried bacon, cured meats and cheese products as well as beer and water. Exposure also occurs through manufacturing and processing of rubber and latex products, as well as fertilizers, pesticides and cosmetics.
Nitrosamines are formed by a chemical reaction between nitrites or other proteins. Sodium nitrite is deliberately added to meat and fish to prevent toxin production; it is also used to preserve, color and flavor meats. Ground beef, cured meats and bacon in particular contain abundant amounts of amines due to their high protein content. Because of the significant levels of added nitrates and nitrites, nitrosamines are nearly always detectable in these foods. Nitrosamines are also easily generated under strong acid conditions, such as in the stomach, or at high temperatures associated with frying or flame broiling. Reducing sodium nitrite content reduces nitrosamine formation in foods.
Nitrosamines basically become highly reactive at the cellular level, which then alters gene expression and causes DNA damage. The researchers note that the role of nitrosamines has been well-studied, and their role as a carcinogen has been fully documented. The investigators propose that the cellular alterations that occur as a result of nitrosamine exposure are fundamentally similar to those that occur with aging, as well as Alzheimer's, Parkinson's and Type 2 diabetes mellitus.
De la Monte comments, "All of these diseases are associated with increased insulin resistance and DNA damage. Their prevalence rates have all increased radically over the past several decades and show no sign of plateau. Because there has been a relatively short time interval associated with the dramatic shift in disease incidence and prevalence rates, we believe this is due to exposure-related rather than genetic etiologies."
The researchers recognize that an increase in death rates is anticipated in higher age groups. Yet when the researchers compared mortality from Parkinson's and Alzheimer's disease among 75 to 84 year olds from 1968 to 2005, the death rates increased much more dramatically than for cerebrovascular and cardiovascular disease, which are also aging-associated. For example, in Alzheimer's patients, the death rate increased 150-fold, from 0 deaths to more than 150 deaths per 100,000. Parkinson's disease death rates also increased across all age groups. However, mortality rates from cerebrovascular disease in the same age group declined, even though this is a disease associated with aging as well.
De la Monte notes, "Because of the similar trending in nearly all age groups within each disease category, this indicates that these overall trends are not due to an aging population. This relatively short time interval for such dramatic increases in death rates associated with these diseases is more consistent with exposure-related causes rather than genetic changes." She also comments, "Moreover, the strikingly higher and climbing mortality rates in older age brackets suggest that aging and/or longer durations of exposure have greater impacts on progression and severity of these diseases."
The researchers graphed and analyzed mortality rates, and compared them with increasing age for each disease. They then studied United States population growth, annual use and consumption of nitrite-containing fertilizers, annual sales at popular fast food chains, and sales for a major meat processing company, as well as consumption of grain and consumption of watermelon and cantaloupe (the melons were used as a control since they are not typically associated with nitrate or nitrite exposure).
The findings indicate that while nitrogen-containing fertilizer consumption increased by 230 percent between 1955 and 2005, its usage doubled between 1960 and 1980, which just precedes the insulin-resistant epidemics the researchers found. They also found that sales from the fast food chain and the meat processing company increased more than 8-fold from 1970 to 2005, and grain consumption increased 5-fold.
The authors state that the time course of the increased prevalence rates of Alzheimer's, Parkinson's and diabetes cannot be explained on the basis of gene mutations. They instead mirror the classical trends of exposure-related disease. Because nitrosamines produce biochemical changes within cells and tissues, it is conceivable that chronic exposure to low levels of nitrites and nitrosamines through processed foods, water and fertilizers is responsible for the current epidemics of these diseases and the increasing mortality rates associated with them.
De la Monte states, "If this hypothesis is correct, potential solutions include eliminating the use of nitrites and nitrates in food processing, preservation and agriculture; taking steps to prevent the formation of nitrosamines and employing safe and effective measures to detoxify food and water before human consumption."
Other researchers involved in the study with de la Monte include Alexander Neusner, Jennifer Chu and Margot Lawton, from the departments of pathology, neurology and medicine at Rhode Island Hospital and The Warren Alpert Medical School of Brown University.
The study was funded through grants from the National Institutes of Health. Two subsequent papers have been accepted for publication in the near future that demonstrate experimentally that low levels of nitrosamine exposure cause neurodegeneration, NASH and diabetes.
Journal reference:
De la Monte, Suzanne M., Alexander Neusner, Jennifer Chu and Margot Lawton. Epidemilogical Trends Strongly Suggest Exposures as Etiologic Agents in the Pathogenesis of Sporadic Alzheimer's Disease, Diabetes Mellitus, and Non-Alcoholic Steatohepatitis. Journal of Alzheimer's Disease, 17:3 (July 2009) pp 519-529
Adapted from materials provided by Lifespan, via EurekAlert!, a service of AAAS.

New Evidence That Vinegar May Be Natural Fat-fighter

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ScienceDaily (July 7, 2009) — Researchers in Japan are reporting new evidence that the ordinary vinegar — a staple in oil-and-vinegar salad dressings, pickles, and other foods — may live up to its age-old reputation in folk medicine as a health promoter. They are reporting new evidence that vinegar can help prevent accumulation of body fat and weight gain.

Tomoo Kondo and colleagues note in the new study that vinegar has also been used as a folk medicine since ancient times. People have used it for a range of ills. Modern scientific research suggests that acetic acid, the main component of vinegar, may help control blood pressure, blood sugar levels, and fat accumulation.
Their new study showed that laboratory mice fed a high-fat diet and given acetic acid developed significantly less body fat (up to 10 percent less) than other mice.
Importantly, the new research adds evidence to the belief that acetic acid fights fat by turning on genes for fatty acid oxidation enzymes. The genes churn out proteins involved in breaking down fats, thus suppressing body fat accumulation in the body.
Journal reference:
Kondo et al. Acetic Acid Upregulates the Expression of Genes for Fatty Acid Oxidation Enzymes in Liver To Suppress Body Fat Accumulation. Journal of Agricultural and Food Chemistry, 2009; 090609114939008 DOI: 10.1021/jf900470c
Adapted from materials provided by American Chemical Society.