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161st Health Research Report 10 AUG 2013

Health Research Report

161st Issue Date 10 AUG 2013

Compiled By Ralph Turchiano

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In this issue:

1.       Plant-Based Compound May Inhibit HIV Infection, Research Shows

2.       Methamphetamine increases susceptibility to deadly fungal infection

3.       Exercise May be the Best Medicine for Alzheimer’s

4.       Study finds evidence of nerve damage in around half of fibromyalgia patients

5.       Blocking sugar intake may reduce cancer risk or progression in obese and diabetic people

6.       Fatty acids could aid cancer prevention and treatment

7.       Illinois scientists put cancer-fighting power back into frozen broccoli

8.       Diets of Pregnant Women Contain Harmful, Hidden Toxins

9.       L-3-n-butylphthalide protects against cognitive dysfunction in vascular dementia

 

Plant-Based Compound May Inhibit HIV Infection, Research Shows

Posted: July 19, 2013 at 5:00 am, Last Updated: July 23, 2013 at 6:49 am

By Michele McDonald

A compound found in soybeans may become an effective HIV treatment without the drug resistance issues faced by current therapies, according to new research by George Mason University researchers.

It’s in the early stages, but genistein, derived from soybeans and other plants, shows promise in inhibiting the HIV infection, says Yuntao Wu, a professor with the George Mason-based National Center for Biodefense and Infectious Diseases and the Department of Molecular and Microbiology.

Still, that doesn’t mean people should begin eating large amounts of soy products. “Although genistein is rich in several plants such as soybeans, it is still uncertain whether the amount of genistein we consume from eating soy is sufficient to inhibit HIV,” Wu says.

Genistein is a “tyrosine kinase inhibitor” that works by blocking the communication from a cell’s surface sensors to its interior. Found on a cell’s surface, these sensors tell the cell about its environment and also communicate with other cells. HIV uses some of these surface sensors to trick the cell to send signals inside. These signals change cell structure so that the virus can get inside and spread infection.

But genistein blocks the signal and stops HIV from finding a way inside the cell. It takes a different approach than the standard antiretroviral drug used to inhibit HIV.

“Instead of directly acting on the virus, genistein interferes with the cellular processes that are necessary for the virus to infect cells,” Wu says. “Thus, it makes the virus more difficult to become resistant to the drug. Our study is currently it its early stage. If clinically proven effective, genistein may be used as a complement treatment for HIV infection.”

Wu sees possibilities in this plant-based approach, which may address drug toxicity issues as well. Because genistein is plant-derived, it may be able to sidestep drug toxicity, a common byproduct of the daily and lifelong pharmaceutical regimen faced by patients with HIV to keep the disease at bay, Wu says. Typically, patients take a combination of multiple drugs to inhibit the virus. The frequency can lead to drug toxicity. Plus, HIV mutates and becomes drug-resistant.

Wu and his team are working at finding out how much genistein is needed to inhibit HIV. It’s possible that plants may not have high enough levels, so drugs would need to be developed, Wu says.

Wu’s research is feeling the financial squeeze these days due to sequestration and budget cuts within the National Institutes of Health, he says. His lab has turned to novel ways to fund the HIV research, including the genistein project. A bicycle ride dubbed NYC DC AIDS Research Ride raised money for Wu’s lab a few years ago and has stepped up its efforts with a new fundraiser.

Other George Mason researchers on the genistein project include Jia Guo, Taban Rasheed, Alyson Yoder, Dongyang Yu, Huizhi Liang, Fei Yi and Todd Hawley.Xuehua Xu and Tian Jin from the National Institute of Allergy and Infectious Diseases in Rockville, Md., and Binhua Ling from Tulane University Health Sciences Center are also working on the research.

Methamphetamine increases susceptibility to deadly fungal infection

Methamphetamine use can make a person more susceptible to the lung infection cryptococcosis, according to a study published in mBio®, the online open-access journal of the American Society for Microbiology.

Researchers found that injected methamphetamine (METH) significantly enhanced colonization of the lungs by Cryptococcus neoformans and accelerated progression of the disease and the time to death in mouse models. C. neoformans is usually harmless to healthy individuals, but METH causes chinks in the blood-brain barrier that can permit the fungus to invade the central nervous system, where it causes a deadly brain infection.

“The highest uptake of the drug is in the lungs,” says corresponding author Luis Martinez of Long Island University-Post, in Brookville, New York and of Albert Einstein College of Medicine in The Bronx. “This may render the individual susceptible to infection. We wanted to know how METH would alter C. neoformans infection.”

Thirteen million people in the US have abused METH in their lifetimes, and regular METH users numbered approximately 353,000 in 2010, the most recent year for which data are available. A central nervous system stimulant that adversely impacts immunological responses, recent studies show that injected METH accumulates in various sites in the body, but the lungs seem to accumulate the highest concentrations, says Martinez, which could well impact how the lung responds to invading pathogens.

To study the impact this accumulation might have on pulmonary infection, Martinez and his colleagues injected mice with doses of METH over the course of three weeks, then exposed those mice to the C. neoformans fungus. In humans, C. neoformans initially infects the lungs but often crosses the blood-brain barrier to infect the central nervous system and cause meningitis. In their experiments, METH significantly accelerated the speed with which the infected mice died, so that nine days after infection, 100% of METH treated mice were dead, compared to 50% of the control mice.

Using fluorescent microscopy to examine lung tissue in METH-treated and control mice, the researchers found that METH enhanced the interaction of C. neoformans with epithelial cells in the lining of the lung. Seven days after exposure to the fungus, the lungs of METH-treated mice showed large numbers of fungi surrounded by vast amounts of gooey polysaccharide in a biofilm-like arrangement. METH-treated mice also displayed low numbers of inflammatory cells early during infection and breathed faster than controls, a sign of respiratory distress.

Martinez says this greater ability to cause disease in the lung may be due in part to simple electrical attraction. Their analysis shows that METH imparts a greater negative charge on the surface of the fungal cells, possibly lending them a greater attraction to the surface of the lung and an enhanced ability to form a biofilm that can protect its members from attack by the immune system. The fungus also releases more of its capsular polysaccharide in METH-treated mice, which can help the organism colonize and persist in the lung.

“When the organism senses the drug, it basically modifies the polysaccharide in the capsule. This might be an explanation for the pathogenicity of the organism in the presence of the drug, but it also tells you how the organism senses the environment and that it will modify the way that it causes disease,” Martinez says.

But the fungus doesn’t stop in the lungs. “The drug stimulates colonization and biofilm formation in the lungs of these animals,” says Martinez. “And this will follow to dissemination to the central nervous system by the fungus.”

C. neoformans in the lung moved on to the bloodstream and then into the central nervous system. The brains of METH-treated mice had higher numbers of C. neoformans cells, greater quantities of the fungus’ polysaccharide, and larger lesions than control mice, indicating that METH has a detrimental effect on the blood-brain barrier, permitting the pathogen to cross more easily from the bloodstream to infect the central nervous system.

“METH-induced alterations to the molecules responsible to maintain the integrity of the blood-brain barrier provide an explanation for the susceptibility of METH abuser to brain infection by HIV and other pathogens,” write the authors.

Martinez and his colleagues plan to follow up on the work by investigating how aspects of the immune system might be involved in changes the drug causes to the blood-brain barrier.

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mBio® is an open access online journal published by the American Society for Microbiology to make microbiology research broadly accessible. The focus of the journal is on rapid publication of cutting-edge research spanning the entire spectrum of microbiology and related fields. It can be found online at http://mbio.asm.org.

The American Society for Microbiology is the largest single life science society, composed of over 39,000 scientists and health professionals. ASM’s mission is to advance the microbiological sciences as a vehicle for understanding life processes and to apply and communicate this knowledge for the improvement of health and environmental and economic well-being worldwide.

Exercise May be the Best Medicine for Alzheimer’s

 

July 30, 2013

Kelly Blake 301-405-9418

COLLEGE PARK, Md. – New research out of the University of Maryland School of Public Health shows that exercise may improve cognitive function in those at risk for Alzheimer’s by improving the efficiency of brain activity associated with memory. Memory loss leading to Alzheimer’s disease is one of the greatest fears among older Americans. While some memory loss is normal and to be expected as we age, a diagnosis of mild cognitive impairment, or MCI, signals more substantial memory loss and a greater risk for Alzheimer’s, for which there currently is no cure.

The study, led by Dr. J. Carson Smith, assistant professor in the Department of Kinesiology, provides new hope for those diagnosed with MCI. It is the first to show that an exercise intervention with older adults with mild cognitive impairment (average age 78) improved not only memory recall, but also brain function, as measured by functional neuroimaging (via fMRI). The findings are published in the Journal of Alzheimer’s Disease.

“We found that after 12 weeks of being on a moderate exercise program, study participants improved their neural efficiency – basically they were using fewer neural resources to perform the same memory task,” says Dr. Smith. “No study has shown that a drug can do what we showed is possible with exercise.”

Recommended Daily Activity: Good for the Body, Good for the Brain

Two groups of physically inactive older adults (ranging from 60-88 years old) were put on a 12-week exercise program that focused on regular treadmill walking and was guided by a personal trainer.  Both groups – one which included adults with MCI and the other with healthy brain function – improved their cardiovascular fitness by about ten percent at the end of the intervention. More notably, both groups also improved their memory performance and showed enhanced neural efficiency while engaged in memory retrieval tasks.

The good news is that these results were achieved with a dose of exercise consistent with the physical activity recommendations for older adults. These guidelines urge moderate intensity exercise (activity that increases your heart rate and makes you sweat, but isn’t so strenuous that you can’t hold a conversation while doing it) on most days for a weekly total of 150 minutes.

Measuring Exercise’s Impact on Brain Health and Memory

One of the first observable symptoms of Alzheimer’s disease is the inability to remember familiar names. Smith and colleagues had study participants identify famous names and measured their brain activation while engaged in correctly recognizing a name – e.g., Frank Sinatra, or other celebrities well known to adults born in the 1930s and 40s. “The task gives us the ability to see what is going on in the brain when there is a correct memory performance,” Smith explains.

Tests and imaging were performed both before and after the 12-week exercise intervention. Brain scans taken after the exercise intervention showed a significant decrease in the intensity of brain activation in eleven brain regions while participants correctly identified famous names. The brain regions with improved efficiency corresponded to those involved in the pathology of Alzheimer’s disease, including the precuneus region, the temporal lobe, and the parahippocampal gyrus.

The exercise intervention was also effective in improving word recall via a “list learning task,” i.e., when people were read a list of 15 words and asked to remember and repeat as many words as possible on five consecutive attempts, and again after a distraction of being given another list of words.

“People with MCI are on a very sharp decline in their memory function, so being able to improve their recall is a very big step in the right direction,” Smith states.

The results of Smith’s study suggest that exercise may reduce the need for over-activation of the brain to correctly remember something.  That is encouraging news for those who are looking for something they can do to help preserve brain function.

Dr. Smith has plans for a larger study that would include more participants, including those who are healthy but have a genetic risk for Alzheimer’s, and follow them for a longer time period with exercise in comparison to other types of treatments. He and his team hope to learn more about the impact of exercise on brain function and whether it could delay the onset or progression of Alzheimer’s disease.

Study finds evidence of nerve damage in around half of fibromyalgia patients

Small study could lead to identification of treatable diseases for some with chronic pain syndrome

About half of a small group of patients with fibromyalgia – a common syndrome that causes chronic pain and other symptoms – was found to have damage to nerve fibers in their skin and other evidence of a disease called small-fiber polyneuropathy (SFPN). Unlike fibromyalgia, which has had no known causes and few effective treatments, SFPN has a clear pathology and is known to be caused by specific medical conditions, some of which can be treated and sometimes cured. The study from Massachusetts General Hospital (MGH) researchers will appear in the journal Pain and has been released online.

“This provides some of the first objective evidence of a mechanism behind some cases of fibromyalgia, and identifying an underlying cause is the first step towards finding better treatments,” says Anne Louise Oaklander, MD, PhD, director of the Nerve Injury Unit in the MGH Department of Neurology and corresponding author of the Pain paper.

The term fibromyalgia describes a set of symptoms – including chronic widespread pain, increased sensitivity to pressure, and fatigue – that is believed to affect 1 to 5 percent of individuals in Western countries, more frequently women. While a diagnosis of fibromyalgia has been recognized by the National Institutes of Health and the American College of Rheumatology, its biologic basis has remained unknown. Fibromyalgia shares many symptoms with SFPN, a recognized cause of chronic widespread pain for which there are accepted, objective tests.

Designed to investigate possible connections between the two conditions, the current study enrolled 27 adult patients with fibromyalgia diagnoses and 30 healthy volunteers. Participants went through a battery of tests used to diagnose SFPN, including assessments of neuropathy based on a physical examination and responses to a questionnaire, skin biopsies to evaluate the number of nerve fibers in their lower legs, and tests of autonomic functions such as heart rate, blood pressure and sweating.

The questionnaires, exam assessments, and skin biopsies all found significant levels of neuropathy in the fibromyalgia patients but not in the control group. Of the 27 fibromyalgia patients, 13 had a marked reduction in nerve fiber density, abnormal autonomic function tests or both, indicating the presence of SFPN. Participants who met criteria for SFPN also underwent blood tests for known causes of the disorder, and while none of them had results suggestive of diabetes, a common cause of SFPN, two were found to have hepatitis C virus infection, which can be successfully treated, and more than half had evidence of some type of immune system dysfunction.

“Until now, there has been no good idea about what causes fibromyalgia, but now we have evidence for some but not all patients. Fibromyalgia is too complex for a ‘one size fits all’ explanation,” says Oaklander, an associate professor of Neurology at Harvard Medical School. “The next step of independent confirmation of our findings from other laboratories is already happening, and we also need to follow those patients who didn’t meet SFPN criteria to see if we can find other causes. Helping any of these people receive definitive diagnoses and better treatment would be a great accomplishment.”

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Other authors of the Pain report are Zeva Daniela Herzog, Heather Downs and Max Klein, PhD, all of MGH Neurology. Preliminary results of the study were presented at the 2012 American Neurological Association meeting, and it was supported by Public Health Service grants NINDS K24NS059892 and UIL RR025758, Department of Defense grant GW093049, and a donation from Jane Cheever Powell.

Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $775 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.

Blocking sugar intake may reduce cancer risk or progression in obese and diabetic people

Findings reveal why patients with metabolism-related diseases are at higher risk for aggressive tumors

Blocking dietary sugar and its activity in tumor cells may reduce cancer risk and progression, according to researchers from the Icahn School of Medicine. The study, conducted in fruit flies and published in the journal Cell, provides insight as to why metabolism-related diseases such as diabetes or obesity are associated with certain types of cancer, including pancreatic, breast, liver, and colon cancers.

Ross Cagan, PhD, Professor of Developmental and Regenerative Biology at Mount Sinai, has developed a cancer model in the fruit fly Drosophila that allows scientists to evaluate diseases in the context of the whole animal and multiple genetic targets, rather than just looking at the connection of one gene to one disease. In the current study, Dr. Cagan used fruit flies to understand the effects of diet and insulin resistance on cancer progression.

Cells use glucose for energy and to grow. When a cell becomes insulin resistant, glucose builds up in the blood instead of being absorbed by the cell, starving the cell and leading to metabolic diseases like diabetes. Because of this dysfunctional growth, scientists have been puzzled about how tumors can thrive in an insulin-resistant environment.

“Previous research has established a strong correlation between metabolic diseases and pancreatic, breast, liver, and colon cancers, but we have not determined how tumors grow so aggressively in this environment if they do not have the energy provided by glucose,” said Dr. Cagan, who is also Associate Dean of the Graduate School of Biomedical Sciences at Mount Sinai. “Using our fruit fly model, we discovered how tumors overcome insulin resistance in the body and turn metabolic dysfunction to their advantage.”

Dr. Cagan and his team engineered fruit flies to express Ras and Src, two important oncogenes, resulting in the development of small head tumors. Next, they fed the flies with a high-sugar diet that promoted insulin resistance. They found that high dietary sugar acts together with Ras and Src to increase insulin sensitivity specifically in tumor cells. By ramping up signaling of an important pathway called Wingless/Wnt, they increased tumor cells’ insulin receptors to further promote insulin sensitivity. This cascade of activity changed these small, weak tumors and caused them to begin growing aggressively.

Armed with three new drug targets—glucose, the Ras/Src oncogenes, and Wingless/Wnt signaling—Dr. Cagan and his team identified compounds that can block the process. They treated the flies with acarbose, a treatment for diabetes; a compound called AD81; and a drug called pyrvinium. Acarbose blocked sugar conversion to glucose; AD81 cut off Ras/Src and caused cell death; and pyrvinium inhibited Wingless/Wnt signaling. Taken together, this cocktail of drugs substantially reduced tumor size and progression.

“Our study shows that sugar activates oncogenes in the tumor, which then promote insulin sensitivity, meaning that the exorbitant glucose levels in the blood pour into the tumor, having nowhere else to go in the insulin-resistant body,” said Dr. Cagan. “We have identified a three-drug combination that stops this signaling activity and tumor growth in its tracks, without affecting normal cell function.”

Next, the research team plans to find out whether the same cascade of events is happening in humans with insulin resistance using tumor samples. Based on those findings, Dr. Cagan and his team will test compounds that exploit this oncogene/sugar cascade.

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Fatty acids could aid cancer prevention and treatment

Omega-3 fatty acids, contained in oily fish such as salmon and trout, selectively inhibit growth and induce cell death in early and late-stage oral and skin cancers, according to new research from scientists at Queen Mary, University of London.

In vitro tests showed omega-3 fatty acids induced cell death in malignant and pre-malignant cells at doses which did not affect normal cells, suggesting they have the potential to be used in both the treatment and prevention of certain skin and oral cancers. Omega-3 polyunsaturated fatty acids cannot be made by humans in large quantities and so we must acquire them from our diet.

The scientists were studying a particular type of cancer called squamous-cell carcinoma (SCC). Squamous cells are the main part of the outermost layers of the skin, and SCC is one of the major forms of skin cancer. However, squamous cells also occur in the lining of the digestive tract, lungs, and other areas of the body. Oral squamous cell carcinomas (OSCC) are the sixth most common cancer worldwide and are difficult and very expensive to treat.

In the experiments, the scientists grew cell cultures in the lab from several different cells lines to which they added fatty acids. The cell lines included both malignant oral and skin SCCs, along with pre-malignant cells and normal skin and oral cells. Professor Kenneth Parkinson, Head of the Oral Cancer Research Group at Queen Mary’s Institute of Dentistry, said: “We found that the omega-3 fatty acid selectively inhibited the growth of the malignant and pre-malignant cells at doses which did not affect the normal cells.

“Surprisingly, we discovered this was partly due to an over-stimulation of a key growth factor (epidermal growth factor) which triggered cell death. This is a novel mechanism of action of these fatty acids.”

While previous research has linked omega-3 fatty acids with the prevention of a number of cancers, there has been very little work done on oral cancers or normal cells.

Dr Zacharoula Nikolakopoulou, carried out the research while studying her PhD at Queen Mary, under the supervision of Professor Parkinson and Professor Adina Michael-Titus, who is co-ordinating a programme of work on the protection of the nervous system with omega-3 fatty acids, in the Centre for Neuroscience and Trauma at Queen Mary’s Blizard Institute.

Dr Nikolakopoulou said: “As the doses needed to kill the cancer cells do not affect normal cells, especially with one particular fatty acid we used called Eicosapentaenoic acid (EPA), there is potential for using omega-3 fatty acids in the prevention and treatment of skin and oral cancers.

“It may be that those at an increased risk of such cancers – or their recurrence – could benefit from increased omega-3 fatty acids. Moreover, as the skin and oral cancers are often easily accessible, there is the potential to deliver targeted doses locally via aerosols or gels. However further research is needed to define the appropriate therapeutic doses.”

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Illinois scientists put cancer-fighting power back into frozen broccoli

URBANA, Ill. – There was bad news, then good news from University of Illinois broccoli researchers this month. In the first study, they learned that frozen broccoli lacks the ability to form sulforaphane, the cancer-fighting phytochemical in fresh broccoli. But a second study demonstrated how the food industry can act to restore the frozen vegetable’s health benefits.

“We discovered a technique that companies can use to make frozen broccoli as nutritious as fresh. That matters because many people choose frozen veggies for their convenience and because they’re less expensive,” said Elizabeth Jeffery, a U of I professor of nutrition.

“Whenever I’ve told people that frozen broccoli may not be as nutritious as fresh broccoli, they look so downcast,” she added.

As little as three to five servings of broccoli a week provides a cancer-protective benefit, but that isn’t true for bags of broccoli that you pluck out of your grocery’s freezer, she noted.

The problem begins when soon-to-be-frozen broccoli is blanched, or heated to high temperatures, to inactivate enzymes that can cause off-colors, tastes, and aromas during the product’s 18-month shelf life, she explained.

The extreme heat destroys the enzyme myrosinase, which is necessary to form sulforaphane, the powerful cancer-preventive compound in broccoli, she said.

“We know this important enzyme is gone because in our first study we tested three commercially frozen broccoli samples before and after cooking. There was very little potential to form sulforaphane before the frozen broccoli was cooked and essentially none after it was cooked as recommended,” said Edward B. Dosz, a graduate student in Jeffery’s laboratory.

In the second study, the researchers experimented with blanching broccoli at slightly lower temperatures instead of at 86ºC, the current industry standard. When they used a temperature of 76ºC, 82 percent of the enzyme myrosinase was preserved without compromising food safety and quality.

Sulforaphane is formed when fresh broccoli is chopped or chewed, bringing its precursor glucoraphanin and the enzyme myrosinase into contact with each other. The researchers first thought that thawing frozen broccoli in the refrigerator might rupture the plant’s cells and kick-start the enzyme–substrate interaction. It didn’t work, Dosz said.

But they had previously had success using other food sources of myrosinase to boost broccoli’s health benefits. So the researchers decided to expose frozen broccoli to myrosinase from a related cruciferous vegetable.

When they sprinkled 0.25 percent of daikon radish—an amount that’s invisible to the eye and undetectable to our taste buds—on the frozen broccoli, the two compounds worked together to form sulforaphane, Dosz said.

“That means that companies can blanch and freeze broccoli, sprinkle it with a minute amount of radish, and sell a product that has the cancer-fighting component that it lacked before,” he said.

One question remained: Would sulforaphane survive the heat of microwave cooking? “We were delighted to find that the radish enzyme was heat stable enough to preserve broccoli’s health benefits even when it was cooked for 10 minutes at 120ºF. So you can cook frozen broccoli in the microwave and it will retain its cancer-fighting capabilities,” Dosz said.

Jeffery hopes that food processors will be eager to adopt this process so they can market frozen broccoli that has all of its original nutritional punch.

Until they do, she said that consumers can spice up their frozen, cooked broccoli with another food that contains myrosinase to bring the cancer-fighting super-food up to nutritional speed.

“Try teaming frozen broccoli with raw radishes, cabbage, arugula, watercress, horseradish, spicy mustard, or wasabi to give those bioactive compounds a boost,” she advised.

Diets of Pregnant Women Contain Harmful, Hidden Toxins

UC Riverside study suggests that prenatal health care professionals do more to advise patients to avoid tap water, certain types of fish, caffeine, and canned goods that may put developing babies at risk

By Bettye Miller on August 6, 2013

A UCR study finds that amid healthy foods consumed by pregnant women are others that contain hidden toxins.

RIVERSIDE, Calif. — Pregnant women regularly consume food and beverages containing toxins believed to pose potential risks to developing fetuses, according to researchers at  the University of California, Riverside, suggesting that health care providers must do more to counsel their patients about the dangers of hidden toxins in the food supply.

In a peer-reviewed study published in the July issue of Nutrition Journal — “Consumption habits of pregnant women and implications for developmental biology: a survey of predominantly Hispanic women in California” — a team of psychologists from UC Riverside and UC San Diego found that the diets of pregnant Hispanic women included tuna, salmon, canned foods, tap water, caffeine, alcohol and over-the-counter medications that contain substances known to cause birth defects.

The study is unique in that it highlights the unseen dangers of consuming toxins in food and beverages that are not typically thought of as unhealthy for a fetus, said Sarah Santiago, a Ph.D. student in psychology at UCR. It also contributes to the body of literature aimed at assessing dietary habits of both Hispanic and non-Hispanic pregnant women.

“Unlike alcohol and nicotine, which carry a certain stigma along with surgeon general warnings on the packaging, tuna, canned foods, caffeine, and a handful of other foods and beverages with associated developmental effects are not typically thought of as unsafe,” Santiago explained. “Hopefully, this study will encourage health care providers to keep pregnant women well informed as to the possible dangers of unhealthy consumption habits.”

The research team — Kelly Huffman, assistant professor of psychology at UC Riverside and the paper’s senior author; Santiago; and UCSD undergraduate student Grace Park — surveyed 200 pregnant or recently pregnant women at a private medical group in Downey, Calif., between December 2011 and December 2012. The women ranged in age from 18 to about 40, with Hispanic women accounting for 87 percent of the group. Nearly all had a high school degree, and about one-fourth had a college or post-graduate degree. More than two-thirds had an annual income of $50,000 or less.

Using a food questionnaire, participants reported how often and when during their pregnancy they ate certain foods, drank certain beverages, and ingested prescription and over-the-counter medications. Nearly all of the women reported eating meat while pregnant, with about three-quarters of them eating fish, typically tuna, tilapia and salmon. All reported eating fresh fruit, but fewer than one-third ate the recommended amount of more than one serving a day. Three-fourths ate canned goods, particularly fruits, vegetables and soup. Most reported drinking water, with 12 percent consuming tap water. Eighty percent consumed caffeinated beverages, and about 6 percent reported drinking alcohol sometime during their pregnancy. Most reported taking prenatal vitamins. Nearly half reported taking an over-the-counter medication — primarily acetaminophen — at least once and most reported taking prescription medications at least once.

The results are concerning, the researchers said.

“Consumption of tuna, salmon, canned goods, sugary desserts, fast foods, and drinking of tap water, caffeinated  beverages, and alcoholic beverages during pregnancy have been deemed unhealthy due to the appearance of environmental toxins found to have harmful effects in the developing offspring,” the researchers wrote.

Tuna contains methylmercury, and prenatal exposure has been associated with numerous developmental deficits involving attention, verbal learning, motor function and delayed performance. “Staggering” levels of polychlorinated biphenyls (PCBs) have been found in farmed salmon. Prenatal exposure to PCBs has been linked to lower birth weights, smaller head circumferences, and abnormal reflex abilities in newborns and to mental impairment in older children. Metal food cans are lined with a plastic that contains Bisphenol A (BPA), which leaches from the lining in cans into the food. Prenatal exposure to BPA has been associated in animal studies with hyperactivity, aggression and reproductive problems.

“This study has found that income is inversely correlated with canned food consumption, suggesting that women of low socio-economic status in particular may be especially at risk,” the UC Riverside psychologists found.

Tap water also contains prenatal toxins. In Downey, eight pollutants found in drinking water exceed the health guidelines set by federal and state agencies. Some of those contaminants are known to result in central nervous system defects, oral cleft defects, neural tube defects, low birth weight and risk of fetal death, the researchers said. Pregnant women should be encouraged to drink filtered or bottled water in areas where contamination levels are high, they advised.

Also problematic was the level of caffeine consumption, the research team found. Caffeine consumed during pregnancy is associated with fetal mortality, birth defects and decreased birth weights. Animal studies have found developmental delays, abnormal neuromotor activity, and neurochemical disruptions.

A handful of women in the study — 5.8 percent — reported drinking alcohol at some time during their pregnancy, less than the national estimate of 7.6 percent. Maternal drinking rates are highest among white women ages 35 to 44.

“We do not know whether this is something unique to Hispanic women, or ubiquitous among women of multiple ethnicities,” the researchers wrote. “The implications of this research are twofold:  Women of childbearing age hoping to conceive should be advised to eliminate all alcohol consumption, as effects of maternal drinking have dire consequences in the first trimester when the mother may not know she is pregnant. … It is also clear that prenatal medical professionals should discourage the consumption of dangerous foods, beverages and medications that women commonly report consuming during pregnancy.”

Not enough research has been conducted on certain substances to merit fail-proof labels of teratogenicity — that is, whether a substance causes developmental malformations. “Because regulation of prenatal consumption demands a very high level of evidence of teratogenicity, little-researched substances often go unregulated and health care professionals assume they are healthy,” Santiago explained. “The problem could also lie in reduced access to health care, or time constraints in prenatal consultations. Perhaps health care providers are informed, but fail to pass the information on to their clients for lack of time or because they assume the clients are already informed.”

Teratogenic substances often have subtle, though serious, effects that manifest later in development. “Research suggesting that a given substance does not cause physical abnormalities at birth may be misinterpreted as a green light for consumption — a grave mistake, considering that other research may exist demonstrating the long-term neural or behavioral abnormalities that result from consuming that substance during pregnancy,” Santiago added.

The research team continues to collect data on beliefs and attitudes about consumption of these substances during pregnancy in a search for clues as to why women continue to eat these substances, and where in the system interventions would be most appropriate.

L-3-n-butylphthalide protects against cognitive dysfunction in vascular dementia

3-N-butylphthalide, a green botanical medicine, is a successfully synthesized and stable chemical drug used for the treatment of ischemic stroke that has independent intellectual property rights in China. The first L-isomer, originally extracted from celery seed, was artificially synthesized from racemic acid, also known as butylphthalide. L-3-n-butylphthalide has been shown to reduce β-amylase-induced neuronal apoptosis and improve cognitive function in Alzheimer’s disease animal models. As a neuroprotective drug for cerebrovascular disease, 3-n-butylphthalide has been confirmed to protect nerve cells in animal experiments of stroke. Because of the significant effects of l-3-n-butylphthalide in the clinical treatment of acute ischemic stroke, Yaping Wei and colleagues from Hebei Medical University also adopted l-3-n-butylphthalide for the treatment of vascular dementia. These researchers are the first to report that pretreatment with l-3-n-butylphthalide can improve cognitive deficits and neuronal loss in the hippocampus of cerebral repetitive ischemia/reperfusion mice. L-3-n-butylphthalide may be a potentially beneficial and promising drug for the treatment and prevention of vascular dementia through upregulation of Akt expression in the hippocampus. These results are published in the Neural Regeneration Research (Vol. 8, No. 19, 2013).

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These reports are done with the appreciation of all the Doctors, Scientist, and other Medical Researchers who sacrificed their time and effort. In order to give people the ability to empower themselves. Without base aspirations of fame, or fortune. Just honorable people, doing honorable things.

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