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Saturday 28 December 2013

New study: High mortality in US Central Southern states most likely due to smoking

 

NEW YORK (26 December 2013) — Between 1965 and 2004, the distribution of states with the highest mortality changed dramatically. In 1965, the states with the highest mortality (Rhode Island, Alaska, Delaware, Pennsylvania, and New Hampshire) were spread across geographic regions. By 2004, however, the states with the highest mortality were geographically contiguous, and located in the south. The Central South (Alabama, Kentucky, Mississippi, and Tennessee) had the highest mortality rates in the United States. A new study by Andrew Fenelon of Brown University explores the possibility that smoking behaviors account for this situation.
Fenelon used US mortality data from vital statistics on cause of death for the period 1965-2004 and, for the purposes of this study, considered lung cancer deaths to be indicative of cigarette smoking. In the US, more than 90 percent of lung cancer deaths among men and more than 80 percent among women result from smoking. Although the prevalence of smoking declined in all states in that time period, southern states, particularly Kentucky, have maintained overall high levels of smoking.
Fenelon found that in the Central South, mortality attributable to smoking peaked later than in other regions and at a significantly higher death rate, indicating a greater and more persistent burden of smoking. By 2004, the gap in mortality attributable to smoking between the Central Southern states and states in other regions was exceptionally large: among men, smoking explained as much as 75 percent of the difference between the Central South and other US regions.
Laws and policies in the Central South do not strongly discourage smoking. There are currently 10 states with no statewide ban on smoking (for example, in workplaces or restaurants); nearly all of these states are in the South. State taxes on tobacco products also remain low in the Central Southern states compared to other states with lower mortality from smoking. Studies have shown that smoking bans and tobacco taxes reduce the prevalence of smoking.
This study highlights geographic inequalities in health and mortality within the US and underscores the importance of narrowing these gaps as a public policy goal.
Source:Population Council

EU Considering a Ban on Danish Cinnamon Rolls

The European Union is considering a ban on Danish cinnamon rolls, or kanelsnegler, after finding that they contain very high levels of cinnamon, which could prove to be harmful for the liver.The 2008 EU regulations limited the amount of cinnamon to 5 and 50 milligrams per kilogram of food. The EU revealed that excess consumption of coumarin, a naturally occurring toxic chemical found in cassia cinnamon, could lead to liver damage. 
A recent study conducted by Danish Food Administration has found that the amount of cinnamon in kanelsnegler exceeds the maximum limit. While Denmark can ignore the EU regulation, with EU countries allowed the freedom to retain certain food privileges for the sake of tradition, the government has gone ahead with plans to restrict cinnamon levels to 15 mg per kilogram of baked products. The move has unsurprisingly drawn criticism from Danish bakers who say that it will be the end of cinnamon rolls as they know it. "Cinnamon rolls are of course a traditional Danish baked product. There is no point in limiting cinnamon. We have used it in Danish baking for as long as I can remember. It's the end of the cinnamon roll as we know it", Hardy Christensen, head of the Danish Baker's Association, said.
 Source:Danish Baker's Association

Survey Says Widows Better Off on Wellbeing Index

 Survey Says Widows Better Off on Wellbeing IndexIn a latest survey by National Australia Bank Wellbeing Index, widowed people have higher levels of well-being than married couples.

Women aged 18 to 29 are the unhappiest age group, added the survey.

When it comes to marital status, widows and widowers had the highest levels of well-being, the survey, that included 2,100 Australians, showed.

"In particular, mental well-being, feeling part of the community and physical health are significantly stronger contributors to the well-being of widows when compared to married couples," NAB economists were quoted as saying in Herald Sun.

Those with no children reported higher levels of well-being than those with children, while the highest earners were happier than those on lower incomes.

Those in regional cities reported the highest levels of well-being, compared with people in capital cities and rural areas, the survey added.

When it comes to age, women aged 18 to 29 reported the lowest levels of wellbeing while women aged 50-plus reported the highest levels.

 Source:Herald Sun.

 

Chitosan Molecule Improves Nerve Cell Adherence

 Chitosan Molecule Improves Nerve Cell AdherenceNerve cell adherence and growth along the surface of a material can now be promoted by the chitosan molecule. It can enhance the adherence and influx of Schwann cells, thus encouraging the growth of axons.
However, physical nerve guidance by a nerve conduit may not be sufficient to foster optimal recovery. Dr. Huawei Liu and colleagues from Institute of Stomatology, Chinese PLA General Hospital in China prepared microspheres containing nerve growth factor for sustained release by a compound method, and implanted them into chitosan conduits to repair 10-mm defects on the right buccal branches of the facial nerve in rabbits.

Researchers found that the sustained in vitro release of active nerve growth factor lasted for at least 90 days. The muscular atrophy induced by facial nerve defects was attenuated, and the nerve conduction velocity and amplitude were significantly increased. Moreover, microspheres for sustained release of nerve growth factor in combination with chitosan conduits improved axon and myelin sheath regeneration of injured facial nerve.

These findings, published in the Neural Regeneration Research (Vol. 8, No. 33, 2013), indicate that the combination of nerve growth factor-releasing microspheres and chitosan conduits exhibits superior effects in repairing facial nerve injury compared with nerve growth factor alone.

 Source:Neural Regeneration Research
 

Study Shows How Plants Evolved to Survive Cold Winters

 Study Shows How Plants Evolved to Survive Cold WintersResearchers have studied how flowering plants evolve specific strategies, like the seasonal shedding of leaves, to move into areas with cold winters, say researchers.
Early flowering plants are thought to have been woody-which maintain a prominent stem above ground across years and changing weather conditions, such as maple trees-and restricted to warm, wet tropical environments.

Lead author Amy Zanne, assistant professor of biology in the George Washington University's Columbian College of Arts and Sciences, said freezing is like a plant's equivalent to frostbite, asserting that their water-conducting pipes can be blocked by air bubbles as water freezes and thaws, and over time, if plants moved into colder climates, they've had to figure out how to get around these problems.

Dr. Zanne and a team of researchers identified three repeated evolutionary shifts they believe flowering plants made to fight the cold. Plants either:

dropped their leaves seasonally, shutting down the pathways that would normally carry water between roots and leaves;

made skinnier water-conducting pathways, allowing them to keep their leaves while reducing the risk of air bubbles developing during freezing and thawing, which would shut down those pathways (the fatter the pathways, the higher the risk); or

avoided the cold seasons altogether as herbs, losing aboveground stems and leaves and retreating as seeds or storage organs underground, such as tulips or tomatoes.

Source:The results have been published in journal Nature.

 

Friday 27 December 2013

Cancer-promoting protein is vital to safe division of tumor cells

PKM2 controls mitosis, saving cancer cells from death and promoting brain tumor growth

HOUSTON – Researchers have caught a protein they previously implicated in a variety of cancer-promoting roles performing a vital function in cell division, survival and development of brain tumors.
In a paper published in Molecular Cell, Zhimin Lu, Ph.D., professor of Neuro-Oncology at The University of Texas MD Anderson Cancer Center and colleagues report how a tumor-specific protein flips a crucial switch in an irregular mechanism for mitosis that allows cancer cells to safely divide.
"Our research shows that tumor cells rely heavily on a distinct mechanism for orderly cell division that's driven by oncogene-induced pyruvate kinase M2," Lu said.
After a cell begins division by replicating all of its chromosomes, mitosis separates them into two identical sets of chromosomes for both cells. After mitosis, cytokinesis completes cell divison.
"Without PKM2 regulating a checkpoint in mitosis, the tumor cell would not successfully divide," Lu said. "Depleting PKM2 led to an uneven distribution of DNA to the two new cells, triggering programmed cell death, or apoptosis, of those cells after division."
"This new, additional role for PKM2 in cancer development and survival may provide a molecular basis for diagnosing and treating tumors with upregulated PKM2," Lu said. He and his colleagues have now identified four specific mechanisms by which PKM2 promotes cancer development.
PKM2 regulation of mitosis worsens tumors in mice; affects human glioblastoma


The key relationship between PKM2 activity and mitosis uncovered by the researchers led to rapid brain tumor growth when activated in mice, while blocking it reduced tumor volume by 83 percent and more than doubled survival from about 20 days to beyond 40 days.
Analysis of 50 human glioblastoma multiforme tumors and 50 lung cancer tumors confirmed the relationship in human cancer and indicated an effect on survival for patients with glioblastoma, the most common and lethal form of brain tumor.
PKM2 can act as a protein kinase, which gives orders to other proteins by attaching phosphate groups to them. While it plays a normal role in sugar metabolism, PKM2 also actively promotes cell growth during infancy when such growth is desired.
Usually, Lu said, it eventually turns off, but tumor cells reactivate PKM2, and it is famously overexpressed in solid tumors. This tumor-specific PKM2 is activated by the epidermal growth factor receptor (EGFR), which is overactive in a variety of cancers.
Deplete PKM2 in mitosis, tumor cells abnormally divide in multiple cancer types
A series of experiments in glioblastoma cell lines revealed that PKM2 phosphorylates a protein called Bub3, activating it to interact with others in a protein complex that assures orderly and equal chromosome separation.
Depleting PKM2 blocked Bub3 activation, leading to an increase in cells with abnormal numbers of chromosomes and programmed cell death.
The team confirmed its findings in human breast, prostate, lung, pancreatic and colon cancer cell lines.
PKM2-induced Bub3 activation was essential for development of brain tumors in mice. Experiments in the 50 glioblastoma and lung cancer tumors confirmed that phosphorylation of Bub3 correlates with phosphorylation of H3-S10, a marker of cell mitosis in tumor cells.
With low Bub3 phosphorylation, glioblastoma patients live longer Among the 50 glioblastoma patients, the 15 with low levels of Bub3 phosphorylation had a median survival of 69.8 weeks, compared to 40.5 weeks for the 35 patients with high levels of Bub3 activation.
Previous research by Lu and colleagues showed PKM2, usually active outside the cell nucleus, slips into the nucleus where it promotes cancer formation, growth and survival by:
  • Activating an important transcription co-factor that, in turn, activates other cancer-promoting genes.
  • Phosphorylating the histone protein H3, loosening the packaging of DNA and leading to the activation of cell division genes.
  • Inducing expression of glycolytic genes (including PKM2 itself) and triggering a glucose metabolism mechanism called the Warburg effect that nourishes tumor cells.
Potential avenues for thwarting these effects identified in their experiments include two classes of drug that inhibit SRC and MEK activity.
"Our research further highlights the importance of PKM2 in human cancers and of developing ways to target its activity and use it as a biomarker to guide treatment," Lu said.
Source:University of Texas M. D. Anderson Cancer Center

Proportion of opioid treatment programs offering on-site testing for HIV and STIs declines

A survey of opioid treatment programs finds that the proportion offering on-site testing for human immunodeficiency virus (HIV) and sexually transmitted infections (STIs) declined substantially between 2000 and 2011, despite guidelines recommending routine opt-out HIV testing in all health care settings, according to a study appearing in the December 25 issue of JAMA.
"Opioid dependence is a risk factor for HIV, STIs, and hepatitis C virus (HCV) infection. Opioid treatment programs, which provide treatment to more than 300,000 opioid-dependent individuals in the United States, are well-positioned to offer testing for these infectious diseases to a high-risk population. They were among the first venues to offer HIV testing and are more likely to offer HIV, STI, and HCV testing than other drug treatment programs. Private for-profit opioid treatment programs are increasingly widespread and such programs offer on-site HIV testing less often than nonprofit and public programs. However, with the 2006 national recommendations for routine opt-out HIV testing, we hypothesized that the percentage of programs offering on-site testing for HIV, STIs, and HCV would increase," the authors write.
Marcus A. Bachhuber, M.D., and Chinazo O. Cunningham, M.D., M.S., of the Albert Einstein College of Medicine, New York, analyzed data from a survey sent to directors of drug treatment facilities and tabulated the percentage of opioid treatment programs offering on-site HIV, STI, and HCV testing from 2000 to 2011.
The number of U.S. opioid treatment programs increased from 849 in 2000 to 1,175 in 2011. The percentage of programs operating as for-profit businesses increased from 43 percent to 54 percent, nonprofits decreased from 43 percent to 36 percent, and public programs decreased from 14 percent to 10 percent. From 2000 to 2011, the absolute number of programs offering testing for HIV, STIs, and HCV increased but the percentage offering on-site testing for HIV declined by 18 percent and for STIs by 13 percent. There was no change for HCV testing. More than 75 percent of public programs offered on-site testing for each infection, with no change over time.
"Declines were most pronounced in for-profit programs, suggesting that persons enrolled in these programs may be at increased risk for delayed diagnosis and continued transmission of HIV, STIs, and HCV," the authors write.
"Opioid treatment programs are important venues for offering testing to high-risk individuals. As the number of for-profit opioid treatment programs increases, and the opioid, HIV, and HCV epidemics continue to intersect, further work is needed to understand and reverse declines in offering on-site testing."
Source:JAMA

NIH study shows enzyme that produces melatonin originated 500 million years ago

An international team of scientists led by National Institutes of Health researchers has traced the likely origin of the enzyme needed to manufacture the hormone melatonin to roughly 500 million years ago.
Their work indicates that this crucial enzyme, which plays an essential role in regulating the body’s internal clock, likely began its role in timekeeping when vertebrates (animals with spinal columns) diverged from their nonvertebrate ancestors.
An understanding of the enzyme’s function before and after the divergence may contribute to an understanding of such melatonin-related conditions as seasonal affective disorder, jet lag, and to the understanding of disorders involving vision.
The findings provide strong support for the theory that the time-keeping enzyme originated to remove toxic compounds from the eye and then gradually morphed into the master switch for controlling the body’s 24-hour cyclic changes in function.
The researchers isolated a second, nonvertebrate form of the enzyme from sharks and other contemporary animals thought to resemble the prototypical early vertebrates that lived 500 million years ago.
The study, published online in PNAS, was conducted by senior author David C. Klein, Ph.D., Chief of the Section on Neuroendocrinology in the NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and colleagues at NIH, and at institutions in France, Norway, and Japan.
Melatonin is a key hormone that regulates the body’s day and night cycle. Dr. Klein explained that it is manufactured in the brain’s pineal gland and is found in small amounts in the retina of the eye. Melatonin is produced from the hormone serotonin, the end result of a multistep sequence of chemical reactions. The next-to-last step in the assembly process consists of attaching a small molecule — the acetyl group — to the nearly finished melatonin molecule. This step is performed by an enzyme called arylalkylamine N-acetyltransferase, or AANAT.
Because of its key role in producing the body clock-regulating melatonin, AANAT is often referred to as the timezyme, Dr. Klein added.
The form of AANAT found in vertebrates occurs in the brain’s pineal gland and, in small amounts, in the retina. Another form of the enzyme, termed nonvertebrate AANAT, has been found only in other forms of life, such as bacteria, plants and insects.
“Nonvertebrate AANAT appears to detoxify a broad range of potentially toxic chemicals,” Dr. Klein said. “In contrast, vertebrate AANAT is highly specialized for adding an acetyl group to melatonin. The two are as different from each another as a Ferrari is from a Model-T Ford, considering the speed of the reaction and how fast it can be turned on and off.”
In 2004, Dr. Klein and his coworkers published a theory that melatonin was at first a kind of cellular waste, a by-product created in cells of the eye when normally toxic substances were rendered harmless. Because melatonin accumulated at night, the ancestors of today's vertebrates became dependent on melatonin as a signal of darkness. As the need for greater quantities of melatonin grew, the pineal gland developed as a structure separate from the eyes, to keep serotonin and other toxic substances needed to make melatonin away from sensitive eye tissue.
“The pineal glands of birds and reptiles can detect light,” Dr. Klein said. “And the retinas of human beings and other species also make melatonin. So it would appear that both tissues evolved from a common, ancestral, light-detecting tissue.”
Before the current study, the researchers lacked proof of their theory, particularly in regard to the question of how the vertebrate form of the enzyme originated because it did not appear to exist in non-vertebrates and had been found only in bony fishes, reptiles, birds, and mammals — all of which lacked the non-vertebrate form.
The first evidence of how the vertebrate form of the enzyme originated came when study co-author Steven L. Coon, also of NICHD, discovered genes for the nonvertebrate and vertebrate forms of AANAT in genomic sequences from the elephant shark, considered to be a living representative of early vertebrates.
This finding indicated that the vertebrate form of AANAT may have resulted after a phenomenon known as gene duplication, Dr. Klein said. Gene duplication, he added, typically results from any of a number of genetic mishaps during cell division. Instead of one copy of a gene resulting from the process, an additional copy results, so that there are two versions of a gene where only one existed previously. The phenomenon is thought to be a major factor influencing evolutionary change.
The researchers theorized that following duplication, one form of AANAT remained unchanged and the other gradually evolved into the vertebrate form. Dr. Klein said that at some point after vertebrate AANAT developed, vertebrates appear to have stopped making the nonvertebrate form, perhaps because it was no longer needed or because its function was replaced by a similar enzyme.
Before the researchers could continue, they needed to confirm their finding, to rule out that the nonvertebrate AANAT they found didn’t result from accidental contamination with bacteria or some other organism. The NICHD researchers sought assistance from other research teams around the world. DNA from Mediterranean sharks and sea lampreys was obtained via fishermen’s catches by Jack Falcon of the Arago Laboratory, a marine biology facility that is part of the CNRS and the Pierre and Marie Curie University in France. Samples from a close relative of the elephant shark — the ratfish — were provided by Even-Jorgensen at the Arctic University of Norway. Finally, Susumo Hyodo of the University of Tokyo contributed samples from elephant sharks he collected off the coast of Australia.
Next, the Hyodo and Falcon groups isolated RNA from the retinas and pineal glands of the animals. RNA is used to direct the assembly of amino acids into proteins. From these RNA sequences, it was possible to assemble working versions of AANAT molecules — both the vertebrate and nonvertebrate forms.
The sequences of the proteins encoded by the AANAT genes were analyzed by Eugene Koonin and Yuri Wolf of the National Library of Medicine using computer techniques designed to study evolution. Peter Steinbach, of NIH’s Center for Information Technology, examined the three-dimensional structures of nonvertebrate and vertebrate AANAT in the study animals and determined that the two forms of the enzyme likely had a common ancestor.
Taken together, their results provide evidence for the hypothesis that nonvertebrate AANAT resulted from duplication of the non-vertebrate AANAT gene about 500 million years ago and that following this event one copy of the duplicated gene eventually changed into the gene for vertebrate AANAT.
In addition to providing information on the origin of melatonin and the evolution of AANAT, the findings also have implications for research on disorders affecting vision. Vertebrate AANAT and melatonin are found in small amounts in the eyes of humans and other vertebrates. Although they may play a role in detoxifying compounds, it is also reasonable to consider that this detoxifying function is shared with other enzymes.
“It’s possible that a malfunction in these other enzymes might lead to an accumulation of chemicals known as arylalkamines — in the same family as serotonin — and this might contribute to eye disease,” Dr. Klein said. “Consequently, research into how these enzymes function might lead to therapies to protect vision.”
The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation.
NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the US Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases.
Source:Pharmabiz

Excitement may be Better Than Relaxation When It Comes to Anxiety-Inducing Situations

People who try to get excited may be better able to face anxiety-inducing situations like public speaking, as opposed to individuals who try to relax, a new study found.
"Anxiety is incredibly pervasive. People have a very strong intuition that trying to calm down is the best way to cope with their anxiety, but that can be very difficult and ineffective," study author Alison Wood Brooks, PhD, of Harvard Business School, said.

"When people feel anxious and try to calm down, they are thinking about all the things that could go badly. When they are excited, they are thinking about how things could go well."

Several experiments conducted at Harvard University with college students and members of the local community showed that simple statements about excitement could improve performance during activities that triggered anxiety.

Since both anxiety and excitement are emotional states characterized by high arousal, it may be easier to view anxiety as excitement rather than trying to calm down to combat performance anxiety, Brooks said.

"When you feel anxious, you're ruminating too much and focusing on potential threats," she said. "In those circumstances, people should try to focus on the potential opportunities. It really does pay to be positive, and people should say they are excited. Even if they don't believe it at first, saying 'I'm excited' out loud increases authentic feelings of excitement."

Source:The study was published online in APA's Journal of Experimental Psychology: General.


 

Researchers Discover How Rho-associated Protein Kinase Modulates Neurite Extension

Thursday 26 December 2013

Study shows Where Alzheimer's starts and how it spreads

Using high-resolution functional MRI (fMRI) imaging in patients with Alzheimer's disease and in mouse models of the disease, Columbia University Medical Center (CUMC) researchers have clarified three fundamental issues about Alzheimer's: where it starts, why it starts there, and how it spreads. In addition to advancing understanding of Alzheimer's, the findings could improve early detection of the disease, when drugs may be most effective. The study was published today in the online edition of the journal Nature Neuroscience.
"It has been known for years that Alzheimer's starts in a brain region known as the entorhinal cortex," said co-senior author Scott A. Small, MD, Boris and Rose Katz Professor of Neurology, professor of radiology, and director of the Alzheimer's Disease Research Center. "But this study is the first to show in living patients that it begins specifically in the lateral entorhinal cortex, or LEC. The LEC is considered to be a gateway to the hippocampus, which plays a key role in the consolidation of long-term memory, among other functions. If the LEC is affected, other aspects of the hippocampus will also be affected."
The study also shows that, over time, Alzheimer's spreads from the LEC directly to other areas of the cerebral cortex, in particular, the parietal cortex, a brain region involved in various functions, including spatial orientation and navigation. The researchers suspect that Alzheimer's spreads "functionally," that is, by compromising the function of neurons in the LEC, which then compromises the integrity of neurons in adjoining areas.
A third major finding of the study is that LEC dysfunction occurs when changes in tau and amyloid precursor protein (APP) co-exist. "The LEC is especially vulnerable to Alzheimer's because it normally accumulates tau, which sensitizes the LEC to the accumulation of APP. Together, these two proteins damage neurons in the LEC, setting the stage for Alzheimer's," said co-senior author Karen E. Duff, PhD, professor of pathology and cell biology (in psychiatry and in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute.
In the study, the researchers used a high-resolution variant of fMRI to map metabolic defects in the brains of 96 adults enrolled in the Washington Heights-Inwood Columbia Aging Project (WHICAP). All of the adults were free of dementia at the time of enrollment.
"Dr. Richard Mayeux's WHICAP study enables us to follow a large group of healthy elderly individuals, some of whom have gone on to develop Alzheimer's disease," said Dr. Small. "This study has given us a unique opportunity to image and characterize patients with Alzheimer's in its earliest, preclinical stage."
The 96 adults were followed for an average of 3.5 years, at which time 12 individuals were found to have progressed to mild Alzheimer's disease. An analysis of the baseline fMRI images of those 12 individuals found significant decreases in cerebral blood volume (CBV) — a measure of metabolic activity — in the LEC compared with that of the 84 adults who were free of dementia.
A second part of the study addressed the role of tau and APP in LEC dysfunction. While previous studies have suggested that entorhinal cortex dysfunction is associated with both tau and APP abnormalities, it was not known how these proteins interact to drive this dysfunction, particularly in preclinical Alzheimer's.
To answer this question, explained first author Usman Khan, an MD-PhD student based in Dr. Small's lab, the team created three mouse models, one with elevated levels of tau in the LEC, one with elevated levels of APP, and one with elevated levels of both proteins. The researchers found that the LEC dysfunction occurred only in the mice with both tau and APP.
The study has implications for both research and treatment. "Now that we've pinpointed where Alzheimer's starts, and shown that those changes are observable using fMRI, we may be able to detect Alzheimer's at its earliest preclinical stage, when the disease might be more treatable and before it spreads to other brain regions," said Dr. Small. In addition, say the researchers, the new imaging method could be used to assess the efficacy of promising Alzheimer's drugs during the disease's early stages.
Source:Columbia University Medical Center

Why is Laughter Not Always the Best Medicine? A Serious Take on Laughter

Laughter may not be the best medicine, after all. The Christmas issue of British Medical Journal (BMJ), one of the world's oldest and most prestigious medical journals, takes a hard and serious take on laughter. Laugh related dangers range from asthma attacks to strokes, says the article. Laughter is not purely beneficial. The harms it can cause are immediate and dose related, the risks being highest for Homeric (uncontrollable) laughter," the authors wrote.

The authors delved deep into researches related to laughter that were published between 1946 and 2013; an analysis was drawn from nearly 5000 studies.

Harms
Psychological harms:

Laughter weakens resolve and promotes your preference for certain brands. Hence it is better for doctors to be sceptical of those cheer laden witty drug reps.

Laughter may not be that good for the
heart:

Hearty laughter can cause syncope, due to neurological changes. It can lead to conduction abnormalities and arrhythmias. 'Laughing fit to burst can cause cardiac rupture,' observes BMJ. There has been a reported case of death after intense sustained laughter in a woman with a condition known as
long QT syndrome.

Respiratory harms:

Laugher may provoke inhalation of foreign bodies. It sometimes triggers attacks of
asthma. Pilgaard-Dahl syndrome is a rare condition in which middle aged smokers can develop a condition called pneumothorax. Exhaled air flow during laughter can disseminate infections.

Harms to the
nervous system:

Laughter can trigger cataplexy, i.e. sudden loss of muscle tone. It may precipitate headaches. In one recorded case, 'a woman with a patent foramen ovale laughed uproariously for three minutes, became aphasic, and had a cerebral infarct.''

Harms to the
digestive system:

Laughter is an unusual precipitant of Boerhaave's syndrome, i.e. spontaneous rupture of the food pipe. It may also make hernia protrude.

Laughter is thus not as light as we think. A strong laughter may dislocate your jaw; it can cause stress incontinence.

Gelastic seizures manifest by laughing, thus laughter can be pathological.

Benefits

Don't panic anyway, laughter also has a brighter side. Laughter can increase pain thresholds. Laughter prevents
heart attacks; it is good for blood vessels. Authors also note that laughter induced by a clown improved lung function in patients with the lung condition called chronic obstructive pulmonary disease.

'A day of merriment consumes over 8360 kJ (2000 kcal), improves glycaemic control, and cures obesity'. Laughter has obstetric benefits; would-be-mothers undergoing treatment for infertility benefitted from the entertainment provided clown, dressed as a chef de cuisine.

The ENT benefits may be deduced from this line, "A surgeon proceeded to read [to me] the diverting history of 'The Lady Rohesia' [from The Ingoldsby Legends], and how she was cured of her quinsy... The story caused me to laugh, and this led to the bursting of the [tonsillar] abscess, and to my cure without the use of cold steel."

The latest revelations 'refute the proposition that laughter can only be beneficial.' Well, now we have been warned decently well about the risks of outbursts of laughter!

Reference: Laughter and MIRTH (Methodical Investigation of Risibility, Therapeutic and Harmful): narrative synthesis. BMJ 2013;347:f7274



 

Study Develops Method for DNA Extraction from the Saliva After Stroke Using Magnetic Nanoparticles

 Study Develops Method for DNA Extraction from the Saliva After Stroke Using Magnetic NanoparticlesA risk factor for stroke is the C677T polymorphism in the methylenetetrahydrofolate reductase (MTHFR) gene. Studies have report a higher C677T homozygosity frequency in Chinese than in Europeans. Usually, the detection of genetic diseases is rather complicated on a large scale owing to the invasive sampling and a cumbersome DNA extraction process.
In a study by Dr. Li Yi and team from Peking University Shenzhen Hospital in China, DNA from stroke patients and healthy controls was extracted from the saliva using a magnetic nanoparticles-based method and from the blood using conventional methods. Real-time PCR results revealed that the C677T polymorphism was genotyped by PCR using DNA extracted from both saliva and blood samples. The genotype results were confirmed by gene sequencing, and results for saliva and blood samples were consistent. Therefore, this noninvasive magnetic nanoparticles-based method using saliva samples could be used to screen for the MTHFR C677T polymorphism in target populations. Source:This study was published in the Neural Regeneration Research (Vol. 8, No. 32, 2013). 

Berries Promote Skin Health

 Berries Promote Skin HealthAn expert has said that berries like raspberries and strawberries will help to achieve a glow this party season. 
"Exposure to pollution, tobacco and toxins, consumed in excess at this time of year, leaves us vulnerable to free radical attack. Berries are powerhouses for cell protection and the perfect snack for skin health," femalefirst.co.uk quoted Caroline Hitchcock, one of Britain's leading facialists, as saying.

They contain manganese, which has the ability to convert toxins within the skin cells into oxygen, reducing skin damage.

You can even prepare a face mask with the fruity ingredient. A ready to glow mask will have a hydrating effect on the skin and also brighten the face. Just follow these three steps:

- Mash four strawberries, half an avocado, a little bit of lemon juice in a bowl and make a smooth paste.

- Apply on face with a mask brush working into skin. Avoid eye area.

- Leave for up to 20 minutes then rinse with cool water.
Source: femalefirst.co.uk        

Wednesday 25 December 2013

These Prescription Drugs Make Your Brain Stop Working

Drugs commonly taken for a variety of common medical conditions negatively affect your brain, causing long term cognitive impairment. These drugs, called anticholinergics, block acetylcholine, a nervous system neurotransmitter.
They include such common over-the-counter brands as Benadryl, Dramamine, Excedrin PM, Nytol, Sominex, Tylenol PM, and Unisom.

Other anticholinergic drugs, such as Paxil, Detrol, Demerol and Elavil are available only by prescription.

Physorg reports:

“Researchers … conducted a six-year observational study, evaluating 1,652 Indianapolis area African-Americans over the age of 70 who had normal cognitive function when the study began … ‘[T]aking one anticholinergic significantly increased an individual’s risk of developing mild cognitive impairment and taking two of these drugs doubled this risk.’”

Many view over-the-counter (OTC) drugs as safe because they don’t require a prescription. Well nothing could be further from the truth.

In fact, many OTC drugs were previously carefully monitored prescription drugs. Many people are not aware that while I was in college in the 1970s, I worked as a full time pharmacy apprentice and helped sell drugs to patients all day long.

Motrin was the first non-salicylate prescription NSAID. Now it is a popular OTC ibuprofen option. Similarly, anti-ulcer drugs like Tagamet, Zantec, and Prilosec used to be carefully controlled. Now they can all be easily purchased in a smaller “OTC strength” that nearly doubles the number of pills required to equal the prescription dose.

Just because a drug is available without a prescription does not make it any less dangerous. It is still a chemical, which in no way, shape, or form treats the cause of the problem and can lead to complications that can seriously injure, if not kill, you or someone you love.

So this is clearly important information that can help you or someone you love reduce your risk of dementia as you get older. Based on the findings of this study, I would strongly recommend that seniors in particular avoid all anticholinergic drugs, like Benadryl (generic is diphenhydramine) which is a pervasive and commonly used in virtually all of the OTC sleeping pills.

Researchers will continue studying the matter to see whether anticholinergic-induced cognitive impairment can be reversed, but don’t hold your breath. Avoidance is really the best solution.

What are Anticholinergic Drugs?

Anticholinergic drugs block a nervous system neurotransmitter called acetylcholine. Those suffering from Alzheimer’s disease typically have a marked shortage of acetylcholine.

Anticholinergic drugs are available both over-the-counter and by prescription, as medications used for a variety of symptoms can have this effect. Examples include night-time pain relievers, antihistamines, and other sleep aids, such as:

-Excedrin PM

-Tylenol PM

-Nytol

-Sominex

-Unisom

-Benadryl

-Dramamine
Prescription drugs with anticholinergic effects include certain antidepressants, medications to control incontinence, and certain narcotic pain relievers.

Examples of prescription meds in these categories include:

-Paxil

-Detrol

-Demerol

-Elavil

A Special Note for Aspartame ‘Reactors’


Many of the drugs listed here, as well as a long list of additional ones, contain diphenhydramine. As an important side note, you need to beware that chewable tablets and rapidly disintegrating tablets that contain diphenhydramine may be sweetened with aspartame.

If you have the genetic disease phenylketonuria (PKU), you must be particularly careful to avoid these types of drugs and all other types of aspartame-sweetened foods and beverages in order to prevent mental retardation.

But many other people also suffer detrimental health effects from aspartame, so you should know that this is yet another potential source of this toxic sweetener.

Anticholinergic Drugs Increases Dementia in the Elderly .

  
 
I’ve previously written about the health dangers of many of these individual drugs. Paxil, for example, is an addictive antidepressant that is well known to increase the risk of suicide in children and teens. It is also known to increase violent behavior.

Benadryl and Sominex have previously been found to cause hallucinations in the elderly, and a number of the drugs on the list also promote dental decay.

The results of this study indicate that drugs with anticholinergic effects may be yet another piece of the puzzle that might explain the sharp rise in dementia and cognitive decline.

According to the University of Michigan, dementia strikes about 50 percent of people who reach the age of 85. Of those, about 60 percent go on to develop Alzheimer’s disease.

In this study, the researchers tracked the intake of anticholinergic drugs and monitored the cognitive abilities of 1,652 African-American seniors, aged 70 and older, for six years. All of the participants had normal cognitive function at the outset of the study.

Fifty-three percent of the participants used a ‘possible anticholinergic,’ and 11 percent used a ‘definitive anticholinergic’ drug.

They found that those who took drugs classified as ‘definite anticholinergics’ had a four times higher incidence of cognitive impairment.

In those who were not carriers of the specific gene, APOE ε4 allele, the risk was over seven times higher. (The APOE ε4 gene is known to influence many neurological diseases, and is considered a high risk factor for Alzheimer’s.)

Taking two of these drugs further increased the risk of cognitive impairment.

PhysOrg reports:

“Simply put, we have confirmed that anticholinergics, something as seemingly benign as a medication for inability to get a good night’s sleep or for motion sickness, can cause or worsen cognitive impairment, specifically long-term mild cognitive impairment which involves gradual memory loss.

As a geriatrician I tell my Wishard Healthy Aging Brain Center patients not to take these drugs and I encourage all older adults to talk with their physicians about each and every one of the medications they take,” said Malaz Boustani, M.D., IU School of Medicine associate professor of medicine, Regenstrief Institute investigator and IU Center for Aging Research center scientist.”

Even More Reasons to Ditch the Sleep Meds


In 2008, Americans filled more than 56 million prescriptions for sleeping pills and spent more than $600 million on over-the-counter sleep aids. But anticholinergic sleep medications in particular may be causing far more harm than good, especially long term, without providing any benefit at all.

In a recent article, CBC News reported that the U.S. Food and Drug Administration has had data for 15 years which shows that over-the-counter sleep aids like Tylenol PM and Excedrin PM do not offer any significant benefit to patients.

There’s no explanation for why the FDA took 15 years to evaluate the industry’s research, but upon final analysis “the data suggests the combination products are statistically better than a placebo but not by much,” CBC News reported.

I guess it can be chalked up as yet another vibrant example of how industry research frequently amounts to little more than corporate wishes and good PR fodder.

Another analysis of sleeping pill studies from 2007 (financed by the National Institutes of Health) found that sleeping pills like Ambien, Lunesta, and Sonata reduced the average time to go to sleep by just under 13 minutes compared with fake pills — hardly a major improvement.

Yet, the participants believed they had slept longer, by up to one hour, when taking the pills.

This may actually be a sign of a condition called anterograde amnesia, which causes trouble with forming memories. When people wake up after taking sleeping pills, they may, in fact, simply forget that they had been unable to sleep!

You would be far better off putting your money toward authentic solutions to help you sleep than on sleeping pills, as it’s now clear that they do next to nothing to help you sleep – in fact, they may actually make it more difficult for you to get a good night’s rest naturally – and may significantly increase your risk of dementia.

Sleeping Pills are NOT a Safe Solution for Sleepless Nights

Please understand that resorting to sleep medications is risky business, and that these pills do not address the underlying reasons why you’re having trouble sleeping in the first place.

In addition to the long-term problems already discussed, there are other serious, not to mention bizarre, risks involved.

For starters, these pills are notorious for being addictive, which means that once you want to stop taking them, you’ll likely suffer withdrawal symptoms that could be worse than your initial insomnia. Some, such as Ambien, may also become less effective when taken for longer than two weeks, which means you may find yourself needing ever higher dosages.

Ambien may also make you want to eat while you’re asleep – and I don’t mean sneaking down to grab a piece of fruit. The sleep eating can include bizarre foods such as buttered cigarettes, salt sandwiches, and raw bacon.

Sleeping pills, and again Ambien in particular, are also known to increase your risk of getting into a traffic accident. Ambien actually ranks among the top 10 drugs found in the bloodstreams of impaired drivers, according to some state toxicology labs.

Among the elderly, using sleeping pills may increase the risk of nighttime falls and injuries, and anyone who takes them may find they wake up feeling drowsy if the effects of the drug have not worn off yet.

You’re far better of finding safe and natural solutions that will actually address the underlying causes of your sleepless nights instead of just cover up the resulting symptoms.

How to Get a Good Night’s Sleep Without Dangerous Drugs


If you are having trouble sleeping, please do not ignore the problem or simply wait for it to go away. Quality sleep just as important as your need for food, water, and pure air — and there are very simple methods to help you get yours.

Please read my comprehensive sleep guide 33 Secret’s to a Good Night’s Sleep for my full set of recommendations, but to start, make certain you are exercising regularly.

A Stanford University Medical School study found that after 16 weeks in a moderate-intensity exercise program, subjects were able to fall asleep about 15 minutes earlier and sleep about 45 minutes longer at night. However, don’t exercise too close to bedtime or it may keep you awake.

Stress is another major reason why people have trouble sleeping, which is why I suggest you start to wind down from your day at least an hour before your bedtime (but preferably two or more).

Calming activities such as journaling, meditating, sipping herbal tea, washing your face, using the Emotional Freedom Techniques (EFT) or reading a book may soothe your mind and help you unwind. Be sure your phone, email, and television are all off during this time.

Make sure your sleeping environment is comfortable and conducive to sleep.


This includes keeping the temperature cool, adding in some white noise if you need it and making sure your room is pitch-black. If there is even the tiniest bit of light in the room it can disrupt your circadian rhythm and your pineal gland’s production of melatonin and serotonin. For this reason, I highly recommend adding room-darkening drapes to your bedroom, or if this is not possible wearing an eye mask to block out any stray light.

Again, by following my 33 Secrets for a Good Night’s Sleep, the majority of people will be able to fall asleep and stay asleep. However, for times when sleep is especially difficult, these eight natural remedies
may also help and are far safer than sleeping pills of any kind.

Source: http://www.realfarmacy.com/studies-prove-that-these-drugs-make-your-brain-stop-working
Drugs commonly taken for a variety of common medical conditions negatively affect your brain, causing long term cognitive impairment. These drugs, called anticholinergics, block acetylcholine, a nervous system neurotransmitter.
They include such common over-the-counter brands as Benadryl, Dramamine, Excedrin PM, Nytol, Sominex, Tylenol PM, and Unisom.


Other anticholinergic drugs, such as Paxil, Detrol, Demerol and Elavil are available only by prescription.

Physorg reports:

“Researchers … conducted a six-year observational study, evaluating 1,652 Indianapolis area African-Americans over the age of 70 who had normal cognitive function when the study began … ‘[T]aking one anticholinergic significantly increased an individual’s risk of developing mild cognitive impairment and taking two of these drugs doubled this risk.’”

Many view over-the-counter (OTC) drugs as safe because they don’t require a prescription. Well nothing could be further from the truth.

In fact, many OTC drugs were previously carefully monitored prescription drugs. Many people are not aware that while I was in college in the 1970s, I worked as a full time pharmacy apprentice and helped sell drugs to patients all day long.

Motrin was the first non-salicylate prescription NSAID. Now it is a popular OTC ibuprofen option. Similarly, anti-ulcer drugs like Tagamet, Zantec, and Prilosec used to be carefully controlled. Now they can all be easily purchased in a smaller “OTC strength” that nearly doubles the number of pills required to equal the prescription dose.

Just because a drug is available without a prescription does not make it any less dangerous. It is still a chemical, which in no way, shape, or form treats the cause of the problem and can lead to complications that can seriously injure, if not kill, you or someone you love.

So this is clearly important information that can help you or someone you love reduce your risk of dementia as you get older. Based on the findings of this study, I would strongly recommend that seniors in particular avoid all anticholinergic drugs, like Benadryl (generic is diphenhydramine) which is a pervasive and commonly used in virtually all of the OTC sleeping pills.

Researchers will continue studying the matter to see whether anticholinergic-induced cognitive impairment can be reversed, but don’t hold your breath. Avoidance is really the best solution.

What are Anticholinergic Drugs?

Anticholinergic drugs block a nervous system neurotransmitter called acetylcholine. Those suffering from Alzheimer’s disease typically have a marked shortage of acetylcholine.

Anticholinergic drugs are available both over-the-counter and by prescription, as medications used for a variety of symptoms can have this effect. Examples include night-time pain relievers, antihistamines, and other sleep aids, such as:

-Excedrin PM

-Tylenol PM

-Nytol

-Sominex

-Unisom

-Benadryl

-Dramamine

Prescription drugs with anticholinergic effects include certain antidepressants, medications to control incontinence, and certain narcotic pain relievers.

Examples of prescription meds in these categories include:

-Paxil

-Detrol

-Demerol

-Elavil

A Special Note for Aspartame ‘Reactors’

Many of the drugs listed here, as well as a long list of additional ones, contain diphenhydramine. As an important side note, you need to beware that chewable tablets and rapidly disintegrating tablets that contain diphenhydramine may be sweetened with aspartame.

If you have the genetic disease phenylketonuria (PKU), you must be particularly careful to avoid these types of drugs and all other types of aspartame-sweetened foods and beverages in order to prevent mental retardation.

But many other people also suffer detrimental health effects from aspartame, so you should know that this is yet another potential source of this toxic sweetener.

Anticholinergic Drugs Increases Dementia in the Elderly

Read more at http://isupportorganic.blogspot.com/2013/12/these-prescription-drugs-make-your.html#OlzWlGCZz67YQ2ba.99
Drugs commonly taken for a variety of common medical conditions negatively affect your brain, causing long term cognitive impairment. These drugs, called anticholinergics, block acetylcholine, a nervous system neurotransmitter.
They include such common over-the-counter brands as Benadryl, Dramamine, Excedrin PM, Nytol, Sominex, Tylenol PM, and Unisom.


Other anticholinergic drugs, such as Paxil, Detrol, Demerol and Elavil are available only by prescription.

Physorg reports:

“Researchers … conducted a six-year observational study, evaluating 1,652 Indianapolis area African-Americans over the age of 70 who had normal cognitive function when the study began … ‘[T]aking one anticholinergic significantly increased an individual’s risk of developing mild cognitive impairment and taking two of these drugs doubled this risk.’”

Many view over-the-counter (OTC) drugs as safe because they don’t require a prescription. Well nothing could be further from the truth.

In fact, many OTC drugs were previously carefully monitored prescription drugs. Many people are not aware that while I was in college in the 1970s, I worked as a full time pharmacy apprentice and helped sell drugs to patients all day long.

Motrin was the first non-salicylate prescription NSAID. Now it is a popular OTC ibuprofen option. Similarly, anti-ulcer drugs like Tagamet, Zantec, and Prilosec used to be carefully controlled. Now they can all be easily purchased in a smaller “OTC strength” that nearly doubles the number of pills required to equal the prescription dose.

Just because a drug is available without a prescription does not make it any less dangerous. It is still a chemical, which in no way, shape, or form treats the cause of the problem and can lead to complications that can seriously injure, if not kill, you or someone you love.

So this is clearly important information that can help you or someone you love reduce your risk of dementia as you get older. Based on the findings of this study, I would strongly recommend that seniors in particular avoid all anticholinergic drugs, like Benadryl (generic is diphenhydramine) which is a pervasive and commonly used in virtually all of the OTC sleeping pills.

Researchers will continue studying the matter to see whether anticholinergic-induced cognitive impairment can be reversed, but don’t hold your breath. Avoidance is really the best solution.

What are Anticholinergic Drugs?

Anticholinergic drugs block a nervous system neurotransmitter called acetylcholine. Those suffering from Alzheimer’s disease typically have a marked shortage of acetylcholine.

Anticholinergic drugs are available both over-the-counter and by prescription, as medications used for a variety of symptoms can have this effect. Examples include night-time pain relievers, antihistamines, and other sleep aids, such as:

-Excedrin PM

-Tylenol PM

-Nytol

-Sominex

-Unisom

-Benadryl

-Dramamine

Prescription drugs with anticholinergic effects include certain antidepressants, medications to control incontinence, and certain narcotic pain relievers.

Examples of prescription meds in these categories include:

-Paxil

-Detrol

-Demerol

-Elavil

A Special Note for Aspartame ‘Reactors’

Many of the drugs listed here, as well as a long list of additional ones, contain diphenhydramine. As an important side note, you need to beware that chewable tablets and rapidly disintegrating tablets that contain diphenhydramine may be sweetened with aspartame.

If you have the genetic disease phenylketonuria (PKU), you must be particularly careful to avoid these types of drugs and all other types of aspartame-sweetened foods and beverages in order to prevent mental retardation.

But many other people also suffer detrimental health effects from aspartame, so you should know that this is yet another potential source of this toxic sweetener.

Anticholinergic Drugs Increases Dementia in the Elderly

 
Drugs commonly taken for a variety of common medical conditions negatively affect your brain, causing long term cognitive impairment. These drugs, called anticholinergics, block acetylcholine, a nervous system neurotransmitter.
They include such common over-the-counter brands as Benadryl, Dramamine, Excedrin PM, Nytol, Sominex, Tylenol PM, and Unisom.


Other anticholinergic drugs, such as Paxil, Detrol, Demerol and Elavil are available only by prescription.

Physorg reports:

“Researchers … conducted a six-year observational study, evaluating 1,652 Indianapolis area African-Americans over the age of 70 who had normal cognitive function when the study began … ‘[T]aking one anticholinergic significantly increased an individual’s risk of developing mild cognitive impairment and taking two of these drugs doubled this risk.’”

Many view over-the-counter (OTC) drugs as safe because they don’t require a prescription. Well nothing could be further from the truth.

In fact, many OTC drugs were previously carefully monitored prescription drugs. Many people are not aware that while I was in college in the 1970s, I worked as a full time pharmacy apprentice and helped sell drugs to patients all day long.

Motrin was the first non-salicylate prescription NSAID. Now it is a popular OTC ibuprofen option. Similarly, anti-ulcer drugs like Tagamet, Zantec, and Prilosec used to be carefully controlled. Now they can all be easily purchased in a smaller “OTC strength” that nearly doubles the number of pills required to equal the prescription dose.

Just because a drug is available without a prescription does not make it any less dangerous. It is still a chemical, which in no way, shape, or form treats the cause of the problem and can lead to complications that can seriously injure, if not kill, you or someone you love.

So this is clearly important information that can help you or someone you love reduce your risk of dementia as you get older. Based on the findings of this study, I would strongly recommend that seniors in particular avoid all anticholinergic drugs, like Benadryl (generic is diphenhydramine) which is a pervasive and commonly used in virtually all of the OTC sleeping pills.

Researchers will continue studying the matter to see whether anticholinergic-induced cognitive impairment can be reversed, but don’t hold your breath. Avoidance is really the best solution.

What are Anticholinergic Drugs?

Anticholinergic drugs block a nervous system neurotransmitter called acetylcholine. Those suffering from Alzheimer’s disease typically have a marked shortage of acetylcholine.

Anticholinergic drugs are available both over-the-counter and by prescription, as medications used for a variety of symptoms can have this effect. Examples include night-time pain relievers, antihistamines, and other sleep aids, such as:

-Excedrin PM

-Tylenol PM

-Nytol

-Sominex

-Unisom

-Benadryl

-Dramamine

Prescription drugs with anticholinergic effects include certain antidepressants, medications to control incontinence, and certain narcotic pain relievers.

Examples of prescription meds in these categories include:

-Paxil

-Detrol

-Demerol

-Elavil

A Special Note for Aspartame ‘Reactors’

Many of the drugs listed here, as well as a long list of additional ones, contain diphenhydramine. As an important side note, you need to beware that chewable tablets and rapidly disintegrating tablets that contain diphenhydramine may be sweetened with aspartame.

If you have the genetic disease phenylketonuria (PKU), you must be particularly careful to avoid these types of drugs and all other types of aspartame-sweetened foods and beverages in order to prevent mental retardation.

But many other people also suffer detrimental health effects from aspartame, so you should know that this is yet another potential source of this toxic sweetener.

Anticholinergic Drugs Increases Dementia in the Elderly

 

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