Friday, January 15, 2010
Friday, January 15, 2010
NEW YORK (Reuters Health) Eating the Mediterranean way can help reduce your risk of stomach cancer, a large study from Europe shows.
"The results add to the evidence for the role of the Mediterranean diet in reducing cancer risk and add further support for the need to continue to promote the Mediterranean diet in areas where it is disappearing," Dr. Carlos A. Gonzalez of the Catalan Institute for Oncology in Barcelona and his colleagues say.
The traditional diets of Greece, Italy and other Mediterranean countries have many health benefits, they point out in the American Journal of Clinical Nutrition, including protection against cancer. But there is less information on how eating this way might influence risk of specific cancer types. Gonzalez and his team looked at gastric cancer, the second-leading cause of cancer death worldwide.
To investigate whether diet might be protective against the disease, the researchers analyzed data from the European Prospective Investigation into Cancer and Nutrition (EPIC) study on 485,044 men and women 35 to 70 years old from 10 European countries.
All had been given a score on an 18-point scale based on how closely their diet adhered to the Mediterranean ideal of being rich in fruit, vegetables, legumes, fish, cereals and olive oil, with a relatively low intake of red meat and dairy products.
During nine years of follow-up, 449 of the study participants developed gastric cancer.
People with the highest relative Mediterranean diet scores were 33 percent less likely to develop the disease than people whose eating patterns were furthest from the Mediterranean ideal. Gastric cancer risk fell 5 percent for every one-point increase in a person's Mediterranean diet score.
Just 23 percent of people diagnosed with gastric cancer will survive for five years, the researchers note. "Therefore, identifying dietary recommendations that can help reduce incidence is important for the effective management of this cancer," they conclude.
Source: American Journal of Clinical Nutrition, online December 9, 2009.
Friday, January 15, 2010
(HealthDay News) -- The thyroid, a small gland at the base of the neck, helps regulate your body's metabolism, including how fast your heart beats.
An overactive (hyperthyroid) or underactive (hypothyroid) gland can lead to a host of health problems, particularly during pregnancy.
The National Women's Health Information Center lists these possible complications of an untreated thyroid problem during pregnancy:
By Ros Krasny
Friday, January 15, 2010
BOSTON (Reuters) The number of children aged 2 to 5 who have been diagnosed with bipolar disorder and prescribed powerful antipsychotic drugs has doubled over the past decade, according to research released on Friday.
The research suggests that while it is still rare to prescribe powerful psychiatric drugs to 2-year-olds, the practice is becoming more frequent.
The data, compiled from 2000 to 2007, and published in the Journal of the American Academy of Child & Adolescent Psychiatry, could inform testimony at the upcoming Boston-area murder trials of the parents of 4-year-old Rebecca Riley. The girl died of an overdose of mood-stabilizing medication in 2006.
A Boston child psychiatrist, Kayoko Kifuji, diagnosed Riley with bipolar disorder and attention deficit hyperactivity disorder when she was 30 months old, and placed her on several powerful drugs: Depakote, an antiseizure medication also used for bipolar disorder, and clonidine, a blood pressure medication.
Kifuji's testimony may be crucial to the fate of Michael and Carolyn Riley, who face first-degree murder charges. A grand jury and a review by the state's medical licensing board cleared the doctor of wrongdoing.
Prosecutors claim the Rileys deliberately overmedicated their daughter to subdue her. The couple say they were following Kifuji's instructions and their daughter died of pneumonia.
The case has shone the spotlight again on a debate within the psychiatric profession about whether bipolar disorder can be diagnosed in very young children and whether it is wise to prescribe powerful medications.
Bipolar disorder, characterized by severe mood swings, was once thought to emerge only during adolescence or later. But Dr. Joseph Biederman, a child psychiatrist at Harvard University, transformed views on the subject by arguing that children could have the disorder at extremely young ages.
He is credited with spearheading a more than 40-fold increase in the number of children diagnosed with bipolar disorder over the past decade.
Biederman was accused in 2008 by Republican U.S. Senator Charles Grassley of failing to fully disclose payments by drug companies, including some that produced medication for bipolar disorder. Biederman declined to be interviewed about the latest study.
"The psychiatric diagnosis of very young children is anything but an exact science," said Harry Tracy, a psychologist and publisher of NeuroInvestment, a monthly publication specializing in central nervous system disorders.
"Such disparate causes as ADHD, depression, bipolar disorder, sexual abuse, and family dysfunction can produce very similar symptoms in a toddler."
The report's author, Mark Olfson, professor of clinical psychiatry at Columbia University, said about 1.5 percent of all privately insured children between the ages of 2 and 5, or one in 70 children, received some sort of psychotropic drug -- whether an antipsychotic, a mood stabilizer, a stimulant or an antidepressant -- in 2007.
If a child is diagnosed with bipolar disorder between the ages of 2 and 5, about half are prescribed an antipsychotic, such as Eli Lilly & Co's Zyprexa, AstraZeneca Plc's Seroquel, and Johnson & Johnson's Risperdal. They are prescribed to about one in 3,000 2-year-olds, according to his report.
"There might be a role for these drugs but only after you've tried other interventions, with the parents, or with the parents and child together, but that is not happening when you examine the billing records," Olfson said.
(Additional reporting by Toni Clarke; Editing by Peter Cooney)
Friday, January 15, 2010
ScienceDaily (Jan. 15, 2010) Nearly 20 years ago Huntington Potter kicked up a storm of controversy with the idea that Down syndrome and Alzheimer's were the same disease. Now the evidence is in: He was right.
And that's not all. Down syndrome, artery-clogging cardiovascular disease, and possibly even diabetes, appear to share a common disease mechanism with Alzheimer's disease, Dr. Potter and colleagues at the Florida Alzheimer's Disease Research Center, USF Health Byrd Alzheimer's Institute, recently reported.
The researchers' two papers -- one in Molecular Biology of the Cell and the other in PLoS One -- implicate the Alzheimer's-associated protein beta amyloid (amyloid protein), which damages the microtubule transport system responsible for moving chromosomes, proteins and other cargo around inside cells. Both studies were done in mice and humans cell cultures modeling Alzheimer's disease. Together, the laboratory discoveries suggest that protecting the microtubule network from this amyloid damage might be an effective way to prevent or even reverse Alzheimer's disease and associated disorders.
Huntington Potter, PhD, was the principal investigator for the studies.
The first paper, by Antoneta Granic and colleagues published online Dec. 23 in Molecular Biology of the Cell, provides the mechanism behind previous work by Dr. Potter's laboratory showing that all Alzheimer's disease patients harbor some cells with three copies of chromosome 21, known as trisomy 21, instead of the usual two. Trisomy 21 is a characteristic shared by all the cells in people with the birth defect Down syndrome. This earlier work demonstrated that Alzheimer's disease could be considered a late onset form of Down syndrome.
By age 30 to 40, all people with Down syndrome develop the same brain pathology seen in Alzheimer's disease, including a nerve-killing buildup of sticky amyloid protein clumps. This contributes to accelerated nerve cell loss and dementia.
With the study reported in MBC, Dr. Potter and his colleagues now show that the Alzheimer's-associated amyloid protein is the culprit that interferes with the microtubule transport system inside cells. The microtubules are responsible for segregating newly duplicated chromosomes as cells divide. "Beta amyloid basically creates potholes in the protein highways that move cargo, including chromosomes, around inside cells," said Dr. Potter, who holds the Eric Pfeiffer Endowed Chair for Research on Alzheimer's Disease.
When the microtubule network is disrupted, chromosomes can be incorrectly transported as cells divide and the result is new cells with the wrong number of chromosomes and an abnormal assortment of genes. For example, Down syndrome cells contain three copies of the beta amyloid gene on chromosome 21 -- leading to more accumulation of the "bad" amyloid protein over a lifetime, Dr. Potter says. "Alzheimer's disease probably is caused in part from the continuous development of new trisomy 21 nerve cells, which amplify the disease process by producing extra beta amyloid."
The second paper by lead author Jose Abisambra and colleagues, published Dec. 31 in the online journal PLoS One, describes another consequence of the damaged microtubule network caused by the amyloid protein.
Many Alzheimer's disease patients also commonly develop vascular diseases and diabetes. Whether this coincidence is bad luck or due to shared disease processes is intensely debated. Research teams have investigated the role that low-density lipoprotein (LDL), the bad cholesterol that causes atherosclerosis, cardiovascular disease and stroke, may play in the development of Alzheimer's with mixed results. However, the USF group focused on the amyloid protein's potential effects on LDL metabolism. The receptor needed to detect and use LDL is among the proteins transported by the microtubules.
As previously reported by their colleagues in the MBC paper, the second USF team found that the amyloid protein inflicts damage to the microtubule network. As a consequence, the receptor needed to pull LDL circulating throughout the bloodstream into the body's cells has trouble getting to the cell surface to retrieve this bad cholesterol. This interference with LDL metabolism may allow bad cholesterol to build up in into plaques that choke off blood supply to the brain and heart in people with Alzheimer's, Dr. Potter said.
Similarly, other key proteins -- including insulin receptors and receptors for brain signaling molecules -- are also likely locked inside cells when the transport system is damaged by amyloid or other factors. "The insulin receptors are needed to get blood sugar inside the cell where it can be used for energy. The nerve cell signaling receptors help promote memory and learning," Dr. Potter said. "So, if these receptors are unable to function properly, it may lead to diabetes and problems with learning and memory."
"We're beginning to understand how conditions like cardiovascular disease and diabetes may manifest some of the same underlying disease processes as Alzheimer's disease," he said, "rather than being independent diseases that just happen to develop in the same patient." The studies were supported by funds from the USF Health Byrd Alzheimer's Institute, the Eric Pfeiffer Chair for Research on Alzheimer's Disease, and the National Institute on Aging, sponsor of the statewide Florida Alzheimer's Disease Research Center at the University of South Florida.
By Amy Norton
Friday, January 15, 2010
NEW YORK (Reuters Health) The popular herbal remedy St. John's wort may help ease menopausal hot flashes, a small study suggests.
St. John's wort is probably best known as an herbal antidepressant, with some clinical trials suggesting that it can help relieve mild to moderate depression symptoms.
A few studies have also investigated the herb's effects on menopausal symptoms, but have focused on its impact on mood -- and not the so-called vasomotor symptoms of menopause, which include hot flashes and night sweats.
"(The) findings of our study suggest that this herbal medicine can be used to treat hot flashes due to menopause, and it is a new finding about the usage of St. John's wort," Marjan Khajehei, of Shiraz University of Medical Sciences in Iran, told Reuters Health in an email.
Khajehei and her colleagues found that among a group of women they randomly assigned to take either St. John's wort or an inactive placebo for eight weeks, those using the herb saw a greater reduction in daily hot flashes.
Among women taking St. John's wort, the average number of hot flashes declined from roughly four per day at the start of the study to fewer than two per day at week eight. In contrast, women in the placebo group were having an average of 2.6 hot flashes per day by the eighth week.
The herb also appeared to lessen the duration and severity of the women's hot flashes, Khajehei and her colleagues report in the journal Menopause.
The study included 100 women who were 50 years old, on average, and had been having moderate to severe hot flashes at least once per day. The women were randomly assigned to take either drops containing St. John's wort extract or placebo drops three times a day for eight weeks.
While women in both groups saw their hot flashes improve, those taking the herbal extract had a better response, on average.
St. John's wort contains estrogen-like plant compounds called phytoestrogens, and it's possible that these compounds explain the benefits seen in this study, according to Khajehei.
However, she said, further research is needed to confirm that the herb eases hot flashes and that phytoestrogens are the reason.
St. John's wort is generally considered safe when taken as directed, Khajehei noted. Still, she added, since phytoestrogens have mild estrogen-like effects in the body, women who have any contraindications to using estrogen -- such as a history of breast or endometrial cancers -- should talk with their doctors before starting St. John's wort.
The herb has also been shown to interact with certain medications, including antidepressants, the heart medication digoxin and the blood thinner warfarin. Experts generally recommend that people on any medication talk with their doctors before starting an herbal remedy.
Source: Menopause, February 2010.
Friday, January 15, 2010
ScienceDaily (Jan. 15, 2010) Taking both calcium and vitamin D supplements on a daily basis reduces the risk of bone fractures, regardless of whether a person is young or old, male or female, or has had fractures in the past, a large study of nearly 70,000 patients from throughout the United States and Europe has found.
The study included data published in 2006 from clinical trials conducted at UC Davis in Sacramento as part of the Women's Health Initiative (WHI). It appears online in this week's edition of the British Medical Journal.
"What is important about this very large study is that goes a long way toward resolving conflicting evidence about the role of vitamin D, either alone or in combination with calcium, in reducing fractures," said John Robbins, professor of internal medicine at UC Davis and a co-author of the journal article. "Our WHI research in Sacramento included more than 1,000 healthy, postmenopausal women and concluded that taking calcium and vitamin D together helped them preserve bone health and prevent fractures. This latest analysis, because it incorporates so many more people, really confirms our earlier conclusions."
Led by researchers at Copenhagen University in Denmark, Robbins and an international team of colleagues analyzed the results of seven large clinical trials from around the world to assess the effectiveness of vitamin D alone or with calcium in reducing fractures among people averaging 70 years or older. The researchers could not identify any significant effects for people who only take vitamin D supplements.
Among the clinical trial results analyzed was Robbins' WHI research, which was part of a 15-year, national program to address the most common causes of death, disability and poor quality of life in postmenopausal women such as cardiovascular disease, cancer and osteoporosis. Those trials were primarily designed to study the effect of calcium and vitamin D supplementation in preventing hip fractures, with a secondary objective of testing the supplements on spine and other types of fractures, as well as on colorectal cancer. The results were published in the Feb. 16, 2006 edition of the New England Journal of Medicine.
Fractures are a major cause of disability, loss of independence and death for older people. The injuries are often the result of osteoporosis, or porous bone, a disease characterized by low bone mass and bone fragility. The National Osteoporosis Foundation estimates that about 10 million Americans have osteoporosis; 80 percent of them are women. Four of 10 women over age 50 will experience a fracture of the hip, spine or wrist in their lifetime, and osteoporosis-related fractures were responsible for an estimated $19 billion in health-related costs in 2005.
"This study supports a growing consensus that combined calcium and vitamin D is more effective than vitamin D alone in reducing a variety of fractures," said Robbins. "Interestingly, this combination of supplements benefits both women and men of all ages, which is not something we fully expected to find. We now need to investigate the best dosage, duration and optimal way for people to take it."
Thursday, January 14, 2010
Thursday, January 14, 2010
NEW YORK (Reuters Health) Diabetes may hasten progression to dementia in older people with mild thinking impairment, new research shows.
So-called mild cognitive impairment, or MCI, increases a person's risk of developing Alzheimer's disease and other types of dementia. But aside from a person's severity of mental impairment, there is currently no way to predict which people with MCI will go on to develop full-blown dementia.
Diabetes has been tied to mental decline and dementia in aging, but it is not currently known whether people with MCI who have diabetes are at greater risk of future dementia.
To investigate, Dr. Latha Velayudhan of the Institute of Psychiatry in London and her colleagues followed 103 men and women with MCI over age 65 for four years, during which time 19 developed dementia. Most of these individuals had "probable or possible" Alzheimer's.
The 16 individuals in the study with diabetes were nearly three times as likely to develop dementia as the study participants without diabetes, the researchers report in the British Journal of Psychiatry.
While the study is small, Velayudhan and her colleagues note, it is fairly representative of the population at large because participants were recruited from primary care centers, not specialized memory clinics.
There are several ways that diabetes could speed mental decline, the researchers say, for example through its effects on insulin, which plays a key role in how the brain uses glucose for fuel.
"Whatever the mechanism, with an expected increase in the prevalence of diabetes in people of all ages including older adults, the risk of developing dementia may increase," Velayudhan and her colleagues say.
"Identification of those at particular risk of progression might help to target early treatment -- both pharmacological and social," they conclude.
Source: The British Journal of Psychiatry, January 2010.
Thursday, January 14, 2010
ScienceDaily (Jan. 14, 2010) For those who do not drink, researchers have found that six essential oils -from thyme, clove, rose, eucalyptus, fennel and bergamot -- can suppress the inflammatory COX-2 enzyme, in a manner similar to resveratrol, the chemical linked with the health benefits of red wine. They also identified that the chemical carvacrol was primarily responsible for this suppressive activity.
These findings, appearing in the January issue of Journal of Lipid Research, provide more understanding of the health benefits of many botanical oils and provide a new avenue for anti-inflammatory drugs.
Essential oils from plants have long been a component of home remedies, and even today are used for their aromatherapy, analgesic (e.g. cough drops), or antibacterial properties. Of course, the exact way they work is not completely understood. However, Hiroyasu Inoue and colleagues in Japan believed that many essential oils might target COX-2 much like compounds in wine and tea.
So, they screened a wide range of commercially available oils and identified six (thyme, clove, rose, eucalyptus, fennel and bergamot) that reduced COX-2 expression in cells by at least 25%. Of these, thyme oil proved the most active, reducing COX-2 levels by almost 75%.
When Inoue and colleagues analyzed thyme oil, they found that the major component -carvacrol- was the primary active agent; in fact when they use pure carvacrol extracts in their tests COX-2 levels decreased by over 80%.
Mariko Hotta, Rieko Nakata, Michiko Katsukawa, Kazuyuki Hori, Saori Takahashi, and Hiroyasu Inoue. Carvacrol, a component of thyme oil, activates PPAR-gamma and suppresses COX-2 expression. Journal of Lipid Research, January, 2010
Thursday, January 14, 2010
(HealthDay News) -- Your body needs the mineral magnesium to properly contract and relax muscles, to produce proteins and to help enzymes function, the U.S. National Library of Medicine says.
Its experts offer this list of dietary sources for magnesium:
Thursday, January 14, 2010
ScienceDaily (Jan. 14, 2010) Researchers from Boston University School of Medicine (BUSM) have found that angiotensin receptor blockers (ARBs) -- a particular class of anti-hypertensive medicines -- are associated with a striking decrease in the occurrence and progression of dementia. These findings appear in the January issue of the British Medical Journal.
Using data from the Decision Support System Database of the U.S. Department of Health System Veterans Affairs (with information on more than 5 million people), the BUSM researchers looked at records from patients who used ARBs, and compared them with subjects who had a similar health status, but were taking different medications. They found patients taking ARBs had up to a 50 percent lower chance of getting Alzheimer's disease or dementia. Patients taking two forms of medications targeting the angiotensin system, ARBs and Angiotensin Converting Enzyme (ACE) inhibitors, had a 55 percent lower risk of dementia.
The researchers also examined patients who were already suffering from Alzheimer's disease or dementia, and found those subjects had up to a 67 percent lower chance of being admitted to nursing homes or dying if they were taking both ARBs and ACE inhibitors. Patients who appeared to benefit particularly well from use of ARBs were those who had experienced strokes before or during the course of their illness.
According to the BUSM researchers these results suggest that ARBs might protect against developing Alzheimer's disease and dementia. "For those who already have dementia, use of ARBs might delay deterioration of brain function and help keep patients out of nursing homes," said senior author Benjamin Wolozin, MD, PhD, a professor of pharmacology at BUSM. "The study is particularly interesting because we compared the effects of ARBs to other medications used for treating blood pressure or cardiovascular disease. This suggests that ARBs are more effective than other blood pressure and cardiovascular medications for preventing Alzheimer's disease or dementia," he added.
Although the researchers are unsure why ARBs might be so beneficial, they believe one possibility suggested by prior studies on animal models is that ARBs help prevent nerve cell injury from blood vessel damage or help promote nerve cell recovery after blood vessel damage. The authors also speculate that ARBs might help protect the blood vessels in the brain against damage related to cardiovascular disease. Damage to blood vessels is thought to reduce brain capacity and promote dementia, so reducing this damage might prevent the occurrence or progression of dementia.
Funding for this study was provided by the Retirement Research Foundation and from the Casten Foundation.
By Joene Hendry
Thursday, January 14, 2010
NEW YORK (Reuters Health) New research hints that how well your lungs function in adulthood and your risk of developing chronic breathing problems is partly determined in childhood.
In a study, researchers found that early childhood "disadvantage factors" -- such as being around someone who smoked or suffering lung infections - seemed to help fuel the development of chronic obstructive pulmonary disease, or COPD, much later in life.
"People with early life disadvantage have permanently lower lung function, no catch-up with age but a slightly larger decline in lung function and a substantially increased COPD risk," Dr. Cecilie Svanes, at Haukeland University Hospital in Norway, and colleagues report in the journal Thorax.
COPD is a progressive lung disease that makes it hard to breathe. It covers emphysema, chronic bronchitis, and severe asthma. COPD is chiefly caused by cigarette smoking.
Among more than 13,000 men and women 20 to 45 years old, Svanes team found that 40 percent had at least one "childhood disadvantage" such as exposure to secondhand smoke, lung infections prior to the age of 5, having parents with asthma, or having a personal history of asthma.
The researchers compared how these early life "disadvantages" associated with lung function tests completed 9 years apart in roughly 7,700 of these individuals.
Compared with those having no "childhood disadvantages," COPD was six- and seven-times more likely, respectively, in men and women exposed to any three such factors, after allowing for multiple other factors, including current smoking and childhood asthma.
Exposure to two "disadvantages" seemed to confer five-times the COPD risk in men and doubled the risk in women.
Moreover, Svanes commented in an email to Reuters Health, "The effects of childhood disadvantage on lung function was as strong for the 50 year olds as for the 30 year olds."
The author of a commentary on the study points out that combining childhood risk factors (such as asthma in the child or parent, or early lung infections) with early exposure to secondhand smoke resulted in a risk for COPD that "rivaled or exceeded that seen from the traditional COPD risk factor of cigarette smoking."
Svanes and colleagues say their findings linking COPD to childhood factors are new and need confirmation in more detailed investigations. However, if confirmed, these findings suggest, "adult respiratory health to a large extent originates early in life," they conclude.
"My hope," Dr. David M. Mannino of University of Kentucky in Lexington wrote in his commentary, "is that a better understanding of the early life factors that increase the risk of disease might lead to better early detection and intervention efforts."
Source: Thorax, January 2010
Thursday, January 14, 2010
ScienceDaily (Jan. 14, 2010) A fast-acting compound that appears to improve cognitive function impairments in mice similar to those found in patients with progressive Alzheimer's disease has been identified by scientists at Wake Forest University School of Medicine and the Vanderbilt University Medical Center Program in Drug Discovery. Researchers hope to one day replicate the result in humans.
The compound -- benzylquinolone carboxylic acid (BQCA) -- has also been shown in previous rodent studies to lessen the occurrence and severity of the behavioral disturbances often symptomatic of Alzheimer's, such as hallucinations, delusions, paranoia and outbursts.
"That makes this compound somewhat novel," said Michelle M. Nicolle, Ph.D., an associate professor of gerontology at Wake Forest and co-researcher on the study, published recently in the Journal of Neuroscience. "We wanted to see if this very specific acting compound was able to change the way the brain works and whether or not it improved memory in our 'Alzheimer's mice,' which are experiencing progressive cognitive decline much like a person with Alzheimer's does."
Other attempts to identify such a specific treatment for Alzheimer's have failed, according to Nicolle.
"Current treatments only treat the symptoms while the underlying disease is still progressing," she said, "so recent research efforts are focusing on stopping disease progression instead of symptomatic treatment."
The researchers' findings suggest that the compound could alter the progression of disease in mice and, ultimately, hold importance for humans, as well.
BQCA activates a specific neurotransmitter receptor in the brain called the M1 muscarinic acetylcholine receptor. M1 receptors have been the focus of research into treatment of Alzheimer's disease because they affect the part of the brain that stimulates the memory and learning functions the disease inhibits. Until now, scientists have not found a treatment selective enough to activate the receptors without producing side effects such as nausea, vomiting and increased frequency of urination.
But in this study, Nicolle said, researchers found that BQCA boosted the weak signals of the M1 receptors in a mouse model of Alzheimer's disease.
"In Alzheimer's disease, the chemical signals -- the little bits of information that are talking to each other in the brain -- are reduced, so you can't do the tasks very well," Nicolle said. "BQCA is only boosting an existing signal, so it's really specific in its action."
BQCA also seemed to inhibit production of amyloid beta, one of the markers of Alzheimer's disease in the brain -- perhaps key to the compound's potential for slowing the progression of the disease.
Moreover, the compound works quickly, Nicolle explained. After just one administration of BQCA one hour before behavioral testing, mice were able to learn new ways to do tasks -- in this case, finding a piece of hidden peanut butter chip in one of two small flower pots that looked the same but smelled different. One of the pots was made to smell like lemon, indicating the location of a food reward, namely the peanut butter chip. The other pot smelled like clove, a smell that if followed, would lead the mouse to a pot with no food reward. All mice learned to locate the peanut butter chip in the pot that smelled like lemon.
However, when the odor stimuli were switched, making clove the indicator of the peanut butter and lemon the indicator of no reward, the BQCA-treated "Alzheimer's mice" were able to forget the old rule and quickly learn the new rule to locate the chip in the clove-scented pot. The untreated Alzheimer's mice had difficulty learning the new rule and persisted in looking for the chip in the lemon-scented pot -- a characteristic of impaired cognitive function known as "perseveration."
Tasks that require the replacement of old rules with new rules are categorized under the broad umbrella of cognition called "executive function" in humans. Examples of executive function such as planning, multitasking and activities of daily living, like cooking and getting dressed, are all capabilities that slip away as Alzheimer's disease progresses.
"In older people and in Alzheimer's disease patients, we call it flexible learning," Nicolle said. "They learn one rule, and they don't want to change the rule to get to the end goal."
Treatment with BQCA in mice allowed a previously learned rule to be replaced with a new one.
Because of the early indications that the compound could treat the behavioral symptoms associated with Alzheimer's, the researchers also believe BQCA could be targeted for treatment of schizophrenia. However, the compound will need further testing in the laboratory before it is ready for clinical trials with human participants.
The study was funded with grants from the National Institute of Mental Health, the National Institute of Neurological Disorders and Stroke, and the Alzheimer's Association.
In addition to Nicolle, the research team included Mona L. Watson, B.S., also of the School of Medicine; Jana K. Shirey, B.S., Ashley E. Brady, Ph.D., Paulianda J. Jones, Ph.D., Thomas M. Bridges, B.S., Satyawan B. Jadhav, Ph.D., Usha N. Menon, Ph.D., Zixiu Xiang, Ph.D., Craig W. Lindsley, Ph.D, P. Jeffrey Conn, Ph.D, and J. Phillip Kennedy, B.S., all of Vanderbilt University; Albert A. Davis, Ph.D., James J. Lah, M.D., Ph.D., and Allan I. Levey, M.D., Ph.D., all of Emory University School of Medicine; and Edward P. Christian, James J. Doherty, Michael C. Quirk and Dean H. Snyder of AstraZeneca Pharmaceuticals.
Wednesday, January 13, 2010
By Joene Hendry
Wednesday, January 13, 2010
NEW YORK (Reuters Health) Women who suffer from depression and anxiety may want to take a look at their diet as possible contributors to these conditions, study findings hint.
Dr. Felice N. Jacka, at the University of Melbourne, Australia, and colleagues report mood disorders were more common among women 20 to 93 years old who, over 10 years, ate primarily processed, refined, high-fat foods.
"There's no magic diet," Jacka commented in an email to Reuters Health. But eating a diet mainly of vegetables, fruit, whole grain foods, low fat dairy products, and lean meat, and reserving processed and sweet treats to "sometimes foods," will aid physical health and may also support mental well-being, she said.
Jacka's team assessed diet and psychiatric evaluations gathered over 10 years from 1,046 women representative of the general Australian population. A total of 925 women were free of mood disorders, whereas 121 had depressive and/or anxiety disorders, the researchers report in the American Journal of Psychiatry.
When they assessed how diet might relate to mood disorders, they found that a "Western" diet -- eating primarily hamburgers, white bread, pizza, chips, flavored milk drinks, beer, and sugar-laden foods -- was associated with more than a 50 percent greater likelihood for depressive disorders.
By contrast, both depression and anxiety disorders appeared about 30 percent less likely among women eating a more "traditional" Australian diet --- mostly of vegetables, fruit, beef, lamb, fish, and whole-grain foods.
These associations remained when the research team allowed for a variety of factors including age, body weight, social and economic status, education, physical activity, smoking, and alcohol drinking habits. But similar "adjusted" analyses in women mainly consuming fruits, salads, fish, tofu, beans, nuts, yogurt, and red wine showed no similar associations.
Taken together, the findings highlight the need for additional investigations to determine whether unhealthy eating leads to declining mental health or vice versa, the researchers say.
Given that diet is modifiable, finding evidence of a causal tie between diet and mental health seems worthy of pursuit, the researchers conclude.
Source: American Journal of Psychiatry, published online January 4, 2010
Wednesday, January 13, 2010
TUESDAY, Jan. 12 (HealthDay News) -- Daily supplements of calcium and vitamin D reduce the risk of fractures in women and men of all ages, even if they've suffered previous fractures, but vitamin D supplements alone don't offer significant protection, a new study has found.
Researchers analyzed data from 68,517 people, average age 70, who took part in seven studies that looked at the effect vitamin D or vitamin D plus calcium had on reducing fractures.
The analysis revealed that vitamin D given alone in doses of 10 micrograms to 20 micrograms per day doesn't prevent fractures. However, calcium and vitamin D given together reduce the risk of hip fractures, total fractures and possibly vertebral fractures.
The study, published online Jan. 12 in BMJ, called for additional studies of vitamin D, especially vitamin D given at higher doses without calcium.
There's a growing consensus that a combination of calcium and vitamin D is more effective than vitamin D alone in preventing nonvertebral fractures, Opinder Sahota, of Queen's Medical Center in Nottingham, England, wrote in an accompanying editorial.
Further research is need to determine the most effective dose, treatment duration and method of taking the calcium/vitamin D combination, Sahota said.
The U.S. National Institute of Arthritis and Musculoskeletal and Skin Diseases has more about calcium and vitamin D.
By Julie Steenhuysen
Wednesday, January 13, 2010
CHICAGO (Reuters) Antidepressants fail to help about half of the people who take them, and a study in mice may help explain why.
Most antidepressants -- including the commonly used Prozac and Zoloft -- work by increasing the amount of serotonin, a message-carrying brain chemical made deep in the middle of the brain by cells known as raphe neurons.
Researchers at Columbia University Medical Center in New York said on Wednesday that genetically engineered mice that had too much of one type of serotonin receptor in this region of the brain were less likely to respond to antidepressants.
"These receptors dampen the activity of these (serotonin-producing) neurons. Too much of them dampen these neurons too much," Rene Hen of Columbia, whose study appears in the journal Neuron, said in a telephone interview.
"It puts too much brake on the system."
Hen said the finding may be useful in giving doctors an idea of whether a patient will respond to an antidepressant.
And it could also help drugmakers populate better clinical trials to help identify new drug compounds that work for people who are unlikely to benefit from conventional antidepressants.
"The goal is to figure out something that is useful for the non-responders," he said.
For the study, Hen and colleagues needed to reach serotonin receptors in just the right part of the brain.
To do this, the team used mice that were genetically altered to have fewer serotonin receptors only in the region where the serotonin-producing raphe neurons are located.
Once the team had mice that had different levels of serotonin receptors in different parts of the brain, they did a behavior test that assesses boldness when mice get food in a brightly lit area.
Mice on antidepressants usually become more daring, but the drugs had no such effect on mice with surplus serotonin receptors.
"The most dramatic finding is that the mice that have high levels of receptors in these serotonin neurons do not respond to fluoxetine or Prozac," Hen said.
But when they reduced the number of these receptors -- or molecular doorways -- they were able to reverse the effect, he said.
"By simply tweaking the number of receptors down, we were able to transform a non-responder into a responder," Hen said.
At least 27 million take antidepressants in the United States, nearly double the number that did in the mid-1990s.
Eli Lilly and Co's Prozac, known generically as fluoxetine, and Pfizer Inc's Zoloft or sertraline belong to a class of antidepressants known as selective serotonin reuptake inhibitors, or SSRIs. Other common antidepressants include Forest Laboratories Inc's Celexa, or citalopram, and Lexapro, or escitalopram; and GlaxoSmithKline's Paxil or paroxetine.
(Editing by Mohammad Zargham)
Wednesday, January 13, 2010
ScienceDaily (Jan. 13, 2010) Being obese could lead to a greater risk of developing the most common form of renal cell cancer, according to research in the January issue of the UK-based urology journal BJUI.
US researchers found that obese patients with kidney tumours have 48 per cent higher odds of developing a clear-cell renal cell cancer (RCC) than patients with a body mass index (BMI) of less than 30. And the odds increase by four per cent for every extra BMI point.
The team at the Memorial Sloan-Kettering Cancer Center in New York, USA, studied 1,640 patients with kidney tumours. They found that 88 per cent had malignant tumours and 61 per cent of these were clear-cell RCCs. The remaining 12 per cent had benign tumours.
When they factored in the patient's weight, they discovered that there was a significant association between obesity and clear-cell RCC, which accounts for up to 80 per cent of RCC cases and is one of the more lethal variants.
"Recent scientific breakthroughs about what causes clear-cell RCC have led to the development of new targeted therapies" says lead author Dr William T Lowrance.
"This makes it more important than ever to identify those people who face an increased risk of developing this variant, which is on the rise in the USA.
"The widespread use of abdominal imaging has definitely contributed to increased detection of RCC, but fails to account for it entirely.
"A number of studies have suggested that obesity could be a risk factor for RCC, but the exact reason is unknown. Researchers suggest it might be secondary to hormonal changes, decreased immune function, hypertension or diabetes in obese patients."
The study looked at all patients who had undergone surgery at the Center between January 2000 and December 2007. Patients with hereditary renal cancer syndrome were excluded and BMI data was missing for a further 64, giving a study size of 1,640.
Key findings included:
· Patients had an average age of 62 years, 63 per cent were male and 88 per cent were white.
· 38 per cent of patients had a BMI of 30 or more, which is classified as obese, and this rose to 42 per cent in the patients with clear-cell RCC. By contrast, only 31 per cent of the patients with benign tumours were obese.
· 67 per cent of the obese patients had malignant tumours with clear-cell RCC, compared with 57 per cent of the non-obese patients.
The rates for the other kinds of malignant tumours -- including papillary, chromophobe and collecting duct -- were similar between the obese and non-obese patients.
"We also looked at other health and lifestyle factors, like diabetes, hypertension and smoking" adds Dr Lowrance. "This showed that the only other factors that were independent predictors of clear-cell RCC were male gender and tumour size."
The researchers conclude that BMI is an independent predictor of clear-cell RCC and that as BMI increases, the odds of having a clear-cell RCC also increases.
"Although we still need to find out more about the pathology of clear-cell RCC, this study is useful as it provides individual predictors of the chance of developing this form of cancer" concludes Dr Lowrance. "Of these, obesity provides the strongest association."
Lowrance et al. Obesity is associated with a higher risk of clear-cell renal cell carcinoma than with other histologies : Obesity Associated With Clear-Cell RCC. BJU International, 2010; 105 (1): 16 DOI: 10.1111/j.1464-410X.2009.08706.x
By Lauran Neergaard,
AP Medical Writer
The Associated Press
Wednesday, January 13, 2010
WASHINGTON Sleeping in on Saturday after a few weeks of too little shuteye may feel refreshing, but it can give a false sense of security.
New research shows chronic sleep loss can't be cured that easily. Scientists teased apart the effects of short- and long-term sleep loss and found that the chronically sleep-deprived may function normally soon after waking up, but experience steadily slower reaction times as the day wears on, even if they had tried to catch up the previous night.
The findings have important safety implications in our increasingly 24/7 society, not just for shift-workers but for the roughly one in six Americans who regularly get six hours or less of sleep a night.
"We know that staying awake 24 hours in a row impairs performance to a level comparable to a blood-alcohol content beyond the legal limit to drive," said lead researcher Dr. Daniel Cohen of Boston's Brigham and Women's Hospital.
But when the already chronically sleep-deprived pull an all-nighter, "the deterioration is increased tenfold," Cohen said.
The National Institutes of Health says adults need seven hours to nine hours of sleep for good health. Regularly getting too little increases the risk of health problems, including memory impairment and a weakened immune system. More immediately, too little sleep affects reaction times; sleepiness is to blame for car crashes and other accidents.
The new work shows how two different sleep drives impact the brain, one during the normal waking hours and the other over days and weeks of sleep loss.
It has critically important ramifications for anyone who works "crazy hours" and thinks they're performing fine with a few hours of weeknight sleep, said Shelby Freedman Harris, behavioral sleep-medicine director at New York's Montefiore Medical Center, who wasn't involved with the new research.
"Don't think you can just bank up your sleep on the weekend, because it doesn't work that way," Harris warned.
Cohen wondered how both acute and chronic sleep loss interact with our bodies' natural circadian rhythms, the 24-hour biological clock that signals when it's time to sleep and wake.
He recruited nine young, healthy volunteers and messed up their normally good sleep habits for three weeks. They stayed awake for 33-hour stretches with 10 hours of sleep in between, a radical enough schedule that their internal circadian clocks couldn't adjust. Their sleep deprivation was comparable to that of someone who gets about 5 1/2 hours of sleep a night, Cohen said, but the extra-long wake-sleep schedule also allowed him to test the value of catch-up sleep.
Cognitive and motor skills tests every few waking hours measured the volunteers' ability to stay alert and attentive, with results compared to similar volunteers getting a normal amount of sleep.
The well-rested can catch up from the occasional all-nighter fairly easily. But as the study wore on and the volunteers became more sleep-deprived, the rejuvenation they felt each time they awoke increasingly proved a facade, Cohen reported Wednesday in the journal Science Translational Medicine.
They functioned OK during their first few waking hours, especially that first week. But then their reaction times steadily worsened with each hour they stayed awake, with a big drop in performance between the first and second weeks of sleep deprivation, he found.
That daytime decline was subtle, and the people's circadian rhythms provided a bit of rescue. Know how most people get a bit tired in the afternoon? Even these sleep-deprived volunteers got an energy boost then, as their circadian rhythms kicked in.
But when they stayed up past bedtime yet again, their performance suddenly plummeted just as their circadian rhythm reached its natural lowest point, Cohen's team found. The drop was so sharp that he concluded these people were increasingly vulnerable to accidents and errors.
"When exposed to the next all-nighter, they really fall apart much faster than they previously would," said Cohen, also a neurologist at Beth Israel Deaconess Medical Center.
Stay tuned: Scientists don't yet know how quickly you recover from chronic sleep loss once you resume a good bedtime, Cohen said.
By Amy Norton
Wednesday, January 13, 2010
NEW YORK (Reuters Health) A new study suggests that a synthetic chemical that is ubiquitous in the environment and in people's blood may affect the liver -- though the significance for human health remains unclear.
The chemical in question is perfluorooctanoic acid (PFOA), which is used to make substances called fluoropolymers. Used in an array of manufacturing processes, fluoropolymers impart fire-resistance and water, stain and grease repellency to everything from carpets to cookware.
According to the U.S. Environmental Protection Agency (EPA), non-stick cookware and other consumer products coated with Teflon or similar trademark products are not manufactured with PFOA. However, some of these products may contain trace amounts of PFOA as impurities.
Research shows that PFOA persists in the environment and at low levels in most people's blood; exactly how it gets into the bloodstream is not clear, but contaminated water, dust and food are possibilities that researchers are currently investigating.
Also unclear are the potential human health effects of such everyday PFOA exposure. In lab animals, the chemicals have been shown to cause developmental problems and other adverse effects, including liver damage. But a number of human studies have found no evidence that PFOA exposure affects the liver.
In the new study, researchers in Taiwan used data from a U.S. government health study to look at the relationship between blood PFOA concentrations and liver enzyme levels. They found that among 2,200 U.S. adults, liver enzymes generally inched up in tandem with PFOA levels, particularly in obese individuals.
Liver enzymes are a marker of the organ's functioning, and significant elevations in the blood can indicate liver inflammation or other damage -- as seen in diseases like hepatitis and cirrhosis, or scarring of the liver.
The increases found in this study, however, were not enough to indicate liver damage, according to senior researcher Dr. Pau-Chung Chen, of the National Taiwan University College of Public Health in Taipei.
Instead, Chen told Reuters Health in an email, "This result particularly challenges other studies (suggesting) that there are no demonstrated liver effects, even among occupational workers, of PFOA exposures."
The findings, published in the American Journal of Gastroenterology, do not prove that PFOA in the blood directly affects the liver, according to Chen. "Nonetheless," the researcher added, "the associations between PFOA and liver enzymes raise concerns given their common presence in the general population."
Only 0.4 percent of adults in this study had undetectable PFOA levels. So it must be assumed that exposure to the chemical is "almost universal" in the general U.S. population, Chen noted.
Much more research is needed to understand the possible health implications of such low-level exposure. For its part, the EPA says it is continuing to investigate the potential risks of PFOA and related chemicals.
"However," the agency states on its Web site, "given the scientific uncertainties, EPA has not yet made a determination as to whether PFOA poses an unreasonable risk to the public, and there are no steps that EPA recommends that consumers take to reduce exposures to PFOA."
Source: American Journal of Gastroenterology, online December 15, 2009.
By Lindsey Tanner,
AP Medical Writer
The Associated Press
Wednesday, January 13, 2010
CHICAGO Raise a glass of diet soda: The nation's obesity rate appears to have stalled. But the latest numbers still show that more than two-thirds of adults and almost a third of kids are overweight, with no sign of improvement.
According to government data from the years 2007-08 published Wednesday, the obesity rate has held steady for about five years, reflecting earlier signs it had stalled after steadily climbing.
Dr. William Dietz, an obesity expert with the Centers for Disease Control and Prevention, cautiously called the results promising. "We're at the corner; we haven't turned the corner," he said.
Not only are the vast majority of adults overweight, 34 percent are obese; and 17 percent of children are obese. Even the youngest Americans are affected 10 percent of babies and toddlers are precariously heavy.
The CDC data were contained in two reports published online in the Journal of the American Medical Association.
"Even though this finding is certainly good news, the statistics are still staggering," said Dr. J. Michael Gaziano, a contributing editor at the journal.
The new data are based on health surveys involving height and weight measurements of 5,700 adults and 4,000 children, surveys the CDC does every two years.
The results in adults, showing 68 percent are too heavy, have been virtually the same in the last three surveys.
In most age groups, black adults had the highest rates of obesity, followed by Mexican-Americans and whites.
Among children ages 2 to 19, 32 percent were too heavy a rate that was mostly unchanged. But disturbingly, most obese kids were extremely obese. And the percentage of extremely obese boys ages 6 to 19 has steadily increased, to 15 percent from about 9 percent in 1999-2000.
CDC researcher and study author Cynthia Ogden said it was disappointing to see no decline, and troubling that the heaviest boys seem to be getting even heavier. The study didn't examine the causes, but Ogden cited the usual reasons soft drinks, video games and inactivity as possible explanations.
"We shouldn't be complacent. We still have a problem," Ogden said.
Gaziano, a cardiologist at Boston's Veterans Affairs hospital and Brigham and Women's Hospital, said getting the nation to turn the corner and reduce obesity requires changing many unhealthy behaviors, and getting restaurants, schools, food manufacturers and communities to support the fight.
That's starting to happen, from efforts to pull soda from school vending machines to campaigns by groups like the NFL to encourage physical activity, he noted.
is also high on the White House agenda. President Barack
Obama has pushed to make obesity prevention part of health care reform. Overhaul measures pending in
Congress include encouraging employer-based wellness programs and requiring large restaurant chains to list calories. And Michelle Obama on Wednesday said fighting childhood obesity will be a top priority this coming year.
In a round-table conversation with reporters about her first year in office and upcoming goals, Mrs. Obama said the new CDC reports suggest a generation of children will be destined for increased rates of heart disease, high blood pressure and strokes "if we don't get a handle on this issue."
"We have a chance to change the fate of the next generation if we get on it," she said.
People like Darrell Pender are paying attention.
Obesity "is constantly in the news," said Pender, a 42-year-old New York City computer technician who decided to get serious about fighting fat after being diagnosed with diabetes three years ago.
Pender was tempted by a TV ad for obesity surgery, but chose a less drastic option a nutrition support group that he credits with helping him make healthier food choices. So far, he's lost 50 pounds over several months. At 350 pounds, he's still very obese, but his diabetes is under control and he feels healthier.
Karen Congro, Pender's nutritionist at the Brooklyn Hospital Center, said obese patients in recent years seem more willing to try lifestyle changes rather than quick fixes doomed to fail.
Fifteen years ago, "I would have said this seems almost hopeless. Patients would say, 'I had an overweight uncle who lived to 99,'" Congro said. "Now I almost never hear that."
Associated Press Writer Nancy Benac in Washington contributed to this report.
On the Net:
By Kate Kelland
Wednesday, January 13, 2010
LONDON (Reuters) Exposure to a chemical found in plastic containers is linked to heart disease, scientists said on Wednesday, confirming earlier findings and adding to pressure to ban its use in bottles and food packaging.
British and U.S. researchers studied the effects of the chemical bisphenol A using data from a U.S. government national nutrition survey in 2006 and found that high levels of it in urine samples were associated with heart disease.
Bisphenol A, known as BPA, is widely used in plastics and has been a growing concern for scientists in countries such as Britain, Canada and the United States, where food and drug regulators are examining its safety.
David Melzer, professor of epidemiology and public health at the Peninsula Medical School in Exeter, England, who led the study, said the research confirmed earlier findings of a link between BPA and heart problems.
The analysis also confirmed that BPA plays a role in diabetes and some forms of liver disease, said Melzer's team, who studied data on 1,493 people aged 18 to 74.
"Our latest analysis largely confirms the first analysis, and excludes the possibility that the original report was a statistical blip," they said in a statement.
BPA, used to stiffen plastic bottles and line cans, belongs to a class of compounds sometimes called endocrine disruptors.
The U.S. Endocrine Society called last June for better studies into BPA and presented research showing the chemical can affect the hearts of women and permanently damage the DNA of mice.
"The risks associated with exposure to BPA may be small, but they are relevant to very large numbers of people. This information is important since it provides a great opportunity for intervention to reduce the risks," said Exeter's Tamara Galloway, who worked on the study published by the Public Library of Science online science journal PLoS One.
U.S. environmental health advocacy groups are urging a federal ban on BPA.
"There's enough research to take definitive action on this chemical to reduce exposures in people and the environment," Dr. Anila Jacob of the Environmental Working Group, a non-profit organization, said in a telephone interview.
The U.S. Food and Drug Administration is considering whether any action needs to be taken.
U.S. government toxicologists at the National Institutes of Health concluded in 2008 that BPA presents concern for harmful effects on development of the prostate and brain and for behavioral changes in fetuses, infants and children.
Canada's government plans to outlaw plastic baby bottles made with BPA. The charity Breast Cancer UK last month urged the British government to do the same because they said there was "compelling" evidence linking the chemical to breast cancer risk.
Experts estimate BPA is detectable in the bodies of more than 90 percent of U.S. and European populations. It is one of the world's highest production volume chemicals, with more than 2.2 million tonnes produced annually.
(Additional reporting by JoAnne Allen in Washington; editing by Mark Trevelyan)
Wednesday, January 13, 2010
NEW YORK (Reuters Health) Women with a family history of diabetes who are free from the disease themselves are more likely to develop pregnancy-related diabetes, a new study confirms.
And the risks associated with having a brother or sister who is diabetic are much higher than having one or even two parents with the disease, Dr. Catherine Kim of the University of Michigan Medical School in Ann Arbor and her colleagues found.
The increased demands placed on the body during pregnancy can cause some women to develop abnormally high blood sugar. The condition, known medically as gestational diabetes, typically gets better after a woman delivers her baby, but it increases her risk of developing type 2 diabetes later on.
The more relatives a person has with type 2 diabetes, the greater their risk of developing the condition themselves. But little is known about how a woman's family history of the condition affects her risk of developing gestational diabetes.
To investigate, Kim and her team looked at 4,566 women participating in the National Health and Nutrition Examination Survey, all of whom had at least one child. Ninety-seven percent had never been diagnosed with diabetes, about 1 percent had gestational diabetes only, and 2 percent had type 2 diabetes.
Having a mother or father with diabetes increased the likelihood of having diabetes or gestational diabetes to a similar degree, the researchers report in the American Journal of Obstetrics and Gynecology. But while having two parents with diabetes boosted the likelihood of having diabetes eight-fold, this only doubled the likelihood of gestational diabetes.
On the other hand, having a diabetic brother or sister increased gestational diabetes risk more than seven-fold, but only slightly upped type 2 diabetes risk.
"The odds of increased most markedly when a sibling was affected," Kim and her team write. And when the researchers accounted for early-life factors such as education and poverty, the risk associated with having a diabetic sibling actually increased. "Sibling-only history may be a greater risk factor than previously documented," they say.
The findings suggest, the researchers say, that gestational diabetes may follow a different pattern of inheritance than type 2 diabetes, which is closely associated with being overweight or obese.
Further investigation of these patterns could help identify women who are at particularly high risk of developing type 2 diabetes after having the gestational form of the condition, they add, "and thus target them for future prevention interventions."
Source: American Journal of Obstetrics and Gynecology, December 2009.
Wednesday, January 13, 2010
TUESDAY, Jan. 12 (HealthDay News) -- New research in mice suggests that loss of smell could serve as an early indicator of Alzheimer's disease.
People with Alzheimer's are already known to suffer from loss of smell. But the new research pinpoints a direct link between development of amyloid plaques -- the bits of gunk in the brain that cause Alzheimer's disease -- and a worsening sense of smell.
The findings are reported in the Jan. 13 issue of the Journal of Neuroscience.
Researchers found that the plaques first develop in the part of the mouse brain that's devoted to the sense of smell. When tested, the mice with the plaques had to spend more time sniffing odors to remember them, and they had a hard time telling the difference between odors.
"What was striking in our study was that performance of the mouse in the olfactory behavior test was sensitive to even the smallest amount of amyloid presence in the brain as early as 3 months of age (equivalent to a young adult)," study co-author Daniel W. Wesson, of New York University School of Medicine and the Nathan S. Kline Institute for Psychiatric Research in Orangeburg, N.Y., said in a university news release.
"This is a revealing finding because, unlike a brain scan, a laboratory-designed olfactory test may be an inexpensive alternative to early diagnosis of Alzheimer's," Wesson said.
The Alzheimer's Association has more on Alzheimer's disease.
Tuesday, January 12, 2009
Tuesday, January 12, 2009
TUESDAY, Jan. 12 (HealthDay News) -- For women under age 70, every 10-beat-per-minute increase in resting heart rate boosts the risk of dying from a heart attack by 18 percent, a new study has found.
Norwegian researchers tracked the health of about 50,000 healthy adults, aged 20 and older, for an average of 18 years. During that time, 6,033 men and 4,442 women died. Heart attack and stroke accounted for more than 58 percent of male deaths and more than 41 percent of deaths among women.
The higher a person's resting pulse, the greater their risk of death from cardiovascular disease, particularly from ischemic heart disease (heart attack and angina). Men with a pulse of 101 beats per minute or more were 73 percent more likely to die of ischemic heart disease than those with a rate of 61 to 72 beats per minute -- the normal healthy range.
Women with a resting heart rate of 101 beats per minute were 42 percent more likely to die of ischemic heart disease than those with a normal pulse. This was particularly true among women younger than 70 with a high resting heart rate -- they were more than twice as likely to die of a heart attack, the study found.
But the study also found that women with higher levels of physical activity had a lower risk of dying from ischemic heart disease, even if they had a high resting heart rate.
Physically inactive women with a resting heart rate of 88 beats per minute or higher were more than twice as likely to die of a heart attack than those with a lower heart rate. But women with a heart rate of 88 beats per minute or higher who did frequent and intensive exercise were only 37 percent more likely to die of a heart attack. However, this protective effect of exercise wasn't seen in men with high heart rates.
The study was published online Jan. 12 in advance of print publication in the Journal of Epidemiology and Community Health.
The U.S. Centers for Disease Control and Prevention has more about heart disease.
By Rachael Myers Lowe
Tuesday, January 12, 2009
NEW YORK (Reuters Health) More than a third of Americans with heart disease may not be getting "guideline-based" treatment for their disease.
Researchers found evidence that patients with coronary artery disease (CAD) -- in which plaque build-up starves the heart of its blood supply -- receive more recommendations for angioplasty and fewer recommendations for coronary artery bypass surgery (CABG) than indicated by current guidelines.
CABG, also known as "open-heart surgery," is a procedure in which the rib cage is spread open and a section of a healthy blood vessel is attached to "bypass" the blocked section of the coronary artery and improve the blood supply to the heart.
Angioplasty is a less invasive procedure used to widen narrowed or blocked arteries. A thin tube, or catheter, is threaded through a blood vessel to the affected area and a small balloon is inflated to open the blockage.
Which therapy is appropriate for a particular patient is outlined in "evidence-based" guidelines developed jointly by the American College of Cardiology and the American Heart Association.
"The guidelines are what a multidisciplinary and representative group of cardiologists and surgeons have determined is the best intervention given the patient's specifics," Dr. Edward L. Hannan, of the State University of New York in Albany, noted in a telephone interview with Reuters Health.
Hannan and his associates wanted to know whether cardiologists were following existing guidelines for use of angioplasty and CABG. They conclude in a report published this month in the journal Circulation that, too often, the answer is "no."
Hannan's team looked at data gathered between 2005 and 2007 at 19 hospitals in New York State involving 10,333 patients treated for CAD. They compared the treatment the professional guidelines called for according to the patient's medical status with the treatment recommended by the physician.
They found that 94 percent of patients for whom angioplasty was indicated by the guidelines were recommended for angioplasty. But only 53 percent of patients for whom the guidelines called for CABG were recommended for the surgery; 34 percent of these patients were recommended for angioplasty.
For patients who had indications for both CABG and angioplasty, 93 percent were recommended for angioplasty and 5 percent for surgery. Among patients for whom neither CABG nor angioplasty was indicated by the guidelines, 6 percent were recommended for CABG and 21 percent for angioplasty.
Hannan and his colleagues say they were intrigued by the frequency with which angioplasty was recommended even though the guidelines suggested surgery. What's also concerning is that the tendency to recommend angioplasty was "more accentuated" at hospitals with angioplasty capabilities, the authors note.
The finding that angioplasty appears to be recommended more often than indicated is "particularly important," Hannan and colleagues say, given that some recent studies have found CAGB surgery outcomes to be better than angioplasty outcomes for some patients.
He and his colleagues plan to follow these patients over time to determine how patients fared after getting treatment different from that recommended in the professional guidelines.
One problem, according to Hannan, is that current guidelines are "kind of complicated and confusing." He and his colleagues favor multidisciplinary involvement in CAD treatment decisions.
In a written commentary, Dr. Raymond J. Gibbons of the Mayo Clinic says the study raises valid concerns, particularly about the way medical tests and procedures are paid for in the current US healthcare system.
Of greatest concern, he writes, is the possibility that "the recommendations for (angioplasty) in patients indicated for CABG reflect a 'grow the business' and 'make it up in volume' mentality in response to declining reimbursement rates."
The current reimbursement system "favors tests and procedures," he notes, and six angioplasties can be performed in the time it takes to complete one bypass.
If these concerns are not addressed, Gibbons told Reuters Health: "We run the risk of losing the confidence of patients" and prompting regulatory interference, "which I personally believe would be a disaster."
Source: Circulation, online January 4, 2010
Tuesday, January 12, 2009
TUESDAY, Jan. 12 (HealthDay News) -- People with a family member who had pancreatic cancer before age 50 face a greatly increased risk for the disease, a new study has found.
Researchers already knew that people with several relatives diagnosed with pancreatic cancer were more likely than others to develop the disease, but it wasn't clear whether the relatives' age when they got the disease played any role.
They found, though, that risk increased ninefold when just one of several family members with the disease developed it before turning 50.
The finding, published online Jan. 12 in the Journal of the National Cancer Institute, stemmed from a review of the medical records of more than 9,000 people in 1,718 families.
The researchers also found that people with multiple relatives with pancreatic cancer were found to have a sixfold higher risk for pancreatic cancer, and chances of developing the cancer doubled if a person had just a single relative with the disease.
"These data should help to further inform risk assessment and subsequent early detection screening of individuals at high risk of developing pancreatic cancer," wrote the researchers, from the Johns Hopkins School of Medicine in Baltimore.
The study, they said, had a caveat: Family members of people with pancreatic cancer may have undergone screening that could have made it more likely that they'd be diagnosed with the disease.
The American Cancer Society has more on pancreatic cancer.
Tuesday, January 12, 2009
ScienceDaily (Jan. 12, 2010) Mango fruit been found to prevent or stop certain colon and breast cancer cells in the lab.
That's according to a new study by Texas AgriLife Research food scientists, who examined the five varieties most common in the U.S.: Kent, Francine, Ataulfo, Tommy/Atkins and Haden.
Though the mango is an ancient fruit heavily consumed in many parts of the world, little has been known about its health aspects. The National Mango Board commissioned a variety of studies with several U.S. researchers to help determine its nutritional value.
"If you look at what people currently perceive as a superfood, people think of high antioxidant capacity, and mango is not quite there," said Dr. Susanne Talcott, who with her husband, Dr. Steve Talcott, conducted the study on cancer cells. "In comparison with antioxidants in blueberry, acai and pomegranate, it's not even close."
But the team checked mango against cancer cells anyway, and found it prevented or stopped cancer growth in certain breast and colon cell lines, Susanne Talcott noted.
"It has about four to five times less antioxidant capacity than an average wine grape, and it still holds up fairly well in anticancer activity. If you look at it from the physiological and nutritional standpoint, taking everything together, it would be a high-ranking super food," she said. "It would be good to include mangoes as part of the regular diet."
The Talcotts tested mango polyphenol extracts in vitro on colon, breast, lung, leukemia and prostate cancers. Polyphenols are natural substances in plants and are associated with a variety of compounds known to promote good health.
Mango showed some impact on lung, leukemia and prostate cancers but was most effective on the most common breast and colon cancers.
"What we found is that not all cell lines are sensitive to the same extent to an anticancer agent," she said. "But the breast and colon cancer lines underwent apotosis, or programmed cell death. Additionally, we found that when we tested normal colon cells side by side with the colon cancer cells, that the mango polyphenolics did not harm the normal cells."
The duo did further tests on the colon cancer lines because a mango contains both small molecules that are readily absorbed and larger molecules that would not be absorbed and thus remain present in a colon.
"We found the normal cells weren't killed, so mango is not expected to be damaging in the body," she said. "That is a general observation for any natural agent, that they target cancer cells and leave the healthy cells alone, in reasonable concentrations at least."
The Talcotts evaluated polyphenolics, and more specifically gallotannins as being the class of bioactive compounds (responsible for preventing or stopping cancer cells). Tannins are polyphenols that are often bitter or drying and found in such common foods as grape seed, wine and tea.
The study found that the cell cycle, which is the division cells go through, was interrupted. This is crucial information, Suzanne Talcott said, because it indicates a possible mechanism for how the cancer cells are prevented or stopped.
"For cells that may be on the verge of mutating or being damaged, mango polyphenolics prevent this kind of damage," she said.
The Talcotts hope to do a small clinical trial with individuals who have increased inflamation in their intestines with a higher risk for cancer.
"From there, if there is any proven efficacy, then we would do a larger trial to see if there is any clinical relevance," she said.
According to the National Mango Board, based in Winter Park, Fla., most mangoes consumed in the U.S. are produced in Mexico, Ecuador, Peru, Brazil, Guatemala and Haiti. Mangoes are native to southeast Asia and India and are produced in tropical climates. They were introduced to the U.S. in the late 1800s, and a few commercial acres still exist in California and Florida.
Tuesday, January 12, 2009
WASHINGTON (Reuters) People with fat in their thighs and backsides may live longer because the fat traps harmful fatty particles and actively secretes helpful compounds, according to a report published on Tuesday.
Many studies have shown that people who accumulate fat around the abdomen and stomach are more likely to die of heart disease and other causes than bottom-heavy people, but the reasons are not clear.
This may be because several different mechanisms are involved, said Konstantinos Manolopoulos of Britain's University of Oxford.
"It is the protective role of lower body, that is, gluteofemoral fat, that is striking," Manolopoulos wrote in the International journal of Obesity.
"The protective properties of the lower-body fat depot have been confirmed in many studies," he added.
Fat on the bottom and thighs appears to store excess fatty acids, said Manolopoulos, who reviewed published scientific studies for his report.
Pear-shaped people also appear to have lower levels of compounds called inflammatory cytokines -- signaling chemicals involved in the body's response to infection that also can play a role in heart disease and diabetes when they are inappropriately active.
Fat on the legs may also absorb fats from the diet, keeping them from overwhelming the body when people overeat, Manolopoulos said.
Cholesterol levels reflect a tricky balance between high density lipoprotein, the HDL or "good" cholesterol that removes harmful fats from the blood, and low-density lipoprotein, the "bad" LDL cholesterol that can harden and block the arteries.
Fat in the thighs may also be more stable, he said, with studies showing abdominal fat breaks down quickly during fasting or stress, releasing potentially harmful components from the fat.
"The exact regulatory mechanisms of fatty acid release and storage and their effect on short- and long-term fatty acid metabolism remain to be analyzed," Manolopoulos wrote.
Leg fat may also be better at producing hormones such as leptin, which are made by fat and affect appetite and metabolism -- although Manolopoulos said this is poorly understood.
Understanding all this could lead to better drugs for treating obesity and related disease such as diabetes and heart disease, Manolopoulos said.
(Reporting by Maggie Fox, Editing by Sandra Maler)
Tuesday, January 12, 2009
ScienceDaily (Jan. 12, 2010) High intakes of calories and sodium appear to be associated with the progression of retinal disease among African American patients with diabetes, according to a report in the January issue of Archives of Ophthalmology, one of the JAMA/Archives journals.
Diabetic retinopathy is the leading cause of blindness among 20- to 64-year-olds with diabetes, according to background information in the article. The condition occurs when diabetes-related changes to the body damage the blood vessels of the retina. Proliferative retinopathy (involving the growth of new blood vessels in the retina) and macular edema (when fluid leaks into the macula, the part of the eye responsible for sharp vision) -- collectively called vision-threatening diabetic retinopathy -- are the two main causes of vision loss in patients with diabetes.
Monique S. Roy, M.D., of New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, and Malvin N. Janal, Ph.D., of the New York University College of Dentistry, assessed 469 African American patients with type 1 diabetes who originally enrolled in the study between 1993 and 1998. Then and after a six-year follow-up (between 1999 and 2004), participants completed a food frequency questionnaire, had a complete eye examination, underwent blood testing and had photographs of the retina taken to determine progression of diabetic retinopathy.
Individuals with the highest caloric intake at the beginning of the study were more likely to develop vision-threatening retinopathy by the end of the six-year period. In addition, high sodium intake at the initial examination was associated with the development of macular edema.
"In African American patients with type 1 diabetes, high caloric and sodium intakes are significant and independent risk factors for progression to severe forms of diabetic retinopathy," the authors conclude. "These results suggest that low caloric and sodium intakes in African American individuals with type 1 diabetes mellitus may have a beneficial effect on the progression of diabetic retinopathy and thus might be part of dietary recommendations for this population."
This work was supported by grants from the National Eye Institute, Bethesda, Md., and a Lew Wasserman Merit Award from Research to Prevent Blindness, Inc., New York.
Monique S. Roy; Malvin N. Janal. High Caloric and Sodium Intakes as Risk Factors for Progression of Retinopathy in Type 1 Diabetes Mellitus. Arch Ophthalmol, 2010; 128 (1): 33-39 [link]
By Alan Mozes
Tuesday, January 12, 2009
TUESDAY, Jan. 12 (HealthDay News) -- Antioxidants in green tea appear to significantly lower the risk for developing lung cancer among smokers and nonsmokers alike, new research from Taiwan reveals.
The study suggests that smokers and nonsmokers who consume a minimum of one cup of green tea per day appear to have a nearly 13-fold and fivefold lower risk, respectively, for developing lung cancer than smokers and nonsmokers who don't drink any green tea.
"The health effect of green tea consumption could modify the risk of lung cancer, particularly among smokers," said study author I-Hsin Lin, of Chung Shan Medical University in Taichung.
Lin and her team are scheduled to present their findings at a lung cancer conference this week in Coronado, Calif. The conference is sponsored by the American Association for Cancer Research and the International Association for the Study of Lung Cancer.
The observed protective effect seems to result from the strong "antioxidative property" of polyphenols found in green tea preparations.
To determine just how strong this effect might be, the authors assessed the dietary intake and lifestyle habits of 170 lung cancer patients and 340 healthy patients.
The participants completed questionnaires outlining their smoking histories, green tea consumption habits, fruit and vegetable intake, and cooking practices. Patients were also asked to note any family history of lung cancer.
Genetic testing was also conducted to assess which particular insulin-like growth factor genotype -- among several -- each participant possessed.
This analysis was considered crucial, given the author's observation that, independent of green tea consumption, genetically determined hormonal differences can affect how quickly cancer cells spread, thereby predisposing people toward a greater or lesser general risk for developing lung cancer in the first place.
While emphasizing that both smoking and nonsmoking tea drinkers generally benefited from green tea consumption relative to non-tea drinkers, the team observed that tea drinkers with particular growth factor genotypes seemed to gain even more protection -- as much as 66 percent greater protection compared with tea drinkers bearing a different genetic background.
The findings reflect solely upon the potential interplay of green tea, genetics and lung cancer risk, the researchers noted, leaving aside potential questions regarding black tea consumption.
"Our results suggest the potential health benefits of green tea consumption," concluded Lin. "However, cigarette smoking can serve as an initiator and promoter of carcinogenesis, [so] cessation of smoking is the best way for cancer prevention."
Dr. Norman Edelman, chief medical officer of the American Lung Association, emphatically agreed.
"First of all, this is not a new concept," he observed. "The idea that various antioxidants are protective to the lung has been around for a while, and green tea is a powerful antioxidant. But for us to really know whether or not just one cup can have such an enormous effect, you really have to look at more data and all the other possibly confounding factors, such as whether patients are obese, whether they are leading otherwise healthy lives, that kind of thing."
"Meanwhile, what the American Lung Association is really afraid of," cautioned Edelman, "is that people will look at this and think, 'Oh, well, I can smoke as long as I have a few cups of green tea.' Nothing could be further from the truth. Smoking is extremely toxic, obviously, and extremely detrimental to your health. And nothing changes this fact. So the most important thing here is that we don't want anyone to get the message that it's OK to smoke so long as I drink green tea."
Meanwhile, another group reported that a diet high in leafy green vegetables, folate and some multivitamins might protect against smoking-related genetic changes that lead to lung cancer.
The researchers from Lovelace Respiratory Research Institute in Albuquerque, N.M., found those substances, including vitamins C, A and K, could influence a chemical modification called cellular gene methylation. Aberrant gene methylation is known to be a mechanism in the development of cancer in smokers.
Their findings were published online Jan. 12 in Cancer Research.
Exploring yet another front in lung cancer science, a second study scheduled for release at the lung cancer conference suggests that lung cancer patients who are smokers seem better able than nonsmoking patients to tolerate higher -- and presumably more effective -- dosages of a standard chemotherapy treatment known as erlotinib.
The research team, from the Wake Forest University in Winston-Salem, N.C., found that while nonsmokers ultimately developed dangerously toxic side effects -- such as rashes, diarrhea and/or dehydration -- when placed on an average daily dose regimen of just 225 milligrams of erlotinib, smokers didn't develop similarly problematic reactions until the daily average dosage reached 300 milligrams.
For additional details on green tea and lung cancer prevention, visit the National Cancer Institute.
Tuesday, January 12, 2009
ScienceDaily (Jan. 12, 2010) Researchers at Wake Forest University Baptist Medical Center and colleagues have identified the first genetic variant associated with aggressive prostate cancer, proving the concept that genetic information may one day be used in combination with other factors to guide treatment decisions.
The research is being reported in the Proceedings of the National Academy of Sciences.
"This finding addresses one of the most important clinical questions of prostate cancer -- the ability at an early stage to distinguish between aggressive and slow-growing disease," said Jianfeng Xu, M.D., Dr. P.H., professor of epidemiology and cancer biology. "Although the genetic marker currently has limited clinical utility, we believe it has the potential to one day be used in combination with other clinical variables and genetic markers to predict which men have aggressive prostate cancer at a stage when the disease is still curable."
According to the authors, prostate cancer accounts for one-fourth of all cancer diagnoses in the United States. Autopsy studies suggest that most aging men will develop prostate lesions that, if detected clinically, would be diagnosed as cancer.
Although most men have a slow-growing form of the disease, aggressive prostate cancers are currently the second-leading cause of cancer death in the U.S., accounting for 27,000 deaths annually.
"The current inability to accurately distinguish risk for life-threatening, aggressive prostate cancer from the overwhelming majority of slow-growing cases creates a treatment dilemma," said Xu.
While researchers, including Xu's team, have identified multiple genetic variants associated with the risk of developing prostate cancer in the first place, until now there have been no genetic factors associated with disease aggressiveness.
Based on existing evidence that some men are genetically predisposed to developing aggressive prostate cancer, the researchers hypothesized that inherited genetic variants exist that could be used as markers to identify these men at an early, curable stage of disease.
"Identifying factors that are associated with a risk of having or developing aggressive disease is urgently needed to reduce over-diagnosis and over-treatment of this common cancer," said Karim Kader, M.D., Ph.D., a Wake Forest Baptist urologist specializing in prostate cancer and a co-author on the paper.
The study involved the analysis of genetic information from 4,849 men with aggressive disease and 12,205 with slow-growing disease to determine if the men with aggressive disease had genetic variants in common. The analysis included participants in the Genetic Markers of Susceptibility study performed by the National Cancer Institute (NCI) as well as additional study populations in the U.S. and Sweden.
The researchers identified a genetic variant (rs4054823) that was associated with a 25 percent higher risk of developing aggressive disease.
"A single variant with a moderate effect such as this is unlikely to be sufficient on its own at predicting risk," said Xu. "But its identification is significant because it indicates that variants predisposing men to aggressive disease exist in the genome."
He said that as more variants associated with aggressive disease are identified, it is possible that doctors could test men to determine their risk of aggressive disease not only at the time of diagnosis, but early enough in their lives to target them for increased screening.
"We speculate that a panel of variants could be an important part of developing a screening strategy that could reduce the number of men requiring screening, thereby reducing over-diagnosis, while also identifying men at risk for developing aggressive disease at a stage when the disease is potentially curable."
The research was primarily funded by NCI.
Co-researchers were: S. Lilly Zheng, M.D., Jielin Sun, Ph.D., Ge Li, M.D., Lina D. Purcell, B.S., Seong-Tae Kim, Ph.D., and Fang-Chi Hsu, Ph.D., all with Wake Forest University School of Medicine; Sarah D. Isaacs, M.S., Kathleen E. Wiley, M.S., Patrick C. Walsh, M.D. and William B. Isaacs, Ph.D., all from Johns Hopkins Medical Institutions; Fredrik Wiklund, Ph.D., Jan Adolfsson, M.D., Ph.D., and Henrik Grφnberg, M.D., Ph.D. all from the Karolinska Institutet in Stockholm, Sweden; Pδr Stattin, M.D., Ph.D. from Umeε University Hospital in Umeε, Sweden; Jeffrey M. Trent, Ph.D., David Duggan, Ph.D., and John Carpten, Ph.D., from Translational Genomics Research Institute in Phoenix, Ariz.; and Jonas Hugosson, M.D., from Sahlgrenska University Hospital, Goteborg, Sweden.
Tuesday, January 12, 2009
NEW YORK (Reuters Health) Children who are breastfed for longer than six months could be at lower risk of mental health problems later in life, new research from Australia
"Breastfeeding for a longer duration appears to have significant benefits for the onward mental health of the child into adolescence," Dr. Wendy H. Oddy of the Telethon Institute for Child Health Research in West Perth and her colleagues report in The Journal of Pediatrics.
Breastfeeding could help babies cope better with stress, the researchers note, and may also signal a stronger mother-child attachment and these benefits may last.
Oddy and her colleagues studied 2,366 children born to women enrolled the Western Australia Pregnancy Cohort (Raine) Study. Each of the children underwent a mental health assessment when they were 2, 5, 8, 10, and 14 years old.
Eleven percent were never breastfed, 38 percent were breastfed for less than six months, and just over half were breastfed for six months or longer.
The mothers who breastfed for less than six months were younger, less educated, poorer, and more stressed, and were also more likely to be smokers, than the moms who breastfed for longer. They were also more likely to suffer from postpartum depression, and their babies were more likely to have growth problems.
At each of the assessments, the researchers found, children who were breastfed for shorter periods of time had worse behavior. Differences were seen for internalizing behavior, in which negativity is directed inwards, for example depression; and in externalizing behaviors, such as aggression.
For each additional month a child was breastfed, behavior improved.
Breastfeeding for six months or longer remained positively associated with the mental health and well-being of children and adolescents after the investigators adjusted for social, economic and psychological factors as well as early life events.
They conclude: "Interventions aimed at increasing breastfeeding duration could be of long-term benefit for child and adolescent mental health."
Source: The Journal of Pediatrics, online December 14, 2009.
Tuesday, January 12, 2009
TUESDAY, Jan. 12 (HealthDay News) -- A combination whole-body PET-CT scan is more accurate than some other commonly used tests in detecting cancer in patients with neurologic symptoms, according to U.S. researchers.
So-called "paraneoplastic neurologic disorders" can occur in people with lung, breast, ovarian and other types of cancer when cancer-fighting antibodies mistakenly attack nervous system cells. Cancers that cause neurological symptoms are often small, restricted to one site and not detected until autopsy, the Mayo Clinic researchers explained.
Routine non-invasive cancer examinations may prove inconclusive in such cases. "These standard evaluations include physical examination; computed tomography of the chest, abdomen and pelvis; mammography in women; and testicular ultrasonography and prostate-specific antigen testing in men," wrote Andrew McKeon and colleagues.
They analyzed the medical records of 56 patients with suspected paraneoplastic neurologic disorders who underwent standard evaluations that did not detect cancer. The patients then underwent whole-body PET-CT, a combination of positron emission tomography (PET) and computed tomography (CT) .
Those scans detected abnormalities suggestive of cancer in 22 patients. Of those, 10 had cancer diagnoses confirmed by biopsy or another method. Of these cancers, two were in the thyroid, one in the tonsil, three in the lungs, one in the colon and three were cancerous lymph nodes with unknown primary cancer sites.
Nine of the 10 cancers were early-stage, and the patients underwent early treatment. After a median follow-up of 11 months, seven patients had cancer remission and five had improvement in neurologic symptoms.
The study was published online Jan. 11 in advance of the March print issue of the journal Archives of Neurology.
The U.S. National Institute of Neurological Disorders and Stroke has more about paraneoplastic disorders.
By Julie Steenhuysen
Tuesday, January 12, 2009
CHICAGO (Reuters) People with a gene linked to long life and good health are also less likely to develop Alzheimer's disease, U.S. researchers said on Tuesday.
They said people with two copies of a certain version of the cholesteryl ester transfer protein or CETP gene had significantly slower memory declines compared with people who had different versions of the gene.
"We've known for a long time that genetic factors matter in Alzheimer's disease," said Dr. Richard Lipton of Albert Einstein College of Medicine at Yeshiva University in New York, whose study appears in the Journal of the American Medical Association.
Lipton said most studies have sought to identify genetic variations that increase the risk of developing Alzheimer's disease, such as APOE4.
"Instead, we looked for genes that protect against Alzheimer's disease, and also for genes that might promote healthy brain aging," Lipton said in a telephone interview.
An estimated 26 million people globally have Alzheimer's disease, the most common form of dementia. The disease starts out with mild memory loss and confusion but escalates into complete memory loss and an inability to care for oneself.
Lipton's team examined a variant of the CETP gene that is already associated with exceptional longevity and cardiovascular health.
They analyzed the DNA of more than 500 people who did not have dementia at the start of the study. The team also did annual memory tests.
After at least three years of follow up, 40 people developed dementia.
"We found in people who carry the longevity variant of CETP, there was a 70 percent reduction in the risk of Alzheimer's disease, and the rate of annual decline on tests of memory was much lower," Lipton said.
"That proved our hypothesis that at least this genetic variant associated with longevity was also associated with successful brain aging and protected against the onset of Alzheimer's," he said.
It is not exactly clear how this gene could protect the brain, but Lipton said people with the longevity variant of the CETP gene tend to have high levels of high density lipoprotein or HDL, the so-called "good" cholesterol that protects against heart disease.
"One possibility is the longevity gene promotes successful brain aging by preventing vascular disease," he said.
Or, he said, the gene may have a direct protective effect against Alzheimer's.
"Understanding the mechanism would allow you to discover drugs that mimic the genetic defect," Lipton said.
Drug companies are already targeting the CETP gene in the hopes of raising levels of HDL or good cholesterol. Pfizer's drug torcetrapib showed early promise, but the drug had excessive side effects, and Merck & Co now has a drug in late-stage clinical trials.
Despite decades of research, doctors still have few effective treatments for Alzheimer's disease, which is expected to affect 100 million people by 2050.
(Editing by Maggie Fox)
Tuesday, January 12, 2009
ScienceDaily (Jan. 12, 2010) A new method of blocking the genesis of blood vessels that feed tumors may start with the nuclear receptor COUP-TFII (chicken ovalbumin upstream promoter-transcription factor II), said a pair of Baylor College of Medicine researchers who have studied the factor for more than 20 years.
In a report in the Proceedings of the National Academy of Sciences, a team led by Dr. Ming-Jer Tsai and Dr. Sophia Y. Tsai, both professors of molecular and cellular biology at BCM, described experiments in which the growth of new blood vessels and tumors themselves were suppressed when COUP-TFII was not present.
Their work demonstrates that the receptor directly regulates an angiogenic factor called Angiopoietin-1, which enhances the development of new blood vessels. (Angiogenesis means encouraging the formation of new blood vessels.) Without COUP-TFII, Angiopoietin-1 does not carry out its job efficiently meaning that neither the blood vessels nor the tumors grow, probably because there is limited vasculature to provide nourishment.
"This is important because it means we may be able to find an antagonist that can intervene to halt tumor growth and metastasis," said Dr. Ming-Jer Tsai. "Metastasis is the reason most cancer patients die."
At present, studies of vascular endothelial growth factor (VEGF) inhibitors are underway, he said. This factor also plays an important role in the growth of new blood vessels, and the drugs work against the tumors only for a short while.
"They only work on one pathway of angiogenesis," he said. This finding identifies another important pathway and another way to fight the tumors.
"We studied breast cancer tumors in this model," said Dr. Sophia Tsai. She said the team plans to look at other kinds of solid tumors in which they believe COUP-TFII plays a role in angiogenesis.
Another benefit of knocking out COUP-TFII is that it is not needed in adult animals, she said. COUP-TFII is important in blood vessel formation in the developing fetus but plays no important role in maintaining the vasculature afterward, except in situations such as pregnancy or wound healing. The blood vessels of adult animals that lacked the factor remained normal.
She, Dr. Ming-Jer Tsai and their colleagues are also looking at ways to screen known biological chemicals for the ability to inhibit COUP-TFII.
Others who took part in this work include Drs. Jun Qin, Xinpu Chen and Xin Xie, all postdoctoral associates in the Tsais' laboratories.
Funding for this work came from the National Institutes of Health.
By Frederik Joelving
Tuesday, January 12, 2009
NEW YORK (Reuters Health) A speedy ticker could increase your chances of suffering a fatal heart attack, according to a new study. But in women, regular workouts might help keep the risk low.
Based on more than 50,000 healthy adults, researchers from Norway found that with each increase of 10 beats per minute in resting heart rate, a woman's risk of dying from a heart attack climbed by 18 percent up to the age of 70 years. For men, the risk rose by 10 percent.
A healthy heart beats about 60 to 70 times a minute, with some normal variation on either side. If the rate exceeds 80 for an extended period, doctors start to worry -- that is, if they notice, because an elevated pulse may go undetected in otherwise healthy people, said Javaid Nauman of the Norwegian University of Science and Technology in Trondheim, who was involved in the new study.
In the U.S., heart disease is the leading killer of both men and women. Each year around 1.2 million people suffer a heart attack, and more than one-third die as a result.
High blood pressure, high cholesterol levels and diabetes are well-known risk factors for heart disease, but so far heart rate has been overlooked, experts say.
"It's important to draw attention to heart rate as a cause of heart attack," University of Western Ontario cardiologist Dr. Malcolm Arnold told Reuters Health. He was not involved in the new study, but said its large number of participants made it stand out.
According to Nauman and colleagues, their study, published in the Journal of Epidemiology and Community Health, is the first to examine the combined effect of pulse and exercise on fatal heart attacks.
For the analysis, they tapped into data from a large population study in central Norway, selecting only people who did not have known heart disease.
At the outset of the study in 1984 to 1986, the participants filled out questionnaires about their lifestyle and general health, and scientists measured their heart rates and a few other physiological parameters.
When the study ended in 2004, more than 10,000 of the participants had died, some 40 percent due to heart disease. Overall, men who had a resting heart rate above 100 beats per minute were 73 percent more likely to die from heart attack than men whose heart rate lay within the healthy range.
For women whose with resting heart rate was above 100 beats per minute, the risk of a fatal heart attack increased by 42 percent as a whole, and in those younger than 70 years, it more than doubled.
People who exercised, however, had a considerably lower resting heart rate than those who were more sedentary.
In women, those who reported higher levels of physical activity had a lower risk of dying from heart disease, irrespective of their resting heart rate. Among the most active, even a heart rate above 87 beats per minute did not lead to a significant increase in heart attacks.
"The most promising thing that we find is that you can keep a check on your resting heart rate by engaging in physical activity," Nauman, an exercise physiologist, told Reuters Health, noting that this will reduce the risk of heart attack.
To his knowledge, he added, medications normally used to treat elevated heart rate, such as beta-blockers, have not been shown to have beneficial effects in otherwise healthy people.
According to Nauman, who is working toward his doctoral degree, the lower heart rate in active people was likely due to exercise's balancing effects on the autonomic nervous system, which can crank our heart beat up and down.
The heart's pace again may influence our cardiovascular health both directly and indirectly. Arnold cautioned that because of the study's design, it is impossible to tease out exactly why active women have a lower risk of heart attack.
For instance, people who exercise often may also have a healthier diet, he said, which has a powerful influence on the heart.
Still, he added, the report "confirms the potential benefit of physical activity as part of a healthy life style."
Source: Journal of Epidemiology and Community Health, online January 12, 2010.
Tuesday, January 12, 2009
ScienceDaily (Jan. 12, 2010) New research has found giving up caffeine does not relieve tinnitus and acute caffeine withdrawal might add to the problem. This is the first study of its kind to look at the effect of caffeine consumption on tinnitus.
The study, by the Centre for Hearing and Balance Studies at Bristol University and supported by a grant from Deafness Research UK, is published online in the International Journal of Audiology.
Researchers carried out the first pseudo-randomised, double-blinded, placebo controlled study of phased caffeine withdrawal and abstention to test for a connection between caffeine consumption and tinnitus. The aim of the study was to provide evidence for therapeutic practice to the tinnitus community.
Sixty-six volunteers who experienced tinnitus and who usually consumed at least 150 mg a day of caffeine took part in a 30-day trial. Their usual caffeinated tea and coffee was replaced with double-blinded supplies, under one of two conditions: usual caffeine consumption followed by phased withdrawal; or phased withdrawal followed by reintroduction then usual caffeine consumption.
The study was designed so that the participants didn't know about the conditions. They knew they would receive caffeine on some days, but not on others, but did not know which days were which. Participants were required to complete a questionnaire to measure their tinnitus three times during the study -- at the start, after they had been withdrawn from caffeine for ten days and after they had consumed their normal amount of caffeine for ten days. The participants also kept a very brief record of their tinnitus symptoms each day.
Dr Lindsay St. Claire, Senior Lecturer in the Centre for Hearing and Balance Studies at the University of Bristol, and the lead researcher on the study, said: "With almost 85 per cent of adults in the world consuming caffeine daily, we wanted to challenge the claim that caffeine makes tinnitus worse. Many professionals support caffeine withdrawal as a tinnitus therapy, even though there is a lack of any relevant evidence, and, in fact, acute symptoms of caffeine withdrawal might even make tinnitus worse.
"Many other dietary restrictions are claimed to alleviate tinnitus without the support from controlled studies. Further work in this area would be of great benefit to people with tinnitus and their clinicians."
Deafness Research UK's Chief Executive, Vivienne Michael, added: "For many years, there has been a commonly held belief that caffeine is a major aggravator of tinnitus symptoms although there is very little evidence to support this. In the UK alone, we estimate that for over half a million people, tinnitus has a negative effect on their quality of life.
"This new paper reports on a detailed analysis of the effects of caffeine consumption, withdrawal, abstinence and the severity of tinnitus symptoms. It provides the first experimental evidence to challenge the theory that caffeine triggers or aggravates tinnitus."
Tinnitus affects nearly 15 per cent of adults in the UK at any one time and caffeine is consumed daily by approximately 85 per cent of adults globally.
Monday, January 11, 2010
By Joene Hendry
Monday, January 11, 2010
NEW YORK (Reuters Health) Young children may be more apt to have high blood sugar, a precursor to diabetes, if they average 8 hours or less of sleep a night, report Chinese and American researchers.
This risk may be even greater among obese youngsters, Dr. Zhijie Yu, at the Chinese Academy of Sciences in Shanghai and colleagues note in Archives of Pediatric and Adolescent Medicine.
Moreover, Yu said in an email to Reuters Health, shorter sleep seemed to influence blood sugar "independently of a large variety of risk factors," such as age, gender, birth-related influences, early life feeding or later diet, recent illness, physical activity, body mass, and waist girth.
Yu's team investigated sleep duration and blood sugar levels in 619 obese and 617 non-obese children who were 3 to 6 years old and free of diabetes or blood sugar problems.
Parental reports showed a greater percentage of the obese (47 percent) than the non-obese (37 percent) kids averaged 8 or fewer hours of sleep nightly. These reports also showed nightly averages of 9 or 10, or 11-plus, hours of sleep less common in obese (37 and 16 percent) versus non-obese (43 and 20 percent) kids, respectively.
High blood sugar levels, defined as 100 milligrams of glucose per deciliter of blood after not eating for 8 hours, appeared about 1.35-fold and 2.15-fold more likely in the shorter-sleeping non-obese and obese kids, respectively. (For comparison, 110 milligrams per deciliter is considered "pre-diabetes," while diabetes is diagnosed at 126 milligrams.)
High blood sugar levels were evident in 23 of the 217 non-obese and in 49 of the 291 obese kids sleeping less than 8 hours. By contrast, 21 each of the 175 non-obese and 229 obese kids getting 9 or 10 hours of sleep nightly had high blood sugar.
Overall, 11 of the children had levels above 126 milligrams per deciliter, the level at which diabetes is diagnosed.
These findings hint that, similar to adults, adequate sleep may help kids, "maintain a healthy body weight and an optimal (blood sugar) level," Yu said.
However, Yu's team highlights the need for further studies to confirm these findings in both Chinese and other populations of youngsters.
Source: Archives of Pediatric and Adolescent Medicine, January 2010
Monday, January 11, 2010
(HealthDay News) -- Vitamin B12 helps maintain healthy blood and aids in making important proteins. People who don't get enough can have memory problems or confusion, and are at greater risk of developing anemia, Children's Hospital Boston says.
The hospital mentions these dietary sources of vitamin B12:
Monday, January 11, 2010
WASHINGTON (Reuters) Tiny amounts of lead are common in the blood of U.S. teenagers and may be damaging their kidneys, U.S. researchers reported on Monday.
They found evidence of early kidney damage in children with lead levels far below what is normally considered dangerous and said this could lead to kidney disease in later life.
"To our knowledge, this is the first study to show that very low levels of lead may impact kidney function in healthy children, which underscores the need to minimize sources of lead exposure," Dr. Jeffrey Fadrowski of Johns Hopkins University in Baltimore, who led the study, said in a statement.
Even though sources of lead have been drastically cut in the United States, the metal may still be damaging the health of some people, Fadrowski's team reported in the Archives of Internal Medicine.
They studied test results from 769 adolescents aged 12 to 20 who took part in the Third National Health and Nutrition Examination Survey from 1988 to 1994.
When divided into four equal groups, those in the quarter with the highest lead levels had evidence of slowing kidney function.
"Our findings were particularly striking because we saw slightly decreased kidney function in healthy children without conditions that could account for it, and this could spell more kidney trouble down the road as these children get older or if they acquire additional risk factors for kidney disease, such as high blood pressure and diabetes," said Dr. Susan Furth of Johns Hopkins Children's Center, who worked on the study.
The teens in the study had a mean lead level of 1.5 micrograms per deciliter, considered safe by the U.S. Centers for Disease Control and Prevention. The CDC's level of concern for lead is 10 micrograms per deciliter of blood.
Better Monitoring Urged
The youngsters with lead levels above 2.9 had slower kidney function. They were also more likely to come from poor families with lower education levels.
The researchers noted that 26 million Americans have chronic kidney disease, which can be caused or worsened by high blood pressure.
Lead exposure has decreased substantially in the United States, primarily due to measures including the 1996 ban on lead in gasoline and a 1978 phaseout of lead in paint.
But most of the U.S. general population still has detectable blood levels, the researchers added.
"Current exposure sources include industry, lead paint, folk remedies, glazed pottery, candy, and drinking water in some urban areas, and certain populations continue to experience high lead exposure, in particular, inner-city children and adults living in areas of low socioeconomic status."
They called for better monitoring of both lead and kidney function in children.
Source: Archives of Internal Medicine, January 11, 2010.
Monday, January 11, 2010
ScienceDaily (Jan. 11, 2010) Researchers at the Indiana University and Stanford University schools of medicine have determined how a "chemical chaperone" does its job in the body, which could lead to a new class of drugs to help reduce the muscle damage caused by heart attacks
Such drugs would work by restoring the activity of a mutated enzyme, rather than taking the more common approach of blocking the actions of a disease-related protein.
The team, led by Thomas Hurley, Ph.D., associate chair and professor of biochemistry and molecular biology at IU, and Daria Mochly-Rosen, Ph.D., professor of chemical and systems biology at Stanford, report in the journal Nature Structural Biology published online Jan. 10 that the compound, called Alda-1, acts much like a shim to prop up a mutated form of a key enzyme, restoring the enzyme's function.
The enzyme, called ALDH2, plays an important role in metabolizing alcohol and other toxins, including those created by a lack of oxygen in the wake of a heart attack. It also is involved in the metabolism of nitroglycerin, which is used to prevent chest pain (angina) caused by restricted blood flow and oxygen to the heart.
However some people, including about 40 percent of people of East Asian descent, carry a mutated form of the ALDH2 enzyme that does not carry out its intended functions well. People with the mutated form of the enzyme are at increased risk of cardiovascular damage.
The IU and Stanford team reported in 2008 in the journal Science that in laboratory tests Alda-1 bypassed the body's usual signaling system and activated the ALDH2 enzyme directly, reducing damage to heart muscle tissue. That finding raised the possibility of new treatments for heart attacks, methods to protect hearts during open heart surgery, organ transplants, stroke and other situations in which blood flow is interrupted.
Their current paper describes how Alda-1 activates the ALDH2 enzyme in a process that Dr. Hurley likens to a woodworking procedure in which Alda-1 attaches to the ALDH2 enzyme at a crucial spot and acts like a shim or wedge to prop it up.
"Because of the mutation in the gene, parts of the protein structure become loose and floppy. Alda-1 reactivates the enzyme by propping up those parts of the structure so they regain normal function," said Dr. Hurley, director of the Center for Structural Biology on the Indiana University-Purdue University Indianapolis campus.
Determining how the Alda-1 compound works will enable the researchers to begin working on alternative compounds that hold more promise as potential drugs. One primary improvement needed is the ability to give the drug orally, rather than by injection, Dr. Hurley said.
"Based on the information from these studies, we're now ready to sit down with medicinal chemists and start designing new analogues by applying our understanding of what we need to leave alone and what we can modify to improve the properties of Alda-1," he said.
He predicted that alternative compounds could be available for testing by mid-2010.
The research was supported by grants from the National Institute of Alcohol Abuse and Alcoholism at the National Institutes of Health.
Monday, January 11, 2010
MONDAY, Jan. 11 (HealthDay News) -- New research shows that PET brain scans can diagnose which type of Parkinson's-related disease a person has.
Between 1998 and 2006, researchers scanned the brains of 167 patients who had signs of Parkinsonism but hadn't been specifically diagnosed. They used PET (positron emission tomography) technology.
The researchers found that the scans allowed them to differentiate between idiopathic Parkinson's disease, multiple system atrophy and progressive supranuclear palsy, although the diagnoses sometimes differed from those of doctors who assessed the patients.
According to the researchers, who report their findings online in advance of print publication in the February issue of The Lancet Neurology, early diagnosis helps doctors place patients in proper drug trials.
In an accompanying commentary, Professor Angelo Antonini of the IRCCS San Camillo, Venice, and Parkinson Institute in Milan, Italy, wrote: "The clinical and research relevance of these findings should not be underestimated. Neuroprotective and disease-modifying drug research is intensifying, and results mostly rely on accurate early diagnosis."
The National Institutes of Health has more on Parkinson's disease.
Sunday, January 10, 2010
By Kate Kelland
Sunday, January 10, 2010
LONDON (Reuters) Researchers have found four new genetic variants that increase the risk of contracting one of the major forms of leukemia, confirming that risk factors for the fatal blood cancer can be inherited.
The findings mean scientists now know of 10 genetic variants associated with chronic lymphocytic leukemia (CLL), scientists at Europe's Institute of Cancer Research who conducted the study said.
The four new genetic factors are all common in European populations and each factor contributes to an increase in the risk of the disease.
CLL is the most common type of leukemia
in adults, accounting for around 30 to 40 percent of all forms of leukemia in
Western countries. Most of those diagnosed are over the age
of 55, and while the incidence of CLL is broadly equal in black and white populations, the disease is rare among Asians.
Richard Houlston, who led the study, said it confirmed the inherited risk of CLL, and showed it was not due to a single gene due to the cumulative effect of many genetic changes.
Each person may carry any number, from a few of the identified risk factors to all of them, he said in research published in the journal Nature Genetics. And the more genetic factors carried, the higher their risk of developing CLL.
"People who have more than 13 risk factors are seven times more likely than the general population to develop CLL," Houlston added in a statement about the study.
The risk factors were identified using a genetic analysis technique that scientists have used previously to find risk genes in breast, prostate, testes, brain and colon cancer and childhood leukemia.
The researchers scanned the genes of 2,503 CLL patients and compared them to 5,789 healthy people, looking for differences in DNA between the two groups.
In previous studies, Houlston's team found that genetic factors could make people more susceptible to CLL, identifying six genetic factors more common among sufferers.
The four new factors add to those findings and the study also found that 87 percent of people with CLL would have at least one of these genetic risks.
David Grant, scientific director of the Leukemia Research charity which funded the study, said it confirmed some long-held suspicions that this form of leukemia may run in families.
"This research is providing the genetic evidence that an increased risk of developing CLL can be inherited," he said in a statement.
"However it is clearly a complex picture and we need to study more families before we can be certain of the particular genetic traits that are most important."
(Editing by Michael Roddy)
Sunday, January 10, 2010
SUNDAY, Jan. 10 (HealthDay News) -- Researchers believe they know why light exacerbates the already debilitating pain of migraines, even in some blind people.
A report published online Jan. 10 in Nature Neuroscience reveals how visual and pain pathways in the brain converge to produce this phenomenon.
Although the findings are unlikely to help migraine patients in the near future, "this gives us a little better insight as to the theory and mechanism behind migraine," said Dr. Michael Palm, an assistant professor of neuroscience and experimental therapeutics and internal medicine at Texas A&M Health Science Center College of Medicine, College Station, and director of the Parkinson's and Headache programs at Texas Brain and Spine Institute in Bryan.
"We are making progress in understanding this phenomenon," he said.
The Boston-based researchers report there are cells in a part of the brain called the thalamus "where information from the visual system and information from the pain system converge, and that anatomic convergence provides the first available explanation for how it could be that light makes pain worse," added Dr. Richard Lipton, director of the Montefiore Headache Center and professor of neurology and epidemiology at Albert Einstein College of Medicine in New York City.
About 85 percent to 90 percent of all migraine sufferers report having photophobia, which is when light makes the pain worse, said study senior author Rami Burstein, an associate professor of anesthesia and neuroscience at Beth Israel Deaconess Medical Center and Harvard Medical School in Boston.
"We had no clue in the world where in the world light and pain talk to each other in the brain," Burstein said. "They have completely different pathways in the brain."
"For light to make pain, those pathways would have to converge at some level," Lipton noted.
To solve the paradox, the team studied 20 blind individuals, all of whom suffered from migraines. Six participants had no light perception at all and no functioning optic nerve. These individuals also experienced no photophobia.
The remaining 14 people could sense light and dark and also experienced photophobia.
"This told us that the optic nerve is critically needed in order to produce photophobia or exacerbation of the headache by light," Burstein explained.
The researchers next discovered that a set of photoreceptors called melanopsin project onto neurons on the thalamus that also process pain signals.
"If we wanted to understand how light makes the pain worse, we needed to follow in the brain the pathways that lead from the eye into the brain using the third group of photoreceptors," Burstein said. "That is the connection so at that point we shifted to animals."
The thalamus is the brain's sensory switchboard, receiving sensory signals from different parts of the body then redirecting them to various sensory, motor and cognitive areas of the cortex.
"We identified a new pathway in the brain that originates in the eye and goes to the brain areas where neurons are found that are active during migraine attacks," Burstein said. "The light can increase the electrical activity in neurons that are active to begin with."
The findings should put to rest any thoughts that patients exaggerate their sensitivity to light, Lipton said. "This provides an anatomic and physiological basis for a common experience -- that light makes pain worse, not because you're a whiner, but because there is an anatomic pathway that links the visual system to the pathway that produces head pain," Lipton said. "That odd bit of clinical symptomatology has a firm basis in brain science."
The National Headache Foundation has more on migraines.