Friday, July 31, 2015

Exciting new drugs for Alzheimer's disease? Nah.

Exciting new drugs for Alzheimer’s disease? Nah.
So, exciting new drugs for treating Alzheimer's disease, right?
Wrong. Or, rather, let's allow for semi-miraculous outcomes and say instead that this recent news is unlikely to be right.
31 july 2015--Most of the news concerned research results on two monoclonal antibody drugs reported at last week's Alzheimer's Association International Convention in Washington. Both drugs attack beta amyloid, the protein that is suspected by some researchers of gumming up the brain. Not a theory embraced by all, however.
The two drugs aren't even new drugs. Solanezumab, from Eli Lilly, has already bombed in two previous clinical trials. Biogen reported some results from aducanumab, adding to data released in March.
There are plenty of hard-nosed critiques out there, so it's difficult to understand the media huzzahs. Unless so-called reporters are just swallowing press releases whole.
Oh, wait . . .
Emily Underwood described the drugs' uneven history at Science, observing of the new results, "the small cognitive benefits and the fact that one trial didn't show any reduction in the amyloid in people's brains left plenty of room for skepticism."
Kevin Lomangino took stock at HealthNewsReview and noted "So why bother to present provisional results that don't even demonstrate that the drugs had any noticeable effect? As Matthew Herper points out at Forbes, the show at this week's conference may have been more about company stock prices than about informing patients and the public."
Lomangino was unhappy at pretty much all the coverage except for a piece at NBC–and even that was damaged, in his view, by a cheerleading hed. Which presumably the writer of the reasonable story had nothing to do with, as is so often the case.
At In the Pipline, pharma researcher Derek Lowe is not happy about the aducanumab study's small size. "And the first thing that has to be learned from watching clinical research (especially for a disease like Alzheimer's) is that you cannot draw conclusions until you see a large, well-run data set. Ignore this advice at your peril. The list of promising-looking Alzheimer's ideas that have evaporated on contact with a larger trial is long and terrible."
As for solanezumab, Lowe says Lilly claims to be seeing more effect in the patients who started the therapy earlier, but "not everyone is buying that interpretation. The effect they're seeing may well be clinically meaningless."
Solanezumab failed to meet its endpoints in two Stage 3 clinical trials. Leading researchers to proclaim, in one of the more tortured arguments ever, that the disappointing outcome must mean that it works not just on symptoms but on the underlying disease itself.
Doc Perry Wilson treats this argument with the contempt it deserves at Medpage Today, saying solanezumab is "unlikely to have any clinical benefit" and calling the announcement "a Master Class in how to spin your drug that failed its original trial."
Recent research is also showing that even if a splendid Alzheimer's drug arrives, it may be splendid for only part of the population. Frederick Kunkle reports at the Washington Post that African-Americans with Alzheimer's disease also seem to suffer from additional brain pathologies less frequent in Caucasians, notably the accumulation of abnormal proteins called Lewy bodies and lesions in tiny blood vessels.
Researchers at the Alzheimer's meeting have also found that older women with cognitive decline seem to get worse and progress to Alzheimer's disease twice as fast as men, Laura Geggel reports at LiveScience.
According to Harry Johns at Congress Blog, Alzheimer's is already the US's most expensive disease, one that threatens to bankrupt Medicare. Today, Medicare spends nearly 1 out of 5 of its dollars on caring for people with the disease. By 2050, a generation from now, it is estimated that will climb to nearly 1 in 3 dollars.
Neuroscientist Douglas Fields, writing at a SciAm Mind guest blog, is optimistic that even the obstructive current Congress will be open to funding more Alzheimer's research. The key, he says, will be early diagnosis. Well, maybe. But until there are effective ways of treating early Alzheimer's, early diagnosis is kinda beside the point, isn't it? Or could even be a bad idea, considering what bombshells like this hopeless news can do to patients and their families?
Bloomberg View attempts a rational economic argument for more research: "Lawmakers may also want to consider that taxpayers will end up paying either way. Medicare and Medicaid will spend $153 billion caring for patients with Alzheimer's and other kinds of dementia this year, or about 261 times what the NIH will spend looking for ways to prevent and cure the disease. Until one is found, these numbers are way out of balance."
This story is republished courtesy of PLOS Blogs:
Provided by PLOS Blogs

Thursday, July 30, 2015

Fats from fish and vegetables may increase longevity

A study that included more than 4,000 Swedish 60-year-olds, showed that high levels of polyunsaturated fats in the blood are linked to increased longevity and decreased risk of cardiovascular disease. The study was a collaboration between Karolinska Institutet and Uppsala University and was published in the medical journal Circulation.
In most studies that investigate the correlation between food and longevity, the subjects report what they have eaten, and this may be inaccurate. In the current study, the level of polyunsaturated fats in the  of the subjects was measured. This has previously been shown to be a good indicator of intake of these fats that are abundant in oily fishes such as salmon and herring, as well as in walnuts, avocado and olives.
30 july 2015--"This is the world's largest study in the area as far as we know, and one of its strengths is that both men and women were evaluated at the same time", says Professor Mai-Lis Hellénius at the Department of Medicine, Solna, Karolinska Institutet, one of the researchers in this study.
The results show that high levels of polyunsaturated fats in the blood are associated with decreased overall mortality in both men and women. In women, polyunsaturated fat intake was also linked to a decreased risk of cardiovascular disease. When the results were calculated, other important lifestyle factors, such as exercise alcohol and smoking, were also taken into account.
"The findings are clinically relevant and support current dietary guidelines that advise us to shift from saturated to unsaturated fats", says Mai-Lis Hellénius.
More information: "Polyunsaturated Fat Intake Estimated by Circulating Biomarkers and Risk of Cardiovascular Disease and All-Cause Mortality in a Population-Based Cohort of 60-Year-Old Men and Women." Circulation 17 June 2015,DOI: 10.1161/CIRCULATIONAHA.115.015607 
Provided by Karolinska Institutet

Wednesday, July 29, 2015

Scientists discover link between common medications and serious falls in older men

old person

29 july 2015--Using data from The Irish Longitudinal Study on Ageing (TILDA), scientists from Trinity College Dublin, St James's Hospital, Dublin, Ireland and three UK Universities have discovered a significant link between serious falls causing injury in older men and a particular group of commonly used medicines. The findings are published today by the Journal of the American Geriatrics Society.
Many medicines which are commonly prescribed for older people for bladder problems, depression, psychosis, insomnia, and respiratory problems, have anti-cholinergic effects. The medications affect the brain by blocking a key chemical called acetylcholine which is involved in passing messages between nerve cells. This can lead to side effects including blurred vision, increased heart rate, sedation and confusion.
Previous studies have shown an impact on cognitive function and mortality from taking multiple anti-cholinergic medicines. In this important new study, the researchers led by Dr Kathryn Richardson who carried out the research at the Department of Gerontology in Trinity and at the Faculty of Medicine and Health Sciences at the University of East Anglia, examined whether the use of such medicines increased the risk of subsequent serious falls (which caused injury) in people aged over 65 years in Ireland.
Using the TILDA data which recorded the medications the participants were taking and the number and type of falls they had experienced, the team found that falls resulting in injury were more than twice as likely in men taking medicines with potent anti-cholinergic activity. The effect remained even after accounting for differences in health and other risk factors for falls. A greater use of such medicines increased the risk for these men further. There was no such association for women, however.
Speaking about the significance of these findings for prescribing practices in older people, lead author Dr Kathryn Richardson, a former PhD student at Trinity, who is now a Research Fellow at the University of East Anglia said: "Our findings indicate the importance for doctors, pharmacists and healthcare professionals to regularly review the appropriateness of medications taken by their older patients. It is however, important that people don't stop taking any medications before speaking with their GP. It is not fully clear why the same link was not found in women and further research is needed to explore this and the reasons behind the findings in men".
Dr Richardson continued: "Experiencing a fall can have a devastating impact on older people's lives and is a major contributor to care home admission and hospitalisation, so it is vitally important for us to find ways to reduce the risk of falls or their severity."
Senior author and Principal Investigator of TILDA Professor Rose Anne Kenny said: "Falls are one of the leading causes of loss of independence as people get older and the principal reason given for admission into nursing home care in Europe. If early risk factors are identified and modified, falls can be prevented. This paper highlights important new risk factors for falls."
Dr Chris Fox, Clinical Reader/Honorary Consultant Psychogeriatrician at the University of East Anglia said: "With the rising levels of frailty in older people we must develop strategies to maintain health and avoid prescribing medicines which could cause a deterioration- such an approach could be simply implemented using tools available"
Dr Ian Maidment, Senior Lecturer in Clinical Pharmacy at Aston University said: "After a fall, an older person may never regain the same quality of life. This research helps us to understand how medication is linked to falls. It is vital that doctors, nurses and pharmacists review medication if someone has suffered a recent fall."
Provided by Trinity College Dublin

Tuesday, July 28, 2015

Insulin resistance increases risk for Alzheimer's disease, study finds

The fact that obesity increases the risk of cardiovascular disease and some cancers is well known. But a new Iowa State University study adds to the growing evidence that memory loss should also be a top concern.
The study, published in the Journal of the American Medical Association Neurology, found a strong association between insulin resistance and memory function decline, increasing the risk for Alzheimer's disease. Auriel Willette, a research scientist in the Department of Food Science and Human Nutrition at Iowa State, says insulin resistance is common in people who are obese, pre-diabetic or have Type 2 diabetes.
28 july 2015--Willette and co-author Barbara Bendlin, with the Wisconsin Alzheimer's Institute, examined brain scans in 150 late middle-aged adults, who were at risk for Alzheimer's disease, but showed no sign of memory loss. The scans detected if people with higher levels of insulin resistance used less blood sugar in areas of the brain most susceptible to Alzheimer's. When that happens, the brain has less energy to relay information and function, Willette said.
"If you don't have as much fuel, you're not going to be as adept at remembering something or doing something," he said. "This is important with Alzheimer's disease, because over the course of the disease there is a progressive decrease in the amount of blood sugar used in certain brain regions. Those regions end up using less and less."
Willette's work focused on the medial temporal lobe, specifically the hippocampus - a critical region of the brain for learning new things and sending information to long-term memory. It is also one of the areas of the brain that first show massive atrophy or shrinkage due to Alzheimer's disease, Willette said.
Cognitive decline can have immediate impact
This is the first study to look at insulin resistance in late middle-aged people (average age was 60), identify a pattern of decreased blood sugar use related to Alzheimer's and link that to memory decline, Willette said. Participants were recruited through the University of Wisconsin-Madison and Wisconsin Registry for Alzheimer's Prevention study, an ongoing study that examines genetic, biological and lifestyle factors that contribute to dementia.
The link between insulin resistance and Alzheimer's disease is important for prevention, but the risk is much more immediate, Willette said. Problems regulating blood sugar may impact cognitive function at any age. Testing for insulin resistance in obese patients and taking corrective action, through improved nutrition and moderate exercise, is a crucial first step, he said.
"We are terrible at adjusting our behavior based on what might happen in the future," Willette said. "That's why people need to know that insulin resistance or related problems with metabolism can have an effect in the here and now on how they think, and it's important to treat. For Alzheimer's, it's not just people with Type 2 diabetes. Even people with mild or moderate insulin resistance who don't have Type 2 diabetes might have an increased risk for Alzheimer's disease because they're showing many of the same sorts of brain and memory relationships."
Understanding the progression of cognitive decline will take additional research. Willette says following those who are at-risk through the different stages of dementia and Alzheimer's will offer insight as to what happens as their cognitive function declines.
More information: JAMA Neurol. Published online July 27, 2015. DOI: 10.1001/jamaneurol.2015.0613 
Provided by Iowa State University

Monday, July 27, 2015

Study identifies challenges of delirium detection in older adults in emergency department

27 july 2015--An estimated one to two million older adults with delirium visit hospital emergency departments in the United States annually. Yet about two-thirds of the cases of this sudden and potentially lethal change in mental status are unrecognized by emergency department clinicians who are under time pressure and almost always managing multiple patients at once. Half a year later, those with undetected delirium who were discharged from the emergency department have significantly higher mortality rates than those whose delirium was recognized.
Researchers from the Indiana University Center for Aging Research and the Regenstrief Institute have conducted what is believed to be the first study to interview providers to identify the barriers and possible catalysts to delirium detection in emergency care situations.
"Delirium is a serious condition that is too often missed in the ambulance and emergency department and we need to improve its detection," said Michael LaMantia, M.D., MPH, an Indiana University Center for Aging Research scientist, Regenstrief Institute investigator and assistant professor of medicine at IU School of Medicine. "Patients sent home from the emergency department with undetected delirium have six-month mortality rates almost three times greater than their counterparts in whom delirium is detected. Unrecognized delirium presents a major health challenge to older adults and an increased burden on caregivers and the health care system."
The researchers, led by Dr. LaMantia, report that the hectic emergency department environment, typically focusing on accident victims and acutely ill individuals rather than older adults with multiple chronic illnesses who are experiencing a sudden need for emergency care, is the largest challenge to delirium recognition and treatment. They also found that emergency department medical staffers were more likely to think of delirium in older adults when patients exhibit agitation, rather than in those who are more withdrawn.
"Emergency Medical Service, Nursing, and Physician Providers' Perspectives on Delirium Identification and Management" appears online ahead of print in Dementia: The International Journal of Social Research and Practice, a peer-reviewed journal.
In focus groups convened by the researchers, emergency physicians, emergency department nurses, and  personnel indicated that delirium recognition is hampered by not having a sense of the baseline cognitive state of the patient, particularly among those with pre-existing cognitive impairment such as Alzheimer's disease.
Doctors indicated a need for a delirium screening test that could be rapidly administered. One physician volunteered. "We're comfortable with obvious delirium. We're all petrified, and we, at least I know my own limitations is that I guarantee you I'm missing patients who have it. And so what would make me comfortable is that when you come back to me and you said, hey we've got a thirty second test that is pretty good at screening for delirium."
Other physicians added that an emergency department dementia screening tool had to be "physician proof," simple to document, not open to interpretation, brief to administer, and "better than our judgment."
Some nurses admitted to more discomfort with treating delirium. Other nurses admitted to feeling overwhelmed by the burden of caring for an older adult with delirium in the busy emergency department environment.
"Clear steps should be taken to improve delirium care in the emergency department including the development of mechanisms by which the medical staff can easily learn about the patient's mental status from family or friends, the adoption of a systematized approach to recognizing delirium, and the institution of protocols to treat the condition when it's identified," Dr. LaMantia said. "The efforts of emergency providers, geriatricians, brain scientists, and implementation experts will be needed to further develop and test these responses to this challenging clinical condition."
Provided by Indiana University

Sunday, July 26, 2015

UK says cure or drug for dementia possible by 2025

UK says cure or drug for dementia possible by 2025

Cameron says he hopes to kick-start an international effort to find a cure or effective treatment for dementia by 2025 .

26 july 2015--British Prime Minister David Cameron says he hopes to kick-start an international effort to find a cure or effective treatment for dementia by 2025.
At a one-day summit on dementia  hosted by the U.K., Cameron declared that discovering a cure or treatment for dementia is "within our grasp."
The Group of Eight health and science ministers signed a declaration agreeing to identify "a cure or disease-modifying therapy for dementia" by 2025, among other goals, including increased funding and greater cooperation.
Globally, about 44 million people are estimated to have dementia, according to Alzheimer Disease International. That number is projected to jump to 76 million by 2030.
Several drugs lessen the symptoms of dementia but none improves the underlying disease. In the U.S., no new drug has been licensed for a decade.
Before the meeting, several British and American scientists called for G-8 countries to commit to investing at least 1 percent of their dementia costs into research. In the U.S., that would mean quadrupling the current $500 million budget to $2 billion.
"I don't think we'll find the silver bullet, but it is possible we will get a signal that a drug may modify dementia in the next three to five years," said Dr. Ronald Petersen, chair of a U.S. advisory council on Alzheimer's and a neurologist at the Mayo Clinic in Minnesota. Petersen attended and said it was possible dementia might one day be treated with a mixture of drugs, like AIDS or high blood pressure.
"The challenge is huge and we are a long way from a cure, but there is hope," Cameron said.
Still, numerous grand declarations to solve health problems have previously flopped. In 1997, U.S. President Bill Clinton promised to find a vaccine for AIDS within a decade. None have yet been discovered.
More information: 

Identifying biomarkers key to early intervention in Alzheimer's disease

Identifying biomarkers key to early intervention in Alzheimer's disease

26 july 2015--Although the term didn't surface until the 1980s, the concept of biomarkers has been around for almost a century. Today, doctors routinely test blood for signs of anemia or the antigen associated with prostate cancer. Urine samples can hint at the presence of infection or diabetes, and EEGs diagnose electrical abnormalities in the brain.
But scientists are now advancing the concept, looking for ways to identify a host of diseases early in the process to provide opportunity for early intervention and improve the chances that treatment will be effective.
This is particularly true for Alzheimer's disease (AD), where evidence points to the fact that the disease process begins long before someone has clinical symptoms, and the ramifications of the disease – both financial and emotional – are disastrous.
At the University of Kentucky's Sanders-Brown Center on Aging, researchers are looking for biomarkers that might serve as an early warning system for AD. The process is not without complications, but these scientists possess a collective "Rosie the Riveter" spirit.
Mark Lovell is one of them. According to Lovell, the only definitive way to diagnose AD is through autopsy, though other options, such as PET imaging to identify the presence of AD pathology, are becoming more widely used. The challenge, explains the bioanalytical chemist and Jack and Linda Gill Professor of Chemistry, is finding a biomarker that 1) is an accepted predictor of the disease and 2) can easily be identified by a physician at the clinic level.
"Multiple studies show alterations in levels of the proteins associated with AD – tau and beta amyloid— in , but a spinal tap to obtain that fluid is often a hard sell for patients", Lovell said. "Furthermore, there appears to be variability in the data connecting the levels of these proteins in CSF and the diagnosis of AD, which has limited the use of beta amyloid and tau clinically."
But in the spirit of Sanders-Brown's iconic first director and Lovell's research mentor, William Markesbery, Lovell is willing to explore unconventional ideas so he started searching for alternative biomarkers.
Working with Bert Lynn, director of UK's Mass Spectrometry Center, Lovell began to sort proteins in CSF samples by weight. As the results came in, two particular proteins (transthyretin and prostaglandin-d-synthase) caught his attention.
"We were able to tease out that these two proteins, when subjected to oxidative damage, tended to stick together and fractionate at a higher molecular weight than expected," said Lovell.
Further study suggested that these proteins may signal dysfunction in the choroid plexus, a brain region responsible for the production and filtration of cerebrospinal fluid.
Since, in AD, current data suggest there are changes in the transfer capacity of the choroid plexus it made sense to Lovell and Lynn that these two proteins might make a good biomarker for AD.
Identifying biomarkers key to early intervention in Alzheimer's disease
The next step, says Lovell, was to go "downstream" to blood or urine, for example to determine whether this same protein combination appears there as well.
"I've historically been skeptical that blood can be as strong a predictor of Alzheimer's disease as cerebrospinal fluid (CSF), but I was pleasantly surprised to see that there was a reasonable correlation in samples of CSF and blood taken from the same patients," Lovell said.
Lovell cautions that further evaluation in larger sample populations is necessary before this can be called a definitive success, but if the hypothesis is borne out, "we will have a blood based biomarker that might be more predictive than amyloid beta peptide."
Ultimately, Lovell thinks AD will be diagnosed by a panel of three or four biomarkers, rather than a single "up or down" test. And that's where Brian Gold comes in.
Gold, a cognitive neuroscientist, is fascinated by CSF protein biomarker findings of Lovell and others and is conducting his own research in the hopes of using brain imaging to find non-invasive AD biomarkers. However, up until now, Gold explains, most MRI studies of preclinical AD have been restricted to structural volumetric characteristics of the brain.
"We've instead been focusing on microstructural brain changes detectable with a form of MRI called diffusion tensor imaging (DTI), which assesses the diffusion of water molecules in the brain," said Gold. "As cellular structures begin to degenerate, tissue barriers degenerate as well, allowing for increased water diffusion DTI-based changes in the brain are thus somewhat analogous to hairline cracks in a house's foundation that precede visible structural damage."
Gold and his colleagues are one of just a handful of U.S. groups exploring how CSF protein biomarkers correlate with microstructural brain changes using DTI and dynamic physiological changes using functional MRI.
His work, published last year in the Neurobiology of Aging, found tantalizing correlations between reduced white matter microstructure in the brain and the presence of CSF markers of AD.
"In other words, if our findings using DTI and functional MRI are highly correlated with Lovell's CSF biomarkers, we have potentially uncovered a minimally invasive way to diagnose pre-clinical AD."
While Gold and Lovell look prospectively for the Holy Grail, others at Sanders-Brown are taking a retrospective look using big data.
Dick Kryscio and Erin Abner help manage the Alzheimer's Disease Center (ADC) database, a collection of thousands of data points from more than 1300 research volunteers enrolled in the Biologically Resilient Adults in Neurological Studies cohort. With literally thousands of blood samples, CSF samples, results from cognitive testing, medication history, physical and neurologicalexaminations, and medical history, the database size probably approaches the inventory of a mid-sized grocery store. Abner and Kryscio troll the reams of data looking for consistencies that might constitute an early warning of disease.
Kryscio notes that biomarkers serve two purposes—as a predictor of disease and as a means to a diagnosis. While most biomarkers today serve the latter function, "a marker truly earns its keep when a person is on his or her way to disease," he says.
And, while not a biomarker in the strictest sense, their most promising work in predicting disease has been in the area of self-reported memory complaints.
Both Abner and Kryscio have published studies in Neurology and Journal of Prevention demonstrating a link between self-reported memory complaints and the development of cognitive impairment later in life.
"In other words, people usually are the best judges of their own memory—they can detect subtle problems years before there are more obvious symptoms," says Abner. She points out that it's an enormous oversimplification. "You aren't likely to have AD just because you can't remember where you put your keys one day," she said but added it has potential as a candidate for the "panel of tests."
Abner and Kryscio's efforts have international ramifications, as they are two of the gatekeepers for the ADC biospecimens, which are shared worldwide.
"The number of data parameters, and the longitudinal nature of the data available, makes this database world-class, but there are nonetheless a finite number of studies for which we can provide specimens before the supply is exhausted," Kryscio said. "It's a service to our research participants to help researchers with a study design that eliminates waste and maximizes the quality of the science, and we don't take that responsibility lightly."
Regardless of the path—whether looking forward or backward—the ability to detect AD at its earliest stages will have huge ramifications on the race to treat and eventually cure the most expensive malady currently known to man.
Provided by University of Kentucky

Saturday, July 25, 2015

Public interest has 'medicalised' vitamin D yet benefits remain uncertain

Public interest has ‘medicalised’ vitamin D yet benefits remain uncertain
Persistent public interest in vitamin D, plus widespread testing of vitamin D status and prescribing by doctors, has led to a significant increase in people taking supplements despite limited evidence of any health benefits – according to new NIHR-funded research from Queen Mary University of London and published in BMJ Open.
25 july 2015--A team of researchers set out to explore public knowledge, beliefs and attitudes to  D by holding a focus group study of 58 adults in East London. The study found many respondents lacked knowledge about vitamin D, including dietary sources and government recommendations. Many had opposing views on the fortification of food products and many were also confused about the risks and benefits of sunshine in association with vitamin D.
In addition, excessive testing and supplementation via health professionals has contributed to a medicalised view of vitamin D. While potentially useful in some high-risk groups (vitamin D deficiency is common and is associated with a range of illnesses) scientists are still unsure about the clinical significance of deficiency and the impact of supplementation. Clinical trials to test the efficacy of vitamin D supplements have largely had inconsistent results and there is no official consensus on the benefits of supplementation.
The study revealed one East London hospital laboratory processed a 10-fold increase in vitamin D test requests – largely from GP practices – over a 5-year period from 2006 to 2010, reaching 44,500 per year. Prescribing of vitamin D preparations has risen dramatically, with eight in every 100 east London patients receiving vitamin D. In the London borough of Tower Hamlets, the number of patients prescribed vitamin D outstripped that for statins, aspirin, and proton pump inhibitors.
Professor Chris Griffiths, who led the study at Queen Mary University of London, comments: "Use of vitamin D as a Google search term increased fivefold over the last decade. It's gone from being a subject of scientific interest to a big public conversation – yet we lack a clear benchmark of the public's knowledge on vitamin D and this is vital to inform professional guidance and public health initiatives.
"Our findings highlight the need for accessible, reliable public information on vitamin D, and clear guidance on the risk and benefits of sun exposure. In particular, this information needs to differentiate between the advice for the general population and those at high risk of vitamin D deficiency."
"Doctors and the general public need to be aware of the limited evidence that vitamin D supplementation improves health, and we encourage doctors to consider this lack of evidence more carefully when testing and prescribing."
Professor Adrian Martineau, Co-Author and vitamin D expert at Queen Mary University of London, added: 'There is growing interest in the potential for food fortification to reduce the prevalence of profound vitamin D deficiency in the UK population, following the lead of countries like the USA and Finland. Our research suggests that, while some members of the general public are open to such an approach, others remain sceptical. We hope that our findings will help the Department of Health to design appropriate and acceptable fortification strategies if a decision is made to go down this road.'
More information: "'Test me and treat me'—attitudes to vitamin D deficiency and supplementation: a qualitative study." BMJ Open 2015;5:e007401 DOI: 10.1136/bmjopen-2014-007401 
Provided by Queen Mary, University of London

Friday, July 24, 2015

'Successful aging' linked to harmful drinking among over 50s

The over 50s who are 'successful agers'—healthy, active, sociable, and well off—are more at risk of harmful drinking than their less successful peers, concludes research published in the online journal BMJ Open.
Harmful drinking is a "middle class phenomenon" which may be a hidden health and social problem in otherwise successful older people, warn the researchers, who call for explicit guidelines on alcohol consumption for this group.
24 july 2015--They base their findings on more than 9000 responses to the two most recent waves (2008-9 and 2010-11) of the English Longitudinal Survey of Ageing (ELSA)—a long term study of a representative sample of those aged 50 and above living independently at home in England.
Given that alcohol consumption is on the rise among older people in England, the researchers wanted to tease out the social and economic factors associated with harmful drinking, and changing patterns of consumption over time.
They used national guidance to define increasing risk of harmful drinking at 22-50 weekly units for men and 15 to 35 weekly units for women; and higher risk, at more than 50 and more than 35 weekly units, respectively, for men and women.
Survey participants were asked about a range of potentially influential factors: income; educational attainment; self reported health; whether they smoked; diet; physical activity levels; whether they felt lonely or depressed; ethnic background; marital status; caring responsibilities; religious beliefs; employment status; and social engagement (civic participation, networks of friends, cultural activities).
Analysis of the responses showed that the risk of harmful drinking peaked for men in their early 60s and then gradually tailed off, whereas for women risky drinking fell in tandem with age.
These patterns suggest that the current group of over 50s may be carrying on levels of higher consumption developed in their younger years, in later life, say the researchers.
Certain factors were linked to a heightened or lowered risk of harmful drinking.
Income was associated with a higher risk, but only among women, while smoking, higher educational attainment, and good health were all linked to heightened risk in both sexes.
Higher risk of harmful drinking was not linked to feelings of loneliness or depression, but it was more likely among men living on their own, including those who were separated/divorced. And it was more common among men of white ethnicity.
Caring responsibilities lowered the probability of being at higher risk among women, but religious belief did not—for either sex.
Employment status did not seem to be a significant factor, but women who had retired were more likely to be at higher risk.
When the researchers looked at changes in  between the two waves of the survey, they found that among women, loneliness, younger age, and higher income were all associated with the likelihood of becoming a higher risk drinker by 2010-11. A healthy diet seemed to lessen the risk.
Among men, these transition patterns were similar, except that caring responsibilities, loneliness, older age and lower income increased the likelihood of no longer drinking at risky levels by wave 2 of the survey.
"We can sketch—at the risk of much simplification—the problem of harmful drinking among people aged 50 or over in England as a middle class phenomenon: people in better health, higher income, with higher educational attainment and socially more active are more likely to drink at harmful levels," write the researchers.
"Our findings suggest that harmful drinking in later life is more prevalent among people who exhibit a lifestyle associated with affluence and with a 'successful' ageing process," they add.
"Harmful drinking may then be a hidden health and social problem in otherwise successful older people," they warn, concluding: "Consequently, and based on our results, we recommend the explicit incorporation of alcohol drinking levels and patterns into the successful ageing paradigm."
More information: BMJ Open DOI: 10.1136/bmjopen-2015-007684 
Provided by British Medical Journal

Thursday, July 23, 2015

New study indicates ankle-brachial index associated with mild cognitive impairment

In a large population-based study of randomly selected participants in Germany, researchers found that mild cognitive impairment (MCI) occurred significantly more often in individuals diagnosed with a lower ankle brachial index (ABI), which is a marker of generalized atherosclerosis and thus cumulative exposure to cardiovascular risk factors during lifetime. Interestingly, this strong association was only observed in patients with non-amnestic MCI, but not amnestic MCI. There also was no independent association of MCI and intima media thickness (IMT) or coronary artery calcification (CAC), two other surrogate markers of cardiovascular risk. Examination of differences by gender revealed a stronger association of a decreasing ABI with non-amnestic MCI in women. This study is published in the Journal of Alzheimer's Disease.

23 july 2015--The concept of MCI describes an intermediate state between normal cognitive aging and dementia. Although people with MCI have a higher dementia risk, very few actually develop dementia. In fact, many persons with MCI convert back to a cognitively normal state. This transitional - and therefore possibly modifiable - characteristic makes the concept of MCI a promising approach in the development of prevention strategies.
What criteria determine MCI? The following four criteria must be met for a diagnosis of MCI: First, participants have a subjective impression of a declined cognitive performance over the last two years. Second, this subjective impression is validated by objective measures (cognitive test battery). Third, participants are capable of handling activities of daily living. Fourth, a diagnosis of dementia is ruled out.
The concept of MCI distinguishes between two subtypes depending on the affected cognitive domain: participants with impairment in the memory domain are categorized as amnestic MCI (aMCI) and those with deficits in non-memory domains are categorized as non-amnestic MCI (naMCI).
The Heinz Nixdorf Recall (Risk Factors, Evaluation of Coronary Calcium and Lifestyle) study is an observational, population-based, prospective study that examined 4,814 participants (50% men) between 2000 and 2003 in the metropolitan Ruhr Area. After five years a second examination was conducted with 90% of the participants taking part.
For this analysis, 490 participants diagnosed with MCI were compared with 1,242 cognitively normal participants. Of participants with MCI, 249 had amnestic MCI and 241 had non-amnestic MCI.
"In conclusion, we found an independent association of a lower ABI with a higher prevalence of MCI and particularly with naMCI, whereas no significant association could be found with aMCI in fully adjusted models," commented lead investigator Christian Weimer, MD, Department of Neurology, University Hospital of Essen, University of Duisburg-Essen, Germany. "This underlines the importance of preventing atherosclerosis by treating cardiovascular risk factors and life style modification to prevent cognitive decline."
More information: "Ankle-Brachial Index but Neither Intima Media Thickness Nor Coronary Artery Calcification Is Associated with Mild Cognitive Impairment"Journal of Alzheimer's DiseaseDOI: 10.3233/JAD-150218 
Provided by IOS Press

Wednesday, July 22, 2015

USPSTF: more evidence needed for visual acuity screening

USPSTF: more evidence needed for visual acuity screening

The U.S. Preventive Services Task Force has concluded that there is currently insufficient evidence to assess the benefits and harms of screening for impaired visual acuity in older adults. These findings form the basis of a draft recommendation statement based on an evidence review published online  by the USPSTF.

22 july 2015—The U.S. Preventive Services Task Force (USPSTF) has concluded that there is currently insufficient evidence to assess the benefits and harms of screening for impaired visual acuity in older adults. These findings form the basis of a draft recommendation statement based on an evidence review published online July 20 by the USPSTF.
In an effort to update the 2009 statement, researchers from the USPSTF conducted a systematic review of the recent evidence on screening for visual acuity impairment in adults aged 65 years or older in the  setting. The investigators examined the benefits and harms of screening, accuracy of screening, and benefits and harms of early vision impairment treatment.
The researchers found that there was inadequate evidence on the benefits of screening, early detection, and treatment to fully examine the overall benefits. Inadequate evidence was also found on the harms of screening. Overall, the evidence was insufficient to assess the balance of benefits and harms for visual impairment screening (I statement). These findings form the basis of a draft recommendation statement, which is available for comment from July 21 to August 17.
"We need more evidence on accurate ways to screen for eye conditions in older adults in a primary care setting and on the link between vision screening and quality of life," Al Siu, M.D., M.S.P.H., chair of the USPSTF, said in a statement.

Tuesday, July 21, 2015

Women descend into alzheimer's at twice the speed of men: study

Women descend into alzheimer's  at twice the speed of men: study
Investigators find gender differences in progression from mild cognitive impairment.
21 july 2015—Women with mild thinking and memory problems—known as mild cognitive impairment—deteriorate twice as fast mentally as men with the same condition, according to new research.
Mild cognitive impairment isn't severe enough to interfere with daily life, but it is linked to higher odds of developing Alzheimer's disease or another type of dementia, the researchers said.
"Our findings do suggest greater vulnerability in women with mild cognitive impairment stage, which is more severe than normal memory loss and is an intermediary stage between aging and dementia," said lead researcher Katherine Lin, a clinical research scholar at Duke University in Durham, N.C.
Several factors may account for this increased vulnerability among women, Lin added. Women may be genetically predisposed to developing more plaque in the brain, which is a hallmark of Alzheimer's, or perhaps there is an as-yet-unknown genetic cause, she said.
To determine the reasons, gender-specific research into Alzheimer's disease needs to become a priority, Lin said. "Potentially, Alzheimer's prevention trials could test treatment effects separately by gender," she suggested.
The results of her study were scheduled for presentation Tuesday at the Alzheimer's Association International Conference, in Washington, D.C. Data and conclusions presented at meetings are usually considered preliminary until published in a peer-reviewed medical journal.
Dr. Luca Giliberto, an Alzheimer's investigator at the Feinstein Institute for Medical Research in Manhasset, N.Y., offered another theory: "Women may have better cognitive reserve than men—that is, more connections between brain cells," Giliberto said.
Because of this greater mental reserve, it's possible that women may start declining later than men, but progress faster once the fall-off begins, he said. In addition, Giliberto said there might be a hormonal component to the speed of decline, perhaps associated with estrogen levels.
For the study, Lin and colleagues collected data on 400 men and women with thinking and memory problems who took part in the Alzheimer's Disease Neuroimaging Initiative. Participants were in their mid-70s at the start of the study.
In up to eight years of follow-up, the thinking and memory of women deteriorated twice as fast as in men, according to a standard test called the Mini Mental State Examination. On that test, the rate of mental slippage in men was 1.05 points a year, in women 2.3 points annually.
For men and women with a specific gene mutation—called the ApoE4 Alzheimer's risk gene—the rate of mental decline was even faster, the researchers said.
Dean Hartley, director of science initiatives at the Alzheimer's Association, agreed that more research is needed to understand gender discrepancies related to Alzheimer's, which is the most common form of dementia.
Hartley said that women make up 75 percent of those who develop Alzheimer's disease. "We also know that 75 percent of the caregivers are women, so women are carrying a big burden," he said.
Women live longer than men. By the time they start having memory and thinking problems, they are at a later stage in life and that might account for the faster decline, Hartley said. It's also possible that biological differences between the sexes are at work, he added.
"The Alzheimer's Association is looking at these differences because it might affect how we need to treat these people," he said.
More information: The U.S. National Institutes of Health outlines the warning signs of Alzheimer's

Monday, July 20, 2015

Defective telomeres are now being linked to dozens of diseases, including many types of cancer

Defective telomeres are now being linked to dozens of diseases, including many types of cancer

Studying telomeres, the structures that protect the ends of chromosomes, has become a key issue in biology. In recent years, not only has their relation to ageing been confirmed; defective telomeres seem to be linked to more and more illnesses, including many types of cancer. The review published by Paula Martínez and María Blasco from the CNIO in Trends in Biochemical Sciences, stresses the importance of investigating these structures to improve diagnoses and develop possible treatments for many diseases. Telomeres, in the opinion of these researchers, will become increasingly important in clinical studies.
20 july 2015--The chromosomes in every single cell are made up of DNA and shaped like strands, with a kind of protective cap at the end of each strand of DNA. Without this end protective cap, the DNA strands would chemically bond to other strands, i.e. the chromosomes would merge and that would be lethal for the cell. The structures that prevent this catastrophe are the telomeres. They were discovered in the 1930s but decades elapsed before someone decided to study them in any depth and since the late 1990s they have always been on the cutting edge of biology research. Biologists are often surprised by their amazing and unexpected complexity, and their health-related significance.
"The biology of telomeres is extremely complex and the more we discover the more we realise what remains to be discovered", says Paula Martínez from CNIO's Telomere and Telomerase Group. "What surprises me most is the high number of factors we are finding that are essential to the preservation of telomeres and, above all, the precise coordination that is required between them all".
The fact that telomeres have been tightly preserved throughout the evolutionary tree -in most eukaryotes: vertebrates, plants and even unicellular organisms such as yeast- indicates their importance. In addition to preventing the merger of chromosomes, telomeres are needed to prevent the loss of genetic information each time a cell divides.
Preventing Information Loss
When a cell replicates, the molecular machinery in charge of duplicating the chromosomes - so that each daughter cell has a copy -cannot reach the tip. This is inherently impossible due to the way the DNA replication machinery works, and it implies that any genetic material at the end of a chromosome with significant information for the cell would be lost. Telomeres prevent this from happening: they consist of a DNA sequence that does not contain genes and that is repeated numerous times- in humans and other species the sequence is TTAGGG; the letters correspond to three of the building blocks that make up the DNA: thymine, adenine and guanine.
Consequently, the shortening of the DNA with every division is not significant. At least not until a certain limit is reached. When the telomeres become too short, we see the problems associated with ageing: cells reach a point where they interpret critically short telomeres as irreparable damage and react by no longer dividing, which prevents tissue from regenerating.
This happens in healthy cells but not in cancer cells. There is an enzyme, telomerase, which is capable of lengthening the telomeres de novo. This enzyme is not present in most cells of an adult organism but it is active in tumour cells. By repairing the telomeres, the telomerase enables cancer cells to proliferate and become virtually immortal.
This link to ageing and cancer, has led to the intense study of telomere-based strategies to combat cancer and diseases associated with ageing. Blasco's group has recently shown that it is possible to make  mortal by acting on the telomeres.
Zooming In To The Tip Of The Buffer
The above-mentioned description of telomeres however is a simplified version of the story. We now know that there is a protective structure enveloping telomeric DNA consisting of six proteins known as shelterins, which are crucial. Another more recent discovery is that there are proteins that, although not in the telomeres themselves, interact with them at specific times to enable them to perform their functions.
These proteins enable the telomeres to unwind, for example; because, the sequence repeated in telomeres, TTAGGG, ends in a single strand of DNA that curves forming a loop and connects to the original strand of the double chain forming a triple chain. "Yes, it is very complicated", admits Martínez. "Structures of up to four chains of DNA can form".
When a cell divides, the telomeres are also replicated. This implies that the end loop must unwind first and then form again. This process also contributes to the shortening of telomeres and we now know that some of the shelterins as well as other associated proteins that interact with telomeres are key elements in this process.
Telomere Syndromes
According to Martínez, "there is now more evidence about relationship between telomere maintenance and several illnesses".
Telomere syndromes, or telomeropathies, have been identified in patients with mutations of the telomerase enzyme. This group includes, for example, pulmonary fibrosis and problems related to the malfunction of the bone marrow. A direct relationship between telomere dysfunctions and many types of cancer has also been found. More recently, we have also discovered that mutations of the proteins that protect telomeric DNA, the shelterins, and those that interact with the telomeres, are linked to various diseases, such as dyskeratosis congenita, Hoyeraal-Hreidarsson syndrome or Revesz syndrome.
"These discoveries underline the plethora of components and pathways that control telomere functions", write the authors in the paper. "In the future, research will bring to light more unknown factors that will improve our understanding of the mechanisms governing cancer and syndromes linked to the shortening of . We hope that this knowledge will be transferred to the clinic in order to improve the diagnosis and treatment of diseases".
Provided by Centro Nacional de Investigaciones Oncologicas

Sunday, July 19, 2015

Combined use of antidepressants and painkillers linked to bleeding risk

Taking a combination of antidepressants and common painkillers is associated with an increased risk of bleeding soon after starting treatment, finds a study published in The BMJ this week.

19 july 2015--The researchers say their results may have been affected by other unmeasured or unknown factors and should be interpreted with caution. However, they suggest special attention is needed when patients use both these classes of drugs together.
Depression produces the greatest decrement in health of all common chronic conditions and depression in older people is an important public health problem.
But concern exists that antidepressants may interact with common  called non-steroidal anti-inflammatory drugs (NSAIDs) to increase the risk of bleeding inside the skull (intracranial haemorrhage).
So a team of researchers based in Korea compared the risk of bleeding among patients treated with antidepressants with and without NSAIDs.
Using the Korean nationwide health insurance database, their study involved over four million people who were prescribed antidepressants for the first time between 2009 and 2013.
NSAID prescriptions were obtained and hospital records were used to identify time to first admission with intracranial haemorrhage within 30 days of a new prescription. Factors that could affect the results, such as age, sex, and use of other medications, were taken into account.
Compared with use of antidepressants alone, the team found that combined use of antidepressants and NSAIDs was associated with a substantially increased bleeding risk.
They found no statistically meaningful differences in risk of bleeding between different types of , or with age. Being male was the most common factor for a higher risk of bleeding with combined use of antidepressants and NSAIDs.
"The addition of NSAIDs to antidepressant treatment increased the risk of intracranial haemorrhage within 30 days of the combination starting, especially in men," conclude the authors. "This result adds to evidence confirming the increase of risk with combination use of antidepressants and NSAIDs."
In an accompanying editorial, Dr Stewart Mercer at the University of Glasgow and colleagues at the University of Cambridge, say the results give some cause for concern.
They point out that both types of drug are widely used, and that co-morbidity of the conditions for which these drugs are used is very high - 65% of those with major depression also have chronic pain.
They urge family doctors to be extra vigilant in terms of prescribing behaviour and discussing the risks with patients, especially in deprived areas where "the combination of mental and physical problems (including chronic pain) is very common." And they say further research is required to extend the findings over longer time periods and in differing populations.
More information: Risk of intracranial haemorrhage in antidepressant users with concurrent use of non-steroidal anti-inflammatory drugs: nationwide propensity score matched study, The
Editorial: Risk of intracranial haemorrhage linked to co-treatment with antidepressants and NSAIDs, 
Provided by British Medical Journal

Saturday, July 18, 2015

New recommendations addresses the diagnosis and management of testosterone deficiency

An expert panel convened by the International Society for Sexual Medicine has developed a detailed "Process of Care" for the diagnosis and management of testosterone deficiency in men.

18 july 2015--After an extensive literature review and in-depth consultations, the panel of 18 experts from a wide range of medical disciplines recommended that testosterone deficiency be defined as a clinical and biochemical syndrome characterized by both a deficiency of testosterone or testosterone action, and relevant symptoms. The panel stressed that the condition may affect multiple organ systems as well as . They also noted that the prevalence of symptomatic testosterone deficiency in  is within the range of 2% to 6%, and it is often associated with obesity and type 2 diabetes, but not necessarily with aging.
The Process of Care provides information on who should be tested for testosterone deficiency, which tests to perform, and which lifestyle modifications or drug interventions are appropriate for different types of patients. It also provides recommendations on when and how to monitor patients after initiating treatment.
The  noted that decisions regarding the appropriate use of testosterone replacement therapy have been complicated by well-publicized controversies about a possible relationship between testosterone replacement therapy and risk of developing prostate cancer and heart disease. The panel found that there were no large-scale, long-term, controlled studies that supported such concerns and that the balance of available evidence is strongly against there being any such relationship in men who are appropriately treated.
"The Process of Care characterizes testosterone deficiency and provides easy-to-follow, evidence-based guidance on its investigation and management, in both general and special populations, such as those with cardiovascular and prostate disease. It highlights the importance of identifying men with testosterone deficiency who want to maintain their fertility, which is likely to be compromised by  therapy, and who need a different approach to treatment," said Dr. John Dean, lead author of the Process of Care, which is published in The Journal of Sexual Medicine. "Very importantly, it should help doctors to make a consistent and reliable diagnosis of a much-neglected problem that may confer a significant health burden on the individual, and to identify the 'worried well' who may request testosterone replacement therapy but do not need it."
More information: DOI: 10.1111/jsm.12952 
Provided by Wiley

Wednesday, July 08, 2015

How does aging affect athletic performance?

How does aging affect athletic performance?

Rowers show the least decline in VO2max compared to other endurance sports. Credit:
I remember the moment a few years ago while watching TV when I realized that if I were riding in the Tour de France, at age 42 I'd be the oldest person in the race. It hit me that my dream of racing in cycling's biggest event was over…it was not going to happen.
08 july 2015--Not that I'd been competing, let alone training seriously, on the bike for a number of years.
Or that not even in my "prime" years for competitive cycling would I have been good enough. It's just that now I had an excuse…. I was too old, too far past my prime years.
So what happened? Is there a physiological reason people in their mid-40's are no longer able to compete at the professional level in most sports, or is it a constellation of challenges, such as the time devoted to training, motivation, managing kids' schedules or busy work demands?
"I'm old" is the common refrain for why we get worse at athletics as we age. But here's what's really happening in the body through the years to make world-class performance less possible. And, interestingly, there are a few physiological elements that contribute to athleticism that don't seem as affected by aging.
The 'sweet-spot' age
In most sports, there is an age "sweet spot," at which the combination of physical, technical and strategic abilities comes together.
In most sports, this age sweet spot falls in the mid-20's to early 30's. Although there have been numerous examples of Olympians competing, and sometimes winning medals, over the age of 50, the vast majority of these come from sports requiring exceptional skill and less aerobic or anaerobic power, such as the shooting events, sailing, equestrian and fencing.
For endurance events, the upper cap for competing at the sport's highest levels appears to be around the age of 40.
Chris Horner won the 2013 edition of the Vuelta a Espana, Spain's version of the Tour de France, just shy of his 42nd birthday, making him the oldest winner of a Grand Tour in cycling.
The oldest Olympic marathon winner was the 38-year-old Romanian athlete Constantina Dita Tomescu, competing at the Beijing Olympic Games.
Dara Torres, at the age of 41 in 2008, is the oldest swimmer to compete in the history of the Olympics, missing the gold medal in the 50-meter freestyle by hundredths of a second. But these examples are the exceptions, not the rule.
Age changes how our bodies use oxygen
One big reason we see declines in aerobic (or endurance) athletic performance with age is that our bodies can't use oxygen as effectively.
The maximal ability to utilize oxygen (VO2max) is a predictor of endurance performance across ages. VO2max is a numerical value that describes how much oxygen your body can use per kilogram of body weight.
VO2max is affected by how well your body can bring oxygen into the lungs, how well this is carried in our blood to the working muscles, and how much oxygen the muscles can use to fuel contraction.
Exercise can improve all of these, and the higher the VO2max, the more "aerobically fit" a person is. That is, they can do more endurance work for their body weight.
In the general population, VO2max tends to decline by about 10% per decade after the age of 30. Athletes who continue to compete and train hard can reduce the drop by about half, to 5% per decade after the age of 30.
The reason VO2max declines with age is that our maximal heart rates go down as well.
Maximal  is the highest heart rate in beats per minute one can achieve during increasing intensity of endurance exercise. It is often roughly predicted as "220 – age = maximal heart rate." Although the actual maximal heart rate for a given person is highly variable, as you age, your maximal heart rate decreases, whether you are a highly fit athlete or a couch potato.
And this decrease reduces both cardiac output and oxygen delivery to the muscles, which translates to a lower VO2max and thus to lower performance in endurance events as we age.
Even if oxygen delivery to muscles goes down, the ability of your muscles to efficiently utilize the oxygen they do get relative to a given workload (this is called exercise economy) is well maintained into our 60's and 70's, though total muscle mass tends to decline as we age, and can contribute to declines in performance as well.
In terms of competitive endurance exercise, rowers have shown the least decline in VO2max with age, but the difference to other sports isn't huge. And it might be because rowing is a lower-impact sport than cycling (with crashes) and running (constant pounding).
Let's not forget the muscles
Some evidence suggest that for sports that require high levels of strength or power, like weightlifting, age-related limitations may reside in our skeletal muscles, those muscles that move our bones and joints.
For competitive weightlifters over the age of 40 (masters level), performance drops more precipitously than it does for endurance athletes such as runners, swimmers and cyclists. That's likely because weightlifting draws on type II muscle fibers (called "fast-twitch" muscles) to produce strength and power. Research indicates that these cells decline in number and function with age.
Not only do these cells decline with age, but so do the cells that support the repair and growth of skeletal muscles in response to exercise decline.
These age-related declines are not as obvious in type I muscles, those muscle fibers most associated with endurance-type exercise.
Recovery can take longer
As they age, many athletes complain that the ability to recover from hard bouts of exercise diminishes.
This can affect the intensity and volume of training of all athletes. But in many contact sports, such as professional American football or rugby, recovering from injuries and the cumulative effects of hard hits becomes the limiting factor in continuing to play at the highest level.
For instance, last season there were only two people in the NFL, Sav Rocca of the Washington Redskins and Adam Vinatieri of the Indianapolis Colts, playing in their 40's.
Injuries take their toll on people playing non-contact sports as well. For masters athletes, experiencing more training-associated injuries leads to reduced training intensity and volume, and thus poorer performance come race day.
Better training can help you stay at your peak longer
Although all athletes will eventually lose the age versus  race, with better training and recovery practices, in the coming years we likely will begin to see more athletes in their 40's remaining competitive at the highest levels of sport. By "training smarter, not harder," athletes can reduce the chances of injuries, maximize gains from training and minimize the effects of aging.
Older athletes need longer to recover and adapt to a training stimulus, so workout planning needs to change with age.
High-intensity interval training, for instance, focuses on the quality of a workout, rather than the sheer volume of training, and can be used effectively by older athletes to improve aerobic capacity.
Cross-training, such as weightlifting and yoga, can help to maintain muscle mass and flexibility, and reduce overuse injuries in endurance athletes.
An emphasis on "active recovery" strategies (an easy run or swim on your rest days) and improved sleeping habits are important for athletes of all ages, but become essential for older athletes.
Performance decline isn't just about physical changes, however. As we age, our intrinsic motivation to train diminishes. Even in athletes, the motivation to train may shift somewhat from setting personal records to remaining active and healthy. And that's a great motivation for any athlete at any .
Source: The Conversation