Category: Ageing

Categories : Ageing Surgeries & ProceduresTags :

Surgical Stabilisation of Odontoid Fractures Linked to Better Outcomes

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In a review of patient treatment data, researchers have found that surgical stabilisation of odontoid fractures was associated with better outcomes than nonsurgical approaches. The article will appear in the September issue of Neurosurgery.

Odontoid fractures (C2 vertebra) are common in elderly patients after a low-energy fall. However, whether the initial treatment should be surgical or nonoperative still isn’t known. Previous studies haven’t accounted for differences in injury severity, or the presence or absence of neurologic impairment, which can affect patients’ results.

Michael B. Cloney, MD, MPH, of the Department of Neurological Surgery at Northwestern University in Chicago, and colleagues have published evidence that surgery should be considered as the initial approach for many patients. Compared with nonoperative approaches to treatment, surgical stabilisation of the fracture was associated with less myelopathy (mobility impairment due to spinal cord damage), and lower rates of fracture nonunion, 30-day mortality, and one year mortality.

“Given the increasing incidence of odontoid fractures with the aging population, we believe our findings could assist with neurosurgical decision-making for an increasingly common and complex problem,” the researchers say.

Accounting for nonrandomised patient groups

Dr Cloney and his colleagues reviewed initial treatment data on 296 patients who were cared for at Northwestern Memorial Hospital between January 1, 2010, and December 31, 2020, because of an odontoid fracture. Their average age was 73. During the hospitalisation, 22% had surgery and 78% had nonoperative treatment (5% were immobilised in a halo-vest and 73% received a cervical collar).

Since the patients weren’t randomised to these treatments, the research team used a type of analysis called propensity score adjustment. They calculated “propensity scores” for each individual – the probability that the patient would have been assigned to receive one of the two treatment approaches based on certain characteristics.

For example, to study the effect of surgery on mortality rates, patients were matched on age, sex, Injury Severity Score, Nurick score (a measure of myelopathy), their number of chronic diseases and chronic conditions such as smoking, and whether they had to be admitted to the intensive care unit.

Surgical stabilisation leads to better results

Follow up with patients lasted an average of 45 weeks. On the propensity score–matched analyses, the group that underwent surgery showed significantly better outcomes than the nonoperative group:

  • Lower rate of fracture nonunion – 39.7% vs 57.3%; treatment effect, 15% less risk of nonunion
  • Lower 30-day mortality rate – 1.7% vs 13.8%; treatment effect, 10% less risk of death
  • Lower one year mortality rate – 7.0% vs 23.7%; treatment effect, 10% less risk of death

Other analyses showed patients in the surgery group were 52% less likely than those in the nonoperative group to have poor Nurick scores at the 26-week postoperative follow-up visit and were 41% less likely to die during the overall follow-up period. Both differences were statistically significant.

“The mortality benefit calculated in the existing literature typically represents an unadjusted mortality rate between two potentially different populations, which leaves it liable to confounding,” the authors note. “Our study represents a relatively large institutional series that suggests a benefit from surgical stabilisation in this population while controlling for confounding factors more thoroughly than existing literature.”

Source: EurekAlert!

Categories : Ageing Obstetrics & GynaecologyTags :

Rethink Needed for the Genetic Cause of Very Early Menopause

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A new study showed that it may be necessary to rethink the genetic cause previously held to be behind very early menopause. Until now, variants in any one of more than 100 genes were thought to cause premature ovarian insufficiency (POI), which results in menopause before age 40. This affects around 1% of women, making it a leading cause of infertility. Under current guidance, a variation in one of these genes is cause for clinicians to consider a genetic diagnosis of POI.

Now, in the largest study to date, published in Nature Medicine, researchers analysed genetic data from more than 104 733 women in UK Biobank, of whom 2231 reported experiencing menopause before the age of 40.

The study found evidence that 98% of women carrying variations in the genes that were previously considered to be causes of premature menopause in fact had menopause over 40, therefore ruling out a diagnosis of POI in these women.

Anna Murray, Professor of Human Genetics at the University of Exeter Medical School is a senior author on the study. She said: “Our research means rethinking what causes very early menopause. The presence of specific genetic variants in multiple women who experience premature menopause has led to the assumption that they are causing the condition – but we have shown that these gene variations are also found in women with a normal age of menopause and therefore in many cases the link could just be coincidence. It now seems likely that premature menopause is caused by a combination of variants in many genes, as well as non-genetic factors. As genomic medicine evolves, we need to apply this standard of evidence to other conditions, so we can tailor diagnosis, treatment and support.”

Dr Julia Prague, Consultant Endocrinologist and Clinical Academic at the University of Exeter, and an author on the paper, said: “Having a very early menopause is often extremely distressing because it means losing fertility and treatment with hormone replacement is required to prevent negative health consequences. Clinicians need to understand the reasons why premature menopause occurs so that they do not miss the true underlying cause and can counsel patients appropriately. Misinterpreting genetic tests could have negative implications for women, such as suggesting that their relatives may also be at risk of very early menopause due to their genes, when in fact they may not be.”

Stasa Stankovic, of the University of Cambridge’s MRC Epidemiology Unit, and co-lead analyst of the study, said: “Each woman’s unique genetic combination shifts menopause timing, either earlier or later. Although genetic variation in the studied genes were not sufficient to cause very early menopause, we did identify genetic drivers that had a much more subtle impact on reproductive longevity. For example, women carrying genetic variation in TWNK and SOHLH2 genes experienced menopause up to three years earlier than the general population. Our future studies will continue using the power of human genomics to better understand the underlying biology of reproductive ageing in women and key genetic drivers of its extreme forms, including very early menopause. With this knowledge, we are also paving the path towards development of next-generation treatments for reproductive disorders.”

Source: University of Exeter

Categories : Ageing CancerTags :

Losing the Y Chromosome to Age Drives Bladder Cancers but Improves Immunotherapy

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Chromosomes. Credit: NIH

As men age, some of their cells lose their Y chromosome and this loss hampers the body’s ability to fight cancer, according to new research from Cedars-Sinai Cancer. The study, published in Nature, found that loss of the Y chromosome helps cancer cells evade the immune system, resulting in aggressive bladder cancer. Somehow, this also renders the disease more responsive to immune checkpoint inhibitors.

Based on their research, investigators are developing a test for loss of the Y chromosome in tumours with the goal of helping clinicians tailor immune checkpoint inhibitor treatment for male patients with bladder cancer.

“This study for the first time makes a connection that has never been made before between loss of the Y chromosome and the immune system’s response to cancer,” said corresponding author Dan Theodorescu, MD, PhD, who initiated the research. “We discovered that loss of the Y chromosome allows bladder cancer cells to elude the immune system and grow very aggressively.”

Lead collaborators on the study also included Johanna Schafer, a postdoctoral fellow, and Zihai Li, MD, PhD, medical oncologist and immunologist, both at The Ohio State University Comprehensive Cancer Center-James Cancer Hospital and Solove Research Institute.

In men, loss of the Y chromosome has been observed in several cancer types, including 10%–40% of bladder cancers. Loss of the Y chromosome also has been associated with heart disease and Alzheimer’s disease.

The Y chromosome contains the blueprints for certain genes. Based on the way these genes are expressed in normal cells in the bladder lining, investigators developed a scoring system to measure loss of the Y chromosome in cancers.  

The investigators then reviewed data on two groups of men. One group had muscle invasive bladder cancer and had their bladders removed, but were not treated with an immune checkpoint inhibitor. The other group participated in a clinical trial and were treated with an immune checkpoint inhibitor. They found that patients with loss of the Y chromosome had poorer prognosis in the first group and much better overall survival rates in the latter.

To determine why this happens, investigators next compared growth rates of bladder cancer cells from laboratory mice.

Cancer cells were grown in vitro and not exposed to immune cells. The researchers also grew the diseased cells in mice that were missing T-cells. In both cases, tumours with and without the Y chromosome grew at the same rate.

In mice with intact immune systems, tumours lacking the Y chromosome grew at a much faster rate than did tumours with the intact Y chromosome.

“The fact that we only see a difference in growth rate when the immune system is in play is the key to the ‘loss-of-Y’ effect in bladder cancer,” Theodorescu said. “These results imply that when cells lose the Y chromosome, they exhaust T-cells. And without T-cells to fight the cancer, the tumor grows aggressively.”

Based on their results derived from human patients and laboratory mice, Theodorescu and his team also concluded that tumours missing the Y chromosome, while more aggressive, were also more vulnerable and responsive to immune checkpoint inhibitors. This therapy, one of the two mainstay bladder cancer treatments available to patients today, reverses T-cell exhaustion and allows the body’s immune system to fight the cancer.

“Fortunately, this aggressive cancer has an Achilles’ heel, in that it is more sensitive than cancers with an intact Y chromosome to immune checkpoint inhibitors,” said co-first author Hany Abdel-Hafiz, PhD, associate professor at Cedars-Sinai Cancer.

Preliminary data not yet published shows that loss of the Y chromosome also renders prostate cancers more aggressive, Theodorescu said.

“Our investigators postulate that loss of the Y chromosome is an adaptive strategy that tumour cells have developed to evade the immune system and survive in multiple organs,” said Shlomo Melmed, MB, ChB, dean of the Medical Faculty at Cedars-Sinai. “This exciting advance adds to our basic understanding of cancer biology and could have far-reaching implications for cancer treatment going forward.”

Further work is needed to help investigators understand the genetic connection between loss of the Y chromosome and T-cell exhaustion.

“If we could understand those mechanics, we could prevent T-cell exhaustion,” Theodorescu said. “T-cell exhaustion can be partially reversed with checkpoint inhibitors, but if we could stop it from happening in the first place, there is much potential to improve outcomes for patients.”

While women do not have a Y chromosome, Theodorescu said these findings could have implications for them as well. The Y chromosome contains a set of related genes, called paralogue genes, on the X chromosome, and these might play a role in both women and in men. Additional research is needed to determine what that role might be.

“Awareness of the significance of Y chromosome loss will stimulate discussions about the importance of considering sex as a variable in all scientific research in human biology,” Theodorescu said. “The fundamental new knowledge we provide here may explain why certain cancers are worse in either men or women, and how best to treat them. It also illustrates that the Y chromosome does more than determine human biologic sex.”

Source: Cedars-Sinai Medical Center

Categories : Ageing Cardiovascular DiseaseTags :

Long-term Daily Aspirin Use in Older Adults Increases Anaemia Risk

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A new study analysing data from the landmark ASPREE trial has found that long-term daily aspirin use increases the risk of anaemia by 20% in people mostly aged 70 and over. The results, which are published in Annals of Internal Medicine, have prompted researchers to suggest considering regular monitoring for anaemia in older adults taking low-dose aspirin. In addition, they should discuss any concerns about their health or medications with their GP.

Anaemia is commonly experienced by older adults, potentially affecting overall function and increasing fatigue, disabilities, depressive symptoms and cognitive problems.

The Monash University-led study followed 18 153 initially healthy older adults in Australia and the USA and recorded incidents of anaemia over an average 4.7 years.

It was the largest study to investigate anaemia in older people as part of a randomised controlled trial, ASPREE (ASPirin in Reducing Events in the Elderly) – with half the participants taking a placebo and the other half a daily low dose (100mg) of aspirin.

The risk of developing anaemia was found to be 20% higher in the aspirin group compared to those in the placebo group.

In addition to a higher risk of anaemia, blood tests revealed a faster decline of haemoglobin and reduced ferritin (a protein that carries iron) levels in the aspirin group compared to the placebo group.

Lead author, Associate Professor Zoe McQuilten from Monash University, said that while bleeding was a known side-effect of aspirin, few previous studies had looked at the effect of prolonged aspirin use on the progressive development of anaemia in older adults.

“This study gives a clearer picture of the additional risk of becoming anaemic with aspirin use and the impact is likely to be greater in older adults with underlying diseases, such as kidney disease,” Associate Professor McQuilten said.

Associate Professor McQuilten said the new data gave doctors insight into the risk of anaemia from prolonged aspirin use by their older patients. “Older adults are more likely to become anaemic generally and now doctors can potentially identify patients at higher risk of developing anaemia,” she said.

Associate Professor McQuilten urged patients to follow the advice of their doctor about their daily use of aspirin. She cautioned that for some older adults, aspirin was recommended as a valuable therapy to prevent recurring heart attacks or stroke. “Patients should not change their aspirin regimen without speaking to their GP,” she said.

Source: Monash University

Categories : Ageing Diet and NutritionTags :

Taurine may Help Extend Healthy Lifespan

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A deficiency of the amino acid taurine is a driver of ageing in animals, according to a new study published in Science. The same study also found that taurine supplements can slow down the ageing process in worms, mice, and monkeys and can even extend the healthy lifespans of middle-aged mice by up to 12%.

“For the last 25 years, scientists have been trying to find factors that not only let us live longer, but also increase healthspan, the time we remain healthy in our old age,” says study leader Vijay Yadav, PhD, assistant professor of genetics & development at Columbia University. “This study suggests that taurine could be an elixir of life within us that helps us live longer and healthier lives.”

Anti-ageing molecules within us

Many studies into ageing have found that various molecules carried through the bloodstream are associated with ageing. Less certain is whether these molecules actively direct the ageing process or are just passengers going along for the ride. If a molecule is a driver of ageing, then restoring its youthful levels would delay ageing and increase healthspan, the years we spend in good health.

Taurine first came into Yadav’s view during his previous research into osteoporosis that uncovered taurine’s role in building bone. Around the same time, other researchers were finding that taurine levels correlated with immune function, obesity, and nervous system functions.

“We realised that if taurine is regulating all these processes that decline with age, maybe taurine levels in the bloodstream affect overall health and lifespan,” Yadav says.

Taurine declines with age, supplementation increases lifespan in mice

First, Yadav’s team looked at levels of taurine in the bloodstream of mice, monkeys, and people and found that the taurine abundance decreases substantially with age. In people, taurine levels in 60-year-old individuals were only about one-third of those found in 5-year-olds.

“That’s when we started to ask if taurine deficiency is a driver of the ageing process, and we set up a large experiment with mice,” Yadav says.

The researchers started with close to 250 14-month-old female and male mice (about 45 years old in people terms). Every day, the researcher fed half of them a bolus of taurine or a control solution. At the end of the experiment, Yadav and his team found that taurine increased average lifespan by 12% in female mice and 10% in males. For the mice, that meant three to four extra months, equivalent to about seven or eight human years.

Taurine supplements in middle age improves health in old age

To learn how taurine impacted health, Yadav brought in other ageing researchers who investigated the effect of taurine supplementation on the health and lifespan in several species.

These experts measured various health parameters in mice and found that at age 2 (60 in human years), animals supplemented with taurine for one year were healthier in almost every way than their untreated counterparts.

The researchers found that taurine suppressed age-associated weight gain in female mice (even in “menopausal” mice), increased energy expenditure, increased bone mass, improved muscle endurance and strength, reduced depression-like and anxious behaviours, reduced insulin resistance, and promoted a younger-looking immune system, among other benefits.

“Not only did we find that the animals lived longer, we also found that they’re living healthier lives,” Yadav says.

At a cellular level, taurine improved many functions that usually decline with age: The supplement decreased the number of “zombie cells” (old cells that should die but instead linger and release harmful substances), increased survival after telomerase deficiency, increased the number of stem cells present in some tissues (which can help tissues heal after injury), improved the performance of mitochondria, reduced DNA damage, and improved the cells’ ability to sense nutrients.

Similar health effects of taurine supplements were seen in middle-aged rhesus monkeys, which were given daily taurine supplements for six months. Taurine prevented weight gain, reduced fasting blood glucose and markers of liver damage, increased bone density in the spine and legs, and improved the health of their immune systems.

Randomised clinical trial needed

The researchers do not know yet if taurine supplements will improve health or increase longevity in humans, but two experiments they conducted suggest taurine has potential.

In the first, Yadav and his team looked at the relationship between taurine levels and approximately 50 health parameters in 12 000 European adults aged 60 and over. Overall, people with higher taurine levels were healthier, with fewer cases of type 2 diabetes, lower obesity levels, reduced hypertension, and lower levels of inflammation. “These are associations, which do not establish causation,” Yadav says, “but the results are consistent with the possibility that taurine deficiency contributes to human ageing.”

The second study tested if taurine levels would respond to an intervention known to improve health: exercise. The researchers measured taurine levels before and after a variety of male athletes and sedentary individuals finished a strenuous cycling workout and found a significant increase in taurine among all groups of athletes (sprinters, endurance runners, and natural bodybuilders) and sedentary individuals.

“No matter the individual, all had increased taurine levels after exercise, which suggests that some of the health benefits of exercise may come from an increase in taurine,” Yadav says.

Only a randomized clinical trial in people will determine if taurine truly has health benefits, Yadav adds. Taurine trials are currently underway for obesity, but none are designed to measure a wide range of health parameters.

Other potential anti-ageing drugs – including metformin, rapamycin, and NAD analogues – are being considered for testing in clinical trials.

“I think taurine should also be considered,” Yadav says. “And it has some advantages: Taurine is naturally produced in our bodies, it can be obtained naturally in the diet, it has no known toxic effects (although it’s rarely used in concentrations used ), and it can be boosted by exercise.

“Taurine abundance goes down with age, so restoring taurine to a youthful level in old age may be a promising anti-ageing strategy.”

Source: Columbia University Irving Medical Center

Categories : AgeingTags :

Muscle Adiposity may Indicate Cognitive Decline in Aging

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New research reveals that the level of muscle adiposity (fat content) may indicate a person’s likelihood of experiencing cognitive decline as they age. In the study published in the Journal of the American Geriatrics Society, a five-year increase in fat stored in the thigh muscle was a risk factor for cognitive decline.

This risk was independent of total weight, other fat deposits, and muscle characteristics (such as muscle strength or mass) and also independent of traditional dementia risk factors.

Investigators assessed muscle fat in 1634 adults 69–79 years of age at years 1 and 6 and evaluated their cognitive function at years 1, 3, 5, 8, and 10. Increases in muscle adiposity from year 1 to year 6 were associated with faster and more cognitive decline over time. The findings were similar for Black and White men and women.

“Our data suggest that muscle adiposity plays a unique role in cognitive decline, distinct from that of other types of fat or other muscle characteristics,” said corresponding author Caterina Rosano, MD, MPH, of the University of Pittsburgh’s School of Public Health. “If that is the case, then the next step is to understand how muscle fat and the brain ‘talk’ to each other, and whether reducing muscle adiposity can also reduce dementia risk.”

Source: Wiley

Categories : AgeingTags :

Immunomodulator Keeps Subclinical Arthritis from Developing into Full-blown Form

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In a 12-month trial involving patients with “preclinical” rheumatoid arthritis, treatment with the immunomodulator abatacept (Orencia) kept the condition from becoming clinical, according to findings presented at the European Alliance of Associations for Rheumatology (EULAR) annual meeting.

Rheumatologists have long sought to nip rheumatoid arthritis (RA) in the bud, with many studies supporting early aggressive treatment on RA diagnosis. This has never been recommended for biologic therapies however.

Nevertheless, some patients show up at arthritis clinics with a few painful joints and other features such as RA-related serum biomarkers that suggest progression to full-blown RA is likely. Would aggressive treatment help slow their decline into RA?

In a phase IIb randomised trial involving patients in the UK and Netherlands who were at high risk for developing RA, only seven of the 110 assigned to abatacept had gone on to develop clinical arthritis after 1 year, compared with 30 of 103 in a placebo group.

The effect waned after abatacept was stopped at the one-year mark, and in the following year, 20 more patients in the abatacept group developed clinical arthritis, as did another eight in the placebo group.

Though the abatacept regimen held the edge for a full two years, projections showed that it was likely that the abatacept group would catch up with additional follow-up. At the same time, abatacept had no particular safety issues and thus could likely be continued.

A decade ago, Andrew Cope, MD, MBBS, of King’s College London colleagues thought about aggressive prevention, registering the current trial, Arthritis Prevention in the Pre-clinical Phase of RA with Abatacept (APIPPRA), in 2014. In a 2019 description of the protocol, they explained the selection of abatacept because “it targets immune reactions early in the chain of events leading to inflammation in RA. It functions by interrupting the interaction between T cells and antigen-presenting cells, attenuating the co-stimulatory signals required for T-cell activation, differentiation and effector responses,” thereby resulting “in downstream immunomodulatory effects on other inflammatory cells of the immune system.”

Participants had to show joint pain but no synovitis, plus either test positive for anti-citrullinated protein antigen (ACPA) antibodies and for rheumatoid factor (RF), or show high levels of ACPA antibodies without RF. The primary endpoint was development of clinically apparent arthritis in at least three joints or diagnosis of RA according to standard criteria.

While the preventive effect seen in the primary analysis did not hold up across the whole sample, Cope noted that it appeared more so in one very-high-risk subgroup: 49 patients who had some level of IgG ACPA antibodies and who were also positive for a series of other biomarkers, including RF, IgA ACPA antibodies, anti-carbamylated protein antibodies, and anti-acetylated peptide antibodies. For this subgroup, only about 10% of those who had taken abatacept progressed to clinical arthritis after two years, versus 50% of those assigned to placebo.

Source: MedPage Today

Categories : Ageing Cardiovascular DiseaseTags :

Oestrogen Pills may Increase Hypertension Risk

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Women ages 45 years and older taking oral oestrogen pills were more likely to develop hypertension than those using transdermal or vaginal formulations, according to new research published in Hypertension.

Less oestrogen and progesterone is produced in a woman’s body after menopause, which may increase the risk for cardiovascular diseases including heart failure, according to the American Heart Association.

Hormone therapy may be prescribed to relieve symptoms of menopause, in gender-affirming care and in contraception. Previous studies have found that some hormone therapies may reduce cardiovascular disease risk in menopausal women under 60 years of age or for whom it has been fewer than 10 years since menopause. The authors of this study noted that while hypertension is a modifiable risk factor for cardiovascular disease, the potential effects of different types of hormone therapy on blood pressure in menopausal women remain uncertain. 

“We know oestrogens ingested orally are metabolised through the liver, and this is associated with an increase in factors that can lead to higher blood pressure,” said lead study author Cindy Kalenga, an MD/PhD-candidate at the University of Calgary. 

“We know that post-menopausal women have increased risk of high blood pressure when compared to pre-menopausal women, furthermore, previous studies have shown that specific types of hormone therapy have been associated with higher rates of heart disease,” Kalenga said. “We chose to dive deeper into factors associated with hormone therapy, such as the route of administration (oral vs non-oral) and type of oestrogen, and how they may affect blood pressure.”

This study involved a large group of over 112 000 women, ages 45 years and older, who filled at least two consecutive prescriptions (a six-month cycle) for oestrogen-only hormone therapy, as identified from health administrative data in Alberta, Canada between 2008 and 2019. The main outcome of high blood pressure (hypertension) was identified via health records.

First, researchers investigated the relationship between route of oestrogen-only hormone therapy administration and risk of developing high blood pressure at least one year after starting the treatment. The 3 different routes of hormone therapy administration were oral (by mouth), transdermal and vaginal application. Additionally, researchers evaluated the formulation of oestrogen used and the risk of developing high blood pressure. For this study, the researchers reviewed medical records of individuals taking oestrogen-only hormone therapy. The two most common forms of oestrogen used by study participants were oestradiol – a synthetic form of oestrogen closest to the naturally produced form – and conjugated equine oestrogen, an animal-derived form of oestrogen and the oldest type of oestrogen therapy.

The analysis found:

  • Women taking oral oestrogen therapy had a 14% higher risk of developing high blood pressure compared to those using transdermal oestrogen and a 19% higher risk of developing high blood pressure compared to those using vaginal oestrogen creams or suppositories. After accounting for age, a stronger association was seen among women younger than 70 years of age compared to women older than 70.
  • Compared to estradiol, conjugated equine estrogen was associated with an 8% increased risk of developing high blood pressure.

Taking oestrogen for a longer period of time or taking a higher dose was associated with greater risk of high blood pressure, the authors noted. According to Kalenga, the study’s findings suggest that if menopausal woman take hormone therapy, there are different types of oestrogen that may have lower cardiovascular risks.

“These may include low-dose, non-oral oestrogen – like oestradiol, in transdermal or vaginal forms – for the shortest possible time period, based on individual symptoms and the risk–benefit ratio, Kalenga said. “These may also be associated with the lowest risk of hypertension. Of course, this must be balanced with the important benefits of hormone therapy, which include treatment of common menopausal symptoms.”

The average age of natural menopause among women worldwide is about 50 years of age. Current evidence supports that initiating menopausal hormone therapy in the early stages may have cardiovascular benefits, though not in the late stages of menopause, according to the American Heart Association’s 2020 Statement on Menopause Transition and Cardiovascular Disease Risk: Implications for Timing of Early Prevention. Previous studies have found that menopausal hormone therapy may help relieve symptoms of menopause, including hot flashes, night sweats, mood changes or sleep disturbances.

Limitations included being based only on medical records, not including women younger than the age of 45 and not collecting data about hysterectomies or menopausal status (which was inferred by taking oestrogen after 45).

The authors will be conducting more research investigating combined oestrogen and progestin, as well as progestin-only formulations of hormone therapy and their impact on heart and kidney diseases.

Source: American Heart Association

Categories : AgeingTags :

Low Sexual Satisfaction in Middle Age Linked to Cognitive Decline

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Low sexual satisfaction in middle age may serve as an early warning sign for future cognitive decline, according to a new study. The researchers, who tracked associations between erectile function, sexual satisfaction and cognition in hundreds of men aged 56 through 68, found that declines in sexual satisfaction and erectile function were correlated with future memory loss.

The study, published in Gerontologist, is the first to longitudinally track sexual satisfaction in tandem with sexual health and cognition, the researchers state, and its findings point to a potential novel risk factor for cognitive decline.

“What was unique about our approach is that we measured memory function and sexual function at each point in the longitudinal study, so we could look at how they changed together over time,” said Martin Sliwinski, professor of human development and family studies at Penn State and co-author on the study. “What we found connects to what scientists are beginning to understand about the link between life satisfaction and cognitive performance.”

The study explored the relationship between physical changes like the microvascular changes relevant for erectile function, and psychological changes, such as lower sexual satisfaction, to determine how the changes relate to cognition. They examined the shifts starting in middle age because it represents a transition period where declines in erectile function, cognition and sexual satisfaction begin to emerge.

Sliwinski added that while the team discovered a strong correlation between the three health factors, they can only speculate as to the cause.

“Scientists have found that if you have low satisfaction generally, you are at a higher risk for health problems like dementia, Alzheimer’s disease, cardiovascular disease and other stress-related issues that can lead to cognitive decline,” he said. “Improvements in sexual satisfaction may actually spark improvement in memory function. We tell people they should get more exercise and eat better foods. We’re showing that sexual satisfaction also has importance for our health and general quality of life.”

For the study, the researchers used survey data from 818 men who participated in the Vietnam Era Twin Study of Aging. Through neuropsychological tests, such as tests of memory and processing speed, they examined cognitive changes of participants over the 12-year span from age 56 to 68, adjusting for participants’ cognitive ability in young adulthood. Their erectile function and sexual satisfaction were measured alongside cognition, using the International Index of Erectile Function, a self-reported assessment for male sexual health. The researchers then built a statistical model to understand how the three variables changed as individuals aged.

“Research on sexual health has historically focused on quantifiable facets of sexuality like number of sexual partners or frequency of sexual activity,” said Riki Slayday, a doctoral candidate at Penn State and lead author on the study. “What we were interested in is the perception of that activity, how someone feels about their sex life, and how that influences cognitive function, because multiple people could be in the same situation physically but experience completely different levels of satisfaction.”

The study found that decreases in erectile function and sexual satisfaction were both associated with memory decline, which the researchers say points to a connection between psychological and physical health.

“When we mapped the relationship over time, we found increases or decreases in erectile function and sexual satisfaction were associated with concurrent increases or decreases in cognitive function,” Slayday said. “These associations survived adjustment for demographic and health factors, which tells us there is a clear connection between our sex lives and our cognition.”

Prior studies have found a link between microvascular changes and changes in erectile function over time. In fact, the active ingredient in Viagra (Sildenafil) was originally developed to treat cardiovascular problems, Sliwinski explained, so the connection between vascular health and erectile function is well understood. How erectile function connects to other aspects of health should be an area of focus for future research, he added.

Increasing the assessment and monitoring of erectile function as a vital sign of health may help identify those at risk of cognitive decline before their 70s, he said. The researchers note that the older adult population in the US is expected to double over the next 30 years, which means twice as many people will likely enter their 60s and experience declines in erectile function and sexual satisfaction.

“We already have a pill for treating erectile dysfunction. What we don’t have is an effective treatment for memory loss,” Sliwinski said. “Instead of the conversation being about treating ED, we should see that as a leading indicator for other health problems and also focus on improving sexual satisfaction and overall well-being, not just treating the symptom.”

Source: Penn State University

Categories : Ageing Cardiovascular DiseaseTags :

Ischaemic Heart Disease in the Elderly Linked to Increased Dementia Risk

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Older people with ischaemic heart disease have an increased long-term risk of dementia and accelerated cognitive decline. Recent research in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association suggests that the heart, the brain, and cognitive function are all connected in the ageing process. Appropriate prevention and treatment of ischaemic heart disease in older people might reduce the burden of dementia, the researchers suggest.

The researchers regularly followed a cohort of 2568 older people aged 60 years or older, without dementia at baseline and living in Stockholm, from 2001–2004 through 2013–2016. Heart diseases at the study entry were ascertained via clinical examination and linkage to the Swedish National Inpatient Register. Dementia status and cognitive function during the follow-up period were diagnosed and assessed regularly following the standard approaches.

“We used statistical methods to link ischemic heart disease at the study entry to an increased risk of dementia and a faster decline in cognitive function during the follow-up period”, says Chengxuan Qiu, at the Department of Neurobiology, Care Sciences and Society, Division of Aging Research Center (ARC) and one of the authors of the study.

Explore cognitive trajectories

Future works should explore cognitive trajectory following the onset of ischemic heart disease and further investigate to what extent medical treatments of ischemic heart disease may affect cognitive decline and dementia onset.

The SNAC-K project on which this study is based is supported by the Swedish Ministry of Health and Social Affairs. This study is supported by additional grants from the Swedish Research Council (VR), FORTE and STINT.