Alzheimer’s

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Heavy Alcohol Use is the Biggest Risk Factor for All Types of Dementia

Heavy Alcohol Use is the Biggest Risk Factor for All Types of Dementia

Heavy Alcohol Use is the Biggest Risk Factor for All Types of Dementia

Chronic alcohol drinking is identified as the biggest risk to the early onset of dementia based on a study involving more than 1 million adults in France affected by the condition. Roughly 46.8 million people worldwide live with dementia and this figure was expected to reach 50 million last year. In 2050, it is predicted that dementia will affect 131.5 million people. Dementia costs the world economy over $818 billion in medical and social care as well as unpaid, informal care (Alzheimer’s Disease International). The results of the study may alert the healthcare sector to pay attention to alcohol consumption as a preventable risk factor for all forms of dementia, especially early onset dementia.

Alcohol Affects Mental Health

Many studies already associate alcohol consumption with negative mental health effects. For example, alcohol and drugs increase the risk of schizophrenia later in life by 3.5 times (Nielsen et al, 2017). Treatment and management of schizophrenia would, therefore, involve elimination of substance abuse. In the case of hospitalized patients involved in the study in France, the effects of alcohol on the brain were studied suggesting several ways the substance could lead to dementia. Ethanol and acetaldehyde (its by-product) are toxic to brain cells and damage their functioning.

Alcohol is also associated with vascular risk factors including cardiovascular diseases, high blood pressure, and diabetes. Chronic drinking was also clustered among those with lower education, depression and smoking habits. All these factors though are independent risk factors for dementia. The research findings revealed that 57% of early-onset dementia cases (before reaching 65 years) affecting 57,000 people was linked to chronic alcohol use.

Implications for Early Health Interventions

The results of this large-scale study have several implications for the healthcare sector. To reduce the burden of alcohol-related dementia, early screening and interventions for heavy drinkers can be implemented. This would decrease the incidence of early-onset dementia. Alcohol use disorders also shorten life expectancies by as much as 20 years and by treating these problems, dementia-related deaths are expected to go down.

Dr. Bruce Pollock, Vice-President of Research at the Centre for Addiction and Mental Health, says, “As a geriatric psychiatrist, I frequently see the effects of alcohol use disorder on dementia, when, unfortunately, alcohol treatment interventions may be too late to improve cognition. Screening for and reduction of problem drinking, and treatment for alcohol use disorders need to start much earlier in primary care.”

Dementia is a brain disease that interferes with the daily life of affected individuals. If risk factors such as alcohol abuse are reduced or eliminated, there is no reason why people should not have a good quality of life as they age and not succumb to the condition or its early-onset.

 

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Nutrient drink for Alzheimer’s has disappointing result in trial

Nutrient drink for Alzheimer's has disappointing result in trial

Nutrient drink for Alzheimer’s has disappointing result in trial


A new study investigating the effects of a nutrient drink for Alzheimer’s disease has led to very different headlines in the media. While BBC News tells us the “Alzheimer’s nutrient drink falters in clinical trial”, the Daily Mirror reports the drink “could help stave off Alzheimer’s disease, according to scientists”.

The trial investigated the effects of Fortasyn Connect – a patented mix of vitamins and minerals, found in the drink Souvenaid – on memory in individuals showing early signs of Alzheimer’s disease.

It was hoped those receiving the drink would experience less memory decline than would usually be expected.

Just over 300 participants were given either Souvenaid or a control drink for two years – both looked and tasted the same, so people didn’t know which they had. The main aim was to see whether those who drank Souvenaid had better results across a range of memory tests than those who didn’t.

The researchers found no difference in this main outcome, but there were some positives in secondary outcomes: those taking the drink had slightly less brain shrinkage and slightly better cognitive scores. However, there was still no difference in the number of people from each group that went on to develop dementia.

Overall, the study provides no evidence that this drink can prevent or slow the progress of dementia.

Regular exercise, a healthy diet, and avoiding drinking heavily and smoking seem to do more to reduce your dementia risk than any nutrient drinks currently available.

 

Where did the story come from?

The study was carried out by researchers from international institutions in Finland, Germany, the Netherlands, Sweden and the US, and was funded by the European Commission 7th Framework Programme. Many of the researchers involved have worked or are currently working for pharmaceutical companies.

The study was published in the peer-reviewed medical journal The Lancet and is free to read online.

There were split reports in the media on this study, with the Mirror and Mail Online claiming the nutrient drink could “stave off dementia”.

Thankfully, BBC News provided a more accurate summary, reporting that the trial found no improvements in memory and thinking.

 

What kind of research was this?

This was a double-blinded randomised controlled trial (RCT) investigating the effects of a nutrient drink on brain function in individuals showing early signs of Alzheimer’s disease.

The trial, called LipiDiDiet, investigated the benefits of the drink Souvenaid, which contains the Fortasyn Connect multinutrient mix. Earlier studies suggested the drink was well tolerated and may improve certain aspects of memory but didn’t slow brain decline overall.

The first part of the LipiDiDiet trial ran for 12 months. This was followed by an optional extension to 24 months, which is what was reported on here.

Double-blind RCTs like this are one of the most reliable ways of assessing the effects of an intervention, as the study design limits the chance that patient characteristics and other confounders are influencing any links.

 

What did the research involve?

The 24-month LipiDiDiet trial was carried out across 11 different sites. Researchers from memory clinics recruited 311 participants, aged 55 to 85 years, who had been diagnosed with “prodromal Alzheimer’s disease”. This term describes people who have normal cognitive function (as defined by the Mini-Mental State Examination) but are experiencing some memory problems and have some physical changes to the brain associated with early-stage dementia.

Eligible participants were randomised to receive either a placebo drink or the Fortasyn Connect-containing Souvenaid drink (125ml) once a day. None of the participants or assessors knew which individuals were taking the treatment.

Participants took their drinks home and reported consumption in a daily diary. To ensure compliance, motivation and safety, participants were contacted by phone once a month during the first 6 months of the trial and once every 2 months thereafter.

Individuals were assessed at baseline, 6, 12 and 24 months using a battery of neuropsychological tests (NTB) – which tested several aspects of cognitive performance, including written memory and visual memory recall – as well as brain scans. Individuals visited the study nurse or physician every 3 months in the first year and every 6 months in the second year.

The main outcome of interest was change in NTB score over the 24 months. A significant decline in NTB score is often indicative of worsening Alzheimer’s.

Other outcomes measured included cognitive change and brain volume. Blood tests were also used to assess the safety of the product.

 

What were the basic results?

The nutrient drink had no effect on the main outcome (change in NTB) at 24 months. The average score change with Fortasyn Connect was -0.028, compared with -0.108 in the placebo group. This gave a between-group difference of 0.098 (95% confidence interval [CI] -0.041 to 0.237), which was not statistically significant.

With regard to the secondary outcomes, there was slightly less reduction in brain volume in the Fortasyn Connect group versus the control group. Overall clinical dementia scores were also slightly worse in the control group than the Fortasyn Connect group. However, there was no significant difference between the number of participants diagnosed with dementia by 24 months, which was 62 people (41%) in the Fortasyn Connect group and 59 (37%) in the placebo group.

Compliance was reported to be high, and there was no difference between groups in the number of adverse events. No serious adverse effects were thought to be related to the drink.

 

How did the researchers interpret the results?

The researchers said: “The intervention had no significant effect on the NTB primary endpoint over 2 years in prodromal Alzheimer’s disease. However, cognitive decline in this population was much lower than expected . group differences on secondary endpoints of disease progression measuring cognition and function [and brain shrinkage] were observed.

“Further study of nutritional approaches with larger sample sizes, longer duration, or a primary endpoint more sensitive in this pre-dementia population, is needed.”

 

Conclusion

This trial provides valuable evidence about the effects of a nutrient drink, Souvenaid, on memory in individuals with early signs that they may develop Alzheimer’s disease.

Importantly, the researchers found no significant effect on the main outcome their study looked at (memory). They did find less brain shrinkage and slightly better cognitive scores in the experimental group, but this still didn’t lead to any reduction in the number who were diagnosed with dementia by the end of the study.

This trial therefore provides no evidence that Souvenaid/Fortasyn Connect can help to prevent or slow Alzheimer’s developing in people with early signs of cognitive decline.

In 2010, Behind the Headlines reported the findings of an early-stage 12-week study of the same Souvenaid/Fortasyn Connect drink. That study found some changes to verbal recall but, again, no overall effect on cognitive outcomes.

As Dr Doug Brown, director of research at Alzheimer’s Society, commented on the present study:

“This trial of Souvenaid did not meet the success criteria that would be needed for developing new drugs, so we cannot be confident of the drink’s benefits . we certainly can’t conclude that the drink slows progression of Alzheimer’s disease.

“People who are worried about their memory should not rush out and buy this drink without first talking to their doctor to find out if it could be suitable for them. There are many causes of memory decline, including normal ageing, so it’s important people are investigated for underlying Alzheimer’s disease before taking this medical drink, or any kind of treatment.”

There’s no guaranteed way to prevent dementia – particularly Alzheimer’s disease, which doesn’t have a fully established cause. However, there are things you can do to try to reduce your risk:

eat a healthy, balanced diet

exercise regularly

lose weight, if necessary

only drink alcohol in moderation

give up smoking, if applicable

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Could a blood test in middle age predict dementia risk?

Blood test for dementia

Blood test for dementia

“Tissue inflammation blood test points to dementia risk,” is the headline in The Times.

Researchers in the US say people who have higher measures of inflammation in middle age are likely to have less brain tissue in some parts of their brain in older age.

The differences in brain volume, seen on MRI scans, were also accompanied by small differences in performance on memory tests.

But the study didn’t find that people with raised inflammatory measures in middle age were more likely to get dementia, as it wasn’t set up to directly measure dementia risk.

Previous research found people with dementia and a smaller brain volume are likely to have higher measures of substances linked to inflammation in their blood.

But it wasn’t clear whether the inflammation happened before the dementia, or afterwards.

The association is further complicated by the fact it’s normal for people’s brains to experience some shrinkage as they get older. And, obviously, not everyone gets dementia as they get older.

While the study is certainly interesting, it doesn’t provide any concrete answers.

For example, we don’t know how people’s inflammatory measures changed over time, or what role factors other than inflammation may have had.

There are steps you can take to reduce your risk of dementia, although these aren’t guarantees.

This includes eating a healthy diet, maintaining a healthy weight, exercising regularly, moderating how much alcohol you drink, and quitting smoking if you smoke.

Where did the story come from?

The researchers came from the Johns Hopkins School of Medicine, the Baylor College of Medicine, the University of Minnesota, the Mayo Clinic, and the University of Mississippi Medical Centre, all in the US.

The study was funded by the US National Heart, Lung and Blood Institute, and was published in the peer-reviewed journal Neurology.

The Times and the Mail Online covered the study in reasonably balanced and accurate stories.

Both made it clear in the article (although not in The Times’ headline) that the study didn’t show a cause and effect relationship between inflammation and dementia.

What kind of research was this?

This was a prospective cohort study.

These types of observational study are good for spotting links between factors – in this case, inflammation and brain volume – but can’t prove that one factor causes another.

What did the research involve?

Researchers recruited more than 15,000 people aged 45 to 65 for an ongoing study principally intended to look at heart disease risk.

As part of the study, they measured 5 substances linked to inflammation in the participants’ blood when they were aged 53 on average.

Twenty-four years later, they selected 1,978 participants to have their brain volume measured by MRI scan and take a word recall memory test.

They then looked at whether higher inflammatory measures were linked to brain volume and memory test performance.

The researchers specifically sought to find out whether age, sex or race might have affected the results, as these have already been linked to dementia risk.

The 5 substances chosen as markers of inflammation were:

fibrinogen

albumin

von Willebrand factor

factor VIII

white blood cell count

Most of these are linked to blood clotting or the body’s response to infection.

The researchers combined people’s scores to give an overall inflammatory marker score.

The memory test involved listening to a list of 10 words and recalling as many as possible after a short delay.

The MRI scans looked at total brain volume, as well as analysing specific areas of the brain known to be affected by Alzheimer’s disease (AD), such as the hippocampus.

What were the basic results?

People who had higher total inflammatory marker scores in middle age (the average age was 53 at the start of the study) were more likely to have a smaller brain volume in certain areas at the end of the study.

These were:

hippocampal volume – the hippocampus is an area of the brain that helps regulate memory

occipital volume – the occipital lobe is an area of the brain responsible for visual processing

AD signature region volume – an area of the brain previously thought to be smaller in people with Alzheimer’s disease; it consists mainly of the cerebrum, which is responsible for higher brain functions

But the people involved in the study did have larger volumes in ventricular parts of the brain (these are cavities in the brain filled with fluid).

Compared with people who didn’t have raised levels of any inflammatory markers at the start of the study, those with raised levels on 3 or more markers had smaller hippocampal (4.6% smaller), occipital lobe (5.7% smaller) and AD signature region (5.3% smaller) volumes.

They also did very slightly worse on the memory test, remembering on average 5 words out of 10, compared with 5.5 words for those without inflammatory markers.

The researchers didn’t see any link between total brain volume and inflammatory markers.

The association between inflammatory markers and brain volume was stronger in people who had higher markers of inflammation at a younger age, and was weaker in African American participants. There were no differences between the sexes.

How did the researchers interpret the results?

The researchers said their findings “provide support” for an early role for inflammation “in the development of neurodegenerative brain changes associated with late-life cognitive decline, AD [Alzheimer’s disease] and other forms of dementia”.

Conclusion

Inflammation in the body is a response to injury or disease. But if the body is constantly in an inflammatory state, it can harm blood vessels and lead to heart disease.

This study suggests high levels of inflammation over the long term might also damage the brain.

That’s not surprising – what’s good for the heart is usually good for the brain, and we already know exercising, avoiding high blood pressure and eating healthily may help protect the brain.

Studies like this will help researchers work out more precisely what’s happening in the brain when people experience memory loss or dementia.

But this study has some limitations.

The first and most important is that researchers didn’t measure people’s brain volume at the start of the study.

This means we don’t know whether the results at the end of the study end represent brain shrinkage, or whether some people had always had smaller brain volume in certain areas.

This makes it harder to be sure that differences in inflammatory markers predated the differences in brain volume. This type of study design can’t prove cause and effect – and in this case, it can’t prove that one situation predated another.

Also, the substances measured may not be very precise measures of inflammation – they’re also involved in other physiological processes.

And the study didn’t look at whether people with higher inflammatory markers were more likely to get dementia, only at their brain volume and performance in one type of memory test.

We don’t know the effect of the smaller brain volume in some areas on those people. The different performance on the memory test was also pretty small.

All in all, it’s far too early to say we could ever have a blood test that accurately predicts dementia risk.

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‘Exercise may help prevent Alzheimer’s disease’

Dementia and exercise

Dementia and exercise

“Cut Alzheimer’s risk by walking,” the Daily Mail recommends. This advice is prompted by a statistical modelling study looking at population attributable risks (PARS) – factors known to influence the prevalence of a disease, such as Alzheimer’s, at a population level.

The seven risk factors researchers looked at included diabetes, smoking, high blood pressure, lack of exercise, obesity, depression and low educational level. In theory, some cases of Alzheimer’s disease might be prevented by reducing these risk factors.

For example, the study estimated physical inactivity accounted for 21.8% of the risk of developing Alzheimer’s in the UK. Another way of saying this is that if nobody was inactive, the risk of Alzheimer’s in the UK population could reduce by 21.8%.

But this is only a theory that applies to an entire population, not individuals. We cannot say for sure that living a healthier life will definitely prevent Alzheimer’s disease.

One of the biggest risk factors for Alzheimer’s is age, and it is possible age will interact with the seven modifiable factors over different stages of a person’s life. This could create a more complex risk profile than the current study was able to describe.

But a healthy lifestyle does have other benefits – regular exercise can reduce your risk of developing heart disease and some types of cancer.

 

Never too late to learn

Although unproven, the hypothesis that keeping the brain active has a protective effect is relatively plausible.

 

Whatever your age, there are many opportunities to learn new things, ranging from weekly evening classes to something more formal, such as an Open University or University of the Third Age course.

 

A good place to find out more is usually your local library, which should be able to provide information about adult education resources in your area.

Where did the story come from?

The study was led by researchers from the psychology department at the Institute of Psychiatry, King’s College London, and was funded by an award from the National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care for Cambridgeshire and Peterborough.

It was published in the peer-reviewed journal, The Lancet Neurology.

The UK media’s reporting was generally accurate, with most focusing on the physical activity risk, which was the most important factor for the UK data.

 

What kind of research was this?

This modelling study used existing data on potential risk factors for developing Alzheimer’s disease, including sociodemographic and lifestyle factors, and health-related factors such as diabetes and high blood pressure.

The researchers then predicted the amount of disease that might be prevented if these risk factors were reduced through changes in lifestyle.

While this type of research can provide useful predictions, they are just that – hypothetical predictions.

Similarly, the predictions apply to entire populations of people, such as everyone in UK. This means the study cannot say that living a healthier life will prevent Alzheimer’s for any specific individual, only that it may prevent some cases across the group as a whole.

 

What did the research involve?

The researchers used existing population-based research to identify the main modifiable risk factors that may be associated with Alzheimer’s disease.

They then predicted how many cases of Alzheimer’s disease might be prevented if the risks were reduced across the US, the UK and the rest of the world.

The main analysis was the calculation of the population attributable risk, or PAR. This is the proportion of cases of a disease in a population that is attributable to the risk factor.

A modifiable risk factor, such as smoking, is a risk you can potentially reduce – for example, by stopping smoking. The main modifiable risk factors linked to developing Alzheimer’s disease were:

diabetes – adult prevalence of diagnosed diabetes between the ages of 20 and 79

midlife high blood pressure – adult midlife prevalence of hypertension between the ages of 35 and 64

midlife obesity – adult midlife prevalence of body mass index greater than 30 between the ages of 35 and 64

physical inactivity – proportion of adults who do not do either 20 minutes of vigorous activity on three or more days, or 30 minutes of moderate activity on five or more days per week

depression – lifetime prevalence of major depressive disorder using Diagnostic and Statistical Manual of Mental Disorders or International Classification of Diseases criteria

smoking – the proportion of adult smokers

low educational level – the proportion of adults with an International Standard Classification of Education level of two or less (pre-primary, primary and lower secondary education)

The researchers made projections for the number of cases of Alzheimer’s disease up to the year 2050. They then modelled risk reductions of 10% and 20% for each decade from now until 2050 to see how many disease cases could be prevented.

They did this for each risk factor both individually (to see which ones had the biggest impact) and combined.

The predictions took account of associations between risk factors – for example, that a person who is obese is more likely to have high blood pressure.

 

What were the basic results?

The study calculated PAR for the world, the US and the UK. We focus on the UK results below.

The largest PAR for an individual risk factor in the UK was for physical inactivity (PAR 21.8% 95% confidence interval [CI], 6.1% to 37.7%).

This meant that 21.8% of the Alzheimer’s cases were predicted to be attributable to physical inactivity, which could potentially be prevented if people were more active.

The next highest PAR was for low educational level (PAR 12.2% 95% CI, 7.6% to 16.9%), followed by smoking (10.6%, 95% CI, 2.9% to 19.4%).

Diabetes, midlife hypertension, midlife obesity and depression gave PARs in the range of 1.9% to 8.3%.

Combining the seven risk factors together gave a UK PAR of 30.0% (95% CI, 14.3% to 44.4%).

This means the researchers predicted around 30.0% of the risk of developing Alzheimer’s disease in the UK was attributable to a combination of these seven modifiable risk factors.

This estimate adjusted for associations between risk factors, such as obesity and diabetes.

 

How did the researchers interpret the results?

The researchers concluded that, “After accounting for non-independence between risk factors, around a third of Alzheimer’s diseases cases worldwide [and in the UK] might be attributable to potentially modifiable risk factors.

“Alzheimer’s disease incidence might be reduced through improved access to education and use of effective methods targeted at reducing the prevalence of vascular risk factors [for example, physical inactivity, smoking, midlife hypertension, midlife obesity and diabetes] and depression.”

 

Conclusion

This study suggests around a third of the risk of developing Alzheimer’s disease might be caused by a combination of seven lifestyle-related risk factors, including low educational level, physical inactivity and smoking. In theory, by reducing these risk factors some cases of Alzheimer’s disease might be prevented.

Predictive studies such as this one are only as good as the assumptions and data used in the calculations. As the researchers themselves acknowledge, despite their best efforts to the contrary, this still involves “substantial uncertainty”. Consequently, there may be some variation in the estimates of the PARs presented because of potential inaccuracies or natural variations in prevalence data.

The strength of the association between the risk factor and the disease may also vary in different groups. This accuracy could be tested by repeating the research using a range of different data sources and assumptions.

The predictions this study makes apply to entire populations of people, such as everyone in the UK. It therefore cannot say that living a healthier life will definitely prevent Alzheimer’s for any specific individual, only that it may reduce the risk and prevent some cases across the group as a whole.

If everyone in the UK was physically active (defined in this study as 20 minutes of vigorous activity on three or more days a week, or 30 minutes of moderate activity on five or more days a week) the study predicts around 20% of the risk of developing Alzheimer’s would be cut, which would reduce the number of people developing the disease overall.

But because we are modelling the effect in large groups, it is not possible to pinpoint which people would get Alzheimer’s and which would not. Other types of test and analysis would need to be developed to be able to predict this.

These predictions assume that all the risk factors tested directly cause or contribute to Alzheimer’s disease. The researchers acknowledge this is open to debate in some areas. This means the risk accounted for by these factors could potentially be lower than estimated in this study.

One of the biggest risk factors for Alzheimer’s disease is age, and it is likely age will interact with the seven modifiable factors over different stages of a person’s life, creating a more complex risk profile than this study was able to describe.

For example, it is unlikely that someone who decides to quit smoking and start exercising regularly at 20 would have the same risk reduction as someone deciding the same thing at 70.

Nonetheless, there are a host of other good reasons for leading a healthy lifestyle, no matter what your age. Keeping active once you reach retirement age can also help you stay more energetic, healthy and independent as you get older.

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Stay With Me campaign launches to improve care for patients with dementia

Stay with me

Stay with me

A new initiative to improve the experience of people with dementia, who come into Leicester’s Hospitals, will be officially launched by Nicci Gerrard, founder of John’s Campaign and Julie Smith Chief Nurse, at Leicester’s Hospitals Champions Celebration Event on Wednesday, 13 September.

This inspiring initiative will be called ‘Stay with Me’, and will be rolled out over the next month into all wards and clinical areas.

The Champions Celebration Event is taking place during Older People’s Month 2017 to celebrate the hard work and support Dementia and Older People Champions provide for older people and people with dementia in and around Leicester’s Hospitals.

The principles of ‘Stay with Me’ were inspired by John’s Campaign, a national initiative founded by Nicci Gerrard in memory of Nicci’s father, Dr John Gerrard.

Justine Allen, from the Patient Experience Team explains:  “We’ve developed our initiative from the campaigns statement of purpose, ‘Stay with Me’. The ethos of ‘Stay with Me’ is to help create a welcoming environment on all hospital wards where there are no barriers for family  who wish to stay beyond visiting times for patients with dementia.  There is a wealth of evidence to suggest patients with dementia who are often frail, vulnerable adults have much more positive outcomes if they are with people they are most familiar with.

“The principles behind this campaign are very simple and similar to that of our existing Carers Charter; to allow family, carers and friends to help support vulnerable patients so it made sense to trial the campaign to see if it could enhance what we already do.”

Throughout June and July 2017, the initiative was piloted on wards 32, 33 and 36 at Leicester Royal Infirmary to see how it works in practice, and to identify possible barriers and difficulties.

During the pilot, staff welcomed carers, friends and family onto the wards beyond standard visiting hours and worked in partnership with families to help provide the best possible care for the patient.

Over 1,400 patients were admitted through the three wards, of which 14 patients had a diagnosis of dementia and had family  who were supported by the scheme to stay beyond visiting times with the patient.

Justine continues: “Where patients may need some extra support, we have found this is often best placed to come from someone they know and love. Being in hospital can be an emotional and overwhelming experience, especially for patients with dementia. Having a familiar face by your side to help with getting dressed, eating or by just simply being there for company and reassurance, can make a huge difference to health and recovery.”

The results of the pilot were overwhelmingly positive and showed excellent engagement with staff from start to finish. Carer and family feedback also suggested they felt more supported and involved.

For further information about John’s Campaign, please visit www.johnscampaign.org.uk