We know the old adage of eating 2 fruit and 5 vegetables every day for our general health. Many of those which are highly coloured, red, yellow and green have been identified as containing high levels of phytochemicals which can have a positive impact for our heart health and brain function.

Researchers have now found that eating the white flesh of fruits appears to be protective versus stroke.
In a Dutch study published in Stroke: Journal of the American Heart Association it was noted that the incidence of stroke in those who ate more white fleshed fruits and vegetables was about half that of those who ate relatively little.

For every 25 grams per day increase in white fruit and vegetable consumption there was a 9% lower risk of stroke.

An average apple weighs around 120grams.

And before you reach for the next plate of hot chips – potatoes were classified here as a starch source.

Apples and pears provided over half the intake of white fruits eaten over the study, which ran for ten years.
What are the other white fruits and vegetable to think about?

Bananas, cauliflower, cucumber and chicory (witlof)

Over twenty thousand people contributed to the study, which took the form of food frequency questionnaires. None had any identifiable cardiovascular disease at the beginning of the study and the average age was 41 years.

Why is this relevant to brain health? Stroke is a major cause of health burden and vascular dementia is the second most common form of dementia.

An editorial published with the article cautions that this research may not be 100% reliable from its use of these type of questionnaires and also did not factor in for the variable that those eating more white fleshed fruits may have been those already leading healthier lifestyles.

Any which way, it is always going to be a good thing to include a wide variety of fruit and vegetables in your diet.

So, next time you take an apple to school for teacher, remember to pack one for yourself as well.

Ref:
Linda M. Oude Griep, W. M. Monique Verschuren, Daan Kromhout, Marga C. Ocké, Johanna M. Geleijnse. Colors of Fruit and Vegetables and 10-Year Incidence of Stroke. Stroke, 2011; DOI: 10.1161/STROKEAHA.110.611152

Are there some things, which really get up your nose?

Well this may be one thing you do want to put up there: a nasal spray capable of protecting your brain from Alzheimer’s disease or stroke.

And before you dismiss that notion as being ridiculous and from “la-la land”, it appears that researchers from Tel Aviv University may be onto something completely novel; a way of effectively preventing and treating Alzheimer’s disease delivering medication via a nasal spray.

This is a story reminiscent of the story of Viagra. The treatment for erectile dysfunction started life as a medication being developed for men with chest pain.
In this case the nasal spray was being developed as a treatment for influenza. The medical scientists were looking to induce an immune response vs. influenza and what they found was that the vaccine, caused the body to activate part of its defence mechanism against viral and other invaders, called macrophages. These macrophages act as large vacuum cleaners gobbling up unwanted proteins such as amyloid from the brain’s blood vessels. Amyloid can build up in the brain and is a pathological finding commonly found in the brain of people with Alzheimer’s disease. In animal studies, once these amyloid proteins had been cleared, then further damage to the brain could be prevented and existing damage repaired.

This means that it may be possible to repair the damage to a brain from a previous stroke and to be able to effectively treat people already experiencing symptoms associated with Alzheimer’s disease.

Previous studies into Alzheimer’s disease have looked at using an immune mediated approach using anti-inflammatory medications and steroids.

Here the immune response being induced is preventing small bleeds causing stroke, which can cause permanent brain damage and contribute to vascular dementia.

The next stage is to look at clinical trials.

So far the animal studies have shown no toxic side effects and fMRI scans on the mice confirmed the effectiveness of the vaccine in returning those mice with cognitive impairment to normal behaviour.

If the drug is found to produce the same effect in humans, this means there may be a simple way of treating up to 80% of those with Alzheimer’s dementia.

Wow, the findings from this study imply we could be looking at a possible breakthrough for a vaccine to guard against and an effective treatment for Alzheimer’s.
Something simple, hopefully inexpensive and literally brain saving.

One small spray for your brain, one giant water cannon of hope for many minds.

Ref: Dr D. Frankel. Tel Aviv Department of Neurobiology Press release

I hate smoking. I hate seeing other people smoke, especially young people.
Smoking kills.
The toxins contribute to heart disease and cancer and stroke.

It also affects our brains.

We all see the messages about why smoking is bad for us. Yet, despite many of us expressing a wish not to smoke, the choice of not smoking remains still too hard for many who prefer to carry on, despite the knowledge that yes they may have an increased risk of lung and throat cancer. And it is frustrating that you are continue to meet people who have lived to a ripe old age who have smoked several packets a day all their lives who will brightly tell you that it hasn’t done them any harm. There are always going to be those who dodge the bullet. But not everyone does.

Does the thought that smoking increases your risk of developing dementia make you think any harder about why it is a good idea to stop?

Heavy smoking in middle age increases the risk of Alzheimer’s disease and vascular dementia in men and women across different age groups. Their risk is doubled for developing a form of dementia within a twenty year period.
This was the finding of a study from Finland recently published in JAMA, Archives of Internal Medicine. They analysed the data from over 21000 multiethnic participants who took part in a survey conducted between 1978 and 1985 when aged between 50 to 60 years. Then from 1994 to 2008 when the average age of this cohort was 72 years, they tracked the number of diagnoses of dementia, Alzheimer’s disease and vascular dementia in the group.

Over the 23-year follow up of these 21,000 people, 25% were subsequently diagnosed with dementia. The heaviest smokers had the greatest risk.
Compared to non-smokers, those smokers who averaged two packs a day had a greater risk of dementia overall and also of the various forms of dementia. i.e. Alzheimer’s disease and vascular dementia.
Those who had given up smoking and those who smoked less than half a packet a day did not appear to be at increased risk.
There was a no difference in the rates by race or sex.

The relevance of this study is that smoking is a double-edged sword. Smoking has long been a well-recognised risk factor for stroke and contributer to vascular dementia. Now it appears that smoking by its contribution to oxidative stress and inflammation, is of significance in the development of Alzheimer’s disease. Smoking through vascular and neurodegenerative pathways can contribute to different forms of dementia.

This is the first study to evaluate the amount of long-term smoking on long-term risk of dementia in all of its forms.
As the world braces itself for the rising tide of dementia from ageing alone, the detrimental effect of smoking is going to become even more relevant.

Convinced yet?

Minna Rusanen; Miia Kivipelto; Charles P. Quesenberry, Jr; Jufen Zhou; Rachel A. Whitmer. Heavy Smoking in Midlife and Long-term Risk of Alzheimer Disease and Vascular Dementia. Archives of Internal Medicine, 2010; DOI: 10.1001/archinternmed.2010.393

It’s now been discovered that our clever brain has more than one way of learning. For the last twenty or thirty years our understanding of the way our brain works to learn or store memories has been that it involves a particular receptor called the NMDA receptor found at the terminal end of brain cell dendrites. This receptor is particularly active in the area of our brain called the hippocampus, which is the area that specialises in helping us to learn and encode memories.

The way it works is that when this particular receptor is activated it allows calcium to enter that brain cell, which then triggers further molecular reactions which results in our brain being able to process, store and then retrieve that information.
Last week Bryce Vissel from the Sydney Garvan Institute of Medial Research was talking on ABC radio discussing the results of the study he had been involved in, that has now been published in the 29th September edition of PLoS One.

Bryce Vissel and other researchers from Australia and the United States had been looking to artificially replicate this NMDA mechanism to provide a way to circumvent the difficulties of memory loss associated with brain injury through stroke and disease. What they found coincidentally was that the brain actually already has a secondary pathway in place, which enables us to store new information. This has been termed “second learning” as this pathway uses a different receptor called AMPA but this is only activated if the information received relates to similar information that has been learnt before. The implication of this finding is that this natural second pathway, may allow us to circumvent the disease, or damaged NMDA receptors, which could prove useful to provide new and alternative ways of treatments for stroke and Alzheimer’s disease.

Among the questions now being raised from this finding, is to work out what allows or triggers this second mechanism to operate. Once that is understood the hope will be to be able to find ways to engage this pathway to take over the role of the NMDA mechanism that isn’t working through disease or injury.
The other potential implication of this finding is that having this second means of learning could have really important effects on how we approach teaching in the classroom in the future as well.

Ref: A Role for Calcium Permeable AMPA Receptors in Synaptic Plasticity and Learning.
Wiltgen BJ, Royle GA, Gray EE, Abdipranoto A, Thangthaeng N, et al. 2010 A Role for Calcium-Permeable AMPA Receptors in Synaptic Plasticity and Learning. PLoS ONE 5(9): e12818. doi:10.1371/journal.pone.0012818

I was sitting in my GP’s office recently, being told something I didn’t want to hear. My blood pressure was too high and I needed to start medication with antihypertensives.

I didn’t want to have to take medication. I had always planned not to be on anything apart from fish oil and glucosamine supplements until I was at least 90 years old. I consider myself fit. I exercise daily, my weight is normal, I eat healthily, I don’t smoke and I keep an eye on how much wine I drink each week.

But my family history includes hypertension and stroke on both my mother’s and father’s side.
And I do recall a conversation with my obstetrician who was managing my pregnancy-induced hypertension a number of years ago. He said, “Jenny, you are likely to develop hypertension as you get older.” Harrumph. I heard, but didn’t want to listen. But who am I trying to kid?

I have what is called “essential hypertension”. The cause is as yet unknown.
I don’t like it. But I can deal with it and take my pills.
The reason why? Because I value my brain cells too highly not to. As a Doctor my medical training has taught me what the consequences of untreated hypertension are.

Hypertension has been described as a silent killer. You can’t feel if your blood pressure is too high. We rely on readings taken with a sphygmanometer to get an accurate idea of the state of our blood vessels.
The blood pressure reading essentially tells us the peak or systolic pressure our heart has to exert with each contraction to pump the blood around our body. The lower reading or diastolic pressure gives us the resting pressure of the circulatory system in between heartbeats.

If the readings are too high we run the increased risk over a period of time of blood vessel rupture causing a stroke or cerebrovascular accident. Other organs are affected as well, including the kidney, eye and heart. None of which is good news.

So, back to the brain and high blood pressure. Sure it’s good not to be at risk of stroke. But what about the effect of high blood pressure on memory and cognition?

Studies have shown that having high blood pressure can contribute to memory loss and other decline in brain function in people over the age of 45.

In one study of over 19000 participants aged 45 or older, they found that with each 10-point increase in diastolic pressure, the risk of cognitive difficulty increases by 7 points.

But how high is high?
We need to keep our diastolic pressure (the lower of the two reading indicating the pressure of the arterial system at rest) at below 90mmHg.

With around 25-30% of the Australia adult population having high blood pressure I am clearly not alone.
For the vast majority of people like myself we have “essential hypertension” where no specific cause is identified. However having high blood pressure causes problems by causing our arterial walls to thicken and lose their elasticity, leading to reduced blood flow and tissue death.

Having reduced blood flow to your brain becomes an issue when you need it to be working harder. For example when you want to be able to pay attention or work out a solution to a problem, the decrease of available blood flow to your brain leads to fewer brain cells being activated and an increased number of memory lapses happening as a result.

In older people, having high blood pressure can predict who is at risk of developing impaired executive function (organising, planning and decision making) and a greater risk of progressing to dementia. One study of 900 octogenarians showed that high blood pressure was associated with an increased risk of developing dementia when frontal lobe functioning was impaired

Because stroke and TIA are leading causes of risk of cerebrovascular disability followed by dementia, controlling hypertension is a simple and effective way to significantly potentially reduce the incidence of forecasted dementia in this group.

So attending to diagnosing and treating hypertension in midlife would appear to be essential to protect you from developing cognitive impairment further down the track.

If you are over 45 and haven’t had your blood pressure checked for a while, now would be a good time to make an appointment and get it checked by your GP.

If it is too high then some simple lifestyle changes could help:

• Keeping your weight in the healthy range
• Don’t smoke
• Reduce your alcohol consumption.
• Do some regular exercise
• Keeping your cholesterol in the normal range
• Eat less saturated fat.
• Use less salt in your diet.

Hypertension has no symptoms, but is easily managed and keeping it in the normal range could make a big difference to being able to save your brain.

References:
Shahram Oveisgharan; Vladimir Hachinski. Hypertension, Executive Dysfunction, and Progression to Dementia: The Canadian Study of Health and Aging. Arch Neurol, 2010; 67 (2): 187-192

JAMA and Archives Journals (2007, December 12). High Blood Pressure Associated With Risk For Mild Cognitive Impairment.

Radiological Society of North America (2007, November 29). High Blood Pressure May Heighten Effects Of Alzheimer’s Disease.