A little ray of sunshine for Parkinson’s disease may lie with Vitamin D.

Vitamin D is the vitamin we obtain through the action of ultraviolet light on our skin. Most of the vitamin D produced is then bound in the blood and only a tiny fraction remains free and able to bind to specific vitamin D receptors now known to be located in a number of target organs in the body including the brain.

Not only that, but the area of the brain with the highest density of Vitamin D receptors is in the Substantia Nigra. This is where highly specialized cells produce Dopamine, the brain neurotransmitter vital for regulating our mood, concentration, motivation and voluntary movement.
In Parkinson’s disease many of these highly specialized cells die and the loss of Dopamine manifests itself in the form of tremor, rigidity of movement, slowness of gait and cognitive decline. Plus, thirty percent of people with Parkinson’s disease develop dementia.
It is the second most common neurodegenerative disease in Australia and remains one of the most poorly understood.

So where does Vitamin D fit in with Parkinson’s disease?

The answer to that is not yet certain, but a recently published study has linked having a higher level of Vitamin D with up to a 65% reduction in the risk of developing Parkinson’s.

These results were in a long prospective study by Paul Knekt in Finland. He showed that in a group of 3173 people aged 50 to 79, followed up over a 29 year period, those with a higher level of Vitamin D had a 65% lower risk of developing Parkinson’s compared to those with the lowest levels.

However it should be noted that all of the subjects in this study actually had lower levels of vitamin D than is recommended. This may reflect the fact that Finland is not a country associated with a lot of sun exposure for its residents. So the suggestion is that having a lower level of Vitamin D may be a predisposing factor to an increased risk of Parkinson’s disease. There is no suggestion that having a low level is in fact a cause. The study remains a starting point to determine whether giving Vitamin D as a supplement would be useful.

One of the problems recognized is that Vitamin D deficiency is widespread, even in a sunny country such as Australia. It has been reported that half to two thirds of teenagers and adults in the US have lower than desirable levels. Because it is very difficult to get sufficient Vitamin D through our diet, having adequate sun exposure is essential to help us achieve and maintain a healthy level.

How much time do we need in the sun?

Five to fifteen minutes of sunlight exposure to the face and upper arms, four to six times a week is thought to be sufficient to prevent deficiency.
Those particularly at risk of deficiency here in Australia include the elderly living in residential care and dark skinned women, especially those who are veiled. The use of sunscreen (essential to protect us from skin cancer) unfortunately prevents the synthesis of Vitamin D in the skin. Application of Factor 8 will prevent up to 95% of Vit D conversion, so a short exposure without sunscreen is recommended and outside the high-risk times of 10 am to 3 pm.

Can we get Vitamin D from our food?

We can derive a limited amount of Vitamin D from food sources. However in cases of deficiency taking a supplement would be recommended.

Vitamin D2 can be found in:

Fatty fish such as mackerel, salmon and herring
Fortified margarines
Cod liver oil
Liver
Eggs

The role of Vitamin D in the brain

The association of Vitamin D and Parkinson’s disease is intriguing and as yet not fully explained. It is believed that Vitamin D acts as a hormone rather than a vitamin, in addition to its role in bone metabolism.

Current thinking is that it may exert a neuroprotective effect through its antioxidant properties, calcium regulation of nerve cells, enhanced nerve conduction, detoxification and immunomodulation.

A UK study looked at Vitamin D levels of a group of 858 Italian men and women over the age of 65 years. Of those with dementia, 50% were vitamin D deficient. Moreover, those with the greatest deficiency had a 60% increased risk of suffering cognitive decline over the 6-year follow up period.

The role of Vitamin D relating to Alzheimer’s disease was looked at in a 2008 study where 100 people with Parkinson’s disease were compared to 100 subjects with Alzheimer’s disease and 100 healthy controls. Here the fraction of patients with the lowest levels of Vitamin D was most marked in the Parkinson’s group (23%) compared to the Alzheimer’s group (16%) and healthy group (10%) indicating support for the notion that Vitamin D plays a role in affording some neuroprotection.

Meanwhile it remains prudent to ensure that we obtain adequate sun exposure to keep our Vitamin D levels up. So go on, it’s time to enjoy some time in the sun.

References:
Emory University (2008, October 17). Lack Of Vitamin D Linked To Parkinson’s Disease.
Archives of Neurology [2010] 67 (7) : 808-811 (Knekt P, Kilkkinen A, Rissanen H, Marniemi J, Sääksjärvi K, Heliövaara M.)

Statisticians have been telling us how Western societies are facing a tsunami of people developing dementia and Alzheimer’s over the next couple of decades. This is associated with our ageing population; we are all living longer, so our relative risk of developing dementia rises as well.

What worries me though is the fact that we seem to be ignoring the impact that the dramatic increase in people living with Type 2 diabetes and obesity will have on these figures.

Both diabetes and obesity are known risk factors for dementia.
Adults who develop diabetes before the age of 65 have twice the risk of developing dementia compared to non-diabetics and also have an increased risk of depression.

It is our children that worry me the most. Twenty years ago the number of kids diagnosed with Type 2 diabetes was in the order of 2%. It was an extremely rare condition. Now 30 to 50% of all those diagnosed with Type 2 diabetes are between the ages of 9 and 19 years. Those aged in their thirties, have seen a 70% increase in the number of people diagnosed.
The scary thing also, is that it is known that there are an even greater number of people with undiagnosed diabetes in the general population.

What is Type 2 diabetes?

When we eat a meal, the carbohydrates in it are broken down and released into our blood stream as sugar, leading to an increase in the blood sugar level. This then stimulates the pancreas gland to release insulin hormone which works to restore the blood sugar level back to normal by sending the glucose to tissues that need it for energy, or for storage. If the body is repeatedly overloaded with excess glucose, the body’s ability to respond to the insulin is diminished, leading to a condition called insulin resistance. Increasing amounts of insulin then get produced, but it can no longer exert its effect. This is the condition of Type 2 diabetes where blood sugar levels are consistently too high and associated with elevated insulin levels.

It is distinguished from Type 1 diabetes where the specialised glands in the pancreas are unable to produce insulin.

When are we going to wake up to this risk?

If you have diabetes, you have a higher risk of cognitive decline and dementia.

In a study of 2300 older women aged 70 to 78, non-diabetics on mental testing scored twice as high as diabetics. It was also found that the longer the person had had diabetes, the more poorly she performed.

In another multiethnic, multicenter study of 10,000 people, the results of cognitive tests taken 6 years apart were compared. In the 40 to 70 year age group, diabetes was again linked to greater cognitive decline.

What does diabetes do to the body and brain?

Diabetes affects multiple organs in the body including the blood vessels, heart eyes, brain and kidneys and is insidious in how it gradually erodes cognitive ability. Elevated blood sugar levels contribute to hardening of the arteries, (atherosclerosis) which increases the risk of heart disease and stoke. In the brain, this vascular damage is linked to an increase in small infarcts (injury to small arterioles in the brain) or tiny strokes. Having persistently elevated blood sugar contributes to damage of our brain cells, brain atrophy and cognitive impairment. The loss of brain cells is especially prominent in the area of the hippocampus, the specialised brain area concerned with memory and learning.
Diabetic patients who have developed diabetic retinopathy have been shown to have twice the risk of developing cognitive impairment.

Excess insulin also contributes to the brain damage. It has been discovered that the brain has it’s own insulin receptors. Increased insulin levels have been linked to increased levels of amyloid, the protein associated with plaques found in Alzheimer’s. Excess insulin also has a role in stimulating inflammation, and reducing the levels of acetylcholine an essential neurotransmitter for memory.

But it’s not just diabetics who are at risk of impaired brain function and reduced mental performance. It has been shown that drinking a sugary glucose drink will adversely affect your ability to perform memory tests. So the key is to avoid big swings in blood sugar levels.

Because we know that diabetes is associated with an increase risk of cognitive impairment and dementia, it is vital that the message gets out to all those at risk.

The good news though, is that we know that good lifestyle choices can have a hugely beneficial effect on blood sugar control.

The aim is to

• Keep blood sugar levels in the normal range
• Maintain a healthy body weight
• Eat a nutritious and brain healthy diet low in saturated fat
• Exercise for 30 minutes a day by walking or other moderate intensity activity.

My question to you is this. Can we afford not be taking immediate steps to educating people to fully understand the consequences of “accepting” the recent global increases in obesity and diabetes?

Our sweet tooth is killing our brain.

Refs:
Roberts et al. Association of Duration and Severity of Diabetes Mellitus With Mild Cognitive Impairment. Archives of Neurology, 2008; 65 (8): 1066 DOI: 10.1001/archneur.65.8.1066
University of Southern California (2009, January 28). Getting Diabetes Before 65 More Than Doubles Risk For Alzheimer’s Disease.

My Dad, who is a retired vet, used to give many of his older canine patients Vitamin E, because he found it seemed to give them a bit more spring in their step and kept them going for longer.

Vitamin E is a powerful antioxidant found in nuts, seeds, eggs, whole grain foods, spinach, avocado, salad dressing and vegetable oils.

The role of Vitamin E in reducing the risk of dementia has been the subject of a number of studies. In the July edition of “Archives of Neurology” the results of a long-term study carried out by the Erasmus Medical Centre in Rotterdam, Holland, revealed the effect of four dietary antioxidants on dementia risk. Over 5000 people aged 55+ (who did not have dementia at the onset of the study), were followed for 9+ years. The study focused the intake of Vitamin E and C, beta-carotene and flavonoids.

In a previous study, the Rotterdam group had found that higher dietary intakes of Vitamin E and C were associated with a lower risk of Alzheimer’s and dementia.

The results of this longer term study though, showed that it was those people who consumed the highest amount of Vitamin E that had 25% less risk of developing dementia compared to those who consumed the least. The dietary intakes of Vitamin C, beta-carotene and flavonoids were not associated with changes in dementia risk. This was an unexpected finding, given the previous positive association link found with Vitamin C.

What about the use of Vitamin E as a supplement ?

Many clinicians routinely give their elderly patients high doses of Vitamin E and often in only one form. Vitamin E is actually a family of eight natural compounds and the one most commonly used is alpha–tocopherol.

A Swedish study looked at the levels of all eight natural vitamin E compounds in the blood of over 200 subjects. Here they found that those with the highest blood level of all of the vitamin E family had a reduced risk of developing dementia. This risk was reduced by between 45 to 54% depending on the individual Vitamin E component level.
Dr Mangialasche in this study noted that the protective effect of the vitamin appears to be related to the combination of the different forms, suggesting that it is the balance of the 8 compounds, which may have the most important neuroprotective effect.

Another study also looked at the role of dietary Vitamin E along with a combination of certain other nutrients which have also been associated with a lower risk of dementia and Alzheimer’s disease.

Columbia University NY revealed the results of a four year study of 200 subjects over the age of 65 (none of whom had dementia). They identified several dietary patterns with varying levels of 7 nutrients, previously associated with Alzheimer’s risk. These included saturated fats, monosaturated fats, omega 3 fatty acids, omega 6 fatty acids, Vitamin E, B12 and folate. One pattern in particular was found to be associated with a significantly lower risk of Alzheimer’s and this was noted to include a high intake of the following:

Salad dressing
Nuts
Fish
Tomatoes,
Poultry
Fruits
Cruciferous vegetables
Dark green leafy vegetables

This is pretty much the basis of the Mediterranean diet, which has previously been associated with a lower risk of Alzheimer’s and dementia.

The authors noted that the nutrients in the low risk dietary pattern reflected the multiple pathways in the development of Alzheimer’s disease.

i.e
• Vitamin B12 and folate help to reduce the body’s levels of homocysteine (a risk factor for Alzheimer’s)
• Vitamin E has a potent antioxidant effect
• Fatty acids assist in normal brain cell membrane function.

So where does that leave us now?

It may well be that including a higher amount of vitamin E rich foods in our diet may have a modest effect on reducing dementia risk. Unfortunately we don’t know yet, how much is to be recommended. Meanwhile eating whole foods in a healthy combination diet based on the Mediterranean model is probably the way to go.
Further studies are likely to continue to evaluate dietary intake of antioxidants and how they may modulate the risk of dementia.

References:
American Academy of Neurology (2008, April 17). Vitamin E May Help Alzheimer’s Patients Live Longer.
Johns Hopkins University Bloomberg School Of Public Health (2004, January 20). Vitamin Supplement Use May Reduce Effects Of Alzheimer’s Disease.
Francesca Mangialasche, Miia Kivipelto, Patrizia Mecocci, Debora Rizzuto, Katie Palmer, Bengt Winblad, Laura Fratiglioni. High plasma levels of vitamin E forms and reduced Alzheimer’s disease risk in advanced age. Journal of Alzheimer’s Disease, 2010
JAMA and Archives Journals (2010, July 13). Eating foods rich in vitamin E associated with lower dementia risk.

P7C3. Remember this name!

Each week I scan different science reports from around the world, which continue to supplement our understanding of how our brain works.
Sometimes one report will leap out from the page when I read it, as it seems to herald a particularly important finding and this week I came across one such report.

The key to maintaining our ability to learn new skills and lay down memory, as we get older is dependent in part in our ability to produce new brain cells.
This is neurogenesis, one component of what makes our brain “plastic”.
The production of new baby brain cells occurs in what is called the dentate gyrus, one region of the hippocampus, which is the area of the brain, associated with learning and memory. However many of the new cells produced don’t necessarily survive to get fully incorporated into our brain.

Think of it in the same way as when turtle hatchlings are released into the ocean. Only a very small percentage actually survive and grow to adulthood. It’s the same with our brain cells. It takes several weeks for new brain cells to fully mature and most of them die off. Plus, the ability for our new brain cells to survive declines, as we get older. So researchers have been looking to identify compounds, which could enhance our newborn brain cells survival.

The results of the recent study could prove to be a breakthrough for potential treatment of Alzheimer’s disease.
A team of researchers at the University of Texas Dallas have found a compound which (at least for rodents) has been shown to increase survival rates of newly formed brain cells and by helping the rats to form new memories, reverse their memory loss.

The compound (given the really sexy name of P7C3) was one of over 1000 molecules investigated by the team. Using genetically engineered mice that lacked a gene needed to allow newborn brain cells to survive, the addition of the P7C3 reduced the expected newborn brain cell death rate.

The next step of the study then looked at whether the compound could slow down age related brain cell death and cognitive decline.
Apparently they used rats for this part of the test because it involved a water maze test, which the genetically engineered mice couldn’t do because they couldn’t swim.
(This conjures up images of mice wearing water wings. But I digress.)
The P7C3 was given on a daily basis to elderly rats with memory problems for two months and they were then subjected to the water maze task. The rats that received the P7C3 performed significantly better than the rats that had not received it. Moreover it was found that the rats given the P7C3 had three times higher than the normal level of newborn brain cells in the dentate gyrus of their hippocampus.

The conclusion was that the P7C3 enhanced new brain cell formation as well as increasing their rate of survival.

This exciting finding indicates that it may be possible in the future to be able to use compounds such as this in humans, because it can be given orally, can cross the blood brain barrier, and can produce long lasting effects for preserving memory and enhancing new brain cell survival. And the compound appears to be safe.

Obviously this is a long way off from being a substance suitable to use in humans, but it heralds an exciting development that we may have treatments in the future that could potentially address some of the core problems associated with Alzheimer’s disease where brain cell death is a marked feature.

And the team have already found that a derivative of the P7C3 called A20 appears to have an even greater neuro protective effect. A20 is apparently 300 times more potent than another compound, which is currently being used in clinical trials as a treatment for Alzheimer’s. The team are now looking to work out how these compounds, P7C3 and A20 produce their effect.
So watch this space.

Reference:
Pieper AA, Xie S, Capota E, Estill SJ, Zhong J, Long JM, Becker GL, Huntington P, Goldman SE, Shen CH, Capota M, Britt JK, Kotti T, Ure K, Brat DJ, Williams NS, MacMillan KS, Naidoo J, Melito L, Hsieh J, Brabander JD, Ready JM, McKnight SL. Discovery of a Pro-neurogenic, Neuroprotective Chemical. Cell, July 8, 2010 DOI: 10.1016/j.cell.2010.06.018

Ladies,

If you could pop along to your local GP’s office and get a blood test which could reveal if you have a higher risk of dementia or not, would you have it?

The results are in from a prospective study, which found that looking at a woman’s level of homocysteine in their blood might be a useful predictor of your relative risk of developing dementia in subsequent decades.

The good news too is that high levels of homocysteine can be treated using folate, vitamin B6 and vitamin B12.

What isn’t known, is whether treating high homocysteine levels would prevent dementia from developing or defer it. More studies would have to be carried out to show if that is the case or not.

But the evidence is now in that having a high homocysteine level is a risk factor for dementia.

What is homocysteine?

Homocysteine is an amino acid that is very important to the body’s metabolism.
It depends on the presence of folate, Vitamin B6 and Vitamin B 12, which we take in with our diet to be kept to a normal range.

Having too much homocysteine has long been known to be associated as a risk factor for heart disease. It appears that some of the risk factors for cardiovascular disease and Alzheimer’s are the same, such as high blood pressure, high cholesterol, smoking, alcohol and obesity.

Other studies have linked dementia and poor cognition with elevated plasma homocysteine levels.
An 8-year study in the Framingham Study again found a doubling of risk of developing Alzheimer’s in those found to have elevated homocysteine.

What hasn’t been determined is whether it is the high level of homocysteine itself or associated vitamin deficiencies, that causes the damage.

But what is known, is that levels of B12 and folate are commonly found to be deficient in the elderly, as is the increased incidence of neurological disease.

In animal studies, folate and Vitamin B12 and 6 deficiencies were linked to poorer memory and spatial learning, and reduced blood supply to the hippocampus, the specialised area in the brain associated with memory.

What are dietary sources of folate and vitamin B12?

Vitamin B12 is found in a variety of commonly eaten foods including meat, fish, milk, eggs and chicken.
Folate is found in green leafy vegetables such as spinach, peas and grains that have been fortified. Many breads and breakfast cereals now have added folate.

Why is this only about the risk for women and not men?

Well basically it is because the study only included women.
So, simply, the results can’t be extrapolated to men.

This was a prospective study that began in the 1960’s on 1500 women (aged between 38 and 60 yrs) who had blood tests done including recording homocysteine levels and filled in a health questionnaire. Thirty-five years later the data is now in, on discovering which of those women subsequently went on to develop dementia or Alzheimer’s disease.

It was those women who had high homocysteine levels, that had twice the risk of developing Alzheimer’s and their relative risk of developing any form of dementia was 70% greater than normal.

We may now be looking at the possibility of being able to use a simple blood test as part of the risk analysis for determining future dementia or Alzheimer’s risk in middle aged women.

And a simple remedy using folate, vitamin B6 and B12 to reduce the levels of homocysteine.