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Science, Lies and B vitamins

‘Wouldn’t it be nice if people could pop a pill to prevent dementia? If ever it comes to pass, that pill won’t contain B vitamins’ declared the Alzheimer’s Forum, a website for pharmaceutical researchers. ‘Taking B vitamins does not seem to cut the risk of developing dementia’ said the BBC last month. Meanwhile, the Alzheimer’s Society launch their prevention plan – but, extraordinarily B vitamins and homocysteine are not even mentioned. Has something happened to questions the advice to take B vitamin supplements? The answer is yes and no.

Last month, to quote the BBC, ‘scientists led by Lisette de Groot, Wageningen University, the Netherlands, found that a supplement containing vitamin B12 and folic acid did not improve cognitive performance in nearly 3,000 volunteers predicted to get a boost from the supplements.’ This comes on the heels of another study two months ago, by Robert Clarke and colleagues discussed later.

What actually happened? The study by Dr Nikita Kwaluw, published in Neurology, gave B12 (500mcg) and folic acid (400mcg) or placebos to almost three thousand people age 65+ without memory problems, but with high homocysteine levels above 12/mcmol/l, which is a risk factor for developing dementia later in life. On testing two years later those on B vitamins versus placebos had a significant one third slower decline in their memory function as measured by the MiniMentalStateExam (MMSE), but no change in other cognitive tests which were run on a much smaller sub-group of participants.  According to Professor David Smith ‘the study was almost certainly underpowered’, in other words the sub-groups were too small to pick up a significant change in two years.

Other than the MMSE, the other test applied to the whole group was for ‘episodic memory’. There was no significant change overall, but when the authors selected those with low B12 status (they measured this in a blood test called HoloTC) those given B vitamins again had a significantly slower rate of decline.

So why the bad press? Nobody in either group developed dementia so how could the BBC say ‘taking B vitamins does not cut the risk of developing dementia’? Why indeed. Both the study authors and Professor David Smith complained to the BBC about their blatant misrepresentation of the study results. 

Let us wind back to 2010 when Professor Smith’s group started publishing results from their Oxford Project To Investigate Memory and Ageing (OPTIMA) cohort. They found it took eight years for memory healthy older people to develop the first signs of dementia, called MCI (mild cognitive impairment). The MMSE, it should be said, is not a very sensitive test and probably the wrong one to use in these kinds of studies, but it is easy to administer. The maximum score is 30. Most older (65+) people score something like 28. By the time you have a score of 25 you are in the dementia zone. The average decline per year in older people is 0.1 points so you’d need a 10 year study to see a 1 point decline. This is the black line in the graph below.

On the basis of this average one would expect a 0.2 decline in a 2 year study such as the recent Dutch trial. But these were not ‘average’ people – they were selected as being ‘at risk’, although their memories were still intact, by virtue of having high homocysteine. Consequently you’d expect a slightly faster rate of decline, which is what happened. Those in the placebo group declined by 0.3 (from 28.2 to 27.9) in the 2 years – 50% faster than you’d expect on average, but completely consistent with previous research. This is the green line in the graph below. Please note I have taken the liberty of extending the results beyond the 2 years to predict what would happen long-term.


The dotted green line is the B vitamin group and the solid green line the placebo group. The decline in the B vitamin group with high homocysteine is much less than the placebo group, at about the average rate of decline in memory healthy people.

What happened to those on the B vitamins? They declined by 0.1, a significant third less (from 28.1 to 28). Put in another way, from this result you’d expect them to take three times as long to develop mild cognitive impairment, leading to dementia. The accurate BBC headline should have been “B vitamins slow risk of developing dementia by a third’.

In the Oxford study, where people already with memory impairment (MCI) were given B vitamins or placebo, the MMSE scores of those taking the placebo dropped rapidly over 2 years by 1.2 (28.4 to 27.2) while those of the B vitamins dropped by 0.3 points (from 28.2 to 27.9), in other words had one quarter the rate of decline. Again, I’ve extended the results beyond the 2 years to predict what would happen long-term:

The dotted blue line is the B vitamin group and the solid line the placebo group. In MCI the speed of decline becomes faster, while in those given B vitamins it slows down to about the same rate as that of ‘memory normal’ people.

In summary, the B vitamins worked in both studies in slowing the rate of decrease of MMSE memory test scores in those with high homocysteine.

There are other relevant studies, such as that of Jane Durga, published in the Lancet in 2007, who gave people with a homocysteine score above 13 either folic acid or placebo over three years. Those on the folic acid had a 0.48 improvement in their memory while those of the placebo had a 0.35 decline. (This was a different memory test, not MMSE, so we haven’t included in the graph.)

Two months ago we reported on another study, in the American Journal of Clinical Nutrition, on B vitamins that was reported to be ‘proof’ that B vitamins don’t work. The press release declared ‘Taking B vitamins won't prevent Alzheimer's disease’. This wasn’t actually a research trial, but an analysis of the combined results from 11 trials that had given B vitamins versus placebo and measured rate of memory decline in memory healthy people. They had the before and after MMSE scores of over seven thousand people over an average of 2.3 years, and the participant’s homocysteine test results. So how did those starting with high homocysteine do on the B vitamins compared to those on placebo? They don't tell you. Instead, they lumped everyone together, with high or low homocysteine, and looked at the difference between those on B vitamins or placebo (without actually showing you how much each group declined by) and declared that the difference overall was not significant. This is simply bad science and, despite having collected good data, have fudged it to imply no effect. Very fishy.

The finding in any of these studies that B vitamins don’t ‘boost’ memory is hardly surprising. Why would they? What we want is for them the arrest or slow down age-related memory decline. If your homocysteine level is high (above 10mcmol/l) all the evidence to date points in the same direction – that B vitamins do either slightly improve, arrest or slow down the rate of memory decline versus placebos. In other words, taking B vitamins works for those at risk by virtue of having high homocysteine, which is about half the 65+ population. This is why we urge you to test your homocysteine level first, then supplement accordingly.

So why all the negative reporting? Could it be that money makes the wheels go round? The last thing big pharma wants is a non-patentable, non-profitable B vitamin supplement cutting dementia risk. They want a patentable, profitable drug. If there was a drug that could reduce the shrinkage of the Alzheimer’s areas of the brain by almost nine times, and virtually stop any further memory, which is exactly what Professor David Smith’s studies have shown in people with MCI and high homocysteine, they would be shouting this from the rooftops. Instead, it appears that the intention is to kill off the competition – B vitamins.

Rather than funding more studies on B vitamins given the consistently positive findings so far, funding is being axed. We wrote to the Prime Minister David Cameron and Secretary of State at the Department of Health, Norman Lamb, to ask if any of the recently pledged £66 million of tax payers money was being ring-fenced for research on prevention? The answer is ‘no’ unlike Australia who has recently pledged $32.5 million for prevention research. Of the total of £140 million spent to date only 0.11%, totalling £156,000, has been spent on prevention research and that was mainly a study giving HRT to see if it would slow down memory decline on the basis that those at risk might be hormone deficient. It didn’t work.

What about the Alzheimer’s charities? The Alzheimer’s Society have pledged £10 million a year for ten years, but their main focus is on genes and fast-tracking existing drugs (such as anti-depressants and anti-hypertensives) to see if they slow decline. ARUK, the other research funding charity, have no interest in B vitamins. Its drugs and biomedical research all the way.

It is better to light a candle than rage against the darkness, says an old proverb, and in that light, we have designed a rather neat prevention study that has the potential to help thousands of people who take part, namely those doing the Cognitive Function Test - perhaps you. We start this ‘Action on Alzheimer’s’ study next year, subject to funds, but you can read the study details here. It’s a good read for those who really want to know the state of play with prevention. We need £59,700 to do this research (which represents one third of the total spent to date on prevention research by all the government funded health research councils), which equates to only a thousand people giving £50. Perhaps you’d like to be one of them?

Please donate here 


December 2014

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How Collette beat the blues and balanced mood swings


From the age of 15 Collette started to become increasingly anxious, depressed and unable to cope with school. At 18 she was given the diagnosis of bipolar disorder. "The years that followed bought with them many high and low moods. It took very little to stress me out and I would become anxious and overwhelmed easily. I used to get frequent infections and have to take antibiotics all the time. I had to take life one day at a time.”

Collette then came to the Brain Bio Centre clinic for help. Like so many people diagnosed with bipolar Collette had been on a number of medications - antipsychotics, anticonvulsants and an antidepressant – and on top of the symptoms related to the disorder she also had to contend with drug side effects which included an extreme lack of energy and memory problems. Collette's programme at the Brain Bio Centre clinic began with a full psychiatric and nutrition assessment. Following the consultations she was tested for neurotransmitter imbalances and food intolerances.

The test results that followed revealed that Collette had low levels of the neurotransmitters serotonin and noradrenalin and was intolerant to a number of foods, including cow's milk and gluten.She started on a protocol that included dietary advice and a supplement programme. Intolerant foods were removed from her diet and her nutritional therapist recommended reduction of...

Read more here.



November 2014

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Don't panic: you are probably adrenalin dominant

At the Brain Bio Centre we see people with a variety of symptoms including anxiety, panic attacks, ADHD, insomnia, but also often with physical symptoms such as muscle aches, cramps, restless legs, hot flushes, feeling cold and having cold extremities and high blood pressure, all of which are classic symptoms of adrenalin dominance. We often measure our patient's adrenalin levels to find out what is going on.

The body produces adrenalin under two circumstances. Firstly, as a response to an actual stress to enable the 'fight or flight' response. This changes your breathing, making you gasp, to get more oxygen in; it pushes up your blood pressure to get rapid circulation, and triggers protein to be turned into glucose so you don't run out of fuel for the fight or flight.

Secondly, adrenalin is produced as a response to low blood sugar levels. The brain is incredibly dependent on a permanent supply of glucose to function. So, when glucose levels in the blood are getting low it triggers an increase in adrenalin, which enables protein to be turns into glucose.

The trouble is that the pace of 21st century living both gives us non-stop stress signals and the way we eat...

Read more here.

September 2014

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Schizophrenia – is personalised nutrition the way forward?

Most people assume that there is no ‘cure’ for schizophrenia yet evidence for a beneficial role for nutritional therapy has been growing. Today a review of effective nutritional interventions has been published in the Nutrition Journal showing a number of important avenues that should be explored.

According to co-author Lorraine Wilder, whose research was gratefully funded by Food for the Brain, thanks to your donations, "There is a considerable body of evidence of benefit from many nutrients. Schizophrenia is clearly a spectrum disorder, and only by assessing a person's unique biochemical imbalances can they be intelligently addressed with nutritional therapy. Given that a third of people don't respond to anti-psychotic medication, and the drawback of their side-effects, it is time for trials testing a personalised nutrition approach to this condition as an adjunct to conventional therapy."

Her research has identified four main areas:

• Oxidative stress, which is higher in those suffering from schizophrenia, and the role, among others, of N-acetyl cysteine and alpha-lipoic acid
• Essential omega-3 and 6 fats
• B vitamins and methylation
• Immune-mediated and inflammatory factors, including allergies

At the Brain Bio Centre we routinely test for all these possibly contributing factors and treat our patients accordingly. Simona is a case in point.
Biochemical tests at the clinic identified a number of nutritional deficiencies, as well as intolerance to dairy. Acting on this information was a revelation for her and has made a real difference to how she feels, "Taking supplements to address the deficiencies has had a direct impact on my energy levels and reduced the sedative effect of my medication, and using niacin (B3) therapy has helped with the ruminations in the evening". With the support of nutritional therapy she has managed to cut down on her medication, of which was one of her main goals.

Often, the onset of problems occurs in teenage years and at times of increased stress. Rachel was diagnosed with psychosis in her first year at university, and was suffering from the side effects of medication as much as from the symptoms of her illness when she first came to the clinic. However, she observed a significant improvement in symptoms within weeks of following her Brain Bio Centre nutritional therapy programme, which included supplementing vitamin C and essential fats. Her mental clarity and concentration is vastly improved and, according to her doctor, she will be completely off medication soon.
Dr Megan Arrol PhD, co-author of this review, is helping us design and run a clinical audit and research trial comparing the effects of treating schizophrenia with a personalised nutrition approach with conventional treatment alone.

We need to raise a further £18,000 for a clinical audit and £44,000 for a randomized intervention trial. If you would like to help please become a Friend of Food for Brain, or make a one-off donation here.

22nd September 2014

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