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food for the brain

Championing optimum nutrition for the mind


Food for the Brain and the Brain Bio Centre clinic

                        

At Food for the Brain we wish to raise awareness of the importance of optimum nutrition in mental health. We are a charitable foundation working to inform organisations and empower individuals to change their diet and lifestyle and take greater control of their own mental health. Find out more about the charity and the work we do

 

Alongside the charity, our not-for-profit clinic, the Brain Bio Centre, helps individuals by utilising nutrition, diet and lifestyle recommendations to assist mental health conditions. Read more about the clinic and hear from our team of specialists.

 

 

Latest News...

Learning the Language of your Genes - Preventing Alzheimer's with Nutrition

It is now well-known that what we eat affects our health in many ways. But did you know that your diet and lifestyle has the ability to influence your genes? This relatively new field of research called Nutrigenomics explores how nutrition can influence our gene expression by merging together the science of genomics, molecular biology, bioinformatics, epidemiology and nutrition. It is essentially a branch of research under the umbrella of Epigenetics, which is the study of how trait variations in our genes are caused by external factors such as diet and lifestyle (1).

Scientists have only just begun to touch the tip of the iceberg of what we know about how nutrients and how our lifestyle can affect the expression of our genes. Genetically we are all very similar, however, our genetic blueprint holds a range of variations that can predispose us to certain health conditions, such as Diabetes Type 2 or Atherosclerosis (2). The way in which we live our lives and what we eat can switch certain genes on or off, thereby affecting what health conditions or diseases we become predisposed to.

This concept is revolutionary, and above all empowering as we are beginning to realise that we aren't necessarily doomed by the genes we have. For example, if your mother or father have suffered with Dementia it doesn't necessarily mean that you too will at some point suffer with the same condition. You are ultimately in control of your own health and can increase your chances of living a long, happy and healthy life by avoiding certain foods and choosing healthy lifestyle habits.

Mark Adam Hyman, an American physician, scholar and New York Times best-selling author, wrote in one of his many books, “The new science of nutrigenomics teaches us what specific foods tell your genes. What you eat directly determines the genetic messages your body receives. These messages, in turn, control all the molecules that constitute your metabolism: the molecules that tell your body to burn calories or store them. If you can learn the language of your genes and control the messages and instructions they give your body and your metabolism, you can radically alter how food interacts with your body, lose weight, and optimize your health”(3).

With that in mind, how can we apply the same principle to avoiding a condition like Alzheimer’s? Scientists have discovered a group of genes that have the potential to affect, to varying degrees, the chances of developing late onset Alzheimer’s. One of these genes which has been identified as having a significant influence on this disease is called apolipoprotein E (APOE). This gene is found on chromosome 19 and comes in different forms, each representing varying risks. For example, around a quarter of the general population inherits one copy of the APOE ε4 gene, which increases their risk of developing Alzheimer’s by up to four times. Research to identify other genes related to this condition continues to unfold more information that was previously not understood (4).

In 2011, four of the largest AD research consortia - the Alzheimer’s Disease Genetics Consortium (ADGC), the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE), the European Alzheimer Disease Initiative (EADI), and the Genetic and Environmental Research in Alzheimer Disease (GERAD) consortium came together to form the International Genomics of Alzheimer’s Project. It is the largest study of the genetics of Alzheimer’s to date with the aim of discovering and mapping the genes that contribute to Alzheimer’s disease. So far, none of the new genes discovered have an effect as big as that of APOE ε4, with most of them influencing the risk of Alzheimer's disease by just a few percent (5).

It is of course understandable for someone who has a relative that suffers with Alzheimer’s to worry whether they too will at some point develop the disease. The evidence does show that people with close relatives diagnosed with the disease are at double the risk of developing it themselves. However, this does not mean that they will inevitably go on to acquire Alzheimer’s later on in life. Having a good, well-balanced diet as well as adopting healthy lifestyle habits can reduce the risk significantly of developing of this disease. For many, over 60’s especially, it is worth taking a homocysteine test as a build up of levels of this amino acid in our blood has been linked to Alzheimer's Disease as well as other chronic conditions. For more information on how you can lower your levels of homocysteine such as by increasing on your intake of B vitamins, follow this link to our webpage.

Our own Cognitive Function Test is a valuable tool for individuals to assess their own cognitive function against others of a similar age and provides a personalised nutrition and lifestyle report, identifying areas, such as low levels of B vitamins or low levels of Omega 3 fats that can increase someone’s risk of cognitive decline. The test aims to empower people who may be concerned about cognitive decline, either putting their mind at rest, or helping them to feel more informed about their circumstances, and in both cases providing them with some positive steps they can take through nutrition and lifestyle to support better cognitive function going forward. To test yourself follow the link here and see what dietary and lifestyle changes you can be making to optimise your cognitive function.

2nd February 2016

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Alzheimer's - drugs or vitamins?

At Food for the Brain we are not against medication and we hope to see a successful drug discovered for health conditions, such as dementia, just like anybody else. It saddens us however to regularly see one-sided news reporting. In terms of disease modifying treatments for dementia/Alzheimer’s Disease, almost all new drug discoveries are hyped-up to be much more effective actually then they in reality are. On the other hand, a number of much more significant studies on the effects of some dietary modification or certain specific supplements on dementia/Alzheimer’s are simply ignored or mis-reported in the mainstream media. The growing emotional and financial cost of dementia (including Alzheimer’s) is so high that we cannot afford to choose sides – there is only one side and that is evidence.

In this case it is the confusing messages sent by the Alzheimer’s Research UK (ARUK). For instance a paper published in 2012 reported that B vitamins given to those with pre-dementia (mild cognitive impairment) dramatically reduces shrinkage of the Alzheimer’s brain areas and reduces further memory loss – so therefore B vitamins represent a disease modifying treatment. This study was part-funded by ARUK, however, last week we are told by ARUK’s Eric Kerran that a new drug, solanezumab is the ‘first disease modifying treatment’! (as reported on www.bbc.co.uk).

If we were to compare B vitamins with solanezumab (designed to clear out amyloid protein from the brain that can build up and contribute to dementia) the effect of solanezumab is very small in comparison to that reported with B vitamins, which mostly work through its effect on lowering homocysteine levels.

In this new drug solanezumab there’s no change in rate of brain shrinkage, which is critical if the drug is going to modify the disease process - not just marginally slow it down. There are also only very minor improvements in memory. Nevertheless, the press coverage reported a different story, “First treatment to slow Alzheimer’s disease unveiled in landmark breakthrough,” in the Telegraph and Newsweek’s title was “New drug shows promise for early-stage Alzheimer’s”, “Hugely significant…first drug actually slowing down the course of the disease …verge of a radical breakthrough.” commented another ARUK spokesman (for the full story: Policy on Alzheimer’s: sure we want a cure, just so long as it’s not cheap click here)

Considering the positive headlines, it surely creates a view that the whole scientific community agrees with the positive media’s stance, however, the press stories were printed even before the study on solanezumab itself was published! Detailed analyses of the complex results of this study by other specialists in the field have since emerged, reporting what actually happened. Margaret McCartney, writing for the British Medical Journal wrote that in one memory test, those on the drug, out of a possible score of 30, scored 1 point higher than those on a placebo. In the other two tests used the difference was also very small. In contrast, there was a virtual cessation of any further memory loss in the B vitamin study over 2 years.

Also, on a very important measure - the Clinical Dementia Rating (CDR), there was no change between Solanezumab and the placebo, which is bad news because it means no-one, actually got better. To give another comparison, the difference between the placebo group (28%) and the B vitamin group (58%) reverting to zero on the CRD was 30%. In other words B vitamin treatment doubled the proportion of people reverting to zero on the CDR according to Dr Celeste de Jager. In the drug study there is no difference between drug and placebo.

The best memory test results for the drug, the MMSE and ADAS-Cog tests, showed a 34% slowing down of decline in scores compared to those on placebo over 18 months. In the B vitamin trial, those starting with high homocysteine had a complete prevention of any further decline in episodic memory and in semantic memory over 2 years.

But perhaps the biggest difference was between the rates of brain shrinkage. Solanezumab treatments resulted in a non-significant 2% reduced rate of brain shrinkage compared to the placebo. In contrast, in the B vitamin study there was an average 30% reduction in the rate of brain shrinkage, which went up to 53% in those with raised homocysteine and 73% in those starting with good omega-3 levels that were supplemented B vitamins, compared to placebo.

Beyond the particular outcome of the solanezumab study, more and more research is indicating that amyloid plaques are not in-fact a cause in Dementia but an effect (leading to more damage).

The brain produces more amyloid protein as a response to a number of neurological conditions. This may be the results of (at least in part) poor methylation (homocysteine levels reflect poor methylation and B vitamins can effectively reduce homocysteine). The solanezumab drug reduces amyloid protein, but if fails to address the cause. A recent study conducted at the University of California has shown that omega-3 supplementation also helps the body get rid of amyloid protein and probably even more effectively together with vitamin D. So omega-3 (and possible more effective with vitamin D) can possibly do what the drug does but without the side-effects, and B vitamins help to reduce the formation of amyloid protein to start off with. Looking at it from this point of view, we already cover three disease modifiable factors, B vitamins, vitamin D and omega-3, albeit there are likely only effective in individuals with low levels.

Considering all this, and that omega-3 and B vitamins to reduce homocysteine levels have with minor-no side effects and solanezumab (a monoclonal antibody drugs which has to be given by injection every few weeks) is associated with haemorrhage (which occurred in a small percentage of people on this study), we find it odd that news, even from respected organisations such as ARUK, can be so unbalanced in favour of drugs. Again we are not against medication but the growing emotional and financial cost of dementias is so high that we cannot afford to choose one over the other, and neither should we have to. In an ideal world solanezumab would have been tested also in conjunction with omega-3, B vitamins, and vitamin D to learn what the best possible outcome is.

One option for now is to try Food for the Brain’s validated free online Cognitive Function Test (only takes around 15 minutes) which also works out your preventable risk factors and gives you a personalised report of key changes to reduce your risk of dementia.

11th August 2015

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'B12 memory study is bad science' written by Patrick Holford

A study published last week, which was rejected by the British Medical Journal, claims that vitamin B12 supplements don’t work for preventing memory decline. One of the authors of the study, published in the American Journal of Clinical Nutrition, is Robert Clarke, who has already published a number of previous papers on the same topic. All of them have concluded that B vitamins are ineffective for dementia prevention, and all have been criticised for bad science and for making the same classic errors.

This study involved 191 people with no memory problems or concerns about cognitive problems. They were described by the authors as being relatively healthy and highly functioning, but with low blood B12 levels. Half the group were given placebos and half were given B vitamins. There was no change in their cognitive function after a year. Neurological tests also showed no change. That’s the gist of it.

So, if the memory of those in the placebo group, who started with good cognitive function, didn’t get any worse why would anyone expect those in the B12 group to respond any differently? If the study had been long enough for the memory of some of those in the placebo group to get worse then the trial might have shown if B12 could help prevent it. But with no change in the placebo group, you know the study is either too short, has the wrong people (eg. without memory issues), using too low a dose or that the memory tests are not sufficiently sensitive.

But there is more that is seriously flawed in this research. The researchers tell us the starting (baseline) homocysteine levels and cognitive function scores of the participants. So it seems to me it would have bI know that reviewers have asked for these calculations to be included in Clarke’s previous studies but, once again, these essential sub-group analyses have not been done. I did contact the lead author, Dr Alan Dangour, to ask why not. He informed me that they were prohibited from doing so, under the ‘Consort’ guidelines (which stands for the ‘Consolidated Standards for Reporting Trials’, giving researchers a set of guidelines for conducting good quality research) given that they had not pre-specified these analyses when they originally designed the trial. The Consort guidelines, however, do allow for relevant post hoc sub-group analyses to be done, since they are so central to the issue being researched I do not understand why they have not been done. The authors say they ‘have clear plans for the conduct and publication of such analyses’ but do not say what they are.

The net result is that the paper is meaningless. It simply shows that supplementing extra B12, if your memory is good, won’t make it better. It’s like finding no benefit from giving insulin to healthy people and concluding it wouldn’t benefit diabetics. Yet Oxford University sent out a press release ensuring the media will pick it up and run more fallacious “no benefits from B vitamins stories”.  The detailed and expert criticism of the trial’s failings no doubt will be published in due course but will inevitably be ignored and so the myth will be perpetuated.

As a result people with raised homocysteine levels will be put off supplementing B12 when there is good evidence that it can help reduce the rate of brain shrinkage and memory loss in those with memory problems and raised homocysteine levels. What is still not nailed down is whether it can help prevent dementia in those without memory problems. This study contributes no useful information at all to that question since it was far too short and no-one in the placebo group was anywhere near the diagnosis of pre-dementia.

It has been funded by the UK government. Why are we taxpayers paying for research that is clearly a total waste of money when there is a desperate need for funding for good quality prevention research?

If you would like to see a summary of evidence for B12 and lowering homocysteine in the context of dementia prevention see www.foodforthebrain.org/hcyevidence.een sensible and useful to have reported on any difference between those starting with high homocysteine versus low homocysteine, or in those starting with worse cognitive function scores.

6th July 2015

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The effects of dietary supplementation on nutrient status in children with Autism Spectrum Disorder

A recently published article assessing the effects of dietary supplementation on nutrient status in children with Autism Spectrum Disorder (ASD) highlights some important considerations when supplementing with a multivitamin and mineral (MVM) supplement. One of the conclusions of the study was that even when a child takes a MVM some deficiencies were not corrected, such as calcium and vitamin D, whilst other vitamins and minerals may lead to levels above the Upper Limit, such as folate, copper and vitamin A. This was particularly true when a child is on a gluten-free and casein-free (GFCF) diet, owing to the fact that these children are more likely to take a MVM.

Some of the recommendations of the study (http://www.andjrnl.org/article/S2212-2672(15)00390-1/abstract), primarily aimed at dieticians and nutritionists, were that multivitamins should not be universally prescribed in children with restricted eating patterns, and that Vitamin D and calcium levels are often low even with a MVM. The author of the study commented that it is important for children with ASD to receive individual assessment for “potential nutritional deficiencies or excess and that when supplements are used careful attention should be given."

Although this research has led to some valuable conclusions and considerations there were a number of other points the authors did not mention.

Due to the common occurrence of limitations in the variety of foods a child with ASD may eat, deficiencies as well as possible excesses in selective nutrients (especially if the preferred food is high in a particular nutrient or artificially fortified) may arise. Research has previously shown that some synthetic nutrients in fortified foods (and some supplement brands) are not so well assimilated and processed by the human body, therefore, possibly acting as a burden rather than a help to address deficiencies.

When choosing a supplement we would recommend visiting your local health food shop for advice rather than using supermarket own brands - often these can have unsubstantial levels of the particular nutrient and use synthetic ingredients rather than natural ones.

At the Brain Bio Centre we can assess every client for their specific nutritional needs and create a supplement and/or nutrition programme supporting any deficiencies and imbalances. For more information on this please visit www.brainbiocentre.com or call 020 8322 9600.The effects of dietary supplementation on nutrient status in children with Autism Spectrum Disorder

18th June 2015

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