Are you addicted to fast food?

Do you crave that next slice of pizza or double beef burger with bacon?
Is your mouth watering at the thought of chicken and chips?

We know that eating too much fat, especially the bad fats such as trans fats and excess cholesterol, is bad for our hearts and our health.
Too much fat in the form of cholesterol is also really bad for our brain.

But surely when it comes to food choices it just boils down to personal taste, convenience, and availability doesn’t it?

Maybe not.

It turns out that many of us have a “fatty” or “salt” tooth rather than a “sweet” one.

Eating a high fat diet over a period of time has been shown to induce irreversible changes in rat studies in relation to the “pleasure centres” of the brain.

These are the same reward or pleasure centres as activated by heroin and cocaine.

So yes, it seems that we can indeed become addicted to fatty foods.

Back to those rats and their high fat diet. Over a six month period, the genes associated with reward were found to be altered, leading to the animals then craving those particular types of food when no longer available.

Which means that if you are trying to lose weight, but have previously being eating a diet high in fat, it is going to be much harder to say “no” to that temptation, next time it is wafted in front of your nose.

This could be why some people find it so hard when trying to lose weight to adhere to healthier eating in the longer term.

Our brain makes its own cholesterol that it uses to form synapses and brain cell membranes. But if our diet incorporates a high level of excess fat over a period of time, this leads to brain damage.

Rats fed excess fat in their diets over a 5 month period produced changes in their brains resembling Alzheimer’s pathology, with the formation of amyloid plaques and neurofibrillary tangles. They also showed evidence of memory impairment, loss of neurons, micro bleeds into the brain and inflammation.

Alzheimer’s is a complex neurological condition, and while cholesterol on its own is not responsible for causing it, it is certainly a contributing factor.

A second study gave rats a high fat, low Omega-3 diet. Omega-3s are essential fatty acids that we have to obtain from our food, as our body does not produce them. They are found in fish, meat, eggs and walnuts. Omega 3s are essential for normal brain function as they form part of the cell membrane around each neuron and help to maintain a healthy brain and normal cognition.

This combination diet led to brains developing x8.7 the amount of amyloid and x1.5 the amount of tau protein build up compared to controls.

So if you have that fat addiction, how can you resist that slice of oh-so-gooey and delicious looking chocolate mud cake?
And how about those piping hot chips sprinkled with salt?
Perhaps understanding that it is an addiction will help those affected to try and tackle the issue differently.

Following on from this research my question now is: what effect is this chronic high fat diet having on our kids’ brains?

Are we setting our children up for a lifetime of difficulty in weight control and contributing to their risk of developing cognitive problems or neurodegenerative disease in the future?

What are your thoughts?

Refs:
Society for Neuroscience (2011, January 19). Long-term, high-fat diet alters mice brains: Brain changes may contribute to cycles of weight gain. ScienceDaily. Retrieved January 20, 2011, from http://www.sciencedaily.com¬ /releases/2010/11/101115112727.htm

Université Laval (2008, October 31). High-fat Diet Could Promote Development Of Alzheimer’s Disease. ScienceDaily. Retrieved January 20, 2011, from http://www.sciencedaily.com¬ /releases/2008/10/081028103107.htm

Celine Ullrich, Michael Pirchl, Christian Humpel. Hypercholesterolemia in rats impairs the cholinergic system and leads to memory deficits. Molecular and Cellular Neuroscience, 2010; 45 (4): 408 DOI: 10.1016/j.mcn.2010.08.001

One of the key findings in Alzheimer’s disease is a loss of synaptic connections.
The synapse is the place where brain cells communicate with each other via their dendritic branches. The cells do not actually touch but are separated by a space called the synaptic cleft. It is across this space that brain chemicals or neurotransmitters cross to stimulate the adjoining brain cells and trigger further electrical messages to be passed along forming neural circuits or pathways.

Without synapses brain cells are unable to communicate to each other.

Sorry, I’m going to get a bit technical here, but it’s important to help understand the article.
Sets of particular proteins that bind together to form a molecular hub called the postsynaptic density or PSD occur at the synapse, in the terminals of the dendrites. Animal studies had previously shown that the PSD plays an important role in brain disease and behaviour. However until now, little has been known about the human PSD.

Researchers from the Welcome Trust Sanger Institute and Edinburgh University have used a technique called proteomics to extract PSD’s from the synapses of patients undergoing brain surgery. Their findings are quite remarkable.

They have discovered a total of 1461 proteins, each encoded by a different gene in these human synapses.
This then allowed them to systematically identify those diseases that affect the human synapse.

Professor Grant who led the research team revealed that over 130 brain diseases involve the PSD including Alzheimer’s, Parkinson’s, some forms of autism and learning disability.

Professor Noebels, Professor of Neurology, Neuroscience and Human Genetics at Baylor College of medicine said that of the 1461 proteins identified, “every seventh protein is involved in a known clinical disorder and half of them are repeat offenders. Researchers will now have a strategic starting point to start to unravel the complexity of brain disorders”

The research group has also created a first molecular network to show just how many of the proteins and diseases are interconnected.

As a sign of tremendous collaboration and desire to accelerate further discovery and use of this data, the scientists have released all of their findings into a public domain at their website G2Cdb
No wikileaks required here. It’s all there to be shared.

They suggest that the proteome of the PSD will help us to gain further understanding of the brain in the same way that the genome assisted our understanding of DNA.

Other fascinating findings Include:

• That the proteins in PSD are important for certain cognitive behaviours such as learning, memory, emotion and mood

• And also for social behaviours, addiction and drug abuse.

Looking at how the PSD has evolved over time and contrary to expectations, the researchers discovered that the PSD has been resistant to change over the millennia.
This means that synapses of rodents are not that dissimilar from humans, making further research using rat and mice models very suitable for studying human brain disease. Looks like we have more in common with our rodent friends than previously recognised.

These findings provide further valuable clues adding to our understanding of the brain and how some brain diseases may develop.

Àlex Bayés, Louie N van de Lagemaat, Mark O Collins, Mike D R Croning, Ian R Whittle, Jyoti S Choudhary, Seth G N Grant. Characterisation of the proteome, diseases and evolution of the human postsynaptic density. Nature Neuroscience, December 19, 2010 DOI: 10.1038/nn.2719

Diabetes is a recognised risk factor for dementia.
It is also associated with a higher risk of depression and eating disorders.
What has now been found is that diabetes affects how much cholesterol our brain can make.

That’s right, our brain makes it’s own cholesterol that it uses to form synapses (the connections between brain cells). It is also used to form the vesicles or storage structures located at the synapse that contain the neurotransmitters, the brain’s chemicals that are passed from one brain cell to the next. We have a “fat” head and it is essential the brain can produce sufficient cholesterol for healthy brain function. Having too little cholesterol in the brain is associated with Alzheimer’s disease and other neurodegenerative conditions.

Studies using mice with type 1 (insulin deficient) diabetes looked at gene expression in an area of the brain called the hypothalamus. It was found that in these mice, gene expression for the synthesis of cholesterol was reduced. Treating them using insulin reversed the problem.
They also found that those mice with unable to synthesise brain cholesterol gained more weight and ate more, indicating that diabetes may affect those brain hormones associated with appetite regulation.

This finding adds to our understanding of the relationship between diabetes, cholesterol and healthy brain function. If you have diabetes, having tight glycaemic (sugar) control and maintaining a healthy weight are essential to help your overall brain health and to protect against future cognitive decline.

Ryo Suzuki, Kevin Lee, Enxuan Jing, Sudha B. Biddinger, Jeffrey G. McDonald, Thomas J. Montine, Suzanne Craft, C. Ronald Kahn. Diabetes and Insulin in Regulation of Brain Cholesterol Metabolism. Cell Metabolism, Volume 12, Issue 6, 567-579, 1 December 2010 DOI: 10.1016/j.cmet.2010.11.006

A study has just been published in JAMA which found that giving supplements of Omega-3 (DHA) to people with mild to moderate Alzheimer’s disease did not produce any reduction in the rate of cognitive decline, indicating that supplementation in this group would not be warranted.
In this study a group of 402 people with either mild to moderate Alzheimer’s disease, 60% of the group received supplementation of 2 gm of DHA, the other 40% received placebo over an 18-month period. They underwent cognitive testing using the Alzheimer’s Disease Assessment Scale and Clinical Dementia Rating. A sub sample of 102 subjects also underwent functional MRI scanning to look for the rate of cortical atrophy.
The study found no benefit of the supplementation on the ADAS-Cog score or rate of brain atrophy during the time of the trial.
Many people currently take Omega-three’s as a supplement, commonly as fish oil capsules and include fish in their diet on the basis of other studies, which have suggested that this is a way to reduce one’s personal risk of developing dementia or Alzheimer’s disease .
So should we stop doing this?

Absolutely not. The difference here in this study is that they were looking at people who had been already diagnosed with Alzheimer’s.

An earlier study in 2006 at the respected Karolinska Institute had previously looked to see if DHA and EPA (Omega-3) supplements given to a group of people with either diagnosed Alzheimer’s disease or a small sub-group with very early cognitive impairment would be useful as a means of slowing the progression of the disease. This study also found no benefit of supplementation in those already diagnosed with Alzheimer’s.
However those who only had mild cognitive impairment did show some benefit. They had less cognitive decline on mental testing than a control group over a 6-month period, and when the control group received the supplements over a second 6-month period their rate of decline decreased as well. Here the authors proposed that is may be because the omega-3 fatty acids exert an anti–inflammatory effect. Inflammation is believed to be part of the neuropathological development of Alzheimer’s. The comment then was perhaps the anti-inflammatory effect of the Omega-3’s could only be of use prior to too much neuropathological change being evident.
The 2006 study only included a very small number of subjects (32 people) Larger studies with bigger cohorts of those with mild cognitive impairment as well as those at risk of Alzheimer’s are needed to see if Omega 3-s may be of benefit in halting the earlier progression of the disease.
The conclusion from the latest study supports the literature that supplementation with DHA is not beneficial in established mild to moderate Alzheimer’s.

Meanwhile there is plenty of evidence to support continuing to enjoy eating fish and taking Omega-3 supplements as a means of reducing our relative risk of developing cognitive decline and dementia.

Bon appetit!

Journal References:
1. K. Yaffe. Treatment of Alzheimer Disease and Prognosis of Dementia: Time to Translate Research to Results. JAMA: The Journal of the American Medical Association, 2010; 304 (17): 1952 DOI: 10.1001/jama.2010.1625
2. J. F. Quinn, R. Raman, R. G. Thomas, K. Yurko-Mauro, E. B. Nelson, C. Van Dyck, J. E. Galvin, J. Emond, C. R. Jack, M. Weiner, L. Shinto, P. S. Aisen. Docosahexaenoic Acid Supplementation and Cognitive Decline in Alzheimer Disease: A Randomized Trial. JAMA: The Journal of the American Medical Association, 2010; 304 (17): 1903 DOI: 10.1001/jama.2010.1510
3. JAMA and Archives Journals (2006, October 11). Omega-3 Fatty Acids May Slow Cognitive Decline In Some Patients With Very Mild Alzheimer’s Disease. ScienceDaily. Retrieved November 4, 2010, from http://www.sciencedaily.com¬ /releases/2006/10/061010022736.htm

Are we getting more intelligent?

That’s a question I’m sure we would all like to assume to be answered with a “Yes”. However is there any proof of this?

Well it turns out that in Sweden there has been an ongoing study doing intelligence tests on 70 year olds and the findings do actually show that, yes the 70 year olds of today do perform better in these tests than their predecessors of thirty years ago.

And there are probably a number of contributing factors such as
• Improved pre and neonatal care
• Improved nutrition
• Better quality of education
• Better treatment of hypertension and other vascular diseases
• Higher intellectual requirements of today’s society with access to advanced technology, the Internet and television.

But that wasn’t the main reason for conducting this study.
What the researchers were looking for was to see if they could find a better way to predict who is most likely to develop dementia and whether the early symptoms have changed over recent generations.

One thing that the study did reveal too is that the incidence of dementia has remained unchanged over this period of 30 years.
People aged 70 to 75 today have the same incidence of dementia as those of that age group 30 years ago. This is important because with the expected explosion of people likely to be diagnosed with Alzheimer’s disease over the next forty years, it would be possible to assume that Alzheimer’s is becoming more common. The increase is actually simply a reflection of the larger proportion of people in our society reaching that age.

In this study of over 2000 people the only predictor of dementia was found to be those with memory problems. But not all of those with memory problems went on to develop dementia.

The researchers were looking to identify those at risk of developing dementia and while they found pointers for a group born in 1901-1902 the same tests did not reveal any clues for the generation born in 1930. It is hoped that finding earlier signs of dementia will enable people more at risk to get diagnosed earlier and receive support more quickly.

S. Sacuiu, D. Gustafson, M. Sjogren, X. Guo, S. Ostling, B. Johansson, I. Skoog. Secular changes in cognitive predictors of dementia and mortality in 70-year-olds. Neurology, 2010; 75 (9): 779 DOI: 10.1212/WNL.0b013e3181f0737c