Archive for May, 2013

Here is a link to my latest article on the Paleo Solution Blog.  It covers how too much exercise can derail health goals.  http://robbwolf.com/2013/05/29/exercise-addiction/

A big piece of starting any nutritional or exercise program is developing a new routine.  What many may not know is the deck of cards is stacked against most of us in this situation.  We actually have habit forming circuits built into our brains.  This is critical for our survival.  For one, it allows us to breathe, blink, and function without having to literally think about it.  It is also set up to get us to do tasks relevant to our survival.

Our habit circuits are set up like such; there is a trigger, followed by an action, and lastly there is a reward.  For example, when eating.  The feeling of hunger is a trigger for us to act.  When we are hungry we seek out food and when we eat our brains flood our system with the feel good neurotransmitters.  The more we take part in this cycle the more it becomes habit.

In that previous example we developed a habit of eating when we are hungry.  How do you feel when you can’t get food when you are hungry?  When that typical routine is broken we get adverse effects such as decreased mood.  The other problem lies in the reward piece.

Highly rewarding foods are readily available everytime we get hungry.  I wrote extensively about this here, http://robbwolf.com/2012/02/15/carb-addiction-cake-is-the-new-crack/ , and http://robbwolf.com/2012/02/29/might-as-well-face-it-youre-addicted-to-food/ .  We eat a food that is highly rewarding and we are going to seek it out more often.  Willpower is a muscle and can be exercised just like any other, but it also gets fatigued like others as well.  At some point you will give into the reward.  Our systems were built like this for survival.

To take that same example from before, when we get hungry we look to eat.  Now instead of the processed sugars and fats we are used to we are eating meat and veggies.  The reward is not quite the same.  This can leave us feeling empty inside, like we weren’t hugged as kids.  Willpower may last for a day, a week, or longer, but at some point everyone falls off the wagon, even me.

How do we fix this problem?  If I had a definite answer I would be a millionaire, but Kenneth Blum and colleagues have done extensive work on neurotransmitter deficiencies and addiction.  The Reward Deficiency Syndrome states that whatever substance we ingest that balances us out biochemically we will become addicted too.

If we have dopamine deficiciencies from lack of sleep, poor diet, and so on, and then we eat a high sugar food such as a bagel and we get that dopamine rush we will be hooked.  This can explain why we all have different food addictions.  Just like with any other addiction, when we get that rush and feel good we are going to want it more and more.  A meal of meats and veggies not giving us that rush is going to leave us wanting that bagel more and more as time passes.  So what can we do?

Here are my suggestions.  We need to identify the triggers that lead us astray.  If it is hunger then we need to make sure we are eating enough at meals and balance out those hormones responsible for that response.  Some people like to eat candy while watching a movie.  They need to identify that as a trigger and maybe have some berries around for those instances.  There are an infinite number of triggers and solutions and that is all individualized.

From there we need to attack that circuit from the reward end.  Being tested and treated for neurotransmitter deficiencies can help balance out our biochemistry and take away that “want” for the addictive food.  Also, those neurotransmitters are largely responsible for our energy and mood and help mitigate stress.  This can lead to better sleep at night and more energy in the morning.  Lastly, neurotransmitters are implicated in just about every disease so they are critical to long term health!

http://robbwolf.com/2013/05/02/glutathione-synthesis-diet/

Remember that Huntington’s Disease is a genetic, degenerative disorder that leads to an increased expansion of the polyglutamine tract called the CAG repeat.  Along with this CAG repeat disorder, people with HD experience excitotoxicity.  In this article I am going to discuss the role that GABA and glutamate play in this part.

Glutamate is our major excitatory neurotransmitter.  It is the chemical messanger that tells us to GO.  GABA is its anithesis as it is our major inhibitory neurotransmitter.  When we release glutamate and all signals are go, GABA then becomes released to calm everything back down and bring us back to homeostasis.  GABA and glutamate activate ionotrophic and metabotropic receptors.

Metapotropic receptors are also known as G-Protein Coupled receptors.  These receptors are the most abundant receptors found in the central nervous system.  In fact, drug companies are looking at drugs that interact with these receptors to aid in the treatment of HD (http://www.ncbi.nlm.nih.gov/pubmed/20708032).

Chorea is one of the early symptoms associated with HD.  This is the involuntary movements that the patients suffer from.  The hypothesis is that decreased GABA leads to the chorea seen in HD (http://www.ncbi.nlm.nih.gov/pubmed/2144428).  Some studies also show an excess of dopamine in the basal ganglia, the area of the brain affected in HD (http://www.merckmanuals.com/home/brain_spinal_cord_and_nerve_disorders/movement_disorders/chorea_athetosis_and_hemiballismus.html).  GABA is needed for inhibition of dopamine.  Also, glutamate and dopamine need to be in balance for proper function.

Studies have found there to be an increase in both dopamine and glutamate in the symptoms of HD and that perhaps balancing them out would have a therapeutic benefit (http://www.ncbi.nlm.nih.gov/pubmed/20406248).  Inhibition of glutamate has been found in autopsies of HD patients.  This would lead to increased receptor sensitivity to glutamate and it directly correlates with CAG expansion size (http://www.ncbi.nlm.nih.gov/pubmed/20406248).  The CAG expansion is a polyglutamine tract.  Perhaps the increased sensitivity in the receptors is leading to an increase in CAG repeats? 

When cells exhibit too much excitotoxicity the mitochondria of the cell will send a message to destroy the cell.  This may be the cause of neurodegeneration seen in HD.  Some theories state that mitochondrial dysfunction is at the center of cell death in HD.  There may be normal amounts of glutamate present, but the mitochondria reads it inappropriately and sends the message to destroy the cell (http://www.acnp.org/g4/gn401000151/ch.html).

The take away from this is we need to address the balance of neurotransmitters to offset the symptoms associated with HD.  A balance of dopamine, glutamate, and GABA are essential to neuroprotection.  Also, a diet that is high in nutrients such as N-acetyl-cysteine, coenzyme Q10, B vitamins, magnesium, and others is essential to maintaining mitochondrial health.