Blame my genetics

I must say, for as hard as I work out I'm always sorely tempted to over eat.  There are so many savory, delicious places to eat in Austin that I'm only beginning to discover.  Gourdough's elaborate donuts covered in all sorts of things (brownies, bacon, gummy worms and more!)  But while I can get myself to salivate over these fabulous treats, I know I can make myself sick from eating too much.  But not everyone can sense that line of where to stop and it's in part due to their genetics.

An example of Gourdough's extravagant donuts.

And while  know the idea that genetics controls your overall body type and weight, I never understood the specifics until now.  Gordon Kennedy was the first to describe the "lipostatic hypothesis" which states brain receives signals about the fat storage of the body and tries to keep it in equilibrium with either feeding behavior or lack of eating.

But sometimes the brain can't receive this signal.  Certain genetic variations lack a specific piece of code that produces a protein.  This protein, now known as leptin, sends the message to the brain that you're full and to stop eating behavior.  But if you lack the genetic code to produce leptin, you're brain thinks you are in a constant state of starvation.  Not only do you feel constantly hungry, your metabolism slows down (as if you are trying to hang on to those last bit of energy producing fat).

Now I'm not here to say that this explains the obesity epidemic in America.   A complete genetic knockout of leptin is fairly rare and can be treated with hormonal replacement therapy.  And of course there are numerous other processes, both in the brain and the gut, that regulate body shape.  But I find it fascinating that we don't have as much control over our appetite.

With all the current hype on the
movie, I couldn't help including
one of my favorite books.

And a special shout out to my friends cutting weight for Taekwondo National Collegiate Competition.  You might be fighting your genetic homeostasis but those few pounds lost will make all the difference in the ring!  Not to mention, we'll be sure to indulge in some of the best food Austin has to offer to bring those leptin levels back up.

Bicycles and the Basal Ganglia

When I first understood that the basal ganglia is necessary for creating procedural memories, I immediately thought of learning to ride a bike.  Nothing could be more iconic of a learned behavior in humans than those first few tentative pedal pushes as you learn to navigate the two-wheeled beast.  Personally, I'm an avid cyclist both as a commuter and for simple pleasure.  I ride my bikes every single day, yet if you asked me I would be unable to explain all the minutiae of adjustments my body makes to keep me in the seat.

One of my friends plans a monthly ride to explore the city and hit up
some of the coolest bars of Austin.

The ability to ride a bicycle, along with many other habitual actions, rely on the processing of the basal ganglia.  This collection of nuclei are vital for what I consider "physical memory."  The basal ganglia receives general input from the cortex, processes it, and then sends it through the ventral lateral nucleus of the thalamus and on to the frontal cortex.  The frontal cortex is then responsible for issuing a command via the motor cortex for the body to actually do something.  This integration with the motor circuit explains why procedural memory is affected when the basal ganglia is damaged and not declarative memories.

The type of damage that the basal ganglia can receive changes how the afflicted person or animal will act.  Two classic diseases- Parkinson's and Huntington's- have symptoms at opposite ends but due to damage in the same structure.  While it's true that each lose function in a slightly different pathway, it would be a little ambitious of me to try to explain the circuitry with only words.

Let's just leave it with the understanding that the diseases cause damage in slightly different ways.   With Parkinson's, the damage leads to a slowing or even lack of movement.  These are called, respectively, bradykinesia and akinesia.  And at the other end of the spectrum is Huntington's where patients experience hyperkinesia.  It's as if they can't stop themselves from making too much movement.

This figure helps identify some of the structures
within the basal ganglia.

In these two diseases, the ability to moderate inhibition or disinhibition seems to be lost.  So there's either a surplus of movement or a dearth of it.  Research into how the damage occurs and ways to prevent it continue.  But I'm happy to say I have a well-functioning basal ganglia and I can continue to ride my bike to my hearts content!