Thursday, August 14, 2014

IT IS SURE TO ASK ONE DAY: "MAY I HAVE THIS DANCE?"


      DOPAMINE'S DEADLY DANCE OF DESTRUCTION:

















SLOW, STEADY, SINUOUS, SURREPTITIOUS...

sur·rep·ti·tious      
     adjective
1   1.     kept secret, especially because it would not be approved of.


DARE WE LOOK AT REALITY?

No one would have ever characterized the late Robin Williams as an ascetic. Quite the contrary, he was the essence of exuberance and manic enthusiasm, manifested as "boundless energy", among other things. Yet, it is very clear that his comic gifts were bestowed 'by the powers that be' as a mystifying double-edged sword. For whatever reason, his ability to make others laugh also came with the capacity to feel other people's pain...perhaps too much so. Now if the human brain were simple enough for us to actually understand it, we'd be so simple [that] we couldn't. What a conundrum! The dopamine tide that also governs both depression and addiction appears to render some kind folks, those with intrinsic hearts of gold, into tortured souls. Then there's the little understood phenomenon of ADHD and severe OCD not naturally cancelling each other out [when one inherits both] but occasionally culminating into a situation of uncontrollable verbiage and gestures.




I truly admire the wisdom of psychiatrists and psychologists pursuant to their clarification of brain chemistry, especially in the wake of Williams' sudden parting. The neurotransmitter dopamine is increasingly cited as much more than a bit player in the genesis of addiction. Perhaps this is knowledge that might be imparted as early on in grade school as is feasibly acceptable. After all, a deep acceptance of our natural conditions only makes sense. Knowledge, as the saying goes, is power.



Dopamine, at its finest, gives us a sense of significance and wholeness. However, too much [of this mood enhancer] and an individual may segue into agitation, restlessness, and full blown hyper-mania. On the other hand, with too little of this key neurotransmitter, the unlucky recipient will experience feelings of depression/misery, inertia, and all sorts of cravings; the latter are an evolutionary brain response to stave the inner emptiness that threatens  to behave much as a bell jar (think Sylvia Plath). It's just that evolution can't do much to prevent so-called 'mis-firings'.
















The cells that produce dopamine occur along three distinct "riverbeds" of the brain. That said, they are prone to periodic flashfloods, if you will, that may result in behavior considered [by many] to be at the outer margins of the proverbial bell curve.







While few of us ever experience the extreme behavioral symptoms that led Robin Williams to end his life, it's fair to say that anomalous behavior is difficult to explain. It does appear that our subconscious thoughts are stronger than we might suppose; furthermore, our actions may also be influenced by chemically mediated synapses that transpired only milliseconds before by our completely UNCONSCIOUS emotional system. In other words, we are truly at the mercy of our unconscious triggers. 


Nature may still be trying to perfect the inner workings of our evolutionary brain; in the past, a very trigger-happy limbic system was a key to survival. Now, the traffic between the cerebral cortex and the limbic system may need to be adjusted, as a key to our survival in a totally different sense.


We, as humans, sometimes have a tendency to describe 'being well' entirely in terms of NOT being 'unwell'. This is partly due to the fact that our emotional roots are, for the most part, fully unconscious.



Embracing the limitless self is, generally-speaking, a noble goal; unfortunately, some do it through the use of mood- or mind-altering drugs or simple alcohol. Even more regrettably, the sense of freedom that alcohol or mind-altering drugs may impart is only temporary. Hence, one who abuses such folly is not free at all; they're actually trapped in a vicious cycle.




Still, an increase in our awareness fosters the ability to change the nature of our unconscious pattern of behavior.


Remember, if you should ever fall, look for a great set of wings; moreover, you simply can't be in continual retreat from this earthly world. And he who has the beauty of a beloved friend can never forget it: especially when the sophistry of dopamine's ebb threatens to catapult one into the rabbit-hole of menacing solipsism!


MAHALO

Sunday, August 10, 2014

TRYING ON A NEW PAIR OF GENES


I.e., GENES EXPOSED FOR WHAT REALLY FITS:

" EYE DREAM
    OF GE-NE..."  



 (WITH MY LIGHT
BROWN HAIR)



How Blue Eyed Parents Can Have Brown Eyed Children
                      yes, that's what I said !!
  (Our grandson Jim...the product of blue-eyed parents)

It's always been known that there are
two different ways to get blue eyes...
but what about brown?

Three of our four children have eyes that would generally be described as "blue" and one has definite brown. The funny thing is that neither of my husband's parents have blue eyes, yet his father's mother and his mother's father most positively DID. As regards my own parents, my father was brown-eyed and my mother's eyes were aqua-blue. Mine turned out turquoise, my middle sister's are brown and my youngest sister's are pale aqua. Now, I would have thought that my daughter's chance of having a truly brunette child were slim to none, when assessing her husband's coloring. That said, 'his' mother is brunette as is my husband. Still, MY offspring's eye color results are probably not as unlikely as my grandson's outcome.


Punnet squares and Hardy-Weinberg, notwithstanding ... the genetics of eye color is much more intricate than what is usually taught in high school or even a college genetics course. Blue eyed parents CAN have a brown eyed child, though this phenomenon is certainly not common!  Brown eyes, as most will recognize, are the result of genetic dominance. However, when 2 genes come into play for eye color, things get shaken up a bit ... and here is where I will hand the metaphorical baton off to a more professorial discussion of the subject:



The take home point is that if someone makes a lot of pigment in the front part of their eye, they'll have brown eyes.  And if they make none there, they have blue. This insinuates that blue eyes are the result of "broken genes". Ergo, there are two ways to produce blue eyes via the above schematic.
The pigment making process involves both OCA2 and HERC2.  A 'working HERC2' is needed to turn on OCA2, and OCA2 helps to actually get the pigment made: in other words, they truly need each other to make pigment.
So someone with only broken HERC2 genes will have blue eyes no matter what OCA2 says or does.  This is because the working OCA2 can't be turned on so no pigment gets made.
The following is true as well.  Someone with broken OCA2 genes will have blue eyes no matter how 'normal' the HERC2 gene is.  Turning on a broken pigment making gene still gives you no pigment.  You need BOTH a working HERC2 AND a working OCA2 to have brown eyes.
But here is the caveat: Because the two genes depend on each other, IT IS possible for someone to actually be a carrier of a dominant trait [like brown eyes].  And if two blue eyed parents are carriers, then they CAN have a brown eyed child!!! 

Carrying a Dominant Trait
People have two copies of most of their genes. They get one copy from their mom and one copy from their dad.
These genes can come in different versions (known as alleles).  For the sake of simplicity and clarity, let's say that OCA2 comes in brown (O) and blue (o) versions, even though reality is actually a bit more complicated. Moreover, let's also say that HERC2 comes in two different versions, brown (H) and blue (h).  Now, since people have two copies of each gene, there are nine different possible genetic combinations with the array of alleles.  

Furthermore, these different combinations give the following eye colors:


Looking at the table, note that any time there are either two lower case h’s or two lower case o’s, a person has blue eyes ... and [again] this is because HERC2 and OCA2 need each other to have an effect; i.e., the blue versions of each gene are essentially broken.
But now let us focus on how two blue eyed parents might have a brown eyed child.  Imagine the following blue eyed parents:



Why OCA2 and HERC2 TRULY Need Each Other

FACT: Eye color depends on how much pigment is in the eye.  A lot of pigment gives brown, some gives green and little or no gives blue.  OCA2 is one of the key genes in determining how much pigment gets made.  If both OCA2 copies are broken, someone would have blue eyes.  Yet, most of the HERC2 gene has very little to do with eye color, per se.  That said, there is one small [critical] section in the middle of this gene that controls whether OCA2 is turned on or not.
If this part of HERC2 ends up broken in both copies, then OCA2 can’t get turned on.  And if OCA2 is off, no pigment gets made. As a result thereof, it is "like" the OCA2 gene is broken.
CASE IN POINT: Think about OCA2 like a light bulb and HERC2 as a switch.  If the light bulb is burned out, it doesn’t matter if the switch is turned on, does it?.  Just like it doesn’t matter if HERC2 works in someone with broken OCA2.  Flipping the switch to a burned out bulb won’t give you any light either!
Same thing with a working OCA2 and a broken HERC2.  A working light bulb gives no light when the switch is off.  Similarly, a working OCA2 makes no pigment when the HERC2 gene is broken.
This is what happens when blue eyed parents carry a brown eye gene.  If they have blue eyes because of a broken HERC2, then they might still have an OCA2 that works!  And if they have a broken OCA2, they might have a working HERC2!
Here is how to think of it in terms of these two parents passing on their genes to the next generation:


When these two have kids, one might pass an on switch and the other a working light bulb.  Now there is light even though neither parent could make light before.  Or in genetic terms, one might pass a working HERC2 and the other a working OCA2.  Now there is pigment where there wasn't any before.  The end result is brown eyes.
BUT WAIT...there's more: OCA2 and HERC2 are Linked!!
An interesting twist to this puzzle is the fact that HERC2 and OCA2 are very close together on chromosome 15.  What this means is that versions tend to travel together in the manner of linked genes.  And this affects the combinations of kids that any two parents can actually have.



To reiterate: Think about OCA2 like a light bulb and HERC2 as a switch.  If the light bulb is burned out, it doesn’t matter if the switch is turned on.  Just like it doesn’t matter if HERC2 works in someone with broken OCA2.  Flipping the switch to a burned out bulb won’t give you any light! Same thing with a working OCA2 and a broken HERC2.  A working light bulb gives no light when the switch is off.  And a working OCA2 makes no pigment when the HERC2 gene is broken. This is what happens when blue eyed parents carry a brown eye gene.  If they have blue eyes because of a broken HERC2, then they might still have an OCA2 that works.  And if they have a broken OCA2, they still might have a working HERC2.


****************************************************

Pretty array of capacitors, don't you think? There are some that will still take physics over genetics any day!


(... and then there are those who truly enjoy their puns.
 In one memorable Loony Tunes episode,
Bugs Bunny clearly emotes,
 "I dream of Jeannie, she's a light brown hare").