Glider RockerThe other night, while rocking my youngest child to sleep, my mind started wandering and I began to think about the distance our rocking chair may have traveled.  No, I am not talking about the number of times we have moved it from one home to another, but the actual distance the rocking motion may have traversed over the years of use it has had in our home.  I bought this chair over 8 years ago with our first child.  It was a little more expensive than we could afford (which wasn’t hard at the time) but I was excited and wanted something nice for mom and baby.  It may have been the most economical purchase I have ever made.

Five boys later this rocking chair is going strong, if not just a tad creakier.  So I decided to actually sit down and calculate, as best as I could, the approximate distance this chair has ‘rocked’.  And after running the numbers, I am feeling a little compelled to give some ‘props’ to the manufacturer, Dutailier[1].

So let’s get to it.  I measured the distance traveled, per rock, to be about 2 feet (1 foot each way).  I used the highest part of the back as the point of reference for the measurement.  This is approximately the height where the child spends most of the time, so I thought it would be a good place to measure.  I then measured about 33 rocks per minute, on average.  With these two measurements alone, I was starting to realize that the distance was accumulating.

Since we have not been keeping an accurate log of how much time each child rocked over the years, the next measurement was an educated guess (although most Mom’s have a pretty clear picture of this measurement).  So after some discussion with my wife, we decided that 60 minutes a day, for the first year and a half, was a pretty good average.  For the first few months, it was quite a bit more than this (hours upon hours).  But it tapers off near the 1.5 year mark.  So 60 minutes a day seemed fair.  Our current child child gets about 4, or more, sessions a day (15 to 30 minutes each) and he is nearly a year.

So how does this all add up?  Well let’s just say that by the time our youngest is 1.5 years old, we will have travelled roughly 2100 miles in that chair.  As the title implies, that is almost the same distance as a trip from Salt Lake City, Utah to New York, New York.  That’s quite a trip (especially is you consider that trip with a baby, screaming or otherwise, on your lap the entire way).  Each kid ended up travelling a little over 400 miles each, which is a little farther than a trip from San Francisco to Los Angeles (California of course).

That’s roughly $0.10 a mile.  I’d say we did alright.

Footnotes    (↵ returns to text)


Partial Heterochromia - E's Awesome EyeConversation on our way to my kid’s school:

T: Dad, I heard people used to marry their cousins and sisters and stuff.  Is that true?

Me: Well yes.  People used to do that for various reasons.

T: I also heard that people who did that have kids with no arms.

After chuckling a bit to myself I started to explain, as simply as I could, the concepts of genetic diversity and how kids have a better chance of not having certain problems if the parents are not related.  This quickly led to a quick discussion about dominant and recessive genes in the over simplified context of eye color.

Me: So Mom has brown eyes and I have blue eyes.  What color are your eyes?

T: Blue. So blue eyes always win?

Me: Not usually.  Mom and I both have two genes for eye color.  But we each only give you one of those.  If you get a brown gene from either of us, then no matter what the other gene is, you get brown eyes; brown is dominant.  I have blue eyes so I must have two blue genes.  I gave you one of those.  Since you have blue eyes, you must have two blue genes.  That means Mom must have both a brown and a blue gene and gave you her blue gene.  If she had given you her brown gene, then your eyes would have been brown, even though you got a blue gene from me.

T: Ok.  But then why does E (his little bother) have an eye that is both brown and blue.

I looked at him and laughed a little more.  I had to admit that I wasn’t 100% sure.  Of course that meant, for the rest of the day, that lack of knowledge was nagging me at the back of my mind until I had time to look into it a little.

So after some research my best guess is that E has Partial Heterochromia Iridum[1].  This condition is associated with a variety of  syndromes.  Fortunately our son exhibits no other signs associated with any of these syndromes.  His appears to be “Simple Heterochromia” that is a congenital hypoplasia of the iris.  In other words, it’s simply a case where parts of his iris are either underdeveloped or just missing melanin (blue eyes are caused by low concentrations of melanin in the iris or ocular fluid[2]).

So while it is somewhat rare, it’s nothing to be concerned about (in our case).  Both he and his brothers think  it is pretty cool and have nicknamed it the “awesome” eye.


The BrainDue to a family history of the disease, I have been interested in keeping track of advances in treating and preventing Alzheimer’s disease for quite some time.  This morning, thanks to Science Friday [1], I learned of a potential new treatment that is showing a lot of promise.  A group of scientists from the Landreth Lab[2], at Case Western Reserve University,  recently published a paper[3] describing the results of their research.  Gary Landreth[4], the researcher interviewed by Science Friday, provided an informative explanation of the research.  The following is a summary of what I took away from that interview.

While there is currently no cure for Alzheimer’s and even its cause is still somewhat unclear, the current theory is that it is closely tied to the deposits of amyloid plaques, or Amyloid Betas (Aβ), that build up in the brain as we age.  Amyloids are “small reddish sticky peptide[s]” which are generated at the synapse during normal brain activity.  A healthy brain relies on proteins called apolipoproteins[5] to clear away the Aβ before it can accumulate.  However as we get older the process for clearing it away becomes less efficient which allows the Aβ to start to accumulate, first into fibrils and then into plaques.  These masses interfere with normal brain activity causing the all too familiar Alzheimer’s symptoms..

ApoE is the principle apolipoprotein of the brain.  In humans there are three different allelic variations of the ApoE gene, ApoE2, ApoE3 and ApoE4[7].  ApoE4 is the variation most commonly associated with Alheimer’s disease.  Dr. Landreth’s research focuses on the use of an FDA approved drug (Bexarotene[6]) to help regulate the ApoE gene expression.    Through a mechanism I would need more time to understand, Bexarotene has proven effective in its ability to help the ApoEs in our brain clear out the Aβ more effectively than they could on their own.  Therefore, for those of us who may have the ApoE4 variation in our genes, some help may be on the way.

Keep in mind that this has only been shown to work in mice and proving the same result in humans will take some time.  But the results are promising. of us, when we think of Oxygen, think of its life giving properties that our bodies rely on continuously.  It makes up 20% of the air we breathe where it is second only to Nitrogen.  Now a smaller group of you (those who may have actually enjoyed their chemistry courses) may have gone somewhere completely different when I said Oxygen.  That’s because you know that these same elements that make up our air have the potential to react with the things they come into contact with (which because its air, is quite a bit of stuff).

When thinking of these reactions, metals often comes to mind.  Some of these reactions are positive, like the green patina that forms on copper when it comes into contact with oxygen.  This coating actually protects the copper underneath from further damage[1].  One well know example of this is the Statue of Liberty and its green hue.  Other reactions, however, can be detrimental.  One of these that we are very familiar with is rust.  Rust is the result of iron reacting with oxygen to form an iron oxide which will eventually completely replace the iron[2].

Now another form of rust (or at least some call it that) is the brown discoloration that occurs if you leave your apple slices out too long.  This also is caused by oxidation[3].  But one reaction that I had never thought of before was the reaction between oxygen and butter.  Oxidized butter, what is that?  Well you know that discolored skin that forms on it if you leave it out on the counter for too long (or the stuff that makes your butter takes like feet)?  Well that’s oxidation as well.  So contact with air is bad for your butter.  But there are two other things which accelerate the oxidization process as well: heat and light.  So obviously keeping butter in a cool dark place (i.e., the refrigerator or freezer) will also retard the process significantly[4].

But for those of us who like to actually use our butter as a spread, keeping the butter at room temperature is ideal.  However in order to keep your butter fresh at room temperature, you need to do your best to remove as much of the other two elements as possible.  So a clear glass butter dish may not be your friend here.  My mother in law recently introduced us to something called a butter bell[5] which is designed to solve this problem.  The history of this device seems somewhat unclear[6] but the principle is simple.  The butter is placed inside a cup which is then inverted and submerged in a larger cup containing water.  The water forms a seal preventing additional airflow into the chamber containing the butter.  Since these are typically ceramic, they provide the additional benefit of blocking out all light.  Ours seems to be working pretty well.  Just keep it out of the sun or you will end up fishing for your butter instead of spreading it.