Rolling a D&D Character

Well, my Dungeons and Dragon’s character, Ollie Oxenfree, was killed over the weekend. A blood golumn got him. We were all very sad.
Anyhow, I got to roll a new character. D&D characters are based on 6 numerical values that are randomly generated by adding together the numbers on three dice. Thus the mimimum score is 3 and the maximum score is 18. There are other ways of getting random numbers between 3 and 18 — for example you could roll a four sided die five times and subtract two. Or you could roll a sixteen sided die and add two. Here is a graph of how likely different rolls are depending on which die/dice you used:

Notice how the more dice you use, the tighter the bell curve appears. You have less than a 1% chance of rolling an 18 (or a 3) and a 12.5% chance of rolling a 10 or 11. For the kind of profession I wanted for my new character (two professions: “Ranger” and “Druid”), I needed at a minimum to roll these scores or higher: 3, 13, 13, 14, 14, 15.
But before I got my hopes up that my character would be able to take on these two professions, I wondered just how likely I was to be able to roll such high scores. I tackled this problem two ways: with a random “monte carlo” simulation, and using statistical analysis.
For the monte carlo simulation, I wrote a perl script that randomly generated scores using a simulated die. It then determined if the rolls met my minimum criteria. After 1000 rolls, it reported the fraction of rolls that were adequate. I had it calculate scores for Ranger+Druid, Ranger only, Druid only, all 3s and all 18s. I know that all 3s or better should be probability of 1 (you always roll a 3 or better). Also, the all 18s should be pretty unlikely (it might not even roll a single one). For those of you following along at home, here is the perl script for this:

@scores = (
[ 3, 13, 13, 14, 14, 15 ],
[ 3, 3, 13, 13, 14, 14 ],
[ 3, 3, 3, 12, 13, 15 ],
[ 3, 3, 3, 3, 3, 3 ],
[ 18, 18, 18, 18, 18, 18 ],
[ 3, 3, 3, 3, 3, 18 ],

foreach $scoresRef (@scores) {
$right = 0;
foreach $i (1..10000) {
my @guess = ();
foreach $b (0..5) {
$guess[$b] = 0;
foreach $a (1..3) {
$guess[$b] += int(1+rand(5.9999999));
@guess = sort(@guess);
my $itsright = 1;
foreach $b (0..5) {
$z = $guess[$b];
if ($z < $$scoresRef[ $b ]) {
$itsright = 0;
$right++ if $itsright;
$total = 1 - ( 1 - $right / 10000 ) ** 6;
print join(", ", @$scoresRef) . " = $total \n";

On Mac OS X, launch, type “perl” and press return. Then copy and paste the code above and press control-D. After a little while it will print out something like this:

3, 13, 13, 14, 14, 15 = 0.0107515164826495
3, 3, 13, 13, 14, 14 = 0.0596604624564983
3, 3, 3, 12, 13, 15 = 0.16341479899658
3, 3, 3, 3, 3, 3 = 1
18, 18, 18, 18, 18, 18 = 0
3, 3, 3, 3, 3, 18 = 0.0214065306042021

Notice the use of the sort function to remove any order issues, also the bit about **6 is because we get 6 tries to roll it right. If we had to roll the scores in the correct order it would be a lot lower probability. What I see is that rolling scores high enough for my ideal character happens about 1% of the time. While this seems pretty unlikely, there are a few things going in my favor. First of all, I get 6 tries to roll (increasing my chances by 6 fold). Furthermore, my montycarlo simulation can easily have some error. Finally, its only 1/2 as likely as rolling an 18 — and I know several of my fellow D&D players have characters with 18s, so shooting for my goal seems perfectly reasonable.
I mentioned that there is a second way to calculate how likely I am to roll my needed scores. The first step will be calculating how likely each sum is. Here is some more perl code for doing that:

foreach $a (1..18) {
$p1[$a] = 0;
$p2[$a] = 0;
$p3[$a] = 0;
foreach $a (1..6) {
$p1[$a] = 1/6;
foreach $a (2..12) {
$p2[$a] = 0;
$start = $a-6;
if ($start < 1) {
$start  = 1;
foreach $b ($start..($a-1)) {
$p2[$a] += $p1[$b]/6;
foreach $a (1..18) {
print "$a : $p2[$a]\n";
foreach $a (3..18) {
$p3[$a] = 0;
$start = $a-6;
if ($start < 2) {
$start  = 2;
foreach $b ($start..($a-1)) {
$p3[$a] += $p2[$b]/6;
$sum = 0;
foreach $a (3..18) {
print "$a : $p3[$a]\n";
$sum += $p3[$a];
print "-" x 32;
print "\n$sum\n\n";

This will print out something like this:

1 : 0
2 : 0.0277777777777778
3 : 0.0555555555555556
4 : 0.0833333333333333
5 : 0.111111111111111
6 : 0.138888888888889
7 : 0.166666666666667
8 : 0.138888888888889
9 : 0.111111111111111
10 : 0.0833333333333333
11 : 0.0555555555555556
12 : 0.0277777777777778
13 : 0
14 : 0
15 : 0
16 : 0
17 : 0
18 : 0
3 : 0.00462962962962963
4 : 0.0138888888888889
5 : 0.0277777777777778
6 : 0.0462962962962963
7 : 0.0694444444444444
8 : 0.0972222222222222
9 : 0.115740740740741
10 : 0.125
11 : 0.125
12 : 0.115740740740741
13 : 0.0972222222222222
14 : 0.0694444444444444
15 : 0.0462962962962963
16 : 0.0277777777777778
17 : 0.0138888888888889
18 : 0.00462962962962963

The first 18 values show the probability that a sum of two dice would be the given value. The second 18 show the values for three dice. Thus rolling three dice and getting a sum of 18 has a P=0.0046. Getting a 10 has P=0.125.
The real complication with calculating the scores for my Ranger/Druid using statistics has to do with figuring out the combinations. Essentially, you need to figure out how likely that *one* of the rolls is 15 or better, but it doesn't matter which. After getting bogged down for quite a while puzzling this out, I decided I would simply trust my monte carlo simulation results 🙂
So I had my dog blow on the dice, and my wife roll them, and sure enough.... I got my scores!


Why are bubbles blue?

Well, if you haven’t tried Mountain Dew Pitch Black, please don’t on my account. It is a disgusting grape flavor. But there is one cool thing about it: It has blue foam. This is kind of interesting because the soda itself appears to be black. One can’t just let strange things like this abide untested.
If you look closely at the drink, it is not actually black — it is a dark purple. However, this is clearly a different hue than the fizzing bubbles. What gives? Your’s truly investigates!
My first hypothesis is that the dye used in the beverage is sensitive to pH, and also that the bubbles in the beverage (which are in close proximity to the off gassing CO2) may be at a different pH than the rest of the beverage. I know that carbon dioxide is a weak acid, but I’m only guessing that the water in the foam is a different pH. To test this hypothesis, I poured a small amount of Mountain Dew Pitch Black into two clear glass containers — one with some baking soda ( a base ) and one with vinegar ( an acid ). The color of the liquid remained the same in both. This shoots down my first hypothesis.
However, when I mixed the two together, the vinegar and baking soda reacted most pleasantly. And the foam turned blue, too…
Next, I hypothesized that there might be two separate dyes in the drink — one of them blue. Somehow the act of foaming up separates these two ingredients. Or, it could be that the blue dye is in much greater concentration, so that when it is diluted in the foam it still appears blue when the other dye no longer is effective. To test this hypothesis, we used paper chromatography. We placed a thin line of soda on a paper towel, and then put a few ice cubes next to the line. With the help of a few drops of water from a wet hand once in a while, the water melted off the ice cubes and wicked through the paper towel. As the water moved through the paper, the dye molecules were dragged along with it. But due to their different molecular weight and affinity for paper, they moved at different rates. The result was a separate band of color for each dye in the soda.


Furthermore, I discovered on The mountain dew website that sure enough, it contains two dyes: Blue 1 and Red 40. With the help of the National Library of Medicine’s Household Products Index, I was able to locate the molecular structures of the two dyes in the Chemical Information Database. Here they are:

FD&C Blue 1 (left) and FD&C Red 40 (right)

There are a few simple things that can be noted by looking at the structures. First, Blue 1 is a bigger molecule. Bigger molecules tend to diffuse more slowly. Interestingly, the blue strip on my paper chromatography experiment moved faster than the red stripe — so the red dye although smaller must interact more strongly with paper.
So why is the foam blue? My hypothesis that the dyes are getting separated in the foam seems highly improbable — purifying mixtures is a very hard thing to do. Try desalinating water, or filtering out a dye sometime. I’m pretty confident that the foam appears blue simply because the blue dye is in the soda at a higher concentration, so that when diluted you see mostly the blue color. The reason the hue can change during dilution is only if the blue dye is over saturated enough so that it remains blue long after the red dye has been diluted away.
We know from experience that soda pop foam is diluted — Coke has creamy white foam even though the drink is caramel colored. Regular mountain dew foam is barely a butter yellow color even though the drink is bright lemon yellow.
I’m waiting for the chance to test this hypothesis, by performing a serial dilution of the beverage. I think that the color should change to blue if you mix the right amount of water with it. Stay tuned.

(Later…) I just had another idea. It might be possible that the blue dye is actually preferentially associated with the foam. I’m thinking of soap as an example. Soap is a long molecule that has different hydrophobicity at each end. One end dissolves very well in water (like sugar or salt) — this end is hydrophillic (water loving). The other end is very oily and would rather be out of the water — that end is hydrophobic (water hating). The result is that the oily end of soap molecules surround greasy dirt and allow water to wash them away. Another side effect of soap is soap bubbles — which are tiny molecular sandwiches with the oily parts of the soap molecules sticking into the air. It never occurred to me before, but soap bubbles may have a higher concentration of soap in them than the rest of the solution.
So, if the blue dye in the Mountain Dew is a soapy molecule (soapier than the red), then it might preferentially stay in bubbles because the oily part of the molecule likes to stick in the air pockets. I can think of two more experiments to test this hypothesis. First of all, we could try to harvest the blue foam off the soda,then let the bubbles go away and compare the color of that liquid with the original. If the liquid is bluer, then we have proof that there was molecular separation.
The second experiment is to add some dish detergent to the Mountain Dew. The dish detergent is most likely a much better soap than the blue dye. It might fill up all the space in the bubbles, and it will also surround the oily parts of the dye — so it might cause the foam to no longer be blue. I’m not really sure this will work, because the soap will also cause there to be a lot more bubbles. That might nullify the first effects.
One other observation supports this latest hypothesis. But FD&C Red 1 is a flat, rigid mostly oily molecule with two water loving sulfates on either end. This probably isn’t a very good soap because the oily part is surrounded by the water loving part (remember soaps need to be polar to work well). FD&C Blue 40, on the other hand has three water loving sulfates, two of which are on floppy molecular connections that allow them to swivel around to the same side. That allows Blue 40 to have an oily side and a water loving side — just the recipie for soap. That oily side will like to associate with the surface of the water — which foam has a *lot* of.


Solar conjunction with Mars

Today the Earth and Mars have moved into an arrangement called a “Solar Conjunction”. This is similar to an eclipse: The Sun is positioned between the Earth and Mars.

The arrangement of the inner planets as of Sept 9

The Earth is the blue circle, and Mars is in red.

The solar conjunction means that the Mars Rovers need to operate without human assistance for two to three weeks. Radio transmissions can’t be sent through the Sun. The rovers will be parked taking spectrograph readings of rocks and dust, and observing how the winds affect a depression in the soil.


What is Cement?

This weekend I was tiling a bathroom. The stuff you stick the tiles to the floor is a mixture of cement, sand and a few other things. That kind of mixture is similar to what is in concrete concrete, which is a remarkable material used in all kinds of construction. The mystery to me was, “Why does cement harden when the water dries?” And also, “Why do they warn not to let touch the wet mixture?” The answers, it turns out, involves the chemistry of Calcium and Silicon — the same element that is used to make computer chips.
Cement is made from powdered di- and tri- calcium silicates. These chemicals react with water to form Calcium Silicate Hydrate. Calcium Silcate Hydrate is insoluable, so it will form solid crystals that glue the cement together. The reaction is remarkable in a number of ways. First, it is slow — as the reaction proceeds, the growing crystals get in the way of the water molecules that are trying to get to the calcium silicates. That slows down how quickly reaction goes. This slowing process allows concrete to be mixed and kept liquid for about three hours as it is shipped to where it is needed.
Another fascinating feature of cement is that it is made from extremely common materials: limestone and sand. At a cement plant, limestone (Calcium Carbonate) and sand (Silicon Dioxide) are ground into a very fine powder. Then they are heated. As the mixture reaches 800°C water boils away from the raw materials. At about 1200°C the limestone breaks down into Calcium Hydroxide, releasing carbon dioxide into the air. At 1400°C the sand reacts with the Calcium Hydroxide to produce molton cement. The cement hardens to form small pebbles called clinker that are then ground up to produce regular cement.
The calcium hydroxide that is produced as an intermediate ingredient is the reason that it’s not good to leave the cement mixture on your skin. More calcium hydroxide is released as the cement is reacting with the water. Calcium hydroxide is a very caustic base, and can cause burns on your skin.
The carbon dioxide that is released is significant: The manufacture of cement in the United States releases about 40 million metric tons of carbon dioxide into the atmosphere each year. Carbon dioxide is suspected to cause Global Warming.
There are a lot of other subtleties in the use of cement. Compounds of aluminum and polymer additives can change the properties of the final product. The diverse properties, inexpensive starting materials and ease of use make cement one of the best building materials in the world.


How do they sequence a gene Part 2: Sequencing

The sequencing reaction is one of the most amazing techniques I’ve seen. Most of the time a molecular biologist gets very little tangible feedback about what is going on: You spend your day mixing up microliter amounts of clear liquids.
However, on the left you see what your film looks like after sequencing. This film has been exposed by radioactively labelled DNA. The DNA is separated by length on the vertical axis, with the longest pieces at the top. Each lane marks a different nucleic acid. You read from top to bottom — thus this sequence of DNA is ggcttcgaaggggactaacaaaggg….
How does the sequencing reaction work? Well, it is similar to PCR — with a few very clever twists. Nucleic acids, which are the building blocks of DNA, can be thought of as really tiny Lego blocks. They have chemically reactive atoms that connect up to other nucleic acids — much like Legos plug into each other. Chemists have invented a new, artificial kind of nucleic acid called a “dideoxy nucleic acid”. Dideoxy nucleic acids are defective legos — they don’t have the bumps on top for another lego to plug into.

The sequencing reaction is very similar to PCR. The DNA polymerase is used to make copies of template DNA out of free nucleic acids. But in sequencing, there are four separate test tubes with almost identical reactions. Each test tube has a little bit of one of the four dideoxy nucleic acids : ddG, ddA, ddT or ddC. In the illustration above, I show the reaction containing ddG. Once in a while as the DNA polymerase is making copies of the template, it will use a ddG instead of a regular G. Since the ddG has no “sticky” end on top (brown arrow), that piece of DNA is prematurely truncated and cannot be extended any more. Furthermore, the length of the truncated DNA will precisely coincide with the position of the G in the DNA sequence.
After the four reactions are finished, the length of the DNA strands in each test tube is measured using electrophoresis. The result is a picture much like the one at the left. Maybe I’ll talk about electrophoresis in a future post.


Science Toys

Becka sent me this link with dozens of science toys. They are made from common Home Despot or Rad Shack items. My favorites so far are the hydrogen bomb and the simplest steam engine. But you’ve got to admit that the morse code radio transmitter is awesome as well…


How do they sequence a gene Part 1: PCR

In response to my discussion about genetic testing, I’ve been asked, “How do they do that?” They do it by sequencing the DNA. In my multi-part answer to this question, I’ll begin with the first step of that process: PCR.
PCR stands for “Polymerase Chain Reaction”. That might be a bit of an exaggeration, as it sounds like molecular biology gone wild. It is actually a very controlled and fascinating technique — quite possibly the most significant innovation in molecular biology in the past twenty-five years.
But first, lets cover some of the principle features of DNA: it is double stranded, composed of a repeating molecular letters that are complimentary and the two strands run antiparallel to each other.
What am I talking about????
Well, as I’m sure you’ve heard, DNA is a double-helix. The double-helix made up of a repeating sequence of a class of molecule known as a nucleic acid. There are four kinds nucleic acids that make up the helix. They are abbreviated as A, T, G and C. Furthermore, the nucleic acids of one strand are complimentary to the molecules in the other strand: An A in one strand is paired with a T in the other strand, and a C in one is paired with a G in the other. The cells of your body read the sequence of nucleic acids much like you read a reference book: you go to the chapter and begin reading the letters from left to right. DNA has a “left to right” direction too (but they call it “five prime to three prime”). DNA is antiparallel because when one strand is going left to right (five prime to three prime), its complimentary strand is going right to left (three prime to five prime). I’ve illustrated this in the diagram: The bottom strand’s letters are upside down.
To begin a PCR reaction, you need two important ingredients: A small amount of template DNA and primers. Template DNA is extracted from the blood of the patient. Each blood cell has the patient’s complete genomic DNA in its nucleus. The primers are short, single-stranded DNA molecules that are manufactured using modern chemistry techniques. Primers are designed to be complimentary to the template DNA. Furthermore, there are two primers that mark where to begin and where to end the manufacturing of DNA through PCR.
Okay, now on to the reaction itself. Here is a diagram illustrating the steps of PCR:

PCR (right click/control click and choose “Zoom In” for more detail)

PCR has three steps: denaturing, annealing and extending.
In the first step, heat is applied to the template DNA to pull the two strands apart to create single stranded template DNA. This process is known as denaturing. Next, the sample is allowed to cool with an excess of primer DNA in the test tube. The primer DNA is perfectly complimentary to the ends of the template DNA, thus it forms short regions of double-stranded DNA with the template. This step is called annealing. Finally some DNA Polymerase is added along with all the necessary nucleic acids, and the remaining single-stranded section of DNA is converted to double stranded as the primer is extended with complimentary bases. From one molecule of DNA, two have been made.
The “chain reaction” occurs when this process is repeated over and over, resulting in first 2, then 4, 8, 16… 2n copies! Most people stop around 15-20 cycles, but some people who are very daring somtimes go up to 30 or even 40 cycles.
Thus from the small amount of DNA that was extracted from the patients blood, a large quantity has been “amplified” using PCR. The amplified DNA will be used in the sequencing reaction… stay tuned!


Olympic Physics

This week the Olympics used the same arena that the original Olympians were at thousands of years ago. I saw them doing the Shot Put. Which got me thinking, of course, what is the best angle to lob a heavy rock in order to get the most distance.
If we start with some simple assumptions we can tackle this problem with algebra. It’s always good to know some boundary conditions just to make sure you can validate your answer. So lets start with these assumptions: We’re launching from ground level on a perfectly level field and there is no air friction. Oh, and as soon as the shot put hits the ground it stops. I think we can all agree that given those conditions, a perfectly horizontal launch won’t go anywhere because it never leaves the ground. Likewise a perfectly vertical launch net any distance either because it will land right where it started. Finally, let’s just take an educated guess: It is going to be somewhere between horizontal and vertical — let’s say 45 degrees as a first approximation.
Now let’s tackle the Algebraic solution to this puzzle. First, I always draw a picture to help me keep track of what’s going on.
The free body diagram.
Here I’ve shown the path of the ball as an arc. The total time (indicated by the stopwatch on the right) is t seconds. The length of the throw is X meters. The initial velocity of the ball is V meters per second at some angle, A, above horizontal. We’ll consider two parts of the velocity: The horizontal speed (Vx) and the initial vertical speed (Vy).
Here is the equation we need to solve this: d = vt + ½at2. We’ll also need to know the acceleration of gravity, G.
Well, the time the ball stays in the air is a function of the vertical component of the throw. So using the above equation we know v is actually Vy. The acceleration, a, is simply G. Finally, the ball is at ground level when the distance travelled is zero. Thus we want to solve:

0 = Vyt - ½Gt2

which has two solutions : t = 0 and t = 2 Vy / G . Hang on, we are making progress!
Using our original equation again, we can see how far the ball has traveled in that time:
X = Vxt

X = 2 VxVy / G

Now we simply use a little trig to relate Vx and Vy to V and A.
Vx = V cos(A)

Vy = V sin(A)

Thus our solution can be shown as this, in terms of V, A and G:
X = 2 V2 cos(A) sin(A) / G

The interesting thing about this result is that it shows that the distance a ball will travel is proportional to the square of how fast you throw it. This means that it is actually easier to differentiate how fast two atheletes can throw a ball based on how far the ball travels than if you were to measure the speed directly. Also, this makes sense in terms of energy, since we know that kinetic energy is proportional to the square of speed.
Moving on with the algebra… We can assume:
sin(2x) = 2 sin(x)cos(x)

That’s some trig I dug up on on the internet. Which gives us.
X = V2 sin(2A) / G

So what it all boils down to is finding the maxima of sin(2A). You need calculus — just a little tiny bit — to do this. What you do is look for a spot on the curve where it’s flat. It gets a little hairy, so I’ll just show you how to set it up and then solve it for you:
dX/dA = 0 = 2 V2 cos(2A)

Which basically boils down to the angle where cos(2A) = 0. The simplest answer is: 45°.
The problem really gets interesting when you factor in the height of the shot put upon throw (since the ball is several feet of the ground when the athelete releases it). Just how much this matters is left as an exercise for the reader. 🙂


Testing for Breast Cancer

Genetic testing is a powerful new way to find out about your risks for certain diseases. One example is the test for one of the “Breast Cancer” genes, for example BRCA1. (BRCA stands for BReast CAncer.)
Before we dive into a discussion of BRCA1, let’s review a little terminology. Perhaps you’ve heard that a person is “made” from their genes. This is true — what makes the human species different from other mammals is the sequences of DNA in our cells. Our genes also play a large role in determining who we are, although genes aren’t everything: Identical twins have the same genes but are still different people. Genes are actually nothing more than sequences of DNA which contain the instructions for building a small molecular machine called a protein. Just like blueprints at a factory, there are different versions of these instructions (as in the “Revision A” and “Revision B” iMacs). These different versions of genes are called “alleles”. Sometimes you’ll hear an allele referred to as a “mutation” or that it is “malformed”. Indeed, often times it is quite clear that the gene is broken (just like a blank blueprint would clearly be broken). Other times it isn’t so clear what the “mutation” does — and in fact it is possible that a mutation would function better than the original (otherwise known as the “wild type”). For example, there may be alleles that make you short (a loss or reduction of function of the human growth hormone) or there may be alleles that make your hair dark (a gain of function in pigmentation synthesis). But no, it is not possible that a single mutation would give you strange super powers or enable you to grow feathers and fly.
A sad fact about mutations is that they are the cause of cancer. Not all mutations cause cancer, but cancer won’t happen without them. Fortunately, cells in your body are full of protection mechanisms to prevent cancer. Mutations can happen at random (due to solar radiation, chemical exposure, time or just bad luck) to any cell in your body. Most of the time a cell’s protection mechanism will either fix the mutation, or cause a cell with a cancerous mutation to die. But once in a while a cell (or the cells that it came from) gets a mutation in the protection mechanism itself. Once a cell’s protection mechanism is disabled, the cell can accumulate more mutations that eventually allow it to become cancerous.
One kind of cellular protection mechanism is called a “tumor suppressor gene”.
Okay, back to BRCA1. What is it, and why does it cause breast cancer? It appears from the literature (a summary can be found at NIH ) that BRCA1 is a tumor suppressor gene. The protein made from the BRCA1 gene acts to suppress cancer! BRCA1 can be dangerous to your health only if it is mutated. The protein made from the mutated gene may be partially or completely broken, leaving your cells more susceptible to becoming cancerous. And remember, your cells can become mutated two ways: Either you inherited that mutation from your parents, or you acquired it.
As researchers have studied BRCA1, they’ve discovered that it is similar to other tumor suppressor genes that have already been studied. In fact, BRCA1 normally protects you from not only breast cancer but also ovarian and prostate cancers. It’s also been discovered that BRCA1 mutations are associated with certain groups of people, for example the Ashkanazi Jews. It appears that over 2% of the Ashkanazi may have a mutation in BRCA1. Indeed the unusually high incidence of breast cancer in a region of New Jersey can largely be attributed to the high number of Ashkanazi descendents living in that area.
BRCA1 is not the answer to all of the Ashkanazi problems, however — it has been shown that even the Ashkanazi who have normal BRCA1 are still three times more likely than other people to develop breast cancer. This just goes to show that cancer is a complex subject and the genetics of this disease are still being figured out.
An example family pedigree.
Let’s look at the example family pedigree above. One woman (marked with an X) is facing a breast cancer triple threat: She’s already had breast cancer, which means she is more likely to get it again than most people. Plus her grandmother was an Ashkanazi Jew. Grandma may have had a mutation in BRCA1; even if she didn’t the Ashkanazi have a higher incidence of breast cancer than most people. X wonders if it would be worthwhile having her BRCA1 and BRCA2 genes sequenced. This is an expensive but painless procedure. It is expensive because the BRCA genes are long, and the entire DNA sequence needs to be verified in order to know if there is a mutation present.
The issue is complicated because it raises questions that don’t affect just her. She has living cousins, some of whom have already had cancer. If X has mutant BRCA1, cousin Y has a 25% chance that she also has that mutation. Should she tell her the results of her genetic screening? There is no simple answer to that question.
Since BRCA1 is also indicated in male breast cancer as well as prostate cancer, should she tell her four sons the results? Each son has a 50% chance of inheriting the mutation — so there is over 90% chance that at least one of them did. What about her granddaughter? Again, there are no easy answers here.
In my opinion, the more information you have, the better. Chances are, X does not have a mutation in BRCA1. Confirming that with sequencing would provide comfort to the whole family. On the small chance that she does have a mutation, that knowledge provides the opportunity to consider more aggressive treatments to prevent future cancer. It also forewarns her relatives to be more vigilant. So her son’s don’t disregard any lumps, or may have their genes sequenced themselves and will seek routine screening for cancer.
Genetic screening is the latest in diagnostic tools that will help us live healthier lives. While intially it is a bit intimidating, once the legal and technical aspects of it are worked out it will become as routine as getting a culture for strep throat or being vaccinated.



Science and technology are responsible for the most dramatic shifts in world culture that our species has ever seen. Thanks to our understanding and application of scientific topics, the human species is able to communicate, travel and work like no other time in history. The last century is rife with monumental consequences of scientific discovery ranging from the atom bomb, to the green revolution to the human genome project. Science impacts every aspect of our lives.
And yet there is very little clear understanding of how science really works. Popular media glosses over scientific details. Statistical analyses are carried to absurd conclusions. Movies will just make things up. The result is a world in which people see science as an impenetrably opaque shrine of doctrine instead of the open realm of debate and knowledge.
I usually rant and rave (my friends are often quoting my remark of, “That’s not science!”) but little else. As of today, I’m starting this blog as an outlet for my frustration. I intend to answer questions about science and to correct the blatant inaccuracies seen in the news or from the entertainment industry. Send me your questions! Let’s dig into the Science Fare!