Saturday, September 7, 2019

Monrovia Library Book Club Discussion Topics for "The Language of Life"

You can see my thoughts in an two earlier blog posts (my first ever blog post in 2010, as well as a more recent blog post in 2019).

However, the book club (at 6:30 PM on Tuesday October 22nd) is really about other people's thoughts (although I hope this non-fiction book helped with understanding about genetics/genomics).

So, here are some discussion topics, which I think could be of interest (even if you didn't already have a passion for genomics):

1) In general, what did you find to be the most interesting part of the book?

2) Did you think this was a good introduction to genetics / genomics? If not, I also recommend reading "The Cartoon Guide to Genetics" (which was required for my AP Bio class in High School, along with a more formal textbook). However, please be aware that the cartoons within the book are in black-and-white.  Also, as with just about anything else, the book isn't absolutely perfect: for example, there is a reference to 200,000 genes in the human genome on page 80 (which was believed at one point, but I would now say we feel much more comfortable with 20,000 genes that can be relatively consistently transcribed).

3) There is a section of the 7th chapter about the influence of genetics on Criminality.  For example, there are a few paragraphs about the X-linked MAOA gene.  While I mostly have to trust the study was fairly presented (and the reproducible in subsequent studies), a study showing decreased expression of MAOA was associated with increased risk of violent behavior and criminal convictions, but only if the individual was abused as a child (page 202).  So, I think this is a good example of a gene-environment interaction, but I don't know how strong / predictive the risk association was.

Likewise, to put things in perspective, Francis Collins also pointed out "approximately half of the US population carries a genetic risk factor that places people at a sixteenfold higher likelihood of imprisonment than the other half.  That happens to be the Y chromosome" (also on page 202).

Would your opinions of someone change if you knew they had a negative genetic predisposition (and you thoroughly understood exactly what has been observed and how much of an effect that has)?  For example, what do you think about giving somebody a lesser or more severe sentence because of their genetics?

4) Also in the introduction, Francis Collins discusses Alzheimer's disease risk, and questions the value of returning results when there is nothing that can be done medically (page xx, as well as illustrated on page 222).

I (Charles Warden) carry one copy of the APOE E4 risk variant (and I know which parent also has that risk variant).

4a) What do you think about a risk assessment for a disease that cannot be prevented or treated?

4b) Does that opinion change if I emphasize the need for you (and your genetic counselor, physician, etc.) to have access to the data to calculate the risk assessments, as well as making sure that you have access to your raw data for re-analysis / evaluation?

If interested, you can see my longer list of informal notes in another blog post.  However, the main message I think I should explain is that it takes some time to get confidence in a risk assessment (and I think there should ideally be some sort of access to the primary data used to come to those conclusions).

While I won't focus on what (from what I understood) were the less representative results here, my impression is that the more robust conclusion was similar to what was reported in my 23andMe report, Genin et al. 2011, and Myers et al. 1996 (which I am using to report the following statistics):

  • ~55% of E4/E4 individuals developed Alzheimer's Disease (with an age of onset ~80 years)
  • ~27% of E4/E3 individuals developed Alzheimer's Disease (with an age of onset ~85 years)
  •  ~9% of E3/E3 individuals developed Alzheimer's Disease (with an age of onset ~85 years)

Likewise, my 23andMe Report says "Approximately 40-65% of Alzheimer's patients have one or two copies of the APOE ε4 variant. However, many people with the APOE ε4 variant will not develop late-onset Alzheimer's disease" (citing Alzheimer's Association 2016).

5) Do you have any direct experiences with genomics results (from 23andMe, AncestryDNA, uBiome, Genes for Good, American Gut, etc)? For example, I have recorded some of my relatively recent experiences in this set of blog posts.

Having 5 questions to guide the discussion may already fill an hour (with a group of 20-30 people).  However, I hope the blog post can help with discussions before the book club (to help me better prepare) as well as after the book club (if anybody doesn't have a chance to express their opinion).

Change Log:

9/7/2019 - public post date
9/8/2019 - revise post from sister's feedback; minor changes
9/9/2019 - trim content
9/10/2019 - fix typo
9/11/2019 - add extra APOE E3/E4 citations (from 23andMe, ClinVar, and accepted middle-author paper; although I think the last of which was also in the pre-print)
9/13/2019 - add CDC links
9/14/2019 - separate blog post for detailed APOE notes
10/1/2019 - minor changes

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