How to study: a re-repost

This seems timely to repost.

Since a new semester is about to begin I think a post on how to study would be apropos. So here is an advice column for students looking for some techniques to improve their study habits. I am not an expert in learning, but I am an expert in being a college student with no fucking idea how to study and had to figure it out over the course of a year or two. I was one of those students who didn't have to do much to maintain an A/B average in high school. Although I was exposed to study skills and habits while in high school, none of it stuck because I really didn't need to study to do reasonably well. So here is what I learned that worked for me. If you have your own successful techniques, please feel free to add them in the comments.

Learning is an active process, it requires energy. It may not be as physically taxing as a 45 minute work out, but then again you may not be doing it right. What I discovered is that I learn when I do things, when I engage the material, when I'm an active participant. If it's a couple of days before the big exam and you're wondering to yourself 'What's the best way I can study? I know, I'll take some time to play online and get some tips.' Well, if this is you, you're fucked or at least I don't have anything for you. Come back after your upcoming exam, my advice might help you for the next exam. Right now, you are in cram mode, so you better start cramming and not wasting your time reading blogs. I will admit that cramming works, to a degree. Cramming is a short term solution, getting enough material under you belt to survive or even succeed at the exam. But it's a long-term problem. Are you really in college to survive exams and classes? That was really high school wasn't it? Cramming is problematic because the material is never actually learned, it may come up again on the final, it will likely be important next semester or the semester after that in your more advanced classes. Learning and cramming both take energy, but the former is far less stressful and provides both short-term and long-term gains.

Step 1. Find an environment to study in. Ultimately this became at my desk in the bedroom of my apartment. I also kept my stereo close by set at police notification level. I learned quickly that I could ignore the music, but sounds from the street, from the kitchen/dining/living room area, or from anywhere outside my room were distracting. To this day, when I'm working on grants or papers and do not want to be disturbed, I  close my office door and crank up some music. Although I am a chaotic person by nature, my desk was neat and organized. I needed a place to work comfortably and that was it. My textbooks and notebooks were stacked in/on some milk crates I used for shelves. (These of course were the store bought kind of 'milk crates' not the easily available sturdy and inexpensive milk crates available behind 7/11s, like the one across the street of my apartment. Although if they were the illicit version, which they weren't, they would have been returned when I moved to go to graduate school.)

$0.69 for 3 in 1989

Step 2. Get a bunch of notebooks. I used spiral bound notebooks available for next to nothing at drug stores. Of course these notebooks will have absurd cover designs or pictures you would never in a million years gravitate towards (see picture of my Molecular Biology notebook). That's not the point. The point is what's inside the notebook, and that will be gold. I mixed up the designs on the notebooks I bought so I could easily identify which one I wanted. The alternative is to be flipping through them wondering if this is the black notebook Im looking for. Get one notebook for every class you take (except maybe for the golf/tennis/etc classes). Any class that has a lecture has its own notebook. No cheating by getting a three-subject notebook. Also, get a couple of additional notebooks.

These things are evidence of evil

Since you're at the drug store all ready, get some pens and pencils. I love pens, but despise cheap ass ball point pens. You'll be using these a lot, so get pens/pencils you are comfortable with. Make sure you get a variety of colors. I survived with black, blue, and red, but there is a veritable palate of colored inks now. Get what you love or at least can tolerate. I prefer mechanical pencils, but if you get classic ones, you better kick in for a decent pencil sharpener or two. Also grab some highlighters also in assorted colors.

Step 3. Do the readings strategically. Chapter 3 is covered Wednesday? Read it through by Tuesday night. That isn't very strategic is it? The strategy is to skim read the text. Get a sense of what's in there and what will be the likely topics and points for the upcoming lecture. You don't need to be more than familiar with the material. (In the case of labs, this is not true. You must be intimately aware of the material, because you will be using that information in the lab. Hell, there may even be a quiz on the lab manual!)

Step 4. Go to class. Although you probably couldn't pass a quiz on the readings material, the vocabulary is familiar. Now you already know a bit about the upcoming lecture. Gather up your pens and pencils and one of the extra notebooks. Leave your textbooks at home, along with the highlighters, and other notebooks. You don't need much.

Get to class on time and get a good seat. In large classes, I recommend a seat near to the front and in the middle where the professor can actually see you. Why? Psychology that's why. Take two students doing equally well, one student the professor recognizes, even if there is no name associated with the face, and one student the professor has barely, if ever, seen. If both come to discuss an issue regarding an examination or writing assignment, which one will have at least a sub-conscious advantage?

Open your notebook to page 1 get out a couple of writing implements and get ready. If the professor has handouts or, god forbid, print outs of the slides, then definitely pick them up, but DONT use them during the lecture (with rare exception). Your job is to take a shit ton of notes. Don't worry about neatness and perfection, just get the stuff written down. Write down the points on the slides, the drawings, incorporate what the professor is saying. The very act of writing things down is helping you learn the material! 'But we have the slide print outs, so why write stuff down?' you ask. In my more youthful days I would have responded with 'Because we didn't have the material presented to us, so stop being so fucking needy.' But in my dotage I think an example is better. What is another name for a television? Did 'idiot box' spring to mind? There's a reason for that. Some people watch tons of TV, these are not inherently the most educated people in the world. My mother loved to watch soap operas during the 70s, hours of soap operas. She was not an expert in social interactions because of this nor was she an expert story teller, she just watched a lot of soap operas. This is one of the biggest impediments to learning, fucking handouts. Remember I said learning was an active process. Lectures are not television. You should be doing something not just watching. The problem with handouts is that it facilitates the TV watching mentality. There are reasons to hand out the notes, which is why you are collecting them, but wait until later to use them. For now, take a shit ton of notes.  Do not be tempted to put notes in the margin of the print outs, you bought the cheap ass notebook, so use it. (Plus you'll want a pristine copy of those hand outs for later.) So, you were in class sitting in a strategic location, you took a shit ton of notes, now what? Go to your next class and repeat using the same notebook.

Notes on chromosomal

melting temps.

Step 5. THE MOST IMPORTANT STEP: The next day. So you went to all your classes, even the ones you think are boring, and you took a bunch of notes, even on things you think you know already. Now what? Hang out with friends, watch TV, play some Xbox, then go to bed and the next day go to all your other classes. At some point on this second day, you need to carve out some studying time. When depends on your schedule. I did this in the mid-late-afternoon, because I was generally done with classes then. Go to your studying environment, get out your notes from yesterday, one of the fresh notebooks that will be specific for a specific class, any handouts, and your textbook. Now you will rewrite your notes in a more organized and legible manner. As you rewrite, you will refer to the text for additional points, and in your class-specific notebook you can either incorporate the textbook material or simple refer to the page numbers/figure numbers. Either redraw or cut out the handout figures you need and add them to your notebook. This could take as long as the original lecture, but probably won't. Regardless, you are now learning some serious material. The act of rewriting helps embed the information into your memory, by organizing the material in a manner that works for you (which is probably like it was presented) you are thinking about the material in total not simply one fact after another. You are also reading the text in a more in depth way, which is easier because you already skimmed it and went to the lecture. Do this for those boring easy classes too. It helps maintain good study habits and instead of simply learning the material, you'll own it. Another benefit is that if you do this, you will know before the next lecture what material you may not understand. This gives you a ton of time to meet with your colleagues, TAs, professor to get things straight.

Step 6. When you finish going through the crappy notes, rip out the page(s) and throw them away. You don't need them anymore because they are rewritten and you'll feel good about the progress you made.

I won't guarantee these steps will improve your grade, but I do guarantee that they will improve your understanding and knowledge of the material.

Additional thoughts:

A. Write in your textbooks, at least highlight important information. I used different colored highlighters for different purposes. Red was for definitions, blue was for what I thought were key concepts, green was for things referring to my class notebook. Will writing in your textbook reduce its value when you resell it? Well hopefully you will not resell it. Having that chemistry textbook could come in handy when you need to revisit something you forgot in your molecular biology class. If you absolutely do not want the book, why buy it in the first place? Probably you could borrow one from a colleague or use the library.

B. Scheduling. You need to prepare ahead of time when things are getting done. If you don't, you will almost certainly get behind or not have enough time. If you want to go to that party or game, you may need to start rewriting your notes earlier than normal to make sure you have enough time to finish before going out. Also, there will be several big assignments due for other classes throughout the semester, you'll need to be prepared for catching up on those notes you couldn't rewrite the day after class. (Don't get more than a class or two behind or you'll defeat the purpose of rewriting.)

C. Turn off your phone. You can survive an hour or two without reading all those awesome texts and facebook postings coming in. A 30 second distraction actually amounts to much longer, because it takes time to get back to where you were before you were distracted. Every time you break focus, you are back to a more superficial level of learning and it takes some time to get back to that deeper level.

D. When it's test time, you'll find it much easier to study. The material is already there in your mind because you've been through it at least twice already. You may have to pull an occasional all-nighter, but it will be different than the cramming you did previously.

Notes for a recently submitted grant

from a relevant paper.

E. For the record, I still use these techniques to prepare grants and papers (see photo). I do a lot of background reading and have notebooks dedicated to taking notes on the papers, complete with different colored pens. This allows me to make connections and think about the material in a much deeper way than I would be able to otherwise. Same for seminars I attend, I bring a notebook.

With those words of advice,

Good luck and have a great semester!

Poor Communication of Essentially Good Research

It is no surprise to see a press release on scientific research that inflates the conclusions of the study or its potential impact. But usually the basic biology is correct, not so with the press release I read today. (I thank the twitterverse for bringing this to my attention.) Since I'll go through the press release paragraph by paragraph, you can thank the twitterverse too,

The release starts out well enough, but quickly goes off the rails. In fact, the writers couldn't get out of the first paragraph, which is also the first sentence, without stating half-truths.

Targeting serious and sometimes deadly fungal infections, a team of researchers at Worcester Polytechnic Institute (WPI) and the University of Massachusetts Medical School (UMMS) has discovered a chemical compound that prevents fungal cells from adhering to surfaces, (This would be a great place for a period.) which, typically, is the first step of the infection process used by the human pathogen Candida albicans (C. albicans). (Red note by AbC.)

The point being made is that 'adherence' is the first step of the infection process. Whatever the hell 'infection process' is escapes me, but it does sound pretty awesome and scary. However, the press release completely misses a key point, Candida albicans is a commensal in humans. C. albicans is easily culturable from 60% of all people and is almost certainly found in all humans. Let me be clear, C. albicans causes serious and sometimes deadly infections as noted in the first line of the press release. However, in the vast vast majority of people, C. albicans is not a problem. Herein lies the problem or obvious question ignored in order to write overimpactful press releases. Does C. albicans only adhere to surfaces during infection? Does C. albicans in most people simply float free in saliva, gastric juices, or vaginal fluids? (The answer to these questions is 'No'.)

After screening 30,000 chemical compounds in a series of tests with liveC. albicans, the team found one molecule that prevented the yeast from adhering to human cells or to polystyrene, a common plastic used in many medical devices. Named "filastatin" by the researchers, this molecule now emerges as a candidate for new anti-fungal drug development and as a potential protective material to embed on the surfaces of medical devices to prevent fungal infections.

This is all pretty good. It hits on the major finding and the potential impact of the research.  What is not explicit here, but comes up later, is that the major source of C. albicans in deadly systemic infections is contaminated medical devices, like catheters.

The team, led by co-principal investigators Paul Kaufman, PhD, professor of molecular medicine at UMMS, and Reeta Rao, PhD, associate professor of biology and biotechnology at WPI, reports its findings in the paper "Chemical screening identifies filastatin, a small molecule inhibitor of Candida albicansadhesion, morphogenesis, and pathogenesis," published online in advance of print by the journalProceedings of the National Academy of Sciences (PNAS).

Again nothing to complain about regarding the press release here. We are basically describing the leaders of the research teams and the source of the article. I do have an issue with part of the title of the paper 'a small molecule inhibitor of...morphogenesis...' The title suggests that filastatin inhibits the formation of cell structure or shape. In actuality, the drug inhibits the ability of yeast cells to form filamentous cells. This is a morphological transition, but it does not encompass the entirety of C. albicans structure and shape. A yeast cell making more yeast cells is an example of morphogenesis. The abstract makes this point clear, but the title is a bit colloquial. This is a problem in the field and not specific to the authors, I have probably used similarly short-hand. 

"In humans, the most widespread fungal pathogen is Candida albicans, which is also one of the most frequent causes of hospital-acquired infections," the authors write. "We conclude that filastatin is not toxic to the human cell line under our assay conditions, but is unique in that it can impair fungal adhesion both to inert surfaces and to cultured human epithelial cells."

I am not sure in what context filastatin is unique as a quick literature search revealed HIV-protease inhibitors, a 23 amino acid peptide, cranberry derived compounds, as well as antibodies have all been reported to inhibit C. albicans adhesion. (This is an issue of the authors inflating their work not of the press release writer(s).)

Infection by C. albicans causes common chronic illnesses like thrush and vaginitis, which affect millions of people globally each year and are not easily cleared by the handful of anti-fungal drugs now available. While most fungal infections do not cause serious harm, if one spreads to the bloodstream it can be deadly.

All good. Minor issue with referring to thrush and vaginitis as chronic illnesses as the vast majority of cases are not chronic.

Hospitalized patients with catheters or central intravenous lines are at risk as the fungi can grow on those devices and enter the body. Similarly, patients with implanted medical devices like pacemakers or prosthetic hips or knees are also at risk if the implant carries a fungus into the body. Also, people with compromised immune systems are at greater risk for serious fungal infections. Because of the lack of effective drugs against C. albicans and other pathogenic fungi, the mortality rate for systemic fungal infections is between 30 and 50 percent.

Again all good, but now we come to it. The paragraphs of FAIL.

Typically, a blood stream infection of C. albicans or a similar pathogen begins with fungal cells attaching to a surface—a catheter, for example, or epithelial cells lining the mouth—to form what is known as a biofilm. Next, the ovoid shaped yeast cells morph into an invasive filamentous form, extending pointed filaments that penetrate and damage surrounding tissues. In the current study, the team found that filastatin curtailed both steps: it largely prevented C. albicans from adhering to various surfaces, and it significantly reduced filamentation (inspiring the name filastatin).

First of all, we have established that C. albicans adheres to things independently of infection. So a basic part of C. albicans lifestyle is to adhere to things, things like epithelial cells which are the structures C. albicans normally finds itself on. This is a function of biology not infection.

Second, this press release builds on a dead mythos that yeast cells are commensals and filaments are infectious. This was the conventional wisdom 20+ years ago, but the field has (or has tried to) move on. It is true the filamentous cells do things related to disease that yeast cells do not. Filamentous cells secrete gobs of proteases which help degrade the host tissues. Filamentous cells are invasive. But you know what, yeast cells do things related to disease that filamentous cells do not. Yeast cells do not stimulate the immune response as much as filamentous cells do. Yeast cell populations grow much faster than filamentous cell populations. Yeast cells can readily disseminate throughout the body via the bloodstream, filamentous cells cannot. But ignoring these facts, there are basic predictions we can make based on the press release premise. For example, we should not observe filamentous cells in non-diseased individuals, but we do. We should not observe yeast cells during bloodstream infections, but we do. Other fungal pathogens should show similar morphological transitions, they don't. In fact, Candida glabrata, the second most common Candida species causing human disease only grows in the yeast form.

Third, filastatin inhibits adherence and filamentation. This becomes problematic because those who work on C. albicans are already aware that filamentous cells are extremely adherent, but yeast cells are not. Thus, if you inhibit filamentation you by definition inhibit adherence. However the press release tells us why this result is really the SHITZ (emphasis mine).

As a next step, the team tested filastatin's impact on C. albicans cells that had grown unfettered in test wells and had already adhered to the polystyrene walls. When the compound was added to the culture mix, it knocked off many of the fungal cells already stuck to the polystyrene. The inhibitory effects of filastatin were further tested on human lung cells, mouse vaginal cells, and live worms (C. elgans) exposed to the fungus to see if it would reduce adhesion and infection. In all cases, the novel small molecule had significant protective effects without showing toxicity to the host tissues.

Based on the bolded statement, you now think 'HOLYFUCKBALLS, that's interesting,' because the cells were already stuck to something. While the press release is technically correct, the implications are flat out wrong. First, in almost every experiment the drug was present throughout the experiment, in other words as soon as the cells were added, aka before adherence occurred. Thus, inhibition of filamentation is an obvious and unsurprising likelihood to explain these data. Second, in the one experiment referred to above, the effect of the drug was minor (see data from paper below). Even this minor effect could be an attribute of growth. 

From PNAS Figure 2D

In one case, the black bars, the cells were kept without (left) or with (right) drug for 8 hours and there is a profound difference between the two conditions. In the other case, the striped bars, the cells were grown for 4 hours and then drug left out (left) or added (right) and cells grown an additional 4 hours. Both samples lacking drug are similar (compare the leftmost of the black and striped bars). The authors suggest that the reduction observed 4 hours with drug (rightmost striped bar) represents a reversal of adherence, but this conclusion is not necessarily the best. How about growth after 4 hours is always ~8000 Fluorescence units, but when drug is added no further growth is observed. Knowing what the Fluorescence looked like at 4 hour in this experiment is lacking and important. Note the press release states the drug did something active, 'it knocked off many fungal cells already stuck to the polystyrene.' I say the drug inhibited growth or prevented additional adherence, like by preventing additional filamentous growth as observed in all the other experiments.

Research is now focused on teasing out the precise molecular mechanisms filastatin uses to prevent adhesion and filamentation. "We need to find the target of this molecule," Rao said. "We have some good leads, and the fact that we aren’t seeing toxicity with host cells is very encouraging, but there is more work to be done."

Why does the target of filastatin need to be found? It seems important, but I am not sure why and I wonder if a general audience reader knows why.

Additional studies on filastatin are underway at both WPI and UMMS. "The molecule affects multiple clinically relevant species, so we're pursuing the idea that it provides a powerful probe into what makes these organisms efficient pathogens," Dr. Kaufman said. "In this era of budget gridlock in Washington, our ability to get funding from the Center for Clinical and Translational Research at UMMS to support this work was essential for allowing us to pursue our ideas for novel ways to approach this important class of hospital-acquired infections."

What makes these organisms efficient pathogens? These organisms are shit pathogens. Virtually no one had issues with deadly fungal infections before the 1960s and even after 1960 that number was minute. It is only recently that these organisms have risen to the forefront of importance and it's not the organism that has changed. Rather it is the host, us, or more specifically modern medicine that is the culprit. Now we have a large and growing population of people who are immunocompromised because of cancer therapy, organ transplants, HIV, even extreme old age. But as noted 'in this era of budget gridlock in Washington,' we must inflate and oversell our studies 'to get funding from the Center of Clinical and Translational Research....' There fixed it.

Look, I agree filastatin is an interesting molecule worthy of additional research and development as a coating for catheters and other medical devices. These are some interesting studies and the fact the drug does not appear to be toxic to human cell lines and in a mouse vaginal model is extremely encouraging. It is important to know how this drug acts systemically in a mouse because the bloodstream infections are the critical ones to combat. But these studies are an important first step. 

The project was also funded by a grant from a WPI/UMMS pilot program established to promote collaborations between researchers at the universities to advance early stage translational research. "Joint research programs, such as the pilot program between our institutions, are central to WPI's work in the life sciences," said Michael Manning, PhD, associate provost for research ad interim, at WPI. "As this collaboration between Professors Rao and Kaufman demonstrates so well, both institutions can leverage their complementary expertise for the ultimate advancement of scientific discovery and public health."

Terence R. Flotte, MD, UMMS executive deputy chancellor, provost, and dean of the School of Medicine, agreed. "The faculty of UMass Medical School and WPI possess scientific knowledge and expertise in disciplines that complement each other," he said. "The creation of this type of multidisciplinary team collaboration between the two universities allows us to work synergistically to solve problems important for improving human health."

Synergistically, √. Novel, √. Translational, √. Paradigm shifting, oops missed that one.

I feel bad, slightly, picking on this press release and the author statements. We often give answers to question that upon reflection wish we had a do over. However, this is my field of interest and C. albicans is the organism I primarily study, so I am intimately familiar  with the issues in the field. I am sure the approach I take here could be applied to many press releases. I would like us, as scientists and communication officers, to work harder at getting the stories out, keeping it interesting and informative without jumping the shark. This likely requires some back and forth between the scientists and communications people with a touch of editorial oversight by an independent scientist.

On the Importance of Science Communication

One thing we often try to teach our graduate students and post-docs, and I believe to a lesser extent our undergraduates, is the importance of being able to communicate science to a general audience. Usually this training is done as part of a research program, which I thin is a mistake. Undergraduates, who are our largest population of trainees, may not be in a research laboratory or not have a laboratory experience that promotes interaction with the public. I believe one of the greatest societal services we (college/university professors) can accomplish is to teach undergraduates how to explain science to society in a competent and confident manner.

In one of my courses students present an aspect of the paper to the rest of the class. However, based on some student feedback and my own goal of teaching promotion of science to the public, this year I am having the student presenters give a 30 second synopsis of the paper that explains the main findings and why these findings are important to a lay audience.

Why is this important? The answer to this question is the point of this post. I spent most of today traveling to a scientific meeting in Calgary. For eight hours, I was in an airport or on an airplane. During the last leg of my travel, which was the longest, a woman sat next to me. We each had our own books and I had my iPod so there was no communication between us. At least there was no communication for most of the flight. Towards the end of this leg, a flight came around offering coffee, to which I said 'yes, please'. After getting my coffee, I asked my aisle mate, if she was worried about getting hot coffee spilled on her when the flight attendant was pouring it. She noted it was a slight concern....and that broke the ice. Shortly thereafter she noted the book I was reading and asked if it was related to a book she read several years previously. I noted that it was and that I had read the same book which got me interested in the series. After some additional small talk, we got around to where we were headed and the purpose of our trip.

I said I was traveling on business and going to a scientific conference...

"What do you do research on?" she asked.

"A fungus that causes disease in people." 

"Which one?" 

"Candida albicans, it lives on the skin and in the intestinal tract of everyone, and is the cause of yeast infections in women." was my standard reply. Maybe you're thinking that bringing up yeast infections (shorthand for vaginal yeast infections) is not the best approach. I disagree, basically all women know what yeast infections are (as do most adult men), and most are familiar with the name Candida albicans. By coming out and saying it directly, you are not unintentionally patronizing the person you are talking to, plus the vagina is not as scary and taboo as society wants us to believe. 

"I know about Candida, is that serious?" she asked. 

"Not really, it lives in all of us normally, but if you are immunocompromised..." 

"I have a friend who had an organ transplant and the doctors were worried about Candida..." 

"Yes, people who are undergoing chemotherapy or had an organ transplant are at risk from a Candida infection. It's a big problem in these patients, but not so much for healthy people, although it can be an annoyance occasionally in some women."

She then started asking me about Candida and why it caused disease. Eventually she told me about her 7 year old son who was suffering from a fungal infection in the cornea of his eye. She told me what the doctors had said the cause was and how to treat it and asked me what I thought. I, of course, told her I was not a medically trained doctor, but that what she told me was in keeping with my knowledge. Then we started talking about these different fungi and how they caused disease and even were able to grow within us. She clearly had some background knowledge in biology, but the important thing is that we were able to talk. I was able to answer some questions and tell her some interesting things she hadn't heard before, and I was able to hear about her son and understand the anguish that comes with being a parent concerned about their child, even when that anguish was over an understood and readily treatable disease.

If I had gone into extreme depth and detail, she may have been turned off, ending our conversation. Maybe not, but we did in fact have a great conversation for the last part of our journey. I was at ease and ready to talk about my research with a lay person. The same could not be said of my interaction with the customs official. When asked abut my business in Canada, I said to attend a scientific meeting. This was fine, but when I was asked about what the meeting was about, what I worked on, and what I was presenting, my answers got more and more detailed and specific. I answered like someone talking to a person in my field and not an immigration officer. I realized I was not making sense, and tried to use less specific language, but it made things worse trying to go back and forth between lay person language and specialized scientist language. My problem here was dealing with a person in authority, which I associate with a leader in my field, not a person ensuring that people are entering their country legally.

So in the course of a few hours, I think I was an effective science communicator 1/2 times. Clearly there is room for improvement. However, these interactions serve to show how easy it is to engage he public on scientific issues and how important it is to be an effective science advocate. We should be spending as much time teaching our students how to communicate science as we do teaching them the facts they need to know. If we continue to fail informing the public, there will soon be no reason to teach the facts.

Happy Birthday Dr. Franklin

Google celebrates Rosalind Franklin's 93rd birthday! Hurray for Science and Hurray for Google's celebration of Scientists!

In Defense of Ignorance: Heffernan Edition

An article making the rounds on Yahoo does a great job of reinforcing societal loathing of science. You know that stupid activity being done everyday by jerk wads and has given us things like clean water, antibiotics, the ability to feed 7+ billion people, wifi, etc.

Heffernan is not a scientist nor someone in a technology field and that's ok. Most people aren't.  But like most people, Heffernan likes the benefits provided by science and technology. For instance you might note she is publishing an article at Yahoo that was certainly written on a computer. She also admits to owning a smartphone. Clearly this is someone who embraces technology, even if she doesn't understand how it works.

She gives up the game in the first paragraph.

As a child I fell in love with technology, but I have to admit I never fell in love with science. I kept hoping that messing around with Macs and Atari and eventually the Internet would nudge me closer to caring about the periodic table, Louis Pasteur and the double-blind studies that now seem to stand for science. As it was, I only cared about the double-blind studies that told me what I wanted to hear—that potatoes are good for you or that people of my height are generally happy—and I liked the phrase “double-blind” when it was on my side because it meant “true” and “take that.” (emphasis mine)

See, she admits to not falling in love with science and what science gave us. She only cared about science when it told her what she wanted to hear. Someone should probably inform her that that is not how science works. That is actually more like how religion works. Interestingly, throughout the early parts of the essay, Heffernan establishes religion as being oppressed by science and those evil practitioners of science. And as you might expect, Heffernan ultimately admits to being a fundamentalist Christian. Of course she is not direct about and does an end around to try to hide her intentions from her 'dear readers.' (As a person who admits to only caring about information that reinforces what she already believes, she likely assumes most people are like her and will not think too deeply about what she is doing.)

Upon admitting that she is a creationist, she tells us that the last person she actually said that to stormed off in a huff. I suspect that is bullshit, a lie, a fabrication. I could be wrong, but I am sure there is more to the story than being said. As a rational skeptic and scientist, I think it is more likely she is lying or leaving out important information than a person up and left a restaurant simply because she said she was a creationist. Based on my reading of Heffernan, I do not think I would like hanging out with her, but if we were at a restaurant having an appetizer and a cocktail, I would still not up and leave simply because she admitted to being a moron.

Upon telling us she read many books, which she seems to read for pleasure and style focusing on the prose not the content, she then states 

I still read and read and listen and listen.

Remember this is the person who tells us she only cares about things that agree with what she wants to hear.

And I have never found a more compelling story of our origins than the ones that involve God.

Ok, for a humanities Ph.D. trained person complaining about scientific prose that is one god-awful sentence. 'than the ones' suggests she is lumping all magical creation stories into this sentiment. Basically suggesting that any mythology is better than reality. But no. Heffernan is clearly only talking about Genesis as interpreted the way she interprets it. We don't need to consider all those silly New England theologians who believe Genesis is metaphor. We can discount all those Catholics and other Christian denominations that believe Genesis is not true, because she has it all figured out.

Heffernan then tries to bring up the fact that science is always changing (it's not, at least not how she believes it does). As we get more information we understand the universe in which we live better, thus we revise our conclusions. Because of this cars get 40+ mpg instead of 2 mpg. Because of this we get more food per acre than we used to. Because of this we have the internet. I don't see Heffernan lamenting the fact she has to upload a crap pile of an article to Yahoo instead of using a good old fashioned telegraph to transmit her thoughts across the country. Stupid science.

See the bible never changes. The book of Genesis is still around in its original form, unlike that pesky science. Genesis has never been translated from the original texts, which we definitely have. And the ideas supported by the bible like slavery and murder of adulteresses have not changed. Ideas that women, even those named Virginia, being responsible for all sin and subject to men haven't changed. Or maybe they have and Heffernan only cares about things that affirm what she wants to hear. But why should I think that.

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It's time to read The Origin of Species....again

I kind of lost the energy to keep up with my Origin of Species (OoS) book club, but I'm restarting it. In part this is to renew my writing here at AbC, but mostly it is to finish reading the OoS. So I have skimmed over chapters 1 through 3 and gone over my notes.

Thoughts on the Prologue.
Thoughts on Chapter 1.
Thoughts on Chapter 2.
Thoughts on Chapter 3.

Now I am rereading Chapter 4 and getting ready to teach incoming College of Biological Sciences undergraduates for 2.5 weeks. Now's you chance to catch up and start. Because I am getting a manuscript to colleagues and teaching a shit ton (by number not weight) next week, the next OoS post will not occur before next weekend. You have time to catch up.

This is the OoS I am reading (it's the 6th edition and it does matter, at least somewhat)

Happy 130th Mr. Kafka

Google celebrates Franz Kafka's birthday. The Trial is one of my favorite literary novels and although I like The Metamorphosis, I don't think it's as good as The Trial.

Google