Sam Brownback should not be president

Sam Brownback, Republican senator from Kansas and a presidential hopeful, gets some free publicity with the publication of his op-ed piece “What I think about evolution” in today’s New York Times. Brownback was one of the three Republican presidential candidates who didn’t raise his hand when asked at a debate if he believed in evolution.

The short summary of Brownback’s op-ed seems to be: science and faith are complementary as long as scientists come up with answers that my reading of the Bible supports.

First, Brownback on the complementarity of science and faith:

“The truths of science and faith are complementary: they deal with very different questions, but they do not contradict each other because the spiritual order and the material order were created by the same God.”

This sounds a bit like Stephen J. Gould’s non-overlapping magisteria (NOMA). The merits of this are strongly debated. Personally, I waffle. The bigger problem with Brownback’s statement is that science and faith absolutely do contradict each other. If faith is telling you that the planet is 6000 years old, then you have a very real conflict with science. Moreover, this seems to represent an over-reaching of faith into the magisterium of science. If you want to know how the natural world (the ‘material order’ according to Brownback) works, ask a scientist, not a priest.

Brownback continues:

“People of faith should be rational, using the gift of reason that God has given us. At the same time, reason itself cannot answer every question. Faith seeks to purify reason so that we might be able to see more clearly, not less. Faith supplements the scientific method by providing an understanding of values, meaning and purpose. More than that, faith — not science — can help us understand the breadth of human suffering or the depth of human love.”

At the risk of sounding uncharitable, what is rational about faith? And what does it mean to say that “faith seeks to purify reason”? Look, I’ll allow that values play a role in making all kinds of decisions – we’re not robots after all. But I’m not so sure I like the notion that reason has to be passed through a purifying filter of faith.

So much for the marriage of faith and reason. Now Brownback gets to what science is OK in his mind:

“If belief in evolution means simply assenting to microevolution, small changes over time within a species, I am happy to say, as I have in the past, that I believe it to be true. If, on the other hand, it means assenting to an exclusively materialistic, deterministic vision of the world that holds no place for a guiding intelligence, then I reject it.”

Is this how faith purifies science: if science contradicts my faith, then the science is wrong? (Didn’t St. Augustine say the exact opposite?)

“Biologists will have their debates about man’s origins, but people of faith can also bring a great deal to the table. For this reason, I oppose the exclusion of either faith or reason from the discussion. An attempt by either to seek a monopoly on these questions would be wrong-headed. As science continues to explore the details of man’s origin, faith can do its part as well. The fundamental question for me is how these theories affect our understanding of the human person.”

Just what, exactly, is faith’s part in exploring human origins? This just sounds like the equal time argument to me. Go play in your own magisterium.

“While no stone should be left unturned in seeking to discover the nature of man’s origins, we can say with conviction that we know with certainty at least part of the outcome. Man was not an accident and reflects an image and likeness unique in the created order. Those aspects of evolutionary theory compatible with this truth are a welcome addition to human knowledge. Aspects of these theories that undermine this truth, however, should be firmly rejected as an atheistic theology posing as science.”

The first couple of sentences remind me of something in Daniel Quinn’s book Ishmael. It’s essentially a retelling of the history of life (as told by a jellyfish) except that it ends, “and then jellyfish appeared.” (I’m paraphrasing…I don’t have the book in front of me.) Obviously, if you look back on a path that you’ve traveled, it will look like that path leads to you. But the notion that the path was preordained is ridiculous. There is no basis for saying that humans are not an accident. This underscores why faith is so detrimental to knowledge: Brownback begins with an untried proposition and he rejects any evidence that puts his proposition in doubt. Knowledge stagnates in such an environment. And read the last two sentences by Brownback again. Can you get more anti-intellectual than that? Have people learned nothing from the colossal missteps of George Bush caused by his lack of respect for actual information about the real world? Believing something to be true in the face of evidence to the contrary is not a laudable position to take.

For other views on Brownback's comments: try Forms most beautiful , Thoughts from Kansas, and Pharyngula

Why we're sometimes thick skulled

In the May 18, 2007 issue of Science, Paul Bloom and Deena Skolnick Weisberg write a short review about why adults sometimes have trouble accepting claims made by scientists. Specifically, they apply findings from developmental psychology to explain the resistance to scientific claims based on two lines of research dealing with “what they [children] know and …how they learn.”

The first line of research has uncovered naïve conceptions that children have about the world. These are things that come pre-wired (if I understand things correctly). Bloom and Weisberg write:

"These intuitions give children a head start when it comes to understanding and learning about objects and people. However, they also sometimes clash with scientific discoveries about the nature of the world, making certain scientific facts difficult to learn.”

This sort of thing comes up a lot regarding the teaching of science – the notion that before you can teach certain topics, you have to understand and deal with the preconceptions that students have about things. If you don’t, students might learn the material as you present it (and they may even give the correct answers on an exam), but if you ask them two weeks later, they will revert to their preconceived idea about the concept. In a video called “A Private Universe,” somebody went around asking Harvard graduates (immediately after commencement, I think) questions about science. One question had to do with where the matter to make plant tissue (wood) came from. Almost all the students said it came from the soil. Actually, it comes from CO₂ in the air. (Makes you wonder about all those student loans you took out to pay the Ivy League tuition, huh? D’oh!) The point is that these students had a preconception, sat through some biology classes that taught something different, and came away without learning anything because the preconception wasn’t dealt with.

Bloom and Weisberg also note that children have a natural inclination to see things “in terms of design and purpose.” They continue:

“For instance, 4-year-olds insist that everything has a purpose, including lions (“to go in the zoo”) and clouds (“for raining”), a propensity called “promiscuous teleology” (15).”

David Gilbert, a Psychology professor at Harvard, wrote a nice little essay at Edge called “The Vagaries of Religious Experience” that dealt with this same sort of thing. (Not promiscuous teleology per se, but how our minds interpret certain events. I’d summarize his ideas, but you’re much better off reading his short essay.)

I wonder how much of this goes back to our ability to see cause and effect? We see what we consider an effect – the universe – and just naturally insert the cause – a bearded guy with grey hair that lives in space.

The second part of Bloom and Weisberg’s article deals with how we learn things. If someone makes a particular claim of truth, how do we deal with it?

“When faced with this kind of asserted information, one can occasionally evaluate its truth directly. But in some domains, including much of science, direct evaluation is difficult or impossible. Few of us are qualified to assess claims about the merits of string theory, the role of mercury in the etiology of autism, or the existence of repressed memories. So rather than evaluating the asserted claim itself, we instead evaluate the claim’s source. If the source is deemed trustworthy, people will believe the claim, often without really understanding it.”

Richard Dawkins wrote an essay published in his book “The Devil’s Chaplain” that addressed the difference in accepting a scientific claim vs. a religious claim, for example. How are the two different? Why is one appropriate (at least sometimes) and the other an indefensible appeal to received wisdom? Dawkins points out that although you, personally, may not independently verify a given scientific claim, it is possible to verify it. A scientific claim is public and open to criticism from anyone who wants to put in the time to verify it. Not so with a pronouncement by the Pope. Born of a virgin? If you say so.

Bloom and Weisberg conclude:

“These developmental data suggest that resistance to science will arise in children when scientific claims clash with early emerging, intuitive expectations. This resistance will persist through adulthood if the scientific claims are contested within a society, and it will be especially strong if there is a nonscientific alternative that is rooted in common sense and championed by people who are thought of as reliable and trustworthy.”

What we need to do now is learn how to break this resistance. Most of the education literature I’ve read suggests that you need to induce “cognitive conflict” in the students. They have to come face to face with the inadequacy of their preconception, then be shown how another explanation is better suited to explaining reality. Unfortunately, this is just very hard to orchestrate, especially with pressures to “cover the material.” And for some people, it's likely true that the only way to replace an emotionally held belief is with another emotionally held belief.

Note: a link to a pdf of the Science article is available online at Adventures in Ethics and Science. A modified version of the paper is available online here. PZ Meyers at Pharyngula also blogs about this article.

Hormone replacement therapy and NSAIDs

I’ll get back to glucagon regulation in a bit. I just got around to reading the latest articles published by PLoS Medical and wanted to mention the findings of an observational study that looked into potential interactions between hormone replacement therapy and traditional nonsteroidal anti-inflammatory drugs (NSAID). (Traditional NSAIDs include things like ibuprofen and naproxen, but aspirin was excluded. Selective NSAIDs like Vioxx were also excluded because they apparently weren’t available in the United Kingdom during the period studied.)

You might recall that hormone replacement therapy made the news in 2002 when a study by the Women’s Health Initiative (WHI) was shut down early because of unacceptable increases in breast cancer. I think there was concern about breast cancer going into the study, however. A more surprising finding was that coronary heart disease (CHD) was higher in women undergoing hormone replacement than those taking a placebo. This was surprising because pre-menopausal women have a much lower risk of heart disease than men, and this difference is thought to be due to some cardioprotective action of estrogen. If estrogen provides cardioprotection, then why were post-menopausal women on hormone replacement at a slightly greater risk for coronary heart disease than women taking a placebo?

One reason, known (or at least suspected) for some time, was that progesterone opposes the cardiovascular benefits of estrogen. (Progesterone – as medroxyprogesterone – was increasingly added to the hormone replacement mix because of an increased risk of uterine cancer. However, a 2002 editorial in the Journal of the American Medical Association cited statistics that in 2000, twice as many prescriptions were written for a pill with just estrogen than a pill with both estrogen and progesterone.)

The article in PLoS Medicine outlines another possibility. This study, which was not a randomized and controlled trial, searched a British database and looked at risks for heart attacks among women who had received (or were still receiving) hormone replacement therapy and those who hadn’t versus a group of “control” patients. This group isn’t really a true control, they were just randomly drawn from some population and matched to the study group by some criteria. They also looked at the use of NSAIDs for those same women.

So, we’ve got two groups of women: our study group and the controls. The authors compared the risk of heart attack (acute MI – myocardial infarction – to be fancy) for women that had undergone hormone therapy (HT) and those that hadn’t, as well as whether they took NSAIDs or not. The relative risks are shown in the table below (as odds ratios). An odds ratio of 1 indicates equal risk; less than one, less risk; and greater than one, a greater risk. The data indicate that the risk of heart attack is reduced for women currently undergoing hormone replacement, but that risk increases for women that are currently undergoing hormone replacement therapy and also taking NSAIDs.

[Click on the image for larger view]

Enough statistics. What’s the physiological reasoning behind this? Like most everything else, it comes down to proteins. Specifically, enzymes known as cyclooxygenases. There are 3 kinds: COX-1, COX-2, and COX-3. The enzyme of prime interest is the COX-2 protein. This enzyme catalyzes a reaction that produces a molecule called prostacyclin (PGI₂). This molecule is a prostaglandin. PGI tends to decrease platelet activity (platelets play a role in blood clotting) and increase the diameter of blood vessels (vasodilation). Estrogen increases the amount of prostacyclin by activating the COX-2 enzyme. Traditional NSAIDs inhibit cyclooxygenases. Inhibiting COX-2 directly opposes the action of estrogen.

This doesn’t mean that women going through menopause should run out and start hormone replacement therapy. The authors of the study are quick to note its limitations. Chiefly, it wasn’t a randomized controlled trial. The data they analyzed wasn’t collected with this issue in mind, it was just a database of patient information. In other words, these data are suggestive but require more controlled studies to draw more definitive conclusions. In any case, hormone replacement therapy still increases risk of breast cancer, so any potential benefits related to minimizing the symptoms of menopause, heart disease or osteoporosis have to be weighed against the risks.

References:

1. Garcia Rodriguez, et al. (2007). “Traditional Nonsteroidal Anti-Inflammatory Drugs and Postmenopausal Hormone Therapy:A Drug–Drug Interaction?” PLoS Medicine
2. Writing Group (2002). “Risks and Benefits of Estrogen Plus Progestin in Healthy Postmenopausal Women: Principal Results from the Women's Health Initiative Randomized Controlled Trial” JAMA 288(3): 321-333. Available free with registration.
3. Fletcher and Colditz (2002). “Failure of estrogen plus progestin therapy for prevention.” JAMA 288(3): 366-368. July 17. Available free with registration.

Devilish details of glucagon regulation

One of the difficult things about teaching science (or any subject, I imagine) is deciding which details to leave out. On one hand, it’s often the details that make things interesting. On the other hand, each layer of complexity often requires more background for it to make sense, and the amount of information necessary for comprehension expands exponentially. As a result, we often present things as cut and dry when they are anything but. I imagine that this often gives students the impression that everything is known. Given that I’m teaching subjects that are a bit outside what I studied in graduate school, I sometimes get to experience this myself as I delve into the research literature. I’m often surprised to find out what we don’t know. As an example, take the regulation of the hormone glucagon.

Glucagon is a hormone produced and secreted by α-cells of the pancreas. The basic role of glucagon is to prevent low blood sugar – it helps maintain adequate levels of glucose in the blood. In effect, glucagon opposes the action of insulin. Insulin decreases blood glucose, glucagon raises it. It does this by triggering the release of glucose from the liver.

According to a common anatomy and physiology text (Tortora & Derrickson):

Decreased blood level of glucose, exercise and mainly protein meals stimulate [glucagon] secretion; somatostatin and insulin inhibit secretion.

From reading that, you might think the regulation of glucagon seems pretty straightforward. But if that’s true, then why did the Endocrine Society publish an article earlier this year by Jesper Gromada and colleagues titled “α-Cells of the Endocrine Pancreas: 35 Years of Research but the Enigma Remains.” (The paper is available online for free as an “author manuscript pdf” here.) Clearly, things aren’t as cut and dry as the textbook leads one to believe.

So, what do we know about glucagon regulation? Before I answer that, perhaps I should mention why this is of anything more than academic interest. If you follow the news, you’ve probably heard discussions of a diabetes epidemic. NPR recently broadcast a story about type 2 diabetes showing up in people in their teens and twenties, much younger than once was common. Traditionally, diabetes is portrayed as a problem with the hormone insulin, but actually, high levels of glucagon also play a role. Moreover, problems with glucagon regulation in people with type 1 or advanced type 2 diabetes lead to problems with low blood sugar (hypoglycemia). In short, being able to control glucagon could help diabetics maintain normal blood glucose levels. (This is important because many of the complications associated with diabetes are a result of chronic high blood glucose.)

Back to what we know about glucagon regulation. From the article in Endocrine Reviews:

The control of glucagon secretion is multifactorial and involves direct effects of nutrients [like glucose and amino acids] on α-cell stimulus-secretion coupling as well as paracrine regulation by insulin and zinc as well as other factors secreted from neighboring β- and δ-cells within the islet of Langerhans. Glucagon secretion is also regulated by circulating hormones and the autonomic nervous system.

Some of that bears explaining. Paracrines can be thought of as local hormones that affect cell types different from the type of cell that made and secreted the paracrine. A regular hormone (as opposed to a paracrine) can be thought of as a circulating hormone – meaning that it circulates throughout the body, not just a local area. β- and δ-cells are other cell types in the pancreas. β-cells release insulin and δ-cells release somatostatin (somatostatin was mentioned in the textbook description of glucagon regulation). Lastly, the islets of Langerhans are clusters of cells including α-, β-, and δ-cells that make up the endocrine pancreas. It’s referred to as the endocrine pancreas because it’s the part of the pancreas that releases hormones (as part of the endocrine system). The rest of the pancreas (the exocrine pancreas) releases digestive enzymes into the small intestine.

If we know all of these things influence glucagon regulation, then what’s the enigma referred to in the article’s title? The uncertainty lies in the relative influence of the factors:

Since the early 1970’s, the mechanism underlying the regulation of glucagon secretion by glycemia has puzzled scientists. The debate continues whether α-cells directly sense and respond to fluctuations in plasma glucose or whether the response is mediated by the autonomic nervous system and/or the paracrine/endocrine effects of secretory products from other islet cell types. Currently, a large body of research favors the latter ‘paracrine/endocrine’ hypothesis.

The ‘paracrine/endocrine’ hypothesis can be summarized briefly as the idea that a drop in insulin triggers the release of glucagon. This portion of the broader paracrine/endocrine hypothesis is often called the β-cell ‘switch-off’ hypothesis because insulin is secreted by β-cells. High levels of insulin inhibit glucagon, so the decline of insulin in the blood will free α-cells from inhibition.

The rest of the paper goes over the evidence for the various controlling factors, explaining why the authors think the ‘paracrine/endocrine’ hypothesis is most likely the major factor regulating glucagon release. One complication seems to be that research conducted on different species can be difficult to compare. Apparently, there are subtle species-specific differences in glucagon regulation. Just because α-cells of mice react a certain way doesn’t necessarily mean that rats (or humans) will too. So, research on one organism doesn’t necessarily translate perfectly to other organisms.

Having written all this, however, I haven’t really gotten much beyond what the textbook said. (Perhaps a good indication that the extra detail isn’t worth going into at the level of class I teach.) But there is something that an inquiring mind still might be wondering: How does insulin prevent the α-cells from secreting glucagon?

This post is already far too long to delve into that in much detail, but the CliffsNotes version is this. The membranes around cells are impermeable to ions like potassium (K⁺), sodium (Na⁺), and calcium (Ca²⁺). It’s still possible for these ions (and others that I haven’t named) to enter cells, but they need passages (called ion channels) through the membrane. Using these channels, cells can control which ions get in and which ions get out. In doing so, the cells set up concentration gradients. For example, K⁺ ions are generally more abundant inside cells than outside them. The reverse is true for Na⁺. A result of this is the generation of an electrical potential across the cell membrane. Changes in the electrical potential can trigger changes in the activities of a cell. (A nerve impulse – the transmission of an action potential – is an example of what can happen when the electrical potential of a cell changes.)

So, to get to the point, insulin opens an ion channel in the membrane of α-cells. The opening of this ion channel changes the electrical potential of the cell, and this indirectly prevents the vessels containing glucagon inside α-cells from releasing the hormone. When insulin levels in the blood decrease, those ion channels close. This changes the electrical potential of the α-cells, and allows the vessels containing glucagon to release the hormone from the cell.

Next week, when I get some time, I’ll take up a new research paper that deals with this issue and comes to conclusions that differ from the ‘paracrine/endocrine’ hypothesis.

RealClimate posts list of links

The good folks over at RealClimate have just posted a list of links for people looking for information about climate change. In addition to basic information about how climate works, they include links to IPCC reports and rebuttals to common denialist arguments.

Restoration work in ANWR

No, not that ANWR. I'm talking about the Arapaho National Wildlife Refuge in northern Colorado. I and 30-40 other volunteers with Wildlands Restoration Volunteers (WRV) spent the weekend planting willows and building fenced exclosures there.

The willows will hopefully provide habitat for migratory songbirds. Previous use of the land resulted in the loss of willows in some areas, and high elk and moose populations have prevented willow regeneration. This is where WRV comes in. They provided the labor to plant willow cuttings and to fence them off so that elk and moose can't browse them down to the ground. The idea is that the exclosures will allow the willows to grow large enough so that parts of the shrubs will be above the reach of herbivores.

I spent Saturday working on building up a fence around one of the exclosures. I can say that my fence building skills are a bit lacking, but I managed not to hurt myself (or anyone else), so that's encouraging. On Sunday, I planted willow cuttings in pots that some high school students in Walden, CO ("Moose watching capital of Colorado") will take care of before planting them at the refuge either this fall or next spring. Other volunteers planted freshly cut or recently cut willows into the exclosures. It will be interesting to see how well the willow cuttings fare over the summer; I think the survivorship of cuttings is fairly low.

In any case, it was good to be outside after being cooped up in my office all spring. The breeding season for birds on the refuge isn't in full swing yet, but there were some snipe around to add entertainment value to the weekend. I'll add a few pictures of the refuge in a week or two. (See what I mean about behind the curve? I don't even own a digital camera.)

What's in a name?

Let's talk about your large intestine. The basic anatomy is pretty simple: a pouch called the cecum at the proximal end, followed by the ascending, transverse, descending, and sigmoid colons, and finally the rectum. The colon is separated into pouches known as haustra (or haustrations). The pouches form due to contraction of segments of muscle that run lengthwise along the large intestine in three bands (known as teniae coli - pronounced TEE-nee-ee KO-lee). The "churning" occurs when circular muscles (perpendicular to the teniae coli) contract. This smushes the feces around, mashing it against the walls of the intestine. Some of the fecal material will also get squirted a little farther down the intestine.

[The figure is from a nice general Anatomy and Physiology textbook by Tortora and Derrickson, 11th Ed. 2006]

I think that's cool. And, it serves as a nice metaphor for what's likely to go on here: No one should expect much in the way of quality from a blog that is named for a process that churns shit.