As part of our discussions of sociality for Thursday, we'll need this short reading. It suggests that passenger pigeons, which once numbered in the billions, were driven to extinction over the course of a few decades in part because their large population size made them more at risk from extinction than if they had existed in smaller populations. This argument is directly counter to what we normally think of, in terms of how population size relates to extinction risk.
The article references a piece of original scientific literature, linked here:
Good evening all,
As I indicated during class on Wednesday, we will not meet for lecture tomorrow (Friday 22 Nov), but instead will consider some topical science news:
We finished one of our recent lectures by introducing the concepts of gene therapy and cloning. Both of these stem from the application of modern genetic methods, and both exist already - but not without controversy.
As described in your text, gene therapy is an attempt to correct defective or missing genes, by using viruses to insert them into a person's cells. It remains very controversial and of relatively limited use, because many of the risks and complications of the technique have yet to be overcome. Indeed, some human gene therapy trials have resulted in patient deaths, and few would say that the technique has been proven to the point at which broad use is possible. Still, for some people with very specific types of genetic defects, gene therapy has proven to be a lifesaver (literally). We can expect to continue to hear much about gene therapy in the years to come.
Related to gene therapy is the concept of gene editing. The goal of this technique is not to replace defective genes with normal copies, but rather to use enzymes to edit (correct) the defective genes in place (e.g., within the cells of the organism). Gene editing utilizes techniques more recent than those employed in gene therapy, so it has been tested, and used, relatively less. Thus, it was of great surprise to the scientific community last Fall when a Chinese scientist (He Jiankui) claimed to have performed gene editing on several artificially (in lab) created human embryos, and then to have implanted those embryos into female surrogates to carry the developing embryos until birth.
The technique of gene editing is new enough that, one year ago, the ethical guidelines governing its use had not been fully developed. Nonetheless, there was a general understanding that the technique was not to be used in human embryonic tissue, that would result in *all* cells in the body inheriting the edited gene. This understanding was very broad, but was not universal, and scientists in several countries did use (or attempt to use) the technique on human embryos, in the hopes of creating a gene-edited person - a "designer baby".
The scientific backlash against this first report of human embryonic (germline) gene editing was relatively swift, and relatively severe. The scientist who conducted these first trials has been stripped of his research position, and charged with violating his country's biomedical research laws. The infants (twin girls) were reported to have been born, but little is known about their condition. Some researchers have suggested that they are at risk of a shortened life expectancy because of the gene editing. The gene that was edited in these now-children is thought to promote resistance to HIV infection, but also seems to play other roles in cells.
The article I am forwarding here comes from a few months ago, when the investigations into this researcher and his colleagues was still in process. In particular, there were a number of scientists here in the U.S. who were implicated as having supported this work. The researchers here have generally been cleared of any wrongdoing, but significant questions remain about who knew what, and the motivations (money? fame? patent-able technology?) for their involvement. This article also includes links to a number of related stories, of which there are many.
It is worth noting that somatic (non-germline gene editing) is gaining ground as a very powerful and promising technique. This variant of gene editing does not change the DNA in every cell in one's body, but only in focal tissues (such as a single organ) that may be malfunctioning due to a defective gene. Indeed, news reports of the promise of this (more-limited) application of gene editing are also prominent in the recent news, including:
I suspect that your generation will be forced to come to terms with the promises and perils of gene editing - it seems both incredibly promising, and incredibly dangerous at the same time. Having a robust set of regulations and ethical guidelines will be very important. If you were faced with the opportunity to correct a gene in yourself, in a loved one, would you? That's a very difficult question to answer a the moment, as we do not yet have enough experience with the pros and cons of these techniques. But, the evidence is beginning to accumulate...
Here's wishing you all the very best Thanksgiving break - please be safe, rest, relax, eat, and enjoy.
Good morning all,
As I noted on Tuesday, we will not meet for lecture today. We have only one textbook chapter remaining, which we will save for our first meeting after the Thanksgiving break.
Instead of lecture today, I'll offer you a reading instead, one that encompasses several of our recent topics. In recent classes, we have considered the degree of cooperation and conflict between reproductive partners, as well as the signaling that occurs to influence each other. When sexual investment is strongly different between the sexes, we expect that sexual selection can drive exaggerated displays, enhance female 'choosiness' of mates, and promote unequal reproductive tactics. But, curiously, sexual displays also are common within pair-bonded species, in which males and females have equal (or nearly equal) roles and should be in cooperative agreement over parental investment, rather than in conflict. An explanation for this paradox has been lacking.
A very recent paper sheds some light on this problem, and present a mathematical model which supports the idea that inter-sexual signaling displays which originate to exploit a sensory bias in the signal receiver can evolve into a cooperative exchange, suggesting that sexual conflict can morph into sexual cooperation. This has significant implications for parental investment and care, as we've noted that the degree of sexual conflict is one of the primary drivers of sexual dimorphism in parental investment.
This paper was published in the Proceedings of the National Academy of Science (PNAS), our national body of 'science experts'. Election to the Academy is reserved for the top thinkers in one's field, and is a prestigious badge of honor. Their Proceedings journal publishes papers submitted by Academy members, as well as those that Academy members recommend for publication.
If you access this link from an IUP campus computer, you can obtain access to the full article and its associated material, through IUP library subscription. If you try to access the article from off-campus, you will be blocked. I've attached the PDF of the article, just in case.
The math of the authors' model is well beyond us. If we accept their model as being sound, it suggests that, instead of females being 'lured' into over-investment in their offspring by male displays, females instead evolve to require (or at least benefit from) the male display in terms of stimulating female condition/motivation to a level of investment which is optimal for the female (but less than that which is maximally optimal for the male). This causes males to remain invested in the pair-bond and their role in parental investment, and reinforces the pair-bond between mating partners. In a sense, the females are now requiring the males to remain present, remain attentive, and to offer displays, in order to ensure that their female partner is providing enough investment of her own.
As do many science journal, PNAS occasionally offers peer commentary on papers which are especially important, or especially difficult (this one is perhaps both). The associated commentary on this paper (link below, PDF attached), describes this result in the context of dove mating pairs, for which male stimulation of female reproductive condition is a well-understood and very necessary component to the reproductive cycle. Interestingly, as the commentary notes, the capitulation of this male-female exchange may ultimately be female self-stimulation of reproductive condition, a result which has been suggested to occur in doves. That may be the current evolutionary end-point to this exchange, but it also has the potential to serve as a type of an "escape clause", which males may now be selected to exploit. It would be interesting to see how much variation exists in this end-point, and whether males can benefit from females which perform more of their own reproductive stimulation.
I hope that you find this article interesting - it represent a nice, theoretical treatment of a difficult (= interesting) problem, and should set the stage for experimental work to come.
I hope that you all have an excellent Thanksgiving break - please be safe, rest, relax, eat, and enjoy. See you early in December for our last chapter.
Good morning all,
As we remain on-schedule, we will not meet in-person for lecture on Friday (15 Nov). I'd like instead to offer you several pieces of recent science news:
We have considered issues surrounding vaping several times this terms, most recently the alarming and poorly-understood severe respiratory distress that has developed in otherwise healthy individuals who vape. After several months of investigation, our CDC (Centers for Disease Control and Prevention) have released a report that appears to identify the likely cause of his distress syndrome: vitamin E acetate, and oily compound used as a additive in some vaping products.
Vitamin E and its derivatives are lipophilic (fat soluble), which allows them to interact with cell membranes more easily than most biological compounds (which are hydrophilic, or lipophobic). Multiple samples of lung tissue from persons afflicted with vaping-associated respiratory distress have revealed this compound adhering to the lung surface. If you remember our discussions on lung structure/function, we described the exchange surface between the alveoli and the capillaries of the lungs as being as thin as possible (essentially, two single-cell layers of epithelium), to allow as much gas diffusion across them as possible. Now, imagine that same surface covered with a sticky, oily residue - it's easy to see that gas exchange could be severely impaired.
There may be other substances contributing to this distress syndrome, and not all experts are convinced that vitamin E acetate is the culprit. But, the evidence is accumulating, and it appears likely to be the primary cause of the cases investigated so far.
If you do vape, check your products - do they list this as an additive? Can you select other materials that do not?
Juul, one of the largest companies producing vaping products, recently agreed to stop making some kinds of flavored vaping products, as they and others in the industry were being accused of improper marketing toward minors:
One young person with vaping-associated respiratory distress recently was forced to undergo a double lung transplant:
Vaping seems like a habit to be avoided at all costs, in my view. Our lung tissue is simply not designed to handle contact with things other than atmospheric gases. In a few years, we may look back at this as a trend that appeared, and briefly flourished, before its significant health implications were well-understood. I suspect that regulations around vaping will get tighter and tighter, and the available evidence suggests that our public health would be best served by limiting access to vaping materials and more carefully regulating their contents.
Have a great rest of the week - see you on Monday for Chapter 22 (DNA Biology and Technology).
Good morning all,
As I noted in lecture on Wednesday, we remain caught-up with our lecture schedule and do not have chapter assigned for today. So, we will not meet in person for class today; instead I will offer this reading which I would like to you to consider.
In our last lecture, we identified the "cell cycle" as a way to describe the normal lifespan of a cell, from its formation, through its functional life, and then its eventual end. All of our body cells are formed from mitotic cell division to begin their life, and, at the end of their functional lives, many of our cells undergo division themselves, essentially being reborn as two new daughter cells.
We also identified important "checkpoints" in the cell cycle, to prevent cells from speeding through the cell cycle too rapidly. Many of our cells have functional lives of months to years, and without these checkpoints, they would otherwise just divide rapidly into new cells. As we noted, failure to stop at these cell cycle checkpoints can lead to tumors caused by uncontrolled growth; some tumors can become cancers, invading otherwise normal tissues and causing them to become cancerous as well.
As you know, cancer is one of the primary causes of human mortality. We experience a variety of cancers: some are slow to progress, others very rapid; some are essentially benign while others are very deadly; some are highly invasive and others less so. The diversity if cancers we experience and the diversity of tissues that they strike represents one the of the primary difficulties in treating cancer: there is no single cure, for cancer is very diverse in its many forms.
That's not to say that there aren't standardized treatments. Most hospitals have oncology boards that carefully document each occurrence of cancer, and they typically made treatment decisions based upon consultation among a team of physicians, including oncologists, radiologists, surgeons, and others. Much of their decision-making is based upon care standards that have been developed by national and international cancer agencies, such as our own American Cancer Society, which suggests treatment guidelines for the different forms of cancer. Still, we know all too well that curing cancer is difficult, and sometime impossible. The best one can hope for is to eliminate the cancerous tissue to the point at which is cannot be detected, but that is no promise that every cancerous cell has been removed, nor that it cannot re-appear.
Because of the burden cancer poses to society, there are many federally-funded research groups investigating potential treatments. These include
Of course, many of the latest treatments combine multiple approaches, such as using immune cells to target delivery of cytotoxic drugs directly to cancer cells.
In the news this week is report of a promising new approach to treating some kinds of cancer, based upon a metabolic starving of cancer cells. Cells that are rapidly dividing (such as those within a tumor or a cancer) are metabolically very demanding, needing large amounts of fuel. Scientists have developed methods to prevent cells from using glutamine (a glucose-like fuel source), to successfully prevent cancer growth. But, earlier formations of this treatment caused widespread side effects, because the cancer cells were not the only ones being starved of fuel.
In this latest test, the scientists successfully "handcuffed" an inactive form of their drug to allow its focal delivery to cancer cells, where it was "unhandcuffed" into an active form by cancer cell enzymes. There it successfully prevented cancer growth. Even better, this new treatment actually improved immune T-cell function, providing an immunological boost to cancer elimination as well.
These initial studies, done in mice, were very promising. While the road from animal studies to human uses is often long and unsure, this could mark the beginnings of a new generation of cancer treatments that are improved in their focused targeting as well as in their effectiveness at cancer elimination.
We'll talk more about cancer in our upcoming lectures, and I hope that this article will put some of the lecture material into practical context. Cancer touches many families, and does not discriminate by race, class, knowledge, or upbringing. May your generation be the one that finally reduces the impact that it has on our individual and our public health.
Have a great weekend - see you on Monday.
Good morning everyone,
Last week I sent you a news report about the prospect of "sugar taxes", extra monetary tax levied against sweetened drinks as a way to reduce their consumption and to (hopefully) induce some improved health in the persons who might normally consume too much sugar in their diets.
The article that I sent you last week considered some of the potential benefits, and potential difficulties, of implementing such taxes. It also described the limited amount of data available thus far, suggesting that it is still too early to know whether these kinds of taxes lead to health improvements.
In this news this week is report of a newly-released study on this very topic. Here, researchers followed the health of a focal group of 200+ people at the University of California-San Fransisco medical school, where a full ban on the sale of sweetened drinks has been in effect. Researchers report improvements in several subject health measures, including reduced waist size, less belly fat, and improved response to insulin. They suggest that these changes were directly a function of reduced sugary drink consumption in these subjects.
Note that this study described subjects under a workplace ban on the sale of sweetened drinks, not those under a "sugar tax". Here, subjects could purchases sweetened drinks elsewhere, or bring them from home, but could not purchase them at their workplace. This is likely to have a larger effect on consumption than a sugar tax itself, but it does suggest that the benefits of lowering the consumption of sweetened drinks is a very worthwhile goal. The available data suggests that most of us consume too much refined sugar (in some form), which suggests that most of us would benefit by reducing our sugar intake. As we have seen many times during the term, our health depends heavily on the choices we make.
Hope that you are enjoying the weekend - see you tomorrow.
As I mentioned in lecture on Tuesday, we are caught-up with our lecture material and will not meet for lecture on Thursday. Instead, I am offering a reading (attached) that I had described earlier, along with some explanation of one of the more important points described in this study.
Last weekend, I sent to our class description (below) of a recent publication examining behavioral-genetic associations in domestic dogs. I hadn't yet seen the original research when I wrote to you last weekend, but forwarded a news report about it that came from the home institution of the senior author on the study. I described in my message to you that some of the behavioral-genetic associations the authors reported were as high as 0.7, near to the limit of those ever reported for narrow-sense heritabilities of behavior.
Over the weekend, I requested a copy of the actual research paper from its senior author, and, upon seeing it, wanted to offer some interpretation.
Early in the term, in chapter 03, we discussed trait variation within species, and we noted (using the canine example) that artificial selection has created an abnormally high amount of trait variation within the single species of domestic dog Canis lupus familiaris.
In our next lecture (Chapter 04), we discussed behavioral genetics and narrow-sense estimates of heritability, describing the upper limit of such associations as around 0.7. We saw in that same chapter (as well as in later chapters, including Chapter 10) some estimates of narrow-sense behavioral-genetic heritability estimates that all were < 0.3, which is typical.
In this new report, the authors report behavioral-genetic associations that are much higher than those typically reported. How can this be? It stems from the artificial (and unusually large) degree of trait variation within this domestic species.
Typically, when one examines associations between traits within a natural (e.g., not artificially-selected) species, we expect some small, defined range of trait values, with correlation (association) between traits of some relatively low magnitude. Here in my Figure 1, I show the trait values and the within-species bivariate trait association for two (hypothetical) different species, such as a fox and a wolf. Within either species, there is some defined range of values for trait X (such as body length) and some defined range of values for trait Y (such as body mass). In my hypothetical example, these traits are correlated somewhat weakly within species A, and uncorrelated within species B. Notice that the two species do not overlap in trait values - a small wolf is always larger than than a large fox.
If domestic dogs were a natural species, chances are good that their trait values would fall somewhere in between these two species, perhaps closer to the 'wolf' end of the spectrum. Nonetheless, they would be expected to occupy only a small potion of the overall trait ranges.
Now, consider what the authors have done in their analysis. They have considered all domestic dog breeds to be of the same species, a fact that is technically true but which ignores the other fact that their range of trait values is anything but normal. They have analyzed behavioral-genetic associations across breeds within this single species, but here the individual breeds represent much more trait variation than natural species might, as size variation across domestic dog breeds is much greater than size variation across canine species in the wild. When associations are evaluated across multiple species (such as in my hypothetical Figure 2), the associations are often of higher magnitude. In the current study, analysis across the very artificially-distributed dog breeds behaves in the same way, resulting in behavioral-genetic associations much higher that those reported within single, natural species. 13/14 of their within-breed estimates (their Figure 1) are <0.3, just as one would expect.
This study is quite interesting, and represent the application of some very modern techniques (canine SNP chip, anyone?) to this interesting question of the heritability of behaviors. It also serves as a very useful reminder of
- the power of artificial selection - modern dog breeds are estimated to have been developed only over the last 300-500 years. For a natural species to evolve as much trait variation in this short time is unheard of.
- the danger of reliance upon secondary news sources - the original news story that I sent to you accurately describes the gist of this research study, and highlights the very strong associations found. But, it also leaves out enough detail that it is not possible to immediately assess why the associations are of such magnitude.
- the importance of proper modeling of evolutionary constraint - as shown in my hypothetical example Figure 2, trait associations across species can be artificially inflated if simple, linear techniques are used instead of methods that account for shared evolutionary history, such as independent contrasts analysis or nested ANOVA. The authors do have a phylogenetic model for their dog breeds; I am not schooled well-enough in the jargon of their analytical models to know if they have fully controlled for relatedness. Whether they have, or have not, these types of broad comparisons should always be examined with an eye for that type of concern.
- the imperfection of any one study - this is a research report describing one body of work on this topic, and I'm certain we could find other, similar/related studies. Is this study perfect? Certainly not. Is it still interesting, and useful? Absolutely. Any one research study can only advance our understanding incrementally. It's too easy, and too common, to dismiss work outright for containing flaws - it's more important to ask, given such flaws, is there anything that we can learn? The latter approach is more fruitful, and provides a much better return on one's investment of time and effort. Here, the traits with the highest across-breed heritabilities are trainability, aggression, and attachment - exactly those traits we might expect to have been key in the artificial selection/shaping of the human-dog relationship. It's a nice confirmation that these are strongly heritable, in ways that have translated into very powerful differences among breeds.
I've spent perhaps too much time dissecting some of these points, but I do so because they put some of our lecture material into sharp relief. Textbook examples are often too carefully culled to represent cutting-edge investigation; it's both fun as well as useful to see where current researchers in these areas actually are working.
Have a great rest of the week - see you on Tuesday for Chapter 11.
Good evening all,
As I noted in lecture on Wednesday, we remain on-schedule with out lecture chapters, and do not have a chapter scheduled for tomorrow (Friday 25 Oct). So, I would like once again to propose that we do not meet in person for lecture tomorrow, and ask instead that you consider the reading that I am forwarding here.
In our last lecture on the endocrine system, we noted the central role of the pancreas and its hormones in the regulation of blood glucose ("blood sugar") levels. When levels of blood glucose rise (such as when we are absorbing digested sugars into our bloodstream after a meal), the hormone insulin is released by the pancreas. Insulin causes our cells (especially liver and muscle cells) to uptake glucose - that is, to take glucose out of the bloodstream and move it into cells by means of membrane transporters. This allows cells to have glucose available for fuel, and also allows cells to store the excess glucose for later use.
On the flip side, when our blood glucose levels decline (such as when we are several hours past a meal and done absorbing nutrients), other cells in the pancreas release the hormone glucagon, which causes our cells (especially liver and muscle cells) to release some of their stored glucose. Together, the use of the two hormones allows us to maintain a relatively even profile of blood glucose levels.
As we discussed yesterday, when blood sugar levels are not well-controlled, diabetes may result. The primary symptom of diabetes is high (and poorly controlled) blood glucose levels. This causes a number of immediate effects, such as excess urination, thirst, and excessive fat metabolism. Over the long term, high levels of blood glucose are very damaging to our tissues, particularly through scarring of the inner lining of our blood vessels. This can lead to the failure of organs with extensive capillary beds (such as the retina of the eye, and the kidney), and has negative effects on circulation in general, especially in the lower periphery. Persons with uncontrolled blood sugar often suffer poor wound healing (especially of the feet), which can lead to infections and, in some cases, require amputation.
In lecture, we distinguished the two general types of diabetes as well. "Type I" diabetes occurs when our own immune system causes the destruction of the insulin-producing cells of the pancreas. This is classified as an auto-immune disorder, as the disease stems from a problem with the immune system. Type I diabetes is often called "juvenile diabetes", because it is typically first diagnosed in one's youth. It can be treated (usually successfully) with injections of insulin - daily, often multiple times. Insulin pumps can also be used - these are small, battery powered pumps that infuse gradual, small amounts of insulin into a catheter. They are expensive and require maintenance, but are effective solutions for many.
"Type II", or "adult onset diabetes" is more challenging. It tends to appear in people with a combination of risk factors: obesity, poor diet, little exercise. Over time, the cells of their body gradually become resistant to insulin, and stop responding to it. Their pancreas produces normal amounts of insulin, but it is ineffective - blood glucose remains elevated, cells become starved for sugar fuels, and metabolize other fuels (mostly fats). Tissue damage accumulates because of the persistently elevated blood glucose levels. Additional insulin (injections) can help somewhat, but the most effective treatment is improvements in diet and exercise. Some people can almost completely reverse their condition through these lifestyle changes, and nearly everyone can benefit at least somewhat from them.
There is a lot of biology associated with diabetes: its causes, effects, and treatments. There also is a lot of sociology to it as well. Diabetes strikes populations very unevenly, and impacts populations of relatively poorer socioeconomic levels most severely. This is believed to be due to a number of factors, including reduced access to high-quality food, more-restrictive employment and familial responsibilities that limit time to exercise, and less access to good information about health. It has also been suggested that food corporations specifically target these populations with advertising and vendors for "fast food", including soft drinks ("soda", or "pop", depending upon where you were raised).
As a food, soda is of very low quality. It is mostly water, but the other primary ingredients are sugar, and often caffeine. It is also quite acidic, and has quite damaging effects on our teeth. So, why do we buy/drink it? We do so at least in part of because of very successful, and very prominent, advertising, which has allowed some soda companies to develop enough clout that they can contractually deliver soda to schools, hospitals, corporations, and even cities.
Think back to your middle- and high-school education: did soda vending machines exist in your school? Were fountain drinks available over the counter in the cafeteria? For most of us, the answer to these questions is "yes". Do you buy bulk quantities of soda? Do you see others around you who do? Again, for most of us, the answers here are "yes" as well.
In recent years, public health experts have recognized the dangers of over-consumption of soda, and more importantly, the danger of exposure to it in our youth. Too often, adolescents develop a "soda habit", and maintain it into adulthood. This, in combination with other lifestyle choices, has led to skyrocketing rates of juvenile obesity. Even more alarming, "adult onset" diabetes is now diagnosed in adolescents at alarming rates.
So what can be done? Well, the debate rages, because to eliminate soda from communities and diets is not really an option. Soda companies are large, and powerful, and they have an avid user base that wants their products. This is a situation similar to that faced years ago with the tobacco industry: large and powerful corporations, well-paid lobbies, a desirous user base, and mounting evidence of the dangerous health effects of the product. Here, too, numerous solutions were discussed and tried. One of the remedies that seemed to be most effective was to implement larger and larger taxes on tobacco, to the point at which fewer people were willing, or able, to financially support their tobacco habit.
Because of the success of this strategy to reduce tobacco usage, we now live in an era of the "soda tax". The idea here is the same: if a popular consumer product is legal, but unhealthy, tax it in order to reduce the number of people using it, and/or the amounts that they use. This remains a controversial idea. Why should companies producing a legal, desirable product be punished? Is this ethical? Does this not also punish the people that work for them, and their suppliers, accountants, and all of the other people who work in associated jobs? Does this also punish consumers of relatively lower income unfairly, because they would be the ones least likely to be able to afford a price increase?
With soda, too, the application of a tax is more complicated. Tobacco and alcohol are relatively uniform in how they are packaged and purchased, but sugary drinks exist across the spectrum (from soda, to sweetened milk, to orange juice and yogurt). Wait -- aren't milk, orange juice, and yogurt good for us? Well, yes, but less so if they have a lot of added sugar. Should they be taxed less than soda, because they are relatively more healthy? What about sugary cereals and granola bars? What about foods with artificial sweeteners? The lines are less clear in this current health debate.
The news report I am forwarding describes a recent assessment of the effectiveness of "sugar taxes". Dozens of other countries, and multiple large cities in this country, have imposed this tax. They have existed for a relatively short time, so there is much yet to be learned about them. They do appear to cause a drop in soda consumption, but whether that translates into improved health of the population is still to be determined. Not surprisingly, the soda companies have responded aggressively, with a variety of tactics. This battle is far from settled.
The next time you are at the grocery store, ask yourself if you are planning to put soda into your cart. And, look around: how many people do? It's common to see people pushing shopping carts with 6-packs of bottled soda (often multiple of them) draped over the edges of the cart. This behavior didn't exist 10 years ago! Have the bottles changed to make this more convenient? Or are we buying more? Our fast food restaurants and convenience stores offer *enormous* fountain drinks - 30, 40, even 50 ounces at a time! Does anyone rally need that much soda at once?
On this, and all of our topics, stay informed. Healthy habits require good information, and wise choices. There is plenty of information available on the health aspects of soda and its social implications. Be wise shoppers and consumers!
And, have a great weekend. See you on Monday for Chapter 17.
Good morning all,
At several points this term, we have discussed the genetics of behavior, including both the ability of single genes to influence behavior, as well as the heritability of individual behaviors and how traits can potentially be mapped onto phylogenetic histories. In the recent behavioral news is a report of a study that used large databases on dog behavior and genetics to look for behavioral traits that were associated with consistent genetic features. The researchers found >100 potential sites in the genome that were strongly associated with dog breed characteristics, including train-ability, aggression, excitability, and others.
One of the strengths of the method used here was that the researchers restricted themselves to a subset of the data pertaining to purebred dogs. This has the advantage of eliminating cross-breed variation which could dilute the strength of the genetic signals they were trying to detect. Dogs also are an advantageous species for a study like this, because they are popular, have long been bred in relatively pure lines, and have been artificially selected for a range of behavioral characteristics.
Some of the associations reported are quite strong, with heritability estimates as high as 60-70%. Those are very high values, near the limit reported for animal behavior-genetic comparisons. It's also surprising, in that, while this study has several strengths in its design, it also has one specific weakness: the researchers did not have genetic and behavioral information from the same individual animals, but instead were relying on databases (and breed averages) assessed across different individuals. That suggests that some of the associations, if tested within individual subjects, could be even stronger.
The human-dog relationship is a long one, and our artificial selection of dogs has been enormously powerful - when you think about all of the different dog breeds in the world, from Danes to dachshunds, Newfoundlands to chihuahuas, they all are the same species. That is testament to an enormous phenotypic plasticity (reaction norm) within their development. I'm going to request a copy of the original research article that this news report references, if anyone would like to see it - I'll bet it is interesting reading. Perhaps it will shed some light on my dog's (a rescue Rottweiler) behavior...
Have a great rest of the weekend - see you on Tuesday.
Good morning all,
During our recent EMG lab, we considered muscle structure/function, and how muscle strength can be improved through enlargement of muscle fibers. We also noted that testosterone can support the development of larger muscles in both men and women. In the news this week is a report confirming that testosterone improves muscle and athletic performance in women, along with news of a strict limit on testosterone in female athletes being imposed by a track-and-field regulatory body.
Testosterone is a potent steroid hormone, produced in abundance by the male gonads (the testes). Testosterone is also found in women. The female gonads (ovaries) do not produce testosterone directly, but do produce several estrogens, which can be converted to testosterone by enzymes (especially in the brain). Both sexes also produce other androgens (male-typical hormones) in the adrenal glands, which also can be converted into testosterone.
So, we tend to think of testosterone as a 'male hormone', but the reality is not so simple. Both women and men have circulating testosterone, although men typically have levels that are 10-30x higher that those found in women. But, here too, our simplistic and convenient categorizations are not always reflected in reality.
While men typically have much more testosterone in circulation than do women, the range of variation in each gender is large. What of women who produce unusually large amounts of testosterone? Will that give them a muscular and a competitive advantage in sporting events? The anecdotal and the experimental evidence say that it will.
It is convenient to think of all persons as being purely binary in terms of their sex, such that all aspects of their sexual make-up (genetic sex, physical sex, physiological sex, gender identity) align to be either purely female or purely male, but the reality is, as always, more complicated. Persons of differential sexual development may not be perfectly aligned in all of their sexual characteristics, causing them to have characteristics which are not purely 100% typical of one gender or another. Apart from the social and physical challenges this poses, how such individuals can be evaluated in regulated sporting events recently has come into question. The most notable case has been that of the South African athlete Caster Semenya, a multi-medal winning foot race champion who has repeatedly been sanctioned because her testosterone levels are higher than the thresholds set for female athletes.
And what of athletes that are making a gender transition? Their testosterone levels are highly variable, and may fall within the male-typical or the female-typical range. Should they be barred from, or limited in, participation in sporting events?
These are important issues, beyond sporting regulation. Most aspects of society long have been male-biased, and it is becoming increasingly apparent that we suffer because of this. In science, it has become very clear that work done largely on male physiology serve females poorly. For decades, the standard experimental models for human physiology have been male mice and rats. Only one gender was used in order to reduce experimental variability. We long have known of differences in the female and male reproductive systems, but we never really appreciated how their influences translate into other systems (including the muscular system). But, now we are learning how surprisingly different male and female physiology outside of reproductive systems can be. And, the fact that this recent study of testosterone supplements in women was one of the first of its kind suggests that we have a lot of catching-up to do:
There is much to be learned about differences in female and male physiology and their implications for our health and well-being, and our scientific community is finally waking up to this fact. How the sporting community deals with the complexities of our physiology is of relatively little importance, perhaps. But the issue of equality in general, in science, health, and society, is one that recent generations have failed to properly address. May your generation be more open, more mindful, and more egalitarian.
Have a great weekend -