Debunking myths on genetics and DNA

Monday, October 29, 2012

GMOs love me, GMOs love me not..

I've been asked to discuss genetically modified foods and I confess I've been procrastinating. Why? Because I don't have an answer on whether or not GMOs are good or bad, and I can't offer one. But, what I can do is offer a few thoughts. Food for thought is usually super-natural, organic, and pesticide-free, so here it goes. :-)

1. What are GMOs?
Technically, all domesticated plants and animals are "genetically modified" since, rather than letting the species evolve through natural selection, mankind has steadily selected offsprings according to some man-made criteria. However, today's technology allows us to artificially modify an organism's genome. The difference between the two is not just in time scale: when selecting crops, or, more in general, any organism, generation after generation based on phenotype, uncharacterized genes are introduced in the species. Genetically engineering, or bioengineering, however, introduces a few well-characterized genes (often from a different species) into the organism. In a way, this is no news: gene therapy creates genetically modified organisms. Humanized mice are created in labs to test drugs and other therapies. The question of whether or not GMOs are good arises in the food industry. Are they safe to eat?

2. The Cartagena Protocol on Biosafety
As California gets ready to cast its vote on Proposition 37 [1] (which would require foods to denote their GMO content on the labels), it is good to review what currently is in act to "protect" us from possible hazards. From Wikipedia:
"The Cartagena Protocol on Biosafety is an international agreement on biosafety, as a supplement to the Convention on Biological Diversity. The Biosafety Protocol seeks to protect biological diversity from the potential risks posed by genetically modified organisms resulting from modern biotechnology."
"The Biosafety Protocol makes clear that products from new technologies must be based on the precautionary principle and allow developing nations to balance public health against economic benefits. It will for example let countries ban imports of a genetically modified organism if they feel there is not enough scientific evidence that the product is safe and requires exporters to label shipments containing genetically altered commodities such as corn or cotton."

3. Why are foods genetically modified?
For a number of reasons, some good and some not so good. Some are just practical reasons in a world that, whether we like it or not, is getting more and more "globalized": the first bioengineered produce was a tomato designed to have a prolonged shelf life. Some crops are genetically modified to resist harsher herbicides and pesticides. Others, are genetically modified to desist bugs from eating them. For example, genes producing Bt toxins have been introduced in cotton and corn. These toxins kill caterpillars that would otherwise eat up the whole crop. Notably, the modification benefits not only the genetically modified crops, but, since it reduces the global population of harmful caterpillars, it also benefits the non-modified crops.

I expect foods that can resist herbicides to be soaked in chemicals. On the other hand, if a crop is genetically modified so its flowers/fruits/seeds no longer offer a viable environment to certain parasites, I expect those foods to be pesticide-free. Yes, I'll take a few modified genes over harmful chemicals. Bottom line: NOTING WHETHER OR NOT A CERTAIN FOOD CONTAINS GMOs DOES NOT HELP. What you should really demand in a label is WHY SUCH FOOD WAS MODIFIED AND WHAT WAS ACHIEVED THROUGH THE BIOENGINEERING. Notice that while the Food and Drug administration currently does not impose any GMO labeling, their guideline recommendations state that the GMO content be noted, as well as the reason why the food was modified, and what was achieved through the modification.

4. Genetic homogeneity is bad
Rice is one of the most consumed crops in the world. Again, from Wikipedia:
"As of 2009 world food consumption of rice was 531,639 thousands metric tons of paddy equivalent (354,603 of milled equivalent), while the far largest consumers were China consuming 156,312 thousands metric tons of paddy equivalent (29.4% of the world consumption) and India consuming 123,508 thousands metric tons of paddy equivalent (23.3% of the world consumption). Between 1961 and 2002, per capita consumption of rice increased by 40%."
Rice is also highly "domesticated", as it has been selected over thousands of years to fit human needs. Currently, there are 20 different kinds of rice, but, according to FAO, the Food and Agriculture Organization, "It is estimated that not even 15 percent of the potential diversity has been utilized." This is a THREAT to food security. If a pesticide-resistant parasite were to attack rice crops, it'd be lethal to the vast majority of rice varieties currently harvested. Heavy use of pesticides favors the selection of pesticide-resistant organisms, while domestication favors genetic homogeneity in crops. This is NOT a good combination. Another reason why, between GMOs and pesticides, I'd favor GMOs. And if GMO research can prevent a pesticide-resistant organism to wipe out 50% of the world-wide food, hey, who's to complain?

5. Knowledge is NOT power if that knowledge is poorly understood
We live in a strange era when technology leaps forward at a higher speed than our ability to comprehend its output, especially in the field of genetics. We have loads of data we don't quite know how to store, let alone analyze. It's getting cheaper and cheaper to have a full human genome typed and companies are advocating that we do it for every individual. But are we capable of understanding the data? Last week I posted a shocking story of a boy discriminated because he carries a recessive mutation for a disease he doesn't have and he's at no risk of contracting (that's what recessive means). The Internet is full of bogus info on genes, genetics, mutations, etc. There's more noise than ever, giving people the illusion that they know when in fact they don't. I fear that the same will happen for GMOs. Once those labels come out, will people be able to understand what they mean? If Prop 37 will only require a "content" statement without a "reason", for example, will the information be really useful or will it just generate a stigma?

You now see why I cannot tell you whether GMOs are good or bad. They can be both! (Aren't we all?)

Food always has a higher impact than other things, but if you think about it, there are so many things that we've introduced in our daily lives in the past few decades that we simply don't know whether or not they are good IN THE LONG RUN: wi-fi, for example. Cell phones. Chemicals in skin products, from sun protection to cosmetics. I'm afraid the next generation will be the test. So the real question is: do we want to experiment with our children as guinea pigs? Sadly, when you put it in these terms, it seems to me it's too late to go back. The experiment has already begun.

If these few thoughts weren't depressing enough, read Pamela Ronald's review, referenced below [2]. One of the great points Ronald makes is that we are changing our climate and environment much faster than ever before (thanks to climate change and an exponentially growing population). Natural selection can't keep up with the pace, hence
"an important goal for genetic improvement of agricultural crops is to adapt our existing food crops to increasing temperatures, decreased water availability in some places and flooding in others, rising salinity, and changing pathogen and insect threats."
The review is clearly biased in favor of GMOs and it lists several benefits from such procedures. While advocating for adequate testing on every newly modified organisms, it also reports that all genetically modified crops tested so far have been deemed safe and substantially no different than conventionally selected crops "in terms of unintended consequences to human health and the environment."

Bottom line: I can't tell you what to vote on Prop 37 and I can't tell you whether or not you should avoid GMOs. Just read as much as you can and be sure to form your own opinion.


[1] Baker, M. (2012). Companies set to fight food-label plan Nature, 488 (7412), 443-443 DOI: 10.1038/488443a

[2] Ronald, P. (2011). Plant Genetics, Sustainable Agriculture and Global Food Security Genetics, 188 (1), 11-20 DOI: 10.1534/genetics.111.128553

Monday, October 22, 2012

Lorenzo's oil got upgraded to stem cell research

Have you seen the 1992 movie Lorenzo's oil? The film portrays the true (and sad!) story of Lorenzo Odone, who, at age 6, was diagnosed with adrenoleukodystrophy, one of the most common forms of leukodystrophies, a family of degenerative diseases that affects the growth of the myelin sheath. Myelin wraps around nerve fibers creating a fatty covering that increases the speed at which impulses propagate. Leukodystrophy is a genetic disorder caused by mutations in the genes that code myelin proteins. When myelin is defective, or not produced in sufficient quantities, it starts degrading, causing the progressive loss of signaling along the nerve. Eventually, the nerve dies.

As shown in the movie Lorenzo's oil, Lorenzo's parents refused to accept the common prognosis they were given at the time for their son (progressive paralysis and death within 2-3 years). Their determination led them to discover an oil mix able to alleviate the symptoms of the disease.

Two papers published in Science Translational Medicine now show that stem cell therapy can partially regenerate neurological function.

Uchida et al. [1] show that stem cell transplantation is effective in the regeneration of the myelin sheath in mouse models. The researchers transplanted human central nervous system stem cells (HuCNS-SCs) into the brains of mice with defective myelination in the central nervous system. The transplanted stem cells generated functional myelin in the mice's central nervous system

In the same issue, Gupta et al. [2] describe how they transplanted the same cells (HuCNS-SCs) into the frontal lobe of four young boys that were affected by Pelizaeus‚√Ą√¨Merzbacher disease (PMD), a form of leukodystrophy. The transplant was followed by a 9-month regimen of immunosuppression to minimize the chances of rejection. One year after the transplant, magnetic resonance imaging (MRI) showed that the transplanted cells had engrafted and successfully myelinated brain cells. The researchers conclude that "modest gains in neurological function were observed in three of the four subjects. No clinical or radiological adverse effects were directly attributed to the donor cells."

Sadly, Lorenzo died in 2008, one day after his thirtieth birthday. His story, though, was and still is an inspiration to many.

[1] Uchida, N., Chen, K., Dohse, M., Hansen, K., Dean, J., Buser, J., Riddle, A., Beardsley, D., Wan, Y., Gong, X., Nguyen, T., Cummings, B., Anderson, A., Tamaki, S., Tsukamoto, A., Weissman, I., Matsumoto, S., Sherman, L., Kroenke, C., & Back, S. (2012). Human Neural Stem Cells Induce Functional Myelination in Mice with Severe Dysmyelination Science Translational Medicine, 4 (155), 155-155 DOI: 10.1126/scitranslmed.3004371

[2] Gupta, N., Henry, R., Strober, J., Kang, S., Lim, D., Bucci, M., Caverzasi, E., Gaetano, L., Mandelli, M., Ryan, T., Perry, R., Farrell, J., Jeremy, R., Ulman, M., Huhn, S., Barkovich, A., & Rowitch, D. (2012). Neural Stem Cell Engraftment and Myelination in the Human Brain Science Translational Medicine, 4 (155), 155-155 DOI: 10.1126/scitranslmed.3004373

Saturday, October 20, 2012

From ABC news: "Boy Ordered to Transfer Schools for Carrying Cystic Fibrosis Gene Mutation"

I'm totally speechless.

Read the article and tell me it's a Halloween prank.


Friday, October 19, 2012

Why extra fat is bad, even when it's in the "right" spots.

Have you been thinking of going on a diet but haven't found the right motivation yet? How about this one: fat feeds tumor cells and enhances their growth. And another question, for the ladies this time: have you ever wondered how those annoying love handles would look so much better inside a bra? No, I don't mean to put a bra around my waist, rather to move that bit of fat up to my chest . . .

Somehow the two things are related. Stay with me and I'll explain.

Numerous studies have shown that obesity not only increases cancer risk, but it's also linked to accelerated progression in numerous types of cancers. A group of researchers from the University of Texas Health Science Center at Houston investigated the reason for such poorer prognosis in obese patients. In a paper published in Cancer Research [1], Zhang et al. show that white adipose tissue (WAT) facilitates tumor growth in mice, and the association was independent of the mice's diet. To show this, instead of overfeeding the mouse to make it grow the fat tissue, they transplanted into the animals adipose stromal cells (ACS) -- cells that can be thought of as the "progenitors" of adipose cells. The transplanted cells increased the proliferation of white adipose tissue. Furthermore, once recruited into tumors, they increased tumor vascularization.

Tumors are basically an uncontrolled growth of cells. It takes a lot of resources to keep cells growing, and new blood vessels are created to "feed" the growth. Zhang et al. showed that the transplanted adipose cells were mobilized in the mouse model and promoted the creation of new blood vessels, thus effectively "feeding" the tumor and promoting its progression. Yuck, right?
"Our results indicate that obesity can accelerate tumor growth irrespective of concurrent diet. [. . .] Our data indicate that ASCs recruited by tumors become perivascular or differentiate into intratumoral adipocytes [1]."
Why did I mention love handles and bras? Because Yoshimura et al. published a paper [2] in 2008 in which they do to humans what Zhang et al. did to mice. For a good reason, of course: in [2] Yoshimura et al. illustrate a new technique called cell-assisted lipotransfer in which they use the aforementioned ACS, the adipose progenitors, to perform cosmetic breast augmentation. Seems like a brilliant idea: no implants needed, no lipoinjection (which carries a high risk of necrosis), just isolate the fat cells, let them grow, then transfer them back. No scars, no complications.
"Final breast volume showed augmentation by 100 to 200 ml after a mean fat amount of 270 ml was injected. Postoperative atrophy of injected fat was minimal and did not change substantially after 2 months. Cyst formation or microcalcification was detected in four patients. Almost all the patients were satisfied with the soft and natural-appearing augmentation [2]."
But now you see why this could present a potential problem: many breast cancer patients seek tissue regeneration after a mastectomy, and while Yoshimura's technique seems innovative and promising, Zhang et al. warn against its possible risks as the fat transfer could potentially feed remaining cancer cells and yield devastating results.

And the moral of the story is: go on a diet, get rid of the love handles, and be happy with a smaller size bra. ;-)

[1] Zhang, Y., Daquinag, A., Amaya-Manzanares, F., Sirin, O., Tseng, C., & Kolonin, M. (2012). Stromal Progenitor Cells from Endogenous Adipose Tissue Contribute to Pericytes and Adipocytes That Populate the Tumor Microenvironment Cancer Research, 72 (20), 5198-5208 DOI: 10.1158/0008-5472.CAN-12-0294

[2] Yoshimura, K., Sato, K., Aoi, N., Kurita, M., Hirohi, T., & Harii, K. (2007). Cell-Assisted Lipotransfer for Cosmetic Breast Augmentation: Supportive Use of Adipose-Derived Stem/Stromal Cells Aesthetic Plastic Surgery, 32 (1), 48-55 DOI: 10.1007/s00266-007-9019-4

Tuesday, October 16, 2012

Reprogrammable cells

Can't remember if I already shared the above picture... it's my favorite sunset shot so far, so forgive me if it's a deja vu.

The Nobel Prize in medicine this year was awarded to John Gurdon and Shinya Yamanaka for pioneering the reprogramming of cells into an embryonic-like state. Embryonic stem cells are cells that undergo asymmetric division, as they divide into an undifferentiated cell and into a specialized cell. This way, they can grow indefinitely while maintaining their undifferentiated state and, at the same time, keep the ability to differentiate into all three germ layers, the cells formed during embryogenesis.

When still a PhD student, in 1958, Gurdon cloned a frog using the nucleus of a cell taken from the intestine of a tadpole. It took another 38 years before the first mammal was cloned: the first cloned sheep, Dolly, was born in 1996 from an unfertilized egg whose nucleus had been replaced with the nucleus of an adult cell. In this case, the adult cell, by being placed into the egg, was effectively "reprogrammed" into an embryonic stem cell. Up until Gurdon's work was published in 1962, general belief was that once cells specialized, they could not revert. The discovery that cells can actually undergo "reprogramming" under special circumstances is quite significant because it gives hope that we can achieve tissue regeneration and treat degenerative diseases or spinal cord injuries.

In 2006 Yamanaka and his colleague Kazutoshi Takahashi published a paper in Cell [1] in which they showed that, activating four genes, they were able to reprogram adult fibroblasts from mouse embryonic cells. They called the new cells induced pluripotent cells, or iPS, and found that they expressed embryonic-state cell markers. In fact, once in the proper environment, they contributed to embryonic development.

Yamanaka is a strong believer that this research will eventually lead to successful regeneration therapies. In fact, he plans to start a bank of induced pluripotent stem cells obtained from 75 different cell lines. Is this the beginning of a new era? A word of caution comes from a paper published in PNAS at the end of 2010 [2]: in this paper, Serwold and colleagues derived mice from reprogrammed T-cells (cells from the immune system) and showed that roughly half of the mice generated this way spontaneously developed T-cell lymphomas.

The mice were generated by transferring T-cell nuclei into enucleate oocytes. As they mature, T-cells undergo genomic rearrangements, and while normally these rearrangements occur in T-cells only during a specific stage of their development, such rearrangements were observed in all somatic cells in the cloned mice. In [2] Serwold et al. show that these rearrangements undergo T-cell lymphomagenesis: in other words, they cause cancer. Though T-cells are not the only cells that currently can be reprogrammed, this study clearly shows that different cell lines can yield different outcomes, some quite deleterious.
"This study suggests that precautions should be taken to ensure that the identity of the reprogrammed cell of origin is known, and that T cells, and probably also B cells, are not inadvertently turned into therapeutic iPS cells. Recent studies have used human blood-derived T cells as sources of iPS cells, and these cells promise to be valuable tools for studying human immune development and disease; however, the results presented here indicate that extra caution is warranted regarding the therapeutic use of such T cell-derived iPS cells [2]."

[1] Takahashi, K., & Yamanaka, S. (2006). Induction of Pluripotent Stem Cells from Mouse Embryonic and Adult Fibroblast Cultures by Defined Factors Cell, 126 (4), 663-676 DOI: 10.1016/j.cell.2006.07.024

[2] Serwold, T., Hochedlinger, K., Swindle, J., Hedgpeth, J., Jaenisch, R., & Weissman, I. (2010). T-cell receptor-driven lymphomagenesis in mice derived from a reprogrammed T cell Proceedings of the National Academy of Sciences, 107 (44), 18939-18943 DOI: 10.1073/pnas.1013230107

Thursday, October 11, 2012

Gene therapy goes... topical

The paper I'm discussing today is so cool, I don't know how I missed it when it came out last July. As the name implies, gene therapy is a technique used to "fix" defective genes either by replacing them with fully functional ones or by silencing them with the use of antisense RNA.

Defective genes either fail to produce the proteins they code for, or produce defective proteins, thus causing genetic disorders. A defective gene can be silenced (so that it will no longer produce the defective protein) using antisense RNA. The antisense RNA binds to the mRNA from the defective gene, thus preventing it from being translated into the protein. Small interfering RNAs, or siRNAs, are short double-stranded RNAs that can successfully deliver antisense RNA to the target genes and effectively suppress gene expression.

There are several ways to deliver either DNA or RNA, each with advantages as well as disadvantages. Viral vectors (genetically modified viruses that instead of carrying viral DNA they carry the therapeutic DNA or RNA to be delivered inside the cell) are great ways to deliver genes, but have to overcome the barrier imposed by the host's immune system. Furthermore, some vectors may have toxic side effects. Other delivery means include conjugate agents, i.e. particles such as lipids, polymers, or nanoparticles that bind to the RNA and have high penetrability. Though such therapies have been quite promising, they pose a challenge: they can be toxic when delivered intravenously or orally, while the topical route is inefficient because the skin won't let through anything greater than a few daltons.

That's too bad, though, because the skin would be the less invasive and easiest way to deliver therapy. Just imagine it: applying genes in the morning just like a daily moisturizer! :-)

In [1] Zheng et al. show that by conjugating siRNAs with inorganic gold nanoparticles, they can defeat the epidermic barrier and successfully reduce the expression of the target genes.
"Recently, we introduced spherical nucleic acid nanoparticle conjugates (SNA-NCs, inorganic gold nanoparticles densely coated with highly oriented oligonucleotides) as agents capable of simultaneous transfection and gene regulation. [. . .] SNA-NCs enter almost 100% of cells in more than 50 cell lines and primary cells tested to date, as well as cultured tissues and whole organs."
The researchers measured uptake, safety, and gene suppression efficacy of SNA-NCs in human keratinocytes, a cell line that constitutes 95% of the epidermis. They found no morphological difference between treated skin cells and controls. Furthermore, they studied the ability of SNA-NCs to aid the silencing of EGFR, or epidermal growth factor receptor, a cell-surface receptor that has been shown to be mutated and up-regulated in several types of cancers, including lung, anus, and 30% of skin cancers. After 3 weeks of treatment, EGFR expression was suppressed by 65% in hairless mice. Human skin is known to be thicker and more difficult to penetrate, so the treatment was also tested on 3D raft cultures that simulate in vivo human epidermis. EGFR mRNA expression was lowered by 52% and EGFR protein expression by 72%.

Zheng et al. conclude:
"Our data from blood serum and mouse skin show that siRNAs, when densely conjugated to the nanoparticles in the form of SNA-NCs, are minimally stimulatory and have far fewer off-target effects than the free siRNAs of the same sequence introduced by traditional methods. Furthermore, our studies show rapid clearance from skin, minimal accumulation in viscera, and no evidence of histological changes in internal organs after topical delivery. The low immunogenicity and few off-target effects, coupled with low toxicity and high efficacy, point to a significant advantage for using SNA-NC technology to introduce siRNAs."

Dan Zheng, David A. Giljohann, David L. Chen, Matthew D. Massich, Xiao-Qi Wang, Hristo Iordanov, Chad A. Mirkina, & Amy S. Paller (2012). Topical delivery of siRNA-based spherical nucleic acid nanoparticle conjugates for gene regulation PNAS DOI: 10.1073/pnas.1118425109

Tuesday, October 9, 2012

Albuquerque International Balloon Fiesta

Every year in October, Albuquerque hosts the International Balloon Fiesta. Here are some shots from the dawn patrol.

Thursday, October 4, 2012

Limb regeneration: a lesson from salamanders

As much as we would love to enlist limb regeneration among modern science's best accomplishments, so far it is still very much confined to science fiction. That doesn't mean it won't happen, though. Key to limb regeneration is cellular reprogramming that allows differentiated cells to return to a germline-like (undifferentiated) state. Genes involved in embryonic development need to be reactivated in order to restart the same process that created the limb during the growth of the embryo.

The vertebrates with the best ability to regenerate limbs are salamanders, making these little critters the most studied in the field. When a salamander loses a limb, a layer of epidermis grows to cover the wound, and beneath this layer new, undifferentiated cells start proliferating, forming a mass called blastema. Recent research shows that this first wave of cell dedifferentiation may recapitulate events occurring during embryogenesis.
"The cells in the limb blastema are believed to be a heterogeneous collection of dedifferentiated cells that have been reprogrammed to achieve varying levels of developmental potential exhibited by the cells involved in embryogenesis [1]."
Germline stem cells are cells that give rise to gametes (the reproductive cells) and have the ability to divide into another stem cell as wells as a more differentiated cell. This mechanism, called asymmetric division, is controlled by a protein called PIWI through small, non-coding RNAs called piRNAs. In [1] Zhu et al. showed that when salamanders regenerate a limb, a germline-like state is established in the growing tissue. In particular, they found that germline-specific genes were expressed in the regenerated limb. In order to show this, they looked specifically at the PIWI proteins.

Zhu and colleagues found a significant amount of upregulated transposable elements in the regenerated limbs. If you remember, transposable elements is a segment of DNA that can move from one locus to another within the genome of the same cell. During the limb regeneration process, transposable elements can impart a deleterious amount of instability, which is counteracted by a corresponding upregulation of the PIWI genes. Conversely, when the PIWI genes were knocked down (i.e. their expression was reduced) in the blastema, limb growth following the amputation was significantly reduced compared to controls.

Zhu et al. conclude
"In the future, further characterization of the subpopulations of these reprogrammed cells with additional germline-specific markers might provide more insight into exactly how far cellular dedifferentiation can proceed and whether there are indeed a small number of cells that could be isolated before a certain developmental threshold and exhibit true pluripotency when isolated from the influence of the partially programmed blastemal cells in the proximity."

[1] Wei Zhu, Gerald M. Pao, Akira Satoh, Gillian Cummings, James R. Monaghan, Timothy T. Harkins, Susan V. Bryant, S. Randal Voss, David M. Gardiner, & Tony Hunter (2012). Activation of germline-specific genes is required for limb regeneration in the Mexican axolotl Developmental Biology DOI: 10.1016/j.ydbio.2012.07.021

Monday, October 1, 2012

The sleep conundrum

How many hours of night sleep do you get? Are you ever surprised at how many more/less hours other people sleep? Well, if you are, you might find comfort knowing that the variation in number of sleep hours across species is huge and, so far, very much an evolutionary mystery.

Common thought is that sleep provides us with a much necessary "recharging" and common that it has an evolutionary advantage. However, it takes time away from foraging/preying and mating, and makes individuals more vulnerable to predators. Furthermore, the huge spread of sleeping hours across species makes it harder to pin point whether it does have a selective advantage or not.

A new paper published in Science [1] shows that at least in one bird species, pectoral sandpipers (Calidris melanotos), being able to sleep less confers an advantage: males compete for fertile females over a period of 3 weeks, during which they sleep very little. Lesku et al. showed that males who slept less were the ones who produced the most offsprings.

The researchers' main hypothesis was that
"variability in sleep duration observed across the animal kingdom reflects varying ecological demands for wakefulness, rather than different restorative requirements. According to this hypothesis, animals can evolve the ability to dispense with sleep when ecological demands favor wakefulness."
Pectoral sandpipers mate with multiple females and are not involved in the raising of their offsprings. Therefore, their mating success is determined solely on how many fertile females they have access to. Furthermore, in the high Arctic, the sun never sets during mating period. Males are awake longer than females and engage in courtship behaviors, competitions with other males, and defending their territory (don't know why, high school just came to mind. . . ahem). Their total wake time was a strong predictor of how many offsprings they ended up having. A caveat the researchers put forward is that this conclusion seems to be at odds with the hypothesis that there is a genetic basis to the duration of sleeping times, as shorter durations would be selected and hence the variation in wake time would progressively lessen. Instead, still a great variation was observed across males.

The bit that I found most intriguing is that at lower latitudes at some point darkness falls, and since most of courtship is based on visual displays, this limits the daily amount of time males can engage in such activities. However, the study was conducted in Alaska, where the sun never sets during mating season. I wonder if the same study on pectoral sandpipers that live at lower latitudes would have yielded the same results. I also can't help but wonder: this behavior was obviously selected by a favorable environment, in this case the fact that the sun never sets during summer days. I think it was this past summer that my dad said, "Would birds have ever learned to fly if it weren't for the wind?"

[1] John A. Lesku, Niels C. Rattenborg, Mihai Valcu, Alexei L. Vyssotski, Sylvia Kuhn, Franz Kuemmeth, Wolfgang Heidrich, & Bart Kempenaers (2012). Adaptive Sleep Loss in Polygynous Pectoral Sandpipers Science DOI: 10.1126/science.1220939