Sci’s not going to lie, she’s a HUGE fan of caffeine

(I mean, duh)

And I remembered only too well many of the things that ERV has said previously about how she uses caffeine before her workouts, to give her the extra boost and improve her workout. So when I saw this abstract on the effects of caffeine on resistance training in humans…well obviously I had to check it out.

Bui et al. “The Effects of Habitual Caffeine Intake on Lead Body Mass and Strength Performance During 12-Weeks of Resistance Exercise Training” Texas A&M, presented at Experimental Biology, 2011.

(Via I can has cheezeburger)

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The latest study out of Brian Wansink’s lab, the man who wrote the book “Mindless Eating”, and whose laboratory focuses on the psychology of how we relate to our food, is already going to have something of a halo. Wansink is a specialist in the field and is very well known for many of his studies on nutrition, including my favorite study, the bottomless soup effect, where a constantly refilling bowl of soup will cause people to slurp up 300 calories more, because their eyes fool them as to how much they’ve eaten (he noted the necessity of using tomato soup, as chicken noodle clogged up the refilling mechanism and caused some very unpleasant gurgling noises that caused people to wonder what was going on).

But recently, Wansink’s lab has begun to study the effects of “health halos” on foods, the idea that a particular health attribute of our food can color our entire perception about that food. Previous work has looked, for example, at the “low fat” health halo--the idea that if you’re told a food is low fat, you will believe that the food is healthier than the regular version.

But low fat changes something about the nutritional value of the food. What about if a food has nothing nutritionally different about it, but has a difference in how it is made? Is there an organic “health halo” effect?

You bet there is.

Jenny Wan-chen Lee et al. “You taste what you see: Organic labels favorably bias taste
Perceptions” Cornell University, presented at Experimental Biology, 2011.

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Heart failure and heart attacks (otherwise known as myocardial infarction) are some seriously scary problems. Myocardial infarction in particular seems to strike without warning, leading either to death or to months of recovery and reduced quality of life. So not only are scientists working on what can help people recovering from heart attacks or living with heart failure, they also want to look at what might protect people who are in danger of cardiac disease.

There's a lot of seemingly paradoxical findings on what can help with cardiac disease. Sometimes people with high cholesterol seem to be protected. Sometimes people on caloric restriction seem to be protected. While the findings seem to be opposites, it's possible that similar physiological mechanisms could be involved (or different ones, that’s possible too).

So how do you find out what changes might protect against MI? One way is to feed a bunch of mice some delicious high fat diets!

Haar et al. "Acute high fat feeding influences cardiac function and confers cardio protection against ischemic injury" University of Cincinnati College of Medicine, presented at Experimental Biology, 2011.

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We all know how devastating a heart attack (known to science as a myocardial infarction or MI) can be. Luckily, science has made great strides, and many people now survive heart attacks and live for many years (though the death rate is still very high). But now that people are SURVIVING heart attacks, the quality of life and ability to prevent another MI is of more concern. Scientists are looking at pharmacological interventions, dietary interventions, etc, etc. And of course, they are looking in to EXERCISE.

Exercise is usually thought to be beneficial to just about everything. But in the case of heart attack, how beneficial is it, what can it help and when should people start?

Guizoni et al. "Cardiac effects of late exercise training in rats with different sizes of myocardial infarction". Internal Medicine, Botucatu Medical School - UNESP, Botucatu, Brazil, presented at Experimental Biology, 2011.

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We have all heard about the problems that can occur when people are exposed to drugs of various kinds as adolescents. The media abounds with stories of "pharming parties", drinking teens, and stories of lives gone wrong. Adolescence is a very tricky period of life. Teens are thought to be at more risk to suffer the negative consequences of drug use, as the adolescent brain is a changing brain, one undergoing extensive neuronal and connective remodeling. We usually think of this in terms of whole cells growing and dying, connections forming or going away. And this does happen, but there are also more subtle effects, like changes in the receptors that mediate signaling in the brain.

One major example of this is the GABA receptor. GABA stands for gamma-Aminobutyric acid, and this chemical is the most important inhibitory neurotransmitter in the brain. Increases in GABA release generally result in decreased cellular activity on the cells where GABA acts directly. But remember (as Sci will tell you often), a chemical is ONLY as good as its receptor! GABA has receptors that are comprised of several different subunits which form up together, and the subunit composition of the receptors determines how a cell will respond to GABA signaling.

And the composition of these GABA receptors is one of the things that changes during adolescence. But what if you take drugs that affect GABA during this time of receptor change? Will this change how you react to drugs such as alcohol (which exerts some of its effects via GABA) during adulthood?

Worrel, Amato, Winsauer. "GABA-A receptor modulation during adolescence alters adult ethanol intake and preference in rats" Louisiana State University Health Sciences Center, presented at Experimental Biology, 2011.

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I'm sure many of you are probably reading this while wearing some kind of corrective lenses. Some of you might be wearing some cool hipster glasses, but many of you are probably wearing contacts. And as you might know, wearing contacts can be a dangerous sport. Putting them in incorrectly can cause you to damage your eye. In fact, there are 42,000 injuries to the cornea (the transparent part of the eye that covers the iris) per year. And what's worse than getting a small scratch in your eye? Getting it infected. The big bug for this is a bacteria called Pseudomonas aeruginosa, and half of the cases of infection will result in poor vision.

So how do we prevent these scratches to our delicate corneas and the infections that can go with them? Well, for starters, take good care of your contacts! But if worst comes to worst, it's possible that there may be a little protein that you ALREADY HAVE, that can help you out.

Griffith, Russell, Pereira. "Cationic antimicrobial protein, 37kDa, mediates corneal wound healing in vitro" Department of Pharmaceutical Science, University of Oklahoma Health Sciences Center, presented at Experimental Biology, 2011.

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People often complain to their friends when others don't "get" something they are trying to say "they can't get it through their thick skulls". Words like "boneheaded" and "numbskull" are things we all recognize. But it might surprise you to realize that our skulls are, on average...very thin. At least compared to our ancestors. In fact, we have in general skeletons that are less robust and skulls that are thinner. And this seems like a kind of odd adaptation. Shouldn't it be GOOD to have a thick skull?

Our ancestors had much thicker skulls, and a more robust skeleton, than we do now. But if it's usually considered a good thing to have a thick skull, what has made our skull so thin? What determines skull thickness? Is it a genetic difference...or is it a matter of how much you use it?

Copes et al. "The effects of manipulating the frequency and magnitude of mastication on system skeletal robusticity in mice" Institute of Human Origins, Arizona State University, Tempe, AZ, presented at Experimental Biology, 2011.

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