July 2008

According to an article in NewsDaily.com, researchers have discovered the miracle pill everyone is looking for. Exercise in a Pill. No more running, no more lifting weights, no more yoga needed. Two compounds have been found to mimic the effects of exercise…

The drugs reproduce many of the biological benefits of exercise, helping cells burn fat better and boosting endurance, said Ronald Evans, a Howard Hughes Medical Institute researcher at the Salk Institute for Biological Studies in California.

One of the pills may some day help people enhance their exercise or training, while the other might be more suited for couch potatoes who need to kick-start themselves, Evans and colleagues reported on Thursday in the journal Cell.

“This is a drug that is like pharmacological exercise,” Evans says. “After four weeks of receiving the drug, the mice were behaving as if they’d been exercised.” ~NewsDaily.com

This sounds great and all, but how does that warning go? What sounds too good to be true usually is….

It sounds as if these drugs are already available on an ‘experimental basis’ but none of the testing has been finished to determine the safety of these products. Although this drug may be useful to people who have legitimate health problems preventing them from being physically able to exercise properly, I see this leading to many problems in the general population.

When will people realize that once you mess with something in your body, other things get screwed up too?  Why not just do some things the old fashioned way and get the results you want without unintended (harmful) side effects…



source: superstock.com

After the big blow up, which is still being discussed, between Tom Cruise and Brooke Shields in 2005, many people wondered whether postpartum depression is ‘real’ or not. A news release from the NIH claims that researchers Istvan Mody and Jamie Maguire may have found a mechanism behind this disease (published in Neuron).



Researchers have pinpointed a mechanism in the brains of mice that could explain why some human mothers become depressed following childbirth. The discovery could lead to improved treatment for postpartum depression. Supported in part by the National Institute of Mental Health, of the National Institutes of Health, the study used genetically engineered mice lacking a protein critical for adapting to the sex hormone fluctuations of pregnancy and the postpartum period. – NIH News Release

Although it was first thought that this depression related to fluctuations in hormone levels, this theory was mostly disproved. Now, it seems that the hormones actually change the levels of a receptor in the brain. A mutation in this receptor in women suffering from postpartum depression may be the cause of this disorder (if women are anything like the mice used here).

The question now is, will this research have Tom eating his words? Probably not, but we have to keep trying…


Honey Bee image: insectidentification.org

There has been much talk in the last few years about the rapid decline of honeybees and what that decline means for farmers. Honeybees are not only used for making honey, but actually pollinate many of the food supply crops we consume. Although a ‘Colony Collapse Disorder’ has occurred before, this time it seems as though it is due to the varroa mite. Unfortunately, this clever little bug is becoming resistant to the pesticides previously used to control their numbers.

ScienceDaily (July 28, 2008 ) — One of the biggest world wide threats to honey bees, the varroa mite, could soon be about to meet its nemesis. Researchers at the University of Warwick are examining naturally occurring fungi that kill the varroa mite. They are also exploring a range of ways to deliver the killer fungus throughout the hives from bee fungal foot baths to powder sprays.

Although this new breakthrough seems encouraging and eco-friendly (no use of pesticides), whenever I hear plans to introduce a new species to control a pest problem I always wonder if the new species will cause more of a problem than the initial menace. In this case, introducing a new fungus to control the varroa mites may have implications for other insects or plants in the area. Hopefully, we learn from past experiences (like introducing the cane toad in Australia to ward off sugar-cane pests) and are more prudent about introducing a new species to places where they do not belong.

At the beginning of the year, I read an interesting book by Dr. Temple Grandin, a professor of animal science who happens to have Asperger’s Syndrom (a form of autism), called Thinking in Pictures. This interesting and enlightening book describes Grandin’s experience with autism and how it helps her relate to animals.

In this book, she touches on the fact that many people who have autism have trouble interpreting the unsaid innuendos, social cues, and sarcastic remarks often used in everyday conversation. This can cause a feeling of confusion and isolation which often times results in the person pulling away from people around them

In a new study published in the journal Social Neuroscience, a team of researchers from Carnegie Mellon University tries to pin point the underlying mechanism of this experience. Here, they show evidence suggesting that this trouble is a result of faulty social network connections and inefficient neuronal pathways. In other words, messages important for understanding non-verbal social cues in an autistic brain are slow or have lower levels of transmission than in a normal brain.

This research highlights an important study published in Science earlier in the month in which the researches searched the genome of families with shared ancestry to find inherited factors for autism. During the course of their research, they noticed that all of the genes in common within a family had high levels of expression in the brain. They go on to show that many of these genes may mediate neuronal synaptic development and plasticity. Here is an excerpt from their conclusions:

Early brain development is driven largely by intrinsic patterns of gene expression that do not depend on experience-driven synaptic activity. Mutations in the genes active in early development can lead to brain malformations or severe mental retardation. In contrast, postnatal brain development requires input from the environment that triggers the release of neurotransmitter and promotes critical aspects of synaptic maturation. During this process, neural activity alters the expression of hundreds of genes, each with a defined temporal course that may be particularly vulnerable to gene dosage changes. The connection between experience-dependent neural activity and gene expression in the postnatal period forms the basis of learning and memory, and autism symptoms typically emerge during these later stages of development. Our finding that deletions of genes regulated by neuronal activity or regions potentially involved in regulation of gene expression in autism suggests that defects in activity-dependent gene expression may be a cause of cognitive deficits in patients with autism. Therefore, disruption of activity-regulated synaptic development may be one mechanism common to at least a subset of seemingly heterogeneous autism-associated mutations.

Every time you learn something new, a new connection forms in your brain. As you are reading this, you are making new connections! So, according to the authors, before you are born your brain develops according to a set plan but during childhood certain genes need to be working to make these new connections.

The findings from this research suggests that in children with autism there may be a defect in early learning due to genetic mutations which makes it more difficult to form new connections and, therefore, to process and learn new things. Although this makes things more difficult, it is not impossible to make these connections but it will take longer and require more repetition, which is why it is so important for this disease to be diagnosed as early as possible and start teaching these children in a way that benefits them the most.

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