Saturday, 18 August 2007

sugar consumption = premature aging

There are several factors which contribute to aging in modern society: mainly genetics, diet, stress and lifestyle factors. I have often wondered whether sugar does really cause aging most especially when i develop sugar cravings usually satiated by chocolate and my newly found craze of Nando's chocolate mousse. However I have never actually looked at these studies which support the findings that sugar induces premature aging but mainly just believed the hype in the media. So, I decided to briefly review a recent manuscript which asks this question and conducts experiments at the molecular level, and confirms previous findings. So as i speak, i believe i am spiralling into premature death by chocolate.
A manuscript by Berge et al. (2007) demonstrated that normal human epidermal keratinocytes (primary cells) treated with 100 mM glucose or 0.1 mM gyoxal* for three days induced premature aging. Their experimental methods included examining the phenotype of cells, cell proliferation and cell viability assays, an assay to examine glycoxidatively damaged proteins, and examination of differentiation markers of the cell.
Findings: Using cell proliferation and cell viability assays, the cell number, proliferation rate and viability was measured and found to have decreased in a dose-dependent manner at a glucose concentration of 100 mM and above relative to controls. In contrast, 0.1 mM of glyoxal and above induced a reduction in the previously mentioned parameters in a dose-dependent manner relative to controls. The LD50 for glucose and glyoxal was 200 mM and 50 uM, respectively. The authors state that the possible reason for the difference in LD50 values could be due to glyoxal having a higher reactivity and easier penetration of the cell membrane. Examination of cell morphology demonstrated that cells treated with the same levels of sugar induced vacuolation (formation of vacuoles) and increase in cell size, both of which are characteristic of senescent** cells. Results from assays targeted to measuring aging cells, including the senescence-associated beta-galactosidase and protein glycoxidation***, were significantly higher in cells treated with the sugars compared to control cells after three days of treatment. Glucose caused a 52% and 58% increase and glyoxal a 44% and 68% increase in the senescence-associated beta-galactosidase and protein glycoxidation assays, respectively. Glycoxidation of proteins targets these proteins to be degraded by the proteasome because they are of no use or unwanted by the cell. Proteasomal degradation is one of a few ways in which unwanted proteins are targeted and removed by our cells. As a measure of unwanted protein removal, the group measured proteasomal activity and found that glucose-treated cells had an 11% increase in proteasomal activity. Glyoxal treated cells had a 3% decrease which the authors state as "unchanged". Differentiation was examined using involucrin level measurement against a differentiation agent, calcium. Using a positive control of 1.2 mM calcium, glucose treatment of cells resulted in involucrin levels lower than the positive control whereas glyoxal treatment resulted in involucrin levels similar to and higher than the positive control.
Conclusions: Glucose concentrations of 100 mM and glyoxal concentrations of 0.1 mM and the above indicators of cell senescence in human epidermal keratinocytes have re-confirmed that sugar is able to induce premature aging.

That Mars bar doesn't look so appetising now, does it?


Source: Berge, U, Behrens, J and Rattan, SI. Sugar-Induced Premature Aging and Altered Differentiation in Human Epidermal Keratinocytes. Annals of New York Academy of Science. Volume 1100: 524-529 (2007).


* The paper refers to the term glyoxal, which i assume is methylglyoxal. Methylglyoxal is a by-product of glycolysis (sugar breakdown).

** Cellular senescence, which is when cells arrest in a non-dividing state, is synonomous with aging in the biological context.

***Glycoxidation is the oxidative alteration of a protein by a sugar and forms advanced glycation end products which are known contributors of aging.

National Science Week 2007

Australia has been celebrating science for the past ten years by running National Science Week (NSW) annually. Today marks the first day of the 10th NSW (18th-26th August). Various science related events will be held throughout the country showing-casing and celebrating science and raising awareness about the importance of science.

http://www.scienceweek.info.au

Happy NSW everyone!

Monday, 6 August 2007

Australian Synchrotron

The Australian synchrotron funded and run by tax payers, opened its doors for the first time last week in Clayton, Victoria. The massive facility which is about the size of a football field cost just over $200,000,000 and almost six years to construct from the time it was proposed to the opening day (31st July 2007). Currently running 24 hours a day for six days a week, the synchrotron is thought to be able to produce synchrotron light a millions times brighter than the sun! Synchrotron light can be used for various applications in biology (eg. protein crystallography), material sciences and physics. The facility which is encased in concrete walls is made up of two circles. The inner circle, named the booster ring is responsible for accelerating electrons very close to the speed of light which are initially fired off by an electron gun. The electrons are then collected by the outer storage ring. There are several catchment areas which come off the circular rings which will eventually represent nine labs. Of the many synchrotrons located around the world, having a local facility will be highly beneficial towards the progress of science in Australia by cutting down travel costs, experimental time and transport problems associated with carrying out experiments overseas.

Sources:
http://www.synchrotron.vic.gov.au/
ABC Radio National (The Science Show, 28th July 2007)

Wednesday, 1 August 2007

Science communication, anyone?

In my readings over the past few weeks I have encountered a few articles directed at scientists describing the complacent attitude of reporting science stories to the media. This may be due to inefficient or misinformed reporting on the part of the scientist or the media, which would be unknown to the reader. An article I read today in “NewScientist” titled “Not all that it seems” (28th July 2007) highlighted this problem once again, describing a story where a reputable newspaper described the discovery of a new gene to be the cause of restless leg syndrome (apparently the actual existence of this conditions is disputed, which is news to me). This reporting was incorrect on the journalist’s part. Anyway, the point being is that the newspaper article was misinforming the public. Another example, closer to home, occurred when a colleague of mine recently identified a new mutation thought to be responsible for a disease which was quite significant to her field of research. The state and several local newspapers published this story with each article being reported differently but accurately. The main gist of one article in particular was correct but there was a line which read something similar to this: “The gene was responsible for attacking a part of the protein”. This statement was incorrect and could never be correct for any matter. First of all, genes don’t attack proteins and secondly, the gene is what encodes the protein ie. the gene is the precursor of the protein. I’m not sure what happened to the lines of communication between the scientist and the journalist in this case. This may be an obvious question but shouldn’t the scientist have read the final result before it had been submitted for publication? A couple of days ago, I read another article in “The Scientist” (“Special feature: How should scientists sell science?”) addressing this issue and even setting up an online survey to get a scientist’s perspective. The article ended with this statement.
With your help we can gauge how the life science community and people who have an interest in life sciences feel about the issue of framing science, and add to the growing debate that could help shape the future of science communication in the media”. ("The Scientist")

There seems to be a missing link between information being passed on from the scientist to the media. To bridge the gap, a scientist not only needs to be able to relay the important messages to his or her colleagues but also the general community at a suitable level that is also truthful. It’s is highly important to keep the public informed on scientific findings; after all, research is publicly funded in a lot of cases and progress in fields of disease research for example is highly encouraging to hear about. In addition, addressing the public on a lay level gives the scientist a different level of understanding and reminds them of the "big picture" which is often forgotten or overlooked because of the specific nature of research.

Unfortunately, this mis-reporting has been on-going for too long now. Fortunately, a new breed of journalists are emerging: there is an increase in jounalists who are also researchers or have expertise in the medical field. In addition, i recently discovered that not only is my own university offering science communication as an elective in a science degree but there is a science communication degree which encompases both journalism and basic science.

PS: A few weeks after writing this post, I had the opportunity to talk to a media consultant of a large medical research institute. One of my questions to her was regarding the misinformation of science in the media and how it could be avoided. She replied by giving me the one reason as to why this occurred: The time delay which occurred for the media to write an article and subsequently get it proof-read by the scientist was too time consuming. If this practice was to occur it would be impractical given the competition between media organisations to report breaking news. She also said that this practice could not be avoided and it was the responsibility of both the scientist and journalist to relay and exchange information as accurately as possible during the interview.


Sources:
NewScientist, 28th July 2007, page 5
The Scientist, 30th July 2007