Saturday, 24 September 2011

Highlights from WCE 2011: Part 1

As I mentioned briefly in my last post I attended the 11th world congress on endometriosis in Montpellier a few weeks ago. It’s a tough life having to travel to beautifully picturesque Mediterranean cities, but hey, somehow I managed to cope. The main body of the conference was run over three days where experts from all over the world presented their latest research and shared up to date knowledge about endometriosis. If you would like to see the whole program for the conference you can download it here. All in all it was a very enlightening few days, but don’t worry if you couldn’t make it yourself because over the next few weeks I’ll be posting highlights from the conference. Unfortunately, I can’t post about everything that was discussed because it would probably take more years to write than I will live, so I’ve gone through the different talks and posters and picked out the ones that I hope you’ll find the more interesting. I’ll start off with the oral presentations that were given then move onto the posters that were presented. I’ll also give a bit of my own interpretation of the science, but I won’t be doing much critical appraisal. So without further ado, let’s jump straight in.

R.S. Bevan from the Brighton and Sussex Medical School, UK (S#1-3) presented their work entitled ‘Alcohol consumption and endometriosis: A multi-centre, case-control study

This study took 1,418 women from 10 countries that were undergoing laparoscopic surgery for either suspected endometriosis or tubal ligation. After surgery the main group were divided into three groups: Those who were found to have endometriosis (745 women), those who had symptoms but no disease was found (565) and those women undergoing sterilisation who had neither symptoms nor endometriosis (86). These women were asked to complete a questionnaire which gave included questions about alcohol consumption.

The results of this study showed that alcohol consumption between the three groups of women did not significantly vary. Although there is still more analysis of this data to be done it is still interest to see these preliminary findings. I think there may have been some expectation that alcohol consumption may be increased in women with endometriosis, perhaps due to the fact alcohol can give pain relief, so the results are interesting from that pint of view. There was also some discussion as to whether alcohol consumption increases the risk of endometriosis. I’m not sure whether or not this is folly. Mainly because the symptoms of endometriosis tend to begin around adolescence, but alcohol consumption doesn’t even seriously start for most people until their late teens, so I’m sure whether there could really be any connection between the two.

S.A. Missmer from Havard Medical School in Boston, US (S#1-4) presented their work entitled ‘Vitamin A and endometriosis risk: A prospective cohort study’

This study analysed consumption of different micronutrients in 1382 women with laparoscopically diagnosed endometriosis. What this study found was that increased consumption of vitamin A seems to reduce the risk of endometriosis. Or rather, I should say, reduced the risk of being diagnosed with endometriosis. These investigators reported a 21% reduction in risk of diagnosis of endometriosis when comparing the highest consumers of vitamin A with the lowest, with the association most prominent in women with no history of infertility, who had a BMI below 25 and who had smoked during their lifetime. The investigations are still undergoing to find out why this reduction in diagnosis risk was observed.

M.Kvaskoff from The Gustave Roussy Institute, France (S#1-5) presented their work entitled

Early life events and the risk of endometriosis: The French E3N cohort’

This study analysed questionnaire data from a large group of women with health insurance in France. The purpose of this study was to see if women with endometriosis had exposure to different factors during childhood that made them more susceptible to endometriosis in later life. This study found that both exposure to cats or dogs at home and living on a farm for more than 3 months during childhood increased the risk of endometriosis in later life.

Girls who started their periods before the age of 12 or who had short menstrual cycles before the age of 17 (a short cycle being anything less than 24 days, were also found to be at a higher risk of endometriosis.

Whilst the level of out if school exercise was unrelated to endometriosis risk, more time spent walking (i.e. greater than 5 hours per week) between the ages of 8 and 15 appeared to increase the risk of endometriosis. Higher exposure to UV radiation at place of birth was found to decrease endometriosis. There were a number of early life factors that were found to have no influence over the risk of endometriosis including: birth height/weight, being born premature, breast feeding and maternal smoking.

So what do we make of this study? Well firstly it is important to distinguish causal factors from incidental factors. What do I mean by causal and incidental? Firstly I’ll stop asking rhetoric questions, then I’ll tell you that a causal factor is a factor that is likely to actually increase the risk of endometriosis, whereas a incidental factor is one that is associated with a causal factor so appears to be associated with endometriosis even though it could have no baring directly on the development of the disease.

Let me give you an example; this study found that young girls who undertook more walking exercise were at higher risk of endometriosis. Does this mean that we should stop all young girls from walking so much? No, because if we look at the rest of the results we can see that girls who lived on a farm were at higher risk; girls who lived on a farm are likely to do more walking, so we can see that walking isn’t directly linked to endometriosis risk, rather it is incidentally linked to endo via other factors (such as childhood environment).

More highlights coming soon!

Wednesday, 14 September 2011

A quick update about emailing blog posts

Just a quick update to let you know about a feature I've enabled. If you've read one of my blog posts and you know someone who you think it may be of interest to, you can now share that blog post by clicking on the little symbol at the bottom of each post that looks like this:

and then filling out all the relevant bits on the page that pops up, easy!

Wishing you all the best


Tuesday, 13 September 2011

My First Publication!

Well it’s been a busy week, I’ve just returned from the 11th world congress on endometriosis in France, where I learnt a lot of new things about endometriosis, met a lot of experts in the field and also had a bit of time to enjoy the Mediterranean weather. I’ll be talking about the conference later, but before that I'm going to wallow in immodesty by talking about my very first proper scientific publication on endometriosis entitled “The emerging role of epigenetics and microRNAs in endometriosis” which was published in the Journal of Expert Reviews of Obstetrics and Gynaecology. You can find a link to the abstract here but unfortunately this isn’t the sort of journal you could go down to your local newsagent and pick up. You may also be slightly disheartened to see that in order to read the full article you have to pay $60 (£30) for the privilege (I hasten to add I don’t receive a penny of that money).

Should you be willing to pay the publisher’s charge then that is all very fine and dandy and I hope you enjoy the drive home to your palace in your gold plated Ferrari. If however, you would like to receive the general gist of the article there is a way to access the information it was based upon which would incur you no extra cost. You see, the article itself is taken from what I wrote in my master’s thesis, so if you could read my master’s thesis, you would have a good idea of what is in my article. Fortunately, my university have started keeping an online repository of all recently submitted theses in an electronic format, including mine, which you can find and download here in PDF format.
However, it would be pretty rude of me to just say “here’s my work, enjoy” then stroll off into the sunset, without putting it in context, particularly because the esoteric nature of scientific literature means it is often inaccessible to the public. It would also be pretty silly of me to dedicate this blog to explaining the scientific work of others without explaining my own, so here goes.
The subject of my work, in this instance, concerns the involvement of epigenetics and microRNAs in endometriosis and how the disease originates and progresses. If you’re reading this then chances are you don’t need me to explain endometriosis, but I’ve had several requests to clarify what are epigenetics and microRNAs. The term ‘epigenetic’ loosely means ‘on top of genetics’, so we should probably explain genetics before we tackle epigenetics.
In broad terms genetics is the study of DNA and the way in which it works. DNA is the universal code for life, some of you may have seem this picture before

That is the structure of the DNA molecule, made from just a handful of different elements joined together in a special arrangement; it is a long list of instructions for making you. Encoded in that double stranded helix is a great deal of information about you; from the colour of your eyes, to the shape of your nose, it dictates the fate of many a feature we use to describe ourselves. Almost every cell in your body contains DNA, and it is a large set of instructions by any account. In total, human DNA contains around 30,000 different individual instructions and each of these instructions we call a ‘gene’. The purpose of most genes is to produce a protein which carries out a specific function. Some of the proteins produced are enzymes that make hormones; others are receptors that allow cells to communicate with one another, the list of functions is quite literally staggering, but all work together to keep your body running. So how do we go from DNA to protein?
Firstly the instructions in the gene have to be read. In order to do this the double strands of the DNA split apart and are transcribed by an enzyme called polymerase. This transcription produces messenger RNA, essentially little pieces of single stranded DNA that contain the information to make a single protein. The messenger RNA then travels to a protein called a ribosome which translates the messenger RNA by bringing in transfer RNAs which have amino acids bound to them. As the transfer RNAs bind to the messenger RNA the chain of amino acids grow longer and as the chain grows it begins to fold into a specific shape that will dictate the function of the protein. Sometimes it is better to visualise these processes as a diagram so below is a picture of the whole transcription and translation process.

An easier way to think about the whole process is to imagine it as a construction site. The gene is like a blueprint to make a house (protein). The information in the blueprint (DNA) is relayed by the foreman (messenger RNA) to the construction workers (transfer RNAs) who, using their building materials (amino acids), build the house (protein).
So where does epigenetics fit into the picture? Well, genetics only tells us what proteins should be made; it doesn’t tell us when they should be made. It is an interesting fact that the DNA in all your cells contains all the genes to make any protein. For example, the cells in your fingers contain the genes to make teeth and the cells in your brain contain the genes to make kidneys. Why is it then, that we don’t have teeth-hands or brain-kidneys? Well this is where epigenetics comes into play. Epigenetic mechanisms are like switches that can turn genes on or off. There are several epigenetic mechanisms, but the ones I have studied most are DNA methylation and microRNAs.
DNA methylation involves sticking methyl groups to DNA which stops the process of transcription; microRNAs on the other hand act by binding to the messenger RNA, either stopping it being read by the ribosome or signalling that the messenger RNA be destroyed. If we go back to our construction site analogy; DNA methylation would be like someone taking a black pen and blanking out all the bits of information on the blueprint that aren’t needed. MicroRNAs would be like lawyers, who stop the foreman and tell him he can no longer build. Epigenetic mechanisms such as these are extremely important for making sure that your cells function properly, any errors in the way these mechanisms work can be disastrous for your body.
I’m hoping my cobbled together explanation of genetics and epigenetics has made at least some sense, but how does it all fit into endometriosis? Well, there have been several studies that suggest that epigenetic mechanisms malfunction in endometriosis. Despite the work of a few pioneering scientists, our understanding of the subject is not complete by any means as epigenetics is a relatively young field of science, having only really existed for the last 20 years or so. Nevertheless, epigenetics has told us a great deal about the way in which complex diseases like cancer work, so the aim of my article was to take what we do know so far and see what it can tell us about some of the mysteries of endometriosis.
I’ll summarise what I wrote about in my paper, and keep it brief for everyone’s sake.
  • There are altered patterns of DNA methylation in endometriotic cells that may explain why they are so resistant to drugs and how they can produce their own estrogen supply
  • The pattern of microRNAs is different in endometriotic cells compared to normal endometrium, this could explain a number of features of endometriosis, including some of the immune system abnormalities associated with endometriosis
  • The altered pattern of microRNAs and DNA methylation could also potentially explain the rare instances when endometriosis of the ovary can turn into ovarian cancer
  • Because microRNAs are also found in the blood, the pattern of microRNAs in women with endometriosis may be different from that of disease free women (I found out only last week that this has been experimentally proven). Therefore, this could lead to a simple blood test for endometriosis
  • · Epigenetic errors can be brought on by exposure to certain environmental toxicants. These epigenetic errors can be passed down family lines. This means that some pollutant that your mother, or even your grandmother, was exposed to may have increased your risk of developing endometriosis.
I’m currently writing another paper where I hope to expand on the role of epigenetic mechanisms in the malignant transformation of endometriosis. But enough of this self-congratulatory ego-massaging, as I mentioned at the beginning of this post, I’ve just returned from the 11th world congress on endometriosis so for the next few weeks I’ll be putting up ‘mini-posts’ about some of the more interesting things discussed at the conference.