I’m channel hopping but it seems to me there’s nothing that I want to watch. I feel like stopping but it’s easier to just sit and drop off.

“Did you know that if you focus really intently on something that takes as much energy as running across North America?”

Last week I helped out on my division’s stand for Science Week. The University of Manchester held a Science Fair for local schools to take part in some simple experiments and find out some new things about “science.” Our stand had a few games including a “Pin the Hormone on the Organ,” and tests to diagnose dogs with diabetes. I’ll just leave that there, I don’t think you need any more information right?..

So, whilst giving our little spiel the question (well statement? I mean I guess it’s a question as it starts with “did you know” but it doesn’t really seem to be asking anything worth while. Is it a rhetorical question? This is why I chose science, English is hard!) above was asked (stated? Goddamn not this again!). My colleague, a practicing clinician, experienced researcher and Head of the Division of Diabetes, Endocrinology and Gastroenterology, nodded politely and said “no I hadn’t heard that.”

Staring at something intently? Like maybe a screen? Is this some nonsense thought up to encourage kids to watch TV or play video games? Well I wasn’t one to let this chubby 10-year old get away with it… Thanks to DiabetesPro literally the day before I saw this little story, “Screen time linked to increased diabetes risk in children.” So, I could shoot down that child with facts!

Obviously, I didn’t as I’m not (that much of) a jerk. But I still think it made interesting reading, and as I don’t have any kids I am in the perfect place to tell people how to raise their children. 1 hour of TV a day folks!

Children who spend 3 hours a day watching TV have increased fat mass, skin folds and insulin resistance. So basically 9-10-year olds are getting pre-diabetic. Even when taking into account factors like physically activity, gender, adiposity (fatness) and socio-economical markers, there is still more insulin resistance in the kids who watch more TV.

It’s likely that the large amount of TV isn’t solely to blame, but the habits which arise from it. Children who consistently watch TV, particularly eating meals in front of the TV, snack more whilst watching TV. Moreover, this policy statement from the American Academy of Pediatrics suggested that children spend 8 hours a day engaging in some sort of media, and teenager more than 11. This included phones, computers and everything else, whilst admitting that a lot of this may overlap and therefore be exaggerated. But still they recommended limiting children’s screen exposure to less than 2 hours a day.

At the moment, it’s all correlative, so could be nonsense until more comprehensive studies are carried out, but stopping your kids snacking whilst watching TV 3 hours a day is probably a good idea.


Today’s quote is by Blakfish


I think part of being a parent is trying to kill your kids

So, I’ve covered a couple of things before about obesity; specifically watching Dr Giles Yeo and leptin. If you don’t know type 2 diabetes is kinda my jam, and obviously obesity can play a big role in causing type 2 diabetes. So obviously I was interested in this article stating that a modern lifestyle is to blame for making y’all chubby.

I’ve covered before (in those links above) that your genes play a massive role in if you put on weight. But Dr Yeo compared them to poker. “You can win with a bad hand, and you can definitely lose with a good hand.” And this study seems to show that especially.

Basically the incidence of the mutated genes isn’t increasing. So why are we getting fatter?

Walter and folks looked at the genes of almost 9000 patients born between 1900 and 1958. They compared 29 mutations, which have been linked to obesity, to generate a Genetic Risk Score (GRS) combining all changes. I won’t go into too much info, as it uses very complicated maths. Basically mutations can take away or add to the risk of obesity, so the GRS is a sum of the positive and negative influences. Get it?

The first cohort of subjects were the oldest, so basically people born before we began feasting for every meal. Interestingly, here was no significant connection between the GRS and the BMI of people. Even though the incidence of mutations and the value of the GRS was the same as for people born later, for some reason people didn’t get fat. As you work your way through the cohorts, looking at people born later, the association increases. This means that the GRS starts to mean more as you get younger patients. Also, the older people got the more likely they were to be obese, potentially due to the increased availability of high-calorie foods, and the sedentary lifestyle old folks tend to have.

This suggests that the modern environment plays a bigger role in whether or not you develop obesity.  So, what’s the happy haps?

The authors suggest a few things. The average calorie intake in the States has increased by a whopping 22% (in woman; only 7% in men – still bad though). Sugar-sweetened drinks increase the risk hugely, and consumption of these bad boys has increased rapidly. I’ve just watched a live cast from Physiology 2016, where Prof John Blundell showed that when given a choice people choose energetically dense food.And now we live in a time when folks can access calorific food simply, and cheaply. Another reason may be because we’ve gotten lazy. Although Prof Blundell mentioned that even exercise cannot undo a high calorie diet. Demereth et al carried out a similar study, but had a more complicated explanation; epigenetics!

I have talked about epigenetics before, but probably in real life rather than here as it’s a bit of a head scratcher. Simply put your DNA contains all the data needed to make you. However, to stop DNA from just being accessed all of the time you need something to control it. This can involve modifying the DNA directly, usually by sticking something onto it. This can increase or decrease the rate of which genes are transcribed (i.e. made) (kind of…). Crucially epigenetics don’t actually change the DNA, just the way it is read. And obesity can cause quite a few epigenetic changes. This means that the expression of the proteins involved in obesity and other nasty things can be changed, simply by becoming obese. It’s like an ironic* perpetual motion machine.

Think of your DNA like a fancy library, like one with a museum. All of the day-to-day books for children and idiots are accessible all the time. But those old, fragile books are kept under lock and key, and can only be used in a controlled environment. Now the easiest way to get access to the books is to bribe the librarian with a pile of greasy donuts. Most of the time anyway; perhaps sometimes the librarian shuns your treats and tells you to do one.

Now imagine your big fat grandad has gone around opening and locking doors and eaten the keys. That’s right, epigenetic changes can pass from one generation to the next. Someone at ENDO 2015 said it can pass over two generations, but I can’t remember who, so let’s just let that hang there…

(Since I originally wrote this piece, this came out. The study shows that incidence of Type 2 Diabetes is increasing, and that the percentage of younger people getting the disease is increasing. If you don’t know, obesity and Type 2 Diabetes usually go hand in hand.)

*American ironic. Not proper ironic


Today’s quote is from Stephen King.

Sometimes you can do things for others that you can’t do for yourself.

A bit of a strange one today.

I received an email just before instructing me that my subscription to a complimentary service has expired. Apparently I had received a two week free trial to DiabetesPro; a free service to health professionals who “need to keep current with what’s happening”. Needless to say I’d never heard of it.

So I trawled back through my emails and it turns out the American Diabetes Association have developed a mobile app to keep you up to date with the latest going on in Diabetes. I assume it’s for medics, but I signed up regardless. Why wouldn’t I?..

“So, you cares?” I hear you asking.

I don’t know, why did you follow the link here in the first place. Don’t hold accountable for your actions!

Oh, wait, I guess I should as I invited you. The point of this was to write about how often I actually use these services. So as well as DiabetesPro, I get updates from the Endocrine, Biochemical and Physiological Societies, PracticeUpdate, Diabetes UK and for some reason the latest in Stem Cell Research and Immunology from Bio-Techne.

I am also on the mailing list for the Lipids MAPS conference, so I receive updates about their conferences, and Keystone Symposia.

A quick look through my Twitter tells me that I follow over 20 accounts dedicated to updating me (and others I assume…) about the latest developments in various topics. That doesn’t even include journals that I follow, or scientists that I know constantly post their latest papers.

A post from Nature summarised some data about whether or not Twitter buzz leads to more citations, and it doesn’t! Interestingly sharing on Mendeley is apparently closer, and as you know, I love me some Mendeley. Apparently, it’s because sharing and analysing things amongst scientists is better than letting the general public have a go at it. Which makes sense really, considering how little some chumps know.

Somewhat crazily in 2012, 20% of biomedical articles were tweeted at least once, and that’s going up, so I assume by the time I get my babies out, I’ll be falling behind if I don’t post it. Who am I kidding, I’ll be posting my Ryan et als like they’re going out of fashion!

Which they might well possibly be considering no-one cares about phosphatidylinositol (4,5)-bisphosphate.

Which brings me onto my next thing. I get updated from Google Scholar every time one of my papers get cited. Unfortunately, as I’ve recently changed my research area (for the second time) I don’t have much to do with the inositol lipids anymore, I tend not to even read those papers. Rude I know.

Similarly, Researchgate lets me know when my papers have been cited, but more importantly it lets me know when people I follow publish more papers. This is useful as I follow my collaborators, competitors and friends a distant third.

I guess there’s also LinkedIn. Look how well I kept a straight face. Get over yourself LinkedIn, you’re dumb.

So, do I use any of these? The Endocrine Society’s “Daily Briefing” is great. The biggest benefit is that it often links to a simply written article. If you want to read the actual papers it clearly supplies references, but other than that a few paragraphs summing up the study is ideal.

Similarly, PracticeUpdate sums up a lot of studies. You know those people who constantly have multiple tabs open on multiple web browsers? Yeah that’s me. And it’s almost definitely PracticeUpdate’s fault. I open at least a tab a day, aiming to read them later, but I rarely get it done.

I have never cited a paper I’ve found on Twitter. I think it’s because when I’m trying to write a paper I don’t generally check Twitter. (I’m a Facebook nerd, not just a better person than you.) I also tend to read papers I find interesting, and not necessarily for their science. Show me a paper about a bunch of nonsense and I’ll probably read that and share it. Even if my friend shares one of their papers I don’t think I’ve ever shared it.

“Why wouldn’t you help your friends?” you scream, somewhat obtusely. Firstly, I’ve just told you it doesn’t help, but I will from now on though! Especially on Mendeley.


Today’s quote is from A.M. Homes.

I hate judgemental people. They’re so mean…and fat.

My first piece is up on the Diabetes UK blog now, so I thought I’d update you on some other stuff I’ve been doing. Namely acting as a referee on a paper.

Now, I have some issues with referees as you’d expect from someone who’s been trying to publish a paper for two years, and I’ve not had the best experiences to be honest.

I’ve had a referee completely misunderstand RT-PCR. It’s basically a method for seeing which genes are expressed, that is it; and that is all we wanted to use it for, to narrow down our options from 13 potential targets. But this chump was adamant that it was quantitative, and we were ignoring these clear differences. Even when we explained that it wasn’t quantitative, and that we only carried it out to see which genes were expressed, they just ignored it and complained about it again. I’m not saying it’s as bad as anti-vax statistics, but it’s pretty close…

I’ve been told that our paper wasn’t novel, despite showing a mechanism that no-one has ever seen before. I know no-one has seen it before, because it’s literally my job to know that. They basically went “A causes B, and we know that C causes D, and all you’ve done it show that they are linked”.

I have had a grant rejected because people already know what PLCs do in insulin resistance, when we applied to investigate PKCs. I mean what can you do with that?! It’s an entire different family of proteins. Obviously you lose novelty if you just decide that investigators want to look at completely different things!

And to top it all off I’ve been called Dr Alexander a fair few times. If someone can’t even understand my name I’m fairly certain they can’t be trusted to understand my science.

Bearing that in mind you can see why I couldn’t wait to be a jerk to someone else’s paper, right? Obviously I won’t tell you which journal or anything it was in, but it’s a higher impact that anything I have published in. So, you’d expect it to be good, hey?

It wasn’t.

It really, really wasn’t.

They missed out control experiments, hid several bits of data, cited their own “Manuscript under review” to back up their conclusions. They even contradicted their own paper that they had just published. They also used a marker for insulin resistance that me and others have shown is inappropriate. As well as using that pesky RT-PCR, but at least they understood how.

I wanted to be a right jerk, but I wasn’t sure if I was just bitter. So, I was “nice” about it. However, my supervisor agreed with all of my criticisms. We sent off a great big “hell no!” and a couple of days later we got to see the other referee’s comments. Now, they take being a jerk to a whole new level. They echoed almost everything we said, but with a heaping scoop of anger and poison.

In the end, it was actually quite comforting to know that my input and comments were valid, and that my belief that this paper wasn’t good was justified. However, you best beware I’m not refereeing your next paper as now I know how mean I can really be!

Today’s quote is from John R. Lindensmith