Author Archives: The Physiological Society

About The Physiological Society

The Physiological Society brings together over 3,500 scientists from over 60 countries. Since its foundation in 1876, its Members have made significant contributions to our knowledge of biological systems and the treatment of disease. We promote physiology and support those working in the field by organising world-class scientific meetings, offering grants for research, collaboration and international travel, and by publishing the latest developments in our leading scientific journals, The Journal of Physiology, Experimental Physiology and Physiological Reports.

Bringing together physiologists from around the world: Europhysiology 2018

In the last two decades physiology events have been challenged by evolving sub-disciplinary and thematic conferences. The Europhysiology series of conferences will bring together the broader European physiology community and promote collaboration among scientists.

‘I am really looking forward to this exciting Europhysiology meeting being able to discuss and networks with colleagues from our European neighbours and hear about the ground breaking research being performed outside of the UK,’ says Charlotte Haigh from the University of Leeds, UK.

The partner Societies value our future leaders in physiology research and so it was critical to find out their opinion of why such a meeting of European physiologists would benefit them.  We asked our Affiliate Working Group what they feel that they will be of most use to them.


A major reason for attending such an event is to foster new collaborative ventures with physiologists from across Europe.  It was strongly felt that in this climate of interdisciplinary research, such a meeting would increase the capacity to tackle complex problems by promoting new research collaborations.

‘When I heard about the opportunity to present as an early career speaker at Europhysiology, I knew this was a great way to share some of the data that our lab collected in the past few years,’ Cas Fuch from Maastricht University, Netherlands told Physiology News.

Interestingly, our early career scientists feel that they are more likely to know who is carrying out research similar to them in the USA rather than Europe and such a meeting would introduce them to researchers and techniques that they were not aware of previously.

It would mean that they could learn how others approach specific research questions and then they could input into these or perhaps change their approaches in the future.  It also opens up new career opportunities.


Indeed early career researchers are also less aware of European differences in career structure and so such a meeting would allow them to probe these differences.  Since Brexit and issues surrounding UK research funding from Europe cannot be totally ignored, it was also considered important to consider how future research collaborations can be worked at this stage.

The structure of the meeting was also very attractive to ECRs with over 100 slots for oral communications; they feel that this is wonderful opportunity to showcase their research.

It is clear that all levels of physiologist are looking forward to this meeting of scientific minds but it is especially rewarding to know how highly our “future physiologists” rate such an opportunity to attend such conferences.


‘For me the conference will be a fantastic opportunity to meet colleagues and friends, to enjoy science in different talks and poster presentations. Discovering new advancements and ideas in the different fields of physiology it will be an opportunity to strengthen already exciting friendships and to make new ones,’ Anaclet Ngezahayo from Leibniz University Hannover, Institute of Biophysics, Germany.

The series will begin in London, UK in 2018 and will subsequently be organised in Berlin, Germany (2020) and Copenhagen, Denmark (2022). FEPS will be a joint organiser of these biennial conferences.

(This article was originally published in Physiology News 110, pg. 19)










Can ketones lower blood sugar, and thus help diabetes?

By Jonathan Little (@DrJonLittle) and Étienne Myette-Côté, University of British Columbia

Low-carbohydrate, high-fat ketogenic diets are gaining popularity as a treatment option for type 2 diabetes because when someone eats less carbohydrates their blood sugar remain low. The diet is named after ketone bodies, compounds that the body produces when someone restricts their carbohydrate intake to very low levels.

Now, new ketone supplements that come in liquid or powder form claim to offer some of the benefits of a ketogenic diet without having to follow such a strict diet. Essentially, they allow you to drink ketones instead of relying on your body to produce them naturally. The appeal is obvious: lifestyle interventions like a ketogenic diet are hard to stick to over the long term. However, these supplements are also interesting for us physiologists because when someone eats a ketogenic diet, so many metabolic changes happen at the same time that it’s difficult to pinpoint which change caused which effect. Using ketone supplements can allow us to study the effects of ketones specifically.


Image from-

Unfortunately there is very little research on ketone supplements, particularly their impact on blood sugar or outcomes relevant to diabetes. To begin to fill this gap in knowledge, our recent research in The Journal of Physiology studied the effect of ketone supplements in healthy adults.

Introducing the ketone star: β-OHB

The most abundant and important ketone body produced by the liver during a ketogenic diet is called beta-hydroxybutyrate (β-OHB). β-OHB can be used as an alternative fuel to carbohydrates by some parts of the body including the brain, heart and muscles. In recent years, β-OHB has garnered substantial media and research attention: studies in cells and animals have shown that β-OHB has glucose lowering, anti-inflammatory, anti-oxidant, and even lifespan-extending effects (1, 2, 3, 4).

In humans, it is difficult to determine the effects of β-OHB itself due to the myriad of physiological and hormonal changes that occur when somebody follows a restrictive ketogenic diet. The first answers come from studies where researchers have infused ketones directly into the blood of participants – like with a drip feed. Several of these studies conducted over the last few decades have consistently observed that when you infuse β-OHB directly into the bloodstream of humans, their blood sugar drops (5, 6).

Although the infusion method provides insight, it lacks therapeutic application: it would be impractical to keep patients with diabetes on a ketone drip in an attempt to lower their glucose. With the blood sugar-lowering effects of β-OHB infusion having been consistently observed in the past, we became interested in studying whether the newly-developed ketone supplements might lower blood sugar levels in humans.


It would be impractical to keep patients with diabetes on a ketone drip.

Do ketone supplements lower blood sugar in humans?

Given that this was the first study (to our knowledge) to directly test this, we started by studying young healthy individuals. We recruited 20 healthy participants (10 males and 10 females, aged between 21 and 29 years) who underwent two oral glucose tolerance tests. This test involves drinking a large quantity of sugar (pure glucose) and measuring blood sugar at several time points afterwards to assess changes in blood sugar level. This test can also be used to diagnose diabetes.

One oral glucose tolerance test was performed 30 minutes following the consumption of the ketone supplement and one was performed after consuming a masked placebo. The order was random – some took the ketone supplement first and some the placebo first – and both the participants and study personnel performing the laboratory analyses were blinded, meaning that they did not know whether the participant had taken the ketone supplement or placebo.

The ketone supplement raised blood β-OHB to just over 3 mM within 30 min, levels normally seen after many weeks on a ketogenic diet or several days of fasting. This suggests that the supplements might be a good method to get β-OHB into the blood, without the hassle of a drip. When we then looked at the spike in blood sugar in response to the oral glucose tolerance test, it was much lower after drinking the ketone supplement compared to the placebo condition. Specifically, when plotted on a graph the area under the curve was decreased by ~16% when participants had the ketone supplement. Additional metabolic benefits of the ketone supplement were a reduction in levels of fatty acids circulating in the blood and an improvement in insulin sensitivity. Thus, consuming a ketone supplement was able to improve aspects of glucose regulation in healthy humans.

This study in healthy humans raises the obvious question of whether the same effects could be seen in individuals with elevated blood sugar, such as individuals with type 2 diabetes, prediabetes, or obesity.

It is not clear if our results will carry over to people with these diseases. However, a major reason for high blood glucose in type 2 diabetes is that the liver is constantly “leaking” too much glucose into the circulation. If the ketone supplement prevents this, which is what we think happens, then ketone supplements might indeed be helpful for diabetes; it’s now up to future studies to build on our findings and hopefully find the answer!


  1. Madison, L. L., Mebane, D., Unger, R. H., & Lochner, A. (1964). The hypoglycemic action of ketones. II. Evidence for a stimulatory feedback of ketones on the pancreatic beta cells. The Journal of clinical investigation, 43(3), 408-415.
  2. Youm, Y. H., Nguyen, K. Y., Grant, R. W., Goldberg, E. L., Bodogai, M., Kim, D., … & Kang, S. (2015). The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease. Nature medicine, 21(3), 263.
  3. Shimazu, T., Hirschey, M. D., Newman, J., He, W., Shirakawa, K., Le Moan, N., … & Newgard, C. B. (2013). Suppression of oxidative stress by β-hydroxybutyrate, an endogenous histone deacetylase inhibitor. Science, 339(6116), 211-214.
  4. Edwards, C., Canfield, J., Copes, N., Rehan, M., Lipps, D., & Bradshaw, P. C. (2014). D-beta-hydroxybutyrate extends lifespan in C. elegans. Aging (Albany NY), 6(8), 621.
  5. Mikkelsen, K. H., Seifert, T., Secher, N. H., Grøndal, T., & van Hall, G. (2015). Systemic, cerebral and skeletal muscle ketone body and energy metabolism during acute hyper-D-β-hydroxybutyratemia in post-absorptive healthy males. The Journal of Clinical Endocrinology & Metabolism, 100(2), 636-643.
  6. Miles, J. M., HAYMOND, M. W., & GERICH, J. E. (1981). Suppression of glucose production and stimulation of insulin secretion by physiological concentrations of ketone bodies in man. The Journal of Clinical Endocrinology & Metabolism, 52(1), 34-37.
  7. Taggart, A. K., Kero, J., Gan, X., Cai, T. Q., Cheng, K., Ippolito, M., … & Jin, L. (2005). (D)-β-hydroxybutyrate inhibits adipocyte lipolysis via the nicotinic acid receptor PUMA-G. Journal of Biological Chemistry, 280(29), 26649-26652.
  8. Reaven, G. M., Chang, H. E. L. E. N., Ho, H. E. L. E. N., Jeng, C. Y., & Hoffman, B. B. (1988). Lowering of plasma glucose in diabetic rats by antilipolytic agents. American Journal of Physiology-Endocrinology and Metabolism, 254(1), E23-E30.
  9. Ferrannini, E., Barrett, E. J., Bevilacqua, S., & DeFronzo, R. A. (1983). Effect of fatty acids on glucose production and utilization in man. The Journal of clinical investigation, 72(5), 1737-1747.
  10. Balasse, E. O., Ooms, H. A., & Lambilliotte, J. P. (1970). Evidence for a stimulatory effect of ketone bodies on insulin secretion in man. Hormone and Metabolic Research, 2(06), 371-372.
  11. Senior, B., & Loridan, L. (1968). Direct regulatory effect of ketones on lipolysis and on glucose concentrations in man. Nature, 219(5149), 83.


#LGBTSTEMDay: Celebrating the diversity of science

By Shaun O’Boyle, founder of House of STEM

Today is the first International Day of LGBT+ People in Science, Technology, Engineering and Maths, celebrating and encouraging diversity in science.

We do better science when our teams are made up of diverse people, with different perspectives, skills, and ideas. To achieve that diversity, however, we must first remove the roadblocks that are causing some minorities to remain underrepresented in science.

These roadblocks can arise early. A recent study by the Institution of Engineering and Technology (IET) found that 29% of LGBT+ young people choose to avoid a career in STEM because they fear discrimination. We know from research published in Science Advances that those who do enrol in STEM courses are more likely to drop out.


Of those who do pursue a career in science, more than 40% are not ‘out’ to their colleagues, and this is having a negative impact on their career prospects. Remaining ‘in the closet’ also takes its toll on a person’s mental health, as they spend every single day monitoring, policing, and editing what they say and do. In the United States, one third of ‘out’ physicists have been told to stay in the closet to continue their career, and half of Trans physicists have experienced harassment in academia. We therefore need to work on the environments LGBT+ scientists work in, to make them more supportive and welcoming.

Take fieldwork, for example. For a scientist, field work can be dangerous—collecting samples near active volcanoes, gathering data in areas of conflict, risking insect-borne diseases while documenting species in the rainforest—and so we prepare as best we can to minimise those risks.

When an LGBT+ scientist is invited to do field work, we must first make sure it’s not to one of the 72 countries where it’s illegal to be LGBT+, or one of the eight where our identity carries the death penalty. Even in countries with no legal barriers, we must make sure that we are not going to a region with a high incidence of hate crime. These are complex risks to minimise. For example, we must make a choice about “coming out” to our colleagues—whether it is better to have their support, or if telling them risks us being accidentally outed on the trip.

LGBT+ scientists and our allies are working to ensure no one struggles to be themselves at work—whether it’s fieldwork or lab work, teaching or studying. Research initiatives such as Queer in STEM and the LGBT+ physical sciences climate survey are doing what scientists do best: gathering data. By having a clearer understanding of the experiences of LGBT+ scientists across different disciplines, we can develop supportive policies, and create more inclusive environments. Initiatives such as LGBTSTEM and 500 Queer Scientists are improving the visibility of LGBT+ scientists, helping to create role models for others in their fields.

Visibility is at the heart of a new initiative to amplify the voices of LGBT+ scientists around the world. Today is #LGBTSTEMDay, the first ever International Day of LGBT+ People in Science, Technology, Engineering and Maths. The initiative is being led by an international collaboration between four groups—Pride in STEM, House of STEM, InterEngineering, and Out in STEM—and supported by more than 40 organisations, including CERN, EMBL, Wellcome, and The Physiological Society.

#LGBTSTEMDay will see live events and get-togethers happen at physical locations from Brazil to Scotland, Toronto to Switzerland. Primarily, however, it will be an online campaign, and an opportunity to highlight the powerful work already being done by people, groups and organisations all around the world to advance the inclusion of LGBT+ people in STEM. We hope you’ll join us in celebrating the diversity of science.

Shaun O’Boyle is a science communicator and producer with a degree in Physiology and a PhD in Developmental Biology. He is the founder of House of STEM, a network of LGBT+ people who work in STEM in Ireland, and one of the organisers of LGBTSTEMDay.

Reflections on Parliamentary Links Day 2018

By Charlotte Haigh, University of Leeds, @LottieHaigh

I was very honoured to be invited to Parliamentary Links Day, by The Physiological Society on the 26th June. The theme this year was science and the industrial strategy. Being Yorkshire, born and bred and still living up north, you don’t often get these opportunities and I was very unsure what to expect.

After arriving early and going through security checks, I found myself in a packed room in Portcullis House ready for the start of the day. Although the event was organised by the Royal Society of Biology, 13 other societies were represented by banners at the event from across the breadth of science, technology, engineering and maths.

The morning session was filled with speakers including five MP’s, the Government Chief Scientific Advisor and a representative from UKRI. These speakers all pulled out key points of how the science and industrial strategy is aimed to be delivered and how increasing the funding of R&D in the UK wasn’t the only challenge. The speeches were broken up by two discussion panels of people from many of the represented societies talking about how they were contributing to influencing and delivering some of the key elements of the strategy.

It was made apparent at the start that not many MP’s are well-versed in science, and this is a problem. We need more scientists and engineers in the House of Commons. This surprised me at first but then on reflection, as scientists, not many of us would aim for that type of profession.

The Chair of the Science and Technology Select Committee, Norman Lamb MP, highlighted how important it is that we continue to get the best people to work in science in the UK. Government is currently working on a blueprint of the pact we need to agree on for science in the Brexit negotiations. I am sure many of us would support this.


Dr Patrick Vallance, The Chief Scientific Advisor, speaking 

Many of the discussions we have been having in the higher education sector at present and for many years were highlighted and discussed. We need to nurture young talent from an early age, right from primary school. We must concentrate on achieving diversity in areas such as gender and ethnicity in all STEM areas, taking it seriously and not just paying lip service to it. We should value technical staff and give them opportunities to flourish. There was also a discussion raised by our own Andrew Mackenzie (Head of Policy and Communications) about the issue of 45% of public spend on R&D going to the golden triangle (Oxford/Cambridge/London) and how we need to focus on getting economic development to poorer regions of country.

So what are my reflections on this day? Well, it was interesting to hear all this and there were no surprises in what was said. Lots of challenges, but not many answers. Many of the discussion points raised resonate and are mentioned within The Physiological Society’s new 2018-2022 strategy which is great to see. Throughout the day, lifelong health (The Society’s policy focus) was mentioned, more than once, as one of the grand challenges for STEM going forward. I think being involved in a day like this is important for The Society and its members, to make the government aware who we are and what we do and promote what I hope is a two-way stream of communication between Government and the scientific community. It was great to hear that ‘scientists on the coal face must be supported’ but the cynic in me questions how the government can really achieve this.

If you wish to see anymore highlights of the event, visit the Royal Society of Biology Facebook page or search #LinksDay18 on Twitter.



Why dieting is bad for you

By Simon Cork, Neurophysiologist, Imperial College London, @SimonCorkPhD

According to a 2016 survey of 2000 people in the UK, almost two thirds of us are on a diet at any one time. For most people, the typical diet consists of eating a salad for lunch, and cutting out desserts and snacks. NHS guidelines for weight loss recommend reducing calorie intake by around 600 calories each day. But is this advice right?

There is a theory among many scientists in the obesity field that body weight is fixed around a “set point”. That means that for the majority of people, body weight is typically static (unless drastic changes are made to exercise or diet). Any fluctuations in our body weight are compensated for by either increasing or decreasing energy input or output. You might feel this if you’re on a low calorie diet by feeling constantly tired and feeling like you just want to sit down. That’s your body’s way of trying to conserve energy.

One method our body uses to keep its weight constant is a hormone called leptin, released by fat cells into our bloodstream. The more fat we have, the more leptin we have flowing through our blood. Normally, leptin acts in the brain to restrict appetite, effectively acting as the brake to restrict major changes in body weight. Minor increases in fat lead to increases in leptin, which reduces appetite. Loss of body fat causes decreases in leptin and thus increases in appetite to compensate. Leptin is therefore the body’s messenger to the brain, informing it of our weight.

The problem occurs when we override the effects of leptin, typically with respect to its appetite-restricting effects. More fat means more leptin, which should reduce our appetite, and thus reduce our body weight back to what our brains perceive as “normal”. However, if we override these effects (e.g. by ordering dessert after starters and a main, or eating large portions, thus eating past the point of feeling full), our brains eventually become resistant to leptin.

simon cork dieting

Leptin levels are directly correlated with body weight. Bronsky et al, 2007.

This leptin resistance effectively means that our brains are tricked into underestimating what our body weight truly is. Although a 150 kg person has more circulating leptin than a 70 kg person, the extra leptin doesn’t decrease appetite as it should because the brain has become resistant to leptin: it needs more leptin to have the same effect. The brain is therefore “tricked” into thinking the body has less fat than it really does.

This has significant consequences when people who want to lose weight go on low calorie diets. As we restrict food intake, we lose body fat. For reasons not fully understood, the levels of leptin fall at a greater rate than body fat. Our brains react by activating mechanisms to restrict any further loss of body fat and promote energy storage. One such reaction is lowering the resting metabolic rate – effectively the minimum amount of energy required to keep us alive.

You may remember a US TV series called “The Biggest Loser”. This show took overweight or obese people and subjected them to a gruelling exercise and diet regime. The contestant who lost the most weight by the end of the show won a significant cash prize. In 2016, the results of a study were released which followed the contestants after they finished the show. They found that almost all contestants regained their weight and found that some regained more weight than before they started.

And this is the crux of the matter. It has been found that people who go on crash diets significantly reduce their resting metabolic rate – effectively, they are using less energy just by being alive than before the diet. And this metabolic rate may never recover – even after stopping the diet.

This may explain why a number of contestants regained more weight after the show than they started with. Their bodies are constantly fighting against a famine. It may also be why most people who go on a diet fail to maintain their low body weight long term. This is the key issue that many people developing weight loss therapeutics are facing.

simon cork dieting 2

Calorie restriction (CR – blue line) results in significant decreases in resting metabolic rate (RMR) Davoodi et al, 2014

For many people, losing weight is relatively easy. Simply restricting calories and/or increasing the amount of energy we use, usually by exercising, will result in weight loss. Maintaining that weight loss is the key issue. Exercise is often the key to maintaining weight loss, but is difficult to maintain the necessary levels of exercise required to compensate for the decreases in energy use that occurs following dieting.

Scientists are currently investigating how to manipulate the body weight set point, by both re-sensitising the body to leptin (i.e. countering the leptin resistance), and/or by increasing the levels of naturally occurring hunger-suppressing hormones that our bodies release after eating.

If decades of dieting advice has told us anything, it’s that dieting doesn’t work to bring about long-term weight loss. But importantly, by permanently reducing the resting metabolic rate, dieting may actually be preventing our bodies ability to lose weight in the future.

Microbiome – fad or future?

By Simon Cork, Neurophysiologist, Imperial College London, @SimonCorkPhD

You may have heard many scientists and media types getting excited over the term “microbiome” recently. There was a series on BBC Radio 4 termed “The Second Genome” recently dedicated to it, and a succession of articles on the BBC News website 1 2. But what exactly is it, what does it do, and should we all be excited?

The microbiome is the term scientists give the community of bacteria that live in your guts (micro meaning small, and biome meaning biological community). People have been studying the microbiome for many years, and there is a remarkable amount of literature around the microbiome of insects. But recently, the microbiome of humans, and specifically the effects our microbiomes have on our overall health, has entered the spotlight.

In insects and other animals, the bacteria that live in and around them have remarkable effects not only on their heath but on their development. For many insects and animals, interactions with bacteria are a requirement for their survival. One particularly powerful example of the influence of bacteria on a host’s behaviour is in the fruit fly.

Feeding fruit flies different diets (and thus altering their gut microbiome composition) causes them to preferentially mate with flies fed on the same diet. When given antibiotics, which wipe out their bacteria, this preference disappears.

In humans, we are only just beginning to understand (or perhaps recognise) the importance that the microbiome has on our health. We are also beginning to understand how changes in our microbiome predispose, or even cause, certain diseases.


Less bacteria, more weight?

Take obesity for example. Worldwide, over 2.1 billion people are overweight or obese. The causes of obesity vary from person to person, but one common factor found in obese individuals is the lack of diversity of their gut bacteria. In a lean individual, the gut bacteria will contain a variety of different strains and species of bacteria. However, in individuals with obesity, this diversity is significantly reduced (with an increase in the ratio of the Firmicutes and a decrease in the Bacteoridates species).

We also know that babies who are born via caesarean section are at a higher risk of developing a number of health conditions in later life, one of which is obesity. The reasons why are not completely understood, but we know that C-section babies do not get the full complement of bacteria that babies born naturally get.

Essentially, in the first few months of life, a baby born via C-section has a gut bacterial population that more closely resembles that found on the skin, as this is often the first bacteria that they come into contact with.

Quite astonishingly, it may be possible that gut bacterial populations that predispose to disease act as a form of non-genetic inheritance of disease. For example, an obese mother, who likely has a bacterial population with a low diversity, may pass this low diversity to her child during delivery, thus predisposing them to obesity in later life.

So what does this mean? Well, the honest answer is we don’t quite know. At the moment, these observations are simply that, observations. We can predict whether or not a person will be obese or lean with 90% accuracy simply by studying the diversity of their microbiome, but what we don’t fully understand is how the bacteria are contributing to weight gain.


What’s in it for them: bacteria causing obesity? And other diseases?

One theory is that certain bacteria have the ability to harvest energy from our diets more effectively than others. Couple this with a sedentary lifestyle and you have the recipe for weight gain.

Another theory is that the bacteria are interfering with our brain chemistry. We know that many species of bacteria can secrete molecules that are either the same or have very similar chemistry to many of the molecules found in our brain, and we know that bacteria are able to secrete these chemicals in response to certain foods.

Could it be then, that our bacteria are driving our food choices? Imagine a population of gut bacteria that have a penchant for sugar; they use this as their main source of energy and want to make sure that it keeps coming. Is it possible that in response to their host eating a sugary meal, the bacteria release chemicals that tells their brain to eat more? This may sound far-fetched, but there’s increasing evidence that this may actually be happening.

There’s also increasing evidence that our gut bacteria may be driving a number of other conditions, including asthma, depression and anxiety, possibly through chemicals they release which interfere with our normal brain chemistry.

To each their own: individual differences and possible ways to shift them

So what can we do about this? Well, the bad news is this area of research is still very much in its infancy.

There are a few things we do know.

Our gut bacterial populations vary considerably from person to person, which makes a one-size fits all approach to fixing a dysfunctional microbiome tricky (although the microbiomes of people living in the same house are more similar than they are to the rest of the population).

The difficulty now is figuring out how we can shift this composition in later life. Unfortunately, downing a yoghurty probiotic drink containing a single strain of bacteria doesn’t really have much of an effect on the overall composition of the community in our guts. Many of the bacteria found in these drinks are not normally found in the guts of anyone – in fact they’re chosen largely because they can survive both the hostile journey from mouth to gut, and through the factory.

Our diets play a large role in the composition of our microbiome. And our microbiome populations become fixed during our early life. Differences in how we were delivered, whether we are breast fed or bottle fed, which country we grow up in and whether we share our house with pets, all affect the composition of our microbiome.

Perhaps the easiest way of shifting our microbiome is related to how much fibre we eat. Our bodies can’t digest dietary fibre on its own, and most of the fibre we eat makes its way to the end of our digestive tracts. This is where it feeds the bacteria in our guts, who in response not only increase their diversity (fibre feeds a lot of different kinds of bacterial species, who can all grow in its presence), but also release chemicals which are beneficial to our bodies’ health.


Poop pills: what do we know about this surprising possible obesity treatment?

However, there is another way we can shift our microbial population – faecal transplants. If we take an obese mouse, and feed its droppings to a lean mouse (thus transplanting its bacteria), that lean mouse will become obese – regardless of what it eats. The same is true if you take the gut bacteria from an obese human and transplant it into the gut of a lean mouse. That in itself is amazing.

But is the same true for humans? Well, faecal transplant (or FT) has been used clinically to treat C. difficile (or C-diff as it’s commonly known) infection. This nasty hospital-acquired infection is difficult to treat with standard antibiotics and, left unchecked, can be fatal. However, FT is an effective treatment for C-diff and is a cure for many people.

On the other hand, the literature surrounding its effectiveness for treating obesity in humans is controversial, and also risky. A lack of proper clinical trials means we don’t fully know whether it works or to what extent. Furthermore, FT has the potential to transmit a number of diseases, and given the increasing number of conditions that are being attributed to gut bacteria, the risk might just be too great given our level of understanding.

The bottom line: the future looks promising

So what’s the take home message? The microbiome is an exciting area of research, and undoubtedly will lead to treatments for a number of diseases in the future.

As it stands, our understanding is largely based on observational data – a case of correlation, rather than causation. But many people are confident causation is there, we just need the definitive proof.

In the meantime, the best thing we can do to feed our hungry bugs is to increase the amount of fibre in our diets and reduce unnecessary antibiotic use. The good news is that a lot of people are getting excited, and the gut microbiome is no longer the playground of just the microbiologists. Gut scientists, lung scientists and neuroscientists are all getting in on the action, and these collaborations are rapidly increasingly our knowledge of how the bacteria in our bowels are affecting our health. The time for the microbiome to really show its potential grows ever closer.




Early to bed and early to rise… makes a teen healthy, wealthy and wise? (Part 2)

By Gaby Illingworth, Rachel Sharman & Russell Foster; @OxTeensleep, @gabyillingwort1, @DrRachelSharman, @OxSCNi

To the possible dismay of parents hoping to start the family day bright and early, teenagers hit the hay and wake up at increasingly later times during adolescence – a delay of between one and three hours compared to pre-pubertal children.

Teenagers struggle to fall asleep early but still need to wake up for lessons during the school week, which contributes to a reduction in time spent asleep. At the weekend, the morning hours may well be spent snoozing to “catch-up” on lost Zzz’s.

In 2015, the National Sleep Foundation recommended that teenagers, aged 14 to 17 years, should be getting eight to ten hours of sleep a night. However, across the globe, teenagers are routinely not getting enough sleep, with older adolescents more likely to have insufficient weekday sleep than early adolescents. One of the consequences of insufficient sleep is that sleepiness during the day is common in this age group.

Sleep researchers have suggested some mechanisms behind this change in teenagers’ sleep timing.

How teenagers become owls: slower clocks, increased light sensitivity, or decreased sleep pressure

Although we don’t know why adolescent sleep changes, we do know that changes occur in the two processes which govern sleep – the circadian rhythm and sleep/wake homeostat. (Catch up on these two concepts in our previous post.)

The teenage biological clock has been proposed to run more slowly at this age, driving their sleep timing later, meaning their chronotype becomes more owl-like.


From DIVA007 on Flickr

Another suggestion is that their biological clock might be more sensitive to light in the evening (delaying sleep) and less sensitive in the morning (making them wake up later).

Adolescent sleep pressure is also thought to accumulate more slowly during the day, making them less tired when they reach the evening.

Jetlag without leaving the country

We know what jetlag feels like when we travel across time zones. Our internal time takes a while to adjust to the new external time.


Teenagers experience something similar with ‘social jetlag’: when their internal time (chronotype) is misaligned with social time (school commitments). At the weekend, they are more likely to be able to sleep according to their chronotype than during the school week. This misalignment of sleep/wake timing has been shown to associate with poorer cognitive functioning.

To blame the bright screens or not?

Teenagers’ lack of sleep is not all down to physiology. They, just like adults, may be engaging in behaviour that isn’t conducive to sleeping well.

The effect of light exposure on sleep has received increasing attention with the proliferation of electronic device use in recent years. However, the results are mixed.

One study on young adults asked individuals to read an e-book at maximum intensity under dim room light for around 4 hours (18:00–22:00) before bedtime on five consecutive evenings, whilst the control group read a printed book.

While the study concluded that those that read the e-book took longer to fall asleep, had lower morning alertness, and a delay of the circadian clock compared to reading a printed book, the effects were relatively small. Those participants who read e-books took only 10 minutes longer to fall asleep (Chang et al., 2015).


As a result, some caution needs to be exercised when the press reports that reading an e-book before bed has unintended biological consequences that may negatively affect performance, health, and safety.

Nevertheless, the impact of using electronic devices prior to sleep does seem to be important. In a large US survey, adolescents were shown to have increased the time spent using electronic media devices from 2009 to 2015.

This was correlated with a decline in sleep duration (Twenge et al., 2017), and light from such devices has been blamed. Such studies have encouraged the use of in-built or downloadable applications that can dim the brightness of screens and/or reduce the light emitted.

Light interventions are now being considered as a tool for adolescents experiencing difficulties with sleep, including reducing their exposure to evening light and increasing morning light to advance the clock to a time more suited for school.

Unfortunately, the evidence showing that such interventions can be helpful is lacking. Furthermore, it is important to stress that game use, social media, and watching TV are all likely to be cognitively arousing so teens may simply feel like staying up when they use electronic media devices.

As a result, disentangling the light effects versus the alerting effects of devices is complex and awaits good experimental studies.

Highly caffeinated



From Austin Kirk on Flickr

Caffeine is a stimulant with a half-life of approximately six hours in healthy adults (meaning that half of it is broken down in our bodies in six hours). It works by preventing the molecule adenosine, which promotes sleep, from having its effect in the brain, thus promoting wakefulness.

Teenagers are advised to consume no more than 100mg of caffeine per day, yet highly-caffeinated energy drinks are popular among teens. Many energy drinks contain higher caffeine levels than 100mg in a single can. Consuming caffeine later in the evening, or consuming it excessively throughout the day may be another contributory factor to delayed sleep.

Correspondingly, the National Sleep Foundation 2006 ‘Sleep in America’ poll found that adolescents who drank two or more caffeinated beverages each day were more likely to have insufficient sleep on school nights, and think they have a sleep problem, than those who drank one beverage or fewer.

We don’t need no early morning classes

School-based interventions are now underway that aim to improve teenage sleep. Sleep education programmes inform teenagers about the lifestyle factors that may be affecting their sleep and how they can improve sleep hygiene.

There is also a movement to delay school start times to better suit the adolescent clock by giving teenagers the opportunity to sleep at hours more aligned with their chronotype and reduce their social jetlag.

Given all the research, one could suggest that “early to bed, later to rise, may help the teen be healthy, wealthy and wise” would be a better amendment to the age-old quote for our average teenager.


Chang, A.M., Aeschbach, D., Duffy, J.F. and Czeisler, C.A., 2015. Evening use of light-emitting eReaders negatively affects sleep, circadian timing, and next-morning alertness. Proceedings of the National Academy of Sciences112(4), pp.1232-1237.

Twenge, J.M., Krizan, Z. and Hisler, G., 2017. Decreases in self-reported sleep duration among US adolescents 2009–2015 and association with new media screen time. Sleep medicine39, pp.47-53.