1.08/ Common Gastrointestinal Conditions
21 Min. 33 Sec. | July 08, 2019
INTRO: Hello and welcome to Clinical Nutrition Notes – a podcast where we speak with guest experts and opinion leaders about the art and science of clinical nutrition – brought to you by Nestlé Health Science Canada. This podcast is intended for health care professionals, for education purposes.
I am your host, Bethany Hopkins, Medical Affairs Manager with Nestle Health Science.
Today we will be talking with Anton Emmanuel M.D. about the nutrition management of four common G.I. conditions clinicians encounter in practice. Dr. Emmanuel is an academic neuro-gastroenterologist at University College London and consultant gastroenterologist at University College Hospital and the National Hospital for Neurology and Neurosurgery at Queen Square. His clinical work encompasses being director of the G.I. physiology unit at University College Hospital as well as providing a gastroenterology service at Queen Square. Dr. Emmanuel's research includes basic gut neurophysiology and the study of the pathophysiology and management of gastrointestinal disorders of the upper and lower gut in neurological disease and functional conditions. He is the editor of the journal Frontline Gastroenterology.
Hopkins: Thank you for joining us Dr. Emmanuel. Nutrition plays a role in the management of a variety of G.I. diseases and disorders. Today we'll explore several common G.I. conditions that gastroenterologists and dietitians encounter in daily practice, and some of the nutrition implications to consider in their management. Namely we will focus on Irritable Bowel Syndrome or IBS, constipation, fecal incontinence and gastroparesis. First, can you talk about the role of fibre in irritable bowel syndrome and constipation.
Emmanuel: Thank you. So, if we look at a very brief review of history, constipation is associated with a low-fibre diet and that kind of observation from the 1920’s became the kind of mantra from Kellogg onwards to then gforce fibre into people. But what we recognize is that constipation is a term which covers a variety of pathologies that can occur and whereas fibre can help some of those, it doesn't help all of those. And in particular there's this question of constipation due to slow transit where in that population of patients who have slow transit constipation, fibre in fact makes their symptoms worse. It makes it worse by making them more bloated, and more windy, and more uncomfortable without increasing the amount of stool they empty. Whereas patients with more normal transit it can be enormously helpful.
So, this notion that there’s a kind of blanket approach saying “fibre, it works, it’s good,” I think is therefore underpinned by thinking about what is causing it to work, how does fibre work. And broadly speaking fibre has two principal mechanisms of action. The first is a physical mechanism where it sits in the gut, doesn’t get absorbed, and osmotically holds on to content and therefore has ability to expand the bowel. And when the bowel is stretched it’s like an elastic band, the more you stretch it the more it pings forward. So, there’s that physical dimension, and that the more fibre there is in one's diet the more that can happen. The other effect of fibre is a chemical one where it forms a nice substrate for colonic bacteria to help digestion. And in that situation what happens there is the metabolites produced by the bacteria are things which may have an effect on gut transit and gut movement, but that effect is maxed out, it's maximal, at very low levels of fibre consumption.
And so, the risk is that you can find yourself taking fibre for the slow transit problem and not actually increasing your stool output and not feeling any more comfortable, in fact getting more uncomfortable. So, of course if you take that in an IBS setting now, if your IBS patient happens to have a slow transit constipation problem, then they'll get more bloated and windy and that's especially troublesome given that some patients with IBS – the bloating and pain is the dominant feature that bothers them.
So, I think this notion of fibre as being a cure-all is something which we need to help patients move away from. Now most professionals know that's the case and we'll try and assess the patient to identify slow transit versus non. But I think it's important to understand there’s that aspect of fibre and the diet, and then specifically we also consider this notion about soluble and insoluble fibres which is, I think would say getting increasingly understood in not just the literature but by our patients. They're familiar with this concept quite often and this emerging concept of a resistant starches and this question of how your gut handles fibre – dependent on whether it's water soluble or not, and that there are certain good soluble fibres from vegetables and fruits and certain more difficult fibres to handle in terms of the cereal-based fibres. And that notion, and how those cereal-based fibres can be more troublesome in people with IBS, is something for which there is a good evidence base now. So, I think the fibre story is not the simple thing that we've had in our minds from time immemorial. It's a more nuanced thing where we’re to think about the sources of fibre and their mechanism of action.
Hopkins: Yes, thank you, and I think that's an important distinction between primarily insoluble fibre sources versus soluble and knowing what's what, and what combination (of fibre) may be in the foods and formulas people are consuming. When you talk about slow versus normal transit, how does one easily figure out what's going on with transit?
Emmanuel: That's an important clinical point, thank you. The key thing is that we need to think about the symptoms. We could put through a transit X-ray but that's often quite difficult for us in the community to get set up and so on. But there are we know two really key symptoms and if you ask our patient and they have both these symptoms they're about 99% likely to have a slow transit X-ray confirming that.
So, what are these symptoms? The first one is the frequency of urge. How often does a patient feel the urge to go to the bathroom? Not how often do they go or how often do they make themselves go, how often do they get that spontaneous, natural call to go. And if that's every 36 hours or more frequent, then it's not slow transit. And the second key symptom is what the stool consistency looks like. If it's the Bristol stool form type 1 or 2, this kind of hard pellet-y stools, that combination of hard pellet-y stools plus infrequent urge is almost diagnostic of slow transit.
Hopkins: Thank you. I think that's very helpful for people to help understand what's happening. I know fecal incontinence is something that you're passionate about, and that probably – I don't know how that's going to come across, but it's something that you feel very strongly about, and you work with people where this is a serious issue. What are the implications with individuals who have fecal incontinence and diet?
Emmanuel: No, thank you. I am passionate about this. I'll say it myself because I think it's such a burdensome symptom to the individual, it's so devastating in terms of what it means in terms of restrictions of life. To focus on the dietary part of it, there is some pretty clear evidence in the literature, really hard evidence, of which we need to be able to access to help our patients and equally not to harm them – because sometimes there is the temptation to give wrong information. The first thing is if the patient is having incontinence to a solid stool or to gas, there is no point to changing the fibre content of their diet.
Changing to a higher fibre diet only helps those incontinent patients who have loose stool incontinence. That's a really critical point because sometimes patients who are losing the occasional pellet into their pads or underwear get told to take more fibre and more fibre, and all you do is make them more uncomfortable and frankly more disenchanted with you as a professional, cause they think “Oh goodness this person has no idea what they're talking about, I'm not doing that anymore,” so there's that aspect.
The second key aspect is sorbitol. And sorbitol is a huge trigger to incontinence in patients, and it's a silent one often because people don't realize they're taking it – sorbitol and most of these artificial sugars, which are especially there in our fizzy drinks, in carbonated drinks. They’re a real issue because they are very osmotically rich, and very poorly absorbed and there's a very strong linear relationship between dose of sorbitol, or artificial sugars in our diet, and stool liquidity. So, reducing the amount of sorbitol in terms of soft scoop ice cream, and chewy sweets, and chewing gum and the litres of carbonated drinks that some of us consume, that's the thing that can really help some patients, to reduce that.
And then the final thing is excessive amounts of caffeine. We know that normal amounts of coffee, that's equivalent of below three espressos a day or six of instant coffees a day, that isn't really associated with any problems. But at higher doses the effect of something called the phosphodiesterase inhibitors in coffee can act to make the sphincters a little bit weaker and the amount of secretion from a gut a little bit more, and that can provoke continence. So, don’t focus on fibre unless the stools are loose, reduce the amount of sorbitol – especially if the stools are loose, and don't worry too much about coffee unless patients are taking massive quantities.
Hopkins: Thank you. And really when you think about it, it's relatively simple when you think about those three things. I guess depending on people's relationship to caffeine, it may or may not be simple for them, but I suppose when you think about the outcome it can have on managing incontinence, people would certainly be willing to do these things if it's going to make their situation better.
Emmanuel: And just to put that in context for 30 seconds. It's worth remembering that even in a tertiary practice like the one I work in, we know that if we just make those observations in diet and those changes, about a quarter of the patients referred to us with their tertiary level incontinence where they've been through the local hospital and local services – that’s all we do to them, do that simple adjustment to their diet and they're sorted out. So, in the aspect of the community the chance of improving continence is even higher because they're less severe patients, so it has a good outcome.
Hopkins: Yeah, it’s really an example of again, a sort of a low-tech intervention. Simple, easy, that can make a profound difference, so thank you. In terms of the next thing I'd like to look at is gastroparesis. Blood glucose, and blood glucose fluctuations may play a role, depending I suppose on the individual and why they have gastroparesis. Can you just comment on gastroparesis in general and then maybe some specific components?
Emmanuel: So, the most common cause of gastroparesis as a symptom of delayed emptying is of course diabetes, and whereas once we used to think it is only people with type 1 diabetes, we know that type 2 diabetics – and that's a huge epidemic in the western world – is also associated with gastroparesis. So, this is an increasingly prevalent problem and what we know is that there's some really elegant data showing that high sugar on its own marginally delays gastric emptying, but the swing from a normal sugar level to high sugar is what critically decelerates the stomach for emptying. It makes the stomach more compliant and makes a pylorus less likely to open up into the intestine. And equally a swing the other way, so people are having recurrent hypos, that can be an issue if they're hovering with a normal blood glucose and every so often dip down, that fluctuation in blood glucose level is what critically affects pyloric emptying.
So, it's an important thing to say. The key thing in diabetic control here is not necessarily to make the sugar normal, it's to – if you can do that of course that's the primary goal – but setting it so it doesn't fluctuate too much. Which means helping the patient educate themselves about fibre sources, and the slow release sugars so they know how to keep their sugar as best as possible from periods of prolonged fasting and so on where they can suddenly dip. So, it's really that information, it's about trying to keep the levels constant rather than the levels low.
Hopkins: Is there a role for – in addition to blood sugar management with diabetic gastroparesis and I suppose even in individuals that have reasonable blood sugar control with diabetes, as well as people that may have idiopathic gastroparesis or other causes of this – is there a role for specific foods or nutrients, ingredients that you see in helping to manage these patients?
So, the first thing to consider is fat. We know that if you have a high-fat diet your stomach holds onto that to take time to emulsify it in the stomach, so that it's released at a nice slower rate into your intestine for the pancreatic and digestive enzymes to be able to handle it. If you dumped fat into your diet quickly, into your intestine, you have a problem with malabsorption quite often. So, we know that a high-fat diet will exacerbate gastroparesis. So, a lower fat content and lower fat density in the diet is a critical thing.
We also know that a protein-based diet is beneficial, the other ways in the way that a high-fat diet is unhelpful, a high protein diet is helpful in accelerating gastric emptying because that allows quicker emptying. The more amino acid there is in your stomach the quicker the pylorus opens and the more, the so-called pyloroduodenal contractions work so that it empties the stomach through that open pylorus better. So low-fat/high protein is one of the key early messages for gastroparesis patients.
Hopkins: Does it matter if when you're thinking about the fat, and here I’m thinking about somebody that may be on enteral nutrition support, if the fat is a long chain triglyceride source or medium chain triglyceride source. Does that make a difference?
Emmanuel: So, there is some data around that, goes back about 20 years now to the 1990s when it was done, but showing that the long chain versions cause more clinical duodenal sensing and therefore they number one, cause more sensitivity of the stomach, but they also cause greater delay in emptying.
Hopkins: Okay thank you. I'd like to come back again just for a moment on protein. Protein, I understand plays a role not only in terms of potentially affecting gastric emptying depending on what type of protein, but protein itself may play a role in attenuating microbial diversity and I find that very fascinating. Can you just elaborate on that for a moment?
So, this is a really interesting area of research and the whole microbiome of course is an interesting area. But you know what scientists find interesting is often not necessarily what's important for clinicians, but what is absolutely emerging is that the diversity of one's gut bacteria is critical to good health. So, not necessarily more numbers, but more families. The greater number of species we harbour in our gut the healthier we are, and what we do about doing that.
Well obviously, the thing that everyone focuses on is to take probiotics, but remember that a probiotic is at this time not something which stays in system for very long. It's like putting a teaspoon into a swimming pool. It may make a small difference for a short while, but it will soon be dissipated. Whereas something in the diet which could do that in a more permanent way, which we change our dietary patterns to, would certainly be a better way of filling the swimming pool up. And in that context, what's emerged is that if you move to a diet which has more protein in it, by implication therefore less carbohydrate in it, that encourages a greater bacterial diversity. And that has all sorts of beneficial effects on general health, but certainly also has effects we know on feeding behavior. So, it improves the search, we don't look so much for fatty unhealthy foods. It’s been shown in an elegant study to reduce the amount of anxiety we experience by having greater diversity.
So, I think the impact of potentially taking that narrative all the way through protein-based diet more, causing greater diversity, causing greater improvements in our food, eating behavior, and our anxiety, may all of that funnel into having greater health effects potentially of all of us. So, this is all early stage phase studies, but there's data for all of those points I mentioned. And we now need to show that it happens in in large groups.
Hopkins: It's fascinating and there's such an interest of course as you mentioned in the microbiome and almost a microbiome mania, if I might say. And in the nutrition world, there is such an interest in protein, usually related to muscle protein synthesis and other aspects. So, it's interesting to see how there's also this connection with the microbiome as another sort of added benefit when you're looking at trying to manage the protein intake of patients on nutrition support.
So, I think I mean I can just sort of maybe finish off my contribution by saying that I think we're moving towards an era where we will be looking at this more personalized approach. I think if it goes against the grain of how we've done physical trials and practice medicine we've relied on sort of mass evidence, which I think actually we're slowly dragging ourselves into thinking about patients having to have things which are going to be more tailored for them, that's for patients. Now whether we move that into the healthy population to keep them healthy that's another big question we don't know.
But a day of saying yes, we know that certain dietary things will suit you better because of your microbiome or your particular metabolism. That would be a really elegant way of looking at how we improve health to complement drugs. It's never instead of, but to compliment drugs and whether we can then apply that as I say to healthy populations to keep them healthy. That's the 22nd century.
Hopkins: Yes. And it's very important implications. So, thank you so much for this for this overview. Before we sign off I would like to take a minute to ask you one last question, so our listeners get to know you a little bit better. We've been talking about nutrition and can you tell us how you first became interested in the field of nutrition.
Thank you. As they say I've never been asked that before. So, I was originally a neurology trainee, I thought my life was nice and set and I was going to be looking at MRI and CT scans the rest of my life. And then went to do a program of research at St. Mark's Hospital in London and fell under the influence of an extraordinary physician and group of physicians at St. Mark’s, who completely changed the way I approached medicine. And began to realize that what I was drawn to, if it's not personal, is the plight of patients who have symptoms which are obscure. What I liked about neurology and what I still like about it is the challenge of working out what a patient is saying and what the subtlety of their nerve function is.
But what I came to realize is that I also liked people's dark hidden corners, the things we don't like talking about, in terms of the things we do and how we behave and what happens to our guts and what happens to our upper intestine, all the things that we think are – because it's such a social organ we use the eating and all this is such so much part of the job. And when it goes wrong we adjust ourselves.
And so, the idea of being a mirror which reflects back to the patient the changes they've made to say, “look you're doing this, that isn't what you have to do.” I sort of though, “this is what I want to do.” And of course, the whole idea of what nutritional things then being something which is then a vector for giving treatment, then sort of came full circle back to my neuro practice where I have these patients with neurological disease who unfortunately develop complications of swallowing or develop sort of malnutrition as part of their disease, which means they need feeding. So, I now practice both, in both aspects of my sort of neurological and G.I. training, which is kind of personally very satisfying but it's a nice circuitous but round story.
Thank you so much for sharing. It’s very interesting, this combination of neurology and gastroenterology, that just does seem to fit so well together. So, you seem to be really onto something here and we may see more neuro-gastroenterologists hopefully in the future as well.
So, on that note we'll conclude this podcast. I'd like to thank you, Dr. Emmanuel for joining us today and thank our audience.
CLOSING: This concludes this episode of our Clinical Nutrition Notes podcast.
To listen to more podcasts or to subscribe to Clinical Nutrition Notes, visit our website at NestleHealthScience.ca
For the Nestlé Health Science podcast team, I'm Bethany Hopkins.