We all know that feeling when we “gut” something out. Whether on the verge of making a difficult decision or undertaking a challenging physical feat, our guts can often be our most reliable allies in getting us through tough times. But what exactly is this “gut feeling” we experience?

 

The “gut feeling” is genuine and based on the connection between our brain and gut. This connection is known as the “gut-brain axis” and is responsible for sending signals between our heart and brain, influencing our mood, appetite, immunity, and ability to think clearly.

 

So how can we ensure our guts are always healthy and send signals to our brains efficiently?

  

Why is gut health important?

By ‘gut health’, we refer to the overall well-being of our gut and digestive system. This may sometimes be easy to forget, but the digestive system is arguably the most crucial system within the body.

Our guts are home to billions of fungi and bacteria – a thought not so pleasant and poetic but one that comprises the reality of us humans. Microorganisms play a fundamental role in preserving the well-being of our gut and entire body. Therefore, a healthy gut can have an array of benefits for both our mental and physical states.

Research exhibits a strong connection between bacteria in our guts (in the colon) and our immune system. Gut bacteria can teach the immune system to spot and recognise benign and harmful microorganisms. This is particularly useful as it means that our immune system will not end up flaring up if it comes across innocuous microbes. Instead, it will identify actual ‘threats’ and intervene accordingly.

Moreover, a healthy gut can positively affect our mood and mental well-being. The stomach produces around 90% of our body’s serotonin, a neurotransmitter that impacts our social behaviour, mood, appetite, and sleep.

Therefore, it is fair to say that a well-nourished gut can work wonders for our general well-being.

Signs of an unhealthy gut

A healthy gut and its microorganisms efficiently carry out many positive functions. Hence, it is no surprise that if – for instance – there is an imbalance in gut bacteria, your overall health gets heavily impacted.

But how do you recognise the signs of an unhealthy gut?

Here are a few symptoms to look out for:

• Upset stomach
• Digestion issues
• Sleep loss
• Migraines
• Skin irritation

How to feed your gut

There is no denying that the symptoms of an unbalanced gut can be rather unpleasant. If you’re experiencing severe gut problems, such as abdominal pain, diarrhoea, or constipation, you must visit your GP. These could be signs of a more severe problem, such as irritable bowel syndrome or celiac disease.

You may consider investing in a private health care plan to avoid lengthy NHS waiting times but be aware that most policies won’t cover pre-existing conditions.

But prevention is better than cure, which in this case is eating the right food.

So, what should you add to the menu?

• Fibre – Plant-based foods and fibre –fruits, vegetables, nuts, and whole grains work wonders for gut bacteria and keep them healthy. A diet that is low in fibre can increase bloating, in contrast.

• Probiotic food – Probiotics are naturally found inside the gut and have a range of digestive benefits, such as helping irritable bowel syndrome. Live yoghurts are a great source of probiotics and can actively encourage more good gut bacteria to develop.

• Antioxidant-rich foods – Antioxidants are compounds that help to protect cells from damage. Foods rich in antioxidants include berries, dark chocolate, and green tea.

• Healthy fats: Healthy fats, such as those found in olive oil, avocados, and nuts, are essential for gut health. They help to keep the gut lining strong and prevent inflammation.

The human gut is home to trillions of microbes. This community of microbes, known as the gut microbiota, plays a crucial role in human health, influencing everything from digestion and nutrient absorption to the immune system and mood. While the gut microbiota is complex and unique to everyone, certain foods can promote gut health and encourage the growth of beneficial microbes. Here are ten gut-friendly foods to add to your diet.

From keeping the body energised to uplifting our mood, a healthy gut can have a significant number of benefits on our well-being. After all, a healthy gut is a happy gut.

Experts from Westfield Health – a leading British health and wellbeing company; have looked at the criticality of gut health while highlighting the possible signs of ailing intestines and what foods could help boost their well-being.

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 As we head outdoors this summer, scientists are working to clip the long, flexible appendages that enable the common bacterium Campylobacter jejuni to make its way from undercooked poultry and natural waterways into our intestinal tract where it makes millions of us sick each year.

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Campylobacter jejuni is the most common cause of diarrhea, vomiting and stomach pain in the United States and the world, with about 140 million cases worldwide and more than 30,000 deaths each year, primarily in children under age 5.

Motility is the “magic bullet” for this bacterium which uses its long, thin, flexible arm-like flagella to maneuver the thick mucus in our gastrointestinal tract, power its way inside our intestinal cells, then wrap itself in a protective biofilm when threatened, says Dr. Stuart A. Thompson, microbiologist in the Division of Infectious Diseases at the Medical College of Georgia at Augusta University.   

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“It’s actually very good at moving, not only because of the flagellum, but because of the spiral shape of the cell itself, so it just travels through mucus,” says Dr. Claudia Cox, postdoctoral fellow, making a whooshing sound that mimics the whirling appendages.

The nimble flagella, each longer than the bacterium’s corkscrew-shape central body, don’t just propel, they help grab and hold onto the cell the bacterium is working to infect and push inside, she says. These essential arms, sticky because of their natural sugar coating, also play a role in building biofilm that will protect it from harsh times like too little food or too much oxygen.

Cox and Thompson want to stop the pervasive bacterium, potentially with a safe molecule that could be given as soon as signs of infection appear, like diarrhea and fever, by targeting elements key to its amazing mobility. But first they have to identify the best points of intervention.

They are looking at the enzyme CbrR, a so-called response regulator of the bacterium that enables it to assess its dynamic environment and make the adjustments it needs to survive. They also are taking the first looks in this bacterium at the “second messenger” cyclic-di-GMP, which the enzyme produces and uses to make those adjustments; and most recently the amino acids that function as building blocks for the bacterium’s long arms.

Thompson is principal investigator on a new two-year $423,500 grant (R21AI164078-01) from the National Institute of Allergy and Infectious Diseases that is helping them better understand those building blocks.

He’s also PI on a two-year, $410,000 grant (1R21AI154078-02) from the NIAID that ends this summer and has helped the scientists better understand how the bacterium uses cyclic-di-GMP to foster bile resistance — bile salt is a powerful antimicrobial — as well as motility/movement and the formation of the slick biofilm the bacterium shelters under when conditions get tough.  

Cox and Thompson have shown that cyclic-di-GMP is produced by CbrR, which in this case is a negative regulator. They reported last year in the journal Microorganisms that when CbrR was present, both the mobility and the ability to produce biofilm were hampered. For example, the bacterium’s general corkscrew form was the same but the long, thin, constantly moving flagella were MIA, Thompson says.

“It turns out, CbrR is a regulator of motility, of flagella,” he says. “Motility is the number one most important virulence factor of Campylobacter. It’s required for colonization, it’s required for host-cell adherence and invasion, and it’s required for biofilm formation,” he says.

Bottom lines: CbrR is a good thing for Campylobacter jejuni because it makes cyclic-di-GMP and because it can downshift motility to help enable the bacterium to survive in a harsh environment, Cox says. That means it’s time to stop moving around so much, to conserve and look for something nearby — they have seen the bacterium pull starch out of a culture medium it was sitting in — to weave into biofilm or take shelter under some other bacterium’s biofilm, she says.

No doubt the super-oxygen sensitive bacterium often needs a port in the storm. Sit a dish of them on a desk for a few days and they are dead, Thompson says, just from the oxygen content in room air, he says. But unlike e coli, Campylobacter jejuni does need some oxygen. Water too, he says, which are some of the reasons why it’s happy in our gut and in the gut of poultry and migratory birds, he says, but notes that in birds, it’s part of their normal flora.

Key to making all these adjustments and the critical function of movement   are amino acids, which combine to form proteins, and changes in amino acids can result in changes in a protein’s structure and function. It’s well known that bacteria use a process called phosphorylation, which is key to regulating many cell processes, to make the alterations needed to build out the flagella, a construction process that works kind of like adding Lego pieces from the ground up until it’s complete. Like with an actual building, there are a lot of regulators involved working to control growth, including stopping it when the time is right, which is where things like a negative regulator become important.

They have evidence that the amino acids serine and threonine, which they found are present in about half of flagella proteins, phosphorylate, or modify, proteins important to motility in that essential, dynamic building process. The new grant is enabling them to learn more about how phosphorylation of serine and threonine modify the bacterium’s proteins and what that does to the bug’s motility proteins with the goal again of finding the most direct target(s) for intervention. That might in this scenario include blocking phosphorylation instead of the resulting actions.

They already have identified two still unnamed proteins, 0215 and 0862, known to remove phosphates from serine and threonine, and have some evidence that 0215 may be involved in both adding and removing a phosphate group. They are looking for others that just add phosphates in this scenario.

This kind of addition and subtraction is important because when a protein has something added to it or taken away, it can change what the protein does, they say. “Sometimes it’s like an on/off switch and sometimes phosphorylation morphs the protein into doing something else,” Cox says.

Clever bacteria can slow down or resume the building of flagella depending on what’s happening in their environment, the scientists say. If they can identify a protein whose loss stops flagella construction, a small molecule that inactivates that protein could mean the important arms don’t get built, Thompson says.

While blocking key survival action of Campylobacter won’t work like a vaccine to try to block initial infection, the idea is that if they can block the growth of flagella needed for the bacterium’s movement, they can stop its progression in its tracks and early in the process, Thompson says.

The initial bacterial invaders would become more vulnerable to the natural immune response and/or simply die off, so the infection would be minor and unable to cause serious disease. 

“It’s more of a targeted therapeutic,” Thompson says. “It’s dead in the water,” Cox adds.

The two also have studied both the primary sugar Campylobacter uses to make slimy, protective biofilm and how the regulatory protein CsrA helps. They showed long ago that when CsrA is missing, Campylobacter can’t move well, stick to each other or the gastrointestinal tract or make biofilm.

While the jury remains out on exactly where the biofilm comes from, they have some evidence it can be made by other bacteria and potentially elsewhere.

But Thompson adds there is also good evidence that the bacterium’s DNA is present in the biofilm but where the sugar, or polysaccharide, a major component, comes from remains unknown.  He notes that the bacterium isn’t always covered in biofilm, like when it’s actively infecting a host and so rapidly replicating. “When our immune cells are spitting all kinds of nasty stuff” at the bacterium would likely be another good time to build biofilm and shelter, particularly when it’s a persistent infection, or when campylobacter runs across bile salt in our gut.

Undercooked poultry is a major source of Campylobacter jejuni, and so is animal poop, including from birds and cows, that ends up contaminating waters in lakes and ponds, Thompson says. While just how it causes disease remains unclear, most people recover in a week, often without antibiotic treatment.

Others develop irritable bowel syndrome, arthritis and the bacterium is the most common cause of Guillan-Barrè Syndrome, in which the immune system harms the nerves causing muscle weakness and potentially paralysis. 

Antibiotic resistance by the bacterium can be a problem because of recent practices of feeding antibiotics to poultry as well as livestock to prevent illness, the scientists say.

Awareness may also be a problem. Despite the fact that it’s far more common than Salmonella, even when Thompson asks a roomful of scientists about Campylobacter jejuni, typically only a handful of hands go up.

Macrophages (green) surrounding enteric neurons (red). CREDIT Laboratory of Mucosal Immunology at The Rockefeller University

A simple stomach bug could do a lot of damage. There are 100 million neurons scattered along the gastrointestinal tract—directly in the line of fire—that can be stamped out by gut infections, potentially leading to long-term GI disease. 

But there may be an upside to enteric infection. A new study finds that mice infected with bacteria or parasites develop a unique form of tolerance quite unlike the textbook immune response. The research, published in Cell, describes how gut macrophages respond to prior insult by shielding enteric neurons, preventing them from dying off when future pathogens strike. These findings may ultimately have clinical implications for conditions such as irritable bowel syndrome, which have been linked to the runaway death of intestinal neurons.   

“We’re describing a sort of innate memory that persists after the primary infection is gone,” says Rockefeller’s Daniel Mucida. “This tolerance does not exist to kill future pathogens, but to deal with the damage that infection causes—preserving the number of neurons in the intestine.” 

Neuronal cause of death 

Known as the body’s “second brain,” the enteric nervous system is houses the largest depot of neurons and glia outside of the brain itself. The GI tract’s own nervous system exists more or less autonomously, without significant input from the brain. It controls the movement of nutrients and waste by fiat, coordinating local fluid exchange and blood flow with authority not seen anywhere else in the peripheral nervous system.  

If enough of those neurons die, the GI tract spirals out of control. 

Mucida and colleagues reported last year that gut infections in mice can kill the rodents’ enteric neurons, with disastrous consequences for gut motility. At the time, the researchers noted that the symptoms of IBS closely mirror what one might expect to see when enteric neurons die en masse—raising the possibility that otherwise minor gut infections might be decimating enteric neurons in some people more than others, leading to constipation and other unexplained GI conditions. 

The researchers wondered whether the body has some mechanism of preventing neuronal loss following infection. In previous work, the lab had indeed demonstrated that macrophages in the gut produce specialized molecules that prevent neurons from dying in response to stress.  

A hypothesis began to take shape. “We knew that enteric infections cause neuronal loss, and we knew that macrophages prevent neuronal cell death,” Mucida says. “We wondered whether we were really looking at a single pathway. Does a prior infection activate these macrophages to protect the neurons in future infections?” 

Bacteria versus parasites 

Postdoctoral fellow Tomasz Ahrends and additional lab members first infected mice with a non-lethal strain of Salmonella, a standard bacterial source of food poisoning. The mice cleared the infection in about a week, losing a number of enteric neurons along the way. They then infected those same mice with another comparable foodborne bacterium. This time, the mice suffered no further loss of enteric neurons, suggesting that the first infection had created a tolerance mechanism that prevented neuronal loss.  

The scientists found that common parasitic infections also have a similar impact. “In contrast to pathogenic bacteria, some parasites like helminths have learned to live within us without causing excessive harm to the tissue,” he says. Indeed this family of parasites, which includes flukes, tapeworms, and nematodes, infect in a way that is more subtle than highly hostile bacteria. But they also induce even greater, and more far-reaching, protection. 

During a primary bacterial infection, Mucida found, neurons call out to macrophages, which rush to the area and protect its vulnerable cells from future attacks. When a helminth insinuates itself into the gut, however, it is T cells that recruit the macrophages, sending them to even distant parts of the intestine to ensure that the whole gamut of enteric neurons are shielded from future harm.  

At the end of the day, through different routes, bacterial and helminth infections were both leading to protection of enteric neurons.  

Next, Ahrends repeated the experiments in mice from a pet store. “Animals in the wild have likely had some of these infections already,” he says. “We would expect a pre-set tolerance to neuronal loss.” Indeed, these animals suffered no neuronal loss from any infection. “They had a lot of helminths in general,” Mucida says. “The parasitic infections were doing their jobs, preventing the neuronal losses that we have seen in isolated animals in the lab.” 

A gut feeling 

Mucida is now hoping to determine the precise impact of neuronal loss in the GI tract. “We’ve observed that animals consume more calories without gaining more weight after neuronal loss,” he says. “This may mean that the loss of enteric neurons is also impacting the absorption of nutrients, metabolic and caloric intake.” 

There may be more consequences of neuronal loss than we expected,” he adds. 

Mucida believes that this research could contribute to a more complete understanding of the underlying causes of IBS and related conditions. “One speculation is that the number of enteric neurons throughout your life is set by early childhood infections, which prevent you from losing neurons after every subsequent infection,” Mucida explains.  

People who for some reason do not develop tolerance may continue to lose enteric neurons throughout their life with every subsequent infection. Future studies will explore alternative methods of protecting enteric neurons, hopefully paving the way for therapies.

Bowel health in children (and adults) depends on the digestive or gastrointestinal system working well. An effectively working bowel is one that, amongst other things, is able to digest food effectively and eliminate the waste (i.e. the poo) easily and with an appropriate frequency (at least 4 times a week). A key sign of how well the bowel is working is the appearance of the poo. But how is poo formed? In other words how does the bowel and digestive work?

How does the digestive system work?

The digestive system is essentially a very long tube that stretches from the back of the mouth to the anus. 

When we eat, the food gets chewed into little pieces that are easy to swallow. In very young children the food is usually provided in a puree or very small pieces until the child can chew adult food. The food leaves the mouth then passes down the food pipe (oesophagus) to the stomach, squeezed by regular contractions along its way. This is called peristalsis. When the food reaches the stomach, it is broken down into a mushy liquid called chyme by acids and enzymes. The chyme then passes into the small bowel (small intestine), which is about 2 metres (7 feet) long in new-born babies and grows to about 6 metres (20 feet) long by adulthood.

The small intestine is made up of three parts. The first section is called the duodenum which is connected to the stomach. The next section is the jejunum which makes up about one third of the entire length of the small bowel. The last and longest part of the small intestine is called the ileum which leads to the large bowel or colon.

The small intestine is where most of the nutrients from our food are absorbed into the bloodstream and used by the body for metabolism, building cells and so on. The remainder of the semi-digested food that cannot be used passes into the large bowel (large intestine). 

The large bowel has strong muscles which squeeze the poo along. The body absorbs water as the poo is squeezed along, so that it turns from a mush into a soft, smooth, sausage-shaped poo. When the poo reaches the rectum, the lowest part of the bowel, the rectum stretches, and a message is sent to the brain saying the child needs to do a poo.

A child with a healthy bowel can pass soft poos (Type 4 according to the Bristol Stool Scale^[1]), at regular intervals without pain or discomfort at least four times a week. 

What can go wrong?

Things can go wrong in the large bowel and the stool becomes too hard (a sign of constipation) or too soft and liquid in consistency (a sign of diarrhoea). Constipation (hard poo that is not easily passed) occurs when too much fluid is reabsorbed into the bowel. This can happen for several reasons:

• withholding the stool (which is when a child avoids emptying their bowels)
• fear of the toilet (sometimes associated with pain or discomfort)
• lack of a toilet routine (some children have such busy lives that it can be difficult to find time to sit and relax on the toilet each day)
• resistance to potty training and an insistence that a nappy be put on to poo in
• an unbalanced diet
• low fluid intake
• a change in routine
• anxiety and emotional upset (for example when starting nursery or potty training)
• some medications

When constipation strikes it is important to be recognise it and treat immediately. Pharmacist, Sultan Dajani says: “Mums need to be able to access an effective treatment for constipation. Several over the counter (OTC) medicines exist for the treatment of constipation in children, but many are only available OTC for children over the age of 12 months or 2 years or over. Following a review by the Committee on Human Medicines (CHM) the Medicines and Healthcare products Regulatory Agency (MHRA) stated that stimulant laxatives (e.g. senna, bisacodyl) should no longer be used in children under 12 years without advice from a prescriber, while stimulant laxative products for children aged 12 to 17 years can be supplied under the supervision of a pharmacist.^[2]”

“Docusol Paediatric is one of very few products that can be taken by mouth and is available OTC for the management of constipation in infants and children from the age of 6 months. Docusol Paediatric works by retaining moisture in the stool from the bowel. With almost no stimulant action (i.e. causing movement (known as peristalsis) in the bowel), Docusol Paediatric is notclassified as a stimulant laxative. Hence the MHRA restrictions on stimulant laxatives are not relevant to Docusol Paediatric.”

Community Pharmacist Sultan Dajani adds: “Docusol Paediatric is efficacious and gentle, quick acting with few side effects. It is sugar free and strawberry flavoured. Plus, it can be mixed with drinks, (e.g. water, juice, milk etc) without changing their consistency and is easy to take. Essential for little ones when it comes to administering an over-the-counter medicine like Docusol Paediatric.”