Gut Health, Allergies and Intolerances Symposium at Nutrition and Health Live

Alex Gazzola reports on several of the Symposium’s talks, held in partnership with the IBS Network and chaired by its Medical Advisor, Dr Nick Reed, on the first weekend of November 2013, at the annual Nutrition and Health Live event.

Food Allergies in Children

“Something has changed over the last century,” said Dr Adam Fox, Consultant Paediatric Allergist at Guy’s and St Thomas’ Hospitals, opening his talk, Food Allergies in Children.

25% of adults have allergies; 40% of children. The rapid increase from rare disease (hay fever was virtually unknown at the end of the 19th century) to epidemic cannot be down to genetics, as relatively speaking the change is too sudden. However, the environmental factors remain unclear. Depressingly, the UK tops the international table of allergic disease, closely followed by New Zealand, Australia, Ireland and Canada. Given the disparate geography of these nations, it must be the cultural similarities that account for the allergy epidemic.

5% of children have genuine food allergy, but 33% of parents believe their child has a food allergy. Medical professionals, said Fox, are dealing with two epidemics: the real food allergy epidemic in children, and the far greater epidemic of parents believing that whatever is wrong with their child – skin problems, headaches, lethargy, behavioural problems – are down to food allergy when they are not.

Atopic children who present with eczema in infancy are more likely to develop food allergy, and later on asthma and rhinitis – a progression known as the allergic march. These allergic conditions influence one another in many ways:

* if you have eczema and egg allergy – then you have a 70-80% risk of asthma;
* if you have asthma – then you have 80% risk of allergic rhinitis;
* if you have food allergy and asthma – then you have a far greater risk of anaphylaxis than if you have food allergy without asthma.

As the overlap between eczema and food allergy is considerable, it is the skin on which the research is focusing. Virtually all peanut- or egg-allergic children have significant eczema in their first year. Research shows that infants with mild eczema have a 10% chance of developing food allergy; those with severe eczema a 70% chance. The earlier the eczema, the greater the risk.

It is unusual to outgrow peanut allergy – only 20% of children manage it. Interestingly, 90% of children with peanut allergy react the first time they eat peanuts. Immunologically, said Fox, this makes no sense, as the immune system must have already been presented the peanut allergen (and subsequently become sensitised to it). Where and when is sensitisation taking place?

Previous speculation – that sensitisation may occur in utero, or during breastfeeding, if the mother consumed peanuts in either case – has since been disproven, leading to the withdrawal in 2009 of the previous cautious Department of Health recommendations to atopic mothers-to-be and mothers that they may want to consider avoiding peanut in pregnancy and during breastfeeding, and to avoid feeding peanuts to their children in the first three years of life.

Focus has shifted to eczema. The use of peanut-containing eczema skincare products (such as Oilatum, which formerly contained it) has been shown to be a significant risk factor, but even after the removal of peanut from most skincare preparations, peanut allergies continue. So there must be exposure to peanut protein via other means – other children handling peanut butter and touching the children, a parent who has eaten peanut butter kissing the child, inhalation of dust with peanut allergen in it, and so on. We know peanut allergen can ‘linger’ in the home, and be carried from room to room easily. Research has shown a tenfold increased likelihood of peanut allergy if there is a lot of peanut in the home environment.

Although nothing has replaced the old 2009 advice, more studies will hopefully address this. Possible prevention strategies include:

* aggressive early eczema treatment. If early and severe eczema is a significant risk factor, aggressive treatment at this stage may reduce risk of food allergies. Fox acknowledged it may be difficult to persuade mothers to put steroid cream on their young infants, however.
* total exclusion of peanut allergen from the home.
* early peanut consumption – might it be better to present peanut to your gut in order to develop tolerance, before the immune system has been presented it via the skin?

A common question, said Fox, was ‘Does it go away?’ It’s tricky to predict whether a food allergy may disappear, but those children more likely to outgrow them are those with lower IgE levels at diagnosis and milder initial eczema.


Priming the Gut: the Role of the Colonic Microflora in Food Allergy and Intolerance

Christine Edwards, Professor of Nutritional Physiology at the University of Glasgow, gave a talk entitled Priming the Gut: the Role of the Colonic Microflora in Food Allergy and Intolerance, in which she explained the revolution that has taken place in how we look at gut bacteria.

We know:
* there are 10 times more bacterial cells in the body than human cells;
* there is 100-150 times more genetic information in those bacteria, than in your body;
* there are at very least 1,000 species of bacteria in the gut.

We also know these bacteria provide us with metabolic functions which we did not evolve ourselves, and which ‘educate’ our immune system.

But the ecosystem is complex. The complexity and variety means there is enormous amounts of data to analyse, requiring the use of difficult-to-access supercomputers, to ‘ask’ even the most basic question. The biggest problem microbiologists face is that these bacteria cannot usually be grown: around 60% are non-culturable, because they either need to grow alongside other bacteria, are anaerobic, or they need something from their human hosts to grow which we have not identified. We cannot study them, or find out what they do.

What we do know is that they are very important for digestion – and we should not be flushing them out with colonic irrigation. Some functions include:

* producing short-chain fatty acids (which may have an impact on satiety and metabolism regulation)
* promoting colonic absorption of water (which is why, when good bacteria levels dip, we get diarrhoea)
* providing energy
* reducing colonic pH
* increasing mineral absorption
* inhibiting pathogens
* producing a wide range of vitamins
* metabolising complex molecules like polyphenols, releasing antioxidants.

Factors influencing gut microbiome and infant colonisation of the gut include:

* genetics
* perinatal antibiotics
* vaginal versus Caesarean birth
* weaning practises
* where you were born / live
* ethnicity
* any digestive disease
* diet
* probiotic intake

Studies show, said Edwards, that allergic infants are less likely to have lactobacilii and bacteroides bacteria, and are less often colonised by entercoccoi bacteria.

Delivery by c-section increased the risk of allergic disease, and a vaginal home birth is more protective than a vaginal hospital birth. There is a decreased risk of food allergy in vaginally delivered babies when parents are atopic.

In conclusion, Edwards said bacterial composition is important for digestion and health, that early diet and environment is very influential on the development on the gut microbiota and allergy, and that there is some evidence linking disturbed microbiota to allergy – but not to intolerance.


Wheat Intolerance

Wheat Intolerance was the simple title of Marianne Williams’ talk. She is a gastroenterologist dietitian specialising in IBS and allergy at Somerset Partnership NHS Foundation Trust.

The subject remains controversial, began Williams, and most people know someone with a gluten or wheat intolerance. 60% of the public believe many people are allergic to wheat or bread. It remains a common source of confusion.

Wheat reactions can be classified into four categories:

* coeliac disease
A well-categorised autoimmune reaction to gliadins in wheat.

* wheat allergy
For instance, reactions to alpha-gliadins in wheat which occur in wheat-dependent exercise-induced anaphylaxis (WDEIA), reactions involving amylase inhibitors from wheat in baker’s asthma. Other gliadins, and lipid transfer proteins in wheat may also be involved. The proteins are generally resistant to acid pH and heat – because of this they are not denatured by cooking and will get through stomach acid and cause systemic reactions in the gastrointestinal tract. Wheat proteins are similar in structure to barley and rye – so there is a risk of cross-reactions with related grains. Wheat allergy only effects 0.4% of children, and 0.2% of adults.

* wheat intolerance
These are reactions due to fermentation of wheat carbohydrates called fructans (chains of fructose units with a glucose end). Fructans in wheat are poorly absorbed in everyone as we do not have the ability to break them down, can ferment in the gut, and can trigger IBS-like symptoms in sensitive individuals. The Low FODMAP diet has yielded excellent results in Williams’ clinic, she said, with around two-thirds of IBS patients improving on the diet.

* non-coeliac gluten sensitivity (NCGS)
… if indeed it exists. This must be a diagnosis of exclusion, argued Williams. Coeliac disease, wheat allergy and wheat intolerance must all be first ruled out, and then a gluten challenge undertaken: if the patient experiences symptomatic relief when gluten is removed from the diet, and relapses with reintroduction, then a NCGS diagnosis can be made. It is vital to rule out gut fermentation because a wheat-free diet is lower in FODMAPs, and patients could be responding to this rather than the removal of gluten. The best current estimates suggest 0.5% have NCGS, and previously higher reported figures may be due to large numbers of undiagnosed / latent coeliacs in previous studies.

But Williams stressed it may not be due to gluten, and we could be looking at something as yet undiscovered. “There are 100 proteins in wheat,” she said. “Why does it have to be gluten? We’re all set in our heads that every problem has to be to with gluten, but if you take gluten out, you’re probably taking wheat out, and therefore your taking all wheat proteins out – and we can’t know it’s not a totally different protein we’ve not previously considered.”



Miranda Lomer, consultant dietitian at Guy’s and St Thomas’ Hospital, spoke on FODMAPs and the low FODMAP diet – as devised by the Australian team of Professor Peter Gibson and dietitan Dr Sue Shepherd – for IBS and other conditions.

FODMAPs are short-chain fermentable carbohydrates and the name is an acronym incorporating several classes of sugars:

Oligosaccharides (fructans, galacto-oligosaccharides – GOS)
Di-saccharides (lactose)
Monosaccharides (fructose)
Polyols (mannitol, sorbitol, xylitol etc.)

Generally, they are not very well digested in the gut. As they pass through the small intestine, they draw water into the bowel, and then as they pass further into the large intestine, they are fermented by gut bacteria, leading to gas production. This excess gas and fluid can, in susceptible individuals, cause predictable symptoms of wind, diarrhoea and bloating.

Fructans are chains of fructose with a glucose end unit. Fructo-oligosaccharides (FOS) and inulin are fructans, and they tend to be found in wheat, onion and garlic. Humans do no not produce an enzyme to digest fructans, so we absorb less than 5% of what we consume. Galacto-oligosaccharides (GOS), such as raffinose and stachyose, are found in beans, pulses and nuts (esp. pistachio and cashews) and again we do not have an enzyme to digest them.

This is a disaccharide made from glucose and galactose, and requires the enzyme lactase to break it down. Not everyone has lactase post-weaning, depending on (mainly) ethnicity. Lactose is a FODMAP in some people, but not all.

This is ingested in three forms:
1. as free fructose
2. via the disaccharide sucrose (a combination of glucose and fructose)
3. via fructans – which are chains of fructose molecules

The main sources are honey and fruit – especially fruit juices and mango – but fruits with equal quantities of glucose and fructose are often well tolerated, as these can be absorbed together.

The main source is sweeteners, sugar-free confectionary, and certain fruits and vegetables. Polyols, again, are poorly absorbed.

The diet works by drastically reducing gas production and fluid in the bowel, and has been shown to be effective in between two-thirds and three-quarters of IBS patients who adhere strictly to it. The diet is challenging, though, and dietitians must work closely with patients in order to teach them the complexities of the diet. Processed foods in the UK are often rich in onion and garlic and high in FODMAPs, so these must often be avoided.

Curiously, spelt bread is lower in FODMAPs than wheat bread, and may account for anecdotally reported tolerance of spelt bread in some patients. Curiously, this is not repeated with spelt pasta, which appears to be just as FODMAP-rich as durum wheat pasta (researchers do not know why). But spelt bread, rather than wheat-free or gluten-free bread, may be a good alternative to those for whom gluten-related disorders have been ruled out.

Resistant starch, said Lomer, as a long-chain fermentable carbohydrate, doesn’t fall into the FODMAP grouping. There is some evidence that a high intake of resistant starch can increase abdominal symptoms, but because the low-FODMAP diet works so well as is, it’s not usually worth excluding resistant starch too – though is an option if it fails. (Resistant starch is found in cold potatoes, cold grains and beans, and under-ripe bananas.)

There are, though, a few down sides to the low-FODMAP diet: generally, calcium intake is lowered considerably, and it seems the diet reduced beneficial bifidobacteria colonies in the gut – though it is not known whether this is a long-term effect.

The low-FODMAP diet might have applications beyond IBS, in that it can reduce output in patients with stomas and relieve gut symptoms in IBD patients in remission.


Probiotics and Gastrointestinal Diseases

“We are in trouble with our guts,” opened Vanya Gant, a microbiologist at UCL Hospitals NHS Trust, opening his talk, Probiotics and Gastrointestinal Diseases.

Our diets contain 1,000 times fewer bacteria than we used to consume several hundred years ago, and our genes have not adapted. We don’t eat dirt or fermented foods. We succumb to monobacterial disease and give ourselves massive quantities of antibiotics.

Such is the level of dysfunctional guts and the appetite for products to help them, that we now have a whole host of probiotic yoghurts, drinks and pills marketed at us to help. Vant argued that “most of these products cannot work”. They are either killed in the stomach acid, merely come out the other end without ‘attaching’ to the lining of the bowel, or are rendered unviable when desiccated for use in tablets. “What’s the point in taking stuff that’s dead or not going to make it past the stomach?”

Antibiotics destroy health and probiotics help it – and the public want probiotics – but what we urgently need, argued Vant, were excellent, randomised, blinded and controlled trials ...

First published November 2013


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