Here at The Journey we are pretty lucky to have the input of some of the leading thinkers and scientists of our generation. All in order to help us navigate the modern challenges of conception, pregnancy and early years. This interview is no exception and is one we were extremely excited to do! In this article we interview one of the leading global scientists and pioneers of allergy prevention: Professor Gideon Lack. We ask him what he thinks is behind the rise in food allergies and how our thinking about allergy prevention is changing. 

First a bit about Professor Lack. He is Professor of Paediatric Allergy at Kings College London. Head of the Clinical Academic Paediatric Allergy Service. He is also Consultant to the Sean Parker Allergy Centre and Stanford University. Crucially, he is behind some of the leading trials that are reversing the way that we approach allergy prevention. Trials such as LEAP (Learning Early About Peanut Allergy) and EAT (Enquiring About Tolerance) studies. He’s a pretty big deal!

Ok, so starting with the basics. Food allergies on the rise: true or false? 

Well for sure something like a peanut allergy has increased over time. In fact the numbers have gone up 2-3x in some areas. We are now in a situation where as many as 8-10% of school children have a food allergy. 10% of which can be life threatening. So yes, it is a real issue. Egg and milk allergies are the two leading food allergies across the globe. That being said there are regional variations. Which is explained in part by the dual allergen hypothesis. (Explained below) 

So, what do you think is causing this? 

Well it cannot be explained by genetics alone, so in some ways we must be responsible for it. There is clearly some environmental component. One thing we do see a lot more of is eczema. We also know there is a clear link between eczema and the development of food allergies. In fact, as many as 80% of children with a food allergy have a history of eczema. (1) 

Ok, so eczema is the first thing we as parents should be watching out for? 

This is where the dual-allergen-hypothesis comes in. Eczema is the first manifestation of the ‘allergic march’. Studies have linked the severity of the eczema with the chance of an allergy developing. So, the more severe the eczema, the greater the chance of a food allergy developing. Interestingly, a study of over 2000 children showed that the risk of egg, milk or peanut allergy was approximately twice as high if eczema was present in the first six months of life compared to the second six months of life. (1) 

What is the connection between development of food allergy and eczema? 

We have seen in various studies that allergic sensitisation occurs after skin exposure. Particularly if the skin is inflamed or broken as is the case with eczema. The allergen basically enters the body via this broken and inflamed skin even at a very low dose. For example it can happen through exposure to the skin from allergens present on tabletops, hands and even in dust. When these are able to penetrate the skin barrier they are met by cells in the skin called Langerhans cells leading to the production of a certain type of antibodies by the immune system: known as Immunoglobulin E (IgE). When the body produces these you get an allergic reaction. Obviously the more vulnerable the skin the higher the chance that the allergen can penetrate. 

So the other route is via eating/drinking a potential allergen? i.e ingestion? 

Exactly. Historically the guidelines were to avoid ingestion of potential allergens through pregnancy, breastfeeding and in the first three years depending on the allergen. The reality however is there was very little evidence to support this and in fact, the incidence of allergies has only been rising despite this practise. In fact, research suggests the opposite to be true. Early introduction of an allergen could be the best way to prevent its development.  The LEAP study and our more recent trial suggests that by exposing a child to an allergen via the oral route at an early stage (as young as 3-4 months) you get a much lower rate of allergy development. 

Ok, so tell us about how this works exactly? What should we know? 

The dual allergen hypothesis in a nutshell suggests that the way and the timing we are exposed to an allergen is critical. Research suggests that if broken/inflamed skin (as happens with eczema) is exposed even in a low dose to an allergen without exposure through the mouth/gastrointestinal tract we are much more likely to get an allergy. 

How does this work? 

The difference between taking an allergen via the mouth/gastrointestinal tract vs the skin is that the gastrointestinal tract is is surrounded by lymphoid tissue which is part of the immune system. The immune system learns very early what to attack and what to tolerate. It learns to recognise ’own’ tissue very early which is key for our survival. Exposure is crucial for the immune system to ‘learn’ what is friend and what is foe. Put it this way. If you do not expose a baby to light or touch studies have shown that leads to failure in the development of certain key areas. It looks as though if you do not expose the immune system to potential allergens there is a higher risk of it not coping appropriately. 

‘A perfect storm…’ 

The trouble is when we have allergens in the environment and then pregnant women and young babies avoiding actual ingestion of the allergen. This is when we get a immune or allergic reaction via the skin but no exposure and ‘learning’ by the immune system within the gut to go with it. Then add in the increase in eczema which makes you more vulnerable and you get an explanation for the high levels of food allergy we are seeing. This explains why we didn’t see allergies to things like Kiwi until they were introduced into our environment in the UK in the 70s and 80s. It is also why we see high incidence of things like peanut allergy in places where peanuts are in the environment but where pregnant women and children avoid eating them. See below: 

So why do you think we’re seeing more eczema which makes the route to food allergy development so much more likely? 

There are many potential causes. Whilst things like the hygiene hypothesis does not really explain the rise in food allergies, there are links to the development of eczema (click here for more on the hygiene hypothesis). There is some moderate link to Caesarean birth and development of eczema in relation to this for example. However, it often starts off as very dry skin. Part of this may be overbathing and some of the skin products that are marketed at babies and children. Many of these products are alkaline but the skin is slightly acidic. So many products have the reverse effect when it comes to moisturizing the skin (click here for more). We also have a whole range of harsh soaps and detergents used in clothes. Many people bathe their children once or more a day. It was unheard of previously to do this so much. 

What about treating eczema? Can that help prevent allergy development?

Prompt intensive treatment of eczema early in order to reduce inflammation in the skin and reduce skin permeability is definitely helpful.

So, given the above, do you think the microbiome has a role to play? 

I have no doubt it plays an important role, but it is not entirely clear at this stage how. It is very complex. An ecosystem within itself where there is an almost evolutionary power struggle going on. We don’t know yet what is cause and what is effect. However, one thing we did see from mice studies was that oral exposure as a route to reduce food allergies did not work in germ free mice which suggests you do need a healthy gut microbiome for this to work. (1) 

What about breastfeeding. Current WHO guidelines suggest exclusive breastfeeding for the first six months, yet the LEAP study and your most recent trial suggest exposing at risk infants as young as three months to oral allergens: 

The guidelines on breastfeeding have perhaps swung too far the other way and now we are perhaps not introducing solids early enough. When formula was invented we swung too far away from breastfeeding, now we have swung in the opposite direction. Perhaps too far. In terms of the argument that the digestive tract is not developed enough to cope with solid food, the reality is that breastmilk is very complex to digest. Our research has shown some compelling evidence that the introduction of allergens to at risk infants (those with severe eczema for example) as early as 3 months old has a significant impact on reducing the development of allergy. (3) 

What about premature babies? Should you work on an age-adjusted basis? 

It is actually child dependent. The child needs to be developed enough to swallow. At this point however we do not exactly know how much, over what period of time in terms of exposure needed to prevent food allergy development. The LEAP study however used 2-6g per week of peanut exposure as a reference point. (2) 

Click here to read more about Professor Lack’s work on the LEAP study as well as here for his most recent trial (EAT) showing significant benefit from early introduction of allergens to at risk infants as young as three months. However the results are pretty compelling with:

• 34% of the standard group of at risk infants went on to develop an allergy vs just 19% of the group who had early introduction.
• 33% of the standard group went on to develop a peanut allergy vs 14.3% of the early introduction group.
• 48.7% of the standard group developed an egg allergy vs 20% of the early introduction group.

References:

(1) Epidemiological risks for food allergies: Gideon Lack

(2) LEAP trial: G Lack et al

(3) EAT trial: G Lack et al 

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