In June 2016 Cell Reports a well-respected science journal published a fascinating paper on the connection between short chain fatty acids and associated nutrient and immune function that collectively reduced food allergy risk and response in their mice population.[1]

For over 20 years (at the time of writing this)  I have been describing the need for a ‘threshold therapy’ approach to the effective manipulation of the common mucosal immune system, in particular the recruitment of metabolic by products derived from food metabolism and microbiome functionality – as well as the specific replacement or supraphysiological supplementation of retinoids or their precursor families, vitamin D and enhancement of SigA are important aspects of this collective approach. Each of the interventions are modest in application and very low in risk, but the collective threshold crossing effect can assist the immune system in its effective maturation and maintainence of tolerance. This can be difficult to demonstrate in studies and as such much of the supportive data requires cross professional communication and data digging. This neat study helps to add credibility to the multiple point intervention through the manipulation of a subset of dendritic cells to favour a regulatory inducing phenotyope. I look forward to seeing how this approach is escalated into human trials in the coming years.

It has been considered over the last few years to advise mothers during pregnancy and whilst breast feeding to avoid allergenic foods such as milk, nuts, and other risky foods to reduce the risk of childhood allergy. Not for the first time researchers say this practice may be doing more harm than good. Research papers presented at a recent American Academy of Allergy, Asthma, and Immunology conference suggests that exposure may be better than avoidance.[1]

A possible link between what a mother eats during pregnancy and the risk of her child developing allergies has been identified in new research published in Septembers; The Journal of Physiology.[1]

This paper identified that if the maternal diet is rich in PUFA’s or poly unsaturated fats such as those found in flaxseed, walnuts and fish their offspring’s digestive tract develops differently than in those progeny lacking these PUFAs.

By Michael Ash, BSc(Hons). DO. ND. FellowDipION

Vitamin D and Vitamin A are essential co-partners in immunological and bone health.[1],[2] I’m particularly excited about vitamin A because of its profound effects on the gut mucosal immune system—a specialty of mine. Just as vitamin D has attracted attention for its ability to increase antimicrobial peptides and help us defeat pathogens, it’s fascinating to me that vitamin A is also essential for the very tissues that protect us from the same pathogens.

The availability of vitamin A in our food is a key factor in a tolerant, highly functional immune system. To quote from the title of a brilliant commentary in the March 2008 issue of Nature’s Mucosal Immunology, “Vitamin A rewrites the ABCs of oral tolerance.”[3]

Vitamin A is crucial to a very sophisticated bi-directional mechanism that takes place in the digestive system and leads to immune tolerance across the entire gut lining. Immune tolerance is the essence of good health. An intolerant immune system will lead to a wide range of illnesses, and the gut is where many people first lose immune tolerance. Vitamin A (retinoic acid) is key to our ability to consume a wide range of antigens (food) and yet not react adversely, and it’s quite fascinating.

As discussed here on many occasions it is well recognised that developed countries are suffering from an epidemic rise in immunologic disorders, such as allergy-related diseases and certain auto-immunities. One of the proposed explanations and one that I feel most convinced about is the changing composition of our intestinal microflora and parasite burden. Our intestinal ecological changes  appear to be altering our ability to manage appropriate immunomodulatory responses to various ingested and inhaled antigens.

The Proceedings of The National Academy of Science Journal published a paper this June 2010 exploring the differences in the microbial communities between those children on a western style diet and those from a rural African community whose diet reflected that of a the early humans – high in fibre.[1]

The saying is ‘what happens in Vegas stays in Vegas’, or if you are English ‘what happens in Blackpool….’ but the same cannot be said about what happens in utero, as increasing evidence supports the understanding that the maternal nutritional environment and early feeding affects the health of the foetus beyond infancy and into adulthood.[1],[2] An article in Nature’s Mucosal Immunology this month explores some of the key events in foetal and neonatal immune management.[3] It stimulated a revisit to the area of what to consider for parents to be and mums of young children when they ask ‘is there anything I can do to prevent or reduce the risk of allergy or atopy in my child’.

The first moments, weeks and months of life can determine the health outcomes of an individual over the duration of their lifetime and this knowledge represents a significant choice for prospective parents. Fortunately the remarkable adaptability of the immune and central nervous system means that there are numerous opportunities in the early years of life to positively influence health outcomes even if the early stages were less than optimal.

The British Naturopathic Association Presents: Childhood Allergies, Diagnosis and Treatment Study day : 21st March 2010 Time: 9.30am – 4.30pm At: Large Lecture Theatre, University of Westminster, 115 Cavendish Street, London, W1W 6UW Directions Cost: BNA members £50, non-members £60, BNA student members £30, non-BNA students £35 Refreshments and light lunch served. CPD certificates provided

An interesting paper published in the Sept 2008 Annals of Neurology described a ‘new to science’ brain aggravating enzyme, triggered by reactivity to gluten, but acting independently of other coeliac symptoms.[1]

Most clinicians understand that overt gluten reactivity is classified under coeliac disease and the the classic constellation of symptoms and signs characterising  malabsorptive syndrome is a readily recognised manifestation  of  coeliac  disease. Frank malabsorptive symptoms include steatorrhea, weight loss or failure to thrive, bloating, and flatulence, with multiple deficiency states. More common but more difficult to recognise, however, are the other diverse ways in which coeliac disease presents.

Coeliac disease may also mimic many common clinical entities. These atypical modes of presentation include deficiencies of single micronutrients; nonspecific gastrointestinal complaints such as bloating, abdominal pain, diarrhoea, constipation, flatulence, secondary lactose intolerance, and dyspepsia; and non-gastrointestinal complaints such as fatigue, depression, arthralgia, milk intolerance, osteomalacia or osteoporosis, and iron deficiency anaemia.

The differing origins of gut dendritic cells — white blood cells that modulate immune responses — may explain how the intestinal immune system manages to destroy harmful pathogens while tolerating beneficial bacteria says an article by Sophie Laffont & Fiona Powrie in Nature journal out on Dec 10th 2009.

The immune system must protect the body from invading pathogens without mounting damaging responses to its own tissues. Dendritic cells, a rare population of white blood cells, have a crucial role in determining the nature of immune reactions and in fine-tuning the balance between tolerance (where the immune system ignores or tolerates an antigen) and the induction of inflammation to destroy pathogenic organisms.

A new twist to the hygiene hypothesis shows that allergic risk can also be modulated by microbial exposure before birth. Mice born to dams that were exposed to bacteria during pregnancy were less likely to develop allergic responses than those born to unexposed mothers. And maternal Toll-like receptor (TLR) signals were required for the transmission of protection.

TLRs are a type of pattern recognition receptor (PRR) and recognise molecules that are broadly shared by pathogens but distinguishable from host molecules, collectively referred to as pathogen-associated molecular patterns (PAMPs).