Gluten-Free and Me.

When I was diagnosed with celiac disease (CD) at the age of 17 (not as dramatic as it sounds) I had no idea what gluten was or how my daily life was about to change. I became a hitchhiker on the journey that is the gluten-free lifestyle. This wasn’t a choice I was making to be ‘healthier’ or because I was ‘intolerant’ or ‘sensitive’ but rather because my immune system would fight me if I fed my body anything containing gluten. For those who don’t know – gluten is a family of proteins found in many cereal grains, especially wheat, barley, malt and rye. These grains are commonly found in pasta, bread, pastry, cereal and a number of alcoholic beverages.

How to speak to someone with Celiac’s
Tip #1

Never say “but can’t you just have a bite?” or “surely you can have it every now and then?”

My Story

This autoimmune disease first became apparent when I developed a skin condition known as dermatitis herpetiformis (DH) – having nothing to do with the herpes virus, might I add. Shortly after a viral infection, I started developing itchy bumps on my skin, especially on my knees and elbows. The itching was like nothing I’d experienced before.

Fortunately, having a medical professional in the family, I was diagnosed relatively quickly after the onset of DH and was able to treat myself by starting a strictly gluten-free diet. In the beginning there were definitely a couple of mishaps but 5 years down the line I’m pretty used to eating gluten free and have mostly forgotten about the world of gluten-rich goodness.

How to speak to someone with Celiac’s
Tip #2
If they decide not to eat at a gluten-unfriendly restaurant:
1 – they’ve probably eaten already or planned their meals around the day.
2 – don’t look at them and the empty space in front of them with sorrow and say “shame” every 10 minutes. We know. It sucks.

Let’s break this down.

Let’s take a step back though. What is celiac disease and how is it different to gluten sensitivity/intolerance or a wheat allergy?

Celiac disease (or coeliac for the Europeans) is an autoimmune disease which manifests when one’s own immune system recognises gluten as a foreign pathogen and mounts a response. This can occur from birth or can be triggered later on in life.

Here are some fun facts that I gathered from the book ‘Living gluten-free for dummies’:

  • Celiac disease is unique in that it can only be treated by diet.
  • It is one of the most common genetic diseases affecting humans.
  • To be at risk of celiac disease you need all 3 of the following:
    • A genetic predisposition.
    • A diet including gluten.
    • Something to launch the disease into activity e.g viral infection (sound familiar?), surgery, emotional stress and more.
  • Because of its strong genetic component – prevalence increases drastically among people who have immediate family with CD.
  • Many classic symptoms include: abdominal pain/indigestion, acid reflux, bloating, nausea, lactose intolerance and much more!

The immune system recognises the gluten proteins as harmful and mounts an attack against the proteins and intestinal cells. This results in recruitment of immune cells and specific antibodies to the small intestine. The immune response damages villi and microvilli. These make up the mucosal lining of the intestine and increase surface area to optimise nutrient absorption. The damage results in the inability to fully digest food and absorb nutrients. This can lead to nutritional deficiencies, malnutrition and other health issues. Testing for CD initially involves a blood test that looks for antibodies only present if you have CD. However, if you have the classic symptoms and test negative, a biopsy can be done.

There seems to be a very fine line between celiac disease and what is known as ‘non-celiac gluten sensitivity’ or NCGS. They share many symptoms and are both treated by a gluten-free diet. When testing for CD, however, a person with NCGS would test negative. There is no antibody or autoimmune response in these cases. It is thought that there may be an innate immune response but this is not fully understood and does not cause any damage to the lining of the intestine like CD does. One mostly has to diagnose it by ruling out CD or a wheat allergy.

A wheat allergy is exactly that – an allergy. This means you react almost immediately after consuming wheat. There is not a risk of further complication and one can be diagnosed with a skin prick test. Being allergic to wheat does not mean one is allergic to gluten containing wheat-free foods.

But where does ‘dermatitis herpetiformis’ join the party?

You might be thinking, well how does an autoimmune reaction in the intestine result in an itchy skin condition?

“When a person with celiac disease consumes gluten, the mucosal immune system in the intestine responds by producing a type of antibody called immunoglobulin A (IgA),” explains John Zone, MD, Celiac Disease Foundation Medical Advisory Board Member and Chairman of the Department of Dermatology at the University of Utah School of Medicine.

These IgA antibodies are directed against epidermal transglutaminase. The antibodies then travel to the skin where they bind with the epidermal transglutaminase protein. Gluten ingestion seems to trigger this reaction.

Not everyone with celiac’s has DH but everyone who has DH has CD. Fortunately, those with DH often do not experience any extreme gastrointestinal issues but may have minor gut inflammation. Of course, there are a variety of manifestations and symptoms of celiac disease, DH being only one of them.

Now that I’ve given some background on me and my favourite disease, we will be diving deeper into the genetics and science behind celiac disease and how complicated it is to predict those at risk of this polygenic disease. So look out for my next post! Coming soon…

Hopefully I’ve helped you understand a bit more about the world of gluten and that you don’t relate too much to the right-hand image!


  • Living Gluten-Free for Dummies : A Wiley Brand (2nd Edition) By Hilary Du Cane, Sue Baic, Nigel Denby and Danna Korn


The Mighty Microbiome

The ‘microbiome’ has become somewhat of a buzzword in the human biology and health world. But what is it exactly? Your microbiome is made up of all the microorganisms in your body which include bacteria, fungi and viruses. These largely exist on the surface of your skin and inside your large intestine. The diversity of microbes in this region begins to increase immediately from birth and is impacted by both the type of delivery and feeding method. The majority of these microorganisms play very important and beneficial roles in digestion and the general health of the gut. There are important bacteria such as Bifidobacteria which help in the digestion of breast milk or others which aid in the digestion of fibre, decrease triglyceride levels and prevent weight gain. Gut dysbiosis occurs when there is an imbalance between the healthy and pathogenic microbes in the gut. This can result in weight gain and an array of other microbiota related diseases.

Fun Fact: Microbiome vs Microbiota

Although used interchangeably, the microbiome refers to all of the microbial genomes that exist in an environment whereas the microbiota are all the microorganisms existing in an environment.

Subtle but significant!

Development of the gut microbiome from birth

Over the last few years, there has been an increase in research regarding the gut microbiome and the implications it has on human health. Not only does it appear to have an effect on weight, heart health and one’s immune system but recent studies have shown that one’s microbiota plays a role in mental health as well. It is believed that the microbiome can have an impact on stress levels, quality of sleep and cortisol release.  In the context of celiac disease, the story of the gut microbiome is that of the chicken or the egg. Does a genetic predisposition for CD result in an affected microbiome or does the microbiome affect risk of CD manifesting. Studies involving identical twins, where one is obese and the other not, have shown that differences in the microbiome are not gene related. This may then suggest that one’s microbiome can contribute to an already existing predisposition to CD.

“Epidemiological data suggest that additional environmental factors, such as type of delivery at birth, milk-feeding practices, intestinal infections, and/or use of antibiotics, could also determine CD risk”.

After coming across a review paper on the implications of the gut microbiome on celiac disease, I became very interested in the idea that environmental factors such as type of delivery and feeding method can have an effect on one’s risk of developing CD through the direct effect on the microbiome. This post will focus on a paper entitled ‘Gut Microbiota trajectory in early life may predict development of celiac disease’. This is hot off the press and published only last year (2018)!

Let’s Review: What do we know

We know that CD only develops in those that have a genetic predisposition to the disease. There is a strong association with the HLA-DQ2 and HLA-DQ8 genes. These are expressed on the surfaces of antigen presenting cells (APCs). When gluten is consumed these APC’s recognise gluten peptides and activate T-lymphocytes which subsequently results in the secretion of pro-inflammatory cytokines and activation of cytotoxic T-cells. This response results in tissue damage leading to the multiple symptoms related to CD. These HLA genes, however, do not guarantee development of CD. They are thus necessary but not sufficient for pathogenesis.

“Although non-HLA variants also contribute to CD risk, studies on the heritability of CD in twins indicate that genetics alone cannot explain CD onset and that non-shared environmental elements also contribute.”

Back to the Paper

This study wanted to investigate “whether alterations in the developing intestinal microbiota and immune markers precede CD onset in infants at familial risk of developing the disease”.

They recruited a cohort of healthy newborns that all had a familial risk of developing CD (at least one first relative having CD). They monitored the progression of the microbiome during the first 5 years of life. After data collection, they compared those infants that developed CD (10 infants) to 10 best-matched controls (regarding type of delivery, HLA-DQ genotype and type of feeding) who did not develop CD by the time the cases did. Their analyses involved DNA typing for the HLA DQ genes, faecal sampling and 16S rRNA sequencing.


The majority of those infants that developed CD, were diagnosed between 16 and 40 months. At the time of diagnosis, all the CD children had elevated tTG antibody levels. Five presented with symptoms (diarrhoea, abdominal distention, constipation, asthenia) while five had no symptoms.

Although the composition and diversity of the microbiota were not very different between the two groups at six months, it seems that the most significant differences between the CD and control group occurred at 4 months of age. The phylum Firmicutes, for example, had significantly higher relative abundance at 4 months in those children that developed CD compared to those that didn’t. The healthy children, however, had a statistically significant increase in Firmicutes between 4 and 6 months while the CD children started with a high basal level at 4 months and then had relatively constant levels thereafter. This meant that at 6 months there were no differences at the phyla level between the two groups but the developmental process had differed. This pattern was similar in the establishment of Enterococcaceae and Peptostreptococcaceae populations. Levels of intestinal IL-6 were also similar between the groups at 6 months despite the CD group having higher levels at 4 months. It is thus the initial establishment of the bacterial communities that may have an impact on the likelihood of CD development


tTG antibody: tissue transglutaminase antibody – only made in people with CD
IL-6: pro-inflammatory cytokine

The important take-way message of this paper is the fact that a timely progressive increase in microbial diversity is an important factor in the development of a healthy gut flora. The group that developed CD thus underwent ‘premature maturation’ as a result of higher basal diversity levels. The differences in the developmental pattern of the two groups could be a lead as to why they developed CD. Although this particular paper did not come to any major conclusions and was limited in case and control numbers, it serves as a springboard off which further, more in-depth studies can base their research.

Still not convinced that celiac disease is worth the research? I’ll leave you with some scintillating stats!

  • An estimated 1 in 133 Americans, or about 1% of the population, has celiac disease.
  • It is estimated that 83% of Americans who have celiac disease are undiagnosed or misdiagnosed with other conditions.
  • 6-10 years is the average time a person waits to be correctly diagnosed. (Source: Daniel Leffler, MD, MS, The Celiac Center at Beth Israel Deaconness Medical Center)