How can bitter foods be good for us when they taste so bad? – Resolving the paradox

Laying out the problem

Our recent post on bitters, left me with a lot of questions.

If bitter tastes indicate the presence of toxins and thereby help us avoid poisonous foods, why do they stimulate such positive physiological responses? Why would some of those responses protect us from metabolic diseases like diabetes and cancer? If bitter taste is merely a warning to avoid a particular food, then why do many traditions revere bitter foods? How do we explain why adults develop a taste for bitter foods that as children they found repulsive? Why does folk law say “Good medicine always tastes bitter”?

After a lot of pondering I think I’ve got an answer but to make sense of it I need to lay out what I see as the relevant parts of the puzzle first.

Read time: 16 minutes (3100 words)

Continue reading

The bitter truth is sweeter than we thought

Cocktail bitters like Angostura and Peychaud’s have pedigrees going back to the 1830’s. Looking like something out of a victorian apothecary these intriguing botanical preparations may indeed have medicinal properties deeper than anyone thought.

Following our recent infographic (Health Hack #1: An alternative to fizzy drinks) in which I recommended using Angostura bitters as a basis for a healthy fizzy drink, I felt I had more to say about bitters in general.

In traditional herbal medicine bitter herbs were considered aids to digestion through stimulation of bile and digestive juices. Taken fifteen minutes before a meal they were used to increase appetite –  the concept behind the idea of the aperitif – or after a meal as a digestive, but they are also thought to stimulate and ‘detoxify’ the liver, and generally are considered a ‘tonic’ to revivify the blood and to ‘enhance the vigour’ of the digestive system. Such vague and ill-defined terminology has led to these claims being largely dismissed. However, recent research is not only confirming the health value of bitter tasting substances but discovering that they have important physiological effects throughout the body.

The story of herbal bitters just took a fascinating turn that is proving to be sweeter than anyone might have imagined …

Read time: 12 minutes (2300 words) Continue reading

Even in the land of barbies and beer vegetarians DON’T live longer

A new study from Australia finds yet again that vegetarians don’t live longer than meat eaters.

We previously reported on a 2015 paper examining mortality among vegetarians in the UK based on data from the large Oxford EPIC study, which found no evidence for reduced mortality compared to the general meat eating population. [see our post UK vegetarians DON’T live longer than meat eaters study finds]

Now a similar analysis from the Australian 45 and Up Study has come to the same conclusions: there is no significant difference in all-cause mortality between vegetarians, semi vegetarians, pescatarians and regular meat eaters in Australia. Continue reading

Gary Taubes on American Heart Association confirmation bias

In our recent post ‘Amazing results challenge guidelines in new study‘, we looked at research that came to exactly the opposite conclusion to that of The American Heart Association who currently recommend replacing saturated fat with MUFAs and omega-6 PUFAs. The researchers concluded:

recommendations of supplementation with these fatty acids in the general diet should be revised.

The public at large are confused by what they see as flip-flopping over dietary issues: butter is bad one week, but ‘back’ the next. Many people find it hard to believe that such an authoritative body as the American Heart Association could be wrong. How can a few small researcher groups and flag-waving bloggers (like us!) possibly be right? Surely august bodies like the AHA sort through the data and discard the poor quality studies? Surely they can be trusted to do due diligence on our behalf?

These are reasonable thoughts for people to have and they are not wrong to think like this, but such convictions rely on our public agencies not slipping into the kinds of confirmation bias that science is supposed to protect us from.

In a recent Op-Ed Gary Taubes (science journalist and author of the best selling book Good Calories Bad Calories) tackles this topic head on. Continue reading

Low fat (but not full fat) dairy associated with increased risk of Parkinson’s disease

Read time: 4.5 minutes (850 words)

Intro

MedPage Today [full article here] drew my attention to a recent Harvard study published in the journal Neurology [abstract herewhich took a closer look at previously identified associations between dairy products and Parkinsons Disease. Their analyses were based on data from two large prospective cohort studies, the Nurses’ Health Study (n = 80,736) and the Health Professionals Follow-up Study (n = 48,610), with a total of 26 and 24 years of follow-up, respectively. An previous study (see below) found an increased risk of Parkinson’s with higher levels of dairy protein consumption.

The latest study looked more carefully at the different types of dairy product. They found that among those who ate 3 or more portions of low fat dairy per day (skimmed milk, low fat cheese and yogurt etc) 4 in 1000 went on to develop Parkinson’s disease, whereas among those who ate no portions of low fat dairy only 3 in 1000 developed the disease.

Comparing the two groups that equates to a roughly 33% increased relative risk. Of course that is only a rather piffling 0.1% absolute risk increase – hardly anything to worry about in the grand scheme of things. What makes this study interesting, however, is that the association did not exist for full fat dairy products only low fat ones.

Uric acid and Parkinson’s disease

The study’s authors speculate that the increased risk seen in the low fat milk group may be due to the ability of milk protein (casein and lactalbumin) to reduce uric acid levels. Parkinson’s disease and uric acid? I wasn’t aware of this link, so started digging into the research…

A particularly helpful review in Practical Neurology [Uric Acid’s Relationship with Stroke and Parkinson’s Disease: A Review] filled me in on the background.

It turns out that there is a growing body of evidence demonstrating an association between low uric acid levels and incidence of Parkinson’s disease. Not only do Parkinson’s sufferers tend to have have low levels of uric acid, but those with higher levels have slower and less aggressive progression of the disease. Importantly, some studies have identified that low uric acid levels four years prior to the onset of Parkinson’s symptoms has a stronger association than levels at onset of symptoms, suggesting that uric acid is linked to the  pathogenesis of Parkinson’s.

Uric acid BTW is an intriguing endogenous antioxidant which although primarily synthesised by the body is also influenced by diet. Excess levels can lead to the formation of crystals which is the basis of the painful condition gout, but can also contribute to kidney stones and kidney damage. Foods containing purines, such as shellfish, offal, meat and beer, can raise uric acid levels, as can alcohol and fructose, so should be avoided if you suffer from gout or kidney stones. The idea that such foods may be protective against Parkinson’s is interesting (although clearly one would not want to go as far as to cause gout!) On the other hand, dairy, cherries and vitamin C are associated with lower risk of gout and are classed as hypouricemic foods as they reduce uric acid levels.

It is believed that uric acid may exert a neuro-protective effect through it’s antioxidant action:

It has been hypothesized that uric acid reduces oxidative stress on neurons. This may have a significant bearing on therapeutic management of disease, as many neurological disorders are believed to result from oxidative stress. As a potentially modifiable risk factor, the prospect for uric acid and its derivatives to play a role in disease modification or prevention has great potential. – Pello et al, 2009

Studies looking at dietary associations with Parkinson’s disease have identified that uric acid lowering foods (e.g. dairy) are always associated with an increased risk of Parkinson’s, except for one. Vitamin C is the only uric acid lowering nutrient associated with reduced Parkinson’s risk: possibly because it is a powerful anti-oxidant itself.

Results from an earlier analysis of the Health Professionals Follow-up Study found clear trends indicating reduced incidence of Parkinson’s disease with increasing consumption of fructose and alcohol (uric acid raising foods) and an increased risk with higher levels of dairy protein consumption (a uric acid lowering food) Adapted from Xiang Gao et al, 2008

Full fat dairy

In the new study the increased risk for Parkinson’s disease was only associated with low fat dairy, not full fat. Why wasn’t full fat dairy associated with an increased risk of Parkinson’s?

For now there is no clear answer, but according to MedPage Today the authors of the study say “The lack of association with full-fat dairy products could be due to a countervailing effect of saturated fats. I think more research is needed to better understand the mechanisms involved in this association,”

The benefits of dairy fats have come up time and again, yet I still know many people who avoid full fat milk, cream, cheese and butter. See our posts:

Bottom Line

The size of the increased absolute risk of Parkinson’s disease associated with consuming low fat dairy products (0.1%) is too small to make it a reason in and of itself to avoid low fat dairy – unless of course, you have a family history of the disease in which case every bit of risk reduction helps.

For all of us, however, this study adds to the evidence of the benefits of full fat over low-fat dairy.

References

  • Intake of dairy foods and risk of Parkinson diseaseKatherine C. Hughes et al, Neurology, June 2017 [Abstract]
  • Low-Fat Dairy Linked to Small Increased Risk for PDKate Kneisel, Contributing Writer, MedPage Today, June 2017 [Full article]
  • Uric Acid’s Relationship with Stroke and Parkinson’s Disease: A Review Scott Pello et al, Practical neurology, Jul/Aug 2009 [Full article]
  • Diet, Urate, and Parkinson’s Disease Risk in Men, Xiang Gao et al, American journal of epidemiology, 2008 [PMC full text]

In the News

  • Why you’re better off eating FULL fat dairy: Consuming three or more portions of the low fat variety of yoghurt, milk or cheese raises the risk of Parkinson’s disease, Daily Mail [Online Article]
  • Low-fat milk linked to Parkinson’s risk, The Times [Online Article]

Amazing results challenge guidelines in new study

  • A new study challenges the dietary guidelines for heart health
  • MUFAs and omega 6 PUFAs not effective at reducing atherosclerosis risk
  • Omega 3 fish oils reverse triglycerides and weight gain in an animal model of insulin resistance, despite increased calories

Read time: 9 minutes (1400 words)

Guidlines for prevention of heart disease have shifted in recent years away from a simplistic ‘reduce total fat’ message towards a more nuanced emphasis on the type of fat. The current American Heart Association (AHA) recommendation is to ‘replace saturated fats with monounsaturated (MUFA) and polyunsaturated (PUFA) fats.’

For the purpose of this post, I am going to put aside my objection to the demonising of saturated fats and instead focus on the MUFA / PUFA alternatives recommended by the AHA. Similarly, I am not going to challenge the cholesterol hypothesis nor debate the merits or otherwise of lowering LDL cholesterol here. Instead I am going to look at a recent paper that studied the effects of MUFAs and PUFAs on atherosclerosis risk.

Note the terms n-3, n6- and n-9 in the title of this paper; these are just shorthand for omega-3 polyunsaturated fatty acids (ω3 PUFAs), omega-6 polyunsaturated fatty acids (ω6 PUFAs) and omega-9 monounsaturated fatty acids (ω9 MUFAs). I’ve made a quick reference guide for these below, showing typical foods high in each kind of fat:

The role of triglycerides in cardiovascular disease

Cardiovascular disease is often preceded by insulin resistance during which changes to the cholesterol delivery system increase the risk of atheroma formation in the artery wall. One of the hallmarks of insulin resistance is an increased production in very low density lipoproteins (VLDL) which are high in triglycerides.

The following is a quick explanation about triglycerides which you can skip if it’s a bit too much or you are already familiar with the subject…

The relevance of triglyceride-rich VLDL

VLDL is a carrier protein, produced by the liver, which transports triglycerides from the liver to the adipose (fat) tissue. It is important to note that these triglycerides are primarily endogenous i.e. manufactured by the body, rather than coming directly from dietary sources.

VLDL and triglycerides are raised principally by (1) Excess caloric intake from any source and (2) Carbohydrates (and especially fructose). In the former case the formation of VLDL can be seen as the body packing away and storing excess calories which are transported to the adipose tissue where they can be stored for a rainy day as fat.

In the case of carbohydrates, triglyceride rich VLDL is manufactured as a response to overwhelming surges in blood glucose that cannot be dealt with sufficiently by insulin induced uptake by the organs, especially muscle and liver glycogen stores. Indeed some have said that raised blood triglycerides are a reliable marker of carbohydrate consumption.

If cells become insulin resistant they stop taking up glucose effectively, increases the need for diversion of calories into the endogenous VLDL pathway. Hence insulin resistance is characterised by raised triglycerides.

Fructose has some unique metabolic problems as it does not trigger insulin, so cannot be taken up by cells as quickly as glucose. Instead it has to be processed by the liver, which can easily be overwhelmed, turning the excess into triglyceride rich VLDL.

It should not be surprising then, that the rats used in the study I am reviewing here, were made insulin resistant by feeding with sugar water (30% sucrose water) for 12 weeks. Sucrose is equal parts glucose and fructose, so their water contained 15% of each of these sugars.

So the aim of this study was to see how different dietary fats affect the dislipidemia associated with insulin resistance, especially the triglycerides. To do this the rats in this study were split into 5 groups: A control group on standard diet, whilst the other four were all made insulin resistant by feeding 30% sucrose water for 12 weeks. Of the four insulin resistant groups one was supplemented with n3 PUFAs, one with n6 PUFAs and one with n9 MUFAs.

It’s a pretty obvious experiment to undertake, and at this point you might rightly be asking why? Hasn’t this has all been done before? Surely the science on such a basic question is settled? With 60 years of American Heart Association advice you would think they had the science to back up their assertions and advice, wouldn’t you?

Well, shockingly, you would be wrong. As the authors note:

To our knowledge no studies have addressed the impact of dietary n-3, n-6 and n-9 fatty acids on VLDL composition and size in the [insulin resistant rodent] model.

There are several reasons why this basic question has not been answered before:

  1. Many previous studies looking at the effects of PUFAs on insulin resistance have applied n6 and n3 together, with only a few addressing n6 alone
  2. Previous studies evaluating n3 fish oils have used cod liver oil, which contains high levels of vitamin A, D and cholesterol, which could affect the findings.
  3. Assessment of MUFAs (n9) have usually used olive oil, which contains a broad range of phytochemicals which may be responsible for the beneficial heart effects observed in those studies, rather than the actual monounsaturated fats it contains.

To get round these problems ithe researchers used the following oils:

  • n3: fish oils from pressing whole fish, hence low in vitamin A and D.
  • n6: linoleic acid rich sunflower oil, low in phytonutrients
  • n9: high oleic sunflower oil

Rodent diets contained 15% w/w of each oil, which represents about 35% by calories i.e. similar to a standard western diet.

Results

What they found was striking and deserves some careful reflection.

To make the findings a little easier to appreciate I have made a graph of some of the key results, but tables with all the study data are provided at the end of the post.

Data is expressed as mean percentage differences compared to the standard rodent chow diet (Reference). All four insulin resistant diets (IR) were sucrose rich; the three intervention diets consisted of supplementing with 15% w/w with n-3: deepwater fish oil; n-6: sunflower oil; n-9: high oleic sunflower oil.

Triglycerides ()  and Liver fat ()

The effects of the high sucrose feeding, as expected was a jump in triglycerides, which can be seen between the Reference and IR results above. Dramatically, supplementation with n3 fish oils almost completely reversed this dyslipidemia, returning VLDL particles to normal. Whilst remarkable, this is in line with previous epidemiological, human and animal studies that have shown n-3 PUFA have positive physiological effects on IR and lipid metabolism.

n6 and n9 oils, however, only weakly attenuated these harmful changes, failing to reverse the atherogenic state of the VLDL particles. This casts doubt on the validity of the American Heart Association recommendations.

In the case of the MUFA (n9), previous studies using olive oil have shown greater improvements in insulin resistance parameters, but as already noted, olive oil contains a broad range of bioactive phytochemicals (e.g. sterols and polyphenols). By using high oleic sunflower oil this study has been able to show that MUFAs do not of themselves produce these beneficial effects.

In relation to MUFAs this is particularly important as many processed food uses high MUFA oils that are low in phytonutrients as these can impart undesirable flavours.

Accumulated liver fat follows a similar pattern to plasma triglycerides. Again, n3 oils produce the best reductions in damage caused by insulin resistance.

Weight gain () and Calorie intake ()

Some of the most surprising results were seen in relation to caloric intake and weight gain. All groups of rats could eat ad libitum, yet in the n3 fish oils and n9 MUFA groups caloric intake was considerably raised. Extraordinarily, despite this those fed the n3 fish oils had no weight gain during this trial, whilst those fed the n9 high oleic oil had the most weight gain.

Rats fed the n6 sunflower oil supplemented diet had lower caloric intake than the n3 and n9 groups, but still gained more weight than the n3 group.

Conclusion

The authors of this study conclude:

In insulin resistance, while n-3 PUFA showed expected favorable effects, supplementation with n-6 PUFA and n-9 MUFA did not prevent atherogenic alterations of VLDL. Thus, the recommendations of supplementation with these fatty acids in general diet should be revised.

The authors seem somewhat nonchalant about the n3 fish oils, but it is worth reflecting for a moment just what those fish oils did: the rats were drinking insane quantities of sugar, eating a hyper caloric diet, yet avoided most of the effects of insulin resistance and weight gain. That’s a pretty impressive feat as far as I can see!

Implications for diet

This study looked at the effects of fat choice in the context of insulin resistant animal models. The results support and extend previous research in humans and epidemiological studies. Taken together these point to certain food choices: fish, seafood and olive oil are good choices based on these results; Omega 6 vegetable oils such as sunflower, safflower, corn and soya oils are best avoided, as are low-polyphenol MUFAs like high oleic oil and possibly filtered rapeseed (Canola) oil. A high quality fish oil supplement seems prudent too.

Based on the ideas suggested by this study cold pressed rapeseed oil is potentially interesting as like extra-virgin olive oil, it contains high levels of phytonutrients, but unlike olive oil it has significant levels of alpha linolenic acid (ALA), a short chain n3 fatty acid. Based on the results above I would expect it to have beneficial metabolic effects possibly similar to or slightly better than Olive oil. Well that’s my prediction. So lets see…

I searched Pubmed for “rapeseed cardiovascular”. Sure enough, in one of the first studies I found [Baxheinrich et al, 2012] patients with metabolic syndrome (which is just one step down from full blown insulin resistance), were placed on a low calorie diet enriched either with olive oil (high n9 MUFA, low n3 ALA) or cold pressed rapeseed oil (high n9 MUFA high n3 ALA) for six months. Although both groups improved similarly on many metabolic measures (body weight, systolic blood pressure, cholesterol, and insulin levels), the cold pressed rapeseed group had significantly lower triglycerides. That said rapeseed oil is probably less suitable than olive oil for high temperature cooking as the ALA it contains is very heat sensitive. Still, its a good choice for salad dressings and mayonnaise!

Additional data

For those of you who like to dig into the data here are some key tables from the study:

(1) Composition of diets; (2) Intakes and body weight; (3) Effects on adipose tissue/liver and serum parameters

References

Gluten Update April 2017

The effects of gluten are not confined to just the 1% of the population that suffer with Coeliac Disease and the estimated 6% who suffer with Non-Coeliac Gluten Sensitivity, but can have detrimental effects in everyone. In these updates we share some of the latest research.

  • Effects of gluten on gluten-tolerant mice
  • Relatives of coeliacs often have gluten related disorders
  • NCGS persists even after 8 years on gluten free diet
  • Gluten free diet prevents progression of potential coeliacs
  • Coeliac disease may be triggered by a common virus
  • Coeliac disease and joint and bone problems

Read time: 11 minutes (2000 words)

Effects of gluten in otherwise gluten-tolerant mice

Dietary gluten causes severe disorders like celiac disease in gluten-intolerant humans. However, currently understanding of its impact in tolerant individuals is limited.

A ground breaking study has undertaken the first detailed investigation into the effects of gluten on metabolism and microbiome in gluten tolerant mice. The purpose of the study was to identify the effects of an obesogenic diet with or without gliadin (a key, immunogenic component of gluten).

The team from The National Food Institute, Denmark (Li Zhang et al, 2017) analysed a huge array of parameters, including insulin resistance, histology of liver and adipose tissue, intestinal microbiota in three gut compartments, gut barrier function, gene expression, urinary metabolites and immune profiles in intestinal, lymphoid, liver and adipose tissues.

Using tightly controlled diets the researchers found that a relatively small change (exchanging casein for 4% gliadin) resulted in a considerable impact on the host response in the mouse model. The levels of gliadin used were comparable to that found in bread. The remainder of the diet was, however, higher in fat than a typical human meal (35g fat/100g).

The headline findings include:

  1. Gliadin Intake Affected Glucose and Lipid Metabolic Homeostasis
  2. Gliadin Intake Altered Gut Microbial Composition and Activity
  3. Gliadin Intake Caused Lower Expression of Gut Barrier Function Related Genes in Ileum
  4. Gliadin Intake Changed the Metabolic Signature of Urine
  5. Gliadin Did Not Affect Systemic Inflammatory Markers but Altered Immune Cell Composition in Liver and Inflammatory Phenotype of Visceral Adipose Tissue

The changes were predominately negative, but there is a huge amount of detail to unpack in this research, cetainly more than I want to go into in this post. That said, I will look a little more into the changes to the microbiome as they are particularly fascinating. If you are interested in going into the other areas more deeply then check out the full free text.

Changes to the intestinal microbiome

After nine weeks on the 4% gliadin diet levels of lactobacillus had fallen by more than 90%. (These are generally considered beneficial bacteria). Conversely, bacteria associated with detrimental health changes including Clostridium XI, Dorea and Coriobacteriaceae increased in abundance by more than ten fold.

Strains belonging to Clostridium XI, including also the opportunistic pathogen C. difficile, are associated with compromised health. Dorea spp. are found to be overrepresented in irritable bowel syndrome patients, and patients with non-alcoholic fatty liver disease. Coriobacteriaceae spp. have repeatedly been shown to be involved in host lipid metabolism, and many bacteria within this group are considered as opportunistic pathogens

One apparently positive change observed in the gliadin consuming mice was an increase in Akkermansia in the colon. This species is usually associated with beneficial effects on metabolic health and inflammation. However, it feeds primarily on mucin secreted from the gut wall, and the researchers suggest its proliferation may be due to increased turnover of the small intestine mucosa due to disrupted gut barrier function.

Another recent paper (The gut–kidney axis in IgA nephropathy: role of microbiota and diet on genetic predisposition, Coppo, April 2017) underscores the importance of gluten-microbiome interaction, in this case to the development of IgA nephropathy (Berger’s disease).

The importance of this research is that it is a major piece of work exploring the effects of gluten relevant to the ‘normal’, apparently gluten-tolerant population. It has shown a large range of measurable effects which will need to be investigated further, particularly to establish their relevance in humans. In terms of the gluten iceberg these researchers are undertaking the deep sea diving necessary to establish the extent of the sub surface portion of the gluten phenomena. I am sure we will see more research like this in the coming years.


First degree relatives of Coeliacs often have gluten related disorders despite testing negative for blood markers 

Here at the clinic we see a disproportionate number of patients who at some point in the consultation declare that one of their parents or siblings has coeliac disease, often as if this is some minor point that is hardly worth mentioning. Nothing could be further from the truth: The biggest risk factors for coeliac disease is being a first degree relative of a coeliac, with nearly four times the incidence than the general population.

The first-degree relatives (FDRs) of patients with coeliac disease are the main risk group for disease development.

– Vaquero et al, 2017

Parents, children or siblings of coeliacs should therefore have blood tests regularly, and if positive should immediately adopt a gluten free diet. A study by Nicola Imperatore et al, which I cover later in this post, has demonstrated the importance of early adoption of a gluten-free diet for anyone with positive coeliac blood tests, even when they have no  symptoms, to avoid progression of intestinal damage and immunological problems.

Some patients, however, claim that they have been screened for coeliac disease and have been told ‘they don’t have it’ – i.e. that their blood markers were negative. In many cases, however, I can tell from their symptoms that they are gluten sensitive despite the test results. Many go on to make remarkable progress once they adopt a properly gluten-free diet, but sometimes it can be an uphill struggle convincing them to give it a try. Such is the power of the medical establishment when it makes its decrees.

These clinical observations have recently received confirmation from a study published in the Journal of Gastroenterology and Hepatology (Vaquero et al, 2017), which investigated the value of a gluten free diet in first degree relatives who were negative for coeliac blood markers (anti-endomysial antibodies and raised anti-tissue transglutaminase ). In this study they invited 205 first degree relatives of known Coeliacs who were negative on blood tests to undergo genetic screening (for the HLA-DQ2/8 genes) and duodenal biopsy to check for intestinal damage. Symptoms were established by questionnaire at the start of the study, after which participants followed a three phase diet: (1) baseline diet (gluten containing) (2) gluten free diet (4 weeks) then (3) gluten ‘overload’ diet

Of 139 who completed the study HLA-DQ2/8 was positive in 78.4% of the participants (homozygous, 15.1%; heterozygous, 63.3%). Alterations to the intestinal mucosa were noted in 37.1% of participants who underwent duodenal biopsy (Marsh I, 32.7%; Marsh IIIa, 4.4%). At baseline more than half of the participants had gastrointestinal symptoms (57.6%), mainly associated with bloating (16.5%), constipation (15.1%), diarrhea (14.4%), and abdominal pain (5.8%). During the gluten-free phase this fell to just one quarter and increased agin during the gluten overload phase.

Symptom improvement during the gluten free diet was twice as common among women as men and three times as common among people with an existing autoimmune disorder. Both of these observations fit clinical patterns at Rosemary Cottage Clinic and are similar to risk factors identified in studies of Non Coeliac Gluten Sensitivity.

In conclusion: First degree relatives of coeliacs have a heightened risk of developing coeliac disease. Of those without coeliac blood markers many have intestinal damage. In addition gluten related symptoms are commonly present independent of intestinal damage. Such people would have to be classified as Non Coeliac Gluten Sensitive as they do not fit the definition of Coeliac.

Non Coeliac Gluten Sensistivity persists even after 8 years of a wheat-free diet

In a paper recently published in Gastroenterology (Carroccio et al, 2017) Italian researchers followed up 200 patients that had been diagnosed with NCGS many years earlier. 88% had experienced improved symptoms following their original diagnosis.

8 years later 148 of these individuals were still on a strict wheat-free diet, with virtually all of them (98%) reporting a continuation of symptom reduction. Among those that had not maintained a strict WFD only 58% had symptoms that were improved compared to the time of diagnosis.

The researchers repeated the double-blind placebo-controlled challenge with 22 patients, and found that 20 reacted to wheat.

This study demonstrates that NCGS is persistent, suggesting that it should be treated as a life long condition and a wheat-free diet adhered to.


A gluten-free diet prevents progression in Potential Coeliac Disease even when asymptomatic

Coeliac disease is diagnosed where patients have positive  blood tests (Anti-endomysial antibodies and raised anti-tissue transglutaminase) as well as evidence of villous atrophy on duodenal biopsy. In some cases, however, blood tests are positive, but there is little or no intestinal damage. Such situations are labelled Potential Coeliac Disease (PCD).

Until now it has not been clear whether such patients simply have a mild form of gluten intolerance, or whether they have early stages of Coeliac disease.  Furthermore, for the subset of PCD patients that have no gastrointestinal symptoms.

To answer these questions recent study an Italian team (Nicola Imperatore et al, Mar 2017) followed patients with PCD either on a gluten free diet or a gluten containing diet for a period of six years.

In short, those on the the gluten containing diet had increased intestinal damage and immune related disorders compared to those on the gluten-free diet. In addition, the asymptomatic patients who continued to consume gluten 69% developed coeliac-related symptoms, 46% developed villous atrophy and 61% immune mediated disorders.

This study underlines the importance of starting a gluten free diet as soon as possible following positive blood tests, regardless of symptoms and presence of villous atrophy.

Routine screening for Coeliac blood markers is not currently undertaken as many people that such tests would identify would prove to have no symptoms nor villous atrophy. It has been assumed that there would be no point in starting them on a gluten free diet as it was assumed that they would not go on to develop coeliac disease. This study challenges this position and demonstrates that many of these ‘false positives’ would indeed benefit from starting a gluten-free diet because they are at risk of developing villous atrophy and autoimmune diseases in the long term..

Coeliac Disease may be triggered by a common virus

It has long been known that the risk of coeliac disease is increased after various infections such as campylobacter, rotavirus and gastroenteritis. One hypothesis is that the presence
of both the pathogen and gluten presented simultaneously to the immune system  is enough to trigger coeliac disease.

Now a team from the University of Chicago, has found that exposing mice to a common reovirus called T1L can induce gluten intolerance. This virus was first identified in humans in the 1950s but has not been associated with any disease.

The team found that when they fed gluten to mice, those that were also infected with the virus produced two to three times as many antibodies to gluten as those that were virus free.

One of the Authors of the study Bana Jabri explained “Instead of mounting a tolerant, non-aggressive response, the immune system in the presence of the reovirus views gluten as being dangerous, promoting a destructive inflammatory response,”

The discovery has led the authors to speculate that a vaccine might be possible to prevent people from developing coeliac disease. Personally I think that’s unlikely, for a number of reasons. 1) gluten seems to cause disease by many pathways not just an aggressive immune response, 2) the researchers did not show that the mice went on to develop coeliac disease they just had a heightened immune response to gluten, 3) there is no evidence that all coeliacs had previously been infected with reovirus, and 4) physiological stressors other than pathogens appear to be able to trigger coeliac disease.

Source: New Scientist, Gluten allergy in coeliac disease may be provoked by virus (04/06/2017)

Coeliac Disease and Joint/Bone problems

In a recent letter to the journal Joint Bone Spine, Coline Daron et al report on their analysis finding 20‐30% cumulative incidence of arthralgia and arthritis among coeliac patients. They also identified an increased risk of osteoporosis:

Out of 11 case‐control studies featuring 1,008 patients with celiac disease and 13,706 controls, we noted a 2.73 [1.86‐3.99] higher risk of osteoporosis at any site in the celiac group. This increased risk was significant for femoral osteoporosis (OR=2.03 [95% CI: 1.11‐3.71]), and most of all for spinal osteoporosis (OR=7.2 [95% CI: 3.42‐15.18]. No increased risk of arthritis was noted in celiac patients compared to controls (OR=0.76 [95% CI: 0.16‐3.66]).

The authors call for physicians to undertake coeliac screening in cases of osteoporosis, arthralgia and arthritis where no obvious cause can be identified.