The main result of this study is that there was a higher prevalence of perceived food intolerance in the exposed group compared to a control group three years after verified Giardia infection. IBS was not an effect modifier for this association. Perceived intolerance to high FODMAP foods and low FODMAP foods were both statistically significantly associated with exposure to Giardia infection.

Limitations and strengths

Some of the limitations regarding the data used in this study have been described before [4, 24]. The response rate in the exposed group (65,3 %) is reasonably high, however, selection bias cannot be ruled out. This may impact the prevalence, but estimates of association are more robust. The exposed group is selected on the basis of having seen a doctor and thus having had giardiasis diagnosed by positive stool samples. The differences in characteristics of this group compared to those who might have had giardiasis without seeking medical attention is not known. Unbiased baseline information about IBS, food intolerance, previous gastrointestinal infections or other illnesses is impossible to obtain, as this may be regarded as a natural, unplanned experiment. However, this problem of missing information is similar for the exposed group and the control group, and most of these factors are presumed to be equally distributed between the two groups prior to the giardiasis outbreak.

The exposed group has had a defined gastrointestinal illness that may lead to increased wariness of possible causes of their abdominal complaints, including food intolerance. Hence they might not actually be more susceptible to intolerance per se.

The response rate in the control group (31.4 %) is relatively low and there is a risk of selection bias. The prevalence of IBS in our control group is 14.0 %, which is a little higher than 8.4 %, the prevalence in the general Norwegian population as found in a large public health survey in 2006 [25]. Our study used the Rome III criteria, which have been shown in a study [26] to find a higher prevalence of IBS than the Rome II criteria used in the above-mentioned study. In sum, this may indicate that our control group is not too dissimilar from the general population. Again, the investigation of associations, with use of relative outcome measures such as OR, depends to a lesser degree on such biases.

The questionnaire items about food have not been validated, and the reliability is not known. They do not constitute a complete assessment of the respondents’ diet. The classification of an open-ended question may be subject to interpreter bias, and there is a potential for misclassification to a varying degree depending on the specific category. All food categories and how the answers were coded were accounted for in a codebook. Although quantitative analyses on qualitative data is not straight forward, one advantage of using an open-ended question instead of a closed-ended one is that it is unguided by any preconceived theory. The respondents were free to answer whichever type of food they perceived as giving symptoms. Also, there were 971 responses to the open-ended question, many of which were readily and unambiguously coded to meaningful food categories. This study was performed in 2007, before the concept of FODMAP-content in the diet was generally known, and the responses will not be biased by the recent interest in this diet. Based on these considerations we found that a quantitative approach was justified.

Interpretation

Perceived food intolerance in a post-infectious setting has been scarcely investigated. Short-term lactose malabsorption after giardiasis has been described, but with contradictory findings [27, 28]. Fat malabsorption with steatorrhoea and diarrhoea can occur in chronic giardiasis, as can folate, B12 and vitamin A deficiency [27], but these are usually resolved with appropriate treatment. In our study the prevalence of perceived intolerance for both dairy products and fatty foods is relatively high, and significantly higher in the exposed than in the control group. Our study is not designed to investigate the mechanisms behind perceived food intolerance.

Recent studies and reviews have elucidated some of the mechanisms behind the development of PI-IBS after infective gastroenteritis [1]. Similar pathophysiologic mechanisms have also been found in sporadic IBS [9]. In this study we find a similar pattern of perceived food intolerance among Giardia exposed respondents with IBS (predominantly PI-IBS) and controls with IBS (sporadic IBS), but with a tendency, sometimes statistically significant, towards the exposed more often reporting intolerance for the specific food categories. Our results do not help clarify whether PI-IBS might be the same entity as sporadic IBS.

The prevalence of IBS and perceived food intolerance were measured at the same time. No inferences about causative pathways between IBS and perceived food intolerance can be made. We found that the exposed had a higher prevalence of perceived food intolerance than controls, and it has previously been found that this group has a higher prevalence of IBS [4]. There was also a significantly higher prevalence of perceived food intolerance among exposed in the no-IBS group. One hypothesis is that giardiasis causes alterations in the gastrointestinal tract that are important in the pathogenesis of both IBS and food intolerance. This does not suggest that the pathogenesis is identical, but there might be some common immunological pathways involved.

In our study 81.3 % of respondents with IBS in the exposed group and 78.4 % with IBS in the control group reported perceived food intolerance when this was defined as light, moderate or severe food-related abdominal complaints. Among respondents without IBS the proportions were 49.0 and 42.3 %, respectively. These results were comparable to a recent dietary survey performed on Irish IBS-patients (89.6 %) and a comparative group (55.0 %) [29]. The results for the non-IBS group is higher than what was found in a general UK population in 1994 (20.4 %) [30]. Other studies on IBS and perceived food intolerances have found prevalence ranging from 25 to 70 % [11, 19, 31, 32]. The reasons for the variance in prevalence of perceived food intolerance reported between studies might be due to different ways of measuring food intolerance, because of differences in the IBS-populations under investigation (e.g. inpatient vs. outpatient), and maybe due to a development in dietary trends over time.

Milk, dairy products, wheat products, caffeine, certain meat, certain vegetables, hot spices, alcohol, fat, fibre, fried food and smoked products are some of the foods stated in other studies to cause symptoms in IBS patients [10, 20]. The first nine of these food categories are also among the quantitatively most important in all investigated groups in our study, whereas the latter three are less frequently reported. Some of the above-mentioned food categories (dairy products, fatty foods and cereals) are significantly associated with IBS both in the exposed group and the control group. There are some similarities between the findings in our study and other studies on IBS and diet [10, 20]. However, as the validity and reliability of our questionnaire-items regarding food have not been tested, the results must be interpreted with caution.

There is a general tendency that the prevalence of perceived food intolerance for the various foods in our study is lower than that in other studies [11, 19, 29]. This could be due to the fact that most of the other studies use questionnaires with a predefined checklist of food items, which is known to overestimate the prevalence of intolerance to the included food items [33]. However, the prevalence of perceived food intolerance in our study is also lower than those reported in another study that used an open-ended question to map food perceived to cause symptoms [29]. This could be partially explained by a stricter coding of some of the food categories in our study, and also due to the fact that the patients included in the study were recruited from a gastroenterology clinic, and might thus be more severely ill than our respondents, who were recruited from the general population.

We found a statistically significant association between exposure status and perceived intolerance to both high and low FODMAP foods. Because the categories of high and low FODMAP foods were not mutually exclusive, the strength of the associations could not be compared statistically, but rather the results had to be interpreted more subjectively. The OR for high FODMAP foods was slightly higher than that for low FODMAP foods both in the unstratified and stratified (according to IBS-status) analyses, but with substantial overlap of the confidence intervals (Tables 3 and 4). The current study does not contradict or support the findings from other studies suggesting that high FODMAP content may add to symptoms among vulnerable individuals.

Food intolerance in IBS should be further investigated, especially with randomized controlled diet intervention studies in primary health care. We would propose that such a diet could be based on the FODMAP concept, but also include a tailor-made diet based on the patient’s perceived intolerances, followed by reintroduction.