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Nutrition and Prevention of Diseases Topic 20

Module 20.5

Nutritional in Prevention and Management of

Irritable Bowel Syndrome, Constipation and

Diverticulosis

Eduard Cabré

Learning objectives

• To get a global understanding of the pathophysiology of irritable bowel syndrome,

idiopathic chronic constipation, and diverticular disease for a more rational use of dietary

tools in these conditions;

• To learn about the true impact of “food intolerance” on symptoms of irritable bowel,

thereby gaining insight into the role of excluding selected food from the diet of these

patients;

• To know the indications and limits for the use of high-fibre diets and fibre supplements in

irritable bowel syndrome, chronic constipation, and diverticular disease;

• To summarise the current evidences for the use of probiotics and prebiotics in these

conditions.

Contents

1. Introduction

2. Irritable bowel syndrome

2.1 Definition

2.2 Epidemiology and healthcare burden

2.3 Pathophysiology

3. Dietary and nutritional issues in IBS

3.1 Adverse reactions to food in IBS

3.1.1 Food avoidance

3.1.2 Food allergy

3.1.3 Carbohydrate malabsorption

3.1.4 Gluten sensitivity

3.2 Nutritional consequences of IBS

3.3 Dietary management of IBS

3.3.1 ‘Primum non nocere’

3.3.2 Exclusion diets

3.3.3 Dietary fibre and bulking agents

3.3.4 Probiotics and prebiotics

3.3.4.1 Probiotics


3.3.4.2 Prebiotics

4. Chronic constipation

4.1 Definition

4.2 Pathophysiology

5. Dietary prevention and management of chronic constipation

5.1 Fibre-enriched diet

5.2 Fibre supplements (bulking agents)

5.3 Probiotics and prebiotics

6. Diverticular disease

6.1 Epidemiology and clinical spectrum

6.2 Pathophysiology

7. Dietary management of uncomplicated diverticular disease

7.1 Fibre supplementation

7.2 Probiotics and prebiotics

8. Summary

Key messages

• Although self-reported food intolerances are frequent in patients with irritable bowel

syndrome, their role on the genesis of symptoms is difficult to demonstrate;

• Thus, in general, patients with IBS could eat a balanced diet without restrictions, and

should be encouraged to do that;

• Sugar malabsorption (i.e. lactose, fructose, sorbitol) is an exception to this rule, and

exclusion of foods containing them (in patients with proven malabsorption and

intolerance) is useful;

• Food allergy account for only a minority of food intolerances in irritable bowel syndrome;

• Increasing fibre intake is useful for preventing and treating functional chronic constipation,

as well as for alleviating symptoms of irritable bowel and diverticular disease (although

evidence is less strong for these indications);

• In contrast, fibre may worsen symptoms in patients with constipation due to colonic inertia

and/or pelvic floor dyssynergia;

• There is growing evidence for the effectiveness of probiotics in irritable bowel syndrome,

chronic constipation, and diverticular disease (depending on the strain used). Data on the

usefulness of prebiotics in these situations are still very scarce.

1. Introduction

Irritable bowel syndrome (IBS), chronic constipation, and diverticular disease of the colon are

clinical conditions with a common pathophysiological basis of disturbed bowel motility.

Furthermore, a pathogenic factor of dietary fibre deficiency has been claimed to occur in most

patients with these gastrointestinal complaints. These is the reason to include them together

in a single educational module.


Although this module is focused on nutritional and dietary prevention and management of

these conditions, a brief epidemiological, clinical, and pathophysiological overview will precede

each section.

2. Irritable Bowel Syndrome

IBS – also referred to as irritable or spastic colon – is one of the commonest seen disorders at

Gastroenterology clinics (20%-50% of referrals) affecting patients physically, psychologically,

socially, and economically. IBS is a combination of chronic or recurrent gastrointestinal

symptoms not explained by structural or biochemical abnormalities. Although IBS is a disorder

of the whole bowel, colonic symptoms usually predominate.

2.1 Definition

The absence of pathognomonic features makes IBS a diagnosis of exclusion. Keeping this is

mind, and to reduce the need for expensive and unnecessary investigations, attempts have

been made for a positive diagnosis of IBS.

Individual symptoms such as abdominal pain, loose or frequent stools associated with pain,

incomplete evacuation, mucus per rectum, abdominal distension or proctalgia fugax all have

limited accuracy in diagnosing IBS. Lower abdominal pain have the highest sensitivity (90%)

but very poor specificity (32%), whereas patient-reported visible abdominal distension have

the highest specificity (77%) but low sensitivity (39%). Therefore, a variety of criteria have

been developed to identify a combination of symptoms to diagnose IBS (Table 1 ).

Table 1 Diagnostic criteria used to define Irritable Bowel Syndrome (IBS)

Criteria

Symptoms, signs, and laboratory investigations

included in criteria

Manning’s (1) IBS is defined as the symptoms given below with no

duration of symptoms described. The number of

symptoms that need to be present for diagnosis is not

reported,, but a threshold of 3 positive is the most

commonly used:

1. Abdominal pain relieved by defecation

2. More frequent stools with onset of pain

3. Looser stools with onset of pain

4. Mucus per rectum

5. Feeling of incomplete emptying

6. Patient-reported visible abdominal distension

Kruis’ (2) IBS is defined by a logistic regression model that

describes the probability of IBS. Symptoms need to

be present for more than two years.


Symptoms:

1. Abdominal pain, flatulence, or bowel irregularity

2. Description of type and severity of abdominal

pain

3. Alternating constipation and diarrhoea

Signs that exclude IBS (each determined by the physician):

1. Physical findings and/or history pathognomonic

for any diagnosis other than IBS

2. Erythrocyte sedimentation rate >20 mm/2 h

3. Leukocytosis >10,000/cc

4. Anaemia (Haemoglobin <12 g/L for women or

<14 g/L for men)

5. Impression by the physician that the patient has

rectal bleeding

Rome I (3) Abdominal pain or discomfort relieved with

defecation, or associated with a change in stool

frequency or consistency, PLUS two or more of the

following on at least 25% of occasions or days for

three months:

1. Altered stool frequency

2. Altered stool form

3. Altered stool passage

4. Passage of mucus

5. Bloating or distension

Rome II (4) Abdominal discomfort or pain that has two of three

features for 12 weeks (need not be consecutive) in

the last one year:

1. Relieved with defecation

2. Onset associated with change in stool frequency

3. Onset associated with change in stool form

Rome III (5) Recurrent abdominal pain or discomfort three days

per month in the last three months associated with

two or more of:

1. Improvement with defecation

2. Onset associated with change in stool frequency

3. Onset associated with change in stool form

The first description of this approach was made by Manning et al (1) (Table 1). Studies

evaluating the accuracy of Manning’s criteria are controversial, but overall, they have a pooled

sensitivity of 78% and pooled specificity of 72%.


The next description of symptom criteria was by Kruis et al (2) (Table 1) and studies on their

accuracy suggested that the Kruis’ symptoms score have an excellent positive predictive value

with a pooled sensitivity of 77% and pooled specificity of 89%.

Subsequently, an international working group developed the Rome criteria, which have

undergone three iterations over 15 years (Table 1) (3-5). These criteria have been heavily

promoted, although there has been only one study in which the accuracy of Rome I criteria

has been evaluated (with a sensitivity of 71% and specificity of 85%) and none describing the

accuracy of Rome II or III.

All studies evaluating the accuracy of diagnostic criteria in patients with IBS face the problem

of lack of a reference standard test for this condition. Notwithstanding, none of the symptom-

based diagnostic criteria have an ideal accuracy and the Rome criteria, in particular, have been

inadequately evaluated, despite their extensive use in the research setting as mentioned.

For these reasons, the American College of Gastroenterology Task Force has recently promoted

a simple, pragmatic, and clinically useful definition incorporating the key features of previous

diagnostic criteria. They have defined IBS as “abdominal pain or discomfort that occurs in

association with altered bowel habits over a period of at least three months” (6).

In addition of the above described symptom-based assessment, a limited screening for organic

disease seems mandatory. This include complete physical examination, haematology counts

and routine biochemistry analysis (including erythrocyte sedimentation rate and, probably,

serum thyroid hormones), a search for ova and parasites in the stool, and a colonoscopy (or

a flexible sigmoidoscopy plus barium enema) in patients older than 50. Additional tests may

be necessary according to the syndromic subtype (see below) or the particular characteristics

of the patient. However, some studies questioned the cost effectiveness of such a routine

work-up, prior to a therapeutic trial for IBS (7,8).

In general, three subtypes of IBS are recognised: 1) IBS with (predominant) constipation (IBS-

C), 2) IBS with (predominant) diarrhoea (IBS-D), and 3) IBS with alternate (mixed)

constipation and diarrhoea (IBS-M).

2.2 Epidemiology and Healthcare Burden

IBS is a prevalent and expensive condition that is associated with a significantly impaired

health-related quality of life (QoL) and reduced work productivity. As mentioned, IBS is one

of the most frequent causes of referral to the gastroenterologist. However, many patients do

not seek for medical care. Thus, the true prevalence of IBS must be estimated by symptom

questionnaire in population surveys.

Based on strict criteria, 7–10 % of people have IBS worldwide (6). Community-based data

indicate that IBS-D and IBS-M subtypes are more prevalent than IBS-C, and that switching

among subtypes may occur. IBS is 1.5 times more common in women than in men, is more


common in lower socio-economic groups, and in people younger than 50 years of age as well.

Patients with IBS visit the doctor more frequently, use more diagnostic tests, consume more

medications, miss more workdays, have lower work productivity, are hospitalised more

frequently, and consume more overall direct costs than patients without IBS. Resource

utilization is highest in patients with severe symptoms, and poor QoL.

2.3 Pathophysiology

A detailed description of the pathophysiological mechanisms thought to be involved in the

development of IBS exceeds the purpose and scope of this educational module. Interested

readers could get complete information in excellent reviews published in recent years (911).

Evidences from investigations of the peripheral and central aspects of the bi-directional brain-

gut axis are shaping a pathophysiological model for IBS. This neurobiological model includes

alterations in autonomic, neuroendocrine, and pain modulatory mechanisms. Altered

viscerosomatic sensitivity (the so-called “visceral hyperalgesia”) seems to play a key role in

these interactions, leading to the development of symptoms of irritable bowel (12). Intestinal

infections and disturbances in intestinal microbiota have also been incriminated as a triggering

factor (13) (see below). The role of dietary components in this pathogenic network will be

discussed in the next section. Psychological stress and/or specific psychological disturbances

(anxiety/depression) contribute to exacerbate symptoms. Indeed, the prevalence of

psychiatric disorders in IBS patients has been found to range from 42% to 93% (14). It seems

likely in IBS that an understanding of the individual, including his or her psychosocial nature

and response to environmental factors influences the expression of any biologic determinants

including dietary factors (Fig. 1).


Fig. 1. A conceptual model depicting the relationship between early life, psychosocial

factors, physiological factors, symptom experience and behaviour, and outcome in IBS

(CNS=Central Nervous System; ENS=Enteric Nervous System). Modified from (9)

3. Dietary and Nutritional Issues in IBS

As shown in Fig. 1, dietary issues are a small part of the pathophysiological network of IBS.

However, dietary counselling is a major component of the therapeutic management of these

patients. In this respect, three aspects deserve special attention:

1) The impact of adverse food reactions on IBS;

2) the nutritional consequences of IBS; and

3) the dietary management of these patients.

3.1 Adverse Reactions to Food in IBS

3.1.1 Food Avoidance

Food adverse reactions consist of any abnormal reaction after ingestion of a food, and include

a) food intolerance, b) food aversions, and c) food allergy.

Food intolerance is and adverse physiological reaction, which is mediated by nonimmunological

mechanisms and may be due to factors within the foods, such as toxins (e.g. food poisoning)

or pharmacological agents (e.g. caffeine or tyramine), enzyme deficiency of the host (e.g.

lactase deficiency) or idiosyncratic responses induced by unknown mechanisms. Food

aversions are psychological avoidance responses to any type of foods.


About two thirds of patients with IBS believe that their symptoms are triggered by specific

foods (15,16). Foods rich in carbohydrates, as well as fatty food, coffee, alcohol and hot spices

were most frequently reported to cause symptoms, mainly bloating and abdominal pain (15).

In spite that this causative relationship is difficult to prove, a majority of patients limit or

exclude food items from their diet, and a small but relevant proportion of them have an

inadequate diet (16). A population-based case-control study (17), however, was unable to

disclose differences in the intake of wheat-containing foods, lactose-containing foods,

caffeinated drinks, and fructose-sweetened beverages between cases with functional

gastrointestinal disorders (n=99) and controls (n=119) (Fig. 2). Cases were slightly more

likely to consume norepinephrine- and epinephrine-containing foods, but not serotonin- or

tryptophan-containing foods. No differences were observed in the amount of calories, fibre,

protein, iron, calcium, and vitamins. Cases reported consuming slightly more fat and less

carbohydrates than controls. Similar results were obtained when the subgroup of IBS cases

(n=65) were compared with controls (17).

Fig. 2. Number of serving per week of frequently suspected “culprit” foods, as assessed by

food frequency questionnaire, between cases with functional GI disorders and controls

(p=NS in every case) (17)

3.1.2 Food Allergy

Only a minority of food avoidance, both in the general population and IBS patients, are due to

true food allergy. The prevalence of food allergy in the general population is greatest in the

first few years of life, affecting about 6% of infants under 3 years of age, and decreases over

the first decade, being lower than 4% in the adulthood.


Food allergy is an abnormal or exaggerated immunological response to a food antigen, which

can be due to 1) a classic type 1 IgE-mediated immediate reaction to the offending food; 2) a

type 4 cell-mediated delayed hypersensitivity response, or 3) a combination of both

mechanisms.

A careful history may establish a suspicion of a food-induced allergic reaction, the type of food

involved and the relationship between the time of ingestion and the onset of symptoms. There

is no gold standard diagnostic procedure for gastrointestinal food allergy. Skin prick test and

the radioallergosorbent test (RAST) for IgE suggest the presence of systemic sensitisation, but

by no means imply food allergy. At present, a double-blind placebocontrolled food challenge

is considered the only conclusive method for diagnosing food allergy. However, it is associated

with several practical problems: a) the lack of a read-out system, b) the variable time between

ingestion and the onset of symptoms, and most importantly c) the lack of discrimination

between food allergy and food intolerance (18,19).

Studies evaluating adverse food reactions in IBS patients have found a poor concordance

between the types of food causing the symptoms and the results of food allergy tests (namely,

skin prick test or serum IgE levels to specific food antigens) (16,20). In a study of 128

consecutive patients with IBS adverse reactions to one or more foods were reported by 80

patients (63%), and skin prick tests were positive in 67 cases (52%). However, there was

little concordance between the specific foods reported to cause intolerance and those positive

to the skin test (11 of 80 patients; 14%) (20) (Fig. 3), suggesting either a lack of accuracy of

skin tests or that type 1 food allergy is not a cause of IBS symptoms.

Fig. 3. Comparison between reported food intolerance and positive skin prick test to the

same allergens in 128 IBS patients (20)


In contrast to IgE, IgG antibodies to food are common in the normal population and often have

been considered physiological. However, IgG-mediated food hypersensitivity has been claimed

to play a role in IBS (21). In a randomised controlled trial, Atkinson et al. (22) assessed the

effectiveness of a food elimination diet based on the presence of specific IgG antibodies as

treatment of IBS patients. One hundred and fifty patients were randomised to receive either

a true diet based on patient’s individual food antibody profile or a sham diet excluding a similar

number of foods, but not those to they had antibodies. Participants remained on the diet for

12 weeks and were then observed during a 4-week food reintroduction phase. After 12 weeks,

the true diet resulted in a 10% greater reduction in symptom score than the sham diet with a

mean difference of 39 points (95%CI: 5–72; p=0.024) with this value increasing to 26% in

fully compliant patients (mean difference 101 points; 95%CI: 54–147; p<0.001) (22) (Fig.

4). Relaxing the diet led to a 24% greater deterioration in symptoms in those on the true diet

(difference 52 points; 95% CI 18–88; p=0.003) (22). The mechanisms by which IgG food

antibodies could mediate this detrimental effect is unclear, and further research in this area is

warranted.

Fig. 4. Mean change in IBS symptom severity score after 12 weeks on true or

sham elimination diets based on specific IgG food profile (22)

3.1.3 Carbohydrate Malabsorption

The role of individual sugar (i.e. lactose, fructose, sorbitol) malabsorption in the development

of symptoms of irritable bowel deserves particular comment. Lactose malabsorption has been

reported to occur in about 25% of patients with IBS in the USA and Northern Europe (7,23),

whereas the prevalence may be as high as 52%-68% in Mediterranean countries (24,25). In

addition to geographical influences, patient selection may account for these differences.


Lactose malabsorption can cause osmotic diarrhoea and bloating, and hence may be more

frequent in the subset of patients in whom these symptoms predominate (24). In a series of

unselected Finish patients, there was a poor relationship between lactose malabsorption,

lactose intolerance and symptoms of irritable bowel (26). A more recent study indicates that

lactose is, indeed, responsible for symptoms in some IBS patients, but these patients can only

be identified by the occurrence of symptoms during the hydrogen breath test, and not on the

individual perception of milk intolerance (27).

On the light of these data, routine investigation of lactose malabsorption in every patient with

IBS does not seem advisable. However, lactose malabsorption should be investigated, by

means of a hydrogen breath test after an oral load of lactose, in those patients in whom

diarrhoea and/or bloating predominate, particularly in countries where lactase deficiency is

highly prevalent.

Fructose and sorbitol malabsorption also occur among patients with IBS. The prevalence of

malabsorption is particularly high when both sugars are administered together (31%-92%)

(24,28,29). Although these figures do not differ from those found in healthy controls (24,29),

the intensity of symptoms after the ingestion of these sugars is significantly higher in IBS

patients (24,29). Such a difference does not appear to be due to intestinal dysmotility and

hypersensitivity to distension (30). Some authors advocate for an increased fermentative

capacity in patients with IBS (24,31), whereas other investigators suggested that intestinal

bacterial overgrowth may account for this phenomenon (32). As in the case of lactose,

hydrogen breath tests using fructose, sorbitol and fructose+sorbitol mixtures as substrate

should be performed in IBS patients with predominating diarrhoea and/or bloating symptoms.

3.1.4 Gluten Sensitivity

Recently, interest has been raised on the potential overlap between celiac disease and IBS.

The prevalence of celiac disease in the general population is about 0.2% to 0.3%, whereas

recent reports indicate that this figure may increase 10%-20% in IBS patients (33-36). It is

possible, however, that this subset of IBS patients simply may represent a cohort of

misdiagnosed patients with celiac disease. To address this issue, it would be helpful to know

the prevalence of IBS in patients diagnosed of celiac disease who are adherent to a glutenfree

diet, as well as to know whether treating celiac disease improves irritable bowel symptoms

(37). The issue of routinely screening patients with IBS for celiac disease is still a matter of

debate (38-40).

3.2 Nutritional Consequences of IBS

Fortunately, malnutrition is not particularly prevalent among IBS patients. In fact, the

diagnosis of IBS must be questioned in the presence of marked nutritional deficiencies or

weight loss. In this setting, the diagnostic work-up for organic disease must undoubtedly be

expanded with specific imaging and laboratory tests to rule-out inflammatory bowel disease,

celiac disease, gastrointestinal neoplasm, chronic pancreatitis, pancreatic cancer, etc.


Despite the rarity of malnutrition in IBS, some patients tend to attribute all his/her symptoms

to the “last meal they ate”. Thus, they would eat a more and more restrictive and imbalanced

diet which can lead them to protein-energy malnutrition or micronutrient deficiencies.

3.3 Dietary Management of IBS

Dietary advice may be a good complement of pharmacological approaches in the treatment of

IBS. It should be kept in mind, however, that excessive dietary restrictions may be the cause

nutritional deficiencies in otherwise ‘healthy’ patients. In the following paragraphs, the

following items will be discussed: a) the role of exclusion diets in IBS , with particular attention

paid to sugar-free diets; b) the role of dietary fibre and bulking agents in these patients; and

3) the impact of modifications of intestinal microbiota in the management of symptoms of

irritable bowel.

3.3.1 ‘Primum non nocere’

The treatment of IBS should be based on the nature and severity of the symptoms, the degree

of physiological disturbance and functional impairment, and the presence of psychosocial

disturbances affecting the course of the illness. Patients with mild symptoms respond to

education and reassurance, whereas antispasmodic (anticholinergics) drugs or low-dose

antidepressant agents (either tricyclic or serotonin-reuptake inhibitors) are recommended in

more symptomatic patients (41-43). However, it should be kept in mind that 40%-70%

respond to placebo alone (44).

In this setting, it is important to avoid restrictive and monotonous diets since, as mentioned,

many IBS patients tend to exclude from their diet a great number of foodstuffs without a firm

reason to do that. After an accurate dietary interview, most patients will realise that a given

foodstuff which apparently caused symptoms on one occasion was well tolerated in many other

instances. Therefore, in general, most patients with IBS could (and should) eat a balanced

diet without restrictions.

3.3.2 Exclusion Diets

A review of the seven clinical trials published from 1980 to 1996, whereby dietary exclusion

was followed by food challenge (45) showed that positive response to an elimination diet

ranged from 15% to 71%, and double-blind placebo-controlled challenges identified problem

foods in 6% to 58% of cases. Milk, wheat and eggs, as well as foods high in salicylates (coffee,

nuts, corn, wine, tomato, etc.) or amines (chocolate, bananas, wine, tomato, etc.) were most

often identified as causing symptom exacerbation. These findings have been confirmed in a

more recent systematic review (46) including eight studies with a total of 540 IBS patients.

However, most studies were uncontrolled and the response rate to exclusion diets ranged from

12.5% to 67% (Fig. 5).


Fig. 5. Response rates in eight studies of exclusion diet in IBS patients. Data from (46)

Although many of these papers claimed that such responses demonstrated the efficacy of

exclusion diets in IBS, such a conclusion is difficult to generalise given the high placebo

response in this condition. Therefore, even realising that exclusion diets may have a

therapeutic role in a minority of selected patients with IBS (47), most recent guidelines state

that “there is insufficient evidence that exclusion diets are efficacious in IBS and their routine

use outside of a clinical trial is not recommended” (42).

While generalised restriction diets are not advisable, specific avoidance of unabsorbed, highly

fermentable, short-chain carbohydrates – collectively termed FODMAPs (Fermentable

Oligosaccharides, Disaccharides, Monosaccharides, and Polyols) – may be useful in IBS

patients (particularly those in whom diarrhoea and/or bloating are the predominant

symptoms). FODMAPs can include fructose and lactose in patients in whom these are

malabsorbed, polyols (such as sorbitol and xylitol) because they are generally poorly absorbed

by humans, and fructo-oligosaccharides (fructans) and galacto-oligosaccharides (such as

raffinose), for which humans do not express suitable hydrolases and are always poorly

absorbed. Major dietary FODMAPs include fructose and fructans. Lactose is mainly found in

dairy products. Common dietary sources of fructose are fruits, honey, and high fructose corn

syrup, and of fructans they are wheat and onions. Tables 2 and 3 describe the lactose,

fructose, and sorbitol contents of dietary sources of these sugars (48,49).


Table 2 Lactose content of milk and some dairy products*

Food Type Lactose (g/100 g)

Milk Whole** 4.6

Semi-skimmed** 4.7

Skimmed** 4.8

Evaporated, whole** 8.5

Condensed, whole, sweetened** 12.3

Dried skimmed** 52.9

Goat 4.4

Sheep 5.1

Cream Single 2.2

Double 1.7

Sour 2.7

Crème fraiche 2.1

Crème fraiche half fat 3.0

Imitation cream (e.g. Tip top, Dream

Topping)

2.3-6.8

Cheese Brie/Camembert Trace

Cheddar 0.1

Cheese spread 4.4

Cheese spread, reduced fat 7.3

Cottage cheese 3.1

Cottage cheese, reduced fat 3.3

Crème cheese Trace

Danish blue Trace

Stilton 0.1

Edam/Gouda Trace

Feta 1.4

Goat’s cheese 0.9

Mozzarella Trace

Parmesan 0.9

Processed cheese slices 5.0

Yoghurt Plain 4.7

Fruit 4.0

Drinking yoghurt 4.0


Fromage frais 4.0

Tzatziki 0.3

*Adapted from (48)

**Cow’s milk

Table 3 Fructose and sorbitol content of some foodstuffs*

Food item Fructose Sorbitol Excess free

fructose**

Fruits (g/100 g edible portion)

Apples, raw 6-8 0.2-1 2-7

Pears, raw 5-9 1.2-4.5 3-8

Mangoes, raw 2-4 ND 0.5-3.5

Kiwifruit, raw 4-5 ND 0

Oranges, raw 2-3 ND 0

Grapes, raw 5-7 0.2 0

Papaya, raw 2-3 ND 0-2

Cherries, raw 5-7 1.4-2.1 0

Plums, raw 1-4 0.3-2.8 0

Plums, dried 14-16 14-16 0

Pineapple, raw 2-3 0 0-1

Grapefruit, raw 1-3 ND 0

Watermelon, raw 3-5 ND 0-4

Peaches, raw 0.2-1.5 0.2-1.3 0

Bananas, raw 2-4 0 0

Strawberries, raw 1-3 <0.1 0

Blackberries, raw 2-3 ND 0

Raspberries, raw 1-3 <0.1 0

Custard apple, raw 8.2 ND 0.7

Passion fruit, raw 2-4 ND 0

Figs, raw 2.8 0 0

Figs, dried 26-28 0 0

Pomegranates, raw 4-6 ND 0-1.5

Coconut, raw 1-3 ND 0-1.5

Blueberries, raw 3-4 ND 0

Melon, raw 2-4 ND 0-3


Fruit juices (g/100 ml)

Apple juice 6-8 0.3-1 2-7

Pear juice 5-9 1.1-2-6 3-8

Grape juice 4 0 0

Prune juice 14 13 0

Grapefruit juice 1-3 ND 0-1

Orange juice 2-6 0 0

Pineapple juice 1.4 0 0

Tomato juice 1-3 ND 0-2

Legumes and vegetables (g/100 g edible portion)

Aubergine, raw 1-3 ND 0

Onion, raw 0.9 ND 0

Beans, raw 1-1.5 ND 0-1

Cabbage, white, raw 1.6 ND 0

Cucumber, raw 0.9 ND 0

Soya, raw 0.5 ND 0.3

Lentils, raw 0.3 ND 0.2

Chickpeas, raw 0.3 ND 0.1

Asparagus, raw 1.4 ND 0.4

Carrots, raw 1 ND 0

Leek, raw 1.5 ND 0.5

Lettuce, raw 0.6 ND 0

Peas, sweet, raw 0 ND 0

Potato, raw 0 ND 0

Tomato, raw 1-1.5 ND 0-0.4

Alcoholic beverages (g/100 ml)

Brandy 16-17 ND 0

Whisky 8-9 ND 0-2

Vermouth 2-6 ND 0

Soft drinks (g/100 ml)

Ginger Ale 3-5 ND 0

Cola drinks 6 ND 0

Lemon drinks 5.2 ND 0

Orange drinks 5.6 ND 0


Other foods (g/100 g)

Honey 41 ND 7

Succedaneum honey 34 25 31

Jams 1-4.5 1-25 0-0.5

Quince jelly 21 27 20

Chocolate 20-60 ND 20-60

Hard nougat 15-30 ND 25-30

Chewing-gum 0 up to 59 0

Biscuits 0 17-33 0

*Adapted from (49)

** Free fructose as monosaccharide in excess of free glucose

Previous uncontrolled studies specifically restricting lactose alone (25), or fructose with or

without sorbitol (49-51) in patients who malabsorbed these sugars showed that this approach

could be useful both in the short- and the long-time (49,50). In a recently published double-

blinded, randomized, quadruple arm, placebo-controlled rechallenge trial Shepherd et al. (52)

have proven that the effect of this dietary change is due to sugar restriction and not to placebo

effect (44). Twenty-five IBS fructose-malabsorber patients who had previously responded to

dietary change were randomly challenged by graded dose introduction of fructose, fructans,

alone or in combination, or glucose (placebo) taken as drinks with meals for maximum test

period of 2 weeks, with at least 10-day washout period between (52). Seventy percent of

patients receiving fructose, 77% receiving fructans, and 79% receiving a mixture reported

symptoms (mimicking previous their previous IBS symptoms) which were not adequately

controlled with rechallenge, compared with 14% receiving glucose (P< 0.002). Similarly, the

severity of overall and individual symptoms was significantly and markedly less for glucose

than other substances (52).

In practice, it is important to keep in mind that 1) unabsorbed sugars induce symptoms in a

dose-dependent manner, and 2) absorption of a sugar may be either facilitated or interfered

by other sugars or nutrients. Table 4 describes some practical issues to optimise the effect of

dietary sugar reduction on the basis of these mechanisms.

Table 4 Dietary strategies for sugar malabsorption designed on the basis of their

small intestinal handling*

Substrate Small intestinal handling Dietary strategies

Lactose Lactase is a saturable enzyme Dairy products with low-lactose

content (mature cheese, yoghurt)

may be tolerated

Fructose Impairment of carrier-mediated

facilitated diffusion of low-capacity

Limit “free fructose” (in excess of

glucose)

Avoid fully mature fruits


Absorption facilitated by glucose Co-ingestion of glucose with high

“free fructose” foods

Absorption facilitated by some

amino acids

Not utilised

Absorption saturable with high

fructose loads

Avoid high fructose load (with or

without glucose) at a single meal

Absorption impaired by sorbitol Avoid co-ingestion of sorbitol

Fructans No small intestinal hydrolysis or

absorption

Limit food with significant (>0.5

g/serving) fructan content

Sorbitol Absorption impaired by fructose Avoid co-ingestion of fructose

*Adapted in part from (51)

3.3.3 Dietary Fibre and Bulking Agents

For years, high-fibre diets and/or the addition of bulking agents (i.e. bran) have been accepted

as effective therapeutic measures to regularize bowel function and to reduce pain in patients

with IBS. However, the quality of the evidence supporting this recommendation is poor.


Fig. 6. Meta-analysis of 12 randomised controlled trials of fibre versus placebo or low

fibre diet in IBS. Events are persistence or unimprovement of either global symptoms of IBS

or abdominal pain. Data from (53)

The most recently published systematic review (53) found 12 randomised controlled trials with

global endpoints dealing with this issue (Fig. 6). Most were over 15 years old and, therefore,

tended to be small (as a whole involving 591 subjects), had suboptimal experimental design,

and utilized a variety of experimental agents and conditions. IBS-C was differentiated from

IBS-D in only three studies; two of these recruited only IBS-C patients and in the other, almost

half of the participants had IBS-C. The other nine studies did not specify which IBS subtypes


were included. Most studies did not use criteria-based diagnosis, concealed allocation,

adequate blinding, or other methods now recommended in modern study design. Nine trials

were double blinded, two were single-blinded, and one was unblinded. Few were at least eight

weeks in duration and none followed patients beyond the period of treatment.

Most studies examined the effect of wheat bran or psyllium hydrophilic mucilloid (Isphagula

or Plantago ovata husk). Taken as a group, treatment with wheat bran provided no global

benefit in patients with IBS. Overall, the relative risk of IBS symptoms not improving with

wheat bran was 1.02 (95%CI=0.82-1.27) (53) (Fig. 6). In contrast, global IBS symptoms

were improved in four of the six studies with Isphagula husk. The relative risk of IBS symptoms

not improving with this agent was 0.78 (95%CI=0.63-0.96) (53) (Fig. 6). Safety issues and

adverse events were not addressed formally in these studies of bulking agents. Clinical studies

and expert opinion suggest that increased fibre intake may cause bloating, abdominal

distension, and flatulence, especially if increased suddenly because, as mentioned before,

patients with IBS appear to have an increased fermentative capacity (24,31).

In spite of the above considerations, high-fibre diets or fibre supplements should not be totally

withdrawn from the therapeutic armamentarium for IBS. Fibre supplements would be

particularly useful in those patients with constipation. Hydrophilic colloids such as Isphagula,

and methyl-cellulose tend to produce less gas (or at an slower rate). In addition, because their

hydrophilic properties, these agents bind water and prevent both excessive stool dehydration

and excess liquidity. Thus, they may be equally effective for patients in whom either

constipation or diarrhoea predominate. In order to minimise bloating, gradual titration is

advised if these agents are used (54).

3.3.4 Probiotics and Prebiotics

In recent years, evidence is growing for a pathogenic role of intestinal microbiota in IBS.

Changes in faecal (luminal) microbiota may lead to increased carbohydrate fermentation and

symptoms such as bloating and diarrhoea. Also, mucosa-associated microbiota may lead to

up-regulation of the intestinal innate immune response in a similar (albeit attenuated) way as

in inflammatory bowel disease (IBD). Indeed it has been suggested that IBS would make part

of a spectrum of intestinal inflammation ranging from “physiological” inflammation in normal

gut to high grade inflammation with macroscopic damage in IBD (Fig. 7). On the other hand,

the well-recognised phenomenon of the development of IBS symptoms shortly after a

gastrointestinal infection is a further argument for a role of bacteria in the pathogenesis of

IBS. The interested reader will found an excellent comprehensive review of the relationship

between gastrointestinal microbiota and IBS in reference #(13).


Figure 7. A “pyramid” of gastrointestinal disorders showing IBS as a part of a spectrum of

inflammation. *IBD=Inflammatory Bowel Disease (ulcerative colitis and Crohn’s disease); #includes lymphocytic and colleagenous colitis. Modified from (13)

3.3.4.1 Probiotics

Probiotics are defined as “live microorganisms, which, when administered in adequate

amounts, confer a health benefit on the host” . Probiotic products widely vary in delivery

systems (e.g., yoghurts, fermented milks, powders, capsules), species (e.g., Lactobacilli,

Bifidobacteria, Streptococci) and strains, and dose (from 108 to 1011 bacteria). Probiotics

may be of benefit in managing the symptoms of IBS via a number of mechanisms such as 1)

increasing mucosal anti-inflammatory and reducing proinflammatory cytokines, 2) directly

modulate intestinal pain (some probiotic species have been shown to up-regulate μ-opioid and

cannabinoid receptors both in vitro and in vivo), 3) blocking the actions of potentially

pathogenic bacteria on toll-like receptors in the innate arm of the immune system, and 4)

enhancing the mucosal barrier function.


placebo in IBS and reporting a dichotomou s outcome. E vents are persistence or

unimprovement of symptoms of IBS. Data from (55)

A very recent systematic review with meta-analysis (55) identified 19 studies including a total

of 1,668 participants that were deemed eligible. The quality of studies was reasonably good

with nine reporting an adequate method of randomisation and six describing appropriate

methods of concealment of allocation. All but three recruited patients according to Rome or

Manning criteria.

Ten trials evaluated 918 participants and reported IBS symptoms as a dichotomous outcome

(Fig. 8).

Taken as a group, probiotics had a statistically significant effect to reduce IBS symptoms

(relative risk of symptoms persisting in probiotic group = 0.71; 95%CI=0.57-0.88). However,

these data probably overestimate the effects of probiotics as there was heterogeneity and

evidence of funnel plot asymmetry, suggesting publication bias with an overrepresentation of

small positive studies in the published literature. Moreover, higher quality studies reported a

more modest treatment effect compared with lower quality trials.

Fig. 8. Meta-analysis of 10 randomised controlled trials comparing probiotics versus


There was no difference among the different types of probiotics used, with Lactobacilli,

Bifidobacteria, Streptococci, and combinations of probiotics all showing a trend toward benefit.

Fifteen publications with 1,351 participants reported IBS symptoms as a continuous variable

(Fig. 9).

Fig. 9. Meta-analysis of 15 randomised controlled trials comparing probiotics versus

placebo in IBS and reporting a continuous outcome. Events are change in symptoms score.

Data from (55)

Probiotics had a statistically significant effect to improve IBS symptoms compared with placebo

(standardized mean difference= -0.34; 95%CI= -0.60 to -0.07). Four trials evaluated

Lactobacilli in 200 patients and found no effect on IBS symptoms. Nine trials evaluated

combinations of probiotics in 772 patients with a significant effect in improving IBS symptoms,

whereas two trials evaluated Bifidobacteria in 379 patients with a trend toward improving IBS

symptoms.


The main limitation of this review (55) is that there were a variety of species, strains, and

doses of probiotics used and, therefore, it was difficult to reach a conclusion about the optimal

probiotic strategy to use in patients with IBS. While the dichotomous data suggest that all

probiotic therapies show a trend for being efficacious in IBS, the continuous data suggest that

1) Lactobacilli have no impact on symptoms; 2) probiotic combinations improve symptoms in

IBS patients; and 3) there was a trend for Bifidobacteria to improve IBS symptoms.

3.3.4.2 Prebiotics

Prebiotics are selectively fermented short-chain carbohydrates that allow specific changes,

both in the composition and/or activity in the intestinal microbiota, which confer a health

benefit. Fructans and galacto-oligosaccharides are able to increase concentrations of intestinal

Bifidobacteria in both the lumen and the mucosa while not increasing the number of

Bacteroides and Clostridia.

Unfortunately, there are very few trials of prebiotics in IBS. A recent randomised controlled

trial (56) of 5 g fructan vs. placebo in 105 patients with mild functional bowel disease found

that those in the therapeutic arm had a significant decrease in the intensity of their symptoms

as assessed by a visual analogue scale. Confusingly, however, the fructan group had a

significant increase in abdominal discomfort compared to controls, probably due to an excess

in gas production. Therefore, the role of prebiotics in the management of IBS is far from being

established.

4. Chronic Constipation

Chronic constipation is not a disease but a symptom. Thus, it may be either secondary to

diseases of the gastrointestinal tract, extraintestinal disorders or drugs (Table 5), or primary

or idiopathic. In this section, dietary approaches for the prevention and management of

idiopathic chronic constipation will be discussed (57).

Table 5 Causes of secondary constipation

Mechanical obstruction

• Colorectal cancer

• Extrinsic compression of the colon

• Benign stricture (inflammatory, ischemic, post-diverticulitis, etc.)

• Hirschsprung’s disease

• Anal fissure

• Severe rectocele

Metabolic causes

• Diabetes mellitus


• Hypothyroidism

• Hypercalcemia

• Hypomagnesaemia

• Hypokaliemia

• Uraemia

• Porphyria

• Lead poisoning

Neurological causes

• Parkinson’s disease

• Spinal cord injury

• Cerebrovascular disease

• Multiple sclerosis

• Autonomic neuropathy

Colonic myopathies

• Systemic sclerosis (scleroderma)

• Intestinal amyloidosis

Drugs

• Opioids

• Anticholinergics

• Calcium channel blockers

• Dopaminergics (anti-parkinsonians)

• Sympathycomimetics

• Phenotiazines

• Antihistaminics

• Antacids (calcium salts)

• Antidiarrhoeal

• Bile salt binders

• Mineral supplements (calcium, iron)

4.1 Definition

According to the Chronic Constipation Task Force of the American College of Gastroenterology,

chronic constipation is a symptom-based disorder based on the presence for at least 3 months

in the last year of “unsatisfactory defecation characterized by infrequent stools, difficult stool

passage, or both. Difficult stool passage includes straining, a sense of difficulty passing stool,

incomplete evacuation, hard/lumpy stools, prolonged time to stool, or need for manual

manoeuvres to pass stool” (58). This definition is broader than the more stringent Rome II

criteria (4). These criteria allow to identify uniform groups of patients for inclusion in

randomised controlled trials, but their use is impractical in clinical practice since most patients

who refer for constipation do not fulfil them. In this sense, the American College of


Gastroenterology definition encompasses the symptoms most commonly expressed by

patients who self-report constipation.

On the other hand, it should be acknowledged that symptom-based criteria for chronic

constipation and IBS-C might overlap. IBS is characterized by abdominal discomfort or pain,

bloating, and disturbed defecation. Most patients with chronic constipation report minimal

abdominal bloating or discomfort. Thus, in some patients it may be difficult, if not impossible,

to differentiate chronic constipation and IBS accurately.

4.2 Pathophysiology

Primary or idiopathic constipation can be broadly divided into three subtypes: 1) slow transit

constipation (the so-called colonic inertia), 2) outlet delay constipation (also known as

obstructive defecation, pelvic floor dyssynergia, pelvic floor dysfunction, defecatory

dysfunction, or anismus), and 3) functional constipation. Physiologic abnormalities in patients

with slow transit defecation include abnormal postprandial colonic motor function, autonomic

dysfunction, and reduced numbers of enterochromaffin cells and interstitial cells of Cajal (59).

Outlet delay constipation occurs as a consequence of the inability to coordinate actions of the

abdominal musculature, the anorectum, and the pelvic floor musculature (60). This prevents

straightening of the anorectal angle, which should precede the normal passage of stool.

Functional constipation include those patients with complaints of constipation but with normal

transit and normal pelvic floor function (61). However, there is a significant overlap between

these subtypes, so that a number of patients with pelvic floor dyssynergia may also have

prolonged colonic transit.

5. Dietary Prevention and Management of Chronic Constipation

Dietary measures to prevent and treat chronic constipation should be implemented in the

setting of wider lifestyle changes, some of them so simple as scheduling a regular time for

defecation and responding to a defecatory urge with no delay.

It has been claimed that a sedentary lifestyle may contribute to constipation. Several

population studies support the idea than people who are more active and perform more

physical activity have a lesser incidence of constipation (62). Physical activity affects colonic

motor function, with changes in function probably proportional to the extent of activity.

Prolonged physical inactivity in those who are normally physically active, especially in the

elderly, can reduce colonic transit, favouring constipation. However, other factors such as

cognitive function, presence of depressive symptoms, use of medications that slow bowel

motility, an inadequate diet, are likely to play a role in the elderly constipation.

In healthy subjects, only vigorous physical activity such as running a marathon increases gut

and colonic activity and can lead to dramatic increases in large bowel function. Modest physical

activity may help subjects with mild constipation, but there is no evidence that it may improve

severe constipation (62).

Increasing fluid intake does not have an important effect on colonic function, and it is not

recommended to treat constipation unless there is evidence of dehydration (62).


5.1 Fibre-Enriched Diet

Virtually all fibres are broken down to a greater or lesser extent in the colon. The extent of

fermentation and the range and nature of the end-products depends on a number of factors,

including the type of fibre, its physical nature (e.g. particle size), solubility, and surface area

exposed to bacterial action.

Different types of fibre have different effects on stool weight (63). The cellulosic fraction of

some cereal fibres has the greatest effect on increasing the stool weight and decreasing transit

time, since it tends to better resist digestion than non-cellulosic polysaccharides (10% of

cabbage fibre is recovered in faeces, compared with 60% of wheat bran). Soluble fibres such

as pectin or guar gum, different forms of resistant starch, and fructans are the less effective

in increasing the stool weight, and some of them are not detected in faeces after consumption,

indicating that they are completely fermented in the colon. Dietary fibre may be classified

according to their solubility, as summarised in Table 6.

Table 6 Classification of dietary fibre according to its solubility*

Type of fibre Examples

Insoluble Lignin**

Insoluble polysaccharides

Cellulose

Hemicelluloses

Soluble Soluble polysaccharides

Pectins β-Glucans

Plant exudates gums

Mucilages

Legume seed gums

Seaweed polysaccharides

Bacterial polysaccharides

Fructans

Fructo-polysaccharides (inulin)

Fructo-oligosaccharides (oligofructose)

Resistant starch

*Adapted from (57)

**Cannot be considered, sensu stricto, as fibre

Increased fibre particle size results in increased stool output. Large particles are more slowly

degraded, whereas reducing the particle size increases the available surface area, resulting in

increasing digestibility, so that the cellulose content of finely ground bran is digested faster

than that in coarse bran. Furthermore, indigestible plastic particles cut to the same size as

coarse wheat bran flakes induce a comparable increase in stool weight.


A diet poor in fibre should not be assumed to be the cause of constipation but could be a

contributing factor. There is not doubt that intake of dietary fibre, mainly insoluble fibre,

increases stool bulk and frequency, and decreases consistency in healthy people. A classical

meta-analysis (64) showed that in 18 of 20 studies stool weight was increased by adequate

fibre supplementation, and there was increased faecal transit. These findings indicate that an

inadequate diet with a diminished intake of dietary fibre may contribute to constipation in

great number of patients. These patients may be considered to suffer from a “relative fibre

deficiency”, as they have not identifiable cause of their complaints. However, there is a subset

of patients with more severe constipation secondary to slow transit and/or pelvic floor

dyssynergia who get worse with an increase in dietary fibre intake (62). Despite that, all

constipated subjects should be advised to increase their dietary fibre intake as an initial

measure since this is the simplest, most physiologic, and cheapest form of treatment (57). In

those people in whom fibre aggravates abdominal distension or in whom fibre lead to

incontinence (mainly in elderly subjects), a reduction in their fibre intake should be

recommended.

On the other hand, gas production from fibre metabolism may limit acceptance. This is

particularly true from extensively fermented fibres (usually the soluble types), which lead to

increased bulk in colon by increasing microbial mass. Less fermentable fibres (usually the

insoluble types) produce less gas and contribute to increasing bulk in the colon by their water-

holding properties. Water-holding appears to be inversely related to solubility and thus to rate

of fermentation by colonic microflora. Highly fermentable have a less pronounced effect of

stool weight than less fermentable ones. Increased bulk in the colon decreases transit time,

which in turn results in decreased water reabsorption, and as a consequence wetter stools and

thus increased stool weight (63).

Therefore, the optimum way of improving colonic function in the majority constipated patients

is to prescribe a diet with a higher fibre content than that ingested previously. The amount of

fibre that is necessary to correct constipation varies in different people, but the effect of fibre

on stool weight is dose dependent. Whereas in some subjects 10 g of fibre per 1000 kcal may

be enough, others may require 20 g per 1000 kcal. In a review of over 100 studies on the

effect of fibre intake on stool weight (65), there was a wide range of the contribution of dietary

fibre to faecal weight (i.e., an increase of 5.7 g faecal bulk per gram of wheat bran fed

compared to an increase of 1.3 g per gram of pectin in the diet). The 2005 Dietary Guidelines

of the US Government recommend a daily fibre intake of 14 g per 1000 kcal to reduce the risk

of cardiovascular disease and promote healthful laxation (for a critical daily stool weight of

160–200 g) (66). In general, patients with chronic constipation require greater doses of fibre

than do healthy subjects in order to produce similar increases in stool weight (64). In starting

a fibre-enriched diet, the total amount of fibre should be progressively increased to improve

tolerance. An appropriately balanced soluble and insoluble fibre intake is likely to be the better

option. However, some patients will tolerate insoluble better than soluble fibre, and vice versa.

5.2 Fibre Supplements (Bulking Agents)


Dietary fibre supplementation can be achieved by increasing the ingestion of fibre-rich foods

as described before, or by providing commercially available fibre supplements. Bulking agents

are a concentrated form of non-starch polysaccharides useful for patients who cannot achieve

adequate dietary fibre intake from conventional foodstuffs. Available bulking agents include

psyllium (Isphagula husk), wheat bran, calcium polycarbophil, methylcellulose, guar gum, and

sterculia (Indian tragacanth or karaya).

A systematic review on the use of psyllium for chronic constipation (67) identified three

randomised placebo-controlled trials. They demonstrated improvements in stool frequency

and consistency at doses ranging from 10 to 24 g/day. However, only one trial was of high

quality and enough duration (>4 weeks), despite including only 22 patients (68). In an

observational study (69), 149 patients were treated with psyllium under the form of Plantago

ovata seeds, 15–30 g daily, for a period of at least 6 weeks. There was an 85% improvement

in patients functional constipation, whereas there was a poor response to treatment among

patients with slow colonic transit or pelvic floor dyssynergia (69).

In it noteworthy that despite the popularity of bran as a treatment of constipation, there is

only one placebo-controlled trial on the effect of wheat bran in chronic constipation, showing

no differences between therapy groups in the improvement of stool frequency or consistency

(67). Also, there are no placebo-controlled trials examining the effect of the other bulking

agents above mentioned. Small trials comparing some of these agents versus psyllium have

failed to demonstrate differences in stool frequency or consistency (67).

In summary, bulking agents may be effective in alleviating chronic constipation in patients

without slow colonic transit or pelvic floor dyssynergia. If the patient is compliant, fibre

treatment may help up to 80%. However, the same results could be obtained by dietary means

encouraging patients to eat either a supplement of natural bran or a fibre-enriched diet (57).

5.3 Probiotics and Prebiotics

Some studies have shown that milk or yoghurt fermented with different types of probiotics

may reduce intestinal transit time and increase the daily stool number in constipated patients.

In a double-blind, randomised, crossover design, Bifidobacterium animalis strain DN-173 010

reduced the colonic transit time as compared to placebo in a group of healthy young women

(70). In a recently published trial (71), 266 women with functional constipation were

randomised to receive this probiotic strain or placebo for 14 days. Treatment with the probiotic

was associated with a higher bowel frequency (6.1±2.7 stools/week vs. 5.0±2.6 dep./week in

controls; P<0.01), an improvement in the quality of the stools according to the Bristol scale

(3.6±1.0 vs. 3.4±1.0; P<0.01), a reduced perception of straining effort (1.9±0.8 vs. 2.2±0.9;

P<0.01) and a reduced perception of pain associated with defecation (0.1±0.2 vs. 0.2±0.3;

P<0.01) (71). Other Bifidobacteria (B. lactis, B. longum) have also proven to normalise bowel

habit in elderly nursing home residents (72).

Promising results have been also obtained with Lactobacillus casei Shirota (73), Escherichia

coli Nissle 1917 strain (74), but not with Lactobacillus GG (75). Thus, probiotics may be

effective in patients with mild to moderate constipation but this effect may dependent on the

bacterial strain used and the population being studied. On the other hand, there are no studies

evaluating the effect of probiotics as compared to fibre supplements (psyllium). The widely


used laxative lactulose is not digested by human disaccharidases, and is a substrate for the

bifidobacteria in the colonic flora. Thus, it is in fact, a prebiotic. Several trials have shown that

lactulose (15–30 ml twice a day) is effective at increasing stool frequency and stool consistency

in patients with mild to moderate chronic constipation. Other prebiotics would be a promising

therapy of chronic constipation.

6. Diverticular Disease

Although diverticula (i.e. pouches protruding outwards the wall of the bowel) may occur

anywhere in the gut, the term “diverticular disease” usually denotes the presence of diverticula

in the large intestine, particularly in the sigmoid colon. In fact, 95% of cases of colonic

diverticula involve this segment, and it is exclusively affected in 65% of patients.

6.1 Epidemiology and Clinical Spectrum

Diverticular disease is very common, particularly in industrialised countries. The prevalence of

this condition increases with the age, being rare in individuals younger than 40, whereas it

occurs in more than one-third of subjects over 65. Diverticular disease is rare in people who

live in developing countries. However, the risk rapidly increases when this people migrate to

Western societies.

About 80% of patients with diverticular disease never have any symptoms. When

symptomatic, patients complain from pain in the left lower quadrant of the abdomen, usually

colic, and changes in bowel habit. In fact, these symptoms mostly resemble those of IBS.

Complications occurs in about 5% of cases and mainly consist of infection of a diverticulum

(diverticulitis) which may lead to bowel perforation or abscess formation. Gastrointestinal

bleeding is rare may also occur, particularly from diverticula arising in the right colon.

A full description of the epidemiology, pathophysiology, clinical presentation, and management

of the entire spectrum of diverticular disease is out of the scope of this educational module.

Interested readers may find valuable information in recent reviews (76,77).

6.2 Pathophysiology

The most widely pathogenic theory for diverticular disease states that this is a consequence

of deficient intake of dietary fibre. This view is supported by data from large prospective

cohorts showing that the combination insoluble component of fibre – mainly cellulose – is

inversely associated with the risk of diverticular disease and that the risk is particularly strong

when low-fibre diets are combined with high-fat and high red meat intake (78,79).

Fibre deficiency would lead to low-volume stools which result in alterations in colonic motility

that produce increased intraluminal pressures (80). High intraluminal pressures are generated

when the sigmoid colon undergoes “segmentation”, a process during which smooth muscle

contraction separates the colon into functionally distinct compartments (81). This normal

physiologic process becomes exaggerated in those with low-volume stools, thereby generating

markedly elevated intrasegmental colonic pressures that are then transmitted to the colonic

wall. The law of Laplace, which states that intraluminal pressure is inversely related to lumen


diameter, has been used to explain the role of low-volume stools in the generation of increased

luminal pressures and development of diverticula (82).

Examination of surgical and post-mortem specimens has offered insight into the structural

changes found in patients with diverticular disease. The term myochosis has been coined to

describe the contracted, thickened appearance of the colon folds. Originally thought to be

secondary to circular muscle hypertrophy, the colon’s corrugated appearance is now known to

be a secondary effect of bowel shortening and increased elastin deposition (83). The exact

reason for elastin deposition in patients with diverticular disease is unknown, although some

have implicated increased uptake of proline from Western diets (82). Further support for the

role of connective tissue changes in the pathophysiology of diverticulosis comes from the

finding that patients with Marfan and Ehlers–Danlos syndromes develop diverticula at an early

age.

7. Dietary Management of Uncomplicated Diverticular Disease

No treatment or follow-up has to be offered to the majority of patients with asymptomatic

diverticulosis, and to those with a single previous episode of symptoms of uncomplicated

diverticular disease due to the low risk of recurrence. Treatment of recurrent uncomplicated

diverticular disease is aimed at relief of symptoms and prevention of major complications, but

the standard approach is still debated. The principal treatments are a fibre-rich diet and non-

absorbable antibiotics, but alternatives include mesalazine and probiotics. In the next

paragraphs the role of dietary approaches to the treatment of diverticular disease (i.e. dietary

fibre, and pro- and prebiotics) will be discussed.

7.1 Fibre Supplementation

The beneficial effects of fibre supplementation in symptomatic diverticular disease were first

reported in 1977 in a double-blind controlled trial of 18 patients assessing the therapeutic

value of increasing the daily dietary fibre intake with 6.7 g/day of bran over 3 months (84).

In this study, significantly greater symptomatic relief was obtained by those on a high fibre

regimen than by those in the control group, despite a marked initial placebo effect (84).

Two subsequent randomized controlled trials reported differing results. In the first one, 85

patients with uncomplicated diverticular disease took bran crispbread (7 g/day fibre),

Isphagula drink (9 g/day fibre), and placebo (2.3 g/day fibre) for four months each in a

randomised, cross-over, double-blind design (85). There were no significant differences on

symptom relief although both active treatments significantly reduced straining at stool,

increased wet stool weight and stool frequency, and significantly softened the stools (85). The

second trial comparing methylcellulose (1 g daily) and placebo in 30 patients also reached a

similar conclusion over a follow-up period of 3 months (86). Both studies did not assess

complication rates related to diverticular disease. Finally, previous observational studies have

reported that a high fibre diet prevents the development of symptomatic diverticular disease

(78,79) and its complications (87,88) despite a compliance rate of only 72% for fibre-

supplementation. However, despite these conflicting data and the certainty that diverticula do


not regress with an increased fibre intake, some amelioration of symptoms in patients with

uncomplicated diverticular disease can be seen with high-fibre diet.

7.2 Probiotics and Prebiotics

The first report on the use of probiotics in diverticular disease comes from a prospective

observational trial on the prevention of complications after acute diverticulitis (89). Patients

with a postdiverticular stenosis of the colon were treated sequentially with rifaximin and

Lactobacilli for a period of 12 months. This treatment proved to be effective in preventing

symptom recurrence and complications (89). The efficacy of probiotic treatment as a single

therapy for uncomplicated diverticular disease has been assessed in one study with 15 patients

(90). The non-pathogenic E. coli Nissle 1917 strain was given for a mean period of 5 weeks

after a course of treatment with an intestinal antimicrobial and absorbent, resulting in a

significantly prolonged remission period and significant improvement of all abdominal

symptoms (90). More recently, a three-arm randomised controlled trial of mesalazine,

Lactobacillus casei DG, or the combination of the above showed that both mesalazine and L.

casei DG are effective in preventing recurrence of symptomatic uncomplicated diverticular

disease, but their association seems to be more promising in this field (91). Although there is

a rationale for using prebiotics in diverticular disease (particularly as maintenance therapy),

to date, there is no data on the effectiveness of these agents in these patients.

8. Summary

Many patients with IBS believe that their symptoms are triggered by specific foods. However,

objective demonstration of these self-reported food intolerances is difficult. True food allergy

account for a minority of intolerances, whereas carbohydrate (i.e. lactose, fructose, sorbitol )

malabsorption is easier to document. In general, patients with IBS could (and should) eat a

balanced diet without restrictions, and (except for malabsorbed sugars) exclusion diets are

not useful in the majority of them.

Increasing fibre intake has been recommended for years as first-line therapy for IBS. However,

the quality of the evidence supporting this recommendation is poor. Despite this, high-fibre

diets or fibre supplements should not be totally withdrawn from the therapeutic

armamentarium for IBS. Hydrophilic colloids (i.e. Isphagula, methyl-cellulose) prevent both

excessive stool dehydration and excess liquidity, and may be equally effective for patients in

whom either constipation or diarrhoea predominate.

Increasing fibre intake is useful for preventing and treating functional chronic constipation,

but this may worsen symptoms in patients with colonic inertia and/or pelvic floor dyssynergia.

Also, fibre intake may help some patients with uncomplicated diverticular disease (although

evidences are not much strong).

There is growing evidence for the effectiveness of probiotics in IBS, chronic constipation, and

diverticular disease (depending on the strain used). Data on the usefulness of prebiotics in

these situations are still very scarce.


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