29 Jul 2020

The effect of feeding on the development of gastric ulcers in pigs

The effect of feeding on the development of gastric ulcers in pigs is anlaysed in this article. It explains the pathogenesis of the disease,  followed by a review of  scientific literature in order to determine the main risk factos for the occurrence of the disease. 

Pathogenesis and aetiology

The pathogenesis of ulcers in the pars oeasophagea of the pig stomach is multifactorial. However, the statement by Schwarz (1910) “without acid there are no ulcers” is still valid. Generally, the pathogenesis of gastric ulcers implies an imbalance between aggressive factors (HCl, pepsin, bile acids) and defensive ones (Friendship, 2006; Martineau et al., 2009; Ichikawa, 2011).

In normal conditions, the proximal region (pars oesopagea) of the stomach tends to maintain a neutral pH, whilst the content on the distal regions (glandular regions) is attacked by hydrochloric acid and digestive enzymes. Any factor that breaks the balance between the neutrality of the proximal region and the acidic, enzymatic secretion of the distal part, constitutes a risk factor for the development of ulceration in the pars oesophagea. 

Alkaline mucus

The thick layer of mucus covering the glandular surface of the stomach is alkaline. This constitutes a natural defense barrier protecting the gastric epithelium from potential damage caused by acid. In contrast with the glandular surface, the squamous epithelium of the pars oesophagea does not contain mucous glands. The absence of mucus makes the squamous epithelium of the pars oesophagea the one most usually affected by gastric ulcers.

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 Absence or inefficiency of epithelial restitution

Epithelial restitution is the process whereby the cells of the gastric epithelium surrounding a lesion could migrate to repair the damaged area. Restitution is not observed in the squamous stratified epithelium of the pars oesophagea (Argenzio &Eisemann, 1996; Argenzio, 1999) or, if it exists, it is much more inefficient than in the glandular region.


The glandular mucosa is also protected by the action of prostaglandins. Among various effects, these substances increase the blood flow in the submucosa and reduce the secretion of HCl. The existence of this effect has not been proven in the epithelium of the pars oesophagea (Argenzio, 1999; Morrisey et al., 2008)


Histopathologically, the lesion is the consequence of thickening and parakeratosis of the epithelium, with nucleated cells present on the surface of the mucosa.

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Ulcers in the pars oesophagea normally involve only the submucosa, but they could reach the muscular layers and, occasionally, even the serosa (Thomson, 2012). 

Experimental observations 

In studies designed to establish the prevalence of gastric ulcers, evaluate preventative strategies, or assess the effect of a treatment, stomachs are collected at the abattoir. After opening and cleaning them, they are classified according to the visual aspect of the pars oesophagea.

There are several score systems to grade the lesions (Kessin et al., 1992; Nielsen and Ingvartsen, 2000b; Kopinski and Mckenzie, 2007). Generally, they are based on the distinction between normal epithelium, hyperkeratosis, erosion, ulcer, scar, and stenosis.

In Denmark, a scoring system with a value scale from 0 to 10 has been proposed (Table 1 and Fig. 1).

Scoring system for gastric ulcers of pigsFigure 1. Scoring system to classify ulcers in the pars oesophagea of the stomach of the pig (Busch 2016).


Table 1. Lesions characterizing the different scores of gastric ulcers in pigs  (Jorgensen and Nielsen, 2015ª)

Scoring system os gastric ulcers in pigs _ meaning of categories

Gastric ulcers: a multifactorial disease

Factors such as feeding and management, among others, could contribute to the pathogenesis of ulcers in variable degrees (Table 2). The impact of some of them has been clearly demonstrated, whilst in others it is not really evident.

 Table 2. Factors contributing to the risk of occurrence of gastric ulcers in pigs.

Animal welfare: Are gastric ulcers painful?

It is not yet clear whether gastric ulcers cause pain in pigs. However, in analogy with what occurs in humans, it is expected that a gastric ulcer can be very painful.

Considering the relationship between ulcers and growth (Fig. 2), it possible that more severe ulcers cause pain since the weight gain suddenly drops as a result of anorexia and the consequent reduction in feed intake. In the same way, the reduced feed intake and growth observed in pigs with an ulcer score of 10 (Table 1) could also be the consequence of the inflammation and/or diameter reduction of the Lower Esophageal Sphincter (LES) (or cardias.

The effect of diets on the occurrence and severity of gastric ulcers Figure 2. The relationship between daily body weight gain and the gastric ulcer score in pigs (adapted from Ref. 1:  Sloth et al., 1998; Ref. 2: Hansen et al., 2006a Ref.3: Jørgensen et al., 2015b)


Effect of feeding

Feed granulometry: coarse vs. fine grinding

According to available data, higher risk of developing gastric ulcers seems to be related to the administration of pelleted feed with very small particle size. In such cases, the prevalence of lesions is higher than in pigs eating mash or coarsely ground ingredients (Reimann et al., 1968, Maxwell et al., 1970, Wondra et al., 1995a, Wondra et al. 1995b, Regina et al., 1999, Nielsen e Ingvartsen, 2000b, Canibe et al., 2005, Liermann et al., 2015).

A homogeneous and firm gastric content, characteristic of pigs eating feed with coarsely ground ingredients, could be the key to protecting the gastric epithelium against ulcers. 

This hypothesis is based on studies showing that pigs consuming feed with coarsely ground ingredients had higher gastric pH, lower concentrations of pepsin and bile acids in the proximal stomach, as well as lower incidence of gastric ulcers.

Contrarily, feed with finely ground ingredients results in a more fluid gastric digesta moving between glandular and non-glandular regions, with low pH, and higher concentrations of pepsin and bile acids in the pars oesophagea. This was accompanied by a higher incidence of ulcers (Regina et al. 1999, Eisemann y Argenzio, 1999a, Nielsen e Ingvartsen, 2000b, Canibe et al., 2005). Withdrawal of feed also was found to decrease pH in the proximal part of the stomach, increasing the prevalence of gastric ulcers (Lawrence et al., 1998, Regina et al., 1999).This confirms the relationship between low pH and increased risk of ulcer development (Lang et al., 1998)

Therefore, coarsely-ground, non-pelleted feed would have a protective effect against the occurrence of gastric ulcers. 

However, this type of feed will impair feed efficiency, lowering productivity. Figure 3 shows that pigs fed a coarse meal had lower prevalence of ulcers, however there is a concurrent increase in feed conversion ratio (FCR); the opposite is true for pelleted, finely ground feed.

relation betwen food presentation, FCR and prevalence of gastric ulcersFigure 3. Relationship between the prevalence of gastric ulcers (scores  6 to 10, according to Table 1) and FCR (Adapted from  Jorgensen y Nielsen, 2015a)

In pigs receiving barley-based feed during fattening, Potkins et al. (1989) observed that fine barley grinding (1.56 vs. 4.68 mm Ø) increased the number and severity of esopageal-gastric ulcers. The same occurred when the feed was pelleted, even with coarse grinding (4.68 mm)

When maize is heated-up in the presence of water, the bonds between starch molecules break, making it more accessible to enzymatic degradation. This process is known as gelatinization. Gelatinised maize, when compared to its raw form, results in a more fluid gastric content, hence predisposing the animal to develop gastric ulcers (Nuwer et al., 1967; Maxson et al., 1968)

Neither heat nor gelatinisation per se­ are responsible for the occurrence of ulcers. Instead, the conditions in which maize expansion is performed may produce certain physical and chemical changes in the starch structure, which would increase ulcerogenic activity (Nuwer et al., 1967).

During pelleting, particle size is reduced and starch gelatinisaton occurs. The thermal treatment applied during pelleting, as well as the reduction of particle size, do not seem to explain the negative effect of pelleting on the ulcers.

These observations agree with the ones reported by Nuwer et al. (1967). The question is what the mechanism capable of explaining the ulcerogenic effect of pellets is.

Fibre content of  the feed

Fiber content of the feed is one of the most studied parameters in relation to the production of gastric ulcers in pigs. Maxwell et al. (1967) demonstrated that, feeding pigs a diet based on oats (85%), or adding a 25% of ground oat husks (2.3 mm Ø) to a maize based ration, there was a reduction in prevalence of gastric lesions respect of pigs eating a maize based diet.

different presentatiopns and inclusion of oats to reduce prevalence of gastric ulcers in pigs

However, the inclusion of 25% oat husks, when ground to a smaller particle size (1.87 mm Ø), did not confer any protective effect against ulcerations. Furthermore, neither the substitution of crushed oat grains (96%) for maize, nor the inclusion of oat bran (9%) on a maize based diet, showed any effect against gastric lesions.

These studies demonstrated that particle size, and not the fibre content of the feed, would be the mechanisms whereby oat husks

However, pigs receiving diets based on oats or oats husks showed growth rate and FCR significantly less favorable. Maxson et al. (1968) arrived to the same conclusion in a study comparing whole oats, crushed oats and oats husks.  

» In fattening pigs eating a diet based on finely ground barley, Potkins et al.(1989) observed that the inclusion of oat husks, but not oat bran, reduced the incidence and severity of gastric lesions due to the change in particle size.

»However, the inclusion of 5% of Lucerne grass (alfalfa) before grinding and pelleting the feed, increased fibre content without any effect on effect on the prevalence of gastric ulcers (Elbers et al., 1995c)

» Substituting corncob silage (15 to 30%) for wheat bran or corn meal, resulted in a level of neutral digestive fibre (NDF)similar to the control, but with higher particle size. This resulted in lower prevalence of gastric lesions (Mason et al., 2013).

» Millet et al. (2012) measured the impact of the fibre inclusion level (3.6 vs. 8.6 %CF), and of particle size (1.5 vs. 6.8 mm Ø) by changing the combination of ingredients. They demonstrated that coarse grinding reduced the incidence of grastric lesions, but only in diets high in fibre.

»Contrarily, Dirkzwager et al. (1998) observed a positive effect when comparing a finely ground diet (2.5 mm Ø) with a coarsely ground one, the combination of both, and the addition of 5% sunflower husks to the first one. Although the proportion of coarse particles was not different between the two diets, the group fed with the intermediate diet showed a higher proportion of severe lesions than the group receiving diet 1, supplemented with sunflower husks. They concluded that the effect on gastric ulcers occurrence was not due the quantity of coarse particles, but to their composition.

» Laitat et al. (2015) substituted beet pulp for wheat, increasing the fibre content (NSP, non-starch polysaccharides) of the feed from 19.0 to 31.4%, resulting in a significant decrease of gastric lesion score (1.55 for standard feed vs. 0.82 for feed supplemented with beet pulp; P<0.05). They hypothesized that fibre content, normally having a higher size of coarse particle, would have reduced the fluidity of gastric digesta. However, the distribution of particle size was not measured in the study,

The fluidity of the gastric digesta could contribute to explain the differences between results from different studies. However, none of the research teams evaluated this parameter (Dirkzwager et al., 1998; Millet et al., 2012; Laitat et al., 2015).

According to studies performed in Denmark (Svane & Pedersen, 1994), an increase in fibre content of the diet (15.1 to 21.5%) did not affect the incidence or scoring of gastric ulcers. However, the increase in particle size had an effect (27% vs 11% prevalence in pigs ingesting feed ground in hammer mill and roller mill, respectively).

Consequently, the fibre content per se does not seem to be a relevant parameter determining the occurrence of gastric ulcers. The beneficial effect would, instead, be associated to the increase of particle size of the feed. This would result in a firmer gastric content, less fluid and with less segregation between solid and liquid phases.  

Although the aetiology of gastric ulceration in the pars oeasophagea in pigs is multifactorial, the contact of this epithelium with very acidic gastric content can be considered crucial in the pathogenesis.

Feeds resulting in a homogeneous gastric content, firm in consistency (not fluid), decreases the risk of ulceration. This is the consequence of a reduced reflux of content form the distal region (acidic and rich in enzymes) towards the par oesophagea.

Among the possible preventative feeding strategies, offering coarsely ground feed is certainly the most efficient way to reduce gastric ulcers in the pig. The structure and type of fibre, rather that its content, could also give some degree of protection.

However, pelleted feed with coarse grinding has a negative effect on FCR. Hence, the choice of grinding size (or sieve size) should be based on two aspects, namely stomach health and animal productivity.

This article was originally published in nutriNews Spain, with the title Influencia de la alimentación en úlceras gástricas de cerdos


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