Nutritionist's Note: How Anti-Nutritional Factors Affect the Gut

Anti-nutritional factors usually form from a plant's own components or metabolites and can hinder a pet's digestion. Legumes are a common source.
What are anti-nutritional factors?
Substances that adversely affect the digestion, absorption and utilisation of nutrients in food, or cause adverse physiological reactions, are collectively called anti-nutritional factors.
They usually form from the plant's own components or metabolites — self-protective substances developed through evolution that help balance nutrients within the plant. Known plant-derived anti-nutritional factors include non-starch polysaccharides (NSP), protease inhibitors, phytic acid, lectins, erucic acid, gossypol, tannins, oxalic acid, glucosinolates, mycotoxins, mimosine, cyanogens, nitrates, alkaloids, photosensitising agents, glycinin and β-conglycinin, among others.
There are also animal-derived anti-nutritional factors — avidin, biogenic amines, gizzerosine — which can arise from raw or stale ingredients. Some factors have special effects on pets, such as dietary fibre, soy isoflavones and soy saponins; eaten in excess these also impair nutrient absorption and can even cause toxicity.
Common anti-nutritional factors that harm canine and feline digestion
1. Protease inhibitors
They bind trypsin in the small-intestinal fluid to form inactive complexes, lowering trypsin activity and reducing protein digestibility and utilisation. They may also cause endogenous protein loss: trypsin bound to inhibitor is excreted in faeces, intestinal trypsin falls, cholecystokinin and secretin release rises, and feedback drives pancreatic hyperactivity, pushing more trypsinogen into the gut.
Excess trypsin secretion causes pancreatic hyperplasia and hypertrophy, disordering digestion and absorption and in severe cases causing diarrhoea. Because trypsin is especially rich in sulphur-containing amino acids, compensatory over-secretion drains them from the body, unbalancing amino-acid metabolism and stunting growth — even causing disease.
2. Lectins
Toxicity varies between legumes. Lectins are not hydrolysed by proteases in the gut and have high affinity for sugar molecules; specific sites on their subunits recognise and bind extracellular polysaccharides on red cells, lymphocytes or intestinal-wall receptor cells, damaging the brush-border mucosa and causing villus lesions and abnormal development.
They interfere with the secretion of many enzymes (enterokinase, alkaline phosphatase, maltase, amylase, sucrase, glutamyl- and peptidyl-transferases), causing malabsorption of sugars, amino acids and vitamin B12 and poor ion transport, severely inhibiting digestion and absorption, lowering protein utilisation and stunting growth.
3. Tannins
Tannins react through hydroxyl groups with trypsin and amylase or their substrates (protein and carbohydrate), reducing their utilisation. They also bind gastrointestinal mucosal proteins, forming insoluble complexes on the mucosal surface that damage the gut wall, interfere with mineral absorption and impair growth. Tannins precipitate with calcium, iron and zinc and complex with vitamin B12, reducing availability.
4. Saponins
Their bitter taste affects appetite and can cause food refusal; they inhibit chymotrypsin and cholinesterase activity, form insoluble compounds with zinc, and have haemolytic effects.