Digestion of starch is effected by hydrolysing enzymes in a complex process which depends on many factors; these include the botanical origin of starch, whether the starch is amorphous or crystalline, the source of enzymes, substrate and enzyme concentration, temperature and time, as well as the presence of other substances in the multicomponent matrix in which starch occurs naturally, e.g. cereal grains. Native starch is digested (i.e. hydrolysed) slowly compared with processed (gelatinised) starch whose crystallinity has been lost and where the accessibility of substrate to enzymes is greater and not restricted by α-glucan associations such as double helices (especially in crystallites) or amylose-lipid complexes (in cereal starches). The restriction of starch digestion (primarily in the human digestive system) due to forms which are resistant to hydrolysis has led to the concept of dietary ‘resistant-starch’. Different forms of resistance can be identified which hinder hydrolysis. With regard to digestibility, whether in the human or animal digestive tract, it is important to understand the mechanisms of enzymatic hydrolysis, and the consequence of incomplete digestion i.e. the potential loss of glucose as a valuable source of energy. This review deals with starch hydrolysis by specific amylases in model (in vitro) and more broadly in in vivo systems. The optimisation of starch hydrolysis and digestion is discussed in the light of modern knowledge.

The alpha-amylase activity in tracheobronchial secretions of 16 consecutive patients with a total laryngectomy was studied. None of these patients had a tracheopharyngeal fistula or pulmonary disorder which might affect the amylase activity. This study proves the presence of amylase in tracheobronchial secretions of laryngectomized patients with a normal lung at a level between x and y and the quantitative analysis of the amylase activity is discussed. The relevance of investigating laryngectomy patients is because of the nature of the surgery the lower respiratory tract is permanently and physically isolated from any other source of salivary amylase. No similar study of the analysis of amylase in normal lung tissue had been reported before.

This information may be of value in order to detect salivary aspiration in patients with a tracheostomy or endotracheal intubation if the level in the aspirate is in the order of a-b times greater than that found in normal tracheobronchial secretions, (x = 35 and y = 1125 i.u./l; a = 31.8 and b = 628.6 i.u./l).

We report an unusual case of bulimia nervosa with bilateral swelling of parotid and submandibular glands as the only symptom of the underlying behavioural disorder. Histologically, sialadenosis was diagnosed in a parotid biopsy. The parotomegaly in bulimia may be a diagnostic primer as these patients often deny their eating disorder. B-scan ultrasonography is an important diagnostic tool to assess the nature of the parotid enlargement. Hyperamylasaemia occurs commonly in bulimic patients and may help to confirm the diagnosis. All patients with suspected bulimia should have a thorough medical history and physical examination to rule out other aetiologies of asymptomatic parotid swelling. As the enlargement is usually transient surgical intervention is only rarely required.