40
Schardinger dextrins were not fermentable and hence not utilized by yeast
(Pringsheim 1928b). In 1931, for the treatment of diabetes, Pringsheim concluded:
“α-dextrin directly utilized would be a suitable source of energy for diabetics since
it only occasionally cause nausea and there is no noticeable increase in urine sugar”
(Pringsheim 1931a).
However, in 1957, French wrote: “It would appear that the Schardinger dextrins
exhibit a toxic effect, possibly by virtue of their remarkable complexing ability, and
in any case, the suggestion of Professor Pringsheim that they be used as an energy
source by diabetics looks risky” (French 1957a). Indeed, the first studies carried out
by him in the rat led to the conclusion that Schardinger dextrins presented a certain
toxicity (French 1957a). In the same paper, it is noted that “In unpublished attempts
to investigate the ability of animals to utilize Schardinger dextrins, B.H. Thomas
and D. French fed rats a diet in which a part of the carbohydrate was supplied by
higher purified β-dextrin. The animals refused to eat the test diet except in very
small quantities and within a week all animals on the ration were dead. Postmortem
examination did not reveal the cause of death” (French 1957a). Their experiments
indeed showed that the rats refused to eat food containing highly refined dextrins
except in very small quantities. In spite of the small doses, rat mortality was 100%
within a week of introducing “highly purified” β-dextrin into the diet (French
1957a). However, in these studies, experimental conditions, such as the purity of
dextrins, the number of rats treated, or the existence of a control group, were not
mentioned. Later, Szejtli suggested that one of the hypotheses was traces of solvent
remaining in the dextrins which the rats could have smelt (Szejtli 1982a, 1988;
Frömming and Szejtli 1994). This was the only result of French’s that posed a problem and which led to extensive debate of the toxicity of the cycloamyloses (French
1957a), and most importantly this result deterred many scientists from developing
cycloamylose-containing products for human use. The observations and conclusions drawn by French were only refuted much later following studies with the
same animal model (Andersen et al. 1963; Lach and Cohen 1963; Lach and Chin
1964; Szejtli et al. 1980a; Chow and Karara 1986).
1.3.12 Other Works During the Period from 1911 to 1970
Other historical landmarks on the discovery of cyclodextrins published by other
researchers during the period from 1911 to 1970 are reported in Table 1.1 (Thoma
and Stewart 1965; Caesar 1968; Szejtli 1998; Loftsson and Duchêne 2007; Kurkov
and Loftsson 2013; Crini 2014; Morin-Crini et al. 2015; Crini et al. 2018).
N. Morin-Crini et al.
Schardinger dextrins were not fermentable and hence not utilized by yeast
(Pringsheim 1928b). In 1931, for the treatment of diabetes, Pringsheim concluded:
“α-dextrin directly utilized would be a suitable source of energy for diabetics since
it only occasionally cause nausea and there is no noticeable increase in urine sugar”
(Pringsheim 1931a).
However, in 1957, French wrote: “It would appear that the Schardinger dextrins
exhibit a toxic effect, possibly by virtue of their remarkable complexing ability, and
in any case, the suggestion of Professor Pringsheim that they be used as an energy
source by diabetics looks risky” (French 1957a). Indeed, the first studies carried out
by him in the rat led to the conclusion that Schardinger dextrins presented a certain
toxicity (French 1957a). In the same paper, it is noted that “In unpublished attempts
to investigate the ability of animals to utilize Schardinger dextrins, B.H. Thomas
and D. French fed rats a diet in which a part of the carbohydrate was supplied by
higher purified β-dextrin. The animals refused to eat the test diet except in very
small quantities and within a week all animals on the ration were dead. Postmortem
examination did not reveal the cause of death” (French 1957a). Their experiments
indeed showed that the rats refused to eat food containing highly refined dextrins
except in very small quantities. In spite of the small doses, rat mortality was 100%
within a week of introducing “highly purified” β-dextrin into the diet (French
1957a). However, in these studies, experimental conditions, such as the purity of
dextrins, the number of rats treated, or the existence of a control group, were not
mentioned. Later, Szejtli suggested that one of the hypotheses was traces of solvent
remaining in the dextrins which the rats could have smelt (Szejtli 1982a, 1988;
Frömming and Szejtli 1994). This was the only result of French’s that posed a problem and which led to extensive debate of the toxicity of the cycloamyloses (French
1957a), and most importantly this result deterred many scientists from developing
cycloamylose-containing products for human use. The observations and conclusions drawn by French were only refuted much later following studies with the
same animal model (Andersen et al. 1963; Lach and Cohen 1963; Lach and Chin
1964; Szejtli et al. 1980a; Chow and Karara 1986).
1.3.12 Other Works During the Period from 1911 to 1970
Other historical landmarks on the discovery of cyclodextrins published by other
researchers during the period from 1911 to 1970 are reported in Table 1.1 (Thoma
and Stewart 1965; Caesar 1968; Szejtli 1998; Loftsson and Duchêne 2007; Kurkov
and Loftsson 2013; Crini 2014; Morin-Crini et al. 2015; Crini et al. 2018).
N. Morin-Crini et al.