Fig. 26
Chart showing descent of Huntington’s chorea in the P—— family (courtesy of Dr. W. F. Lorenz). Squares represent male, circles female; shaded figures are choreic members of the family; partially shaded figures, slightly affected or very “nervous” members. The members of the last generation are for the most part still too young to show their condition. The cross indicates the individual in the asylum from whom the record was traced back.
CASES OF RECESSIVENESS IN MAN
Recessive Conditions More Difficult to Deal With Because They Are Frequently Masked.—Coming now to the question of recessive conditions in man, we find that defects are more likely to be of recessive than of dominant type. Apparently normality usually means the presence of normal determiners and abnormality, the absence of some essential determiner. In the latter case, a unit-factor has seemingly been lost out in some way in the germ-plasm, and the product of such germ-plasm is therefore incomplete. As long as the loss is counterbalanced by the presence of a single determiner from the other line of ancestry, that is, as long as the simplex (Aa) condition prevails, the loss may not be in evidence, except in cases of incomplete dominance (taints, etc.), but any mating which permits of the production of the nulliplex condition will bring the defect to expression again.
Fig. 27
Chart showing inheritance of Huntington’s chorea in the R—— family (courtesy of Dr. W. F. Lorenz); 1, 2 have been patients at Mendota Hospital for the Insane; 3, died of “paralysis”; the fourth or last generation indicated by the cross, ranging in age from 6 to 14, are too young yet to show their condition as regards this malady.
The obscure nature of recessives makes such conditions more difficult to deal with than dominant defects. For as regards the latter we have seen that marriage of unaffected members of the family as far as that particular trait is concerned, is perfectly safe, even to a cousin, for once the germ-plasm is purged of such a positive factor, it, in so far as we know, remains pure. But in the case of a recessive character due to the absence of some necessary determiner a normal offspring of simplex constitution (Aa) will probably transmit to half of his children the capacity for handing on the defect, or if mated to another normal individual of simplex constitution (Aa) is likely to have the actual defect revealed again in one-fourth of his children and latent in two-thirds of the remainder.