| (_a_) FROM TABLE III, VS × M (S). |
+-------+-----------------------------------------+-------------------+
| | Parentage. | Offspring. |
| +----+----+--+--------+---+---+--+--------+---+---+---+---+---+
| Ref. | | | |Father’s| | | |Mother’s| | | | | |
| | FF | FM |F | sibs. |MF |MM |M | sibs. |VS | S | M | F |VF |
+-------+----+----+--+--------+---+---+--+--------+---+---+---+---+---+
|Ach 2 | 32 | 33 |32| |32 |27 |25| | | 1 | 2 | | |
|Bic 1 | 29 | 35 |34| |M |S |25|4t | | 1 | 2 | | |
|Gru 1 | M | M |31|1t |M |S |24| | | 1 | 1 | | |
|Ise 2 | 26 | 31 |31| |31 |27 |23| | | 2 | 5 | | |
|Mil A | 39 | 28 |36|1S 1M 3F|35 |30 |22| | 1 | | 3 | 3 | |
|Wit 2 | 26 | M |33| |M |t |22|2t | | 2 | 1 | | |
| | | | | | | | | +---+---+---+---+---+
| Total | | | | | | | | | 1 | 7 |14 | 3 | |
+-------+----+----+--+--------+---+---+--+--------+---+---+---+---+---+
| A, 32.34 ± 0.59. S. D., 4.38 ± 0.42. |
+---------------------------------------------------------------------+
| (_b_) FROM TABLE IV, VS × F (S). |
+-------+----+----+--+--------+---+---+--+--------+---+---+---+---+---+
|Hol A | | |39| | | |23| | 1 | 2 | 4 | 1 | 1 |
|Law A | 34 | |43| |35 | |24|1S 1M 2F| | 2 | 1 | 1 | |
|Wat 5 | | |37|1F | |S |25|4S | | 1 | 3 | 1 | |
+-------+----+----+--+--------+---+---+--+--------+---+---+---+---+---+
| (_c_) IN PART FROM TABLE VIII, S × F (S). |
+-------+----+----+--+--------+---+---+--+--------+---+---+---+---+---+
|Gui 3 | | |27| |34 |30 |39| | | 1 | 3 | 3 | |
|Hok 1 | 36 | S |37| |31 |35 |27| | | | 2 | | |
|Hot 1 | M | S |30| |S |S |40| | | | 1 | | |
|Hul 2 | 34 | 25 |30| |35 |27 |37| | 2 | 4 | 1 | | |
|Kie | | |S | | | |F | | | 2 | | 2 | |
|Leo (a)| S | S |S |4S |F |S |51|3S 3F | | | | 1 | |
|Leo (b)| | |S | | | |51| | | 2 | | 1 | 3 |
|Lyn 2 | S | F |37| |S |M |29| | | | 1 | | |
|Mer B | 47 | 27 |40| |37 |36 |25| | | 1 | 3 | 1 | |
|Mor (a)| | |50| | | |S | | | |10 | 3 | |
|Mor (b)| | |S | |F |F |F |2S 2F | | 4 | | | |
|Mor (c)| F | M |F |1S 1M 4F| | |S |1S | | 2 | | | |
|Pad 1 | 31 | 35 |28| |33 |23 |37| | | | | 1 | |
|Rid 1 |F(?)|M(?)|42|3F |S |S |S | | | 2 | | | |
|Rom 1 | S | F |38|3t |F |M |28| | | | 6 | 1 | |
|Van | | |42|1S 1F | | |S |1M | | 2 | | 3 | |
|Wat | S | F |27| |26 |45 |40| | | 1 | 1 | 1 | |
| +----+----+--+ +---+---+--+ +---+---+---+---+---+
| Total | | | | | | | | | 3 |26 |36 |20 | 4 |
+-------+----+----+--+--------+---+---+--+--------+---+---+---+---+---+
| A, 33.67 ± 0.40. S. D., 5.58 ± 0.28. |
+---------------------------------------------------------------------+
ACH-2 FAMILY.
A family of English and probable Scotch stock. The family residence
is now located in Oregon, in which State the 3 children of the third
generation were born. The Father, a mechanic, inclined to rheumatism and
nervousness, has at 50 years the formula 150/69 inches; build 2.3 (32).
His sibs are all tall (and presumably slender). His father, a farmer,
died when 78 years old, having at 40 years the formula 150/69 inches;
build 2.2 (32). His mother, after having borne 6 sons and 5 daughters,
died of cancer at 70 years. At that time she had the formula 125/62
inches; build 2.3 (33). Thus, the Father’s fraternity, though their
parents were of medium build, apparently carries a slender tendency.
The Mother suffers from “rheumatism”; she is “always busy” and is living
at 51 years, with the formula 93/61 inches; build 1.8 (25). Her father,
a farmer, died at 82 with the formula 150/69 inches; build 2.2 (32). Her
mother, having had 5 sons and 4 daughters, died of “heart trouble” at 42
years. She had the formula 100/61 inches; build 1.9 (27). Thus this side
of the house inclines toward slenderness. The 3 children are:
1. Female, a bookkeeper and “nervous,” at 26 has the formula 95/65
inches; build 1.6 (23); adjusted to 50 years, 112/65 inches; build 1.8
(27).
2. Female, a bookkeeper, and “energetic” and “nervous,” at 22 has the
formula 120/67 inches; build 1.9 (27); adjusted to 50 years, 139/67
inches; build 2.2 (31).
3. Female, a bookkeeper and “energetic, impulsive, and agile,” has at 23
the formula 112/63 inches; build 1.9 (28); adjusted to 50 years, 129/63
inches; build 2.3 (33).
_Comment._—A medium Father of medium and slender stock marries a
slender, nervous woman who has a slender mother. One of the children is
exceptionally slender and two are slender according to the unadjusted
index. It is very doubtful if the most slender child would ever acquire
the adjusted index of 27, though children Nos. 2 and 3, energetic and
agile at 23 and 22 years respectively, with builds 1.9 (28) and 2.0 (27),
may well acquire a medium build by maturity if they become less active
(R: Ach-2).
BIC-1 FAMILY.
A family of English and French extraction living mostly in Kentucky
and Indiana. The Father, a newspaper publisher, suffered in youth from
typhoid fever. He is living at 52 years, having at 45 years the formula
175/72 inches; build 2.4 (34). His father, a justice of the peace, died
at 39 years from pulmonary tuberculosis contracted during the Civil War.
At 26 years he had the formula 140/70 inches; build 20 (29). His mother,
who had 4 children, suffered in middle age from cancer. She is living at
76 years. At 40 years her formula was 160/68 inches; build 2.4 (35). Thus
the father is of mixed ancestry; he is probably heterozygous in respect
to build.
The Mother has been subject to tuberculosis of throat and lungs. She is
living at 51 years, having at 45 years the formula 102/64 inches; build
1.7 (24). Four of her sibs died from tuberculosis of throat and lungs.
Her father, a revenue collector, suffered in youth from rheumatism and in
middle age from “very bad throat trouble.” He died at 85 years from old
age. At 45 years he was of medium build. Her mother, who had 9 children,
always well, died at 85 years from malignant tumor. At 45 years she was
slender. This side of the house is very slender, largely on account of
tuberculosis. The grandfather is of medium build; the grandmother was
nervously active and slender. The 3 children:
1. Female, a social worker, who in youth suffered from diphtheria,
tonsillitis, and adenoids, has at 23 years the formula 105/64 inches;
build 1.8 (26); adjusted to 45 years, 2.1 (29). (R: Bic-1.)
2. Female, a college graduate, who in youth suffered from tonsillitis,
scarlet fever, and appendicitis and had a tendency to consumption, has
at 22 years the formula 126/66 inches; build 2.0 (29); adjusted to 45
years, 142/66 inches; build 2.3 (33).
3. Female, a student, who has a “nervous temperament,” has at 18 years
the formula 124/67 inches; build 2.0 (28); adjusted to 45 years, 143/67
inches; build 2.3 (32).
_Comment._—The tuberculous tendency of the Mother’s fraternity and of the
Father’s father reappears in at least one of the children. None is as
slender as the Mother, and all approach the medium grade (R: Bic-1).
GRU-1 FAMILY.
A family of English and German extraction living mostly in Pennsylvania
and New Jersey. The Father, a school-teacher and principal, is living
at 52 years, having had at 45 years the formula 134/66 inches; build
2.2 (31). One of his brothers died of “consumption” and was apparently
slender. His father, a farmer, often mentally depressed, is living at 75
years, and has a “medium” build. His mother, who had 10 children, and who
suffered in middle age from rheumatism, is living at 73 years, and is of
“medium” build. Thus the paternal inheritance is toward medium build; the
father possibly heterozygous.
The Mother suffered in middle age from inflammatory rheumatism; she has
at 40 years the formula 106/66 inches; build 1.7 (24). Her father, a
farmer, of medium build, died at 77 years from pneumonia. Her mother, who
had 6 children, died at 77 years from arterio-sclerosis; she was slender.
Thus the maternal build is prevailingly slender, though the grandfather
is of medium build. The 3 children:
1. Female, a teacher, who in youth suffered from diphtheria, has at 20
years the formula 110/65 inches; build 1.8 (26); adjusted to 42 years,
125/65 inches; build 2.1 (30).
2. Female, a student, who in youth suffered from infantile paralysis, has
at 18 years the formula 120/64 inches; build 2.1 (29); adjusted to 42
years, 136/64 inches; build 2.3 (33).
3. Female, at 13 years, has already the build of her next older sister.
_Comment._—All the children have a heavier build than the slenderer
parent and approach a medium build (R: Gru-1).
ISE-2 FAMILY.
A family of Swiss and French origin living in Kansas. The Father, who is
of Swiss parentage, a farmer, is living at 86 years, having the formula
150/68 inches; build 2.3 (32). His father, a farmer, died of consumption,
having the formula 120/68 inches; build 1.8 (26). His mother, who had
8 children, died at 82 years from pneumonia, having the formula 130/65
inches; build 2.2 (31). This side of the house is of mixed slender-medium
build.
The Mother, who has had 11 children, is of French-Swiss stock and has
been a farmer’s wife in Kansas. She has been operated upon for glaucoma,
is living at 72 years, and has the formula 88/62 inches; build 1.6 (23).
Her father, a farmer, died from neuralgia of heart, having the formula
130/65 inches; build 2.2 (31). Her mother, who had 3 children, died at
46 years, suddenly, perhaps from appendicitis, having the formula 115/65
inches; build 1.9 (27). The maternal side of the house has thus a build
ranging from very slender to slender-medium. The 8 children about whom
information is given are:
1. Male, a college professor, died at 42 years after an operation for
appendicitis, having the formula 125/68 inches; build 1.9 (27); adjusted
to 55+ years, 129/68 inches; build 2.0 (28).
2. Female, a librarian, who in youth suffered from pneumonia, in middle
age from a nervous breakdown, has at 47 years the formula 112/60 inches;
build 2.2 (31).
3. Female, a stenographer, who in middle age suffered from fever (in
Africa), has at 45 years the formula 117/63 inches; build 2.1 (30).
4. Male, a college professor, always well, has at 41 years the formula
170/70 inches; build 2.4 (35); adjusted to 55+ years, 175/70 inches;
build 2.5 (36).
5. Male, a merchant, has at 39 years the formula 160/70 inches; build 2.3
(33); adjusted to 55+ years, 166/70 inches; build 2.4 (34).
6. Male, a merchant, who in youth suffered from acute rheumatism and
leakage of heart, has at 36 years the formula 165/72 inches; build 2.2
(32); adjusted to 55+ years, 172/72 inches; build 2.3 (33).
7. Male, an editor, who in middle age has suffered from pleurisy and
pneumonia, has at 33 years the formula 150/71 inches; build 2.1 (30);
adjusted to 55+ years, 159/71 inches; build 2.2 (32).
8. Male, a newspaper reporter, of unknown build.
_Comment._—All children, except the first, who was of a nervous, active
type and died prematurely, are of medium build, mostly slightly fleshier
than the stockier parent (R: Ise-2).
MIL-A FAMILY.
A family probably of old American (English) stock, living in Los Angeles,
California. The Father, at 70 years, had the formula 170/68.5 inches;
build 2.5 (36). Of his sibs, 1 is slender, 1 medium, and 4 are fleshy.
His father, at 70 years, had the formula 180/68 inches; build 2.7 (39).
His mother, at 70 years, had the formula 120/66 inches; build 1.9 (28).
Thus the Father is of mixed fleshy and slender origin.
The Mother, at 85 years, had the formula 100/67 inches; build 1.6 (22).
Her father, at 70 years, 175/70 inches; build 2.5 (35). Her mother, at 70
years, 135/67 inches; build 2.1 (30). Thus, the maternal parent is very
slender with slender to medium grandparents. The 6 children are:
1. Male, at 56 years, has the formula 224/72 inches; build 3.1 (43).
2. Male, at 53 years, 190/72 inches; build 2.6 (37).
3. Female, at 27 years, 130/67 inches; build 2.0 (29); adjusted to 55
years, 148/67 inches; build 2.3 (33).
4. Female, at 64 years, 100/68 inches; build 1.5 (22).
5. Female, at 50 years, 140/67 inches; build 2.2 (31).
6. Female, at 59 years, 190/67 inches; build 3.0 (42).
_Comment._—The children vary from slender to fleshy; thus two have a
heavier build than any ancestor described (S:Mil-A).
WIT-2 FAMILY.
A family of English and Irish extraction; paternal grandparents living
in the Middle States and California. The Father, a merchant, suffered
in middle age from pneumonia. He is living at 75 years. At 70 years his
formula was 155/69 inches; build 2.3 (33). His father, a farmer, died
at 86 years from dropsy. At 70 years his formula was 140/73 inches;
build 1.8 (26). His mother, who had 8 children, died from consumption.
At 50 years she was of medium build. Thus this side of the house is
prevailingly of medium build, but the Father’s father was slender,
consequently the Father is probably heterozygous for build.
The Mother suffered in middle age from insanity and consumption, having
the formula 100/68 inches; build 1.5 (22). Two of her 4 sibs who reached
maturity died from consumption. Their father, a farmer, died at 74
years from bladder trouble. At 50 years he was of medium build. Their
mother, who had 4 children, died from consumption. In this family the
very slender stature is probably controlled by lung tuberculosis. The 3
children are:
1. Male, a machinist, who was accidentally killed at 19 years, 145/69
inches; build 2.1 (30); adjusted to 55 years, 168/71 inches; build 2.4
(34).
2. Male, retired, who in youth suffered from dysentery and pneumonia;
in middle age from indigestion, internal catarrh, tuberculosis,
appendicitis, and malaria, has at 44 years the formula 140/69.5 inches;
build 2.0 (29).
3. Female, who was “very healthy” in youth, but in middle age had mental
“nervous troubles,” has at 40 years the formula 100/64 inches; build 1.7
(24); adjusted to 55 years, 106/64 inches; build 1.8 (26).
_Comment._—The children of this mating are mixed slender to medium; one
of the children is feeble-minded and is very slender; one who is slender
has had active tuberculosis and much other illness; the third, who died
at 19, had an average build. The record is complicated by disease (R:
Wit-2).
HOL-A FAMILY.
A family from Illinois. The Father at 55 years has the formula: 180/68
inches; build 2.7 (39).
The Mother, at 50 years, has the formula: 100/66 inches; build 1.6 (23).
The 9 children are:
(1) Female, at 30 years, has the formula 180/65 inches; build 3.0 (43);
adjusted to 55 years, 194/65 inches; build 3.2 (46).
(2) Male, at 30 years, 130/66 inches; build 2.1 (30); adjusted to 55
years, 139/66 inches; build 2.3 (32).
(3) Male, at 27 years, 170/68 inches; build 2.6 (37); adjusted to 55
years, 183/68 inches; build 2.8 (40).
(4) Male, at 25 years, 165/74 inches; build 2.1 (30); adjusted to 55
years, 184/74 inches; build 2.4 (34).
(5) Male, at 29 years, 140/68 inches; build 2.1 (30); adjusted to 55
years, 151/68 inches; build 2.3 (33).
(6) Male, at 26 years, 125/72 inches; build 1.7 (24).
(7) Female, at 24 years, 140/69 inches; build 2.1 (29); adjusted to 55
years, 161/69 inches; build 2.4 (34).
(8) Female, at 22 years, 110/72 inches; build 1.5 (21); adjusted to 55
years, 130/72 inches; build 1.8 (25).
(9) Female, at 20 years, has the formula 100/64 inches; build 1.7 (24);
adjusted to 55 years, 119/64 inches; build 2.0 (29).
_Comment._—The children vary greatly from very slender to stout or even,
adjusted, to very stout. One of them is much stouter than either parent.
Probably the Father is heterozygous (S:Hol-A).
LAW-A FAMILY.
A family from Georgia. The Father, at 30 years, had the formula 200/68
inches; build 3.0 (43). His brothers were “all stout.” His father, at 30
years, had the formula 160/69 inches; build 2.4 (34). The fleshy father
carries factors for at least medium build.
The Mother, at 30 years, had the formula 100/65 inches; build 1.7 (24).
Her brothers were all of “medium” build. Her sisters are: 1 slender, 1
medium, and 2 fleshy. Their father, at 30 years, had the formula 170/70
inches; build 2.4 (35). The 4 children:
1. Male, at 30 years, had the formula 190/68 inches; build 2.9 (41).
2. Female, at 30 years, 110/61 inches; build 2.1 (30).
3. Female, at 30 years, 100/60 inches; build 2.0 (28).
4. Female, at 30 years, 130/61 inches; build 2.5 (35).
_Comment._—A fleshy man of medium stock has by a very slender woman of
mixed stock in respect to build, 4 children—2 slender, 1 medium, and 1
fleshy (S:Law-A).
WAT-5 FAMILY.
A family of English extraction; grandparents living in Massachusetts,
Michigan, England, Utah, and Montana; parents and children living in Utah
and Montana. The Father, a miner, suffered in middle age from pneumonia
and died at 64 years from chronic bronchitis. At 60 years his formula was
190/72 inches; build 2.6 (37). His father, a farmer, died at 37 years.
The Father had a fleshy sister, at least 3 of whose children were fleshy.
His mother died at 38 years. Apparently, a fleshy strain on the Father’s
father’s side; Father’s mother’s side unknown.
The Mother, who had 7 children, suffered in youth from scarlet fever and
lung fever, is living at 60 years, having the formula 107/65.5 inches;
build 1.8 (25). Her 4 sibs are “thin.” Their father, a lawyer, suffered
at 23 years from scarlet fever, died from an accident at 42. Two of his
sibs were “very large” and tall. Her mother, who had 9 children, died
at 76 years from pneumonia; she was slender and so was her sister. Thus
the slender Mother has both slender and fleshy close relations. The 5
children who grew up are:
1. Female, married, who in youth suffered from scarlet fever, has at 37
years the formula 109/67 inches; build 1.7 (24); adjusted to 55 years,
119/67 inches; build 1.9 (27).
2. Male, a miner, who in youth suffered from scarlet fever, tonsillitis,
and throat trouble, has at 34 years the formula 185/71 inches; build 2.6
(37); adjusted to 55 years, 193/71 inches; build 2.7 (38).
3. Female, married, who in youth suffered from scarlet fever, has, at 31
years, the formula 128/66 inches; build 2.0 (29); adjusted to 55 years,
143/66 inches; build 2.3 (33).
4. Female, married, who in youth suffered from throat trouble, underwent
a tonsillectomy and appendectomy, has at 25 years the formula 120/65.5
inches; build 2.0 (28); adjusted to 55 years, 138/65.5 inches; build 2.3
(32).
5. Female, married, has at 21 years, the formula 120/65.5 inches; build
2.0 (28); adjusted to 55 years, 140/65.5 inches; build 2.3 (33).
_Comment._—The adjusted build of the children show 1 slender (unadjusted,
very slender), 3 medium, and 1 fleshy, suggesting a heterozygous
parentage. This family has been placed in this category, despite
absence of information about the Father’s parents, because of the great
variability of the children (R: Wat-5).
GUI-3 FAMILY.
A family of Scandinavian extraction, living mostly in Kansas. The Father,
a farmer, who suffered in middle age from asthma, has at 74 years the
formula 125/68 inches; build 1.9 (27).
The Mother has at 60 years the formula 150/62 inches; build 2.7 (39). Her
father, a farmer, died at 83 years from senile dementia. At 75 years his
formula was 150/S inches; build, say, 2.4 (34). Her mother, who had 6
children, died at 84 years, “probably senility.” At 75 years her formula
was 120/M inches; build, say, 2.1 (30). The 8 children:
1. Female, married, suffered in youth and middle age from heart trouble,
following rheumatism. At 40 years she has the formula 110/62 inches;
build 2.0 (29); adjusted to 55 years, 116/62 inches; build 2.1 (30).
2. Male, a farmer, who in youth suffered from rheumatism, has at 33 years
the formula 135/67 inches; build 2.1 (30); adjusted to 55 years, 144/67
inches; build 2.3 (33).
3. Male, who died at 16 years from operation for rectal tumor.
4. Male, a real-estate dealer, who in youth suffered from asthma, has
at 33 years the formula 135/67 inches; build 2.1 (30); adjusted to 55+
years, 144/67 inches; build 2.3 (33).
5. Female, a nurse, who in youth suffered from anterior poliomyelitis
(complete recovery), has at 31 years the formula 150/64 inches; build 2.6
(37); adjusted to 55 years, 162/64 inches; build 2.7 (39).
6. Male, a farmer, has at 29 years the formula 153/70 inches; build 2.2
(31); adjusted to 55 years, 166/70 inches; build 2.4 (34).
7. Female, has at 27 years the formula 150/65 inches; build 2.5 (36);
adjusted to 55 years, 166/65 inches; build 2.7 (39).
8. Male, a farmer, has at 24 years the formula 150/67 inches; build 2.3
(33); adjusted to 55+ years, 164/67 inches; build 2.6 (37).
_Comment._—One-half of the children may be expected to exceed the mean
build of the parents, and 2 to equal or exceed the fleshy build of the
Mother (R: Gui-3).
HOK-1 FAMILY.
A family of German and English extraction, living in Illinois, Colorado,
and Iowa. The Father, who is a carpenter, always well, is living at 63
years, having the formula 180/70 inches; build 2.6 (37). His father, who
was a manufacturer, always well, died at 72 years from a fistula. At 72
years his formula 175/70 inches; build 2.5 (36). The father’s mother died
at about 48 years; was of slender build.
The Mother, always well, has at 62 years the formula 105/62 inches;
build 1.9 (27). Her father, who was a coal-mine owner, died at 46 years
from exposure during Civil War. At 45 years his formula 140/67 inches;
build 2.2 (31). Her mother, always well, died at 87 years from old age.
Formula, 145/64 inches; build 2.5 (35). Two grown children:
1. Male, a surveyor, who in youth suffered from typhoid, has at 34 years
the formula 160/70 inches; build 2.3 (33); adjusted to 55+ years, 168/70
inches; build 2.4 (34).
2. Male, always well, has at 26 years the formula 165/72 inches; build
2.2 (32); adjusted to 55 years, 181/72 inches; build 2.5 (35).
_Comment._—Both children are of medium build, fairly close to that of the
fleshier parent (R: Hok-1).
HOT-1 FAMILY.
A family of English extraction, living mostly in New York State. The
Father, who is a carpenter, suffered in middle age from pneumonia. He is
living at 51 years, having the formula 150/71 inches; build 2.1 (30). His
father, who was a farmer, died at 69 years from apoplexy; was of medium
build. His mother, who had 6 children, at 50 years was slender.
The Mother is living at 50 years, having the formula 150/61 inches;
build 2.8 (40). Her father, who was a grocer, suffered in youth from
rheumatism; in middle age from typhoid fever. He died at 61 years from
Bright’s disease. At 61 years he was slender. Her mother, who had 3
children, was always well. She died at 79 years from cerebral hemorrhage;
she was said to be slender.
One son, a teacher, always well, has at 25 years the formula 140/67
inches; build 2.2 (31); adjusted to 50 years, 151/67 inches; build 2.3
(33).
_Comment._—The son is intermediate in build between the parents (R:
Hot-1).
HUL-2 FAMILY.
A rural New York family of prevailingly English origin. The Father, a
business man, always well, had, at 50 years, the formula 140/68 inches;
build 2.1 (30). His father, who died of “rheumatism of the stomach” at
80 years, had the formula 160/69 inches; build 2.4 (34). His mother, who
died at 82 years of old age, with dropsical tendencies, had the formula
95/62 inches; build 1.7 (25). This family has a build at or below the
average.
The Mother, who suffered much from sick headache and “rheumatism,” and in
later years from diabetes mellitus, had, at 50 years, the formula 150/64
inches; build 2.6 (37). Her father, who suffered from migraine, had the
formula 155/67 inches; build 2.4 (35). Her mother, always well, died at
78 years of gradual decay; her formula, at 50 years, 115/65 inches; build
1.9 (27). The Mother is doubtless heterozygous. There are 7 children:
1. Female, who has had pneumonia and suffers from migraine, has, at 38,
the formula 100/62.5 inches; build 1.8 (26).
2. Female, a teacher, married, at 37 years, 115/65 inches; build 1.9 (27).
3. Female, married, and died at 35 years of Addison’s disease, 105/65
inches; build 1.8 (25).
4. Female, who has been operated on for tubercular neck glands, at 34
years, 115/62 inches; build 2.1 (30).
5. Female, who suffered in youth from tachycardia, at 28 years, 100/65.5
inches; build 1.6 (23).
6. Female, who has suffered from migraine and rheumatism and had an
attack of pneumonia, at 27 years, 115/64 inches; build 2.0 (28); adjusted
to 50 years, 119/64 inches; build 2.0 (29).
7. Male, well, at 20 years, 140/67 inches; build 2.2 (31); adjusted to 50
years, 158/68 inches; build 2.4 (34).
_Comment._—On the whole the children are _below_ the average build, like
the slender parent (R: Hul-2).
KIE FAMILY. (Fig. 43.)
II 1 ♂, a slender German. His wife, II 2 ♀, fleshy. Their 4 children of
whose build something is known: III 1 ♂, fleshy; III 2 ♂, slender, over
6 feet tall, married to a fleshy woman, has 6 tall, slender daughters.
III 4 ♀, died of “heart disease”; slender. III 7 ♂, died at 56 of cancer
of the lungs, weight in health 82 kg. (180 pounds); stature 178 cm. (70
inches); build 2.6 (37), fleshy. Thus 2 are fleshy and 2 slender.
_Comment._—From the variability of the offspring we infer that the fleshy
Mother was heterozygous in build (73-670).
[Illustration: FIG. 43.—Pedigree chart showing distribution of build in
the KIE family.]
LEO FAMILY, A. (Fig. 23.)
II 7 ♂, slender with 4 slender sibs. Their parents both slender. His
wife, II 8 ♀, at 36 years, has a stature of 152 cm. (60 inches); weight
84 kg. (184 pounds); build 3.6 (51); very fleshy; relative chest-girth
112/52, or 74 per cent. She has 3 fleshy and 2 slender sibs. Of their
parents one was fleshy and one slender. Thus II 8 is heterozygous.
III 4, the only child, at 9 years, has a relative chest-girth of 57 per
cent; fleshy.
LEO FAMILY, B.
I 5 ♂, slender, and I 6 ♀, whose build is about 3.6 (51), or very fleshy,
have 6 children of whom something is known, as follows: II 8 ♀, build 3.6
(51), very fleshy; II 11 ♀, fleshy; II 15 ♀, slender; II 16 ♀, slender,
married to a slender man and has 3 slender children; II 12 ♂, of medium
stature and 95 kg. (210 pounds) weight; build, say, 3.2 (45); very
fleshy; II 13 ♀, of tall stature and 91 kg. (200 pounds) weight; build,
say, 3.2 (46); very fleshy. Thus there are 3 very fleshy, 1 fleshy, and
2 slender children. The Mother’s heterozygosity is inferred from the
variability of the progeny in build.
II 14 ♂, fleshy, and II 15 ♀, slender, have 2 sons, both slender (73:676).
LYN-2 FAMILY.
A family of prevailingly English stock, living in Illinois and Nebraska.
The Father, who was a farmer and school-teacher, died at 65 years from
cancer of stomach. Formula, 150/64 inches; build 2.6 (37). His father,
who was a farmer, died at 76 years from pneumonia; he was slender. His
mother, who had 10 children, is living and is corpulent. Thus the Father
is heterozygous.
The Mother, who has 1 child, has at 49 years the formula 120/64 inches;
build 2.1 (29). Her father, who is a carpenter, always well, is at 70
years slender. Her mother, who had 4 children, died at 36 years from
pneumonia; she was of medium build. One child, female, a kindergarten
teacher, has at 19 years the formula 110/63 inches; build 2.0 (28);
adjusted to 55+ years, 130/63 inches; build 2.3 (33).
_Comment._—The child is now like the slender parent and will probably
increase somewhat in build (R: Lyn-2).
MER-B FAMILY.
A family of English extraction from Rochester, New York. The Father, at
21 years, had the formula 200/71 inches; build 2.8 (40). His father had
the formula 250/73 inches; build 3.3 (47). His mother had the formula
130/70 inches; build 1.9 (27).
The Mother, at 21 years, had the formula 96/61 inches; build 1.8 (25).
Her father had the formula 170/68 inches; build 2.6 (37). Her mother had
the formula 150/65 inches; build 2.5 (36). Five children:
1. Male, at 21 years, had the formula 175/68 inches; build 2.7 (38).
2. Male, at 21 years, 170/72 inches; build 2.3 (33).
3. Female, 140/64 inches; build 2.4 (34).
4. Female, 130/65 inches; build 2.2 (31).
5. Female, 130/67 inches; build 2.0 (29).
_Comment._—All 5 children are intermediate between the parents; 1 is
fleshy, 1 slender (S:Mer-B).
MOR FAMILY. (Fig. 24.)
(_a_) II 1 ♂, stature 181 cm. (71 inches); weight 13 kg. (200 pounds);
build 3.5 (50); very fleshy. Married II 2, a slender woman. They had 7
sons, 2 fleshy, 5 medium, and 6 daughters, 1 fleshy and 5 medium. Thus 3
fleshy and 10 of medium build. To save space only 5 are represented in
figure 24.
(_b_) IV 16 ♂, slender, married IV 17 ♀, fleshy, who has 2 fleshy and 2
slender sibs; and both parents fleshy. They have 4 living children, all
slender.
(_c_) IV 5 ♂, fleshy with 4 fleshy, 1 medium, and 1 slender sibs and a
fleshy and medium parent; married IV 6, slender, with a slender sister.
They had 2 sons, both slender (73:690).
PAD-1 FAMILY.
A family of English extraction, living in the middle West. The Father, a
horticulturist, subject in middle life to catarrh, is living at 55 years,
having had at 50 years the formula 145/72 inches; build 2.0 (28). His
father, a farmer, who in youth suffered from measles and bronchitis, and
in middle age from liver trouble, died at 59 years from complication of
stomach and liver diseases. At 55 years his formula 145/68 inches; build
2.2 (31). His mother is living at 80 years, having the formula 160/68
inches; build 2.4 (35).
The Mother, at 49 years, had the formula 145/63 inches; build 2.6 (37).
Her father, a merchant and farmer, suffered in youth from typhoid fever
and congestion of the brain. He died at 86 years from old age, having had
at 70 years the formula 170/72 inches; build 2.3 (33). Her mother died at
83 years of old age, having the formula 95/64 inches; build 1.6 (23). The
only grown child is a male, a student, who in youth suffered from measles
and catarrh, has at 21 years the formula 155/67 inches; build 2.4 (35);
adjusted to 50 years, 171/67.5 inches; build 2.6 (37).
_Comment._—The only grown child is like his stouter parent in build (R:
Pad-1).
ROM-1 FAMILY.
A family of prevailing English stock, living in Ohio, Indiana, Illinois,
and Kansas. The Father, who is a lawyer, has at 72 years the formula
170/67 inches; build 2.7 (38). Three of his brothers died at 26 years, 41
years, and 22 years respectively, from tuberculosis; all were of medium
height. Their father, who was a “farmer and blacksmith,” died at 76 years
from Bright’s disease; was slender. Their mother, who had 5 children,
died at 55 years from “tuberculosis of the liver”; was corpulent. The
Father is doubtless heterozygous in build.
The Mother has at 67 years the formula 119/65 inches; build 2.0 (28).
One of her sisters, who was tall, died from “quick consumption”; another
from diabetes; another from dropsy. Two of her brothers, tall, died from
hardening of the arteries, another from “leakage of the heart,” and
another from dropsy. Their father, who was a miller, died at 76 years—“a
complication of diseases (asthma).” He was corpulent. Their mother, who
had 10 children, died at 72 years from pneumonia; was of medium build.
The 7 children are:
1. Female, married, who in middle age suffered from rheumatism, has at 44
years the formula 155/64 inches; build 2.7 (38); adjusted to 55 years,
158/64 inches; build 2.7 (39).
2. Male, a farmer, who in youth suffered from malarial fever, has at 41
years the formula 150/68 inches; build 2.3 (32); adjusted to 55 years,
155/68 inches; build 2.4 (34).
3. Male, a farmer, has at 38 years the formula 155/68 inches; build 2.4
(34); adjusted to 55 years, 161/68 inches; build 2.5 (35).
4. Male, who died at 18 years from diphtheria, having the formula 145/72
inches; build 2.0 (28); adjusted to 55 years, 171/72 inches; build 2.3
(33).
5. Female, married, has at 31 years the formula 115/65 inches; build 1.9
(27); adjusted to 55 years, 132/65 inches; build 2.2 (31).
6. Male, a farmer, has at 28 years the formula 160/71 inches; build 2.2
(32); adjusted to 55 years, 174/71 inches; build 2.4 (35).
7. Female, a student, who in youth suffered from tonsillitis, scarlet
fever, and other “children’s” diseases, has at 22 years the formula
118/64 inches; build 2.0 (29); adjusted to 55 years, 136/64 inches; build
2.3 (33).
_Comment._—All except one on the adjusted weights equal or exceed the
mid-parent index. One of the 7 children is as fleshy as the fleshier
parent (R: Rom-1).
RID FAMILY. (Fig. 48.)
III 9 ♂, at 59 years, stature 157 cm. (62 inches); weight 73 kg. (160
pounds); build 2.9 (42); fleshy; “as fat as butter when a child.” He
has 3 fleshy sibs and his parents are dissimilar in build; hence he is
heterozygous; married to III 10 ♀, slender, of two slender parents.
Of their 2 children, IV 3 ♀, at 30 years is slender; IV 4 ♂, at 16 years,
slender (73:727).
VAN FAMILY. (Fig. 44.)
I 3 ♂, died at 51 years of heart disease, stature 170 cm. (67 inches);
weight 86 kg. (190 pounds); build 3.0 (42); fleshy. He was one of a
fraternity of 8 of whom something is known of the following: I 1 ♂,
slender; I 2 ♂, stature 183 (72 inches); weight 90 kg. (200 pounds);
build 2.7 (38.5); fleshy; slender as a child. I 3, married I 4, who died
at 32, was tall, slender, angular. A brother is of medium build.
They have 5 children: II 1 ♂, died at 53 years of indigestion; stature
189 cm. (74 inches); weight 90 kg. (200 pounds); build 2.6 (37); fleshy.
II 2 ♀, always slender. II 3 ♀, slender. II 4 ♂, at 54, stature 175 cm.
(69 inches); weight 88 kg. (194 pounds); build 2.9 (41); fleshy. Relative
chest-girth 108 ÷ 175, or 62 per cent. He first began to increase in
build at 22 years and at 30 years had his present build; loses weight
after vigorous exercise. He married a woman (II 5) who, like himself, was
slender in youth, but began to grow fleshy at 39, and now has a build
of 2.9 (41). She has 2 slender, 2 fleshy, and 2 very fleshy sibs, and
her parents were both very fleshy. The foregoing couple (II 4, 5) have
2 children who grew up. III 1 ♀ at 28 years, keeps slender by constant
dieting. III 2 ♂ (one of twins) at 25 years, very slender, nervous, and
irritable. The children have not yet reached the age when their mother
became fleshy.
Finally, II 7 ♀, at 50 years, is 170 cm. (67 inches) tall and weighs 88
kg. (195 pounds); build 3.1 (43); fleshy. She was slender up to 27 years
of age. She is married to a somewhat fleshy man and their daughter at 27
is of medium build, but beginning to grow fleshy.
_Comment._—The mating of a man of build 3.0, of a fraternity that is
variable in build, and a woman of slender build yields grown children
with following builds: 2.6, “slender,” “slender,” 2.9 (slender in youth),
and 3.1 (slender in youth). Three of the five become fleshy, but probably
only late in life—the heterozygous reaction (73:745).
[Illustration: FIG. 44.—Pedigree chart showing distribution of build in
VAN family.]
WAT FAMILY.
A family of English extraction living in Wyoming. The Father, who has
tuberculosis, has the formula 125/68 inches; build 1.9 (27). His father
was slender and of average height. His mother was fleshy and of average
height.
The Mother had at 50 the formula 165/64 inches; build 2.8 (40), but
averaged usually from 120 to 128 pounds. She had stomach trouble. Her
father, an invalid and sufferer from tuberculosis, rheumatism, neuralgia,
heart trouble, and dropsy, had the formula 120/68 inches; build 1.8
(26). His weight varied from 102 to 120 pounds; very slender. Her mother,
who had a goiter of which she was cured, and quinsy, had the formula
140/56 inches; build 3.1 (45). The mother’s father’s father had the
formula 180/73.5 inches; build 2.3 (33). His weight varied from 180 to
200 pounds. He was muscular, not fat. The Mother’s father’s mother was
always thin and had the formula 115/65 inches; build 1.9 (27). She had
liver trouble and cancer of the face. The Mother’s mother’s father had
cancer of the face and underwent an operation for it. His formula was
125/65 inches; build 2.1 (30). The Mother’s mother’s mother had at 70
years the formula 160/67 inches; build 2.5 (36). She grew heavier in
middle age. The children are:
1. Male, liable to tuberculosis, has at 24 years the formula 134/67.5
inches; build 2.1 (30).
2. Male, has weak lungs; has at 22 years the formula 170/67.5 inches;
build 2.6 (37).
3. Male, has at 18 years the formula 126/68 inches; build 1.9 (27).
_Comment._—The children show the usual variability that arises from this
type of mating (D:Wat.).
Mating 2. FLESHY × HETEROZYGOUS FLESHY PARENTS.
This includes matings between a heterozygous parent of fleshy build and a
very fleshy (or fleshy) parent of fleshy stock; a back-cross to the more
nearly dominant type.
The matings of this type are as shown in table 33.
TABLE 33.—_Matings between a probably homozygous fleshy and a
heterozygous fleshy parent, together with the progeny of this back-cross._
+--------+---------------------------------------+---------------------+
| | Parentage. | Offspring. |
| +--+--+---+---------+--+--+---+---------+--+---+----+----+----+
| Ref. | | | | | | | | | | | | | |
| |FF|FM| F | Father’s|MF|MM| M | Mother’s|VS| S | M | F | VF |
| | | | | sibs. | | | | sibs. | | | | | |
+--------+--+--+---+---------+--+--+---+---------+--+---+----+----+----+
| | | | | | | | | | | | | | |
|Hud |28|46| 45| |38|35| 40| | | | 1 | 1 | 2 |
|Jon 11c |29|49| 39|1VF 3F 5M|37|42| 39|2F 4M | | | 1 | 8 | 1 |
|Pal |F |M | 43|1S 3F 1VF| | | 40| | | | 2 | | 1 |
|Rec (a) |S | | 40|2F | | |100|2F 1S | | | 1 | 2 | 3 |
|Rec (b) |F |S |40F| |F |VF| 57|2VF 2F 1M| | | | | 1 |
|Rid | |F | 56| |S | |49±|4F 2M | | 1 | | 3 | 3 |
|Smi |VF| | VF| |M | | 48|1F | | 1 | | 3 | 3 |
|The 1 |30|31| F |1F 4S |33|33| 34|2S 1M | | | 3 | 4 | 3 |
|Wen |46|M | 46| |M |M | 37|2F | | | 6 | | 2 |
| +--+--+---+ +--+--+---+ +--+---+----+----+----+
| Total | | 2 | 14 | 21 | 19 |
|Proportions | |3.6|25.0|37.5|33.9|
+--------+--+--+---+---------+--+--+---+---------+--+---+----+----+----+
A = 40.48 ± 0.57.
S. D. 6.36 ± 0.41.
These 9 matings yielded 56 children, with the following percentage
distribution: 4 S, 25 M, 37 F, 34 VF. The 6-zygotic-factor mating 5 × 3
(both possibilities) gives a percentage distribution of 3 S, 25 M, 43 F,
28 VF, which approximates that found.
Attention is called to the distribution of offspring in the Pal, Rid,
Smi, and Wen families. In these families the children are of two extreme
types; intermediates are absent. The result may be due merely to small
numbers, but it suggests the presence of two sorts of gametes in the
heterozygous parent and hence a tendency to segregation in the offspring.
HUD FAMILY. (Fig. 45.)
The Father’s (II 7) build is 3.2 (45); very fleshy; his father’s (I 1)
was 2.0 (28) and his mother’s 3.2 (46). Thus the Father is heterozygous.
The Mother’s (II 8) build is 2.8 (40). Her father’s build was 2.7 (38),
fleshy; and her mother’s 2.5 (35); medium fleshy. The Mother’s 7 sibs
have builds ranging between 2.5 (35) and 3.2 (46); principally fleshy to
very fleshy. So this may be regarded as a back-cross of a heterozygous
parent with a fleshy one of fleshy stock. Of the 4 children, 1 is
medium-fleshy (III 11) with a build of 2.5 (36), 1 is fleshy (III 10)
2.7 (38), and two very fleshy; build 3.2 (45); thus the build of the
offspring is varied, but prevailing very fleshy.
[Illustration: FIG. 45.—Pedigree chart showing distribution of build in
the HUD family.]
JON-11C FAMILY. (Fig. 46.)
A family of Welsh extraction living chiefly in New York State and Ohio.
The Father (II 10), a farmer, suffered in middle age from “rupture,” and
died at 88 years from “old age,” having the formula 150/62 inches; build
2.7 (39). Of his 9 sibs:
1. Brother, died at 70 years from “dissipation,” having the formula
175/68.5 inches; build 2.6 (36).
2. Brother, who died at 53 years from “inflammation of kidneys and
dyspepsia,” had the formula 125/63 inches; build 2.2 (31).
3. Sister, who died at 68 years from Bright’s disease, 140/57 inches;
build 3.0 (43).
4. Sister, who died at 74 years from “flux,” 150/58 inches; build 3.1
(44).
5. Sister, who died at 75 years from Bright’s disease, 120/59 inches;
build 2.4 (34).
6. Sister, who died at 60 years from Bright’s disease, 118/59.5 inches;
build 2.3 (33).
7. Sister, who died at 73 years, 135/64 inches; build 2.3 (33).
8. Brother, who died from typhoid fever at 44 years, 175/68 inches; build
2.7 (38).
9. Brother, 150/62 inches; build 2.7 (39).
Their father, a farmer, suffered in middle age from “hernia”; died of
heart trouble at 65 years, having the formula 120/64.5 inches; build 2.0
(29). Their mother died at 77 years from pneumonia, having the formula
160/57 inches; build 3.5 (49).
The Mother suffered from “nervousness” before marriage, then not troubled
with it again till menopause. She died of “heart trouble, dropsy,
paralysis, and nervousness” at 80 years, having the formula 150/62
inches; build 2.7 (39). Of her 8 sibs:
1. Brother, who died from “congestive chill,” was 67 inches in height.
2. Brother, who died at 56 years from “old age,” 180/71 inches; build 2.5
(36).
3. Brother, who died at 81 years from “poor circulation” and stomach
trouble, had the formula 170/71 inches; build 2.4 (34).
4. Brother, who died from pneumonia at 45 years, 180/70 inches; build 2.6
(37).
5. Brother, who died from “kidney trouble” at 40 years, 170/70 inches;
build 2.4 (35).
6. Brother, who died at 57 years from “abscess on liver,” 160/69 inches;
build 2.4 (34).
7. Sister, who died at 25 years from “child-birth.”
8. Sister, who died at 72 years from “overdose of medicine,” 165/67
inches; build 2.6 (37).
Their father, a farmer and cabinet-maker all his life, died at 83 years
from paralysis, having the formula 200/74 inches; build 2.6 (37). Their
mother, who in middle age suffered from dropsy and palsy, died at 83
years from “old age.” Her formula was 160/62 inches; build 2.9 (42).
The 10 children:
1. Male, a farmer, recorded as always well, has at 66 years the formula
165/67 inches; build 2.6 (37).
2. Female, who in youth suffered from “ague, flux, erysipelas, cholera
morbus,” has at 65 years the formula 130/59 inches; build 2.6 (37).
3. Female, who in youth suffered from asthma, has at 63 years the formula
150/61 inches; build 2.8 (40).
4. Male, a lawyer, who in youth suffered from scarlet fever, and middle
age from “acquired neurasthenia,” has at 59 years the formula 190/70
inches; build 2.7 (39).
5. Female, a school-teacher, who died at 20 years from typhoid fever, had
the formula 120/61 inches; build 2.3 (32); adjusted to 55 years, 139/61
inches; build 2.6 (37).
6. Female, who suffered in youth from scarlet fever and in middle age
from typhoid and kidney trouble, has always been “nervous,” has at 55
years the formula 150/61 inches; build 2.8 (40).
7. Male, a farmer and “shopman,” who in youth suffered from Bright’s
disease, has at 53 years the formula 170/67.5 inches; build 2.6 (37).
8. Female, who at 17 years had fever, lost her mind, has not been well
since—“gradual mental deterioration.” At 51 years she has the formula
170/62 inches; build 3.1 (44).
9. Female, who in youth suffered from “thrush,” and in middle life from
malarial fever and gradual mental deterioration, has at 51 years the
formula 116/57.5 inches; build 2.4 (35).
10. Female, who at 48 years has the formula 165/63 inches; build 2.9 (42).
_Comment._—This is an extraordinarily valuable pedigree furnished by a
member of the family who has taken great pains with the record. Both
parents are of middle-fleshy build (39). The Father’s fraternity shows
sibs: 5 medium, 4 fleshy, and 1 very fleshy. This is associated with
semi-dwarfishness, one of the sisters being only 57 inches in stature and
one of the brothers only 63 inches. _One of their parents is slender;
one obese._ The Mother’s fraternity comprises 4 persons of medium
build and 3 stout. Their _parents are both fleshy_. The “children” are
remarkably uniform. Since they all, except one, reached the parental age,
no “adjustment” is necessary; they can be compared directly. One is of
medium build, 8 are stout like their parents (including the adjusted age
of the girl who died at 20), and 1 is just over the line of being very
stout (44), like her paternal aunt and a little less than her Father’s
mother. Here the obesity has skipped a generation in the direct line,
possibly because the Father was phenotypically reduced in build, perhaps
because of his advanced age (88). This circumstance offers, however,
no theoretical difficulty. The uniformity of the progeny favors the
hypothesis that in this family there are only two independent factors for
fleshy build (R: Jon-11_c_).
[Illustration: FIG. 46.—Pedigree chart showing distribution of build in
the JON-11C family.]
PAL FAMILY. (Fig. 25.)
A family living in a small town in good circumstances. III 9 ♂, a farmer,
who at 67 years is 173 cm. (68 inches) tall, weighs around 90 kg. or 200
pounds; build 3.0 (43); fleshy; net relative chest-girth 120/173, or 71
per cent. This near-obese man was slender as a boy and began to grow
fleshy at 30 years of age. There are 5 others in his fraternity: (1)
III 7 ♂, a physician, at 71 years is 178 cm. (70 inches) tall, weighs
over 90 kg. (200 pounds); build 2.9 (41); fleshy; relative chest-girth
119/178, or 67 per cent. He is doubtless heterozygous for build, since,
by a slender wife, he has 2 fleshy and 2 slender children. (2) III 8 ♀,
married, at 69 years has stature 157 cm. (62 inches); weight 75 kg. (155
pounds); build 2.8 (40); fleshy; relative chest-girth 107/157, or 68 per
cent. By a man of medium build she has 1 fleshy, 1 medium, and 3 slender
children.[10] (3) III 11 ♂, at 65 years has a stature of 175 cm. (69
inches); weight 61 kg. (135 pounds); build 2.0 (28); slender. (4) III 5
♂, at 62 years, stature 178 cm. (70 inches); weight 95 kg. (210 pounds);
build 3.0 (43); fleshy. His relative chest-girth 117/178, or 66 per cent.
As a boy he was of medium build; at about 30 years, like III 7, he began
to grow fleshy, and is now dieting for diabetes (?). By a fleshy wife,
whose sibs vary in build, he has 2 fleshy children and 1 of medium build.
(5) III 12, at 59 years has a stature of 168 cm. (66 inches) and weight
of 102 kg. (224 pounds); build 3.6 (52); very fleshy. By a husband of
medium build she has 1 slender and 1 medium child.[10]
[10] Not shown in figure 25.
The father (II 5) of this fraternity, who died at 87 years of cancer of
the face, was fleshy. He had 5 brothers, all of whom lived to be over 80
years of age and who all, save 1, weighed over 90 kg. (200 pounds). The
mother (II 6) of the man’s fraternity died at 64 of pneumonia; she was of
medium build, and her 4 sibs were of medium build. Thus all her children
were probably somewhat heterozygous, including III 9, the father of 3.
III 10, the wife of III 9, is 178 cm. tall and weighs over 90 kg.; build
2.8 (40+); fleshy.
Of the 3 children: (1) IV 7 ♂ at 44 is of medium build. By a slender wife
he had a daughter who at 22 years has a build 2.4 (34); medium build. (2)
IV 10 ♀, at 42 years, has a stature of 163 cm. (64 inches) and weight of
over 115 kg. (250+ pounds); build 4.3 (61+); obese. She married a slender
man, and 1 of their 9 children, at 19 years, weighs over 90 kg. (200
pounds). (3) IV 11 ♂ is a medium weight; he married a slender woman and
has 4 children who are of medium build.
_Comment._—A fleshy Father, who is heterozygous for build, and his fleshy
wife (of unknown gametic composition) have 1 obese child and 2 children
of medium build (73:704).
REC FAMILY, A. (Fig. 47.)
II 5 ♂ died at 84 years of “heart disease.” His stature was 188 cm. (74
inches) and weight 100 kg. (220 pounds); build 2.8 (40); fleshy. He had
a fleshy brother and sister. Their father was a slender man, but nothing
is known about their mother. II 5 married II 6, who died at 58 years of
bronchial pneumonia. Her formula, 360/60 inches; build of 7.0 (100); very
obese. She has 1 very fleshy and 1 fleshy sister and a slender brother.
This fleshy pair had 6 offspring, as follows: (1) III 2 ♀ (plate 9,
fig. 2), build 4.0 (57), relative chest-girth, 90 per cent. She is the
obese mother (by a fleshy, 2.8 (40), consort) of a slightly less obese
daughter, of build 3.7 (53) (plate 9, fig. 3). (2) III 3 ♂, 170 cm. (67
inches) tall, and weighing 91 kg. (200 pounds); build 3.1 (45); very
fleshy. He is now at a State institution and weighs some 20 or 30 pounds
less. (3) III 4 ♂, build about 2.4 (34); medium. (4) III 5 ♂, very
fleshy. (5) III 6 ♂, about 183 cm. (72 inches) tall, weighs over 90 kg.
(200 pounds); has very large shoulders and abdomen; build, say, 2.8 (40).
(6) III 8 ♀, at 36 years has a stature of 168 cm. (66 inches) and weight
of 71 kg. (157 pounds); build 2.7 (38); fleshy. Her relative chest-girth
is 52 per cent. She married a man of build 3.4 (48) and has 3 sons—2
slender and 1 fleshy.
_Comment._—The parents II 5 and II 6 were probably heterozygous, so that
they produced 1 in 6 of medium build. Also, their children are mostly
heterozygous. Of 8 grandchildren, 2 are slender, 2 are stout (73:714).
[Illustration: FIG. 47.—Pedigree chart showing distribution of build in
REC family.]
REC FAMILY, B. (Fig. 47.)
III 1 ♂, fleshy, with a fleshy father and slender mother, married to
III 2 ♀ (plate 9, fig. 2), who at 53 years has a stature of 150 cm.
(59 inches) and weight of much over 90 kg. (200 pounds); build 4.0
(57); obese. Her relative chest-girth is 135/150, or 90 per cent;
extraordinarily obese. At 16, when married, she weighed 110 pounds; build
2.2 (32); medium. 4 of her 4 sibs and both parents are exceedingly obese
(her mother weighs 163 kg. [360 pounds] and has a build of 7.0 [100]).
The foregoing pair had 5 children, 4 of whom died young. The other, IV
2 ♀, at 36 years has a stature of 168 cm. (66 inches) and weight of 104
kg. (229 pounds); build 3.7 (53); very fleshy. Her relative chest-girth
is 130/168, or 77 per cent. She had at her marriage, when 23 years old
(to a slender man), a build of 2.3 (33), medium grade. After marriage
she increased rapidly in weight, menstruation became scant, she lost the
sex-instinct, and is barren (plate 7, fig. 3).
_Comment._—A tendency to extreme obesity runs in four generations. This
is apparently of the adiposo-genitalis type, with sterility in the latest
generation. Obvious dominant factors are at work here (73:714).
RID FAMILY. (Fig. 48.)
II 2 ♂ died at 54 years; short and weighed 110 kg. (240 pounds); build,
say, 3.9 (56); very fleshy. A brother who died at 52 of apoplexy was
fleshy, married a fleshy woman, and had a fleshy son. The mother of this
fraternity was fleshy; about her consort’s build nothing is known, but he
had a fleshy sister (I 1).
II 3 ♀, wife of II 2, died of senility at 89; she weighed over 90 kg.
(200 pounds). She had 7 sibs: (1) II 4 ♀ died of epilepsy, was of medium
weight, married, and had 5 children, 4 of medium weight and 1 fleshy. (2)
II 5 ♀ of unknown build. II 6 ♀ of medium weight, her children slender.
II 7 ♂ weighed over 90 kg. (200 pounds); build, say, 2.9 (41), or fleshy.
II 8 ♂ weighed over 90 kg.; fleshy. II 9 ♂ also fleshy, like his two
brothers. II 10 unknown. Thus of this fraternity of 6 known persons, 4
are fleshy, 2 medium. Their father was slender; their mother “short and
plump.”
There are 7 offspring from this mating between II 2 and 3: (1) III 1
♀, at 66 years, is bedridden from a broken hip; tall, weight 77 kg.
(170 pounds); chest-girth 108 cm. (42 inches); build, say, 2.8 (40);
fleshy; she was fleshy as a child of 10 years. (2) III 2 ♂, died at 60 of
paralysis, was always slender. (3) III 3 ♂, at 62 years, is tall (say, 71
inches) and weighs 97.5 kg. (235 pounds); build 3.3 (47); very fleshy.
(4) III 4 ♀, at 56 years has the formula 91 kg. (200 pounds); 161 cm.
(63.5 inches); build 3.4 (49); very fleshy; relative chest-girth 74 per
cent. She was fleshy from the age of 16 years. (5) III 5 ♀, at 51 years,
is very fleshy; was a slender child. (6) III 6 ♀ is fleshy. (7) III 8 ♀,
at 35 years weighed 86 kg. (190 pounds), but now at 50 she is a helpless
invalid and has grown slender; she was somewhat slender as a girl. Thus
the offspring are 3 very fleshy, 2 fleshy, 1 always slender, and 1
formerly fleshy but reduced by illness (73:727).
[Illustration: FIG. 48.—Pedigree chart showing distribution of build in
the RID family.]
SMI FAMILY. (Fig. 26.)
I 1 ♂ died at 72 years of acute indigestion; said to have been very
fleshy, like his father. His wife, I 2 ♀, died at 68 years of paralysis.
She was less than 155 cm. (61 inches) tall and weighed 82 kg. (180
pounds); build 3.4 (48); very fleshy. She had 3 sibs, of whom it is known
that 1 was fleshy; the other 2 unknown. Her father was of medium build
and had 3 children by an earlier marriage, and of these 2 were slender
and 1 fleshy. There were 7 children from I 1 and 2. (1) II 1, a man
who died at 69 of pneumonia and diabetes and whose stature is 173 cm.
(68 inches) and weight about 95 kg. (210 pounds); build 3.2 (45). (2)
II 3 ♀ at 75 years is 155 cm. (61 inches) tall and weighs 82 kg. (180
pounds); build 3.4 (48). By a stout consort she has 2 stout and 4 slender
children. (3) II 9 ♀, married, at 74 years is 163 cm. (64 inches) tall
and weighs 49 kg. (107 pounds); build 1.8 (26); slender. By a slender
husband she had one slender daughter, build 1.9 (27), a slender son, and
2 other children who died young. (4) II 5 ♀, fleshy. (5) II 6 ♀, fleshy.
(6) II 7 ♀ said to be 157 cm. (62 inches) tall and to weigh 82 kg. (180
pounds); build 3.3 (47); very fleshy. (7) II 4 ♂, at 55 years, fleshy.
By a medium wife he had a son who at 26 years weighs 77 kg. (170 pounds)
and was fleshy as a growing boy. Of the 7 children, 1 is slender, 3 are
fleshy, and 3 very fleshy (73:736).
THR-1 FAMILY. (Fig. 33.)
A family of English and French stock living in the middle western States.
The Father (II 8), whose occupation has been very shifting, who suffered
from “weak lungs” at 35 years, and who died at 81 years, had in middle
life the formula 140/72 inches; build 1.9 (27). But in answer to special
inquiry it appears that he “took on flesh” in later years. He has to
be recorded as fleshy. Of his 3 sisters, two are slender (both with
cardiac hypertrophy), and 1 is of fleshy build. The fat sister had 2
daughters who weighed over 225 pounds each. His 2 brothers are slender.
His father (I 1), a blacksmith, died at 90 years, having the formula
150/71 inches; build 2.1 (30). His mother, always well, died at 68 years,
having the formula 130/65 inches; build 2.2 (31); medium. This side of
the house carries both fleshy and slender strains, some of the slender
individuals being so, probably, through disease. Apparently the Father is
heterozygous for fleshiness, perhaps one reason why he became fleshy late
in life.
The Mother (II 9) suffered from arthritis deformans and died at 79
years. Her formula was 135/63 inches; build 2.4 (34). Two of her sibs
are slender and one of medium build. Her father (I 3), who suffered
from arthritis deformans, was confined to his chair from rheumatism the
last 15 years, and died at 72 years, having the formula 160/70 inches,
build 2.3 (33). Her mother, who died at 50 years, had the formula 140/65
inches; build 2.3 (33). She had a sister (I 5) who weighed about 250
pounds, “an enormous woman.” This side of the house is of prevailingly
medium build but with a tendency to obesity in one line. The children are
10 in number:
1. Male (III 3), a clerk, has at 66 years the formula 150/69 inches;
build 2.2 (32).
2. Male (III 4), a physician, who has always had a rheumatic tendency
and is liable to sciatic neuritis, at 25 years had the formula 180/68.75
inches; build 2.7 (38). He is the Father of Thr-2 family, page 79.
3. Male (III 6), a preacher, has at 69 years the formula 170/68 inches;
build 2.6 (37). He has a daughter with a build of about 3.2 (45).
4. Male (III 7), a physician, who in middle life suffered from
inflammatory rheumatism, has at 59 years the formula 170/68 inches; build
2.6 (37).
5. Female (III 8), who died at 34 years from appendicitis, has the
formula 225/67 inches; build 3.5 (50). She was “a big overgrown woman in
her teens.”
6. Female (III 9), married, who has a rheumatic tendency, has at 55 years
the formula 190/64 inches; build 3.3 (46).
7. Female (III 11), married, who has 9 children, suffered in middle age
from rheumatism. At 53 years her formula was 225/67 inches; build 3.3
(46).
8. Male, a merchant, well, has at 51 years the formula 155/67 inches;
build 2.4 (35).
9. Male, a merchant, well, has at 49 years the formula 165/68.5 inches;
build 2.5 (35).
10. Male (III 14), a doctor and dentist, has at 47 years formula 180/68
inches; build 2.7 (39). One of his daughters has a build of about 3.2
(45).
Child No. 2, a physician, writes: “Many of my relatives, both on Father’s
and Mother’s side, were afflicted with so-called muscular rheumatism
(cousins, uncles, and aunts), pains in the limbs and muscles (not in
the joints); especially those of robust and fleshy build, who possessed
extraordinary good appetites and digestion, who liked good things to eat
and much of it; the women being good cooks and the men generally marrying
good cooks, they always had plenty to eat (rich food) and to spare. None
of them are users of alcohol, simply being extra-hearty eaters” (R:
Thr-1).
WEN FAMILY. (Fig. 49.)
IV 10 is the Father; his formula is 260/74 inches; build 3.2 (46);
very fleshy. His father (III 10) had the formula 245/73 inches; build
3.2 (46); very fleshy. This father had a brother of just his build
(who eventually died of tuberculosis) and a brother of formula 250/74,
build 3.0 (43); fleshy. The Father’s father’s father (II 5) had the
formula 200/70, build 2.9 (41); fleshy; one of his brothers was fleshy
(38), and one very fleshy, build 3.2 (45). The latter had a very fleshy
son. The Father’s father’s father’s father had a build of 2.9 (41) and
a brother of the same build. These brothers of Gen. I were products
of a first-cousin marriage. The Father’s father’s mother was a woman
whose formula was 200/68.5 inches; build 3.0 (43); fleshy. Hence the
Father’s father and his brother, both of build 3.2 (46), got the fleshy
tendency from both sides of the house. The Father’s mother was a second
cousin of the Father’s father and her line also contained many fleshy
representatives, but she herself was of medium build. Thus the Father
belongs to a fleshy strain, but he probably carries some non-fleshy
gametes.
IV 11 is the Mother; her formula is 160/65.5 inches; build 2.6 (37);
fleshy; she has 2 sibs, both fleshy; her parents are of medium build;
they have some slender grandchildren.
There are 8 children, V 3 to 12, whose sex and indices of build are as
follows: ♂ 3.6 (51), ♀ 3.1 (44), 2 ♂ ♂ 2.5 (35), 3 ♀ ♀ 2.3 (32), ♀ 2.2
(31). Thus 2 are very fleshy and 6 are of medium build. The interval
between the two groups is a wide one, indicating a clear genetic
difference between them. The very fleshy brother, who weighs 265 pounds,
was able to reduce about 60 pounds to be accepted for army service, but
since being discharged from the army he has rebounded to his former
weight. (A:032-25.)
[Illustration: FIG. 49.—Pedigree chart showing distribution of build in
the WEN family. (Gen I 1 should be square ruled, indicating fleshiness).]
SUMMARY AND DISCUSSION.
In a simple monohybrid with complete dominance the back-cross upon the
recessive gives 50 per cent of the heterozygous dominant and 50 per cent
of the recessive allelomorph. In a monohybrid with imperfect dominance
the back-cross upon the recessive gives 50 per cent of the intermediate
and 50 per cent of the recessive. Where 2 or 3 multiple factors are
present and the heterozygote is nearly intermediate but shows a slight
tendency toward imperfect dominance, we may expect an approximation to
a symmetrical distribution of grades about the intermediate condition,
with a skewness toward the recessive condition. That is what is got
in both parts of table 32. This result supports the conclusion that
there is segregation in the gametes of the heterozygous parent, so
that the progeny tend prevailingly to fall again into the slender and
medium-fleshy grandparental types. The results of table 33 similarly
support the conclusion of segregation in the gametes of the heterozygous
fleshy parent.
C. GENERAL DISCUSSION.
HEREDITY AND ENVIRONMENT IN BUILD.
That a tendency to slenderness or fleshiness of build “runs in families”
and characterizes different races is a matter of common observation. But
this fact is far from satisfying the clinician that heredity plays any
part in this result. Thus, von Noorden, who occupies a leading position
among Teutonic investigators of metabolism in general and obesity in
particular, denies the importance of an hereditary anomaly of metabolism
in different families and races. Rejecting “anomaly of metabolism” or
“peculiarity of protoplasmic metabolism,” he stresses “inheritance” of
habits of life that favor obesity, the quantity and quality of food,
and the ideals of bodily activity. For example, the Eskimo are fat
because they eat blubber and huddle in narrow spaces, undergoing little
movement throughout the long, dark winters. It is true that von Noorden
speaks somewhat guardedly; he recognizes exceptions; suggests a possible
hereditary hypofunction of the thyroid. But clearly constitutional
peculiarities are, for him, exceptional as causes of overweight, and here
is where he fails to recognize sufficiently the fact that usually only
particular individuals of a fraternity are fleshy; the others may be
slender.
But besides anomalies of protoplasm and family traditions of feeding,
there are obviously other possibilities. It is well known that different
varieties of cattle differ greatly in their capacity for fattening.
Armsby and Fries (1911) have inquired into the influence of type upon
the fattening of cattle. They used a pure-bred Aberdeen-Angus steer and
a “scrub,” part Jersey, steer for comparison. As is well known, the
former belongs to the easily fattening beef type; the Jersey to the
difficultly fattening milk type. During over 2½ years, beginning at under
1 year of age, these steers were under nearly continuous observations.
They were fed on ordinary growing rations, the same for each steer. The
digestibility of the total ration was determined at intervals; four tests
were made of each animal in the respiration calorimeter to determine the
percentage availability of the energy of the feeds consumed by each. The
results were as follows: Analysis of feces and urine failed to show any
difference in percentage digestibility of the food by the two animals,
and calorimeter tests failed to show any difference in the proportion
of the food-energy which was being metabolized. But the two animals did
not metabolize in the same way. Thus, in the scrub, a larger proportion
of the gain made was of protein than in the case of the beef steer; and,
conversely, the gain of the beef steer was more largely fat than in the
case of the scrub. Reduced to common weight, the energy requirement for
maintenance of the scrub steer was nearly 19 per cent greater than for
the beef steer. Since the beef steer would eat more than the scrub and
tended to store fat rather than protein, the greater tendency of the beef
steer to fatten received a biochemical explanation. The results seem to
show a difference between the two varieties in the working over of the
assimilated materials.
Indeed, it is easily appreciated that steers of the beef and dairy types
of cattle should metabolize differently when we consider the marked
difference in the milk production of the cows of these two types. The
cow of the highest dairy type is capable of manufacturing 20 kilograms
of milk containing 1.2 kilograms of butter fat in one day, or 6 per cent
(Bailey, Encl. Am. Agric., III, 365). The cow of the meat type, of larger
size, produces up to 30 kilograms of milk, and this contains, perhaps,
1.3 kilograms of butter fat per day, or only 4.3 per cent (Sinclair,
1904, p. 740-42). There is here, obviously, a difference in the metabolic
processes in the cows and this is reflected in the steers also.[11] There
is an internal biochemical difference as well as a difference in the
feeding instinct. The latter is not merely a matter of family tradition,
of the family economics or mores; it is a physiological phenomenon as
much as internal metabolism.
[11] I am indebted to Mrs. C. D. Walcott for calling my attention to this
point.
Indeed, even von Noorden (1907, III, p. 700) seems to be forced to this
conclusion by cases of failure to reduce weight at a diet far below that
which appears to be essential to maintenance. Thus a man of 39 years, who
exercised freely in the open air, had a weight of 102 kg. For 3 months
his diet never exceeded 1,720 calories (estimated at 1,000 calories short
of normal requirements) and at the end of this period he weighed 101 kg.
That a relation between ingested food and activity is not the entire
explanation of obesity is recognized by medical men of experience.
Heckel (1920, p. 371), referring to recurrent obesity, remarks on its
frequency and says: To constitute an obesity there must be organic
and hereditary tendencies: “Ne devient pas obèse qui veut.” “Aussi la
guérison accidentelle ou thérapeutique d’une obésité n’indique-t-elle pas
la disparition définitive des tendances personelles ou congénitale.”
Gulick (1922) has lately undertaken experiments to throw light on the
question why some persons fatten easily and some with difficulty. He
had noted that he himself belongs to a non-fattening strain and that
his inclination toward a very copious diet of predominantly starchy
nature did not lead him to put on weight, even though his round of
activity was moderate. So he undertook biochemical, nutritional studies
on himself. His observation covered nearly 21 months. During part of
this time his caloric intake was low, 1,875 to 2,780; during another
part high, 3,400 to 4,100. He found that he fattened somewhat during
the period of heaviest feeding. There was, however, always an excess of
intake over predictable need, and this excess increased absolutely and
probably even relatively as the intake increased. The fecal nitrogen was
2½ to 3½ times greater during over-feeding than under-feeding. The basal
metabolism during maximum feeding was normal. Gulick concludes that a
person belonging to the difficultly fattening type shows a wasteful rate
of oxidation, whether under or over fed, but especially at the latter
time. “It seems clear,” concludes Gulick, “that throughout the entire
experimental series there was some factor at work which caused fuel food
to be burned more freely than in the average individual. This factor was
not an over-active thyroid, as attested by the entirely normal basal
metabolism.” Gulick concludes that it was “some factor in the chemistry
of nutrition” which caused extravagance. This he thinks may very possibly
be comparable to the “secondary effect” of protein enrichment, which,
according to Rubner, can raise the specific dynamic action of the food
without raising the basal rate. It is also possible, he says, that the
spare type may be accounted for by any factor that produces a high “cost
of digestion,” just as the obese may be supposed to suffer from an
abnormally low “cost of digestion” (von Noorden).
Whatever the fundamental cause may be, the fact remains that in certain
families there is a widespread inclination to the production of slender
individuals, while in other fraternities certain proportions (though
usually not all) of any fraternity are fleshy or even obese. Perhaps,
as in the case of the Jersey as contrasted with the beef steer, the
two kinds of individuals do not metabolize their food in the same way;
some are spare and muscular, others lay on fat. In any case we can not
disregard the constitutional factors in build.
Looking at the matter broadly, we can see that no other theory than that
constitutional differences as well as nutritional differences determine
build is sufficient to meet all the facts. In other species of animals we
have precisely the same kind of differences between hereditary strains of
slender and stout build that we have among humans. Thus, among dogs, the
slender greyhound or Dachshund and the robust “Chow”; among horses the
Thoroughbred and the stocky Percheron; among swine the “razor-back” and
the Berkshire; among poultry the slender Leghorn and the stocky Cochin.
Slender and stocky as racial traits appear quite as white and black do
and they doubtless have similarly a genetic basis.
A careful study of the families described in this paper must convince
anyone, it seems to me, of the importance of the genetic factors. The
Fun. family is of a wholly different type from the Thr-1 family. Even
if the latter eat more, it is because of a constitutional urge like the
constitutional urge that leads the Aberdeen-Angus steer to eat more
than the Jersey steer. Very probably the Fun. family metabolizes in a
different way from the Thr-1 family, building more protein and less fat.
In other cases it is not the whole fraternity that is fleshy or slender.
This is well illustrated by the Wen. family, where 2 of 8 of the main
fraternity are very fleshy and all the others of medium build. We have
here to do not merely with a family habit of eating, but a differential
constitution that provides one-quarter of the children with a large
appetite that leads them to eat heavily and manufacture fat and provides
three-quarters of them with a small appetite that leads them to eat
lightly and to manufacture protein instead of fat. Constitutional
differences in the appetite and method of metabolism are the essential
factors; and these are the things that are inherited. Only on such
an hypothesis can we account for the clear evidence presented of
constitutional factors in build—not always one only, but sometimes three
or more acting together to produce the end result of obesity.
A scientific man, interested in nutrition, who has a build of 3.6 (51)
himself and one of whose sisters has a build of 3.1 (44), whereas his 4
other sibs have builds of 2.5 to 2.1 (35 to 30), writes that his brother
(of medium build, but about 75 inches tall) consumes daily about 2,700
calories; he himself and his fleshy sister about 2,500, and the others
of his fraternity, who are of medium build, 2,000 to 1,800. He is a
professional man, who does a good deal of office or laboratory work. He
drinks about 3 to 4 quarts of water per day. His son, who is nearly 11
years of age, weighs just over 120 pounds, is 63 inches tall, and fairly
fleshy. Though he is active, “never still a minute,” yet he has to be
urged to eat, willingly misses a meal, and uniformly declines a second
helping; “he eats much less than his 6-year-old cousins, who are actually
under size for their age; he has never been a heavy eater from the time
he was weaned.” This boy, the son of a very fleshy man, seems to afford
an example of the easily fattening type in whom the slight excess of
calories produces a striking result in build.
ENDOCRINE GLANDS AS LINKS BETWEEN CHROMOSOMES AND SOMATIC QUALITIES.
When it is concluded that there are constitutional, genetic factors for
build, the validity of this conclusion is not weakened by the known rôle
of endocrine glands on metabolism and build. Thus the experiments of
recent years have emphasized the importance of the rôle that the thyroid
gland plays in growth and development. As Uhlenhuth (1922, p. 182) says:
“The ontogenetic development of the individual is controlled by the
thyroid hormone.” Since in cretins the thyroid functions imperfectly or
not at all, the differences between the development of a normal child and
that of a cretin are supposed to indicate the scope of the control by the
thyroid hormone. In the cretin, growth is slowed up almost to cessation.
In the long bones the centers of ossification develop slowly. “The
epiphyses may be absent many years after they are due to appear and their
union with the shafts of the long bones indefinitely delayed. Periosteal
as well as endochondral bone formation may be greatly reduced and
delayed. The cranial bones are thin, poorly ossified, and osteoporotic:
mottling is sometimes evident ontogenologically.”... Incomplete closure
of the fontanelles is very common (Janney, 1922, pp. 391, 392). The
genito-urinary system is undeveloped; the external genitalia remain
infantile. The brain shows defective convolutions and all parts of the
central nervous system show deficient development. Owing to the fact
that the long bones of the leg develop imperfectly, while the chest may
continue to enlarge, the build of the cretin is usually large for his
age. Thus, in general, the specific metabolic changes are retarded. When
the thyroid functions imperfectly after maturity the victim puts on fat.
The fat is usually distributed nearly uniformly under all parts of the
skin. One of Janney’s cases weighed 212 pounds at 12 years. Some degree
of hypothyroidism is doubtless responsible for many of the “very fleshy”
persons referred to in the preceding pages. The frequent recurrence of
obesity in a family is in accordance with the tendency for hypothyroidism
to recur in different members of a family; a tendency shown remarkably in
Barrett’s (1919) family.
The hypophysis, especially its anterior lobe, is believed to exercise an
important control over differential metabolism and the resulting form.
The results of hyperfunctioning of the gland are very different from
those of hyperfunctioning of the thyroid. An extraordinary enlargement
of certain parts of the skeleton, especially of the base of the skull,
the hands, the feet, and the ribs, occurs. There is, indeed, in growing
persons a tendency to the production of giants. In the underfunctioning
of the hypophysis before puberty an extraordinary obesity is apt to
appear, known as dystrophic adiposo-genitalis; because, the more
the fat increases in amount the more the external genitalia appear
under-developed—infantile. The obesity frequently affects the region
of the pelvis only or chiefly, though the thighs also may be involved.
Disfunctioning of the pituitary in later years is believed, likewise,
to induce obesity. Of this disfunctioning there are, doubtless, all
degrees corresponding to the variety of grades of obesity. Thus a second
factor of obesity must be recognized; and this also “runs in families”—is
hereditary.
The other endocrine factors in obesity are less precisely known. It is
believed that the interstitial cells of the gonads secrete hormones that
regulate, especially inhibit, the production of fat. This is inferred by
the frequent tendency of women after the menopause to grow fat and of
eunuchs (of one type, at any rate) to become fleshy. Also, the secretions
of the islands of Langerhans of the pancreas are known to influence
carbohydrate metabolism, so that when they do not function properly sugar
is eliminated unchanged in the urine, and “diabetes,” usually accompanied
by fleshiness in its early stages, ensues. Of course, it can not be
stated that pancreatic insufficiency is responsible for the prediabetic
obesity; but the relation of the two phenomena is undeniably close.
Thus there come clearly to view two links in the chain of causes
connecting chromosomal factors (such as are present in “Mendelian”
heredity), on the one hand, and build, on the other. First, two or
more of the endocrine glands play a great rôle in metabolism and when
disturbed usually result in an abnormal build; and, secondly, just the
condition of endocrine disfunctioning is an hereditary one and seems to
depend on the condition of the enzymes or catalyzers that must be in the
chromosomes.
That other constitutional conditions than those of the larger endocrine
glands may play an important rôle in metabolism can not be denied;
probably the quality of the protoplasm of every active cell influences
the bodily metabolism; but the endocrine glands proper seem, as it were,
to be told off for this specific purpose, and thus peculiarities in their
functioning lead to striking results.
EVIDENCE OF SEGREGATION IN THE HEREDITY OF BUILD.
The best single criterion of Mendelism in any hereditary distribution is
segregation. If there is sufficient evidence of segregation in our study
of build, then we are justified in concluding that build is inherited
in “Mendelian fashion.” There have been several occasions to refer to
evidence of segregation in this work; some of this evidence may be
brought together here and other added.
1. The difference in variability of the progeny of different matings. The
offspring of slender parents are least variable, of fleshy parents most.
This is evidence that the fleshy parents carry gametes for slenderness
and thus that condition reappears in the offspring; but slender parents
rarely carry gametes for fleshiness (p. 56).
2. As a corollary of the above, regression takes place in the progeny
of fleshy parents to a markedly greater degree than in the progeny of
slender parents (p. 39).
3. The progeny of heterozygous parents are significantly more variable
than the progeny of parents belonging respectively to slender and to
fleshy stock. This is evidence that the heterozygous parents carry a
greater variety of gametes than those of “purer stock.”
4. In different matings of the same type the variability of the progeny
differs; apparently, because some parents belong to a special biotype and
others simulate the biotype merely through heterozygosity. Thus, if the M
× M mating be considered (table X), one finds some families characterized
by slight variability of the offspring. The indices of build (English) in
such families are given in table 34.
TABLE 34.—_Indices of build of the progeny of M × M matings, in which the
parents belong to the M biotype._
+------------+---------------------------------------+------+------+
|Reference. |Indices of build of children. |Mid |Total |
| | |range.|range.|
+------------+---------------------------------------+------+------+
|Bat 2 |32, 33, 33, 35 | 33.5 | 3 |
|Bea 7 |31, 32, 32, 34 | 32.5 | 3 |
|Dic 4 |29, 31, 32, 33 | 32 | 4 |
|Kel 4a |31, 32, M, M, M, 34 | 32.5 | 3 |
|Old 2 |33, 33, 33, 35 | 34 | 2 |
|Rig 1 |30, 32, 32, 34 | 32 | 4 |
|War 3 |30, 30, 30, 31, 32, 32, 32, 33, 33, 36 | 33 | 6 |
+------------+---------------------------------------+------+------+
The slight fluctuation in build of progeny of table 34 is obvious. The
modal index of the progeny is close to 33. On the other hand, there are
matings of this type which show a much greater variability. These are
listed in table 35.
TABLE 35.—_Indices of build of the progeny of M × M matings in which the
parents are probably heterozygous._
+------------+------------------------------------------+------+------+
|Reference. |Indices of build of children. |Mid |Total |
| | |range.|range.|
+------------+------------------------------------------+------+------+
|Cas 4 |32, 34, 34, 37, 41, 43 | 37.5 | 11 |
|Coo 5 |31, 33, 35, 36, 36, 36, 37, 37, 38, 38, 41| 36 | 10 |
|Eat A |33, 34, 35, 36, 36, 38, 38, 42 | 37.5 | 9 |
|Fis 2 |33, 35, 37, 37, 37, 39, 40 | 36.5 | 7 |
|Ill 1 |33, 34, 35, 35, 37, 37, 38, 39 | 36 | 6 |
|Mar 22 |31, 32, 33, 36, 36, 40 | 35.5 | 9 |
|Mer 8 |33, 36, 37, 40, 41 | 37 | 8 |
|Nes 1 |32, 33, 33, 37, 41, 51 | 41.5 | 19 |
|Tet A |30, 30, 36, 41, 43, 49, 49 | 39.5 | 1 |
|Rup 1 |30, 30, 31, 31, 33, 36, 38, 40 | 35 | 10 |
|Smi 33 |31, 31, 32, 36, 36, 36, 36, 37 | 34 | 6 |
|Sto 13 |33, 34, 36, 38, 38, 38 | 35.5 | 5 |
|A 01:29 |29, 39, 41 | 35 | 12 |
+------------+------------------------------------------+------+------+
These series of progeny fluctuate in build around 36. It seems probable
that the variable progeny are the offspring of heterozygous parents, but
this can rarely be proved, since the build of the grandparents is not
often available in the present series.
That there are really at least two kinds of matings of the M × M type is
shown more conclusively by figure 50, in which two modes, at 33 and 36,
respectively, are clearly seen. The conclusion seems to be justified that
the mode at 33 is that of progeny derived from the M biotype and the mode
at 36 is that of the progeny of heterozygous M parents. The existence of
these two modes in figure 50 is thus evidence of segregation.
[Illustration: FIG. 50.—Polygon of distribution of offspring of M × M
matings (from Appendix table X) for males, females, and sexes combined.
Abscissæ: index of build, English system. Ordinates: absolute frequencies
for males and females and their half sum for the sexes combined.]
Additional evidence is found in other matings, likewise. Thus the M ×
F mating shows two modes, at 33 and at 36 (fig. 51). There is also one
other, possibly significant, mode, namely, at 38, in the fleshy group.
Since F parents are sometimes homozygous, mating with M would tend to
produce medium-fleshy progeny (i. e., 36). The F parents are, however,
frequently heterozygous, containing both slender, medium, fleshy, and
even very fleshy gametes; and, accordingly, we should expect somatic
segregations at about the points 30, 33, 36, and 38 as centers, just
where we find them.
Again, the S × M mating yields (fig. 52) modes at 32 and 35 respectively,
a shade lower than those of the M × M or M × F matings; but the male
offspring (taken alone) gives modes at 33 and 35. Where the mode is at
33 it is probable that an S and an M gamete have met; and this condition
is relatively common just because M gametes are common. The mode at 35
may arise from an F gamete carried in a heterozygous M uniting with an S
gamete. The S gamete carried in heterozygous M may be responsible for a
probable mode which is hidden in the form of a hump at 28 in figure 52.
[Illustration: FIG. 51.—Polygon of distribution of offspring of M × F
matings (from Appendix table XI), sexes separate and combined. See also
legend of fig. 50.]
Attention is called to the probable influence of these modes on the two
modes shown in figure 7, at 33 and 35 respectively. These two modes are
strong evidence for a segregation in the factors for build. Thus the
very irregularity of the polygon of figure 7 is evidence of the presence
of segregating factors for build. Moreover, these two modes appear at
every age from birth to maturity, as is clearly shown in figure 53.
This bimodality is easily accounted for on genetical grounds, but is
inexplicable upon the bare nutritional hypothesis of build.
ON THE NUMBER OF FACTORS INVOLVED IN FLESHY BUILD.
It is by no means an easy matter to determine the number of independent
factors which are active in the case of a trait that is due to multiple
factors. This matter is still less easy if there is only very imperfect
dominance approaching intermediacy of the trait in the progeny of the
F₁ mating. Yet that is the situation that has to be met in the study of
heredity of build.
An attempt has been made in this paper to test the relative probability
that there are only two, on the one hand, or three or more independent
factors, on the other, involved. We have seen, in each of the various
matings, that the result is, on the whole, more closely in accord with
the 3-factor hypothesis than that of 2 factors. But this is not to insist
that never more than 3 independent factors are involved in build, or
never less than 3.
An attempt was made to apply Dr. Sewall Wright’s formula (Castle, 1922,
p. 22). Using the data of tables 12, 27, and 31, the value for _n_ (the
number of factors) was calculated by the formula
_N_ = _D_² / 8(σ₂²-σ₁²)
where _D_ is the difference between the means of parental pure races, σ₁
is the standard deviation of F₁ and σ₂ is standard deviation of F₂.
[Illustration: FIG. 52.—Polygon of distribution of frequencies of build
of offspring of S × M matings (from Appendix table VII), sexes separate
and combined. See also legend to fig. 50.]
Substitution for the letters of their values given _n_ = (39.20-28.50)²
÷8[(6.78)²-(5.02)²] = 0.69. We can only conclude that, owing to small
numbers, this formula is not applicable here.
Returning, then, to our conclusion that the assumption of at least
3 gametic factors for some, probably most, cases of build accords
best with the results of the various matings, we may inquire what
is the nature of these factors. It seems probable that two of them
may correspond to dystrophies of the pituitary and thyroid glands
respectively and the other or others to other regulatory mechanisms
of metabolism in the organism. It may well be that one of our factors
is the same as that which causes hypothyroidism; another as that which
causes hypopituitarism, and the third that which inhibits the normal
development of the genitalia, such as we see functioning in dystrophia
adiposo-genitalis. This is, indeed, speculation. However, the speculation
is an attempt to give a concrete form to the ideas of multiple factors in
build.
[Illustration: FIG. 53.—Solid figure (model) giving distribution of
relative chest-girth for various ages from birth to 20 years, reading
from left to right. The mean index of build at each age is centered on
the curve of development of relative chest-girth. The relative chest
girth is indicated in percentages passing from the bottom to the top of
the figure. The solid figure is illuminated from the upper part of the
page.]
If we assume three independent factors for build, it does not follow that
these are present in all families. Just as it has been demonstrated that
in different strains of mice there are in some cases 3, in others only 2
factors for susceptibility to cancer, so, apparently, it is with build.
In certain families the distribution of build in the progeny is best
accounted for on the hypothesis that, in such families, there are only
two gametic factors for build. In other families there appears to be only
one gametic factor for build.
It has been repeatedly pointed out that in many cases where multiple
factors are invoked to explain the genetical results, the results can
be equally well explained on the theory of blended inheritance. The
advantage of the factorial theory is that it brings under one type
of heredity even these most difficult cases of apparently blending
inheritance. More than that, however, the theory of multiple factors
explains a number of phenomena that the theory of blending inheritance
does not, such as the greater variability of the F₂ as contrasted with
the F₁ generation, and the skewness in distribution of progeny in the
back-cross. Thus an F × S mating should produce a “medium” progeny with
symmetrical distribution of deviating types on the theory of blending
inheritance; actually it produces not only mediums, but an excess of
fleshy over slender, which is readily accounted for on the hypothesis
that fleshiness is partially dominant over slenderness. In this and
other ways, especially in focussing attention on gametes, the doctrine
of multiple factors is essential to an adequate interpretation of the
results of mating between persons of dissimilar build.
D. SUMMARY OF CONCLUSIONS.
1. Two types of variation in build are to be distinguished: (1) the
change in average build that accompanies ontogeny and (2) variations in
adult build.
2. The popular idea of build is best expressed as the ratio of transverse
chest diameter to stature, or (since the chest diameter is rarely
known) chest-girth to stature. When only weight and stature are known,
the closest approximation to the chest÷stature ratio is given by the
weight÷(stature)² ratio, and this is taken as the standard index of build.
3. The correlation between the standard index of build and the relative
chest-girth is, for males, about 0.45.
4. The index of build of adult males is slightly greater than of females,
because of the relatively greater chest-girth of males. The average index
of build for males is 2.52 (35.8) and for females 2.43 (34.5).
5. There are marked racial differences in build; but they are not so
great as the differences in ontogenetic stages.
6. There are geographical differences in build; the heavy build of
northern peoples may be due to a physiological reaction or, in part, to a
selective survival of the fleshier individuals or strains.
7. The ontogenetic curve of build, expressed by relative chest-girth, is
expressed by figure 1 and (for infancy) figure 2. It shows that at birth
chest-girth is about two-thirds of stature and diminishes in the male to
the age of 12 years; thereafter, on the average, it rises to complete
maturity.
8. Build declines temporarily during the first month of life, owing to
the physiological difficulties attending adjustment to new conditions.
It declines temporarily, again, at about 8 months, probably due to the
cutting of the incisor teeth.
9. The heavy build of the infant corresponds to that of the short-legged
anthropoids. The long-legged, slender-build stage of the boy of 12 years
persists in the Nilotic negroes and many low-grade feeble-minded.
10. In adult life the changes in build vary with families. In those
characterized by slender build there is typically little change. In those
characterized by fleshy build there is typically progressive increase
in weight to 50 years. In some families weight fluctuates greatly at
different periods of adult life. In general, though with numerous
exceptions, a fleshy adult build is foreshadowed in plump build in
childhood.
11. Mass studies on adult build give a polygon of distribution which is
skew, the mode being toward the slenderer end of the polygon. There is
evidence of more than one mode, and hence that there are two or more
types of build. For purposes of description five classes of build are
recognized—very slender, slender, medium, fleshy, and very fleshy.
12. The diseases associated with very slender and slender build are:
tuberculosis, pneumonia, “nervousness,” melancholia. The diseases
associated with very fleshy or fleshy build are: diabetes, nephritis and
dropsy, apoplexy, and arterio-sclerosis and paralysis accompanying it;
also numerous diseases of the alimentary tract.
13. Fleshy parents have, on the average, in our data, larger families
than slender parents.
14. Regression toward mediocrity is less striking in the offspring of
slender than of fleshy parents, suggesting that fleshy parents carry not
only genes for fleshiness but also for slenderness, while slender parents
more rarely carry genes for fleshiness.
15. The offspring of two fleshy parents are twice as variable as those of
slender parents.
16. The hypothesis is indicated that genetically build is controlled
by multiple factors, with fleshiness tending slightly to dominate over
slenderness.
17. There is a marked tendency for persons of similar build (or with
potentialities for such) to intermarry. Dissimilar builds are selected
against.
18. Two slender parents of slender stock have rarely any progeny whose
index of build exceeds 2.2, or just above the upper limit of the slender
group. In general, the progeny of slender parents are relatively slightly
variable.
19. The slender parents are apparently of two kinds: those carrying
only one kind of factor for fleshy build and the other two such gametic
factors. The progeny of the former are very slightly variable; those of
the latter more variable.
20. By comparing coefficients of variability instead of indices, and
by making allowance for the greater range of the fleshy class than the
slender class, it still appears that the progeny of fleshy parents are
relatively and per unit range more variable than the progeny of slender
parents. Absolutely the offspring of the fleshy parents are, as stated,
twice as variable as of slender parents.
21. The matings of slender parents and fleshy parents of fleshy stock
yield a variable progeny, such as is typically found in the F₁ generation
when multiple factors are concerned. The variability is between that of
the progeny of slender matings and that of the progeny of fleshy matings.
22. The F₁ generation has not a mode of build that is intermediate
between that of the parental stocks, but one that is about the same as of
the fleshy matings. This is evidence of partial dominance of fleshiness.
23. The mating of two heterozygous (F₁) parents produces, in general, an
exceptionally variable progeny. This is one of the strongest evidences of
the presence of genetical factors in build.
24. Many, if not most, parents of medium build belong to biotypes with 1
or 2 independent factors for build. Consequently the progeny of medium ×
medium matings is often strikingly invariable.
25. The “back-cross” of a heterozygous parent with a slender parent, on
the one hand, or with a fleshy parent of fleshy stock, on the other,
gives a variable progeny, whose mode is shifted toward fleshiness; but
which shows a tendency to fall again into the slender (or fleshy) and
medium-fleshy grandparental types.
26. Variations in build are not to be accounted for merely by variations
in intake and out-go of calories, but also by the endogenous factors that
determine the “economy of nutrition” or the cost in energy of adding
an additional kilogram of weight to the body. The factors involved in
producing differences in these respects are hereditary factors.
27. The hereditary factors probably work through the intermediacy of
special organs that influence metabolism, notably the endocrine glands.
The latter thus intermediate between the chromosomal constitution, on the
one hand, and control of metabolic processes, on the other.
28. The number of factors involved in very fleshy build is, in some cases
at least, three independent ones. But the number is probably not the same
in all biotypes. Probably in some there is only one, in others four or
more.
29. The factors probably influence the functioning of the thyroid,
pituitary, and perhaps other glands.
APPENDIX.
I-XV. Tables of matings and progeny based on the original family
histories.
XVI. Indices of build, weight ÷ (stature)², for weights from 100 to 225
pounds and 45.4 to 102 kg.; statures from 55 to 78 inches and 140 to 198
cm.
XVII. Equivalent values of index of build by four different systems of
ratios between weight and stature, English system.
XVIII. To transmute the English system of index of build to the metric
system.
ABBREVIATIONS.
In top line of tables: F, father; M, mother; FF, father’s father; FM,
father’s mother, etc.
In body of tables: ca, cancer; E, epilepsy; F, fleshy; hf, heart failure;
I, insane; M-D, mania-depressive insanity; M, medium build; S, slender;
su, suicide; t, tuberculosis; V, very (slender, etc.); yg, young; † or d,
died; * refers to special families not included in the construction of
figure 7, or tables 11 and 12.
TABLE I.—_Very slender × very slender matings and their progeny._
This mating is not represented in our data. This table is nevertheless
indicated and numbered in order to secure the proper ordinal position of
the following tables.
TABLE II.—_Slender × very slender matings and their progeny._
+-----------+--------------+--------------+
| File | Male | Female |
| ref. | children. | children. |
+-----------+--------------+--------------+
|Cod 1 |26 |26 |
|*Fun |29 |28 |
|Jos 1 |39 |32 |
|*Leo |VS S S |27 S |
|Nob 1[12] |25 |26 23 |
|*Pal[13] | |43 VS[13] |
|Sch 37 |31 27 |30 29 |
+-----------+--------------+--------------+
+-----------+---+---+---+--------------+---+---+---+--------------+
| File | | | | Father’s | | | | Mother’s |
| ref. |F. |FF.|FM.| sibs. |M. |MF.|MM.| sibs. |
+-----------+---+---+---+--------------+---+---+---+--------------+
|Cod 1 |29 |35 |33 | |25 |30 |30 | |
|*Fun |27 |27 |29 |26 27 29 |25 |32 |27 |27 31 31 |
|Jos 1 |24 | | | |27 | | | |
|*Leo |VS | | | |S | | |2 S |
|Nob 1[12] |26 |M |M | |24 |M |M | |
|*Pal[13] |S |M |F |S F |VS |M |M | |
|Sch 37 |29 |29 |33±| |25 |27±|29t| |
+-----------+---+---+---+--------------+---+---+---+--------------+
Average build of parents (excluding families with *) 26.13
Number of matings: 4 + 3* = 7
Total number of progeny: 11 + 9* = 20
VS S M F
Classification of progeny 4 12 2 2
Proportional frequency per mille 200 600 100 100
[12] Four adolescents are all below standard weight but 1, who is 5
pounds above.
[13] An invalid.
TABLE III.—_Very slender × medium matings and their progeny._
+-----------+--------------+--------------+
| File | Male | Female |
| ref. | children. | children. |
+-----------+--------------+--------------+
|Ach 2 | |27 33 31 |
|Bic 1[14] | |29 33 32 |
|Gay 3 |32 |36 |
|Gru 1[15] | |30 33 |
|Hil 8[16] |34 |31 |
|Ise 2 |28 36 34 33 32|31 30 |
|Mil A |43 37 |33 22 31 42 |
|Wit 2[17] |33 29t |26 |
+-----------+--------------+--------------+
+-----------+---+---+---+--------------+---+---+---+--------------+
| File | | | | Father’s | | | | Mother’s |
| ref. |F. |FF.|FM.| sibs. |M. |MF.|MM.| sibs. |
+-----------+---+---+---+--------------+---+---+---+--------------+
|Ach 2 |32 |32 |33 | |25 |32 |27 | |
|Bic 1[14] |34 |29 |35 | |25 |M |VS |t, t, t, t |
|Gay 3 |35 | |t |I |24 |M |S | |
|Gru 1[15] |31 |M |M |t |24 |M |S | |
|Hil 8[16] |34 | |33 | |23 |28 | | |
|Ise 2 |31 |26 |31 | |23 |31 |27 | |
|Mil A |36 |39 |28 |S M F F F F |22 |35 |30 | |
|Wit 2[17] |33 |26 |M | |22 |M |t |t, t |
+-----------+---+---+---+--------------+---+---+---+--------------+
Average build of parents, 28.38
Total number of matings, 8
Total number of progeny, 28
VS S M F
Classification of progeny 1 7 17 3
Proportional frequency per mille 36 250 607 107
[14] F died, 39 years, pulmonary tuberculosis. M liable to tuberculosis
of throat and lungs.
[15] Female, 13 years, has already the build of her next older sister
(33?).
[16] F died, 39 years, tuberculosis.
[17] FM died, tuberculosis. M insane and tuberculous in middle life:
died, 51 years.
TABLE IV.—_Very slender × fleshy matings and their progeny._
+-----------+--------------+--------------+
| File | Male | Female |
| ref. | children. | children. |
+-----------+--------------+--------------+
|Hol A |32 40 34 33 27|46 34 25 29 |
|Kut 1[18] | |35 |
|Law A |41 |30 28 35 |
|Olm A |43 51 41 32 37|40 |
|Wat 5[19] |38 |27 33 32 33 |
+-----------+--------------+--------------+
+-----------+---+---+---+--------------+---+---+---+--------------+
| File | | | | Father’s | | | | Mother’s |
| ref. |F. |FF.|FM.| sibs. |M. |MF.|MM.| sibs. |
+-----------+---+---+---+--------------+---+---+---+--------------+
|Hol A |39 | | | |23 | | | |
|Kut 1[18] |43 |M |S | |24 |S |M | |
|Law A |43 |34 | | |24 |35 | |F M S M F |
|Olm A |38 |38 |34 |F |24 |34 |28 |M F |
|Wat 5[19] |37 | | | |25 | |S |4 S |
+-----------+---+---+---+--------------+---+---+---+--------------+
Average build of parents, 32.00
Number of matings, 5
Total number of progeny, 25
VS S M F VF
Classification of progeny 1 5 10 7 2
Proportional frequency per mille 40 200 400 280 80
[18] Tendency to tuberculosis on maternal side.
[19] FF had one sister who had at least three F children. Apparently
there is an F strain on Father’s side. MF had two sibs who were large and
tall. MM had both S and F close relatives; one sister was S.
TABLE V.—_Very slender × very fleshy matings and their progeny._
There is only one example of this mating described at page 97.
TABLE VI.—_Slender × slender matings and their progeny._
+-----------+--------------+--------------+
| File | Male | Female |
| ref. | children. | children. |
+-----------+--------------+--------------+
|Ada 4 |28 27 | |
|Bec 9 |30 |31 |
|Fel 1[20] |27 | |
|Hay 4[21] |29 |27 |
|Hay 12[22] |32 27 |M S |
|Hen 12 |32 28± |22 26± |
|Ker 5 |25 31 | |
|Law 4 |28 |25 |
|Law 7 | |32 |
|Lou 2 | |25 26 |
|McA 2 |28 29 |27 |
|McC 11 |33 |30 |
|Ran 4 |27 |27 25 |
|Sch 8 |30 32 | |
|Sco 5 |32 30 30 | |
|Shi 5 | |32 |
|*Smi |S |28 |
|Ste 9 |29 30 |29 S |
|Wil 23 |27 33 28 27 |29 |
|You 9[23] | |27 |
|A: 01-44 |29 | |
|A: 01-19 | |28 |
|A: 01-60 | |26 |
|A: 01-63 |27 | |
+-----------+--------------+--------------+