LETTERS
Dear
with
Sir:
Experimentation using human subjects is difficult at best. Nevertheless, conclusions from experiments with humans must meet the same tests as experiments with any other animal. When the numbers and uniformity of subjects are limited, and controls impossible, the data should be presented modestly and conclusions adequately hedged. The paper by Friedman and Goldberg (1) is an inadequate test of the theory that a high cholesterol intake during development of the mammal establishes the balance in enzyme systems for control of serum cholesterol concentration in the adult. In humans such systems could require perturbation for 3 years or longer for irreversible adverse development, not 4 months. Furthermore, since few teen-agers (15-19 years), except those with familial hypercholesterolemia, have high risk levels of serum cholesterol even on a high-cholesterol diet, the failure of the authors’ subjects to demonstrate adult hypercholesterolemia is predictable. The value of approximately 155 mg/lOO ml for both groups is not surprising in such juveniles, since the control system does not seem to break down until the third decade or so. Although the first impression is that this is a longitudinal study, more careful perusal makes it appear that different children represented each age group, though this is not clear. It is certainly true of the 15- to 19-year-old group (Table 2 of (1)) which admittedly did not even have the same dietary history as the younger groups. Statistics do not correct for this because of the small numbers involved. The authors do not know how carefully the mothers controlled the cholesterol intake of the children, simply saying that “egg yolks were discouraged.” We are not even sure of the difference in cholesterol intake of the two groups during the 4.month suckling period since the volumes of milk and amounts during that period babies may have milk per day while
of nonmilk food consumed are unknown. The bottle-fed received a fixed volume of no one knows how much the
TI-IF
EDITOR
breast-fed babies got. It may have been much less than the bottle-fed by some and more by others. There may not even have been much difference in total cholesterol intake. As pointed out above, the 15- to l9-year-olds admittedly had unknown infant dietary antecedents. The data on two children, one 3.5 and one 5.5 years old, who were breast-fed for 19 and 37 months, respectively, only add uncertainty since they must be considered independently of the other groups. The authors assume unjustifiably that the breast milk was high ill cholesterol. To publish these fragmentary data, improperly controlled, would only add to the confusion of a subject already overburdened with very questionable conclusions from improperly designed reports, misleading people to assume that unsolved problems are settled. Raymond Reiser Distinguished Professor Department of Biochemistry Texas A&M University College Station, Texas 77843
& Biophysics
Reference 1.
FRIEDMAN, G., AND S. J. GOLDBERG. rent and subsequent serum cholesterols and formula-fed infants. Am. J. Clin. 42-45, 1975.
Protein-calorie nonhuman Dear
deficiency primates
Concurof breast Nutr. 28:
in
Sir,
In the most interesting article by Dr. C. 0. Enwonwu and co-workers on ‘Protein-energy deficiency in nonhuman primates: biochemical and morphological alterations” (Am. J. Clin. Nutr. 26: 1287, 1973), figure 2 is described as “liver section from protein-calorie-deficient monkey showing profound replacement of the cytoplasmic content with fat In fact, what this photomicrograph shows is the typical picture of a liver loaded with glycogen, with no excess fat. Fatty infiltration gives a completely different appearance: com.
.
.“.
Downloaded from https://academic.oup.com/ajcn/article-abstract/28/1/2/4716311 by East Carolina University Health Sciences Library user on 10 January 2019
Experimentation human subjects
TO
Dear
with
Sir:
Experimentation using human subjects is difficult at best. Nevertheless, conclusions from experiments with humans must meet the same tests as experiments with any other animal. When the numbers and uniformity of subjects are limited, and controls impossible, the data should be presented modestly and conclusions adequately hedged. The paper by Friedman and Goldberg (1) is an inadequate test of the theory that a high cholesterol intake during development of the mammal establishes the balance in enzyme systems for control of serum cholesterol concentration in the adult. In humans such systems could require perturbation for 3 years or longer for irreversible adverse development, not 4 months. Furthermore, since few teen-agers (15-19 years), except those with familial hypercholesterolemia, have high risk levels of serum cholesterol even on a high-cholesterol diet, the failure of the authors’ subjects to demonstrate adult hypercholesterolemia is predictable. The value of approximately 155 mg/lOO ml for both groups is not surprising in such juveniles, since the control system does not seem to break down until the third decade or so. Although the first impression is that this is a longitudinal study, more careful perusal makes it appear that different children represented each age group, though this is not clear. It is certainly true of the 15- to 19-year-old group (Table 2 of (1)) which admittedly did not even have the same dietary history as the younger groups. Statistics do not correct for this because of the small numbers involved. The authors do not know how carefully the mothers controlled the cholesterol intake of the children, simply saying that “egg yolks were discouraged.” We are not even sure of the difference in cholesterol intake of the two groups during the 4.month suckling period since the volumes of milk and amounts during that period babies may have milk per day while
of nonmilk food consumed are unknown. The bottle-fed received a fixed volume of no one knows how much the
TI-IF
EDITOR
breast-fed babies got. It may have been much less than the bottle-fed by some and more by others. There may not even have been much difference in total cholesterol intake. As pointed out above, the 15- to l9-year-olds admittedly had unknown infant dietary antecedents. The data on two children, one 3.5 and one 5.5 years old, who were breast-fed for 19 and 37 months, respectively, only add uncertainty since they must be considered independently of the other groups. The authors assume unjustifiably that the breast milk was high ill cholesterol. To publish these fragmentary data, improperly controlled, would only add to the confusion of a subject already overburdened with very questionable conclusions from improperly designed reports, misleading people to assume that unsolved problems are settled. Raymond Reiser Distinguished Professor Department of Biochemistry Texas A&M University College Station, Texas 77843
& Biophysics
Reference 1.
FRIEDMAN, G., AND S. J. GOLDBERG. rent and subsequent serum cholesterols and formula-fed infants. Am. J. Clin. 42-45, 1975.
Protein-calorie nonhuman Dear
deficiency primates
Concurof breast Nutr. 28:
in
Sir,
In the most interesting article by Dr. C. 0. Enwonwu and co-workers on ‘Protein-energy deficiency in nonhuman primates: biochemical and morphological alterations” (Am. J. Clin. Nutr. 26: 1287, 1973), figure 2 is described as “liver section from protein-calorie-deficient monkey showing profound replacement of the cytoplasmic content with fat In fact, what this photomicrograph shows is the typical picture of a liver loaded with glycogen, with no excess fat. Fatty infiltration gives a completely different appearance: com.
.
.“.
Downloaded from https://academic.oup.com/ajcn/article-abstract/28/1/2/4716311 by East Carolina University Health Sciences Library user on 10 January 2019
Experimentation human subjects
TO
