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Biomedical subjects

S M Garn

Publications and source records attributed to S M Garn.

At least 19 recordsLinked to original sources

From the Miocene to olestra: a historical perspective on fat consumption.

Given the extraordinary dietary and geographic diversity of Pleistocene hominids, there is no single "Paleolithic diet" or average pre-Holocene fat intake. Even the Neanderthals initially were scavengers, possibly becoming seasonal hunters of large game at a later period. Fat intakes of greater than 20 g/day (11% of total caloric intake) developed after the domestication of mammals and then by selective breeding of genetically fatter animals in suitably temperate climates. By the late 1940s, the percent of fat in the diet rose to more than 40% in many Western countries (including France), decreasing somewhat to about 35% by the late 1980s in the United States, following reduced consumption of whole milk, fried meats, and other high-fat foods. Overall, fat reductions to less than 30% may be facilitated by no-fat or low-fat substitutes or texturizers or (perhaps more effectively) by increased intakes of fiber and calcium and greater reliance on fats that are poorly absorbed because of their stearate content.

Animals↗

Fractionating healthy weight.

Any discussion of healthy weight necessarily starts with body composition and its relation to long-term mortality and morbidity and then goes on to consider the limited range of ages for which we have epidemiologic data, the time span involved, the criteria used to define "healthy," and the possibility that a weight that is advantageous with respect to one outcome criterion may be disadvantageous for another. One may therefore ask, weight of what? healthy weight for whom? by what criteria? and question whether a simple weight-for-height ratio is sufficiently effective for the task.

Adult↗

Arch dimensional changes in children with idiopathic short stature treated with recombinant growth hormone: a five-year study.

Recombinant human growth hormone (rhGH) increases stature when administered to non-GH-deficient idiopathic short statured children. The aims of this investigation were to determine pretreatment arch dimensions of short statured children (height > or = 2 S.D. below mean for age) and to evaluate their response to rhGH administration by measuring arch-dimensional changes over 5 years of rhGH treatment. Dental casts of 28 short subjects (22 male, 6 female) and of age/gender-matched controls of normal stature were analyzed using a digital imaging system. Four measures of arch width and one of arch depth were calculated for each maxillary and mandibular cast. Subjects receiving orthodontic care were eliminated from the study at the initiation of treatment. Z-scores were calculated to allow for pooling of data. Prior to rhGH treatment, all arch dimensions of the short statured subjects were smaller than the controls, with the exception of mandibular arch depth. Arch dimensions of the rhGH subjects did increase with the continued administration of rhGH. The control group also showed a significant trend for the arch dimensions to increase over time. The influence of rhGH treatment on arch dimensional changes over time remains equivocal based on the results of this investigation.

Adolescent↗

The influence of growth hormone (rhGH) therapy on tooth formation in idiopathic short statured children.

The purpose of this preliminary study was to evaluate tooth formation in children with idiopathic short stature, before and during treatment with recombinant growth hormone (rhGH). Twenty-nine short-statured children ages 6 to 13 years were assigned into two treatment groups, an "experimental" group (n = 18), which received rhGH, and a "control" group (n = 11), which was observed for 1 year before commencing rhGH treatment. Clinical and radiographic records were obtained at the initial, year 1, and year 2 visits. Tooth formation and stature were assessed by calculating Z-scores, appropriate for the age and gender of each child. Delta-Z scores, which measure the change in Z-score over time, were also calculated between annual visits. Height was measured and recorded every 3 months, and Z-score statural norms for age and gender were derived from the 1977 National Center for Health Services national probability sampling. Tooth formation standards were derived from Moorrees et al. A matched control sample for tooth development was derived from untreated children. Tooth formation was initially delayed although the degree of reduction in stature exceeded the initial degree of delay in tooth formation. During this 2-year study, rhGH therapy had a significant influence on acceleration or gain in stature, but did not have a significant influence on tooth formation.

Adolescent↗

Carpo-metacarpal growth disturbance and the assessment of carpal narrowing in children with juvenile rheumatoid arthritis.

Second metacarpal length (M2), radio-metacarpal length (RM), and intermetacarpal width (W) were measured on 96 radiographs in 52 children with polyarticular juvenile rheumatoid arthritis (JRA), and compared with body height and skeletal maturation in order to: (1) differentiate between processes resulting in retardation of bone growth and those producing delay in skeletal maturation; (2) assess the severity and progression over time of such retardation; and (3) assess the impact of retardation of the second metacarpal on the assessment of carpal narrowing in children with JRA. All measurements were converted into z scores (the units of standard deviation above or below the normal mean for each measurement) based on published norms. Retardation of M2 (mean z scores -0.91) began earlier and was more severe compared with retardation of height (mean z score -0.25). This disproportion widened with increasing duration of disease. That this primarily represents a disturbance in M2 growth rather than a secondary effect due to altered maturation is suggested by the bone ages being normal (mean z score 0.14) and the absence of premature closure of the metacarpal physes. Z scores for RM/W (mean -3.53) were at least 1 Z more negative than for corresponding measurements of RM/M2 (mean -2.41) in 47 (90.4%) children and the mean difference between the z scores for RM/W was -1.12. This discrepancy between RM/W and RM/M2 was eliminated by correcting for the reduction in M2.

Adolescent↗

The juvenile-onset, adolescent-onset and adult-onset obese.

As shown in more than 8000 proband-parent pairs derived from a total-community sample and followed in longitudinal fashion, the 5-year incidence of obesity (new cases per 5-year period) approximates 8 percent for the juvenile-onset, adolescent-onset and adult-onset obese alike. Parents of juvenile-onset (ages 5-9), adolescent-onset (10-19) and adult-onset obese (20-39) tend to be of above-average fatness level, +0.25Z scores, overall, regardless of the age at onset of obesity in their progeny. Except for the parents of the juvenile-onset obese, educational level of the parents tends to be below average for the sample as a whole. These new data acquired in longitudinal context and explored in retrospective-prospective fashion do not substantiate the notion that different onset ages of obesity indicate separate etiologies and different family constellations.

Adolescent↗