Search

To compare basal metabolic rate (BMR) calculated by the Harris-Benedict, Ravussin, Cunningham, World Health Organization (WHO) and Schofield equations to BMR determined in an obese pediatric population. The second objective is to derive a new equation, based on measured BMR in obese children, for calculating BMR in obese pediatric patients.The study included 110 (50 male/60 female) healthy obese subjects (BMI28) (11.7 +/- 2.8 years, 73 +/- 27 kg, 152 +/- 14 cm and 38 +/- 6% fat) who had preprandial BMR determined by indirect calorimetry. These results were compared to BMR calculated with the five above mentioned equations. Fat-free mass was determined by bioelectrical impedance and body composition was calculated using the appropriate equation. The age groups analyzed were as follows: males 3 to 10 and 11 to 18 years old; females 3 to 10 and 11 to 18 years old. A new equation was derived by stepwise multiple regression analysis using 100 randomly selected subjects from our test group and tested using the remaining 10 subjects.Basal metabolic rate calculated by the Ravussin and Cunningham equations in all subgroups was lower (p0.05) than measured BMR. Basal metabolic rate calculated by the Harris-Benedict equation was lower (p0.05) than measured BMR in male populations ages 3 to 10, 11 to 18, and in the entire cohort. Measured BMR was overestimated by the Harris-Benedict equation (p0.05) in females 11 to 18 years old; by the WHO equation (p0.05) in both male and females 3 to 10 years old and by the Schofield equation (p0.05) in males 11 to 18 years old. In comparison to measured BMR, the WHO equation appeared to be the most accurate for estimating BMR in males and females 11 to 18 years old. However, BMR calculating using our new equation in the 10 test subjects was similar to measured BMR.The WHO equation was the most accurate of the prediction equations studied. However, our new prediction equation may be more appropriate for calculating BMR in an obese pediatric population.

Nutritional dwarfing, a form of suboptimal nutrition, has been identified as a frequent cause of short stature and delayed sexual development in children. Retarded growth is an adaptive response to suboptimal nutrition.To assess whether recombinant human growth hormone (rhGH) may promote growth during various levels of suboptimal nutrition.Using a previously developed rat model of suboptimal nutrition, six groups of rats (six rats/group) were fed a balanced 1:1 carbohydrate:fat ratio diet for 4 weeks. Three of the groups were administered daily injections of rhGH (0.1 mg/100 g BW) subcutaneously in the back while the other three groups were kept as controls and were given similar dosages of normal saline solution (NSS). Restricted rats within each treatment group were pair fed 80 and 60% of the ad-libitum rats intake. Daily intake of the 80 and 60% fed groups were determined based on the intake of the ad-libitum fed groups. Serum IGF-I and insulin were determined after 4 weeks of dietary treatment by radioimmunoassay while IGFBP-3 was determined by an immunoradiometric assay. Body composition was assessed in all rats by carcass analysis.After 4 weeks, total weight gain and tail growth were higher (p0.05) in the rhGH treated group at 80 and 60% of-libitum energy intake. Serum levels of IGF-I and IGFBP-3 were higher (p0.05) in rhGH treated rats fed at 60% of ad-libitum. In comparison to the NSS groups, administration of rhGH in rats fed ad-libitum increased total body water. Energy restriction caused decreased fat percentage (p0.05) in both rhGH and NSS groups without differences among treated groups.These results suggest that the anabolic effects of rhGH may overcome mild to moderate energy restriction.

Background: A “cooling off” period (COP) of 40 days after MI and 90 days after coronary revascularization or non-ischemic CM (NICM) diagnosis is customary to allow clinical improvement prior to assessing the need for ICD implantation. The COP creates a clinical dilemma that requires balancing ongoing sudden death (SD) risk and the cost of potentially unnecessary ICD implants. We reviewed our wearable defibrillator (WD) experience to assess its clinical utility during this period of uncertainty. Methods: Medical records from 27 patients with EF≤35% requiring a COP who were offered WD (LifeVest, ZOLL Lifecor) were reviewed for clinical indication, EF before and after WD use, sudden cardiac arrest (SCA) or treated VT/VF, and subsequent outcome. Results: Wearable defibrillator indications were: recent MI (n=7), ischemic CM (ICM) with recent revascularization (n=10), untreated NICM (n=9), and tachycardia-CM (n=1). Twenty-five of 27 patients agreed to WD and 23 complied. Two patients had 3 clinical events: 1 (not wearing WD) was resuscitated from SCA; 1 (treated by WD) survived sustained syncopal VT/VF but later died suddenly not wearing the WD. One patient was shocked for AF. After the COP (n=24), 6/24 (25%) patients had EF>35% (3 ICM and 3 NICM) and no ICD was implanted. Eighteen of 24 (75%) had an EF ≤ 35% and received an ICD. Three of 24 (12.5%) patients that received an ICD ultimately had an EF ≥35% over continued follow-up. Conclusions: During the COP, patients with EF ≤ 35% had a 12% clinical event rate (3 events in 25 patients). WD protected patients during this high-risk period but non-adherence was associated with death/cardiac arrest. While ICD implantation was safely avoided in 25%, unnecessary ICD implantation still occurred. Prolonged WD therapy beyond the COP may be more prudent in some to observe for delayed recovery (12%). In patients with newly diagnosed LV systolic dysfunction or after revascularization, risk and recovery are in flux. We suggest that this continuum is not confined to the COP. In patients with low EF, prolonged application of WD may provide additional SD prevention beyond the initial high-risk period and may prevent unnecessary ICD implantation.

BackgroundEnergy and Zinc (Zn) deficiencies have been associated with nutritional related growth retardation as well as growth hormone (GH) resistance. In this study, the relationship between suboptimal energy and/or Zn intake and growth in rats and their response to immunoreactive exogenous recombinant human GH (GHi), was determined.ResultsRats treated with GHi and fed ad-libitum energy and Zn (100/100) had increased IGFBP-3 (p < 0.05) as compared with NSS (215 ± 23 vs. 185 ± 17 ng/ml) along with similar body weight gain. Rats treated with GHi and fed suboptimal energy and full Zn (70/100) had significantly increased weight gain (109.0 ± 18.2 vs. 73.8 ± 11.0 g) and serum IGF-I levels (568 ± 90 vs. 420 ± 85 ng/ml), along with decreased total body water (TBW; 61.0 ± 1.6 vs. 65.7 ± 2.1%) as compared to NSS controls. However, body weight gain was reduced (p < 0.05) as compared with rats fed ad-libitum energy. Growth hormone treated rats fed only suboptimal Zn (100/70), had increased weight gain (217.5 ± 13.2 vs. 191.6 ± 17.9 g; p < 0.05) compared to those given NSS. These rats gained weight in similar amounts to those fed full Zn. Rats treated with GHi and fed both suboptimal energy and Zn (70/70) showed similar results to those fed suboptimal energy with appropriate Zn (70/100), along with significant increases in IGFBP-3 levels (322 ± 28 vs. 93 ± 28 ng/ml). All restricted rats had reduced 24-h EE (kcal/100 g BW) and physical activity index (oscillations/min/kg BW) and GHi did not overcome these effects.ConclusionThese results suggest that GHi enhances weight gain in rats with suboptimal energy and Zn intake but does not modify energy expenditure or physical activity index. Suboptimal Zn intake did not exacerbate the reduced growth or decrease in energy expenditure observed with energy restriction.

Exogenous Growth Hormone (GH) Effects During Simultaneous Suboptimal Energy and Zinc Intake 477