Disordered eating is not associated with musculoskeletal injury in university athletes.

TAKE HOME MESSAGE: Musculoskeletal injuries and disordered eating are prevalent in varsity-level athletes but are not associated in our participants.

Postprandial peptide YY is lower in young college-aged women with high dietary cognitive restraint.

Acylated ghrelin and peptide YY (PYY3-36) are involved in appetite-regulation and energy homeostasis. These gastrointestinal hormones provide peripheral signals to the central nervous system to regulate appetite and short term food intake, and interact with leptin and insulin to regulate energy balance. Dietary restraint is an eating behavior phenotype that manifests as a conscious cognitive control of food intake in order to achieve or sustain a desired body weight. The purpose of the current study was to determine if college-aged women (18 to 25 years) with different eating behavior phenotypes, i.e., high vs normal dietary restraint, differ with respect to circulating concentrations of gastrointestinal hormones during and following a test meal. We hypothesized that women with high dietary cognitive restraint [High CR (score ≥ 13, n=13)] would have elevated active ghrelin and PYY3-36 concentrations after a test meal compared to women with normal dietary cognitive restraint [Normal CR (score < 13, n=30)]. Gastrointestinal hormones were assessed before (-15 and 0 min) and after (10, 15, 20, 30, 60, 90, 120 and 180 min) the consumption of a mixed composition meal (5.0 kcal per kg/body weight). In contrast to our hypothesis, mean PYY3-36 concentrations (p=0.042), peak PYY3-36 concentrations (p=0.047), and PYY3-36 area under the curve (p=0.035) were lower in the High CR group compared to the Normal CR group after controlling for body mass index. No group differences were observed with respect to acylated ghrelin before or after the meal. In conclusion, PYY3-36 concentrations were suppressed in the women with High CR compared to the women with Normal CR. While the current study is cross-sectional and cause/effect of high dietary restraint and suppressed PYY3-36 concentrations cannot be determined, we speculate that these women with high cognitive restraint may be prone to weight gain or weight re-gain related to the suppressed circulating PYY after a meal. Further investigations need to explore the relationship between dietary cognitive restraint, circulating PYY, and weight gain.

Estrogen and peptide YY are associated with bone mineral density in premenopausal exercising women.

BACKGROUND: In women with anorexia nervosa, elevated fasting peptide YY (PYY) is associated with decreased bone mineral density (BMD). Prior research from our lab has demonstrated that fasting total PYY concentrations are elevated in exercising women with amenorrhea compared to ovulatory exercising women. PURPOSE: The purpose of this study was to assess the association between fasting total PYY, average monthly estrogen exposure and BMD in non-obese premenopausal exercising women. METHODS: Daily urine samples were collected and assessed for metabolites of estrone 1-glucuronide (E1G) and pregnandiol glucuronide (PdG) for at least one menstrual cycle if ovulatory or a 28-day monitoring period if amenorrheic. Fasting serum samples were pooled over the measurement period and analyzed for total PYY and leptin. BMD and body composition were assessed by dual-energy X-ray absorptiometry. Multiple regression analyses were performed to determine whether measures of body composition, estrogen status, exercise minutes, leptin and PYY explained a significant amount of the variance in BMD at multiple sites. RESULTS: Premenopausal exercising women aged 23.8±0.9years with a mean BMI of 21.2±0.4kg/m(2) exercised 346±48min/week and had a peak oxygen uptake of 49.1±1.8mL/kg/min. Thirty-nine percent (17/44) of the women had amenorrhea. Fasting total PYY concentrations were negatively associated with total body BMD (p=0.033) and total hip BMD (p=0.043). Mean E1G concentrations were positively associated with total body BMD (p=0.033) and lumbar spine (L2-L4) BMD (p=0.047). The proportion of variance in lumbar spine (L2-L4) BMD explained by body weight and E1G cycle mean was 16.4% (R(2)=0.204, p=0.012). The proportion of variance in hip BMD explained by PYY cycle mean was 8.6% (R(2)=0.109, p=0.033). The proportion of variance in total body BMD explained by body weight and E1G cycle mean was 21.9% (R(2)=0.257, p=0.003). CONCLUSION: PYY, mean E1G and body weight are associated with BMD in premenopausal exercising women. Thus, elevated PYY and suppressed estrogen concentrations are associated with, and could be directly contributing to, low BMD in exercising women with amenorrhea, despite regular physical activity.

High prevalence of subtle and severe menstrual disturbances in exercising women: confirmation using daily hormone measures.

BACKGROUND: The identification of subtle menstrual cycle disturbances requires daily hormone assessments. In contrast, the identification of severe menstrual disturbances, such as amenorrhea and oligomenorrhea, can be established by clinical observation. The primary purpose of this study was to determine the frequency of subtle menstrual disturbances, defined as luteal phase defects (LPD) or anovulation, in exercising women, with menstrual cycles of 26-35 days, who engage in a variety of sports, both recreational and competitive. Secondly, the prevalence of oligomenorrhea and amenorrhea was also determined via measurement of daily urinary ovarian steroids rather than self report alone. METHODS: Menstrual status was documented by daily measurements of estrone and pregnanediol glucuronide and luteinizing hormone across two to three consecutive cycles and subsequently categorized as ovulatory (Ovul), LPD, anovulatory (Anov), oligomenorrheic (Oligo) and amenorrheic (Amen) in sedentary (Sed) and exercising (Ex) women. RESULTS: Sed (n = 20) and Ex women (n = 67) were of similar (P > 0.05) age (26.3 +/- 0.8 years), weight (59.3 +/- 1.8 kg), body mass index (22.0 +/- 0.6 kg/m2), age of menarche (12.8 +/- 0.3 years) and gynecological maturity (13.4 +/- 0.9 years). The Sed group exercised less (P < 0.001) (96.7 +/- 39.1 versus 457.1 +/- 30.5 min/week) and had a lower peak oxygen uptake (34.4 +/- 1.4 versus 44.3 +/- 0.6 ml/kg/min) than the Ex group. Among the menstrual cycles studied in the Sed group, the prevalence of subtle menstrual disturbances was only 4.2% (2/48); 95.8% (46/48) of the observed menstrual cycles were ovulatory. This finding stands in stark contrast to that observed in the Ex group where only 50% (60/120) of the observed menstrual cycles were ovulatory and as many as 50% (60/120) were abnormal. Of the abnormal cycles in the Ex group, 29.2% (35/120) were classified as LPD (short, inadequate or both) and 20.8% (25/120) were classified as Anov. Among the cycles of Ex women with severe menstrual disturbances, 3.5% (3/86) of the cycles were Oligo and 33.7% (29/86) were Amen. No cycles of Sed women (0/20) displayed either Oligo or Amen. CONCLUSIONS: This study suggests that approximately half of exercising women experience subtle menstrual disturbances, i.e. LPD and anovulation, and that one third of exercising women may be amenorrheic. Estimates of the prevalence of subtle menstrual disturbances in exercising women determined by the presence or absence of short or long cycles does not identify these disturbances. In light of known clinical consequences of menstrual disturbances, these findings underscore the lack of reliability of normal menstrual intervals and self report to infer menstrual status.

O2 uptake and muscle deoxygenation kinetics during the transition to moderate-intensity exercise in different phases of the menstrual cycle in young adult females.

O(2) uptake (VO2) kinetics were examined during the follicular (F) and luteal (L) phases of the menstrual cycle to determine if there was an effect of altered sex hormones on the (VO2) response to moderate-intensity exercise. Seven healthy women (age 21 +/- 2 years; mean +/- SD) performed six transitions from 20 W to moderate-intensity exercise (approximately 90% theta L) during the F and L phase. VO2 was measured breath-by-breath and deoxyhemoglobin/myoglobin (Delta HHb) was determined by near infrared spectroscopy. Progesterone and estrogen were significantly (P < 0.05) elevated during the L compared to F phase. VO2 kinetics (tau VO2) were not different in the two phases of the menstrual cycle (F, 22 +/- 5 s; L, 22 +/- 6 s; 95% confidence intervals +/-4 s) nor was the time course of the Delta HHb response (F, TD 11 +/- 2 s, tau 11 +/- 3 s; L, TD 12 +/- 2 s, tau 12 +/- 11 s; tau HHb 95% confidence intervals +/-3 s). Respiratory exchange ratio (RER) was not different between phases for baseline or steady-state exercise and the blood lactate response to exercise was not different. In conclusion, VO2 kinetics at the onset of moderate-intensity exercise are not affected by the phase of the menstrual cycle in young females suggesting either no change in, or no effect of metabolic activation on the on-transient kinetics of moderate-intensity exercise. Additionally, the similar adaptation of Delta HHb in combination with unchanged VO2 suggests that there were no differences in the adaptation of local muscle O(2) delivery.

Depressive symptoms in mid-pregnancy, lifetime stressors and the 5-HTTLPR genotype.

Few studies of gene-environment interactions for the serotonin transporter promoter polymorphism (5-HTTLPR), life stressors and depression have considered women separately or examined specific types of stressful life events. None have looked at depression during pregnancy. In the Pregnancy Outcomes and Community Health (POUCH) Study, women were queried about history of stressful life events and depressive symptoms at the time of enrollment (15-27 weeks gestation). Stressful life events were grouped a priori into "subconstructs" (e.g. economic, legal, abuse, loss) and evaluated by subconstruct, total subconstruct score and total stressful life event score. The effect of genotype on the association between stressful life events and elevated depressive symptoms was assessed in 568 white non-Hispanic participants. The relationship between exposure to abuse and elevated depressive symptoms was more pronounced in the s/s group (OR = 24.5) than in the s/l group (OR = 3.0) and the l/l group (OR = 7.7), but this significant interaction was detected only after excluding 73 (13%) women with recent use of psychotropic medications. There was no evidence of gene-environment interaction in analytic models with other stressful life events subconstructs, total subconstruct score or total stressful life events score. These data offer modest support to other reports of gene-environment interaction and highlight the importance of considering specific stressful life events.

Effect of repeated boluses of intravenous omeprazole and primed infusions of ranitidine on 24-hour intragastric pH in healthy human subjects.

The aim of this study was to identify dosage regimens using intravenous omeprazole and ranitidine that would elevate and consistently maintain intragastric pH > 6 in the first 24 hr of therapy. In 19 healthy, fasting human subjects using continuous 24-hr gastric pH-metry, we studied two dosages of primed infusions of ranitidine (50 mg bolus followed by infusion of either 3 or 6 mg/kg body wt/24 hr) and six regimens of intravenous omeprazole (80-200 mg in 24 hr in two to five boluses). Only the two ranitidine infusions and high doses of omeprazole (> or = 160 mg/day as four or five boluses) raised the intragastric median pH above 5.4. There was no significant difference in the median intragastric pH after high dose ranitidine and high doses of omeprazole. Considerable interindividual variation in intragastric pH was observed after omeprazole therapy. The percentage of intragastric pH > 6.0 during the 24-hr study was lower after omeprazole (35-42%) than after high-dose ranitidine (58%). We conclude that it is possible to raise intragastric pH > 6.0 by use of either primed ranitidine infusion or by repeated boluses of omeprazole. However, maintenance of this high pH in the first 24 hr is difficult with both, more so with omeprazole.

Risk assessment of antibiotic residues of beta-lactams and macrolides in food products with regard to their immuno-allergic potential.

In human medicine drug allergy is a well-established side-effect of the therapeutic use of antibiotics, especially the beta-lactams. Side-effects caused by macrolides are uncommon and only a very few of these seem to be caused by allergic mechanisms. Clinically, drug allergy is characterized by a spectrum of reactions ranging from mild skin rashes to angio-oedema or life-threatening anaphylaxis. Concern has been expressed that antibiotic residues in meat and other foods might be responsible for similar hypersensitivity reactions in a small number of individuals. This review assesses the potential risk of such reactions in general, but focuses on allergy to penicillin and macrolide residues in particular. In relation to the risk of primary sensitization, it is unlikely that residues could contribute to the overall immune response in view of the very low levels that are likely to be encountered in comparison with the high levels received during therapeutic use. No evidence has been found that any individual has become sensitized by residues of either penicillins or macrolides. Furthermore, the oral route is much less sensitizing than parenteral administration and immunochemical studies with penicillin indicate that hapten-protein complexes formed in vivo are unlikely to be immunogenic because of their low dose, low epitope density and binding to autologous carrier proteins. For performed allergens, the epitope density was also too low to be immunogenic. Because of the ubiquitous nature of penicillin-producing moulds in nature and the extensive use of beta-lactam antibiotics in human medicine, it is unlikely that epidemiological studies could be undertaken that could allow quantification of the minimal risk. The risk of allergic reactions in pre-sensitized individuals can be assessed similarly and again it is concluded that factors such as dose, oral administration and low epitope density make it unlikely that a significantly antigenic derivative could be formed. However, a review of the literature on penicillin hypersensitivity revealed a very small number of previously sensitized individuals from whom there is reasonable clinical and documentary evidence that penicillin residues in milk triggered an allergic reaction, usually a rash. Although these cases are very rare (less than 10 cases reported in the last 25 years), they illustrate the continuing need to control antibiotic residues vigilantly. Animal models have not proved useful for predicting the risk of hypersensitivity reactions to drugs, since allergy in man is determined by genetic and other factors and no validated methods exist to determine a no-effect level.(ABSTRACT TRUNCATED AT 400 WORDS)

Use of PCR amplification of cDNA to study mechanisms of human cell mutagenesis and malignant transformation.

PCR is widely employed to amplify short segments of genomic DNA to determine if a specific change has occurred. But some investigators need to sequence the entire coding region of mammalian genes to determine what specific changes have occurred. In 1989, we [Yang et al: Gene 83:347-354] described a method to copy mRNA of the hypoxanthine (guanine) phosphoribosyl transferase (HPRT) gene directly from the lysate of a clone of 6-thioguanine-resistant mutant diploid human fibroblasts without the need for RNA extraction or DNA template purification. To avoid detecting random changes introduced by polymerases, 100 to 500 cells from an individual clone, each containing the identical mutation, are lysed and the cDNA is amplified 10(10)-to 10(11)-fold to obtain 5 to 10 micrograms of DNA. The consensus sequence of the cDNA is determined by direct nucleotide sequencing. Using this method, we have investigated the kinds of mutations induced by carcinogens in the coding region of the HPRT gene and their location in the gene and examined the role of DNA repair in this process. Normal repair-proficient human cells and cells deficient in DNA repair were exposed to mutagens in exponential growth or synchronized and exposed at the beginning of S phase or in G1 phase several hr prior to DNA replication. The kinds and location of mutations in the HPRT gene were determined and knowledge of the nature of the DNA lesions formed by the various mutagens allowed assignment of the DNA strand in which the premutagenic lesion that gave rise to the mutation had been located. Related assays involving PCR have been used to determine the nature of mutations in the coding region of the H-, N-, or K-ras genes of tumor-derived malignant human cells and to determine whether or not such cells express specific growth factor genes.

Induction of mitochondrial metabolism and pH-modulated ammoniagenesis by rocking LLC-PK1 cells.

In an effort to find a model system in which the regulation of renal ammoniagenesis could be delineated, the LLC-PK1 line of cultured pig kidney epithelial cells was examined. Ammonia production by normally cultured LLC-PK1 cells (monolayers on 75-cm2 flasks, under 6 ml still serum-containing medium) was found to be neither modulated by direct (3 h) nor adapted by chronic (3 day) manipulation of medium pH (production at pH 7.05, 7.40, or 7.60 not significantly different). Considering that the mitochondrial glutamine to alpha-ketoglutarate pathway is the major regulatory site of ammoniagenesis, and that mitochondrial metabolism might be restricted under the normal lactate-generating or hypoxic culture conditions, we examined ammonia production by rocked flasks of LLC-PK1 cells. Flask were rocked continually at a rate of 2.5 oscillations/min, thereby exposing the cells to the atmosphere 40-50% of the time and also maximizing medium O2 tension and nutrient-waste exchange. Mitochondrial enzyme activities in rocked LLC-PK1 cells were shown to be consistently 1.5-fold greater than those in normally cultured cells. Ammonia production by rocked cells was not only directly modulated by short incubations with low and high pH media (production at pH 7.05 greater than 7.40 greater than 7.60) but was adapted by chronic (3 day) manipulations of medium pH (16 h after return to pH 7.40 medium production by pH 7.05- greater than 7.40- greater than 7.60-adapted cells). Thus rocker culture of the LLC-PK1 cell line both induces mitochondrial metabolism and converts cellular ammoniagenesis to a pH-sensitive phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)