Welfare reform consequences for children: the Wisconsin experience.

BACKGROUND: The Temporary Assistance to Needy Families, enacted under the Personal Responsibility and Work Opportunity Reconciliation Act of 1996, is a reality for many working families. As public policies are enacted, unintended consequences for infants/children must be minimized. Child advocates in Wisconsin, leading this nation in reforming Aid to Families with Dependent Children (AFDC), are concerned about supporting eligible infants/children as safety-net programs are unlinked. OBJECTIVE: This study reviews the enrollment status of 4 linked programs over time in Wisconsin, from January 1995 to August 1998. Eligible infants/children in programs, such as Medicaid/AFDC, Medicaid/Healthy Start, and Food Stamps, were analyzed and compared with enrollment in Special Supplemental Nutrition Program for Women, Infants/children (WIC), a nonlinked program. DESIGN: A cross-sectional analysis of monthly enrollment for infants/children was subdivided into 3 periods: prewelfare reform or AFDC (January 1, 1995 to December 31, 1995), the welfare reform pilot or Pay For Performance (January 1, 1996 to August 31, 1997), and welfare reform better known as Wisconsin Works (W-2), (September 1, 1998 to August 31, 1998), periods 1, 2, and 3, respectively. PARTICIPANTS: Infants/children in Wisconsin from birth to 18 years of age enrolled in W-2 and/or other safety-net programs were monitored: AFDC or W-2, WIC, Food Stamps, Medicaid/AFDC, and Medicaid/Healthy Start. RESULTS: The average number of infants/children removed from AFDC and Medicaid/AFDC during periods l and 2 were -1210 increasing to -3128 per month, respectively, almost tripling the rates of decline during the pilot period (see ). By the end of this study, >100 000 (111 198) infants/children were removed from AFDC/W-2 enrollment and 51 559 fewer infants/children benefited from Medicaid. This rate of decline slowed during period 3, averaging -687 per month, while W-2 enrollment continued to decline significantly at a rate of -2692 per month. In contrast, Medicaid/Healthy Start enrollment, targeted to infants/children <6 years of age, increased significantly over all periods by +332, +1327, and +266, respectively. Food Stamps enrollment also declined throughout all 3 consecutive periods, -603, -2462, and -1450, respectively. However, enrollment in the WIC program did not decline significantly to the same degree as other certification-linked programs with AFDC or W-2, as indicated by the consecutive slopes of -60, -111, and -183, respectively. CONCLUSION: Wisconsin infants/children were rapidly removed from welfare rolls in unprecedented numbers during the periods January 1995 and August 1998. Comparisons of periods before W-2 implementation and 1 year after implementation support the fact that certification-linked programs, such as Medicaid and Food Stamps, were sufficiently aligned to AFDC/W-2 to significantly impact infants/children enrollment. Historically, WIC certification in Wisconsin has not been linked to AFDC, and infants/children traditionally eligible for Medicaid and Food Stamps are also eligible for WIC. Yet, contrary to the AFDC-linked safety-net programs, declines in WIC enrollment were not statistically significant during all study periods. Statewide and local interventions within Wisconsin, such as outreach activities, targeted to Medicaid/Healthy Start and more recently Title XXI (State Children Health Insurance Program), slowed the reductions of Medicaid enrollment for Wisconsin infants/children. These findings support that altering safety-net programs can result in unintended consequences if not carefully transitioned as demonstrated in Wisconsin welfare reform.

Transcription of the amylin gene in newborn dogs.

To understand the role of amylin, the novel pancreatic hormone, in fuel metabolism of neonatal mammals, the transcription of the amylin gene in newborn dogs was studied under different conditions, such as fasting, hyperinsulinemia, and hyper IGF-1. Our results showed (1) The amylin mRNA level decreased during a 24-h fasting period after birth, 59.1 +/- 4.5% at 4 h, 80.1 +/- 7.9% at 10 h, and 44.5 +/- 3.0% at 24 h, compared to 0-h-fasted controls, respectively. In this period, the decreased mRNA level of the amylin gene and the increased mRNA levels of the gluconeogenic genes showed an inverse ratio relationship. (2) Euglycemic hyperinsulinemic clamp did not alter the amylin mRNA level, 39.6 +/- 1.2% (hyperinsulinemia) vs 41.4 +/- 3.1% (controls), in newborn dogs, but lowered the amylin mRNA by 35.3%, 64.7 +/- 12.5% vs 100.0 +/- 12.0%, in adult dogs. (3) Euglycemic hyper-IGF-1 clamp had no effect on the amylin mRNA levels of either newborn or adult dogs, 52.4 +/- 9.1% (hyper IGF-1) vs 47.9 +/- 4.3% (controls) in newborns and 95.2 +/- 12.6% (hyper IGF-1) vs 100.0 +/- 14.0% (controls) in adults. The data from the present study showed that amylin may be involved in carbohydrate homeostasis, but may not be able to stimulate gluconeogenesis in newborn dogs during a 24-h fasting period after birth. Whether amylin action may be another mechanism for neonatal hyperglycemia by inducing insulin resistance in peripheral tissues needs further investigation.

Insulin resistance and the transcription of the glucose-6-phosphatase gene in newborn dogs.

In the present report changes in the mRNA level of glucose-6-phosphatase (G6Pase; EC 3.1.39) in newborn and adult dogs in vivo were studied to further test the hypotheses that neonatal hyperglycemia may be due to unsuppressed gluconeogenesis by insulin and that the antidiabetic role of insulin-like growth factor-1 (IGF-1) may be intact in newborn dogs who have consistently demonstrated insulin resistance. Our results were the following: (i) Both renal and hepatic G6Pase mRNA were expressed at birth and increased with time during a 24-h period of fasting after birth. (ii) The renal G6Pase mRNA levels in newborn dogs did not respond to either insulin or epinephrine. (iii) Hyperinsulinemia lowered the liver G6Pase mRNA by only 16.3% in newborn dogs, but reduced the liver G6Pase mRNA to an undetectable level in adult dogs. (iv) Hyperglycemia decreased the hepatic G6Pase mRNA by 14.3% in newborn dogs under hyperinsulinemia. (v) Infused epinephrine did not elevate the hepatic G6Pase mRNA level in newborn dogs in the presence of hyperglycemia and hyperinsulinemia. (vi) In newborn dogs, hyper-IGF-1 rapidly reduced the hepatic G6Pase mRNA level by 50%, and hypoglycemia was unable to elevate the hepatic G6Pase mRNA level under the hyper-IGF-1. We concluded that the reduced rate of suppression of transcription of the liver G6Pase gene by insulin in newborn dogs may reflect the unsuppressed neonatal hepatic gluconeogenesis due to insulin resistance and that the physiological roles of IGF-1 seemed to be intact in newborn dogs and may be not responsible for neonatal hyperglycemia.

Developmental aspects of transcription of fructose-1,6-bisphosphatase in newborn dogs.

Our previous investigations demonstrated that unsuppressed gluconeogenesis under hyperinsulinemia in newborn dogs may be a mechanism of neonatal hyperglycemia. In the present study, the transcription of the gene for fructose-1,6-bisphosphatase (fru-1,6-P2ase; E 3.1.3.11) of newborn dogs was studied under various metabolic perturbations (age, suckling, fasting, and hyperinsulinemia). Total RNAs isolated from livers and kidneys were hybridized with a rat fru-1,6-P2ase cDNA probe. We observed that (i) fru-1,6-P2ase mRNA was expressed in both kidney and liver at birth and was about 40 and 80% of those in kidney and liver of adult dog, respectively; (ii) suckling decreased the kidney fru-1,6-P2ase mRNA level to 77.8 +/- 1.7% (24 h) from 100.0 +/- 8.0% (4 h), but increased liver mRNA to 158.6 +/- 11.4% (24 h) from 100.0 +/- 2.3% (4 h); (iii) during a 24-h period of fasting, the kidney fru-1,6-P2ase mRNA level did not change in the first 10 h and then increased 18.5% at 24 h, whereas the liver fru-1,6-P2ase mRNA increased ca. 20% during the first 10 h and then up to 161.1 +/- 18.0% at 24 h compared to that at 100.0 +/- 11.4% (0 h); (iv) euglycemic hyperinsulinemia did not change the renal fru-1,6-P2ase mRNA level, but lowered the hepatic fru-1,6-P2ase mRNA level to 56.0 +/- 8.7 from 100.0 +/- 11.8% (fasted controls) in newborn dogs, which was identical to that in adult dogs. These data suggest that the fru-1,6-P2ase in liver may play a more important role in glucose homeostasis of newborn dogs than that in kidney during the first day of their lives and that the incomplete suppression of transcription of the hepatic fru-1,6-P2ase gene by insulin in newborn dogs may not contribute to neonatal hyperglycemia due to insulin resistance.

Hyponatremic seizures secondary to oral water intoxication in infancy: association with commercial bottled drinking water.

In recent years, hyponatremic seizures resulting from water intoxication have been reported in the United States with an increasing frequency that some have likened to an epidemic. Infants of parents living in poverty and uninformed of the risks of feeding fluids other than infant formula to their babies are particularly at risk. Young infants with vomiting and diarrhea are especially prone to developing hyponatremia if fed fluids lacking sufficient sodium, but even those who are otherwise well may develop symptomatic hyponatremia as a result of being fed excess solute-free water. Most often tap water, either in the form of supplemental feedings or overly dilute formula, has been given in excessive amounts over relatively short periods of time. Less frequently, water in other forms such as juice, soda, or tea has been implicated. This report includes the cases of two infants treated at our institution for hyponatremic seizures and water intoxication after being fed with the same bottled drinking water product marketed for use in infants. The medical records of all infants

Differential effects of insulin-like growth factor-1 on neonatal canine gene expression.

To determine the effects of insulin-like growth factor-1 (IGF-1) and amylin on glucose homeostasis in vivo in newborn dogs, euglycemic hyper-IGF-1 clamps and hypoglycemic hyper-IGF-1 clamps were performed in newborn dogs. Northern blotting and radioimmunoassays were used to study the effects of the infused IGF-1 and/or hypoglycemia on the mRNA expression of the genes for phosphoenolpyruvate carboxykinase (PEPCK) and on the expression of the amylin gene in newborn dogs. Our results were that (1) Infused IGF-1 (plasma IGF-1 >/=1000 ng/ml) rapidly lowered the plasma glucose level, and 120 +/- 38 mg glucose/pup was co-infused during a 105-min clamp to maintain the plasma glucose at the basal level. (2) The infused IGF-1 rapidly reduced the liver cytosolic mRNA for the PEPCK gene to an almost undetectable level. (3) Hyper-IGF-1 had no effect on mRNA level of the amylin gene in pancreas, 106.7 +/- 14.2% vs 100.0 +/- 5.9% (controls), or on plasma amylin concentration, 56. 0 +/- 5.7 pg/ml vs 52.1 +/- 5.7 pg/ml (basal). (4) The amylin mRNA level, 127.8 +/- 3.9% vs 100.0 +/- 5.9% (controls) (P = 0.017), and the plasma amylin concentration, 132.3 +/- 18.3 pg/ml vs 110.0 +/- 10.8 pg/ml (controls) (P = 0.371), showed a parallel stimulation by hypoglycemia in the presence of hyper-IGF-1. We concluded that (1) IGF-1 acutely suppressed cytosolic PEPCK gene expression in liver of newborn dogs. (2) IGF-1 does not effect the expression of the pancreatic amylin gene. (3) Amylin may be involved in glucose homeostasis in newborn dogs and may play a role as a counterregulatory factor during the neonatal period. Unsuppressed amylin production may contribute to neonatal hyperglycemia.

Transcription of hepatic cytosolic phosphoenolpyruvate carboxykinase gene in newborn dogs.

Physiological studies hypothesized that unsuppressed gluconeogenesis by insulin in newborn dogs may be a mechanism responsible for neonatal hyperglycemia. In the present study, we determined the effects of fasting and the infusion of insulin, glucose, and/or epinephrine on the liver cytosolic mRNA levels of the gene for the key regulatory enzyme of gluconeogenesis, phosphoenolpyruvate carboxykinase PEPCK (PEPCK; EC 4.1.1.32), in newborn dogs in vivo to further test the hypothesis. We observed the following: (i) Fasting increased the hepatic PEPCK mRNA level in newborn dogs. The hepatic PEPCK mRNA level was not detectable at birth; the PEPCK mRNA level at 4 h was arbitrarily determined as 100.0 +/- 27.8%, was 108.1 +/- 18.4% at 10 h, and stayed at the same level at 24 h (109.1 +/- 8.2). (ii) Euglycemic hyperinsulinemia did not significantly reduce the hepatic PEPCK mRNA levels in newborn dogs; however, the same treatment resulted in the repression of the liver PEPCK mRNA to undetectable levels in adult dogs. (iii) Under hyperinsulinemia, a moderate hyperglycemia lowered the liver PEPCK mRNA in newborn dogs to undetectable levels. (iv) In newborn dogs, despite the presence of hyperinsulinemia and hyperglycemia, the infused epinephrine was still able to elevate the liver PEPCK mRNA from undetectable levels to 79% of the control levels. We suggest that unsuppressed neonatal gluconeogenesis in the presence of hyperinsulinemia may be evidence of insulin resistance in newborn dogs and that the stimulatory effect of epinephrine on gluconeogenesis overriding insulin and glucose in the liver of the newborn dogs may be a mechanism for inducing neonatal hyperglycemia.

Effects of insulin, epinephrine, and glucose on regulation of transcription of the serine dehydratase gene in newborn dogs.

Our previous investigation showed that hyperinsulinemia incompletely suppressed the transcription of the gene encoding L-serine dehydratase (SDH) (EC 4.2.1.13), a gluconeogenic enzyme, in newborn dogs. To test another hypothesis that insulin resistance in newborn mammals may be partially due to counterregulatory factors, such as epinephrine, euglycemic hyperinsulinemic clamps, hyperglycemic hyperinsulinemic clamps, and hyperglycemic hyperinsulinemic hyperepinephrinemic clamps were performed in newborn dogs in the present study. The infusion rates of insulin and epinephrine were 30 m U/kg/min and 150 ng/kg/min, respectively; the glucose infusion rate was adjustable. The SDH mRNA levels in kidney and liver of newborn dogs were quantitatively analyzed by using rat SDH cDNA probe and by a personal densitometer. The results showed that insulins, glucose, and epinephrine did not change the kidney SDH mRNA level; hyperinsulinemia and hyperglycemia reduced the liver SDH mRNA level by 8.5 and 29.2%, respectively; in the presence of hyperglycemia and hyperinsulinemia, epinephrine was able to increase the liver SDH mRNA by 27.8%, almost offsetting the reduction of the liver SDH mRNA level induced by the combination of insulin and glucose. We conclude that the enhanced regulatory effect of epinephrine counteracting insulin on SDH gene transcription in liver of newborn dogs may be one of the mechanisms responsible for the neonatal insulin resistance which contributes to neonatal hyperglycemia.

Neonatal technology, perinatal survival, social consequences, and the perinatal paradox.

Exogenous surfactant therapy for premature infants with respiratory distress syndrome has had a significant impact on infant mortality and on some complications of prematurity. Yet the total number of low-birthweight infants has not declined, resulting in a high-risk population who would require surfactant therapy and long-term child care. Surviving low-birthweight infants (despite surfactant therapy) remain at risk for the consequences of premature birth, such as neurosensory impairment, cerebral palsy, and chronic lung disease. In addition, because of the close association between poverty and low birthweight, surviving premature infants are at increased risk for the new morbidities such as violence, homelessness, child abuse and neglect, and addictive drug use. A goal should be to reduce the risk of being born with a low birthweight, rather than having to treat the consequences of premature gestation. Despite the marvelous advances that permit us to treat respiratory distress syndrome, the continuing high low-birthweight rate places a significant strain on our health care system. The goal should be redirected to identifying large population-based efforts to reduce the number of low-birthweight infants.

Increased psychological distress in post-partum, cocaine-using mothers.

This study investigated psychological symptoms, self-reported postpartum by poor, primarily African American women who used cocaine during pregnancy. Ninety-nine cocaine-using mothers (COC+) were compared to 44 noncocaine-using mothers (COC-) on standardized measures of psychological distress and verbal comprehension. Mothers were interviewed to determined extent of drug involvement. COC+ mothers reported using alcohol, marijuana, and tobacco at two to three times the rate of comparison mothers during pregnancy and reported earlier initiation of marijuana use. COC+ women were more likely to admit to interpersonal difficulties and to report phobic anxiety and paranoid ideational symptoms. The COC+ group was also more likely to have clinically elevated scores on subscales indicating feelings of personal inadequacy, phobic anxiety, and paranoia. The use of cocaine, in combination with either alcohol or marijuana, was the best predictor of psychoticism, hostility, and total number of distress symptoms.

Direct and indirect interactions of cocaine with childbirth outcomes.

OBJECTIVE: To evaluate neonatal sequelae of maternal cocaine use during pregnancy. METHODS: One hundred women positive for cocaine use during pregnancy were compared with 100 matched controls who did not use cocaine. Maternal characteristics and infant neonatal outcomes were compared. We used t tests, chi 2, and multiple regression analyses to evaluate the contributions of cocaine vs other drugs to outcome. RESULTS: Cocaine was the best predictor of increased incidence of abortions, higher maternal gravidity, and poorer prenatal care. Cocaine was also the best predictor of preterm birth and of lower birth weight, after controlling for prematurity. Maternal use of cocaine and alcohol in combination was the best predictor of decreased linear growth, after controlling for prematurity. CONCLUSIONS: Maternal cocaine use predicts negative birth outcomes directly, as well as through obstetric risk factors of abortion history and less prenatal care. Interactive effects of cocaine and alcohol should be considered in future studies of birth outcomes.

Relation of maternal cocaine use to the risks of prematurity and low birth weight.

To determine whether maternal cocaine use at the time of delivery of the infant is an independent risk factor for low birth weight or prematurity, we performed a prospective anonymous urine toxicology screening study among 425 women in a large urban university-based maternity hospital. The data were subjected to univariate analysis with the Fisher Exact Test and odds ratio determination, and to multivariate analyses by logistic regression. Of 11 variables analyzed, cocaine use near delivery, no prenatal care, marijuana and cigarette use, black race, a previous preterm infant, and staff service were significantly associated with premature birth by univariate analysis. No prenatal care (odds ratio, 9.89; 95% confidence intervals, 3.74 to 26.17) and cocaine use (odds ratio, 7.31; 95% confidence intervals, 2.87 to 18.61) demonstrated the greatest risk associated with premature birth by univariate prediction. After analysis by multivariate logistic modeling, only cocaine use detected at birth remained a significant predictor of prematurity (odds ratio, 13.4; 95% confidence intervals, 1.23 to 145.0). Staff service, black race, cocaine use near the time of delivery, marijuana and cigarette use, a previous preterm infant, and no prenatal care were significant univariate predictors of low birth weight. Cocaine use (odds ratio, 4.14; 95% confidence intervals, 1.18 to 14.56) and marijuana use (odds ratio, 4.52; 95% confidence intervals, 1.42 to 14.39) were the strongest univariate factors. After analysis by multivariate logistic modeling, cocaine use near the time of delivery demonstrated the highest odds ratio (9.90) for predicting low birth weight, but the 95% confidence intervals included 1 (0.53 to 184.0). We conclude that independent of potentially interrelated covariables, a positive result on a cocaine urine toxicology test at the time of delivery is the most dominant factor that was tested to predict prematurity and possibly low birth weight. The effect of cocaine on the duration of gestation or fetal growth may be due to its pharmacologic properties, or cocaine use during pregnancy may identify a subgroup of women whose risk is due to as-yet-unidentifiable socioeconomic or cultural characteristics.

Increased incidence of intraventricular hemorrhage and developmental delay in cocaine-exposed, very low birth weight infants.

This study sought to determine whether very low birth weight (VLBW) infants (< 1500 gm) with fetal cocaine exposure differed from non-cocaine-exposed VLBW infants in incidence of neonatal medical complications and in later developmental outcome. Forty-one cocaine-exposed, VLBW infants, followed in a longitudinal study, were compared with 41 non-cocaine-exposed, VLBW infants of comparable race, social class, age, and incidence of bronchopulmonary dysplasia. Cocaine-exposed infants were identified on the basis of combined findings of maternal and/or infant urine immunoassay and on the basis of maternal self-report. At birth, groups did not differ on medical risk factors except that cocaine-exposed infants had a higher incidence of mild (grades I to II) intraventricular hemorrhage. Cocaine-using women were also more likely to use other drugs, especially alcohol, marijuana, and tobacco. At follow-up, at mean corrected ages of 16.5 +/- 8 months for 30 cocaine-exposed infants and 18.5 +/- 7 months for 37 non-cocaine-exposed infants, standardized assessments of cognitive (Mental Development Index) and motor (Psychomotor Development Index) development were administered. Cocaine-exposed infants had lower mean cognitive (83 +/- 27 vs 91 +/- 19), and motor (85 +/- 25 vs 96 +/- 18) scores; the incidence of developmental delay was significantly higher even after control for the effects of intraventricular hemorrhage and chronologic age. Cocaine-exposed VLBW infants were also more likely to be living with relatives or in foster homes. We conclude that these VLBW, cocaine-exposed infants were at increased risk of intraventricular hemorrhage, were more likely to be placed outside maternal care, and had higher incidences of cognitive and motor delays at follow-up.