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I don't know if the article will come trough without registration so here's an excerp. One of my son's who was adopted at 2 days old and was exposed to fat soluable marijuana throughout the pregnancy. He is disabled. His memory problems I attribute to MJ.
http://www.medscape.com/viewarticle/515684_5
"Physiologic Effects of Prenatal Cocaine Exposure in Neonates

The fetus is at significant risk from cocaine exposure secondary to maternal use. Cocaine has a low molecular weight and is both hydrophilic and lipophilic. These properties allow significant levels of cocaine to cross the placenta and pass through the blood brain barrier. The metabolism of cocaine in the fetus is known to be considerably slower than that of the adult. Fetal exposure to cocaine is, thus, prolonged (Schenker et al., 1993; Wagner et al., 1998). A study by Mahone and colleagues (1994) found cocaine and its derivatives to not only be transferred to the fetus via diffusion into the umbilical cord and within the placental vessels, but also to be in the amniotic fluid and then swallowed by the fetus. The dose, the duration of drug ingestion, and the point in gestation at which the fetus is exposed to cocaine determines the effect the drug may have on the fetus. The majority of research on the topic points to a myriad of clinical manifestations that present in the infant/young child.
Intrauterine Growth (Birth Weight, Length, and Head Circumference) and Prematurity

Variations in intrauterine growth in infants with a history of prenatal cocaine exposure have been observed. IUGR and prematurity of the newborn have been associated with maternal cocaine use. Most studies have found increasing rates of low birth weight, deficits in birth length and head circumference for gestational age, and prematurity among cocaine exposed newborns despite differing methodologies (Bada et al., 2002; Chiriboga, Brust, Bateman, & Hauser, 1999; Richardson, Hamel, Goldschmidt, & Day, 1999; Singer et al., 2002). However, other studies have found limited or no significant associations in birth weight, length, head circumference, and/or prematurity (Bandstra et al., 2001; Bateman & Chiriboga, 2000; Eyler, Behnke, Conlon, Woods, & Wobie, 1998).

Singer and colleagues (2002) compared 218 infants who were prenatally exposed to cocaine and 197 who were not and reported that cocaine use during pregnancy was associated with an increase in premature labor and delivery, lower birth weight, smaller head circumference, a decrease length at birth, and shorter gestational age. Similarly, Bandstra et al. (2001) noted cocaine-associated deficits in birth weight and length but not head circumference. Prematurity was not found by Bandstra et al. (2001), as the infants studied were full-term. Both Singer et al. (2002) and Bandstra et al. (2001) included a target population of primarily African American pregnant women of low-socioeconomic status with cocaine use, identified confounding variables including poly-drug use (i.e., alcohol, marijuana, tobacco, etc.), and controlled for these variables in comparison groups.

In a study examining 295 infants prenatally cocaine-exposed whose mother received no prenatal care as compared to 98 infants whose mother did receive prenatal care by the fifth month of pregnancy, Richardson et al. (1998) noted that during early pregnancy infants from both groups exhibited a reduction in their gestational age, birth weight, length, and head circumference. The authors concluded prenatal cocaine-exposure was associated with IUGR regardless of prenatal care. Confounding factors (alcohol, tobacco, marijuana, other illicit drugs, maternal and infant variables) were controlled for and at the end of each trimester both groups were questioned about their use of cocaine/crack, alcohol, marijuana, tobacco and other drug use.

In contrast to the findings of Richardson et al. (1998), a secondary analysis of data from the Maternal Lifestyle Study (MLS) found that only after 32 weeks of gestation did infants prenatally cocaine-exposed exhibit a decline in their birth weight, length, and head circumference (Bada et al., 2002). Covariates controlled for included clinical site, opiate use, alcohol, tobacco and marijuana use, and maternal and infant characteristics.

In contrast, Eyler et al. (1998) discovered that no significant differences were found between infants prenatally exposed to cocaine and non-exposed infants in terms of birth weight and length while examining 154 pregnant women identified as cocaine users with a matched control group. However, smaller dimensions in head and chest circumferences were found in infants whose mothers used cocaine and who also smoked tobacco. Cocaine users were found to have more infants born prematurely in comparison to the control group. All pregnant women were from a rural population, and the majority were African American and of low-socioeconomic status. Subjects were excluded if illicit drugs were used besides cocaine and marijuana; alcohol and tobacco were statistically adjusted for. The authors also reported that pregnant women were more likely to use a larger amount of cocaine during their first trimester. This is of great concern because this period of gestation is most critical for proper fetal development.

Bateman and Chiriboga (2000) investigated the relationship between birth weight and head circumference with the quantity of cocaine exposure in 240 non-randomized full-term infants from a well-baby nursery in a single inner-city hospital. Levels of cocaine exposure were measured using radioimmuno-analyses of the hair (RIAH) in the third trimester of pregnancy. Measurements indicated: no exposure (136 infants), low exposure (52 infants), and high exposure (52 infants). Adjustments were made for the confounding variables of use of alcohol, tobacco, marijuana, and opiates during pregnancy as well as infant and maternal characteristics. A dose-response effect of cocaine on the neonates' head circumference or, as they defined it, "head wasting" was only found in the high exposure group. Chiriboga et al. (1999) and Kuhn and colleagues (1999) reported similar findings. Chirboga et al. (1999) also found a decrease in birth lengths among infants prenatally exposed to cocaine at high levels of exposure.

In summary, research indicates prenatal exposure to cocaine may affect the infant's gestational age at birth, length, weight, and head circumference, although the findings are not conclusive or consistent."