Mind-Body Maturity

Psychological Approaches To Sports, Exercise, And Fitness

Louis Diamant

• Publisher: Taylor & Francis
• Year: 2019
• ISBN:
  9781317737773
• Edition: 1
• Topic: Psychology
• Subtopic: Mental Health in Psychology
• Index: Psychology

A description of the ways in which sport, exercise and fitness affect human psychology and development from before birth to old age. The contributing authors cover psychological attitudes to fitness, environmental factors, adolescent identity and moral development.

II

DEVELOPMENT: GROWING AND MATURING

2

Environmental Effects on the Fetus: The Examples of Alcohol, Cocaine, and Exercise

Lisa Eisen, Tiffany M. Field

University of Miami School of Medicine

Sandra K. Larson

University of Denver

During pregnancy, a mother-to-be often continues living her life as if nothing has changed, engaging in activities that might directly or indirectly affect the fetus. The nine months of gestation are a period of rapid and extensive growth and development as well as one of enhanced susceptibility and sensitivity. Many factors may influence the course of prenatal development. Whatever a pregnant woman eats or drinks and whatever drugs she takes may be transmitted to the fetus. Whether she is healthy or ill, whether her diet is nutritious or not, and whether she is exposed to environmental toxins or not may affect the development of the fetus. These agents that may produce malformations in the fetus are called teratogens. They include maternal diet, disease, drugs, hormones, and irradiation. In addition, maternal characteristics such as age, emotional state, number of previous pregnancies, and exercise influence prenatal development.

Until the 1940s, it was generally accepted that the human embryo was protected from environmental agents by the fetal membranes and the mother’s abdominal walls and uterus. In 1941 Gregg documented that maternal rubella infection could cause malformations in human fetuses, leading to the first generally accepted realization that human embryos were susceptible to environmental influences. However, it was the thalidomide tragedy of the late 1950s and early 1960s (McBride, 1977) that first focused attention on the role of drugs during pregnancy in the cause of fetal malformations. Still, the potential harmful effects of more commonly used drugs and alcohol were generally ignored. It was not until 1973 that the issue of prenatal effects of alcohol consumption was raised and the fetal alcohol syndrome (FAS) (Jones & Smith, 1973) was defined. Today there is an increased interest and awareness in both the lay and scientific communities of the impact of environmental influences on prenatal development. Not only is there an awareness of teratogens resulting in gross physical abnormalities and mental retardation, but there is also an awareness of more subtle behavioral and cognitive teratogenic effects.

One of the best ways to understand environmental risks to the embryo or fetus is by the use of examples. This chapter discusses three different environmental influences on prenatal development: alcohol, cocaine, and exercise. Alcohol is one of the most extensively researched teratogens, and is a commonly used substance. Cocaine-exposed infants are the new epidemic in hospital neonatal units. The problem has spurred research, but it is still in the preliminary stages. Maternal exercise during pregnancy is a presumed healthy activity made popular by increased health consciousness; but in reality very little is known about the effect of maternal exercise on the developing fetus.

Alcohol

Drinking is often considered less lethal for the fetus than heroin or cocaine. However, alcohol, like other legal drugs such as nicotine and caffeine, has its undesirable effects on the fetus.

In 1968, Lemoine and his colleagues in Paris reported in a French medical journal on abnormalities observed in 127 children of alcoholic parents (Lemoine, Harousseau, Borteyru, & Menuet, 1968). They found these children to have common characteristics including: highly distinctive facial features; considerable growth retardation; high frequency of malformations, including cleft palate, limb malformations, and heart defects; and psychomotor disturbances. Lemoine and colleagues findings went virtually unnoticed until 5 years later when Jones and his associates, working independently in Seattle, discovered the same set of characteristics in children of alcoholic mothers (Jones & Smith, 1973; Jones, Smith, Streissguth, & Myrianthopoulos, 1974a; 1974b; Jones, Smith, Ulleland, & Streissguth, 1973), and termed this pattern of altered growth and morphogenesis FAS (Jones & Smith, 1973). The striking similarities in the independent findings of Jones and Lemoine in two different populations lent much credibility to these observations of the prenatal effects of alcohol.

Over the next several years, studies of the offspring of alcoholic mothers confirmed initial findings of altered growth and morphogenesis (Clarren & Smith, 1978; Jones, Smith, & Hanson, 1976; Smith, Jones, & Hanson, 1976; Ulleland, 1972). Several studies reported mental deficiency of varying degrees in children with FAS (Jones et al., 1976; Shaywitz, Cohen, & Shaywitz, 1980; Streissguth, 1976; Streissguth, Herman, & Smith, 1978a, 1978b). They also found a significant relationship between severity of morphogenesis and mental dysfunction, suggesting that the intellectual handicap, like the morphogenesis and growth deficiency, is of prenatal origin.

Behavioral problems, as well as growth deficiency, morphogenesis, and mental retardation, were reported in children with FAS (Iosub, Fuchs, Bingol, & Gromisch, 1981). These behavioral problems included irritability, hyperactivity, and feeding problems during infancy and the preschool years. A high incidence of speech and language problems ranging from mild to severe dysfunctions was also found. Impaired development of speech and language is a common early indicator of cerebral dysfunction, and behavior problems such as hyperactivity are indicators of minimal brain dysfunction. These problems are believed to be a result of the teratogenic effects of alcohol on the brain.

Effects of the Central Nervous System (CNS)

Alcohol readily crosses the placenta and enters the fetus’ bloodstream. Alcohol is metabolized and eliminated much more slowly in the fetus and in the newborn than in the mother (Idanpaan-Heikkila et al., 1972). Thus, blood alcohol levels of the fetus may reach or surpass those of the mother. Even a small oral dose of alcohol exerts a depressant effect on the Fetal CNS. As little as one ounce of 40% alcohol consumed by the mother was found to significantly decrease infants’ breathing movements within half an hour (Fox et al., 1978). After birth, the nursing newborn may continue to receive alcohol from the mother because alcohol is present in breast milk at the same concentration as in maternal blood (Borges & Lewis, 1981).

The potential effects of alcohol on the developing CNS are devastating. Studies reporting on autopsies of infants who died during the neonatal period whose mothers had a history of alcohol use have described extensive developmental anomalies of the brain, which resulted primarily from aberrations of neuronal migration (Clarren, Alvord, Sumi, Streissguth, & Smith, 1978; Jones, 1975). It is believed that interference with normal cerebellar and brainstem development occurred before 45 days gestation, and that cerebral abnormalities were initiated before 85 days gestation (Clarren et al., 1978). The level of maternal alcoholism in these cases ranged from chronic alcoholics to a binge drinker, who reported drinking at least five drinks at one time at approximately weekly intervals. Thus, intermittent high doses of alcohol can also cause severe damage. It is interesting that only a few of the infants from these studies were considered to have FAS from external criteria, indicating that abnormalities of CNS development can occur without external anomalies.

The effects of maternal alcohol use on fetal development have been investigated by controlled animal models as well (Streissguth, Landesman-Dwyer, Martin, & Smith, 1980). Despite differing methodologies, studies using animal models have the common findings of increased fetal mortality and decreased birth weight being related to maternal alcohol intake. For example, Reyes, Rivera, Saland, and Murray (1983) found alcohol-treated rat offspring to exhibit growth retardation, microcephaly, low birth weight, and decreased survival rates. Offspring from the alcohol group had brain weights that were 10% to 15% smaller than the control group. Further examination showed a decrease in dendritic spines and vacuolated area in layer V of the parietal cortex in the alcohol-treated pups. These findings parallel human findings of autopsies of FAS infants revealing incomplete brain development and lack of normal neuronal migration (Clarren et al., 1978; Jones, 1975).

Animal models have allowed a more controlled means of studying the mechanism of CNS damage related to maternal alcohol consumption. In monkeys, an impairment of the fetal-placental circulation system was found following administration of ethanol to the mother (Mukherjee & Hodgen, 1982). This impairment of umbilical function produced hypoxia and acidosis in the fetus. Although this condition was transient, brain cells are extremely sensitive to low oxygen levels, and significant brain damage may occur despite a short duration of severe hypoxia.

It seems clear that maternal alcohol consumption can have a dramatic effect on the developing CNS. Abnormalities of the CNS can occur in the absence of external anomalies. In addition, binge alcohol drinking may produce damage similar to chronic alcohol drinking.

Dosage And Critical Period

The questions of how much alcohol a mother can drink before damaging her baby and when during pregnancy is the fetus vulnerable to alcohol still remain unanswered. The susceptibility to teratogens varies with developmental stage (Wilson, 1973). There is a degree of vulnerability to teratogenesis throughout the total span of development, but research has demonstrated that the greatest danger is associated with a relatively short period between germ-layer differentiation and completion of major organ formation. This period of tissue and organ differentiation occurs between Gestation Days 18 or 20 to 55 or 60 (Wilson, 1973).

Two vulnerable or “critical” periods have been identified in the development of the human brain (Abel, 1980). The first occurs between 12 and 18 weeks of gestation during a period of neuronal multiplication. The second occurs during the third trimester and continues through the first 18 months after birth. This period is characterized by dendritic branching and formation of synaptic connections. Thus, a teratogenic agent may have maximal effects on the developing brain in the first and third trimesters.

These “critical periods” have some implications with regard to alcohol consumption during pregnancy. External anomalies characteristic of the full-blown FAS are likely to occur in children of chronic alcohol drinkers and those who drink heavily during the first trimester. CNS damage such as mental retardation and more subtle brain damage may occur without external anomalies when maternal alcohol intake occurs before or after the period of organogenesis. Before organogenesis, heavy alcohol intake may produce death, which is one explanation for the higher rate of miscarriages in alcoholic mothers. In the third trimester, after organogenesis is complete, the fetus is still susceptible to alcohol intake. Even a single binge during this period may lead to irreversible brain damage (Mukherjee & Hodgen, 1982). In addition, there may be little structural alteration to be found in the fully formed brain, yet the functional effects may be significant, and obvious behavioral deficits may result (Rodier & Reynolds, 1977).

Whether a particular developmental deviation is produced depends not only on the period of development but also on dosage. The susceptible early embryo is readily malformed or killed by a relatively small dose of suitable agents, but much larger doses may be needed to harm the fetus (Wilson, 1973). Higher levels of alcohol intake may be required at some periods during prenatal development than at others to produce deviant development. What may be a “safe” level of alcohol intake during one period of prenatal development may not be at another period.

Manifestations of deviant development increase in frequency and degree as dosage increases, from the no-effects level to the totally lethal level (Wilson, 1973). Whether there is a threshold below which no manifestation of abnormality is seen is still unresolved. This threshold is bound to change with the period of prenatal development, as well as with the genotype of the individual fetus and mother. Although there may be a theoretical safe level for any agent, finding it is a very difficult task. For alcohol it is even more so because of the many confounding variables associated with chronic maternal drinking: maternal health, maternal nutrition, poverty, physical stress, and other drug use. Further, as yet there has been no teratogen studied that clearly shows a threshold above which the substance is teratogenic and below which the substance is safe (Smith, 1979).

What is a “safe” level of maternal alcohol consumption remains unanswered. It is known that chronically alcoholic mothers and mothers who binge drink often produce offspring with FAS. Researchers have now begun investigating the effects of moderate alcohol consumption or social drinking on the developing fetus. They are not only looking for death and external anomalies in these infants of social drinkers, but for differences in growth and behavior as well.

Social Drinking During Pregnancy

Since 1974, several prospective studies have focused on the question of whether social drinking during pregnancy is harmful. Among the largest and most prolific were the Boston and the Seattle studies. In addition, there have been several epidemiological studies that have dealt with the prenatal effects of alcohol.

Boston Studies

A pilot prospective study at Boston City Hospital, which serves a poor inner-city area, began in 1974 interviewing 633 women and examining 322 babies (Ouellette & Rosett, 1976; Ouellette, Rosett, Rosman, & Weiner, 1977; Rosett, Ouellette, & Weiner, 1976). They found that the frequency of abnormalities was twice as great in offspring of heavy drinkers as that in offspring of abstinent or moderate drinkers. Congenital anomalies were found in 32% of the infants of heavy drinkers compared with 14% in moderate drinkers and 9% in abstinent drinkers (Ouellette et al., 1977). Infants of heavy drinkers had smaller birth lengths, birth weights, and head circumferences, and were more likely to be born prematurely, than infants of abstinent or moderate drinkers. Infants of mothers who drank heavily were significantly more likely to be jittery, have poor muscle tone (hypotonia, and have poor sucking ability compared with infants whose mothers were classified as moderate drinkers or abstainers (Ouellette & Rosett, 1976; Ouellette et al., 1977).

Maternal drinking was also related to neonatal sleep state regulation (Rosett et al., 1979; Sander et al., 1977). Sleep state organization is generally considered an indicator of infant CNS organization and maturity. Heavy alcohol consumption throughout pregnancy was associated with a decrease in the total time spent sleeping, more quiet sleep periods in...

Table of contents

• Cover
• Half Title
• Title Page
• Copyright Page
• Contents
• Contributor
• Preface
• I Introduction
• II Development: Growing and Maturing
• III Theoretical Contributions
• Index