When Health Begins

Prenatal Factors and Lifelong Health

Here are some examples describing the long-term consequences of prenatal events. There is no substitute at any age for a well balanced diet and avoiding exposure to harmful substances.

Folic Acid and Neural Tube Defects

Supplementation with folic acid before and during early pregnancy decreases the risk of neural tube defects1 —the most common of which is spina bifida.2 Neural tube defects occur within four weeks after fertilization—before most women even know they are pregnant. The Centers for Disease Control and many other organizations have long recommended daily folic acid supplements in women of childbearing age.3

Folic Acid and Prematurity

Folic acid deficiency before and during pregnancy has additional consequences beyond the risk of neural tube defects. It is also associated with an increased risk of low birth weight and premature birth.4 In fact, a recent study found that pregnant women who take folic acid supplements beginning one year prior to conception experienced a 70% reduction in the incidence of severe prematurity (prior to 26 weeks postconception) and a 50% reduction in moderately severe prematurity (prior to 30 weeks postconception).5

Iodine Deficiency and Mental Retardation

It is well established that iodine deficiency during pregnancy and early childhood impairs the production of thyroid hormone and may lead to hypothyroidism and brain damage.6 This is the leading cause of preventable mental retardation in many parts of the world.7 For this reason, table salt is supplemented with iodine in many parts of the world in an effort to address widespread iodine deficiency.

Vitamin D and Osteoporosis

Vitamin D deficiency during pregnancyis associated with lower bone mass at birth8 and lower bone mass by ages 8 or 9 years old,9 which raises the risk later in life of developing osteoporosis10, a condition particularly common in women.

Vitamin E, Zinc, and Asthma

Asthma, the leading cause of school absenteeism among chronic illnesses,11 has recently been linked to low vitamin E intake during pregnancy. A 2005 study reported a five-fold increase in the risk of asthma or asthma-like symptoms among five-year-old children whose mothers reported low Vitamin E intake as compared to children of mothers with high Vitamin E intake.12 Giving vitamin E to these five-year-old children did not improve their asthma.

The same study also reported a nearly two-fold increased risk of asthma in five-year-olds whose mothers had the lowest zinc intake during pregnancy.13

Low vitamin D intake during pregnancy is associated with increased wheezing symptoms in five-year-old children (but not asthma), independent of their vitamin D intake after birth.14

Maternal Stress and ADHD

An increased risk of ADHD and anxiety was reported among 8- and 9-year-olds whose mothers experienced high stress levels between 12 and 22 weeks of postmenstrual age (or between 10 and 20 weeks postfertilization).15

High levels of stress later in pregnancy did not translate into increased risks in the children under study.

Prenatal Tobacco Exposure

It is well known that smoking during pregnancy impairs fetal growth,16 and is associated with a higher risk of miscarriage17 and premature birth.18 It also slightly increases the risk of certain brain cancers in young children.19

Prenatal tobacco exposure is also linked to a higher risk of obesity at ages 3,20 4½,21 5 to 7,22 and 33.23 This effect appears to be dose related—the more a pregnant woman smokes, the higher the risk of obesity in her children.24

Other reported complications include: a two- to six-fold greater risk of Sudden Infant Death Syndrome (SIDS),25 and an increased risk of Attention Deficit Hyperactivity Disorder (ADHD),26 noninsulin-dependent diabetes,27 and tobacco experimentation during childhood.28 The risk of nicotine dependence in adults is also elevated.29

Additionally, prenatal tobacco exposure is linked with an increased risk of conduct disorder,30 a collection of emotional and behavioral disabilities.

Prenatal Alcohol Exposure

Prenatal alcohol exposure is widely known as the sole cause of Fetal Alcohol Syndrome, which is the most common preventable cause of mental retardation in the United States31 and other developed countries. It is also associated with lower IQ and a higher rate of fetal mortality.

Less well known is the increased risk of ADHD,32 conduct disorder,33 and intrauterine growth retardation.34 Prenatal alcohol exposure is also associated with an increased risk of alcohol use during adolescence,35 a higher risk of alcohol dependence in early adulthood,36 and lower academic performance.37 Heavy alcohol use during pregnancy is associated with very early premature birth.38

Intrauterine Growth Retardation and Adult Life

Inadequate nutrition during pregnancy is a major cause of intrauterine growth retardation (IUGR) and low birth weight, which are associated with decreased adult height39 and cognitive ability,40 and an increased risk of hypertension or high blood pressure,41 stroke,42 non-insulin dependent diabetes,43 and coronary artery disease leading to heart attack.44

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Footnotes


1	Williams JL et al., 2006. S67; Williams LJ et al., 2005. 580; Blencowe H et al., 2010. i118.
2	Bukowski R et al., 2009. 6.
3	Coming Soon, 2010. 100.
4	Scholl TO, Johnson WG, 2000. 1295s; Ashworth CJ, Antipatis C, 2001. 532.
5	Bukowski R et al., 2009. 6.
6	Coming Soon, 2010. 100.
7	Ashworth CJ, Antipatis C, 2001. 533.
8	Coming Soon, 2010. 100.
9	Cooper C et al., 2005. 2730S; Javaid MK et al., 2006. 36.
10	Coming Soon, 2010. 100.
12	Devereux G et al., 2006. 502; Litonjua AA et al., 2006. 853.
13	Coming Soon, 2010. 100.
14	Devereux G et al., 2007. 855.
15	Van den Bergh BR, Marcoen A, 2004. 1092.
16	Fasting MH et al., 2008. 2.
17	Chatenoud L et al., 1998. 524; Cunningham FG et al., 2001. 859; Brown DC, 1996. 102.
18	Spong CY, 2007. 407; Cnattingius S et al., 1999. 947.
19	Brooks DR et al., 2004. 1000.
20	Adams AK et al,, 2005. 396-397.
21	Dubois and Girard, 2006. 610.
22	von Kries R et al., 2002. 954.
23	Power C, Jefferis BJ, 2002. 416-417; Montgomery SM, Ekbom A, 2002. 26-27.
24	Bergen HT, 2006. 6; von Kries R et al., 2002. 954&956.
25	Salihu HM, Wilson RE, 2007. 717-718; Chong DS et al., 2004. 471, 478.
26	Linnet KM et al., 2003. 1028; Braun JM et al., 2006. 1904; Millichap JG, 2008. e360.
27	Montgomery SM, Ekbom A, 2002. 26-27.
28	Cornelius MD et al., 2000. 45.
29	Buka SL et al., 2003. 1983; Al Mamun A et al., 2006. 457.
30	Wakschlag LS et al., 1997. 670; Fergusson DM et al., 1998. 726; Langley K et al., 2007. e-article.
32	Millichap JG, 2008. e360.
33	Fryer SL et al., 2007. e737.
34	Little RE, Streissguth AP, 1981. 160.
35	Griesler PC, Kandel DB, 1998. 297.
36	Baer JS et al., 2003. 377, 383.
37	Goldschmidt L et al., 1996. 766-767; Streissguth AP et al., 1994. 253.
38	Coming Soon, 2010. 100.
39	Victora CG et al., 2008. 340; Case A, Paxson C, 2006. 8,11,19,32,40.
40	Case A, Paxson C, 2006. 6.
41	Leon DA et al., 1996. 405.
42	Eriksson JG et al., 2000. 873.
43	Ong KK, Dunger DB, 2002. 202; International Diabetes Federation website, 2002. e-article.
44	Barker, Winter, et al., 1989. 579; Barker DJ, 1999. 305.

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