Prevent Birth Defects

High quality diet (based on Mediterranean or USDA standards) associated with fewer birth defects

The data were collected in 10 states from pregnant women with estimated due dates from October 1997 through December 2005. Information was collected via telephone interviews with 72 percent of case and 67 percent of control mothers. Included in the analysis were 936 cases with neural tube defects, 2,475 with orofacial clefts, and 6, 147 controls without birth defects. Mothers reported their food intake using a questionnaire. The researchers developed two diet quality indices that focused on overall diet quality based on the Mediterranean Diet (Mediterranean Diet Score or MDS) and the U.S. Department of Agriculture Food Guide Pyramid (Diet Quality Index or DQI). "...Increasing diet quality based on either index was associated with reduced risks for the birth defects studied," the authors found.

http://www.infozine.com/news/stories/op/storiesView/sid/49231/

Unhealthy diet nearly doubles risk of cleft palate

The Western dietary pattern, eg, high in meat, pizza, legumes, and potatoes, and low in fruits, was associated with a higher risk of a cleft lip or cleft palate (odds ratio 1.9). This risk remained significant after adjustment for potential confounders of maternal education and smoking at the time of the study, and periconception use of folic acid or multivitamins. This dietary pattern was associated with lower red blood cell folate, vitamin B6, vitamin B12, and higher homocysteine concentrations. The use of the Prudent pattern, eg, high intakes of fish, garlic, nuts, vegetables, increased vitamin B12 and serum folate levels, was not associated with cleft lip or cleft palate risk compared with the Western diet.

http://www.ncbi.nlm.nih.gov/pubmed/17666614

Obesity increases risk of neural tube defects

Mothers who are obese when they get pregnant have a higher risk of serious birth defects of the brain and spine (neural tube defects).

http://www.cdc.gov/ncbddd/bd/research.htm

High dietary glycemic index increases risk of several birth defects

Data from the National Birth Defects Prevention Study were used to investigate the association between the maternal dietary glycemic index and the risk of birth defects among nondiabetic women. Among the 53 birth defects analyzed, high dietary glycemic index was significantly associated with encephalocele (adjusted odds ratio (aOR) = 2.68), diaphragmatic hernia (aOR = 2.58), small intestinal atresia/stenosis (aOR = 2.97) including duodenal atresia/stenosis (aOR = 2.48), and atrial septal defect (aOR = 1.37). Using quartiles to categorize dietary glycemic index, the authors identified associations with cleft lip with cleft palate (aOR = 1.23) and anorectal atresia/stenosis (aOR = 1.40). The joint effect of high dietary glycemic index and obesity provided evidence of a synergistic effect on the risk of selected birth defects. High dietary glycemic index is associated with an increased risk of a number of birth defects under study. Obesity coupled with high dietary glycemic index appears to increase the risk further for some birth defects.

http://www.ncbi.nlm.nih.gov/pubmed/23171874

Low selenium and zinc increases risk of neural tube defects

Neural tube defects are important causes of infant mortality and childhood morbidity. We investigated the relationship between zinc, selenium, copper, and lead concentrations and neural-tube-defect occurrence in women with a second-trimester termination due to fetal-neural-tube defects in this case-control study. Cases had significantly low serum zinc and selenium levels (62.48 vs 102.6 and 55.16 vs 77.4, respectively). Serum copper and whole-blood lead levels were significantly high when compared to controls. There was a negative correlation between serum zinc and selenium levels, and serum copper levels. Our results are consistent with some previous reports. The etiology of neural tube defects cannot be explained with one strict etiologic mechanism. On the contrary, an interaction among environmental, genetic, and nutritional factors such as trace elements and vitamins would explain these anomalies. If folic acid supplementation is given, additional zinc supplementation should be considered for the further decrease in the recurrence and occurrence of neural tube defects.

http://www.ncbi.nlm.nih.gov/pubmed/14997023

Multivitamins may prevent neural tube defects

Women who had previously given birth to one or more infants with a neural-tube defect were recruited into a trial of periconceptional multivitamin supplementation. 1 of 178 infants/fetuses of fully supplemented mothers (0.6%) had a neural tube defect, compared with 13 of 260 infants/fetuses of unsupplemented mothers (5.0%).

http://www.ncbi.nlm.nih.gov/pubmed/6101792

High homocysteine, low folate, low vitamin B12 associated with neural tube defects

The firm association between increased homocysteine concentration and neural tube defects has led to the hypothesis that high concentrations of homocysteine might be embryotoxic and lead to decreased fetal viability. There are several genetic polymorphisms that are associated with defects in folate- and vitamin B12-dependent homocysteine metabolism. The methylenetetrahydrofolate reductase (MTHFR) 677C>T and 1298A>C polymorphisms cause elevated homocysteine concentration and are associated with an increased risk of neural tube defects. Additionally, low concentration of vitamin B12 (cobalamin) or transcobalamin that delivers vitamin B12 to the cells of the body leads to hyperhomocysteinemia and is associated with neural tube defects. This effect involves the transcobalamin (TC) 776C>G polymorphism. Importantly, the biochemical consequences of these polymorphisms can be modified by folate and vitamin B12 supplementation.

http://www.ncbi.nlm.nih.gov/pubmed/14969589

D-chiro-inositol prevents spina bifida birth defect in mice

Although D-chiro- and myo-inositol both reduced the frequency of spina bifida in curly tail mice by all routes of administration, D-chiro-inositol consistently exhibited the more potent effect, reducing spina bifida by 73–86% in utero compared with a 53–56% reduction with myo-inositol. Pathological analysis revealed no association of either myo- or D-chiro-inositol with reduced litter size or fetal malformation. CONCLUSIONS: D-chiro-inositol offers a safe and effective method for preventing folic acid-resistant neural tube defects in the curly tail mouse. This raises the possibility of using inositol as an adjunct therapy to folic acid for prevention of neural tube defects in humans.

http://www.ncbi.nlm.nih.gov/pubmed/12202440

High homocysteine levels cause birth defects

Evidence suggests a connection between the amino acid homocysteine and a variety of pregnancy complications, including recurrent miscarriage, pre-eclampsia and placental abruption as well as adverse neonatal outcomes such as neural tube, heart and limb defects, intrauterine growth restriction and stillbirth.

http://lpi.oregonstate.edu/infocenter/vitamins/fa/

Metabolic disorders (diabetes, hypertension or obesity) increase risk of autism or developmental delay

Children aged 2 to 5 years (517 autism spectrum disorder, 172 developmental delays, and 315 controls) were enrolled in the study, a population-based, case-control investigation. RESULTS: All metabolic conditions (diabetes, hypertension, and obesity) were more prevalent among case mothers compared with controls. Collectively, these conditions were associated with a higher likelihood of autism spectrum disorder and developmental delays relative to controls (odds ratio: 1.61; odds ratio: 2.35, respectively). Among autism spectrum disorder cases, children of women with diabetes had MSEL expressive language scores 0.4 standard deviations lower than children of mothers without metabolic conditions. Among children without autism spectrum disorder, those exposed to any metabolic disorder scored lower on all MSEL and Vineland Adaptive Behavior Scales subscales and composites by at least 0.4 standard deviations. CONCLUSIONS: Maternal metabolic conditions may be broadly associated with neurodevelopmental problems in children. With obesity rising steadily, these results appear to raise serious public health concerns.

http://www.ncbi.nlm.nih.gov/pubmed/22492772

Hormonal imbalances in the mother may cause autism

The androgen theory of autism proposes that autism spectrum conditions are in part due to elevated fetal testosterone levels, which are positively correlated with a number of autistic traits and inversely correlated with social development and empathy. Compared to controls, significantly more women with autism spectrum conditions reported (a) hirsutism, (b) bisexuality or asexuality, (c) irregular menstrual cycle, (d) dysmenorrhea, (e) polycystic ovary syndrome, (f) severe acne, (g) epilepsy, (h) tomboyism, and (i) family history of ovarian, uterine, and prostate cancers, tumors, or growths. Compared to controls, significantly more mothers of autism spectrum conditions children reported (a) severe acne, (b) breast and uterine cancers, tumors, or growths, and (c) family history of ovarian and uterine cancers, tumors, or growths. These results suggest current hormone abnormalities in women with autism spectrum conditions and their mothers. Direct investigations of serum testosterone levels and genetic susceptibility to high testosterone production or sensitivity in women with autism spectrum conditions would illuminate the origin of these conditions. The relationship between fetal testosterone and current testosterone levels also needs to be clarified. The present results may be relevant to understanding the increased male risk to developing autism.

http://www.ncbi.nlm.nih.gov/pubmed/17462645

High saturated fat intake may cause reduced memory and learning ability in offspring

Eighteen pregnant mice were randomly divided into three groups of six each and fed with chow or high lipid diet composed of either flaxseed oil (polyunsaturated fat)(chow diet 84%, cholesterol 0.2%, flaxseed oil 15.8%) or lard fat (saturated fat)(chow diet 84%, cholesterol 0.2%, lard fat 15.8%). After weaning, the offspring were fed the same diet as their mothers were fed during the experiment, and their spatial memory and learning ability were evaluated by Morris water maze when they were 8 weeks old. Compared to chow diet (control), high flaxseed oil diet increased high density lipoprotein cholesterol level in the mothers but not in offspring; high saturated fat diet increased serum total cholesterol level and low density lipoprotein cholesterol level both in mothers and offspring. Brain fatty acids profile was altered by high saturated fat diet compared with chow diet. The changed fatty acids composition affected the spatial memory and learning ability of adult offspring. CONCLUSIONS: A long-term high saturated fat diet increased offspring serum total cholesterol and LDL-C levels and affected the brain's fatty acid composition, and memory and learning ability.

http://www.ncbi.nlm.nih.gov/pubmed/20015474

Pesticides and soy may cause hypospadias

A study in the United Kingdom found no relationship between a maternal organic vegetarian diet and hypospadias frequency, but women who consumed nonorganic vegetarian diets had a greater percentage of sons with hypospadias. Because nonorganic diets can include residues of pesticides such as vinclozolin, we sought to assess the interaction of realistic daily exposures to genistein (found in soy products) and vinclozolin and their effects on the incidence of hypospadias. Pregnant mice were fed a soy-free diet and orally gavaged from gestational days 13 to 17 with 0.17 mg/kg/day of genistein (equivalent to 5.5 mg for a 120 lb woman), 10 mg/kg/day of vinclozolin, or genistein and vinclozolin together at the same doses, all in 100 microL of corn oil. The controls received the corn oil vehicle. The incidence of hypospadias was 25% with genistein alone, 42% with vinclozolin alone, and 41% with genistein and vinclozolin together. These findings support the idea that exposure to these compounds during gestation could contribute to the development of hypospadias.

http://www.ncbi.nlm.nih.gov/pubmed/17905137

Progesterone use may cause hypospadias

This analysis included 502 subjects diagnosed with second- or third-degree hypospadias and 1286 male, live-born, nonmalformed control subjects. Forty-two case mothers (8.4%) and 31 control mothers (2.4%) reported any pregnancy-related progestin intake from 4 weeks before through 14 weeks after conception, resulting in an odds ratio of 3.7. Among the 10 cases and 13 controls who did not report any fertility-related procedures or treatments other than progestins, the odds ratio was 2.2. Progestin intake for the purpose of contraception was not associated with increased risk. Conclusion: This study found that pregnancy-related intake of progestins was associated with increased hypospadias risk.

http://www.ncbi.nlm.nih.gov/pubmed/16203941

Clomid may cause birth defects; Metformin does not appear to cause birth defects

The available data suggest that clomiphene treatment, especially after several cycles, might be associated with a slightly higher risk of neural tube defects and severe hypospadias in the offspring. Letrozole and metformin do not appear to be teratogenic.

http://www.ncbi.nlm.nih.gov/pubmed/18519067

Beef consumption associated with low sperm count in sons

A mother's high beef consumption while pregnant was associated with lower sperm counts in her son, according to a study led by researchers at the University of Rochester. Among the 51 men whose mothers were the highest beef eaters, almost 18 percent had sperm counts classified by the World Health Organization as "sub-fertile" (20 mill/ml or lower). By comparison, sperm concentrations were 24 percent higher for men whose mothers ate less beef, and only about 5 percent had sperm counts that could be classified as sub-fertile.

http://www.sciencedaily.com/releases/2007/03/070328073237.htm

Low protein diet during pregnancy associated with coronary heart disease in offspring

In conclusion, a maternal low protein diet throughout gestation significantly impairs recovery of the 6-month-old adult rat heart to myocardial ischaemia-reperfusion-induced injury. Undernutrition during development may increase susceptibility to coronary hard disease by impairing recovery from coronary events.

http://www.ncbi.nlm.nih.gov/pubmed/17445339

N-acetyl cysteine may prevent birth defects and miscarriage caused by diabetes

We found decreased Bcl-2, increased Bax and cleaved Caspase 3 proteins in embryos from diabetic rats. Moreover, we found increased activation of Caspase 3 in cells from embryos previously exposed to a diabetes-like environment (in vivo, in vitro) compared to cells from control embryos, which was normalized by supplementation of N-acetylcysteine or apoptosis inhibitor. Additionally, we found increased dysmorphogenesis in embryos exposed to a diabetic environment in vivo and in vitro. Exposure to a diabetic milieu during organogenesis increases apoptosis in embryonic cells and dysmorphogenesis in embryos. Enhanced apoptotic rate may have a role in diabetic embryopathy by inducing disturbed embryonic maturation, increased rates of resorptions and congenital malformations.

http://www.ncbi.nlm.nih.gov/pubmed/17034987