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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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DES (diethylstilbestrol) is a drug that mimics estrogen, a female hormone. From 1938 until 1971 doctors prescribed this drug to help some pregnant women who had had miscarriages or premature deliveries on the theory that miscarriages and premature births occurred because some pregnant women did not produce enough estrogen naturally to sustain the pregnancy for full term . An estimated 5-10 million pregnant women and the children born during this period were exposed to DES. Currently, DES is known to increase the risk of breast cancer, and cause a variety of birth-related adverse outcomes exposed female offsprings such as spontaneous abortion, second-trimester pregnancy loss, preterm delivery, stillbirth, neonatal death, sub/infertility and cancer of reproductive tissues . DES is an important developmental toxicant which links the fetal basis of adult disease.
A number of studies have shown that tobacco use is a significant factor in miscarriages among pregnant smokers, and that it contributes to a number of other threats to the health of the fetus. Smoking and pregnancy, combined, cause twice the risk of premature rupture of membranes, placental abruption and placenta previa. Also, it causes 30% higher odds of the baby being born prematurely.
Methylmercury and inorganic mercury is excreted in human breast milk and infants are particularly susceptible to toxicity due to this compound. The fetus and infant are especially vulnerable to mercury exposures with special interest in the development of the CNS since it can easily cross across the placental barrier, accumulate within the placenta and fetus as the fetus cannot eliminate mercury and have a negative effect on the fetus even if the mother does not show symptoms. Mercury causes damage to the nervous system resulting from prenatal or early postnatal exposure and is very likely to be permanent.
Cannabis in pregnancy is the subject of various scientific studies, usually regarding whether it has effects on the child later in life.
Effects found by Fergusson, D. M., Horwood, L. J., & Northstone, K. (2002) where that cannabis had a negative effect on babies. They were found to weigh significantly less, as well having shorter birth lengths, and had smaller head circumferences than babies who were not exposed to prenatal cannabis. Marijuana use has been shown to affect global motion perception by considerably increasing it, unlike alcohol that significantly decreases it.
Based on recent (2005) US NCHS data, the rate of multiple births is now approximately 3.4% (4,138,349 total births, of which 139,816 were twins or higher-order multiple births).
The majority of identical twins share a common (monochorionic) placenta, and of these approximately 15% go on to develop TTTS.
By extrapolating the number of expected identical twins (about one-third) from annual multiple births, and the number of twins with monochorionic placentae (about two-thirds), and from these the number thought to develop TTTS (about 15%), there are at least 4,500 TTTS cases per year in the U.S. alone: 139,816 X .33 X .66 X .15 = 4,568 cases of TTTS per year in U.S. (involving more than 9,000 babies.)
Since spontaneous pregnancy losses and terminations that occur prior to 20 weeks go uncounted by the C.D.C., this estimate of TTTS cases may be very conservative.
Although infertility treatments have increased the rate of multiple birth, they have not appreciably diluted the expected incidence of identical twins. Studies show a higher rate of identical twins (up to 20 times with IVF) using these treatments versus spontaneous pregnancy rates.
One Australian study, however, noted an occurrence of only 1 in 4,170 pregnancies or 1 in 58 twin gestations. This distinction could be partly explained by the "hidden mortality" associated with MC multifetal pregnancies—instances lost due to premature rupture of membrane (PROM) or intrauterine fetal demise before a thorough diagnosis of TTTS can be made.
Some doctors recommend complete bed-rest for the mother coupled with massive intakes of protein as a therapy to try to counteract the syndrome. Research completed shows these nutritional supplements do work. Diet supplementation was associated with lower overall incidence of TTTS (20/52 versus 8/51, P = 0.02) and with lower prevalence of TTTS at delivery (18/52 versus 6/51, P = 0.012) when compared with no supplementation. Nutritional intervention also significantly prolonged the time between the diagnosis of TTTS and delivery (9.4 ± 3.7 weeks versus 4.6 ± 6.5 weeks; P = 0.014). The earlier nutritional regimen was introduced, the lesser chance of detecting TTTS ( P = 0.001). Although not statistically significant, dietary intervention was also associated with lower Quintero stage, fewer invasive treatments, and lower twin birth weight discordance. Diet supplementation appears to counter maternal metabolic abnormalities in monochorionic twin pregnancies and improve perinatal outcomes in TTTS when combined with the standard therapeutic options. Nutritional therapy appears to be most effective in mitigating cases that are caught in Quintero Stage I, little effect has been observed in those that are beyond Stage I.
The use of recreational drugs in pregnancy can cause various pregnancy complications.
- Ethanol during pregnancy can cause fetal alcohol syndrome and fetal alcohol spectrum disorder. Studies have shown that light to moderate drinking during pregnancy might not pose a risk to the fetus, although no amount of alcohol during pregnancy can be guaranteed to be absolutely safe.
- Tobacco smoking during pregnancy can cause a wide range of behavioral, neurological, and physical difficulties. Smoking during pregnancy causes twice the risk of premature rupture of membranes, placental abruption and placenta previa. Smoking is associated with 30% higher odds of preterm birth.
- Prenatal cocaine exposure is associated with premature birth, birth defects and attention deficit disorder.
- Prenatal methamphetamine exposure can cause premature birth and congenital abnormalities. Short-term neonatal outcomes show small deficits in infant neurobehavioral function and growth restriction. Long-term effects in terms of impaired brain development may also be caused by methamphetamine use.
- Cannabis in pregnancy has been shown to be teratogenic in large doses in animals, but has not shown any teratogenic effects in humans.
Intrauterine exposure to environmental toxins in pregnancy has the potential to cause adverse effects on the development of the embryo/fetus and to cause pregnancy complications. Air pollution has been associated with low birth weight infants. Conditions of particular severity in pregnancy include mercury poisoning and lead poisoning. To minimize exposure to environmental toxins, the "American College of Nurse-Midwives" recommends: checking whether the home has lead paint, washing all fresh fruits and vegetables thoroughly and buying organic produce, and avoiding cleaning products labeled "toxic" or any product with a warning on the label.
Pregnant women can also be exposed to toxins in the workplace, including airborne particles. The effects of wearing N95 filtering facepiece respirators are similar for pregnant women as non-pregnant women, and wearing a respirator for one hour does not affect the fetal heart rate.
Vaccinating the majority of the population is effective at preventing congenital rubella syndrome.
In low-risk pregnancies, the association between cigarette smoking and a reduced risk of pre-eclampsia has been consistent and reproducible across epidemiologic studies. High-risk pregnancies (those with pregestational diabetes, chronic hypertension, history of pre-eclampsia in a previous pregnancy, or multifetal gestation) showed no significant protective effect. The reason for this discrepancy is not definitively known; research supports speculation that the underlying pathology increases the risk of preeclampsia to such a degree that any measurable reduction of risk due to smoking is masked. However, the damaging effects of smoking on overall health and pregnancy outcomes outweighs the benefits in decreasing the incidence of preeclampsia. It is recommended that smoking be stopped prior to, during and after pregnancy.
Studies suggest that marijuana use in the months prior to or during the early stages of pregnancy may interfere with normal placental development and consequently increase the risk of preeclampsia.
Known risk factors for pre-eclampsia include:
- Having never previously given birth
- Diabetes mellitus
- Kidney disease
- Chronic hypertension
- Prior history of pre-eclampsia
- Family history of pre-eclampsia
- Advanced maternal age (>35 years)
- Obesity
- Antiphospholipid antibody syndrome
- Multiple gestation
- Having donated a kidney.
- Having sub-clinical hypothyroidism or thyroid antibodies
- Placental abnormalities such as placental ischemia.
Pregnancy also poses as another high risk factor for vitamin D deficiency. The status levels of vitamin D during the last stages of pregnancy directly impact the new borns first initial months of life. Babies who are exclusively breastfed with minimal exposure to sunlight or supplementation can be at greater risk of vitamin D deficiency,as human milk has minimal vitamin D present. Recommendations for infants of the age 0–12 months are set at 5 ug/day, to assist in preventing rickets in young babies. 80% of dark skinned and or veiled women in Melbourne were found to have serum levels lower than 22.5 nmol/L considering them to be within moderate ranges of vitamin D deficiency.
There is conflicting evidence to suggest whether obesity contributes to vitamin D deficiency.Obese individuals have an increased risk of being vitamin D deficient likely caused by lack of sun exposure from reduced mobility and or low levels of physical activity. The serum levels of obese Australian were 8.3- 9.5 nmol/L lower in both genders comparable to those of healthy weight ranges. During the AusDiab study conducted throughout Australia serum levels within obese people were shown to be 57% lower than with normal weight after receiving the same amount of UV exposure.
Inconsistent to the findings of AusDiab Study, The Australian Bureau of Statistics (ABS) found there to be no correlation between weight levels and vitamin D serum level. According to ABS the Vitamin D supplementation was said to not be a contributing factor as supplement use was similar across all weight ranges.
Fertility following ectopic pregnancy depends upon several factors, the most important of which is a prior history of infertility. The treatment choice does not play a major role; A randomized study in 2013 concluded that the rates of intrauterine pregnancy 2 years after treatment of ectopic pregnancy are approximately 64% with radical surgery, 67% with medication, and 70% with conservative surgery. In comparison, the cumulative pregnancy rate of women under 40 years of age in the general population over 2 years is over 90%.
When ectopic pregnancies are treated, the prognosis for the mother is very good in Western countries; maternal death is rare, but most fetuses die or are aborted. For instance, in the UK, between 2003 and 2005 there were 32,100 ectopic pregnancies resulting in 10 maternal deaths (meaning that 1 in 3,210 women with an ectopic pregnancy died).
In the developing world, however, especially in Africa, the death rate is very high, and ectopic pregnancies are a major cause of death among women of childbearing age.
The data presented is for comparative and illustrative purposes only, and may have been superseded by updated data.
According to current recommendations by the WHO, US CDC and U.S. Department of Health and Human Services (DHHS), all individuals with HIV should begin ART. The recommendation is stronger under the following conditions:
- CD4 count below 350 cells/mm
- High viral load (>100,000 copies/ml)
- Progression of HIV to AIDS
- Development of HIV-related infections and illnesses
- Pregnancy
Women are encouraged to begin treatment as soon as they are diagnosed with HIV. If they are diagnosed prior to pregnancy, they should continue with ART during the pregnancy. If the diagnosis of HIV is made during the pregnancy, ART should be initiated immediately.
Vitamin A plays a role in the immune system and is a low-cost intervention that has been suggested to help with preventing mother-to-child transmission of HIV. A Cochrane review summarised the evidence of five trials conducted in Malawi, South Africa, Tanzania and Zimbabwe between 1995 and 2005, where none of the participants received antiretroviral therapy. They found that giving vitamin A supplementation to pregnant women or to women after they delivered a baby probably has little or no effect on mother-to-child transmission of HIV. The intervention has been largely suspended by antiretroviral therapy.
Congenital rubella syndrome (CRS) can occur in a developing fetus of a pregnant woman who has contracted rubella, usually in the first trimester. If infection occurs 0–28 days before conception, the infant has a 43% risk of being affected. If the infection occurs 0–12 weeks after conception, the risk increases to 51%. If the infection occurs 13–26 weeks after conception, the risk is 23% of the infant being affected by the disease. Infants are not generally affected if rubella is contracted during the third trimester, or 26–40 weeks after conception. Problems rarely occur when rubella is contracted by the mother after 20 weeks of gestation and continues to disseminate the virus after birth.
It was discovered in 1941 by Australian Norman McAlister Gregg.
For many adopted or adults and children in foster care, records or other reliable sources may not be available for review. Reporting alcohol use during pregnancy can also be stigmatizing to birth mothers, especially if alcohol use is ongoing. In these cases, all diagnostic systems use an unknown prenatal alcohol exposure designation. A diagnosis of FAS is still possible with an unknown exposure level if other key features of FASD are present at clinical levels.
Amount, frequency, and timing of prenatal alcohol use can dramatically impact the other three key features of FASD. While consensus exists that alcohol is a teratogen, there is no clear consensus as to what level of exposure is toxic. The CDC guidelines are silent on these elements diagnostically. The IOM and Canadian guidelines explore this further, acknowledging the importance of significant alcohol exposure from regular or heavy episodic alcohol consumption in determining, but offer no standard for diagnosis. Canadian guidelines discuss this lack of clarity and parenthetically point out that "heavy alcohol use" is defined by the National Institute on Alcohol Abuse and Alcoholism as five or more drinks per episode on five or more days during a 30-day period.
"The 4-Digit Diagnostic Code" ranking system distinguishes between levels of prenatal alcohol exposure as "high risk" and "some risk". It operationalizes high risk exposure as a blood alcohol concentration (BAC) greater than 100 mg/dL delivered at least weekly in early pregnancy. This BAC level is typically reached by a 55 kg female drinking six to eight beers in one sitting.
Cannabis consumption in pregnancy might be associated with restrictions in growth of the fetus, miscarriage, and cognitive deficits. The American Congress of Obstetricians and Gynecologists recommended that cannabis use be stopped before and during pregnancy, Cannabis is the most commonly used illicit substance
among pregnant women.
Although it is difficult to draw firm conclusions, there is some evidence that prenatal exposure to marijuana may be associated with deficits in language, attention, cognitive performance, and delinquent behaviors. THC exposure in rats during the prenatal developmental phase may cause epigenetic changes in gene expression, but there is limited knowledge about the risk for psychiatric disorders because of ethical barriers to studying the developing human brain. While animal studies cannot take into account factors that could influence the effects of cannabis on human maternal exposure, such as environmental and social factors, a 2011 review of rodent studies by Campolongo "et al." said there was "... increasing evidence from animal studies showing that cannabinoid drugs ... induce enduring neurobehavioral abnormalities in the exposed offspring ..." Campolongo "et al." added that "clinical studies report hyperactivity, cognitive impairments and altered emotionality in humans exposed in utero to cannabis". Martin "et al." investigated recent trends in substance abuse treatment admissions for cannabis use in pregnancy in the US, based on Treatment Episodes Data Set (TEDS) from 1992 to 2012, and discovered that, while the proportion of treatment admissions for pregnant women was stable (about 4%), the admissions for women who were pregnant and reported any marijuana use grew from 29% to 43%. A 2015 review found that cannabis use by pregnant mothers impaired brain maturation in their children, and that it also predisposed their children to neurodevelopmental disorders.
The role of the endocannabinoid system (ECS) in female fertility has long been suspected and studied. Most studies through 2013 linking development of the fetus and cannabis show effects of consumption during the gestational period, but abnormalities in the endocannabinoid system during the phase of placental development are also linked with problems in pregnancy. According to Sun and Dey (2012), endocannabinoid signaling plays a role in "female reproductive events, including preimplantation embryo development, oviductal embryo transport, embryo implantation, placentation, and parturition". Karusu "et al" (2011) said that a "clear correlation ... in the actual reproductive tissues of miscarrying versus healthy women has yet to be established. However, the adverse effects of marijuana smoke and THC on reproductive functions point to processes that are modulated by ECS."
Keimpema and colleagues (2011) said, "Prenatal cannabis exposure can lead to growth defects during formation of the nervous system"; "[c]annabis impacts the formation and functions of neuronal circuitries by targeting cannabinoid receptors ... By indiscriminately prolonging the "switched-on" period of cannabinoid receptors, cannabis can hijack endocannabinoid signals to evoke molecular rearrangements, leading to the erroneous wiring of neuronal networks". A report prepared for the Australian National Council on Drugs concluded cannabis and other cannabinoids are contraindicated in pregnancy as they may interact with the endocannabinoid system.
Morning sickness may be an evolved trait that protects the baby against toxins ingested by the mother. Evidence in support of this theory includes:
- Morning sickness is very common among pregnant women, which argues in favor of its being a functional adaptation and against the idea that it is a pathology.
- Fetal vulnerability to toxins peaks at around 3 months, which is also the time of peak susceptibility to morning sickness.
- There is a good correlation between toxin concentrations in foods, and the tastes and odors that cause revulsion.
Women who have "no" morning sickness are more likely to miscarry. This may be because such women are more likely to ingest substances that are harmful to the fetus.
In addition to protecting the fetus, morning sickness may also protect the mother. A pregnant woman's immune system is suppressed during pregnancy, presumably to reduce the chances of rejecting tissues of her own offspring. Because of this, animal products containing parasites and harmful bacteria can be especially dangerous to pregnant women. There is evidence that morning sickness is often triggered by animal products including meat and fish.
If morning sickness is a defense mechanism against the ingestion of toxins, the prescribing of anti-nausea medication to pregnant women may have the undesired side effect of causing birth defects or miscarriages by encouraging harmful dietary choices.
A vitamin deficiency can cause a disease or syndrome known as an avitaminosis or hypovitaminosis. This usually refers to a long-term deficiency of a vitamin. When caused by inadequate nutrition it can be classed as a "primary deficiency", and when due to an underlying disorder such as malabsorption it can be classed as a "secondary deficiency". An underlying disorder may be metabolic as in a defect converting tryptophan to niacin. It can also be the result of lifestyle choices including smoking and alcohol consumption.
Examples are vitamin A deficiency, folate deficiency, scurvy, vitamin D deficiency, vitamin E deficiency, and vitamin K deficiency. In the medical literature, any of these may also be called by names on the pattern of "hypovitaminosis" or "avitaminosis" + "[letter of vitamin]", for example, hypovitaminosis A, hypovitaminosis C, hypovitaminosis D.
Conversely hypervitaminosis is the syndrome of symptoms caused by over-retention of fat-soluble vitamins in the body.
- Vitamin A deficiency can cause keratomalacia.
- Thiamine (vitamin B1) deficiency causes beriberi and Wernicke–Korsakoff syndrome.
- Riboflavin (vitamin B2) deficiency causes ariboflavinosis.
- Niacin (vitamin B3) deficiency causes pellagra.
- Pantothenic acid (vitamin B5) deficiency causes chronic paresthesia.
- Vitamin B6
- Biotin (vitamin B7) deficiency negatively affects fertility and hair/skin growth. Deficiency can be caused by poor diet or genetic factors (such as mutations in the BTD gene, see multiple carboxylase deficiency).
- Folate (vitamin B9) deficiency is associated with numerous health problems. Fortification of certain foods with folate has drastically reduced the incidence of neural tube defects in countries where such fortification takes place. Deficiency can result from poor diet or genetic factors (such as mutations in the MTHFR gene that lead to compromised folate metabolism).
- Vitamin B12 (cobalamin) deficiency can lead to pernicious anemia, megaloblastic anemia, subacute combined degeneration of spinal cord, and methylmalonic acidemia among other conditions.
- Vitamin C (ascorbic acid) short-term deficiency can lead to weakness, weight loss and general aches and pains. Longer-term depletion may affect the connective tissue. Persistent vitamin C deficiency leads to scurvy.
- Vitamin D (cholecalciferol) deficiency is a known cause of rickets, and has been linked to numerous health problems.
- Vitamin E deficiency causes nerve problems due to poor conduction of electrical impulses along nerves due to changes in nerve membrane structure and function.
- Vitamin K (phylloquinone or menaquinone) deficiency causes impaired coagulation and has also been implicated in osteoporosis