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Correlation between genetic distance and birth defects

Correlation between genetic distance and birth defects


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It is folk knowledge that in-breeding causes birth defects due to similarity of genetics between parents. Consequently, is there a similar correlation between genetic distance of parents and probability of birth defects?

The best reference I can find of this is this handout by the Australian Centre for Genetics Education which says:

If parents are unrelated, their chance of having a child with a birth defect or disability is between 2% and 3%.

If parents are first cousins, the chance is a little higher at 5% to 6%. This is due to the increased chance that they will both carry the same autosomal recessive mutation, passed down through the family.

However this doesn't talk about genetic distance in particular.

This question is really just a more specific version focused on a single metric (genetic distance) and outcome (birth defects) of two previously answered questions:


For humans the closest argument may come from observational studies (since experiments aren't possible due to ethical reasons).

One example for the correlation of genetic distance and "defects" comes from a recent study of Chagnon et al. PNAS, 2017 http://www.pnas.org/content/114/13/E2590.full . Rather than asking for birth defects directly they however survey the number of children, and survival of children to age 15 (which would be one example of the term "inbreeding depression" that is more general than "birth defects")

Note that their study also sheds some light on the underlying big question, why certain types of kin relationships can be common despite their effect on the creation of healthy offspring - and why certain types of cousin relations are different from others.


Genetic risk maternal age

The table below shows the correlation of maternal age (mother's age) and the potential risk of human genetic abnormalities in children.

Australian Average Maternal Age Change

The first column shows maternal age, the second column shows the most common human chromosomal abnormality, trisomy 21 (Down syndrome), the third column shows all chromosomal abnormalities. The data below are from papers published in the 1980's. Ώ] ΐ] Α]


Interestingly, recent studies suggest that increasing paternal age (father's age) can also have affects on childhood mortality Β] and neurodevelopmental outcomes. Γ]


The Oocyte Mosaicism Selection theory Δ] suggests that "the incidence of trisomy 21 mosaicism in a cohort of normal fetal ovarian samples, indicating that an accumulation of trisomy 21 germ cells does indeed take place during fetal oogenesis, i.e., from the first to the second trimester of pregnancy. We presume that this accumulation of trisomy 21 (T21) cells is caused by their delay in maturation and lagging behind the normal cells. We further presume that this trend continues during the third trimester of pregnancy and postnatally, up until ovulation, thereby explaining the maternal age effect in Down syndrome." A similar selection model and ageing has been suggested for Trisomy 13. Ε]


Population Genetics

СТЭ лучше расшифровать как "стандартная теория эволюции": до настоящего синтеза там далеко, и сейчас разные авторы пробуют дополнить еë аспектами, упущенными — или совсем неизвестными — при создании СТЭ, но важными для эволюционирования в природе, чтобы действительно двигаться к "новому синтезу". Слишком уж много их в «стандартной теории» игнорируется ради нескольких ключевых абстракций, безусловно работающих, но дьявол в деталях, при учëте которых их придëтся менять — может, и не намного, но в значимых элементах.

Так, стержневой момент СТЭ, еë можно сказать, удерживающий камень — представление, что "никто и ничто не "подсказывает" организации, в какую сторону изменяться", по блестящему замечанию Б.Б.Жукова. Она реализует все возможности, а дальше вступает в действие отбор, оптимизирующий её для каждого следующего «шага» развития, причём безотносительно к любой более дальней перспективе, он «близорук», как пишут А.В.Марков и Е.Б.Наймарк в «Эволюции. Классические идеи в свете новых открытий» (2013). Селективные давления, фиксируемые в природе, неизменно реакция на «здесь и сейчас» без каких-либо попыток — и даже возможностей — прогноза более долгосрочных последствий и приспособления именно к ним.

Что выглядит достаточно странно, ибо здесь СТЭ противоречит сама себе: особи, составляющие популяцию, находясь под отбором, выбирают модель поведения (и модулируют внутреннее состояние, скажем, физиологическое) так, чтобы максимизировать итоговую приспособленность, для чего «оценивают» среду обитания и друг друга, скажем, по соответствующим сигналам — и здесь-то они, безусловно способны и на долгосрочный прогноз, и на опережающее отражение, хотя бы отчасти или частично. То и другое должно стать массовым, когда (или если) под отбором оказывается вся популяция? Однако же — см. написанное выше: отбор не «даёт» индивидам, успешным в борьбе за существование, сколько-нибудь долговременных выигрышей, лишь краткосрочный, и (что то же самое) не меняет их организации, исходя из «прогноза последствий» средовых изменений, только из «современных проблем» жизни в изменённых условиях.

Следовательно, везде, где мы ни обнаружим (в стремлении продолжать и улучшить синтез, родивший СТЭ!)

1) «подсказки» экологической или социальной среды, в какую сторону особям разного качества (или с разными признаками, связанными с приспособленностью) «лучше меняться», или

2) изменения организации «в сторону» сколько-нибудь долгосрочного выигрыша (т.е. исходящие из более или менее долговременных «прогнозов» ею средовых изменений и вызванных ими проблем размножения и выживания, а не только текущих), мы будем вынуждены говорить о номогенезе — направлении эволюции неселективными факторами, происходящими из разных источников: внешней среды, сложившейся организации особей или популяционной структуры, организующей их перемещения и взаимодействия «внутри» эволюционирующей популяции.

Замечу, что эти «подсказки», направляя изменения, меняя их скорость, интенсивность элиминации и другие параметры, отнюдь не отменяют отбора — он остаётся «топливом» происходящего движения по эволюционной траектории, но вот «руль» переходит в другие руки, да и «мотор» отчасти меняется. Причём это мы обнаруживаем, отнюдь не отрицая СТЭ а, напротив, делая второй шаг в синтезе, пытаясь детальней исследовать формирование локальных адаптаций, межпопуляционную дифференциацию и другие «штатные» для неё темы. Мы вынуждены его сделать, когда представления «первого шага» - нивелирующий эффект переселений особей между группировками и его случайный характер (в смысле независимый от их признаков, связанных с приспособленностью, и от средовых различий в месте оседания vs в месте исхода) — оказываются опровергнуты. С ростом тщательности исследования разных видов это оказывается всё чаще, почему их приходится рассматривать как нулевую гипотезу, опровержение которой требует от нас в качестве общего объяснения конкретных ситуаций развивать уже номогенетические представления, поскольку таких ситуаций оказывается всё больше и больше. В статье дан обзор соответствующих исследований


How radiation exposure affected health

Studies in Hiroshima (shown on map below) and Nagasaki conducted over the past 75 years have yielded important insights into the health effects of radiation. Researchers went to great lengths to determine survivors’ exposure, which depended partly on their distance from the hypocenter of the bombings.

Younger and more vulnerable

The younger an individual was at the time of the

bombings, the greater their risk of developing

cancer. But the risk decreased over a survivor’s

Women were at higher risk of developing

radiation-associated cancer, largely because of

additional cases of breast cancer.

Estimating the combined gamma and neutron radiation exposure for each individual was a challenge. Scientists began by calculating the expected radiation at various distances from the hypocenter, then verified those numbers in several ways. They cut samples from the copper roof ornaments of temples, for instance, and used mass spectrometry to check for a nickel isotope created by the bombs’ neutron bombardment. To study the degree to which buildings might have shielded victims, Oak Ridge National Laboratory built several typical Japanese houses at the Nevada Test Site and measured radiation levels inside and outside during atomic bomb tests in 1957 and 1958.

In the 1960s, ABCC also interviewed 28,000 survivors, asking for details on their exact location at the time of the blast, what sort of building they were in and on what floor, and even which way they were facing and whether they had been sitting or standing. The investigators used those details to assign a dose for every person in the LSS. (In the 1980s, they refined their work down to the level of individual organs.)

Year after year, the researchers have tracked the incidence of more than a dozen different types of cancers in the survivors, along with mortality. “Radiation risk is very complex,” says RERF epidemiologist Alina Brenner. It depends on sex and age at exposure and can be influenced by genetic susceptibility and lifestyle factors such as smoking. And risks “change over time as a population ages,” she says. But the sheer size and duration of the LSS, along with its detailed data on exposure, age, and sex, allowed researchers to draw many conclusions as the decades passed.

Dose was clearly very important. Among those who were within about 900 meters of the hypocenter and received more than 2 grays of radiation, 124 have died of cancer. (That dose is about 1000 times the average annual radiation dose from natural, medical, and occupational sources combined.) In its latest LSS update, RERF scientists conclude—based on comparisons of cancer deaths between the exposed group and unexposed controls—that radiation was responsible for 70 of those deaths (see graphic, above). Scientists call this number, 56.5%, the attributable fraction. The numbers of deaths are low because few who were close to ground zero survived the blast, explains Dale Preston, a biostatistician at Hirosoft International who previously worked at RERF. But among these people, “Most of the cancers are due to the radiation,” Preston says.

At 1 gray of exposure, the dose roughly 1100 meters from the hypocenter, the attributable fraction is 34.8%, and it decreases linearly for lower doses. Women suffered more radiation-associated cancers than men, largely because of cases of breast cancer. Both men and women exposed at a younger age were more at risk as they aged: “It’s thought that actively dividing cells are more susceptible to radiation effects, so younger people are more sensitive,” Ozasa says. Radiation most increased the risk of leukemia among survivors, followed by cancer of the stomach, lung, liver, and breast. There was little impact on cancers of the rectum, prostate, and kidney. Exposure also heightened the risk of heart failure and stroke, asthma, bronchitis, and gastrointestinal conditions, but less so for those with a 2-gray exposure, 16% of noncancer deaths were deemed attributable to radiation.

Katsuhiro Hirano, a Hiroshima area schoolteacher, heads an association of second-generation bomb survivors that is pushing for greater recognition of their health concerns.

The findings have had an “outsized influence” on policies and practices to make the use of ionizing radiation safer, says Kimberly Applegate, a radiation health expert retired from the University of Kentucky and a member of the International Commission on Radiological Protection (ICRP). The shielded rooms now routine for x-ray procedures and the dosimetry badges that track the accumulated exposure of health care and nuclear power plant workers are based in part on RERF data. ICRP is also using the data to develop recommendations for space tourists and astronauts traveling to Mars.

Whether RERF’s findings—based on one-time exposure—can shed light on the risks for those exposed to low doses over long periods of time is still a topic of debate. “Nobody really knows” what happens at low doses, says Robert Ullrich, RERF’s head of research. But so far, RERF’s conclusions are consistent with studies of those exposed to low doses at work, he says.

Participants themselves didn’t reap benefits from the studies, at least at first. Many joined expecting treatment for their ills, Iida says. But ABCC did not offer treatment because it might be seen as an admission of responsibility for their suffering by the United States. “ABCC did not have a good reputation among the hibakusha,” Iida says. Its top positions were held by U.S. scientists, adding to strains that led to a reorganization of ABCC into RERF in 1975. Japan and the United States now have equal representation on the Board of Councilors, key positions are split, and both countries contribute roughly half of its annual budget, now $31 million.

RERF now shares tests results and other individual data with study participants and provides them with counseling and referrals the Japanese government subsidizes health care for most hibakusha. In 2017, at a ceremony marking the 70 th anniversary of the commission’s founding, Niwa expressed regret that ABCC had studied bombing victims without treating them. “Survivors still feel there is an asymmetrical relationship” with RERF, says Akiko Naono, a sociologist at Kyoto University who studies hibakusha issues. They are the source of data but still see little in return.

U.S. researchers studying Hiroshima and Nagasaki bombing victims in 1945 initially worked from train cars. The research continues to this day.

New data are still coming in. In papers published in 2018 and 2019, for example, RERF scientists reported that women exposed to bomb radiation at the age of menarche, the first occurrence of menstruation, were at a higher risk of developing breast or uterine cancer later in life than those exposed before or after puberty. The proliferation of breast and uterine tissue during puberty provides “a lot of potential for DNA damage induced by radiation,” Brenner says.

The breast cancer study also gives a glimpse of RERF’s future agenda. The first analysis did not try to distinguish among the several major breast cancer subtypes, which vary in their biological mechanisms and prognoses, Brenner says. RERF is now analyzing cancerous tissue collected from patients to determine whether any of those subtypes occur more frequently in radiation victims. If so, that could provide hints about just how radiation damages tissue and raises cancer risk.

Samples are one resource RERF has in abundance. During detailed biennial health examinations of more than 23,000 of the survivors (including some exposed in utero), researchers have collected and preserved blood and urine samples, some dating back to the late 1950s. RERF has also amassed frozen cell lines from parents and children in 500 families in which at least one parent was exposed to radiation, plus an equal number of control families.

DNA in those samples—which so far has not been sequenced—could provide a check on the early data about the health of survivors’ offspring. Despite the reassuring findings about birth defects, some researchers worry radiation may have caused mutations in testes and ovaries that children born years later might have inherited. Researchers plan to compare the number and types of mutations found in the families to see whether any are more common in children of radiation-exposed parents, Ullrich says.

To estimate survivors’ exposure, U.S. scientists measured radiation inside and outside Japanese style houses during atomic bomb tests in the Nevada Desert in the 1950s.

RERF hasn’t yet seen any evidence of radiation-linked health effects in a study of 77,000 children of survivors. That could be “because we may not have the statistical power to be able to see” an impact, Ullrich says. Based on the findings, the Japanese government has refused to provide health care or screenings to the second generation.

But the possibility of harm still haunts survivors’ children, including Hirano. His mother, then 20, went searching for relatives in Hiroshima 2 days after the bombing, exposing herself to residual radiation. Hirano has no medical problems, but like many children of survivors, he has stories about health issues in his family. His mother had two stillbirths before he was born, and a cousin, also a second-generation survivor, died of leukemia in his 30s. “Many second-generation A-bomb survivors have great anxiety about their health,” he says. And those directly exposed to the bomb are often wracked with guilt if their children get sick or die, he says. Kodama is an example. Her youngest daughter died of ear canal cancer at age 45 in 2011. Ever since, she has wondered: “Was it because of the damage to my genes?”

Hirano’s association of survivors’ children is now taking the matter to court, seeking recognition as hibakusha and the health care that goes with it. “But the biggest hope of our movement,” he says, “is that there never again be second-generation victims” of atomic bombs.


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Chapter 19 - Introduction to Human Genetics

This chapter reviews the basic principles of human genetics to serve as a basis for other studies that deal with specific genetic approaches in clinical research. Genetics is the science that deals with the storage of information within the cell, its transmission from generation to generation, and variation among individuals within a population. Human genetics research has a long history, dating to the study of quantitative traits in the nineteenth century and to the study of Mendelian traits in the first decade of the twentieth century. Medical applications have included such landmarks as newborn screening for inborn errors of metabolism, cytogenetic analysis, molecular diagnosis, and therapeutic interventions such as enzyme replacement. Medical applications historically have been limited to relatively rare disorders caused primarily by mutations in individual genes or structural abnormalities of chromosomes. Recent advances, and especially the sequencing of the human genome, have opened the possibility of understanding genetic contributions to more common disorders, such as diabetes and hypertension. Genetic approaches are now being applied to conditions in virtually all areas of medicine. Genetic information is stored in the cell as molecules of deoxyribonucleic acid (DNA). Each DNA molecule consists of a pair of helical deoxyribose–phosphate backbones connected by hydrogen bonding between nucleotide bases. There are two types of nucleotide bases, purines (adenine [A] and guanine [G]) and pyrimidines (cytosine [C] and thymine [T]).


Classification and aetiology of birth defects

Birth defects are encountered frequently by paediatricians and are important causes of childhood morbidity and mortality. Paediatricians may be called upon to see children with single- or multiple-system birth defects. Birth defects can be classified based on their severity, pathogenetic mechanism or whether they involve a single system or multiple systems. This article reviews the classification of birth defects and gives a flavour of our current understanding of the aetiology of the complex developmental processes involved in the formation of these anomalies.


R esults

Residency and population density.

The number of male and female prairie voles classified as residents based on nest trapping data and MNKA estimates of population density were highly variable between study sites and among years ( Table 1 ). The total number of residents in Indiana in each of the 3 years of study was greater than that in every year in Kansas. Densities tended to be higher in Indiana than in Kansas, but in every year, population densities at both sites were considered “low” (< 100 voles/ha) according to the criteria established by Getz et al. (1993).

Microsatellite loci analyses.

For the microsatellite loci used to estimate pairwise relatedness, the proportion of loci typed ranged from 0.94 to 0.98 per year per population, and the probability of identity between 2 randomly chosen full siblings varied from 2휐 𢄣 to 3휐 𢄣 . The number of alleles per locus ranged from 9 to 23 in the Kansas population ( Table 2 ) and 4 to 21 in the Indiana population ( Table 3 ). In the Kansas population, observed heterozygosity ranged from 0.40 to 0.97 while expected heterozygosity ranged from 0.42 to 0.94 ( Table 2 ). In Indiana, the observed and expected heterozygosity ranged from 0.08 to 0.89 and 0.09 to 0.90, respectively ( Table 3 ). After Bonferroni correction, only a single locus in 1 population in 1 year (Indiana 2008 Table 3 ) deviated significantly from Hardy−Weinberg expectations, likely due to a null allele. Since we used a small number of loci to assess relatedness in this study, the influence of a single locus on estimates of spatial genetic structure could potentially be substantial. Therefore, we did not include the genotypic data from the locus (MSMM3) that was not in Hardy−Weinberg equilibrium in the Indiana population in 2008, in our spatial autocorrelation analyses to examine the relationship between genetic and geographic distance among same-sex voles in Indiana.

Table 2.

Number of prairie voles (Microtus ochrogaster) genotyped (n), number of alleles per locus, and observed (H o) and expected (H e) heterozygosities for the 2005, 2006, and 2008 field seasons in Kansas.

Locus nNumber of alleles H o H e
200520062008200520062008200520062008200520062008
AV1357311431716140.740.810.830.910.920.87
MOE255291431515160.910.930.870.880.920.89
MSMM254291361717170.960.970.900.920.940.92
MSMM356301401316150.880.930.790.890.890.87
MSMM557311382019230.770.610.870.930.900.93
MSMM65730144910100.460.400.460.460.500.42

Table 3.

Number of prairie voles (Microtus ochrogaster) genotyped (n), number of alleles per locus, and observed (H o) and expected (H e) heterozygosities for the 2006, 2007, and 2008 field seasons in Indiana.

Locus nNumber of alleles H o H e
200620072008200620072008200620072008200620072008
AV131092833261414130.880.850.850.870.860.87
MOE21192823281617150.760.820.850.860.850.84
MSMM21202763281614140.880.850.890.880.870.89
MSMM31172592991112100.870.820.810.850.860.85 a
MSMM51022723272120210.820.820.860.900.900.89
MSMM612028532881040.140.080.090.170.100.09

a Locus not in Hardy–Weinberg equilibrium.

Relationship between relatedness and geographic distance.

Estimates of pairwise relatedness among males and females in Kansas ranged from 𢄠.4 to 0.47 and 𢄠.36 to 1.0, respectively. In Indiana, pairwise relatedness ranged from 𢄠.45 to 0.71 among males and 𢄠.75 to 1.0 among females. The mean distance separating unrelated females in Kansas (78.2 m ± 6.4) was more than twice the mean distance separating related females (35.5 m ± 6.4 P < 0.0001 Fig. 1 ). No significant differences were detected between the mean distances separating unrelated and related males in Kansas (P = 0. 483), or voles of either sex in Indiana (females: P = 0.256 males: P = 0.852).

The mean distance (± SE) separating related (r ≥ 0.25, ■) versus unrelated (r < 0.25, □) resident adult voles (Microtus ochrogaster) for males and females compared separately within the Kansas (KS) and Indiana (IN) populations. Means were determined by combining the 3 years of data collected for each sex within each population. Sample sizes listed on bars.

The spatial autocorrelation coefficient r was significantly greater than expected by chance for both females (P = 0.001 Fig. 2a ) and males (P = 0.013 Fig. 2b ) at 20 m in the Kansas population, indicating that prairie voles separated by less than 20 m were significantly more related to same-sex conspecifics than expected by chance. None of the values of r were significant at distances greater than 20 m for males, but females showed significant negative spatial autocorrelation at distances of 80 m (P = 0.002) and 100 m (P = 0.002). In the Indiana population, we detected a significant positive spatial autocorrelation among females at distances less than 20 m (P = 0.033 Fig. 3a ) but females appeared to be randomly distributed with respect to relatedness at all greater distances. Among males in the Indiana population, spatial autocorrelation analysis revealed a significant negative spatial autocorrelation at 80 m (P = 0.008 Fig. 3b ), and a significant positive spatial autocorrelation at 220 m (P = 0.031 Fig. 3b ).

Correlograms illustrating the genetic correlation coefficient (r) as a function of geographical distance for resident adult a) female and b) male prairie voles (Microtus ochrogaster) in Kansas. Upper and lower permuted 95% CI (dashed lines) about the null hypothesis of no genetic structure (r = 0), and bootstrapped 95% CI error bars about r are shown. Sample sizes for each distance category are indicated at top of correlograms.

Correlograms illustrating the genetic correlation coefficient (r) as a function of geographical distance for resident adult a) female and b) male prairie voles (Microtus ochrogaster) in Indiana. Upper and lower permuted 95% CI (dashed lines) about the null hypothesis of no genetic structure (r = 0), and bootstrapped 95% CI error bars about r are shown. Sample sizes for each distance category are indicated at top of correlograms.


ACKNOWLEDGMENTS

We thank the Ministries of Education and Water and Forests of the Central African Republic government and the Ministry of Scientific Research and Ministry of Forest Economy of the Republic of Congo for giving us the permission to conduct this research project. We are very grateful to the staff of the Dzanga-Sangha Project and the World Wildlife Fund (WWF) Central African Republic, as well as to the staff of the Wildlife Conservation Society (WCS) Congo Program in the Nouabalé-Ndoki National Park for supporting our research and providing logistical support. Thanks to the invaluable and numerous Aka gorilla trackers from Bai Hokou and Mongambe, who have been crucial for habituation and daily follows of the gorillas. We also thank the whole Mondika team (Mike Stucker, Erlych Obecki Bayanga, Jaslin Bounzanga, Stevy Pebou, Franck Moutengue, Philemon Bembo and all the trackers) for their help. We thank Benjamin Robira for calculating the center point of the home range of the study groups. Long-term monitoring of gorillas at Mondika was made possible through funding by US Fish & Wildlife Services, US AID, TNS Foundation, GRASP LifeWeb, and WCS. We thank the platform "Paléogénomique et Génétique Moléculaire" from the French National Museum of Natural History (MNHN) at the Musée de l'Homme in Paris, for providing technical assistance and funds for the experiments conducted in this study. We thank also the MNHN in France, the Labex BCDiv, the Action transversal du Muséum (ATM), SAFAPE ANR, and the Projets Fédérateurs of the Human and Environment Department of the MNHN for financing the field data collection.


Conclusions

These simulations indicate that when all species are adequately represented in the reference data sets, genetic methods can give reliable species identifications. The degree to which species are genetically differentiated appears to be a critical determinant of success. When all species are represented in the reference data set, BLAST, distance, and liberal tree-based methods will be equally successful and make more correct identifications than the strict tree-based method, which requires that the query sequence must fall within, and not sister to, a single-species clade. The strict tree-based method is conservative, making ambiguous or false-negative identifications at a rate inversely proportional to the number of reference sequences per species.

When the correct species has not been included in the reference data set, only the tree-based methods, especially the strict method, coupled with a distance threshold will protect against false positives. The other methods are ubiquitously poor or have a rate of error determined by empirical thresholds.

One of the prime motivations for the development of genetic methods is their large-scale application to species identification. A major criticism of these methods has been that they will be unreliable because of inadequate sampling of genetic variation and incorrect taxonomy. These concerns can be mitigated by applying a conservative approach, by using the strict tree-based method. However, once the specific taxonomic group is well understood and its genetic diversity is fully sampled, this conservative approach is no longer warranted. It would be appropriate to switch to whichever of the other methods, BLAST, distance, or a more liberal tree-based approach, are the computationally most efficient and provide the greatest speed. The requirement for both well-differentiated species and multiple reference sequences per species, in order to achieve an acceptable level of successful identifications, may render these techniques inappropriate in some circumstances. In a finite world, there will always be a trade-off between the accuracy and the cost, measured in both time and money, of species identification. It is important that the reliabilities of different approaches are fully understood so that an informed decision may be made.