Even if the fetus is not a person,abortion is immoral: The impairment argument

Much of the debate about the ethics of abortion has centered on whether the fetus is a person. In an attempt to sidestep this complex issue, I argue that, even if the fetus is not a person, abortion is immoral. To arrive at this conclusion, I argue that giving a fetus fetal alcohol syndrome is immoral, and that if this is so, then killing the fetus is immoral. Roughly, this is because killing the fetus impairs it more than giving it fetal alcohol syndrome. Since abortion (in most cases) amounts to killing the fetus, this means that abortion (in most cases) is immoral. I defend the premises of this argument against a plethora of objections, concluding that they either do not work, or commit their proponent to a controversial position.     

The impairment argument for the immorality of abortion revisited

Eric Vogelstein has defended Don Marquis' ‘future-like-ours' argument for the immorality of abortion against what is known as the Identity Objection, which contends that for a fetus to have a future like ours, it must be numerically identical to an entity like us that possesses valuable experiences some time in the future. On psychological accounts of personal identity, there is no identity relationship between the fetus and the entity with valuable experiences that it will become. Vogelstein maintains that a non-sentient fetus nonetheless has a future like ours because it is numerically identical with a future organism that has a mind that bears valuable experiences. Skott Brill, drawing on Jeff McMahan's embodied mind account, denies that human organisms directly have experiences, claiming that they only have experiences derivatively by virtue of their thinking part, and the loss of a future like ours is not transferred to the organism. I show that on McMahan's account, a strong case can be made for the organism having experiences directly, and the subject having these experiences derivatively. This negates Brill's reasoning, although it does imply that non-sentient fetuses do not have a future like ours in quite the same way as we do. I conclude that this is not problematic for Marquis' argument.     

Violinists,demandingness, and the impairment argument against abortion

The ‘impairment argument’ against abortion developed by Perry Hendricks aims to derive the wrongness of abortion from the wrongness of causing foetal alcohol syndrome (FAS). Hendricks endorses an ‘impairment principle’, which states that, if it is wrong to inflict an impairment of a certain degree on an organism, then, ceteris paribus, it is also wrong to inflict a more severe impairment on that organism. Causing FAS is wrong in virtue of the impairment it inflicts. But abortion inflicts an even more severe impairment (death), and so, ceteris paribus, is also wrong. Notably, Hendricks thinks that this argument does not require the claim that the foetus is a person. Here, I respond to Hendricks by arguing that the ceteris paribus clause of the impairment principle is not met in ordinary cases of pregnancy. Carrying an unwanted pregnancy to term is much more burdensome than is refraining from excessive drinking for nine months. This provides a pro tanto justification for obtaining an abortion that does not apply to causing FAS. If the foetus is not a person, it seems fairly clear to me that this justification is strong enough to render abortion permissible. Hendricks is therefore incorrect in claiming that the impairment argument can go without claims concerning foetal personhood. If the foetus is a person, then whether burdensomeness justifies abortion depends on certain questions relating to Thomson’s famous violinist argument. I will not attempt to answer those. But anyone who is otherwise sympathetic to Thomson’s argument should not be moved by the impairment argument.     

Against the impairment argument: A reply to Hendricks

In an article of this journal, Perry Hendricks makes a novel argument for the immorality of abortion. According to his impairment argument, abortion is immoral because: (a) it is wrong to impair a fetus to the nth degree, such as causing the fetus to have fetal alcohol syndrome (FAS); (b) it is wrong to impair a fetus to the n+1 degree (to cause the fetus to be more impaired than to have FAS); (c) killing the fetus impairs the fetus to the n+1 degree (causes it to be more impaired than to have FAS); (d) abortion kills the fetus; (e) therefore, abortion is immoral. The impairment argument is a promising account for the wrongness of abortion because it does not rely on the controversial metaphysical premise that a fetus is a person. This article aims to show, that despite some immediate advantages over the rival theories of the immorality of abortion there is a reason to believe that the impairment argument is untenable. That is because there are goods that can be achieved by abortion but that cannot be achieved by impairing the fetus.     

Abortion is incommensurable with fetal alcohol syndrome

A recent article argued for the immorality of abortion regardless of personhood status by comparing the impairment caused by fetal alcohol syndrome to the impairment caused by abortion. I argue that two of the premises in this argument fail and that, as such, one cannot reasonably attribute moral harms to abortion on the basis of the moral harms caused by fetal alcohol syndrome. The impairment argument relies on an inconsistent instantiation, which undermines the claim that personhood is irrelevant, and it does not fulfill its own ceteris paribus clause, which demands that no additional benefit be gained from abortion that would not be gained from causing fetal alcohol syndrome.     

Boonin on the future-like-ours argument against abortion

I argue that David Boonin has failed in his attempt to undermine Donald Marquis's future-like-ours argument against abortion. I show that the ethical principle advanced by Boonin in his critique to that argument is unable, contrary to what he claims, to account for the wrongness of infanticide. Then I argue that Boonin's critique misrepresents Marquis's argument. Although there is a way to restate his critique in order to avoid the misrepresentation, the success of such restatement is precluded by the wrongness of infanticide.     

The parenthood argument

Don Marquis is well known for his future like ours theory (FLO), according to which the killing beings like us is seriously morally wrong because it deprives us of a future we can value. According to Marquis, human fetuses possess a future they can come to value, and thus according to FLO have a right to life. Recently Mark Brown has argued that even if FLO shows fetuses have a right to life, it fails to show that fetuses have a right to use their mother's body, evoking Judith Jarvis Thomson's famous violinist case. In the wake of Brown's conclusion, Marquis presents a new argument—the parenthood argument (PA)—which he believes shows that abortion is seriously morally wrong. Here I argue that the PA fails to show abortion is seriously morally wrong for the same reasons FLO fails to show abortion is seriously morally wrong.     

The effects of alcohol on fetal development

Prenatal exposure to alcohol has profound effects on many aspects of fetal development. Although alterations of somatic growth and specific minor malformations of facial structure are most characteristic, the effects of alcohol on brain development are most significant in that they lead to substantial problems with neurobehavioral development. Since the initial recognition of the fetal alcohol syndrome (FAS), a number of important observations have been made from studies involving both humans and animals. Of particular importance, a number of maternal risk factors have been identified, which may well be of relevance relative to the development of strategies for prevention of the FAS as well as intervention for those who have been affected. These include maternal age >30 years, ethnic group, lower socioeconomic status, having had a previously affected child, maternal under-nutrition, and genetic background. The purpose of this review is to discuss these issues as well as to set forth a number of questions that have not adequately been addressed relative to alcohol's effect on fetal development. Of particular importance is the critical need to identify the full spectrum of structural defects associated with the prenatal effects of alcohol as well as to establish a neurobehavioral phenotype. Appreciation of both of these issues is necessary to understand the full impact of alcohol on fetal development.     

The pro-life argument from substantial identity and the pro-choice argument from asymmetric value: a reply to Patrick Lee

Lee claims that foetuses and adult humans are phases of the same identical substance, and thus have the same moral status because: first, foetuses and adults are the same physical organism, and second, the development from foetus to adult is quantitative and thus not a change of substance. Versus the first argument, I contend that the fact that foetuses and adults are the same physical organism implies only that they are the same thing but not the same substance, much as living adults and their corpses are the same thing (same body) but not the same substance. Against Lee's second argument, I contend that Lee confuses the nature of a process with the nature of its result. A process of quantitative change can produce a change in substance. Lee also fails to show that foetuses are rational and thus have all the essential properties of adults, as required for them to be the same substance. Against the pro-choice argument from asymmetric value (that only the fact that a human has become conscious of its life and begun to count on its continuing can explain human life's asymmetric moral value, i.e. that it is vastly worse to kill a human than not to produce one), Lee claims that foetus's lives are asymmetrically valuable to them before consciousness. This leads to counterintuitive outcomes, and it confuses the goodness of life (a symmetric value that cannot account for why it is worse to kill a human than not produce one) with asymmetric value.     

Genetic polymorphisms: impact on the risk of fetal alcohol spectrum disorders

Clinical reports on monozygotic and dizygotic twins provided the initial evidence for the involvement of genetic factors in risk vulnerability for fetal alcohol spectrum disorders (FASD) including fetal alcohol syndrome (FAS). Research with selectively bred and inbred rodents, genetic crosses of these lines and strains, and embryo culture studies have further clarified the role of both maternal and fetal genetics in the development of FASD. Research to identify specific polymorphisms contributing to FASD is still at an early stage. To date, polymorphisms of only one of the genes for the alcohol dehydrogenase enzyme family, the ADH1B, have been demonstrated to contribute to FASD vulnerability. In comparison with ADH1B*1, both maternal and fetal ADH1B*2 have been shown to reduce risk for FAS in a mixed ancestry South African population. ADH1B*3 appears to afford protection for FASD outcomes in African-American populations. Other candidate genes should be examined with respect to FASD risk, including those for the enzymes of serotonin metabolism, in particular the serotonin transporter. By its very nature, alcohol teratogenesis is the expression of the interaction of genes with environment. The study of genetic factors in FASD falls within the new field of ecogenetics. Understanding of the array of genetic factors in FASD will be enhanced by future genetic investigations, including case-control, family association, and linkage studies.     

The future‐like‐ours argument,animalism, and mereological universalism

Which metaphysical theories are involved—whether presupposed or implied—in Marquis’ future‐like‐ours (FLO) argument against abortion? Vogelstein has recently argued that the supporter of the FLO argument faces a problematic dilemma; in particular, Marquis, the main supporter of the argument, seems to have to either (a) abandon diachronic universalism (DU) or (b) acquiesce and declare that contraception is morally wrong. I argue that the premises of Marquis’ argument can be reasonably combined with a form of unrestricted composition and that the FLO argument is better viewed as including animalism, i.e., the thesis that we are animals.     

Selective abortion in Brazil: the anencephaly case

This paper discusses the Brazilian Supreme Court ruling on the case of anencephaly. In Brazil, abortion is a crime against the life of a fetus, and selective abortion of non-viable fetuses is prohibited. Following a paradigmatic case discussed by the Brazilian Supreme Court in 2004, the use of abortion was authorized in the case of a fetus with anencephaly. The objective of this paper is to analyze the ethical arguments of the case, in particular the strategy of avoiding the moral status of the fetus, the cornerstone thesis of the Catholic Church.     

The Rubinstein–Taybi syndrome: modeling mental impairment in the mouse

Mental impairment syndromes are diagnosed based on below-average general intellectual function originated during developmental periods. Intellectual abilities rely on the capability of our brain to obtain, process, store and retrieve information. Advances in the past decade on the molecular basis of memory have led to a better understanding of how a normal brain works but also have shed new light on our understanding of many pathologies of the nervous system, including diverse syndromes involving mental impairment. The recent multidisciplinary analysis of various mouse models for Rubinstein–Taybi syndrome has shown the power of animal models to produce an important leap forward in our understanding of a complex mental disease while simultaneously opening new avenues for its treatment. These studies also suggest that some of the cognitive and physiological deficits observed in mental impairment syndromes may not simply be caused by defects originated during development but may result from the continued requirement of specific enzymatic activities throughout life.     

Biomarkers for detection of prenatal alcohol exposure: a critical review of fatty acid ethyl esters in meconium

BACKGROUND: The objective of this study was a review of published studies utilizing measurement of fatty acid ethyl esters (FAEE) in meconium as biomarkers for prenatal alcohol exposure. METHODS: We completed a literature search of PubMed using the terms meconium, fatty acid ethyl esters, biomarkers, and prenatal alcohol exposure. We included only peer reviewed studies utilizing analysis of meconium for the presence of FAEE in humans through the year 2007. RESULTS: We found 10 articles reporting on original research examining the relationship of FAEE from meconium and prenatal alcohol exposure (PAE). The 10 articles used six different PAE assessment strategies and four different analytical techniques for determining FAEE endpoints. The articles included 2,221 subjects (range 4 to 725) with 455 (20.5%) subjects identified as exposed using the methods stated in the articles. FAEE levels above the studies' respective cutoffs were reported for 502 (22.6%) subjects. CONCLUSIONS: The accurate identification of alcohol‐exposed pregnancies represents a significant challenge in the development of FAEE detection cutoffs to maximize the sensitivity and specificity of the test. We present several options for the improvement of exposure assessment in future studies of FAEE as biomarkers for PAE. Birth Defects Research (Part A), 2008. © 2008 Wiley‐Liss, Inc.     

酒精诱导突触发生期神经元凋亡的分子机理

在突触发生时期,酒精诱导的神经元凋亡可能是胎儿酒精综合征产生的原因之一。酒精可能通过增加自由基的产生,影响神经递质受体的功能、干扰神经营养因子信号通路、激活内源性的细胞凋亡信号途径等分子机制,促进发育过程中的神经元凋亡。酒精影响发育的另一个重要机制是抑制蛋白质合成。新近的研究显示,双链RNA激活的蛋白激酶介导酒精引起的蛋白翻译受阻和神经元死亡。     

Risk for congenital anomalies associated with different sporadic and daily doses of alcohol consumption during pregnancy: a case-control study

BACKGROUND: The classic clinical criteria for the diagnosis of fetal alcohol syndrome (FAS) include a "characteristic" facial appearance, pre- and postnatal growth deficiency, microcephaly, mental retardation, and occasional major malformations. However, diagnostic constraints, especially in the newborn period, lead to an underestimate of their prevalence. We report an epidemiological study of the potential risk of congenital defects in the offspring of mothers who ingested different sporadic and daily amounts of alcohol during pregnancy. METHODS: The study was based on the data from the ECEMC hospital-based case-control study and surveillance system, with a methodology aimed not only at the surveillance of congenital anomalies, but also at investigating their characteristics, clustering, and causes. For the purposes of this study, we considered as exposed those infants whose mothers reported the ingestion of any amount of alcohol during gestation (4705 mothers of cases and 4329 mothers of controls), and classified them into five groups according to their levels of alcohol consumption. Two groups consisted of mothers who consumed increasing sporadic levels and the other three consisted of mothers who consumed increasing daily levels of alcohol. RESULTS: Our study showed that even low sporadic doses of alcohol consumption during pregnancy may increase the risk of congenital anomalies in the offspring and that this risk increases with increasing levels of alcohol exposure. CONCLUSIONS: The results of our study suggest that it is necessary to generalize the preventive norm and recommend complete abstinence from alcohol during gestation. Birth Defects Research (Part A), 2004.     

Illegal abortion and reproductive injustice in the Pacific Islands: A qualitative analysis of court data

The Oceania region is home to some of the world's most restrictive abortion laws, and there is evidence of Pacific Island women's reproductive oppression across several aspects of their reproductive lives, including in relation to contraceptive decision-making, birthing, and fertility. In this paper we analyse documents from court cases in the Pacific Islands regarding the illegal procurement of abortion. We undertook inductive thematic analysis of documents from eighteen illegal abortion court cases from Pacific Island countries. Using the lens of reproductive justice, we discuss the methods of abortion, the reported context of these abortions, and the ways in which these women and abortion were constructed in judges' summing up, judgements, or sentencing. Our analysis of these cases reveals layers of sexual and reproductive oppression experienced by these women that are related to colonialism, women's socioeconomic disadvantage, gendered violence, limited reproductive control, and the punitive consequences related to not performing gender appropriately.     

Intracellular calcium plays a critical role in the alcohol‐mediated death of cerebellar granule neurons

Alcohol is a potent neuroteratogen that can trigger neuronal death in the developing brain. However, the mechanism underlying this alcohol‐induced neuronal death is not fully understood. Utilizing primary cultures of cerebellar granule neurons (CGN), we tested the hypothesis that the alcohol‐induced increase in intracellular calcium [Ca²⁺]_i causes the death of CGN. Alcohol induced a dose‐dependent (200–800 mg/dL) neuronal death within 24 h. Ratiometric Ca²⁺ imaging with Fura‐2 revealed that alcohol causes a rapid (1–2 min), dose‐dependent increase in [Ca²⁺]_i, which persisted for the duration of the experiment (5 or 7 min). The alcohol‐induced increase in [Ca²⁺]_i was observed in Ca²⁺‐free media, suggesting intracellular Ca²⁺ release. Pre‐treatment of CGN cultures with an inhibitor (2‐APB) of the inositol‐triphosphate receptor (IP₃R), which regulates Ca²⁺ release from the endoplasmic reticulum (ER), blocked both the alcohol‐induced rise in [Ca²⁺]_i and the neuronal death caused by alcohol. Similarly, pre‐treatment with BAPTA/AM, a Ca²⁺‐chelator, also inhibited the alcohol‐induced surge in [Ca²⁺]_i and prevented neuronal death. In conclusion, alcohol disrupts [Ca²⁺]_i homeostasis in CGN by releasing Ca²⁺ from intracellular stores, resulting in a sustained increase in [Ca²⁺]_i. This sustained increase in [Ca²⁺]_i may be a key determinant in the mechanism underlying alcohol‐induced neuronal death.