Is cloning human beings morally wrong? The basis for the one serious objection to cloning is that, because of what a clone is, clones would have much worse lives than non-clones. I sketch a fragment of moral theory to make sense of the objection. I then outline several ways in which it might be claimed that, because of what a clone is, clones would have much worse lives than non-clones. In particular, I look at various ideas connected with autonomy. I conclude that there is no basis to the claim that, because of what a clone is, clones would have much worse lives than non-clones. I therefore reject the claim that cloning human beings is morally wrong. (+info)
Equality and selection for existence.
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It is argued that the policy of excluding from further life some human gametes and pre-embryos as "unfit" for existence is not at odds with a defensible idea of human equality. Such an idea must be compatible with the obvious fact that the "functional" value of humans differs, that their "use" to themselves and others differs. A defensible idea of human equality is instead grounded in the fact that as this functional difference is genetically determined, it is nothing which makes humans deserve or be worthy of being better or worse off. Rather, nobody is worth a better life than anyone else. This idea of equality is, however, not applicable to gametes and pre-embryos, since they are not human beings, but something out of which human beings develop. (+info)
Can we learn from eugenics?
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Eugenics casts a long shadow over contemporary genetics. Any measure, whether in clinical genetics or biotechnology, which is suspected of eugenic intent is likely to be opposed on that ground. Yet there is little consensus on what this word signifies, and often only a remote connection to the very complex set of social movements which took that name. After a brief historical summary of eugenics, this essay attempts to locate any wrongs inherent in eugenic doctrines. Four candidates are examined and rejected. The moral challenge posed by eugenics for genetics in our own time, I argue, is to achieve social justice. (+info)
Genetics of mouse behavior: interactions with laboratory environment.
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Strains of mice that show characteristic patterns of behavior are critical for research in neurobehavioral genetics. Possible confounding influences of the laboratory environment were studied in several inbred strains and one null mutant by simultaneous testing in three laboratories on a battery of six behaviors. Apparatus, test protocols, and many environmental variables were rigorously equated. Strains differed markedly in all behaviors, and despite standardization, there were systematic differences in behavior across labs. For some tests, the magnitude of genetic differences depended upon the specific testing lab. Thus, experiments characterizing mutants may yield results that are idiosyncratic to a particular laboratory. (+info)
Genetically determined obesity in Prader-Willi syndrome: the ethics and legality of treatment.
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A central characteristic of people with Prader-Willi Syndrome (PWS) is an apparent insatiable appetite leading to severe overeating and the potential for marked obesity and associated serious health problems and premature death. This behaviour may be due to the effects of the genetic defect resulting from the chromosome 15 abnormalities associated with the syndrome. We examine the ethical and legal dilemmas that can arise in the care of people with PWS. A tension exists between a genetic deterministic perspective and that of individual choice. We conclude that the determination of the capacity of a person with PWS to make decisions about his/her eating behaviour and to control that behaviour is of particular importance in resolving this dilemma. If the person is found to lack capacity, the common law principles of acting in a person's "best interests" using the "least restrictive alternative" may be helpful. Allowing serious weight gain in the absence of careful consideration of these issues is an abdication of responsibility. (+info)
The genetic basis of cognition.
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The molecular characterization of single-gene disorders or chromosomal abnormalities that result in a cognitive abnormality (predominantly mental retardation) and of the genetic variants responsible for variation in intellectual abilities (such as IQ, language impairment and dyslexia) is expected to provide new insights into the biology of human cognitive processes. To date this hope has not been realized. Success in finding mutations that give rise to mental retardation has not been matched by advances in our understanding of how genes influence cognition. In contrast, the use of engineered mutations in mice to study models of learning and memory has cast new light on the molecular basis of memory. A comparison of studies of human and mouse mutations indicates the limitations of current genetic approaches to the understanding of human cognition. It is essential to interpret a mutation's effect within a well-characterized neural system; mutations can be used to define gene function only when the mutation has an effect on a system whose constituents form a serial causal chain, such as the molecular components of a signal transduction pathway. Typically, however, genetic mutations with a cognitive and behavioural phenotype are characterized by specific effects on different systems whose inter-relationships are unknown. Genetic approaches are currently limited to exploring neuronal function; it is not yet clear whether they will throw light on how neuronal connections give rise to cognitive processes. We need a much greater integration of different levels of understanding of cognition in order to exploit the genetic discoveries. In short, a rapprochement between molecular and systems neuroscience is required. (+info)
General kin selection models for genetic evolution of sib altruism in diploid and haplodiploid species.
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A population genetic approach is presented for general analysis and comparison of kin selection models of sib and half-sib altruism. Nine models are described, each assuming a particular mode of inheritance, number of female inseminations, and Mendelian dominance of the altruist gene. In each model, the selective effects of altruism are described in terms of two general fitness functions, A(beta) and S(beta), giving respectively the expected fitness of an altruist and a nonaltruist as a function of the fraction of altruists beta in a given sibship. For each model, exact conditions are reported for stability at altruist and nonaltruist fixation. Under the Table 3 axions, the stability conditions may then be partially ordered on the basis of implications holding between pairs of conditions. The partial orderings are compared with predictions of the kin selection theory of Hamilton. (+info)
Familial influence on variation in age of onset and behavioural phenotype in Alzheimer's disease.
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BACKGROUND: Alzheimer's disease manifests considerable heterogeneity, the cause of which is unknown. AIMS: To determine the familial (genotypic) influence on phenomenology (phenotype) in Alzheimer's disease. METHOD: Affected sibling pairs with Alzheimer's disease were assessed for a range of cognitive and non-cognitive symptoms. Resemblance for phenotypic characteristics was estimated using intraclass correlations for continuous traits and by pairwise concordance for dichotomous traits. The relationship between age of onset and APOE genotype was examined using linear regression analysis. RESULTS: Significant familial effects on age of onset (intraclass correlation 0.41) and mood state (intraclass correlation 0.26), and a relatively high pairwise concordance for agitation (excess concordance 0.1) were found. The APOE locus was found to account for 4% of the variance in age of onset. CONCLUSIONS: Substantial familial influence on age of onset, depression and agitation suggests that genotype does influence phenotype in Alzheimer's disease. Establishing the molecular basis for this phenotypic variation may prove relevant to other neuropsychiatric disorders. (+info)