What Genes Cant Do
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Studying thin individuals might help develop new treatments to help others avoid becoming overweight, Kathiresan said. The study looked primarily at people with European ancestry. Additional research is needed into different ancestral backgrounds, researchers stated. Skip to content. You may have obesity genes to blame. Researchers have found a genetic predisposition for obesity. Inquirer Morning Newsletter. Sign Up Inquirer Morning Newsletter. Mari A. Schaefer MariSchaefer mschaefer inquirer. Never Miss a Story.
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Aubrey Whelan. Stay away from tea, coffee and lavatory water on flights, report recommends. Natalie B. This strongly reinforces the DNA metaphor by suggesting that genes must be contributing to risk in important ways. The reason is that the fabric of genetic causation is probabilistic both in terms of the inheritance of genes, and their effects. However, most studies of such specific hypotheses have come up empty. In keeping with the DNA metaphor, the idea of the genomic approach is to assume that genes simply must be causing a trait of interest, and to look across the entire genome to find variants that are more common in individuals with the trait than in those without it.
The hope was that we would soon eliminate the debilitating or fatal diseases to which most of us now fall victim, once we had exhaustive knowledge of genome-wide variation. Genomic studies searching for causal genes have grown ever larger and more expensive, but commensurately important results have yet to roll in. Most of the estimated overall genetic influence on the traits or diseases of interest is still unidentified.
However, the most recent study, by Heather Elding and colleagues at University College London, published in The American Journal of Human Genetics , estimates that the number of genes associated with the disease is around , most with very small effects, which explains only a small amount of the genetic background of this disease. Height is an easily measured trait that clearly runs in families, and many studies have been done looking for genes for this trait.
More than contributing genetic regions, from an estimated or so, have been found but, again, none with very large effects. In fact, to date, only 10 per cent or so of the variation in height has been explained, as a study from Exeter University published in Nature in October demonstrated.
Many more genes will be found to contribute, but environmental factors such as diet or illness will as well. Behavioral and psychiatric traits are proving to be just as intractable, and the story is similar with the same kinds of studies in other species, as varied as yeast, insects, and plants. What is being documented is the blunt reality of the state of nature. These environmental factors are themselves quite complex and elusive to assess, or even identify. Perhaps the most important single fact lurking in all of this is that when numerous genes contribute to a trait, the specific set of contributing variants is different for every individual.
What Genes Can't Do // Reviews // Notre Dame Philosophical Reviews // University of Notre Dame
This is a many-to-many causal relationship: there are many genetic paths to a single height, blood pressure, triglyceride, or cholesterol level. Equally, a given genotype is consistent with many different trait values. This makes another aspect of the DNA metaphor problematic. By cooperation we do not necessarily mean the social, emotional variety.
Cooperation describes the way in which a trait is produced by many factors, the countless genes and lifestyle aspects that contribute to the trait.
If these factors do not work adequately together, the trait will not successfully be built into an embryo in the first place. Extensive webs of cooperation within us — genes with genes, organelles with organelles, cells with cells, tissues with tissues, and so on — mean that except for the rare disastrous instances, individual contributing genes neither spell doom nor success on their own. If there are many ways to fail — as the rare, serious genetic mutations show — there are a great many more ways to succeed.
Another way to view cooperation among genes is that evolution has provided a kind of redundancy that protects individuals from harmful mutations and overly harsh screening by natural selection. If each gene is, in itself, not a deterministic cause of some useful trait, then the organism can often do just fine with modification of or even loss of that gene, because other contributing genes cover for it, or any one modification has only a trivial effect.
We know, for example, that many well-known variants that are clearly associated with very serious human disease are the normal state in other species.
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Indeed, whole-genome sequence studies have consistently shown that all of us carry a significant number of defunct or seriously disrupted genes, and this can include genes whose mutations are clearly implicated in some disease contexts, even if we ourselves are healthy. All this might seem confusing: genes are molecules and hence fundamental causal agents of life, yet their effects are highly probabilistic and very hard to pin down or predict.
As we have tried to explain, although genetics and evolutionary research are often very technical, the issues are actually reasonably simple. In this light, we can return to the intriguing topic of behavior and, particularly, of free will. C omplex organisation arises from webs of interaction among causal factors. Even if individual factors cannot be held responsible for particular developments, complex phenomena such as people, skills, skulls, languages, and even football teams clearly do exist, and have a material rather than any mystical or immaterial basis.
In fact, emergent complexity takes essentially the same form , and presents the same challenge, in the very different contexts of biology, ecology, anthropology, sport — and free will.
The 3230 genes you can’t do without
Political preference? You name it — even our moral decisions must, in principle , be predictable from our inherent, inherited genome. Is this just a temporary limit in scientific knowledge, or is something more profound going on here? Perhaps as we are evolved biological organisms, uncertainty is unsettling to us. Dualism asserts that mind and consciousness, whatever they are, are free from the usual material constraints.
In other words, we have free will, just since we feel that we do. Free will is at the heart of assumptions that we are morally responsible for our actions, which in turn affects social and legal policy as well as religious notions of earned salvation.
Even if genes affect intelligence, we can’t engineer cleverness
Yet, how can they not be the product of their genes? An answer might lie in the understanding of complex causation that we have presented here. Mind, wondrous though it might be, is in fact the product of molecular forces, including genes. Yet the mind seems fundamentally unpredictable from genes. We should not be at all surprised that, just like most other traits, behaviour is not specifically predictable from genes.
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Our mental activities feel as if they are free, and their unpredictability supports that feeling. But the reason is that the causation involved is so complex and deeply probabilistic that it is, in effect, unpredictable even if we were to try to enumerate all the contributing factors. In that sense, for all practical purposes, we are indeed free. It is sobering to point out that none of these issues about determinism, probability, complex causation — and even their implications for free will — are new.
They can be traced back to the classical philosophers, and were vigorously debated along with the development of probability and statistics in the 18th through to the 19th centuries, and then reinforced by discoveries in sub-atomic physics in the 20th century. The significance and challenge of probabilistic multifactorial causation have been recognised.
bbmpay.veritrans.co.id/gay-dating-de-villanueva-de-la-torre.php What is new is that we have a much better documentation of this problem from a genetic point of view. But, conceptually, we have not advanced very much in our understanding of what are deeply puzzling aspects of the way the cosmos — including life — works. We want the comfort and sense of safety that comes from predictability.
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And, in the scientific era, we assume a material understanding of causation. We want to be in control, to be able to manipulate nature to alleviate the problems that we face in a finite life in a finite world.