J2014

I think this is good principle. I think the problem comes though when give rights to humans that protect us against things which could produce more benifit than harm. Consider for example experimenting on babies or the mentally disabled. This could result in scientific discoveries that save thousands of lives. Consider slavery, We consider it wrong even if it were to bring benifits to our economy. The point is that human lives are protected by rights that mean we should not be treated as property ie as a slave . Yet when it comes to animal experimentation we treat animals as property. To be consistent then we must either accept that experiments on babies could be permissible or that animal experiments are wrong.

I don't think we need to prove animals have feelings for the original argument to be accepted, merely that we have as much evidence to support this as to support the belief that other humans have feelings

Yes, perhaps it was premature to say they induced depression. Perhaps it would be better to say they induced experiences which resulted in a change in the perception of ambiguous stimuli. The same thing was done in another study using chronic stress to affect their preferences. http://www.ncbi.nlm.nih.gov/pubmed/23847501 I suppose the difference between a plant and an animal like a rat is that rats can learn about the 'what, where and when' of events. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3690604// They combine multiple sensory inputs to form a new representation of the world. So while a plant expresses reflex behavior, they cannot learn associatively. If the ability to be conscious is defined as the ability to bind together multiple sensory imputs to one continuous experience , then it appears animals express behavior consistent with this. I think you are right that we cannot prove that animals have sentience based on behavior, but then again all I have to judge other humans have sentience is that they behave as if they did have it. By the principle of equal consideration then, on what basis do we discriminate between the sentient like behavior of animals and the sentient like behavior of humans?

If we accept the wikipedia definition of sentience as the abilty to experience perceive or feel subjectivity, then I would say there is evidence. For example in this study ... http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055368/ "Rats were trained to press a lever to receive a food reward contingent to one tone and to press another lever in response to a different tone to avoid punishment by electric foot-shock. In the ambiguous-cue test, the lever-press responses to tones with frequencies intermediate to the trained tones were taken as indicators for the rats' expectation of a positive or negative event." The authors then induced the animals to become depressed, and found the animals were more likely to respond to the ambiguous stimuli pessimistically, ie. they experienced subjectivity. They also expressed preferences behaviorally, showing they have interests.

Hi, l have previously been very pro animal experimentation based on a utilitarian argument. Recently I have however come across the animal rights argument of Gary Francione that as animals are sentient and have interests, these interests deserve to be protected to the same degree as we protect the interests of humans of comparative sentience, ie. babies or the mentally disabled. To conduct animal research therefore seems to disregard the interest of animals to not be treated as property (that is have their interests to continue to live be subservient to our own interests). Do you have any argument to refute this? Do you think animal research is justifiable, and why?

In E.coli new phospholipids are synthesised from dihydroxyacetone phosphate, which is it self made from fructose 1,6-bisphosphate. http://www.annualrev...7.030502.090851 Essentially cells grow their membranes through the metabolism of sugers.

I am not a climate scientist, however from my understanding what you describe would be the the ideal experiment. Obviously that cant be done. The climate models are not however simple statistical correlations that lack controls. They are complex computer simulations that take data from experiments that approximate the relative effects of as many variables as possible that would have an effect on the climate, thereby controlling for them. They then run these models to see how well they match past climate conditions, and how CO2 has affected the past climate. They then run them forwards in time to see how predicted value of CO2 will affect the climate. The potential effects of all the variables we can think of that could also produce global warming are controlled for, yet CO2 emission still are still shown to be causing global warming. Citing specific processes that may act to reverse climate change, or be misconstrued as human climate change, is pointless unless you have knowledge of the statistical and computational models of climate change, and know whether or not those specific processes that can affect the climate have been included in climate models. for example for the whole its the sun argument.... http://cc.oulu.fi/~usoskin/personal/nature02995.pdf http://arxiv.org/PS_cache/arxiv/pdf/0901/0901.0515v1.pdf http://www.warwickhughes.com/agri/lockwood2007.pdf

This review does suggest epigentics may play a role in autism, however I have never seen any evidence to suggest the epigenetic changes were induced by "overstimulation of the information age". Schanen NC. 2006 Epigenetics of autism spectrum disorders. Hum Mol Genet. 2006 Oct 15;15 Spec No 2:R138-50 http://www.ncbi.nlm.nih.gov/pubmed/16987877?dopt=Abstract

What control in that experiment distingueishes between their hypothesis, that placental status can influence IQ, and the alternate hypothesis that genetics influenced them both? There was none. That is becasue natural experiments are limited in controls. The researchers do not randomly induce the experimental manipulation to see what the effects are, rather they find "natural" experimental manipulations. Because the induction of the experimental manipulation in not random, other factors can lead to both the assumed controled experimental manipulation being merely correlated with an effect, rather than there being a causal relationship. Surely the only way to investigate if an effect is causal or spurious is to perform a control? Since you appear not to understand what confounding factors are, or why the are so prevalent in observational studies, I conclude that you don't understand the research. This article makes some of the arguements i put forward very well Why Twin Studies Are Problematic for the Study of Political Ideology: Rethinking Are Political Orientations Genetically Transmitted? http://sites.lafayette.edu/suhaye/files/2010/01/plugin-critique_of_twin_studies_-_suhay__kalmoe__mcdermott_101007.pdf also Twin Studies of Political Behavior: Untenable Assumptions? Jon Beckwith and Corey A. Morris DOI: 10.1017/S1537592708081917

I did the above and now you dont want to accept the logical conclusion to save face. as for the pitiful attempt to disparage my argument by saying I do not understand what I am talking about, or the progress of science, I have already explained how I think epidemiology fits into the progress of science, providing important insight in to what genes may be important that can be further explored in animal models. If you actually think that any statement in science is obviously correct, or any experiment can find conclusive evidence then you really have no idea how science works. I think it is you who has no idea what you are talking about. You certainly have very poor debating skills. You asked me for epidemiological evidence that could show, in principle, that the twin studies data could be due to developmental factors. I did and now you only respond with vague insults. As for the iq twins study, I don't think it does necessary show that placental status affects iq. There could for example be a gene, or collection of genes, that both increase the chances of two embryos sharing a placenta, and quite independently of that effect, also have an effect on iq.

IQ is not a normal trait? Firstly you should be asking about the competence of the delivery teams because a traumatic birth can also be correlated with schizophrenia. The disposition of the family dog is not relevent because, it would, i assume, not be a shared by twins reared apart. Futhermore there is no mechanism that you can extrapolate from animal models that would give rise to such an effect. There is however for the effects of share experience in the womb (see the previous schizophrenia review paper) I really dont. The fact that the epidemiolgists in the journal say "Although epidemiological studies cannot establish causality," should show you why it is not correct to imply that twin studies could show "conclusively" genetic inhevitance of behaviour traits. I used your terms to show that epidemiology is very poor at showing causation, because when controled for something else... in the schizophrenia case, infection with influenza...... a different result can be attained. This shows that epidemiolgy is by its nature poorly controled. It can show correlation, it is excellent at identifing possible genes involved in disease, but because it is poorly controled, it cannot show causation. Hmmmm, i really dont think you were. I am pretty sure you were implying that twin studies could show "conclusively" genetic inhevitance of behaviour traits. They showed it is not neccessary conclusive at all. They gave one example of an environmental factor that can be misconstrued as a genetic factor, as I suggested could be the case. There could therfore be many other environmental factors also misconstrued for genetic factors. We cant know because epidemiology and natural experiments lack proper controls.

I think you dont understand my arguement. You're the one who claimed that twin studies showed "conclusively" the result of genetic inheritance. It sounded a bit like naive verificationism so I gave an possible alternative interpretation of the data that is not falsified by that experiement. If we are to come at this question from an unbiased perspective then all the twin studies you metioned give support to the shared placenta hypothesis. At least to the extent that they also give support to the shared DNA hypothesis. I might as well ask you if you could give me any evidence that the shared DNA of twins is not down to shared developement. The only way would be to implant the embryos of monozygotic twins into different women and then see if their behaviour still has a high degree of correlation. Or alternatively implant two genetically unrelated embryos into one person, and see if that increases the likelyhood of similar characteristics. Obviously neither experiment has or will be done. Can you give me an example of a genetic change that was induced in a human to see if it changed behaviour? Since natural experiments are very poorly controled i think you would have a hard job. Anyway as for some epidemiology on the effects of sharing a placenta, below is a study showing that approx 12% of the variance in IQ in monozygotic twins derives from sharing or not the same placentas Jacobs et al 2001, Heritability estimates of intelligence in twins: effect of chorion type. Behav Genet. 2001 Mar;31(2):209-17. http://www.ncbi.nlm....pubmed/11545537 and here is a short review with respect to schizophrenia http://www.its.calte...erspec%2007.pdf some good links in that too if you're interested. This paper ( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2632220/?tool=pubmed ) suggests that up to "14% of schizophrenia cases would not have occurred if influenza infection during early to mid-gestation had been prevented". If that is true, then could this have been misconstrued in the twin studies as a genetic cause? What other environmental factors in the womb could also be misconstrued as genetic? I don't know. However looking for alternate explanations for what has apparently been "conclusively" shown to be true IS the job of a real scientist, and indeed you should attempt to argue that it may have been down to other factors, but you should not belittle other explanations because it doesn't fit within your narrow view of science.

Indeed that is exactly what i am saying, it does not conclusively show the result is due to genetic inheritance. It could also be due to sharing the exact same conditions in the womb. Non identical twins could have a lower correlation bacause although they share the same womb, they do not share the same placenta. I am not saying that this shared developement hypothesis is true, but it should not be disregarded either.

The problem with natural experiments tho is that they are very poorly controled, and that is what prevents these corralative studies showing causation. In the twin studies for example, monozygotic twins do not just share the same DNA, they also share the same placenta. Surely any correlation between genetics and behaviour could then be due to shared developement in the womb rather than shared genetics? Similar lack of controls can be found in genome wide association studies, genes may be correlated with unknown environmental factors rather than behaviour itself, eg people with a specific mutation may just happen by chance to be more likely to be part of a specific socioeconmic group. While that specific example could be controled, what if the environmental factor with which the gene was correlated was unknown? I do not think twin studies or GWAS are worthless, they are very good at identifying possible genes that may infulence behaviour, but by themselves they do not show causation. John

I don't think this is necessarily true. Lemarckism could still occur without a selection pressure from the environment, each member of a species could acquire more characteristics enabling it to be more specialised at exploiting its niche simply by exploiting its niche.

I think SamTheSkeptic is right in that using observation exclusively is inadequate to show that a correlation is actually a causation. I think that is the main criticism, hypotheses can't be test in humans because we would have to induce the genetic lesion to see if that results in the predicted change in behaviour. If there were no ethical consideration one could of course just remove a gene for a serotonin and see if that increases the chances of aggression later in life, like it does in mice. Or we could induce the mutations in the monoamine oxidase gene,that have been shown to increase the likelihood of aggression in humans, in a normal individual and see if that leads to the same effect. We can't obviously. So how could we see if the correlations found between genes and behavious are in fact causative. One approach could be pharmacogenomics. Since we can't induce negative behavioural changes genetically, we could instead see how the effects of drugs on behaviour varies with genetics. But then again as no genetic manipulation is being induced, causation would still be difficult to prove. But if the drug directly affect the mechanism perturbed by the genetic lesion, that does bolster the argument that it was the underlying genetic mutation that induced the behaviour. Gene therapy could be another way one could get at this problem. Correct the genetic lesion and see if that changes behaviour. The same critique could be said of determinism in general. If we don't have free will then we can blame anything for our behaviour... environment, upbringing, genes, I could even imaging a murder appealing to a judge that he did it cause "the random firing of a neuron in complex network lead to a the emergent phenomena of me swinging an axe at someones head"! The solution is that we shouldn't lock a murderer up because they are ultimately responsible for all the decisions they make, but because the decisions they make violate the rights of other people. Jail is not then an revenge, but a protection for others and a punishment to correct the offender's behaviour. Therefore, saying we should not believe that genes affect behaviour bacause it could lead to bad effects is nonsense. John

The below study shows its possible to stimulate parts of the visual cortex using arrays of micro electrods and induce the perception of points of light in blind people. The same thing is also possible using TMS. It is concieveable therefore using very complex mutielectrode arrays or some advanced form of TMS that these points of light could be turned in to patters that represent some virtual reality...... long time from that tho. I think the same same is true for stimulation of the somatosensory cortex and the inducition of tactile perceptions. http://www.ncbi.nlm.nih.gov/pubmed/19660667 http://www.ncbi.nlm.nih.gov/pubmed/1891194

The majority of material in your body is water(60%). An average male weighs approx. 72 kg. Therefore about 43.2kg is water. As 1 mole of water is about 18g, thats 24000 moles. 94 half lives later there will be 1 or less water molecule remaining. The biological half life of water in the body is between 4 and 18 days. If we take the max half life, 18, multiplied by 94 gives about 4 and a half years. Of course some of the hydrogen and oxygen present in that water will still be present due to its incorporation into proteins, lipids and DNA so there you go, 4 and a half years and the majority of material in your body will be replaced.

I agree, it remains unknown. However, the possibility remains that more than 10,000 people may be infected with the abnormal prion. http://www.ncbi.nlm.nih.gov/pubmed/15221931?dopt=Abstract Then again other studies suggest the number may be considerably less http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2685439/?tool=pubmed An interesting editorial on the subject can be found here http://www.bmj.com/content/338/bmj.b435.full

I know there was a article publised in the lancet a few years ago that looked at incubation periods of kuru, suggesting that prion diseases in humans may have an incubation period of 50 years or more! If this is the case, a CJD epidemic could be just waiing to happen.... Collinge et al (2006) Kuru in the 21st century—an acquired human prion disease with very long incubation periods The Lancet, Volume 367, Issue 9528, 24 June 2006-30 June 2006, Page 2034, doi:10.1016/S0140-6736(06)68930-7

Except that epigenetics now shows there is some truth to lamarckism, though i think no one has suggested epigenetics could explain speciation.

Yeah, i suppose the misconception could come from the fact that your body is constantly rebuilding the same cell, proteins are constantly being degraded and produced in all cells. Protein in the body has a half life of about 80 days, which means most of the protein in your body will be "new" after a few years. John

No, the 7 year rule is not true. This can be shown by analysing the amount of carbon 14 that is incorporated in to DNA. Carbon 14 is a radioactive form of carbon that is present in the atmosphere such that any plants that absorb carbon dioxide will contain a ratio of carbon 12 to carbon 14 that matches that in the atmosphere. As animals then eat plants, they too will be made up of a ratio of carbon 12 to 14 that matches that in the plants they eat. Now, between 1955 and 1965 testing of atomic weapons caused a dramatic increase in carbon 14 levels in the atmosphere. In 1963 with the test treaty ban coming into force, the amount of carbon 14 in the atmosphere slowly reduced. Measuring the ratio of carbon 12 to carbon 14 in cerebral cortex neurons from people born before the cold war, he earliest was born in 1933, and died in 2000's, showed that the most of DNA in these neurons had carbon 14 levels that caresponded to the levels in the atmosphere before 1955, and that therefore DNA synthesis had occurred before 1955, ie during childhood. DNA synthesis during adulthood made up less than 1%. Therefore most of the carbon atoms that form your DNA in neurons as a child are the same atoms that make up your DNA throughout your entire life. John source... Bhardwaj et al. (2006) Neocortical neurogenesis in humans is restricted to development. PNAS August 15, 2006 vol. 103 no. 33 12564-12568 http://www.pnas.org/content/103/33/12564.full