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S**A
No Blueprint to Be Found
Robert Plomin implies in this book that genetic studies, beyond just twin studies, have definitively established that much of who we are is related to genes and that this fact portends a “DNA revolution.” This is not an accurate representation of the literature to date. As even Plomin acknowledges, these genetic studies (genome-wide association studies) trying to tie genetic variants to specific traits like mental disorders, personality traits and IQ, despite a lot of fanfare, are rarely if ever reproduced in follow-up studies. This has led to a “replication crisis” in the field of Behavioral Genetics. He attempts to side-step this ongoing issue by asserting that “polygenic risk scores” are effectively a kind of replication. This involves finding hundreds or even thousands of genetic variants that are in slightly higher proportion for a trait (schizophrenia, autism, etc.) and looking at all those that a particular person possesses and “adding” them up. If the score is high, then the person would theoretically be more likely to have or get the trait in question.Plomin’s apparent obsession with polygenic risk scores is far in excess of its actual utility, and his timing for the book might be a bit off, as these polygenic risk scores are being called into question in numerous recent papers, noting both their inherent mathematical limitations and the possibility that they are largely skewed by population stratification (when your population is too homogenous, say all white European, then you might get false positive results). Without polygenic risk scores, the book offers nothing new, and is otherwise a rehash of twin studies from decades ago.In my view, he goes in a dangerous direction with this focus on polygenic scores, suggesting, for example, that such scores for I.Q. could be used as admission criteria for elite schools. Leaving aside their lack of validity, this borders on eugenics. Moreover, because polygenic risk scores tend to distribute in a “bell curve,” he concludes that a disorder like schizophrenia is a matter of degree, with only the highest scores receiving the diagnosis. Thus, it’s a matter of how many schizophrenic genetic variants someone has, with only those at the extreme end currently receiving the diagnosis. “Who has not sometimes experienced these symptoms [hallucinations, delusions, disorganized thoughts, etc.],” he asks? This would imply that, in addition to those we diagnose with schizophrenia, there is a larger population of somewhat schizophrenic individuals, an even larger population being a little bit schizophrenic and another half of the bell curve for those with gradations of “un-schizophrenia.” As a psychiatrist, I treated schizophrenia for many years and find this notion absurd. No psychiatric diagnosis is perfect, but schizophrenia is a relatively distinct diagnosis, as are most other psychiatric diagnoses. They do not tend to fall into a bell curve continuum. Thus, it appears that Plomin embraces his theory at the expense of reality. His claim that, “psychiatric diagnoses are not supported by genetic research,” does not lead him to question the validity of the genetic research. Instead, he proposes scrapping current diagnostic criteria, asserting that, “Genetics offers a causal basis for predicting disorders, rather than waiting for symptoms to appear.” This strikes me as science fiction. Plomin argues that most environmental factors such as parents, schooling and life experiences “don’t make a difference” in regards to the traits a person has when they reach adulthood. Because siblings and even identical twins often can be very different, he explains this by saying that it is related to unnamed, “non-shared environment,” guided by “...unsystematic, idiosyncratic, serendipitous events with lasting effects.” He is effectively saying that, say, which side of the crib a twin is on is potentially more important than parents, schools and life experience and such undefined experiences account for 50% of our phenotype. That’s hardly a “blueprint,” and really is absurd on its face.A telling portion of the book is Dr. Plomin’s attempt to evaluate his own polygenic scores. This starts out well, since his score for height is high and he is tall, however he also has a high score for body mass index and schizophrenia (he is relatively thin and, presumably, not schizophrenic). Rather than just admit the fallacy of these scores, he doubles down, stating “I came to accept that my high BMI polygenic score makes sense...[and] had a good effect on my attempts to persevere with my never-ending battle of the bulge...” Even more ridiculous, related to his high score for schizophrenia, he states “...I wonder if my need for a highly structured, scheduled working life may be an attempt to keep myself on an even keel.” This seems little different than my “New Age” friends trying to justify their horoscope.Plomin is old enough that he need not concern himself about suddenly becoming obese or schizophrenic, but I would ask him if he thinks his life would have been different if he had been told (erroneously) as a youth that he was likely to become fat and schizophrenic? What an irresponsible and reckless idea he is promoting. His motivation appears to be to promote his world view, rather than an interest in helping humanity. His book is speculative, utopian, meandering and, in some ways, frightening. This book is of little value, and reinforces views that are already being touted by some rather unsavory characters. Other than his unsupported proclamations, it presents no real evidence to his “blueprint” claim.
B**C
Important Work with Some Flaws
This book discusses an important topic and one that should inform our policy decisions. Unfortunately it does not and this topic is generally taboo. The bottom line, supported by massive amounts of evidence by the way, is that the most important systematic influences on who we are and what we become our our genes.I give the author high marks for the courage to write this book and the first part of it was really outstanding. I was a little disappointed in the second part because I don't think the author's evidence support some of his conclusions. As of yet the correlations are not strong enough and there's way too much individual variation. To his credit Plomin admits and even shows in graphs the massive amount of overlap between individuals of different groups, but then he makes statements that seem to ignore what he just demonstrated.For example he says based on DNA alone you could predict that he is tall. His polygenic score for height is in the 90th percentile. And he is tall, however his own scatterplot shows a significant portion of the individuals in the 90th percentile of polygenic scores for height around the normal range. And there are plenty of people even below normal. So what you can predict from his DNA alone is that it is more likely than not that he is tall but not with a great deal of confidence. A significant portion of the people in his percentile are not tall. The same problem runs through much of the second part of his book.I do happen to believe that his general theme is correct and that EVENTUALLY polygenic scores will become much more predictive as the data accumulates. When he talks about how genes are responsible for approximately 50% of psychological traits, and how even a significant part of the so-called environmental effect is driven by genes, and finally how most of the rest of the environmental impacts are not systematic and unknown his analysis is outstanding and has powerful implications. This is important and we need to come to terms with it. We just aren't there yet with the predictive power of polygenic scores. And he way over plays its predictive power at the present time.Despite this flaw, overall I think this is an outstanding work and it's very important. I wish this information was much more widely known and accepted because it has important policy implications. I can't give it five stars but I do highly recommend this book.
J**E
A real game-changer
Very insightful and readable. I wish he had responded to some critiques of twins studies but otherwise there is more than enough making this book worth a read. Pay attention since this topic will become increasingly important with time.
L**D
Wild claims, but Plomin's statistical approach to genetics is seriously flawed
There are battles going on in Science between key people with strongly held opposing views on complex subjects. One such battle recently was between Richard Dawkins and Edward O Wilson over 'group selection' or more accurately, 'multi-level selection' in evolution. Here, Robert Plomin, a long-time researcher in psychology known for his twins studies has written a book that challenges the equally polemical book 'Not in Your Genes', by well-known psychologist Oliver James (A book I have given a very critical review). The general consensus on the 'nature versus nurture' debate is that both genes and environment, especially early upbringing, almost certainly play a role in making us who we are, but these two men go much too far in fighting their corner, each looking desperately for evidence to support their case.The simple fact is that both get the genetics wrong. In the case of Oliver James this has been pointed out by others, he gets some things hopelessly wrong, though when it comes to early upbringing he makes good points. In the case of Plomin, it's harder for most people to see the errors because they exist partly in a misrepresentation of current genetic knowledge, but also largely in the inappropriate assumptions made right at the start of his analysis.Plomin says, (p112), 'we have 3 billion rungs in the double helix of DNA, which is called the genome.' That's actually the 'haploid' genome, only found in sperm and egg, and not capable of making anything on its own. A bit later he says, 'we actually have 6 billion nucleotide bases because our DNA consists of two genomes'. No, we actually have 3 billion rungs, on the haploid genome, but 6 billion RUNGSs (base pairs) on our DNA. On the haploid genome we have 6 billion bases (because there are two per rung) and on our (somatic cell) DNA, which is diploid, we have 12 billion bases! This might seem a pedantic point; this sloppy use of the 3 billion figure appears all over the place and in research papers, but it is hugely important to remember that the human genome is Diploid; that we have two lots of DNA, two lots of 'homologous' genes, and that in every case where the two stretches of DNA differ (and they differ in many many stretches) they 'compete' to make us. Do not confuse the two sets of chromosomes with the two strands of bases in the double helix of DNA. The two strands, known as the 'sense' and 'antisense' strands, contain the same information, though one is the negative image of the other - vital to the copying mechanism. The two sets of chromosomes contain quite different information and constitute two 'machines' churning out proteins in each of our cells. In many cases these will be different proteins, and to confuse matters further some of those proteins are structural but many are 'transcription factors' that turn on other genes in the 'gene cascade' that makes us what we are. Those transcription factors can cross over between the two 'machines', complicating things even more. Put another way, we have two different 'genomes', two machines that are kept apart in each of our somatic (body) cells, but whose products can interact. Confusion arises because the word 'genome' is used to refer to several things - to the haploid genome found in sperm and egg, to the diploid genome that is really two genomes, in somatic cells, and finally to a sort of reference genome of only 3 billion base pairs that is called 'haploid' but is actually derived from a mix of cells from the diploid cells of many humans (as was the case in the human genome project) , and which ignores the fact that our real genomes contain two sets of different chromosomes that operate independently, yet combine their protein product to make us, only coming together in the first stage of the making of sex cells (meiosis), before being halved again, but in a random way.Plomin forgets what he surely knows, and effectively pulls the wool over the reader's eyes when he says blatantly (p 131) 'these DNA differences can be genotyped with whole-genome sequencing that sequences all 3 billion base pairs of DNA.' No they can't! What he does not tell us is that no mammal (humans included) has yet had it's DNA fully sequenced (see Wikipedia) and that attempts to sequence the full diploid sequence of humans have been few so far, and very limited in accuracy. The Human Genome Project gave us a rough 'quasi haploid' sequence in 2001 which has been greatly improved on since, but there still remain regions that cannot be sequenced because of the 'shotgun' methods used which cannot cope with short repetitive DNA. The big revelation of the Human Genome Project was that humans only have 21,000 protein coding 'genes' (a dubious term that has almost lost all meaning, but that's another matter). The ENCODE project in 2012 brought more huge surprises. Firstly, what had been known as 'junk DNA' was found to be highly functional, transcribed into RNA, and conserved. Secondly, certain types of DNA, especially short repeating sequences were found to be present in huge numbers, in fact they are the main feature of the genome! Gene Expression became the thing to study, not 'genes'; and a whole new mysterious world of RNA products opened up to be explored.Sequencing the diploid genome is difficult - though it has been done a few times, the results are inaccurate. Most sequencing machines start by breaking up the DNA into short lengths, read the resulting fragments, and then use computer power to match the fragments up in the final result - a process that is confused by lots of repeats. Only when the new 'Nanopore' sequencing machines come into use, actually threading their way along the entire DNA molecules (which are around half a metre long and one molecule thick!) will we get to know our genome properly. Most current sequencing takes in both lots of chromosomes and then 'blends' them into one result. It is impossible to know what sits next to what, and on which version of the chromosome, yet the most important thing about a gene is it's expression level, determined by it's start sequence and many other factors. The expression of a gene product is also determined by the two 'alleles' which may each produce their protein product independently (or not - if one is methylated). One may swamp the other (Mendel's 'dominance'), or they may add (see hemizygous diseases), or one may block a process by forming a toxic product, etc etc. It's complicated, even as we currently understand it! An article entitled 'First Diploid Human Genome Sequence Shows We're Surprisingly Different' (available online) described new discoveries from sequencing the genome of Craig Venter (originator of the shotgun method in the USA who raced against the British with their slower method). This was one of few attempts to get an actual diploid genome sequence, and it revealed that differences between the two sets of chromosomes in him were seven times greater than expected! The researchers commented that it was to be expected that most people would have a similar level of differences. Plomin should take note!Plomin chooses to ignore all this complexity - he chooses to think (because he can, and because I don't think he has questioned our current understanding of mechanisms deeply enough) that whatever it is in our genome that determines who we are, this thing is linked to SNPs. SNPs (single nucleotide polymorphism or 'snip') are single base pairs that differ from the 'reference genome' (whatever that is - see Wikipedia - it is full of holes and a dubious concept) anywhere in the DNA. Early investigations showed, as he admits, that this didn't seem to be so. There were pretty much no significant effects traceable to one SNP. Determined, Plomin postulates that perhaps they work in concert, and hey presto, he finds that 'genome wide association studies' seem to confirm this - though not very convincingly. Surprisingly, he tells us, it turned out that traits were determined by the combined effects of 'many thousands' of 'genes'. But hang on - there are only twenty thousand to play with - how does that work? Nobody has an answer! We do know a lot about the mechanisms of how DNA makes us, that's the field of Developmental Genetics, and morphology; but those fields just do not match up with the idea of SNPs being major determinants of how we end up!Just about everything Plomin says from there on has no validity, simply because of one huge error, and the clue is in the name, 'genome wide association studies'. Association is not causation - one of the first rules of scientific research. To move from association to causation we look for several things. Ideally, we change one thing and observe the effect - change a base pair in the DNA and look for it's effect. This would not currently be allowed in humans though it is becoming possible with the new CRISPR tools. Failing that, we look for a mechanism of cause, as I have just explained, but Plomin has chosen not to look. Secondly, and less convincingly, we may look for a linear relationship - does more of something cause a bigger effect, if so it is perhaps more likely to be causing that effect.. Plomin says (p133), 'we can use inherited DNA differences to PREDICT individual differences in psychological traits without knowing anything about the myriad pathways connecting genes and behaviour.' No! We can't! That's wrong science, and statistics based on totally wrong assumptions. We could do that if we knew for sure that those DNA differences (specifically multiple SNPs) did indeed determine behaviour, or were at least linked to other DNA factors that determine behaviour, but we don't know that, and we have increasing evidence to suggest that other aspects of DNA along with Epigenetic DNA modification and a whole world of RNA revealed by the 2012 ENCODE project are in fact more likely to be the real determinants. Most SNPs, which arise due to random mutation, have no effect on the functioning of the genome. Many SNPs in protein coding genes change nothing because of the redundant coding inherent in the triplet coding scheme (64 possibilities 20 amino acids). Where they do change the protein, they are likely either to make no difference to it's binding properties (important in transcription factors that control gene expression), or to render it totally non-functional.To demonstrate what Plomin has actually found, lets take a lesson from Autism. Autism has been found to be linked to many genes. It has also been found to be associated with many environmental effects - from watching TV to staying indoors, to taking paracetamol, to ultrasound scans, to immunisation, to mercury, to sprays, . . . . . . TO MODERN LIFE. All these things are just things that are in turn associated with modern life. Groups like the Amish, who avoid modern life, and the Cubans, who get less of it, don't get autism (seems pretty true though it has been disputed). Is Plomin simply finding SNPs that are associated with something other than the condition he is testing for? Are his SNPs for Schizophrenia actually more present, for whatever reason, in people who choose to live in cities, or near airports (known major risk factors). I think it's very likely!I could go into a lot more detail over his errors of statistics and genetics, but this is stuff for a paper or a book by me. I will though point out just one, because it is startling. He says (p 112), 'It is random which of your mother's pair of chromosomes you received for each of the twenty three chromosomes, and similarly for your father. For each of your chromosomes, your sibling has a fifty-fifty chance of getting the same chromosome as you, which is why siblings are, on average, fifty percent similar. Well firstly we have 46 chromosomes not 23, but ignoring that slip we simply DO NOT inherit chromosomes. Basic genetics teaches that in meiosis, the process of egg or sperm production, the DNA copying process 'crosses over' multiple times at random between the two available templates while copying a chromosome, producing a new, novel, chromosome in which stretches of DNA from both sides (your grandparents) are incorporated alternately. This crossing over only occurs at certain spots between 'genes' (remarkably) otherwise the DNA would be rendered useless and garbled. If we did inherit whole chromosomes, then we would tend to resemble one or other of our grandparents much more than we do. Even statements like 'we all inherit fifty percent from each parent', are invalid. On average, yes, but in reality it is perfectly possible (though unlikely) to inherit half of our DNA from one GRANDPARENT! I think this is true, and that it is observed in reality in some families, though it is not talked about.Finally, I want to consider the case of Schizophrenia, the 'mental disease' that always crops up and which Plomin thinks is a major trait that proves his point because it is one for which he can find a more significant association with a group of SNPs than for most mental traits. He says (p134), 'GWA studies have shown that there are no associations that account for more than 1 percent of the differences between individuals'. Assuming that he meant to say, 'psychological differences', is this true, or has he not looked for the obvious? One of the most important pieces of evidence we have regarding the cause of schizophrenia is the fact that it is around TEN times more prevalent in the Afro-Caribbean population of the UK. A simple look at DNA would therefore surely reveal a huge association between many genes and Schizophrenia - genes for skin colour (just a few), for hair, and many other 'Afro Caribbean' genes. Does this mean that we have found simple genes for Schizophrenia. No, we have found genes that are highly associated with Schizophrenia, but the real reason why this is so is, (most likely) that Afro-Caribbeans especially, and probably other groups, suffer loss of feelings of self - who they are - at the shock of coming into a very different culture from the one they grew up in; it's a phenomenon of migration. The Psychiatrist R D Laing was the expert on this - see his books, 'The Divided Self', and 'The Self and Others'. This important evidence actually tells us, straight away, that Schizophrenia is not, primarily, genetic, since Afro-Caribbeans do not experience this excess of Schizophrenia in their own country. Some people may be slightly more likely to go Schizophrenic under culture shock, just as many people are more likely to suffer mercury poisoning (down to genes for detoxification), but it is folly to call the genes the cause of such things.To understand the implication of what I have just said, imaging taking a sample of people in the UK and looking at their DNA. Certain genes would surely stand out as heavily associated with schizophrenia - genes for skin colour etc. The degree to which they stood out would be a function of the proportion of Afro-Caribean immigrants in our population. Now take a sample population from a Caribbean island, and do the same experiment. They would all carry the genes, but you would find very little Schizophrenia! Those genes, which appeared so associated with Schizophrenia in the UK, have in fact nothing to do with the condition. They are not predictive in any way, yet despite his careful explanations that association is not causality, he undoubtedly thinks his findings are predictive in some way (see his introduction about fortune telling). They are not even predictive of the proportion of schizophrenia to be found in a population, because the result is a spurious feature of the population chosen.I have just used the word 'schizophrenia', though in fact I don't believe it exists - another problem for Plomin's ideas.. As Prof. Richard P Bentall, a key researcher into so-called mental illness has explained in his excellent books, 'Madness Explained' and 'Doctoring the Mind', schizophrenia is just a catch-all term for a syndrome of traits - auditory hallucinations, visual hallucinations, paranoia, catatonia, etc, that originated a long time ago with Emil Kraepllin. Bentall has used statistics (convincingly I think) to show that correlation is better between diagnosis and effect, in blind trials, if we consider the individual traits and not the imagined 'disease' of schizophrenia.I do think that DNA probably accounts for a lot of what we are, including mental traits, but I also agree with Oliver James about the huge significance of early upbringing, and attachment, when it comes to emotional and mental difficulties. Both men though, present a totally worthless argument to support their case!! I listened to Plomin on 'Start the Week' (BBC Radio 4) on the day his book was released, and then watched him interviewed on Newsnight by Kirsty Wark. He seems a genuine man, passionate about his subject, and of course he is held in high esteem as recipient of many awards and titles, but it's a pity he got such publicity by making outrageous claims for genetics when the reality is that we are just at the start of the real DNA adventure and most experts know this.
D**E
Highly flawed
This would be one star, apart from the fact that Plomin’s style is very easy to read. The overriding assumption in this book is that Plomin believes the reader will agree with his thesis, despite offering no evidential studies beyond his own. He appears to have got an idea in his head as a young graduate student (probably largely to explain his weight and being the first person in his family to go to university, as he won’t shut up about either) then spent the next four decades conducting studies to prove himself correct.If you believe in nature over nurture, save yourself £9.99 because this book will only confirm your position and does not provide any meaningful discussion of the subtleties of the human condition.Essentially, Plomin’s view boils down to it doesn’t matter what happens in your life, your genes rule your head. It’s not a far step from accepting this kind of genetic determinism to a dystopian nightmare where criminals are never challenged because they can’t help themselves, or we don’t allow children to develop intellectually because they don’t have the ‘right genes’. Plomin skates over the ethical implications of imposing his position on the inevitability of inherited personality traits, and this is the worst aspect of his book.
S**Y
Nature and nurture
Nature and nurture are both effective in making a person but Nature it seems is by far the dominant actor and the secret of this is written in DNA.Robert Plomin is at great pains to point out the model used is to discover probabilities and genes are not deterministic. He discusses the fact that he discovered he was genetically prone to Schizophrenia but never succumbed to the disorder. At present therefore the knowledge of this blueprint would suggest it is a blueprint of probabilities.The environment he suggests is light touch and we are subjectively active how we interpret the world and correlate our experiences according to our genetic propensities....we psychologically manipulate the environment to "get what our DNA whispers what it wants.".Some may view this new world with foreboding. Like the internet it probably will be horrendously abused, and like the internet it will be difficult to regulate in the best interests of the individual and society. Plomin suggests people will not tolerate paternalistic regulations that will prevent them from learning about their own genomes. That may be so, and acceptable as long as it their own genomes they seek to learn about. Parents should not be allowed access to their children's genomes, except when medically necessary. Genomes are the ultimate in private property if you like. The discovery of their offspring' s genetic propensities is not their business. Their business is to respond to the child's self expression, not to bend it to their own ambitions, or reject it. Accordingly it should be forbidden by law to have access to the genome of someone who is legally still a child, except as I said, where medical therapy would be informed and guided by such.An exciting and thought provoking book. Plomin suggests research in DNA is going at such a pace that it my be last week's news at the time we read his book. Well I look forward to the next episode!
R**D
Genes are only half the story
Blueprint states that our inherited genetic blueprint accounts for only half of the differences between individuals and even after thirty years of research, the nature of those non-shared environmental factors that appear to account for the other half of this difference, are still something of a mystery.The author seems somewhat disappointed that we cannot yet extend statistical correlation to our genes and what we become to 100% accuracy.The book describes these non-shared environmental effects as mostly random – unsystematic and unstable – which means we can’t do much about them. But the book misses the point, because this is precisely how it should be.The main problem with this book is that it purely focuses on the small differences in inherited genetic code and fails to acknowledge those other (more important) factors that account for how and why we are all different.Evolution tells us that our main objective as a species is to survive and to pass on our genes to the next generation. Such a process favours variability, flexibility and adaptability in the response to our environment and therefore we have developed some important mechanisms to do just that.The first mechanism (which is the one discussed in the book) is the variability of our genetic code that we inherit and how the genes we receive from each parent are shuffled to produce differences in siblings. To this can be added the random mutations that increase diversity, which together, account for the 50% difference between individuals.However, it’s not just our genes that are important, but it’s also how they become expressed that create who we are. Our knowledge of epigenetics tells us that our genes are not just pre-programmed, but also respond to the environment. But our genes are not just switched on or off but have set-ranges and can operate at any point in between these two extremes. This gives our genes an infinite number of combinations and permutations to respond to any environment.However, all the above effects pale into insignificance compared to a further evolutionary development of our species: conscious awareness. This gives us the opportunity to review our situation and responses in all situations and to make changes as we see fit. It is this real time adaptive capability that marks our species as unique.This directed awareness also gives us the opportunity to lessen the impact of any genetic pre-dispositions to certain illnesses, physical or psychological and also gives us an amazing opportunity to improve as individuals by pushing our genes to the limit.For example, two individuals may have different genetic potentials for playing table tennis and if they both practice and focus on developing their skills in exactly the same way, the individual with the highest genetic potential (if we could measure such a thing) would tend to achieve better results.However, if the genetically deficient individual practiced more and put in more focused work on developing their skills than their more gifted counterpart, it is likely they would become the better player. In this way, nurture would trump nature. This example shows is that epigenetics gives us all the capability to improve and even to perform better than our original genetic profile might imply.However, this is not yet the end of the story of conscious awareness, as there is now increasing evidence of the power of our mind. We already know that our beliefs and expectations (a combination of genes and life experience) create a filter through which we perceive our world and affect how we all experience reality. We therefore see what we expect to see etc, etc.Furthermore, the Placebo Effect has shown that our beliefs and expectations do not just colour our perceptions but can also create physical and chemical changes in the brain. Therefore, an increasingly important area will be how to utilise mechanisms that can change our beliefs and expectations and therefore our perceptions of ourselves and our world. One such mechanism is Suggestion/Guided Visualization. As our brain cannot tell the difference between what is real and what is imagined, we can create conscious thoughts and feelings that effectively “mimic” the external environment, which can then become subconsciously hard-wired through repetition.Without these further evolutionary adaptations, we would all be identical and no more sophisticated than robots, all of us bumping blindly into each other and into the outside world in response to our inherited genetic programmes. This is the reason why the author of Blueprint cannot find those elusive genes that create the “lost” 50% in the difference between individuals, as it is this random, unsystematic and unstable environment that works from the outside to stimulate our genes.So, what does all this mean? Well the author goes on to raise some profound points when he says: …Instead of trying to mould children in our image, we can help them find out what they like to do and what they do well. In other words, we can help them become who they are… Rather than striving for an ideal self that sits on an impossibly tall pedestal, it might be worth trying to look for your genetic self and to feel comfortable in your own skin…This is the realm of Positive Psychology, that provides a proven prescription for Happiness and Personal Fulfilment (Positive Emotion/Engagement/Relationships/ Meaning/Accomplishments) which in essence, advises us to identify our Signature Strengths and Core Values and to apply these to all areas of our lives.
A**R
Fascinating...I just wish I understood the writing.
I found this both a really interesting and impacting read....and a really frustrating one. I’m no dummy but I didn’t really understand large portions of it. Of course, an important book on a very important matter has to be precise....but given its purpose was (I think) to communicate this stuff to a wider audience, I’m sure it could have been written better from that perspective.
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