There's a really interesting phenomenon I've observed with people who end up developing let's just call it a chronic illness and whenever they tell the story about how the illness began they always describe it the same way and they'll say things like you know before this event or before this time I was always fine or even I was always very healthy and very strong and I never got sick and since that time they say those words since that time since that event sometimes the event is they took antibiotics a few times sometimes the event is a divorce or a postpartum but they say the same words and ever since then and they're never the same and I want to share why I've observed this is often happening and some personal thoughts on this because I find that people very often get obsessed with the event without fully understanding why that happened in the first place and that it may not be related to the event at all. Hey guys Dr. Alex Hine author of the health book master of the day doctor of Chinese medicine now before we jump into this video two very important links right below it the first is if you'd like to get my free weekly video newsletter and a free guide for daily rituals that can potentially help you add years to your life with Chinese medicine it's right below the video and the second is if you'd like to become a patient with mine locally or online via telemedicine the contact info for my private practice and what I'm seeing patients is right below as well. Let's talk about this idea of the healing crisis versus the breakdown you know I had this patient once and she was telling me the story this was in school years ago she was telling you the story of how her main complaint was panic attacks and she said that she went to an amusement park and while she was on a roller coaster she ended up effectively having a panic attack at the peak of this roller coaster so it's building it's building it's building she felt like she freaked out and since then she had been having real panic attacks true panic attacks regularly and had developed anxiety and sleep problems and she said that before that time she was pretty good and had never had a panic attack in her life so all of us the students we all thought this was very interesting right how could a roller coaster trigger a panic attack and then permanently alter her physiology in a way that gave her panic attacks was she just reacting to that initial panic attack over again was there something else going on what was really happening here and I see this a lot in many many different kinds of illnesses not just panic attacks and anxiety obviously that's a telltale example because once you have a panic attack you become scared of the next one but in other illnesses as well even just depression in general and people will often say things like after that time I've never been the same and I wanted to take a second to point out a distinction between what led up to the event and the actual event and that what often happens is that we ascribe the problem to the event not knowing that what came before was really the build-up the susceptibility to that event happening and that's very important to distinguish so let's talk about recognizing the crisis right this is the event the event was the roller coaster ride the event was the divorce the event was becoming an entrepreneur and exhausting yourself from stress and worry and anxiety and being up all night the event was a breakup the event was moving to a new city alone whatever it was we often ascribe the commencement of our illness to that event but it is not the event that caused that it's the event that is merely the trigger what we almost always see behind the scenes if you look at the preceding year or preceding years is that there has been an underlying pattern of long-term exposure to stress or long-term something that leads to in Chinese medicine a depletion of your resources that then makes you more susceptible to that event being catastrophic so for many of us if the resources are healthy we maintain good health regular exercise good sleep we're careful of our stress then when those events happen they will often not lead to catastrophic illness that lingers for years but when we are already depleted and run down more Chinese medicine perspective one thing I see is that that event just kicks off you know it is the straw that broke the camel's back when I see someone and they're saying ever since I've been an entrepreneur since that stressful period ever since that postpartum ever since that divorce whatever that event is when they come in and I feel their pulses the pulses are almost always so deep and so weak they're not going to happen like that from something that just happened a month ago unless the person hasn't slept in a week the pulses are very unlikely to be that depleted so that is a significant amount of resource depletion over months or years and so what happens is let's just say this let's just say these are vital resources right I'm creating a concept not a not a tangible thing these are resources and your the last three years been killing it going through grad school working you get divorced when your parents get sick or dies your resources are like this they're at 20% and then suddenly the divorce hits your health goes to crap you haven't slept well in years anxiety and depression that started three years ago is still there today how could that be how could that event have kicked that off and you've never gone back to feeling normal again because all of this was never fixed all of this deep resource depletion has not been restored and so this pattern of where people are experiencing the symptoms years later they come to see me it's as if the pulse has not regained any of the volume or the quality or the strength and this is why these things become chronic so let's talk about recognizing the breakdown because the breakdown remember is this this is the event that you attribute to the beginning of this illness and some I'm sure do start that way but a higher percentage that I see the events just to trigger and the event because it's big is what we focus on because we did not have a good job or it's difficult to observe all of the breakdown before because it's subtle you know it's sleeping poorly every now and then to well I generally am not a good sleeper or yeah I've had digestive problems a little bit low grade for a while or a little bit of anxiety and every now and then a night where I don't feel like I slept at all recognizing these little canaries in the coal mine is essential to understand how susceptible am I to a trigger an event derailing me potentially for years and there's even interesting research that I was reading that people who experience depression and anxiety who have for example no close social ties or they have a 75% chance of developing depression in the years following that difficult event and the majority of them the preceding years to developing depression anxiety were very stressful high stress years and I know we can't always control the stress in our lives but understanding that there is almost always a preceding sequence before that leads to a susceptibility to that event being catastrophic and that was my point of this video today even though it's a bit long-winded understanding that the event you attribute to why you develop depression anxiety panic attacks postpartum whatever it is is often years before that time and that the event most likely did not cause that unless it is very linear easy correlation to observe most likely didn't cause that but we had been depleting those resources and creating these dysfunctions in the body baby little pathologies were building right the flywheel was spinning in the wrong direction already and so very unbalanced on one leg on one toe it's easy for something to push you off and to go down hard and to stay that way for a long time so I thought I would talk about this today because it's something I see a lot it's very very important to understand and it's also important to understand why after that event healing hasn't happened in a year why it feels incremental and years later you may not feel the same that's where you have to intervene and dedicate your life towards more aggressively healing if that makes sense all right guys that's all I have for today something very important to observe again before you go I have that free download below this video for daily rituals that can possibly help you add years to your life with Chinese medicine and if you'd like to become a patient of my locally online via telemedicine the link to my private practice is right below this video


And outside Africa, the White House has defended the U.S. decision to provide Australia with advanced technology for nuclear-powered submarines that's rejecting criticism from both China and France over the deal. A White House spokeswoman, Jen Psaki, said the agreement is not aimed at China, and the U.S.'s mounting concerns about Chinese influence in the Indo-Pacific region. As we've said, I would first say that we value our relationship and our partnership with France on a variety of issues facing the global community, whether it's economic growth or whether it's the fight against COVID or addressing security throughout the world, and that has been a long-standing partnership for many, many years. We don't see this from our end as a regional divide. We see this as areas and security issues that we want to take on together.


If you're retiring or leaving the military soon, it's safe to assume you're planning for what to do next. Petty Officer Gabriel Cotico shows us how one retired sailor at Fleet Activity, Sassabo, chose to pass on her knowledge, training and skills to our country's future generations. My name is Deb Jenkins. I teach science and social studies here at E.J. King, Sassabo. I've been teaching now, I'm going into my 10th year. I was part of the Women and Navy program. I was one of the first set of women on board ships, spent 22 years, loved every minute of it. It was a very good career that set me up for my career today. My long-term goal was to get my degree in teaching. I'm a Navy person and I felt that I would be best suited for working with military students. This was the best scenario for me is to go back and give back to a military. I wouldn't change my life for the world. The best decision I ever made was to join the Navy because it made me a person I am today.


Good afternoon ladies and gentlemen and welcome to the Nature Press Briefing. My name is Faye and I'll be a coordinator for today's conference. With the duration of the call you'll be on listen only, however at the end of the call you will have the opportunity to ask questions. Is there any time needed assistance? Please press star zero on the telephone keypad and you'll be connected to an operator. I'm now handing you over to Ruth Francis to begin today's call. Thank you. Hi everybody and welcome to the Nature and Science Press Briefing concerning two papers. Firstly a map of human genome variation from population scale sequencing which will be published by Nature this week and a second paper diversity of human copy number variation and multi-copy genes published by science. We've also got on the phone today the side pack director Cassie Wren. Before we begin can I remind you all that the papers and this press briefing subject to our usual embargo of 1800 London time, 1300 US Eastern time tomorrow, Wednesday the 27th of October. First of all we're going to hear from three of the authors of the papers. We've got first Dr Richard Durbin of the Welcome Trust Sanger Institute, then Evan Eithler Professor at the University of Washington and we've also got we're going to hear from Professor David Altschuler of the Broad Institute of MIT in Harvard. We also for the purposes of the Q&A session have Dr Lisa Brooks from the National Human Genome Research Institute. So we're going to start off with some comments from three of the seekers and then we'll go to questions. I'm handing over to Richard now. Thank you and hello everybody. So 10 years ago the draft human genome reference sequence was published but we know that individual genomes differ and a main focus of human genetics is to identify which of these differences or genetic variants contribute towards our tendencies to disease and in the last 10 years DNA sequencing technology has advanced dramatically so it has become feasible to systematically sequence many people to find genetic variants and build a catalog which we can use as a basis for investigations into disease genetics and which which variants may be functional. So a few years ago an international consortium was founded the Thousand Genomes Project to carry out this plan to produce a catalog of genetic variation and in this week's nature we issue we are publishing the results of the initial pilot phase of the Thousand Genomes Project. Already just in the pilot phase we've identified over 15 million genetic differences by looking at 179 people. Over half of those differences have never been seen haven't been seen before and in doing so these have already provided a more complete catalog of variation than was available previously and an example is that if you look at one person's genome amongst the three million variants which that individual will have over 95 percent of them would be present in our catalog. So just as important as discovering the variation this has been a real shift in how we can approach human genetics and we've developed in conjunction with the manufacturers of machines who also were part of the project methods for using sequencing effectively and efficiently in human genetics and we've tested three different approaches and are taking two of them forwards to the full-scale project to produce a deeper and broader catalog which is already underway which will study 2,500 people and I think David at the end will come back to this later. So the paper primarily describes the new sets of variants we find and the methods that we use or initially describes those but also describes analyses that we can perform now. We have a more complete dataset than which were previously not accessible and there are a number of key points which are picked out in the paper and in the press release in particular we can see that each individual is carrying a significant number of deleterious mutations maybe 250 or 300 genes which have defective copies. We can also look at the effects of recent evolution on the human genome and the effects of natural selection around genes and between populations but this is in fact only a start a key property of the project is that all the results are being made publicly available on the web just as the original reference genome was and then people both within the project and outside are already beginning to use the data for many different approaches and in particular because we're looking at all the DNA when we do DNA sequencing rather than just looking at known places of variation as has been used in the in GWAS studies it's possible to examine more complex types of genetic variation and so Evan Eichler who is going to talk next has been his group have been looking using the thousand genomes data for particular analysis of copy number variation so I'm over to Evan okay hello everyone this is Evan Eichler I'm going to discuss the companion piece that was published in science I'm really going to pick up where Richard left off talking about really an effort to try to extract more information from the roughly 15 percent of the genome that has been very difficult to assay but is generally described as inaccessible the work I'm going to describe is really the work primarily of two third-year students Peter Sudmont and Jacob Kitzman and at the University of Washington so the focus of the science piece like I said is to pick up on looking at more difficult regions of the genome we focus specifically on the copy and content of duplicated genes and these have been particularly difficult because of the repetitive nature so there's a roughly about a thousand genes within the human genome that I would argue have been largely inaccessible to traditional genetic study as a result of the repetitive nature so what did we do in this pet paper we essentially take all the data from the thousand genomes project in addition to about a dozen other genomes that are not part of the thousand genomes project and we essentially remap it using our own computational measures when we do this we essentially assay two properties of that data we measure the read depth as an indicator of how many copies there are of a given gene family so this can range from zero copies to dozens in some cases you know many dozens of copies and then we identify unique sequence tags a total of 4.1 million of them that allow us to essentially distinguish one copy from each of its its nearest neighbors so this provides us the ability to assay both the copy and content for any region of the genome and in principle any gene in the genome really I think for the first time I think what's different from this paper in addition to where we're focusing and a much more narrow focus than the thousand genomes project per se is that we're looking at individual level variation as opposed to variation at the population level so what did we find for us it was particularly exciting we think the veil has been lifted for us in terms of a whole new level of genetic diversity and this is really back to copy number differences over gene families and we find three things which I think are worth highlighting first we find that the most copy number of variable genes in the human species map to historically duplicated regions of the genome so you can think of these almost as accordions of the genome expanding and contracting in terms of their copy number when we look at the the four populations that we have access to in this study from the thousand genomes we show that when we compare populations we see that there is more genetic difference between the populations in these particular regions at least in terms of copy number when compared to unique regions of the genome and we compare these roughly 159 humans that we've analyzed to date and compare them to that of the great apes we have the ability I think pretty clearly to identify the genes and the gene families which have expanded specifically in our lineage of evolution since we separated from that of chimpanzee and gorilla and what we find here and even though the numbers are quite small we find a particularly tantalizing set of genes that are important in terms of neural development in terms of a neuronal migration and we want to focus on these going forward as potential candidates for helping to define some aspect of the human condition so what we plan to do going forward I think there are two really big things that are exciting in our lab and and hopefully others as well is that by developing these methods I think we can now explore the functional properties of these what I can call untouchable genes of the of the human genome we can look at expression differences we can look at changes in terms of methylation we can look at changes in terms of chromatin configuration I think the second and perhaps the most important is that is that now we can assay the copy and content of these genes we can begin to do association studies for these gene families which have often been difficult to assay previously and look for a particular particular associations with phenotypes such as disease disease susceptibility and thank you hand it over now to David Schubert yes hello thank you for calling in and for the chance to speak with you so I've been asked to comment briefly on the application of the project and its relevance for medical research so start just by saying that it's clear from the history of genetics of humans but also many model systems that following the genetic contributors to disease can be a powerful tool to discover new clues about the genes and underlying biological basis of diseases both rare and common it's also clear that with evolving technology and given the true complexity of the genetic base of disease that a more complete understanding will require uh knowing the entire genome sequence of individuals and of populations and the routine deployment of this information in medical and clinical research from this uh application standpoint to medical research the key challenge in the first phase of discovery is to be able to distinguish those genetic variants that contribute to each disease from a background of many millions per genome that are not involved in that particular disease a problem of a needle in a haystack in addition it's important technically to avoid false positive discovery claiming their variants that aren't there or missing important variants as evan was saying that you otherwise couldn't assess so i think there are three ways in which this project contributes uh the first is that as richard mentioned the project has been a laboratory in which many members of our field have worked together on the methods for sequencing whole genomes these individuals have come from many countries they've come from academic institutions and also private companies and the work has been done in a public private partnership and with all the data available in the public domain and the methods available and this i think has contributed greatly we hope to increasing the efficiency and the accuracy and the broad availability of these methods so that they can be deployed in many quarters second uh while each of our genomes contains many millions of variants and some of these are unique to each individual and i'll turn to those in a second it's also the case as our paper describes and has has actually been clear for many years that most of the variation in each individual's genome in each single person's genome most of it is common variation meaning that it is shared by people who are apparently unrelated in the general population and so one approach that the project is enabling is to systematically and accurately and efficiently test these what are called polymorphisms variants seen in apparently unrelated individuals for their relationship to disease a early first draft of this approach was what are known as genome-wide association studies built on an earlier map of genome variation built by the Snipkin Sorsham and the hat map project and those genome-wide association studies tested only very common genetic variants those with high frequencies of five and ten percent and above and those studies have been successful in identifying hundreds of new clues about the genetic basis of disease the thousand genomes project makes this approach much more complete and much more powerful by going down to much lower frequencies and also broader range of populations and much more complete data in each frequency range in each population second some diseases are caused not by variants that are common or that are shared by individuals but actually variants that are very rare spontaneous even arising in an individual as in the case of a cancer or a very rare arising in a recent ancestor the mother or the father grandparent of someone those will never be contained in a catalog however in DNA sequencing is used to discover all the variation in such individuals or families the first step in analysis under that model of rare genetic variants is to know which of the millions of genetic variants are in the category of common variants which can be studied with the other approach conceptually and which are very rare and it turns out that that requires a catalog of which are common or else all one gets out of those sequencing studies in rare genomes is millions of candidates and no real way to hone in on the ones that you care about and so already the earliest data from the thousand genomes project has been used in multiple published papers in which individual sequenced in one case from evans institution but there are other cases well they sequenced a family and they were able to quickly hone in on the disease mutations and if you read those paper that paper and others like it the first step is to look in the public database and the thousand genomes database and say which are the common variants we're going to set those aside for study under different genetic model and we can hone in on the small number that a unique teach individuals that's the second way so three ways actually in which we think the project contributes to medical research one the methods data and uh and uh standards that have emerged from this public private partnership two a complete a much more complete database of polymorphisms of all sorts of single base changes copy number variants as Evan told you about other kinds of structural changes that can be tested systematically for disease and then third as if you will a a lookup table to allow people whose diseases might best be studied under this different genetic model of rare variants to focus in on those i'd like to make one final comment before turning it over to questions which is a just a personal perspective on genetics in medical research it's clear that disease is influenced by inheritance but also by environment by behavior and by chance moreover it's clear and been clear for a long time long before the current era that most diseases are influenced by many genes and moreover by many variations in many genes it is not a simple problem nonetheless uh we continue to uh drive as a field towards using DNA technology and we do this to understand or to eliminate disease we do this despite knowing each success it's just the first step towards the biological investigation of that disease it's not an answer it just frames the hypothesis i think the reason we do this is because we live in a time when one of the great scientific opportunities is to use this new ability to read DNA in our population and to follow up the inherited portion and it is a technical ability and a conceptual ability that i think has great fruit but we want to be very careful as a project not to uh suggest that this uh framework project is itself medical research because it is simply a foundational tool it is not being done in disease samples nor to suggest that there are any easy answers that will come but we do believe that in the long run this is a very valuable and promising approach to learn new things about the basis of disease and that if we do that as a field and then biological follow-up occurs that this has promised to contribute to improvements in the long run in human health thanks very much David and thanks to uh Richard and Evan also um so we're going to go over to questions now um just to remind you that we've also got Dr Lisa Brooks from the NHGRI on the phone if anybody wants to ask her anything thank you ladies and gentlemen if you'd like to ask a question please press seven on the telephone keypad if you change your mind i wish to destroy your question please press seven again it will be advised when to ask the question we have a question from the line of a look to her from the guardian please go ahead hi this is Alec Johnson the guardian um i've just got a couple of questions about numbers actually um which i hope you could just clarify for me um you mentioned that you have a database now 15 million uh snips and um there are also some other numbers in the papers about um the number of genetic changes an average person carries there that's between 250 and 300 um i just wondered if you could tell me how this compares to what we knew already um so it's just to put into context of how much further this new set of papers takes us in working out diversity between humans well this is uh Richard answering so the numbers of uh a total variance per person is actually about three million um but the numbers of genes which appear to have a a complete loss of function defects in them is is the 250 to 300 those numbers are not that new but what we've done here is by sequencing by looking at many people um we've each variant that you find in an individual will only be in some members of the population so uh the 15 million number is a substantial increase over previous uh uh list and means that we can cover more of the variants present in any one individual in fact the project as a whole is moving onwards from the 200 or so people studied genome-wide in the pilot um and now it's sequenced over uh a thousand people uh so that data on a thousand people are available and we can already see this number of 15 million is going to go up and we're going to get a deeper and richer picture going forward so we're moving um that number is increasing and will uh at least double over over the next year so this is David Altshuler let me um uh just add one other thing to that which is um a number that i personally find uh just just useful as a way to think about this because after a while millions of variants whether it's one million or ten million or fifteen million it's hard to have context if you're not if but here's a number that i think is easy for people to understand uh this idea of the number of genetic variants in each individual so what we mean by that is if we were to take a DNA sample if a DNA sample was taken from a reader or any of us and we sequence it and we just define as the variation in that genome the sites at which the month the copy one inherited from one's mother and the other copy of the genome you inherited from your father differ all right that's the number Richard said there's some three million or so differences between those two copies or another way of thinking about it is the differences between an individual uh and a copy of the genome and that uh human genome reference sequence that came out of the human genome product that number is the same it's just a comparison of any two chromosomes and it's about uh three million letters or one in a thousand letters because there's three billion letters so one to thousand of three million three billion is three million so now the question is how much is our knowledge of that variation that we might find in each individual increased over time so we go back to ten years to uh that what Richard started at the uh announcement of the human genome sequence that number would have been that if we sequenced any person's genome and said what fraction of the variation in that genome was in the public database it would have been five percent or less in other words 95 percent of what was found in the next person's genome was new not previously seen at the time of half map maybe five years ago that number was on the order of 40 percent or so 40 or 50 percent so in other words you'd sequenced the next if one had had that technology it wasn't available at that time but we now know um that if you had sequenced the person's genome said how much of that variation in that person is in that uh database for SNPs for these single base changes would have been 40 or 50 percent much less for the kind of structural variant that Evan was telling you about if you look today for single nucleotide polymorphisms in the pilot data of the thousand genomes project 95 percent of what you find in the next person's genome is already in this database still lower for the kind of variants that Evan's uh studying because they're harder to study and we see these numbers going to 98 percent or something like that for many types of variation that in other words by the time the thousand genomes project's done each person if they had their genome sequenced the vast majority greater than 95 percent maybe as much as 98 or 99 percent of the variation that person would already be in the public database and therefore it could be referenced back and then perhaps one or a few percent of the variation would be unique to that individual not in that database a lot did you want to follow up on that no that's fine thank you okay thanks next question please thank you and we have a question from the line of Tina say from science me please go ahead uh yes i wanted to follow up on that just a bit so how many SNPs are currently in the database and then i have a question about the loss of function genes um so i i can so in the the pilot um coming out of the pilot project there are 15 just over 15 million SNPs 15 million 275 thousand uh these many of those yeah these are not exactly the same as the set of variants which are in dbSNP which come from all other projects um i don't have a number number for the total union across all research available today um and then uh so you see that each person um has about 250 to 300 genes that are basically inactivated uh in their genome um do those tend to be some of the same genes or would they be unique genes in each person and what does that say about disease risk and um how necessary these genes are so the mix some of those genes uh are commonly inactivated and maybe genes which uh are not strongly required um but uh there are also a a more gene in the category of these loss of function variants which include uh premature stop codons uh frame shift mutations and uh changes in splicing so that uh the exons don't get put together properly um in that category is substantially enriched for uh rarer variants for things that are present just perhaps in one of the uh 179 people um so it is true that and that indicates two things first that these probably many of these are functional and that the reason why they're not more common is that they've been selected uh away there's this negative selection against them or purifying selection uh it also says that we are each probably carrying um more or less private certainly rare uh defective copies of genes they don't necessarily lead to disease directly in the individual they may um we have two copies of most genes one from the mother one from the father and so if one is defective you're just a carrier that can sometimes have a a a phenotypic effect i think i was just i was just gonna add that the there's been much speculation over the years about the relative contribution of different kinds of genetic variants to the basis of disease but ultimately these are questions that can only be answered empirically because all the speculation is based on different assumptions about uh how the genes and pathways and biology of disease works what's truly exciting is to live in a time when we have the methods and data to ask those questions empirically and i think that uh what you will the answer to your question for example about what role do these genes that are in activated plane disease can be rather straightforwardly evaluated now not just because of the thousand genomes project but the general approach by identifying them and relating them to patients and disease and so rather than speculate i think we'd say we are helping to create a foundation to answer that question and anyone who does speculate i think is speculating there's no way to know short of doing the experiment and what's exciting is that we now are going to have the tools and methods increasingly to just answer those questions through actual empirical data rather than speculations and people are beginning to do that yes absolutely and just to follow up on the last part of what Richard Durbin was saying when we talk about a gene being inactivated it's one of the two copies of the gene that the person has so we don't so for for most people one version doesn't work these loss of function variants but generally the other version of the person inherited from the other parent will work so this would be recessive mutations then well there's one copy of them if the other one works and the person is perfectly fine because of it then they are recessive yet no but most of the most of the variants that we're seeing in this way are for our carrier status of uh diseases known as recessive diseases although it's not always the case in fact in very few examples has has there ever been large-scale study of people who are carriers to know if they have any uh any disease risk okay one of the surprising things um is that actually um most disease genes have been studied either uh in to the extent disease genes meaning those that cause rare strong genetic diseases have largely not in every case but in most cases only been studied people who have those diseases so the broader population relevance of the of having a variant in those genes is actually not well characterized because it hasn't been possible to do studies of this sort until now and so when you sometimes read about someone saying someone had a part of their genome or their whole genome sequence and they were found to have a mutation that causes a disease and yet they're apparently healthy that's more a statement about it not having been possible previously to do that kind of empirical study rather than a shocking finding this is um Ruth i'm just going to remind the speakers if you can say who you are when you run through and i think i've got a bit confused uh but um next question please thank you the next question comes from the line of nicholas wade from the new york time please go ahead hi david can i ask you to clarify the cutoff point between common and rare variants and i think it was like what you just said now it was five percent in the hat map days so when you've reached the point of having ninety eight percent of variation in your database um what will be the uh uh the definition of a of a snip at that stage sure so let me let me just there's a couple of ways to answer this question um first of all i think that the uh personally well there's the classical definition sort of in the textbooks of what is a common variant or what's known as a polymorphism and that number is one percent or higher in the population and um in the era of a hat map and the snip consortium given the technology that was available at the time um there were the the sort of uh frequency to which that resource went was down to between five or ten percent and the first uh a set of genome wide association studies were a variance of five ten percent and above um things below that frequency first of all would still be down to one percent would still be classical polymorphisms that's the term that's been used but i think actually the most meaningful conceptual framework is the one that i used in my opening comments which is there are two types of variants there are those that are present in apparently unrelated individuals from inherited from shared ancestors uh that can be cataloged and then studied for relationship to disease and that goes down somewhere below one percent uh and then there's ones that are unique to each family or individuals which i think would be well called rare or private mutations and those are much much less frequent the numbers i cited to answer your question about 98 99 percent is for a frequency of one percent and above so it's not the 99 98 percent in your database uh what percentage of the quote missing inheritability do you believe you will have captured i have no idea because that calls for speculation i really i really consider it a complete a question of empirical data and i think that frankly there's been too much speculation i think that what we know is that there are rare variants that influence disease because that's been documented for decades and we know that there are common variants that influence disease uh because they're documented examples and i think the question of sort of a complete understanding is probably many years in the future where we've explained every if we ever will explain all the inheritance but i think the promising and exciting thing is we are actually for the first time as a field making progress at least honing in on the many genes that contribute to each disease but they just may want to comment if a major part of the burden is is borne by these very rare variants which i see mostly sort of spontaneous mutations then it could be we will come up pretty empty-handed i eminently rational as this approach is um our catalog might help us i mean i can't well here this is good i think it's i think this idea that this divide in the sand that we have in terms of percentage is really i think to be honest totally bogus what we want to be able to do is we want to be able to look at genomes comprehensively not just as a function of frequency of small variants but in terms of the full spectrum variation ranging from single base pair changes to insertion deletion events to larger c and v events so copy number variant changes and i think i mean i can't imagine that we come up came up empty-handed if we just look at things for example from the copy number variation perspective you know at the at this point today now with technology that we have we can pretty much uh diagnose about 20 percent of kids with mental retardation or intellectual disability as having a large copy number variation event sometimes it's sporadic sometimes it's been inherited for a very few gen and i think there's a lot of yield to come from studies of genetic variation but i think the point that we have to keep our you know keep the keep our eye on is that we need to actually divorce yourself from this idea of frequency and move to really a comprehensive assessment of all forms of genetic variation and i think if we do that we'll be able to actually link that's where we are right now with the technologies that are coming online to sequence genomes to you know comprehensively assay structural variations to sequence exomes i believe that this is this is the era where we're going to actually make huge huge inroads in terms of genetic basis or understanding the genetic basis i think the last point and i made this in my opening comments is that i think that the thousand genomes project that we mentioned each of us in our own way three different things three different ways in which this project contributes one of which is methods standards part of sort of a public private collaboration of companies and academics all working together to make the technology work for any application i think that that is a contribution under any disease model and then i think that as evan said we want to be comprehensive in the exact deployment of the resource will differ depending on the different approaches people take but i actually think that the actually the documented value of the thousand genomes project for medical research just in the first year is actually more under the model that nick way just mentioned of rare genetic variants it's a necessary step in how you interpret a rare a rare variant model to know the common variants so i think it would be missed just so people aren't confused this project is not about any given model it's about what evan said which is a comprehensive approach it's not about any particular underlying model it's about testing all the models thanks everyone um next question yeah next question comes from the line of michael price from the washington examiner please go ahead hi yes my question is for evan i'm getting away from the diseases a little bit when you're talking about the genes associated with neural development i was wondering if you could um let me know if those were related to specific regions of the brain or or processes or connections or anything like that um i think it's how you tied that back to neural development yeah so i mean what we did is actually we did a formal test to see which genes were you know enriched or which genes had been specifically duplicated in the human lineage and we use some of these programs that have been developed to look at gene classes and neural development came up significant but only modestly so but when you actually look at the specific examples they're actually quite striking so as as an example there's this gene known as surgap 2 it's actually duplicated specifically in the human lineage we don't know the function or we actually don't know the role or even if the the duplicated copies are totally functional but what we do know is that there are multiple copies of surgap 2 and the parent gene surgap is in fact important in terms of neural neuronal migration in the cortex and so it's expressed and there's a beautiful paper published in cell about a year ago that looked into this and it's really the kind of the spatial temporal expression of surgap 2 which dictates how far neurons actually migrate in the cortex and then begin their kind of arborization or lateralization it's to me it's just an anecdote and you got to be careful not to get too excited about these anecdotes but when you start looking at all the genes that that we find that are duplicated and pretty much often fixed in all humans that we look at but not so in the chimp or gorilla we see a significant number of genes that that would be particularly sexy candidates for I don't know if the right word is human mentation but they're neurogenesis and so this is something that we like to pursue and I think it's an understudied area where people have been looking at you know human evolution they've been focusing mainly on again the tractable regions of the genome that 90 that's easily a thank you next question thank you ladies and gentlemen please be reminded if you do wish to ask a question please press seven on the telephone keypad now and a final reminder to ask a question please press seven on the telephone keypad now we have no further questions coming through take the time then to say thanks to everybody for dialing in to today's briefing and thanks to the speakers for their time and if you need any more information please don't hesitate to consult us or once again I can want to remind you of the nature and science embargoes on these papers which is 6 p.m. London time 1 p.m. US Eastern tomorrow Wednesday the 27th of October there'll be a recording of this briefing on the Nature Press site and science will make that available to you under embargo many thanks


Esteemed colleagues, thank you for inviting me to this webinar and I would like to present myself. My name is Sam Vaknin. I'm a professor of psychology in Southern Federal University in Dostov-on-Don, in the Russian Federation. I'm also a professor of finance and a professor of psychology in the Global Outreach Program of SEAPS, Center for International Advanced Professional Studies. Today I would like to discuss with you a much neglected topic in psychology and more specifically in psychopathology and even more specifically in psychopathology of personality. And that is a topic of twins. Now it's very surprising that there's such a dearth that there are so few studies of twins in this particular niche of psychology. Twins share the same ovum, identical twins share the same appearance, they have the same age, they have the same set of parents, they experience the same upbringing. They, by definition, ipsofactor, they constitute the perfect case study. If we want to distinguish and discern individual effects upon the etiology and pathogenesis of personality disorders, nothing comes more natural than sets of twins. And yet you would be hard pressed to find such studies. Is it a question of political correctness? Is it a question of logistical difficulties, like finding a large population of twins to work on and to work with over an extended period of time? I'm not quite sure what the reason is. Twins are not that rare, as we might imagine. And there have been numerous other studies on groups of people and populations which are much more rare than twins. Why not twins is one of the unresolved mysteries of clinical psychology? At any rate, twins present a very interesting conundrum when it comes to narcissism, especially primary narcissism, the type of narcissism that is nascent and incipient in early childhood, the type of narcissism that allows the child to gradually separate from the parent, more specifically from mother, the primary object, the type of narcissism that allows individuation, the type of narcissism that endows the child with sufficient grandiosity and fantastic capacity to take on the world. The world is hostile, the world is unknown, the world is frightening. And so to take on the world, to assume risks, to seek novelty, to explore, to satisfy curiosity, this requires a lot of grandiosity. Mother, a good enough mother, provides a safe base, but that's not enough. It's only one of the conditions. She encourages the child to be grandiose. Actually a good enough mother colludes with the child's primary narcissism. And so there is a very clear narcissistic universe in the good sense. This is healthy narcissism, that's the kind of narcissism that later on underlies the regulation of self-esteem, self-confidence, and the sense of self-worth, it's a kind of narcissism that allows us to take on new tasks, new missions, new assignments, new jobs, to embark on undertakings such as having a relationship, siring children, these all require a modicum, a modicum of suspension of disbelief and a lot of grandiosity. So these are the roots of healthy primary narcissism and this process, which Jung called the constellation of the self via introversion and Freud called by other names, never mind all that right now, this process of primary narcissism, constructing one's individual, constructing one's self, becoming a person. This process is heavily disrupted in twins and it's disrupted in twins because there is triple or double mirroring.  At a very, very early stage, it starts with the kind of omnipotence, omniscience, and omnipresence that are essentially divine. The child experiences a unitary universe, the child is the world, the world is the child, there are no boundaries, there are no separations, there are no distinctions. The child does not realize that there is something external, external and internal are one. It's what Freud called an oceanic feeling and it also manifests in mental health disorders in adults such as psychotic disorders with hyperreflection.   This chism is the first major psychological trauma in life. Break apart this universe and realize that there is external and internal. The formation of the boundary between these two worlds is, starts us on the way to maturation, personal growth, personal development and ultimately adulthood via another phase, another narcissistic phase which is adolescence. But what happens if this unified universe doesn't include only one person, mother, but includes yet another person, the twin. And that other person is a mirror, a spitting image, a mirror image of the child. So the child has to confront two extensions of himself. One extension is the mother from which he has to separate and individuate on the way to becoming an adult, an individual adult. And the other person is a copy, a clone of oneself.  First, the child has to separate from mother and then the child has to separate from himself. Twins self as reflected in the other twin. The separation from the other twin is perceived unconsciously and intuitively as a divorce from oneself, as divorcing oneself. That is even much more traumatic than the experience with mother. Theoretically, such a cataclysmic break will be perceived as internal, not external indeed. Twins form a narcissistic union. They consider themselves one organism with two heads, one organism with two souls and two psyches. Throughout life, twins maintain this pseudo or quasi-telepathic capacity where they actually share a life. It reminds me that in quantum physics we have a phenomenon called entanglement where two particles share the same molecules and then they're broken apart, they're separated. One of them is cast away light years into the universe. But when the first one changes on Earth, this particle changes somehow, for example, changes his spin, changes one of its characteristics, the particle at the very end of the galaxy will change instantaneously. This is called entanglement. It has been demonstrated in laboratory experiments. It's not speculation. This is an entanglement among twins. Twins are like these two particles. Never mind how further away the second twin is going to go. They maintain this union, this narcissistic union. And breaking it apart somehow is an apocalyptic, super traumatic event which no twins don't go through, don't have to endure. Now, if this is the case, we should expect to see a much higher level of secondary pathological narcissism among twins. If twins have to endure a trauma in order to individuate, many of them theoretically would opt not to go through this process, to remain entangled with their twin. Twins may decide to not become individuals, but to become a colony, a colony of two, to become a hive, a hive mind, to become an organism with two heads. In other words, many twins, we can speculate that many twins would get stuck somehow in the transition from primary narcissism to individuation. And when this happens, this is what Freud called secondary narcissism, and today we call this pathological narcissism. When the child who is not a twin cannot separate from the parent and individuate, we have on our hands a narcissist. When the twin cannot separate from his or her twin and individuate, when the twin remains engulfed and meshed, merged, fused and entangled with another person who is a replica of him, a copy, a clone, we should definitely anticipate much higher rates of secondary narcissism because of the failure of separation and individuation in this case from oneself. Because exactly as Jung had observed very early on, and today, many other scholars in object relations theory, in the object relations school and so on, it's not enough to separate individuate from the parent. At some stage, one needs to separate and individuate from the self. Jung called it the constellation of the self. The self becomes like an alien object, a separate object, an autonomous entity. Freud described it as the ego. He said that the ego has an interface with reality, the ego helps us to maintain reality testing. And he made it very clear that the ego and the person are not coterminous. Jung went even further. He said the ego is not the self and the self is not the ego. There are structures and constructs inside us, like introjects, like the self. And many people say that the self is an introject, like what Freud called the superego, the inner critic or whatever you want to call it. There are structures and constructs inside our psyche, which are essentially alien to us. And this is why many of us experience estrangement. We feel that we are not ourselves in certain situations under extreme duress or stress or anxiety. If the twin, if one twin cannot separate from the other twin, ever mentally, psychologically, they may have a problem in maturation, a problem in becoming an adult. Is this true? And here is the agony, in a way, of the theoretical psychologies, because the experimentalists failed him or her. I work in theoretical psychology. I'm not an experimentalist. And when I try to go to the literature to see studies which will substantiate or falsify some of my ideas, I can't find any. So I would like to propose a mini review of the literature somehow. Let's start with a general statement. It's taken from an article titled, Beyond the Diet, How Thinking About Twins Expands Psychoanalytic Theory. It was written by Dr. Ruth Simon, it was published not long ago, in Fort Da. Fort Da is a psychoanalytic newsletter and it's published in volume 26. So she starts by asking the question, who is older? You know, this is a classic question, everyone asks twins, who is older? And the answer is, we are both older. She asks, why think about twins? Why at all? And here is her answer, concisely. She says, psychoanalytic theory and practice have conceptualized psychology and identity in highly individualistic ways. We have, I take a break here just to elucidate. Our modern psychology is founded on the principle of individualism, a psychology which would have reflected a more collectivist approach, would have been totally different. A psychology, a psychology started in China or in Japan and not in Germany and the United States. Had it started in Asia, it would have looked completely different, it would have emphasized social relationships, interactions, interpersonal dynamics rather than the individual. But it's a fact that psychology started in countries where the individual was the organizing and explanatory principle. So all our psychology, modern psychology revolves around the concept of personality or individual. It's a construct, there's no veracity to it. It's not something that is essentially testable or falsifiable. It's simply a convenient way to organize knowledge, but one should not mistake a convenient way to organize knowledge a classificatory system, a taxonomic system with the truth or with reality. No one had ever captured an ego or spoken to a super ego. We use the tri-lateral, Freud's tri-lateral model, those of us who do, to talk about the world. It's a language element. It is not pretensions to reality or truth. Well, at least if you are not seriously primitive in your approach to psychology. So I continue from Simon's article. The limitations of these conceptualizations, individualism, become particularly apparent when we try to apply them to patients who are twins. It used to be fairly rare to encounter twins in a therapy practice, but that is becoming less and less true as the birth rate of twins has risen dramatically over the past several decades. Interrogating the ways in which current psychoanalytic theory falls short of addressing the unique psychological needs of twins and other multiples elucidates a fundamental individualistic bias in the field. In lieu of understanding the unique psychology of people who were born as twins, those who were born as singletons, parents, friends, partners, teachers and therapists, singletons tend to impose and interpolate our own majority cultural, political and psychological biases on the minority twin population. By the way, she's not the first to say this, Louis Althusser, the famous post-Marxist social theorist and psychologist, I think he was psychologist, I'm not sure, but he made contributions to psychology. Althusser in 1971 made the same observation that actually singletons, people who are born as single newborns, they are the majority and twins are a repressed minority, akin for example to black people or Native Americans or women in many cultures. They are a repressed minority and the value system and the language and the constructs and the assumptions and the theories that pertain to single people, people who had never grown up in a dyadic cell with another twin, these are imposed on twins. It's like twins at a certain stage should become singletons. This can never happen, because twinship is not a state of birth, it's a state of mind. There is a, we should establish a separate psychology for multiples, which is divorced from the psychology of individuals. Simon continues, contemporary American neoliberal ideologies, psychoanalytic theories and our own familial experiences have led us to think in individualistic and binary terms that do not readily apply to healthy twin psychology and have led twins to feel misunderstood by those who care for and try to help them. The relational identities and psychologies of twins fundamentally challenge our understanding of psychic health, with significant implications for twins and non-twins alike. One recent study of twins was conducted by Vernon, Vilani and Vickers together with Harris, it was published in 2008 and the title was a behavioral genetic investigation of the dark triad and the big five, big five is a personality factor, personality factor theory. It was published in personality and individual differences, volume 44. So Philip Vernon and Vanessa Vilani in 2008, they examined the behavioral hereditary aspect of three dark triad factors. Today we have dark tetrads, the concept has evolved a little, but in those early days the dark triad was comprised of narcissism, Machiavellianism and psychopathy. It was an open question whether these are acquired, whether these were acquired or learned behavioral trait complexes or whether they reflect brain abnormalities. What is a genetic contribution or template? So there was a lot of, there were a lot of open questions about heredity and their relationship between heredity, brain functioning and behavior. And this was one of the first studies to examine dark triad elements. And what they did, they used the big five factor analysis theory of personality to sort of map the characteristics and then they tried to correlate them with genetics. And of course the easiest way to do this was to study twins. So they selected 278 adult grown-up twins and they subjected them to surveys and to structured interviews and tests and so on and so forth and then they took the results and they grouped them together in terms of the dark triad, Machiavellianism, narcissism, psychopathy and in terms of the big five factors of personality. What they discovered is that there was a very strong relationship. They even used the word huge, huge relationships among a few dark triad factors and each of the dark triad factors and the big five. In other words, there was internal correlation between the dark triad factors which shows that the dark triad is a valid construct. It has internal validity, internal consistency and there was a high correlation between the dark triad and the big five factors of personality. So it seems that personality somehow interacted with dark triad elements. So in terms of genetics, this is phenotype. It's not genotype. So these factors were somehow connected to the phenotypic level. These relationships probably had to do with heredity because the correlation was consistent across the sets of twins, across the various twin couplets, it was consistent. It was predictable if you knew, if you created a picture, created an analysis, analyzed the big five factors, you were able to predict dark triad and vice versa. And so the strong indication was that there was a hereditary kind of variable, series of hereditary variables, which together constituted a template upon which two phenotypes emerged. One phenotype was the big five factor analysis of personality, but it was closely correlated with dark triad factors which were correlated among themselves. In other words, dark triad factors in twins were derived from their personality, which was clearly strongly correlated with their genes, with the fact that they shared the same genes. This was an astounding discovery because if dark triad, if dark triad properties and traits and behaviors are correlated in twins with their phenotype, which by definition is correlated with their heredity, with a genetic baggage or material, why not make the same reasonable assumption when it comes to non-twins? Can we learn from this about non-twins or is there something in twins that predisposes them to manifest or to express certain clusters of traits and behaviors? It's very unlikely. It's very likely. Twins simply provide a crystal lens. Twins are laser. It's like studying laser rather than a diffused light from a bulb. We can see things much more clearly, but these things are valid. A light is light. Whether it's a laser beam or a bulb, it's still light. It's still photons. It's still these personality traits and characteristics and phenotypes and factors that appear in twins in a very discernible and emergent way that is very easy to observe and to analyze, but this means in all probability that it's the same with non-twins. The same Vernon collaborated with Petrides and Schermer and Wesselka three years later, 2011. They published an article called Trade Emotional Intelligence and the Dark Trier Trades of Personality, and it was published in a journal that is dedicated to the study of twins, Twin Research and Human Genetics, Volume 14. They wrote, and this time I would quote because there are many technical terms, so they wrote, for instance, in one way to deal with twin investigations, scientists analyze the identity scores of monozygotic or indistinguishable twins raised together to disygotic or friendly twins raised together. Since the two sorts of twins, so we have monozygotic twins, they're identical, they share the same ovum, they grow, they come out of the same egg, maternal egg, essentially they are one person, one person divided in two. In many cases, by the way, one of the twins dies in uterus in the womb and the other twin survives and when he's born he carries parts of his, of his, of the other twin, the dead twin carries them with him. So the surviving twin would have two sets of some organs, which are actually inherited from the dead twin, but some monozygotic twins, of course, we have identical twins. So Petritis and Vernon studied indistinguishable twins, monozygotic twins, and studied dizygotic twins. These are twins that develop at the same time, two fertilized eggs in the womb develop at the same time, they're born at the same time, but they're not identical. Yet they are raised together. These are two, these are two perfect, perfect study conditions, pure unadulterated situations. And they continue to write, since the two sorts of twins in this plan are raised together, all twin sets are viewed as having shared a 100% regular condition. Conversely, the monozygotic twins share 100% of their qualities, while the dizygotic twins just offer around half of their qualities. So the monozygotic twins have 100% identity. The dizygotic twins are 50-50. Yet both sets of twins, both types of twins, were raised in the same environment that was critical, critical for the experiment, for the study. In this way, the authors continue, in this way, for any given identity attribute, it is conceivable to divide impacts by first getting the monozygotic connection, reflecting 100% normal condition and 100% shared qualities. And then subtracting the dizygotic relationship, reflecting 100% regular condition, but only half the shared qualities. And this distinction speaks to half of the hereditary impact. Multiplied, this number is said to represent 100% of the hereditary impact, and is one approach to infer a file of heritability. Now and then, called the heritability coefficient, we designate it by each two. So you see that if we study simultaneously, twins who are 100% the same raised in the same environment, and twins who are only 50% the same and raised in the same environment, we can clearly eliminate the environment and remain only with a genetic hereditary difference between the two groups. Any quality they have, any trait, any behavior, any psychological construct can then clearly be attributed to a genetic predisposition or foundation. It's a brilliant approach, absolutely brilliant approach. So H2 is the heritability coefficient. The authors continue, essentially monozygotic H2 might be viewed as a gauge of the impact of the normal condition. At long last, since singular contrasts and the earth should represent the totality of conduct, it is said that subtracting the entirety of H2 and the normal condition impact from one is equivalent to the impact of extraordinary or non-shared situations. The year before, in the International Journal of Methods in Psychiatric Research, the July 2010 edition, an article was published titled Measurement Non-Variance of DSM-4 Non-Cecistic Personality Disorder Criteria Across Agents 6 in Population-Based Sample of Norwegian Twins. I don't know why everyone goes to Norway to get twins for psychological studies. Must be a secret there, which I am not a privy to. Anyhow, the authors in this case were Kubaric, Egen, Kendler, Torgersen, Reichborn, Kjernoud and Niel. Quite a few. And they wrote the following. We investigated measurement non-invariance of DSM-4 non-ecistic personality disorder criteria across age and sex in population-based cohort sample of 2,794 Norwegian twins. That's a very big study. And so they discovered amazing things. I would even say counter-intuitive things. First, age had a statistically significant effect on the factor mean for NPD. Sex had a statistically significant effect on the factor mean and variance. Sex was more important than age. Controlling for these factor-level effects, item-level analysis indicated that the criteria were functioning differently across age and sex. Now this defies the DSM. Defies even the alternate model in the DSM-5 published in 2013. Because the assumption is that narcissistic personality disorder is stable across the lifespan, all pervasive and stable across the lifespan. And this study shows it's not. The assumption also is that it is gender-neutral, sex indifferent. And this study clearly shows it's not. So they continue. After correcting for measurement differences at the item level, the latent factor mean effect for age was no longer statistically significant. So when they tweaked the measurement effect, they discovered that age is much less important than sex. The mean difference for sex remained statistically significant after correcting for item threshold effects. The results indicate that DSM-4 NPD criteria, which are still valid in DSM-5 by the way, perform differently in males and females and differently across age. Differences in diagnostic rates across groups may not be valid without correcting for measurement non-variance. But of course, in all this, there's another hidden conclusion, surprisingly not enunciated and promulgated in the study. These were twins. It seems that being a twin, the state of twinship, which intuitively and theoretically should have affected primary narcissism, should have encouraged pathological secondary narcissism, didn't. Being a twin is not a good predictor prognosticator of having NPD in later life.  What matters is age.  That's a pretty conclusive study, the foundational study, I would say. The number of people studied was enormous. It seems that biological factors, because age and sex are totally genetic. They're totally biological. This is not gender, mind you. This is sex. Male, female. Yeah, male, female, not men, women. Men, women, these are gender constructs, gender roles which we acquire, learn, emulate via socialization and otherwise, imitating role models and figures. It's not men and women. It's male and female gametes. It's totally biological. It seems that whether you're male or female and your range determine your propensity for acquiring or developing NPD and then determines the progression and trajectory of the disease, not whether you're a twin or singletoe. It seems that the role of environment here is really seriously minimized, because if we were to rely on environment only, all twins should have ended up being narcissists. They have this narcissistic, self-contained universe which they cannot extricate themselves from. They are solipsistic. They are enclosed, self-sufficient, self-contained. Their communication patterns are very, very interesting. I think they have a private language, so they should have developed into rank narcissists with autistic features and if they didn't, being a twin has a biological foundation, but it's mostly an environmental thing. The way other people react, acquisition of language, parental changes, modifications in behavior. In a study published entitled Narcissism and Object Relations in Monozygotic Twins, studied by Haussier, Weiber, Aikis, Philippine, Prigent, Quistake and Ahdaba. It was published in Research in Psychoanalysis last year. They did discover that the mother of twins becomes a third-party symbiotic object. A twin goes through libidinal investment, investment in the self and later investment in other people. Always accompanied by two people, not one.  He had all the time the dialogue is with the mother figure or the main caregiver and this dialogue never stops, of course, but at some stage, via various stages of individuation and separation, the mother becomes totally internalized, she becomes an introject, the voice, not so with twins. Twins have to contend with mother but also with another copy of themselves. This is a highly unusual situation and none of the psychological theories we have. Not one of them has any tools to describe this or to cope with this. Is it symbiosis? Is this second twin a reflection, a mirror, and if so, what are the dynamics that are created, for example, in the constellation of the self? Does every twin create a twin self, a twin ego? Is everything doubled? Is it a state of constant resonance, vibration, life-long vibration, lifespan vibration? And what's the role of the mother, who is more dominant at any stage? Is the separation and individuation mainly from the mother or mainly from the twin? And if a separation and individuation with the mother succeed but fails with the twin, what happens? If it succeeds with the twin but fails with the mother, what happens? What is the meaning of Nazism in a twin set, among a couple of twins, especially identical twins? Imagine two identical twins, one of them is a narcissist. Nazism is a confusion of external objects with internal objects. The narcissist mistakes external objects and treats them and relates to them as internal objects. The other twin is internalized up initial from the very beginning. So what happens then when there is essentially no external object?  And then he has two internal objects. And of course, the other twin is a personality of her own and this personality diverges from the inner representation. How does the first twin cope with the divergences and idiosyncrasies and emerging personality of the other twin? We don't have any information about this or little information about Nazism in twins. In an article published in February this year titled the behavioral genetics of the dark triad core versus unique trait components pilot study was published in personality and individual differences volume 154 was written by offered by eight consumer and Jones. So they wrote recently there has been the suggestion that the dark triad traits Machiavellianism Nazism and subclinical psychopathy share a common overlapping core in this exploratory investigation. A secondary data analysis were conducted to extract common dark triad core which they call the dark factor. So they try to find a dark factor that underlies all three manifestations of the dark triad, Nazism, Machiavellianism, subclinical psychopathy. And so they continue. We found that Machiavellianism and psychopathy had higher factor loadings of the dark factor than Nazism. The dark factor was best explained by genetic and unique environmental factors when sex and age effects were removed. Genetic and unique environment models best fit the residuals for Machiavellianism and psychopathy. And Nazism, but only when sex and age were removed. Again we see the critical importance of sex and age. You have to remove them which I find to be totally unacceptable. I mean removing sex and age from the equation is like removing the individual. I would have never done this had I designed a study but okay they did. And even then they discovered that the dark factor actually creates Machiavellianism and psychopathy, not so much Nazism. Nazism had much more to do with sex and age. These results suggested that further behavioural genetic studies should be conducted on the common and unique variances of dark triad. And finally I would like to quote from Caliguria's article the influence of childhood rearing of the separation and individuation process of tweens Pace University. It's a doctoral dissertation published last year. A critical sentence, a single sentence to round up the presentation. Similar to the intrauterine environment the infant is in a state of absolute primary Nazism and is contained within kind of a bubble. With the mother, as Hoel suggests, they have a shared sense of self. They have a self-contained narcissistic system in which both tweens feel incomplete. So he sustains, he believes that there is a trilateral system with twins. Mother and the other tween fulfill an identical psychodynamic role. I think this is pretty indisputable. The importance, crucial importance of tweens in each other's lives has been documented numerous times and amply. What we fail to study is how is this connected intimately and inexorably to the emergence of primary Nazism, which is a precondition for separation and individuation, and to the emergence of secondary Nazism, which is the pathological kind that we find in narcissistic personality disorder. These questions, regrettably and egregiously, we don't have an answer. Here's something for you to do. A research agenda. Thank you for listening. And now, if you have any questions, I will pick.


Can you tell me what it is you feel is helpful about this doorway for those coming to it? It's wide open. What do you feel is helpful for them? Yeah, well this doorway, it seems to be hidden to the everyday perceptions of the world, the linear perceptions. So it's almost like an esoteric doorway into mysticism. And it can be quite disturbing to the ego. So I would say don't be alarmed as you come close to this doorway, because the ego may have some reactions. But it's very gracious doorway. It's God's love and grace coming into awareness. And there still seems to be steps to take. The mind is very addicted to linear time, so it has to come in a form of steps. But each step leads happily on to the next step and the next. And with each step inward that you take through this doorway, through this portal or gateway, every step gets lighter and lighter. And you become less aware of the elements of time and space. So in order to come and to experience God's grace, you have to meet the conditions of grace. You can't bring judgments through the portal. You can't bring these attachments of the past into the portal. You have to leave them at the door. And so in that sense it's a very light journey as you enter into the portal. So you get lighter and lighter because you're not carrying the weight of past thoughts and beliefs and perceptions.


Hi everyone, it's MJ the Fellow Actuary and in this video I want to talk about my art. So I've been exhibiting since 2016 and I've been at a different gallery every single year doing an exhibition and now in 2020 I have moved to Super Rare which is digital art on the blockchain and you can actually go to their website and place a bit on this piece but what I want to do in this video is just maybe talk a little bit more about this piece that we have over here. So let's just jump straight into it. So first of all you're probably wondering what is that background that keeps going red? Well those are the tectonic plates of earth and the red is to actually symbolize the fact that you know there's lava under the earth. We've then got this really cool map made by one of my favorite academics called Cholesander's Purse and I don't even know how to pronounce this. It's a quintessential projection but it's a way to do the map of the earth without distorting any of the land masses. Of course the only awkward thing about this map is that New Zealand gets chopped up into the top four corners but what's nice about it is that Africa my continent isn't shrunk like on normal maps. Then I've got this little thing which is like a mermaid flying a stingray. It's from the Garden of Earthly Delights a very famous painting by Hieronymus Bosch. I hope I am pronouncing that Dutch artist's name correctly and I'm really am inspired by a lot of the work that he does. Speaking about artists this is Abraham and Isaac. This is a big religious scene from an artist called William Blake who again I really get a lot of my inspiration from. Then seeing that I'm based in Cape Town I've got a few of the some of the famous boats that visited Cape Town back in the day. So we've got the St Gabriel which Vasco de Gama from Portugal sailed to Cape Town with and then we have the Dramadyrus which Jan van Riebeck from the Netherlands came down to Cape Town with. So yeah took quite a bit of time drawing these boats and then they've got very small little parts in this piece but yeah I'm all about the detail. Then yeah I mean the fact that I'm from Cape Town well I'm living in Cape Town now originally from Johannesburg which is based here in South Africa and that is kind of the view from my parents place where I was kind of like thinking of this art piece. So you'll see us in the bottom corner all the bottom there I'm just kind of showing you where the inspiration or where this piece was conceived in the world. Then I was looking through Leonardo da Vinci's notebooks for for inspiration and I came across this unknown drawing which I just thought was cool. I have no idea what it is but I was like you know what it has to go into the piece. Then this is a very famous ancient Greek computer. Again my pronunciation is a little bit dodgy but we're going to try the Antikathira mechanism and it's a little bit of an enigma when it comes to science because why did the ancient Greeks have like this fancy technology back in the day. So we'll see we've used this as a pattern just to create a little bit of layers in the piece. Then like I said I started this piece actually back in 2016. I remember starting it before Pokemon Go and that's why I didn't want to release it straight away because then Pokemon came back with quite a bit of vengeance and the piece was supposed to have a little bit of nostalgia so I've waited a little bit longer and done a few more additions to the piece and now only releasing it in 2020. The problem with that though is I got these scientific waves from a really really old source and I have forgotten where it comes from. I did a Google reverse image search on this and I think my sketching of the waves is a little bit too bad because yeah they couldn't they couldn't pick up where this is from. It could have been from one of Isaac Newton's books like I said it was this is four years ago. This was really cool. Again my pronunciation is going to let me down but this is a dwarf planet that is in our solar system. It's flying around Neptune it's got an egg shape and it's got this weird rotating frame orbit which I've kind of represented in the in the egg shape planet. It's named after like I said the Hawaiian goddess so we've got the Hawaiian islands there but I just thought it's really cool. I mean this is a dwarf planet in our solar system that I didn't know about and I was like wow um and I guess maybe it's one of the things we want to talk about in this piece is you know we're so focused on Pokemon and pop culture that we sometimes don't spend enough time learning about yeah our own our own solar system and all the crazy stuff that's happening around us. Anyway moving on another artist that really influenced me is Joseph Kapik. This is his piece Melinda Zena. I really do need to work on my pronunciation. Again very very small piece a little you know detail in this piece but really am influenced by his style. You should check out the original of this piece it's you know I haven't done it justice by just you know tracing out the outline it really really is a stunning piece. Then we've got those two heads the Julia Caesar and Herodotus. I think we all know Julia Caesar as the Roman leader and then Herodotus is a Greek historian which is maybe a little bit of an unknown guy but he's just got such a cool face. Then this big piece at the bottom is a Viking compass. I just love that pattern and those sharp angles it is it is really a nice design. Then there's a lot more computers in this. You can see this is the Charles Babbage machine. Babbage is that how you pronounce it I don't know. Very much an early computer we having a top down look of this thing. Again it just it fascinated me this the whole pattern that this thing kind of created and then of course let's talk about you know who's that Pokemon. It's not actually a Pokemon instead it is a North mythology devil that I found while Google searching ruins in the Viking Scandinavian area and I just thought it's so cool how yeah I think most of us have never seen this thing before yet we've all yeah we all know Pokemon and I thought I don't know Pokemon they keep releasing new Pokemon so this could become a Pokemon. Probably it will be a ghost type or a dark type Pokemon but yeah I just wanted to have that question of you know who's that Pokemon people think hey you know have I seen that before and I don't know it's maybe it's a call for education that's what I like to do on my YouTube channel is I do like to teach and I think that's coming across in the arts as well is to try and get a little bit of that curiosity get people interested in North mythology because I don't know it's very rich there's a lot a lot of joy to be had from it and then yeah I mean people like to always ask me what exactly is the meaning of the piece I've given a few clues to it now but of course I mean what would an art piece of me be if it didn't have some sort of secret cryptic code so there's a little bit of a clue it's in the piece try and decipher that and that'll of course give you a little bit of an answer to the meaning of this piece. Anyway that's I don't want to take too much of your time so once again my name is Michael Jordan based here in Cape Town you're probably coming from the link from Super Rare but if you're not if you're watching this on YouTube then see the link in the description to go to Super Rare where you can see this piece on the blockchain and you can actually make a bid to purchase it and yeah who knows this might be a really good investment for you. Anyway thanks so much for watching and I will see you guys soon. Cheers!