No Two of Us Are Alike–Even Identical Twins

Press Release, University of Western Ontario, March 28, 2011

Just like snowflakes, no two people are alike, even if they’re identical twins according to new genetic research from The University of Western Ontario. Molecular geneticist Shiva Singh has been working with psychiatrist Dr. Richard O’Reilly to determine the genetic sequencing of schizophrenia using identical or monozygotic twins.

The study is published in this month’s PLoS ONE.

Singh looked at about one million markers of identical twins (and their two parents) where only one twin had schizophrenia. “The most informative feature of schizophrenia is that it sometimes runs in the family. So, for example, the risk of developing schizophrenia is much higher if your brother, sister, mother or father have the disease,” says Singh, noting in the general population about one percent have schizophrenia. “We started with the belief that monozygotic twins are genetically identical, so if one member of identical twins has schizophrenia, then the risk for the other twin should be 100 percent, if it’s all due to genes. However, studies over the years have shown that the risk of the disease in both twins is only 50 percent.” That means either the twins are genetically not identical or the familial disease involves non-genetic (random) effects.

Singh and his team have now demonstrated that the monozygotic twins are not genetically identical. “So if schizophrenia is in the genes, then the difference in the genetic makeup of monozygotic twins, with only one disease twin, must have something to do with the disease.” Singh found about 12 per cent of DNA can vary across individuals, “Cells are dividing as we develop and differentiate. More importantly, these cells may lose or acquire additional DNA. The genome is not static.”

Dr. O’Reilly hopes this research will lead to better understanding and improved treatments for schizophrenia. “If we had a genetic test for schizophrenia, it could be applied early in the disease when it’s hard to make that diagnosis,” says Dr. O’Reilly.

The research was funded through the Canadian Institutes of Health Research, the Ontario Mental Health Foundation and the Schizophrenia Society of Ontario.

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  • Anonymous

    If it is the case that twins ARE genetically identical and yet their physical, psychological and physiological characteristics could STILL manifest differently then this would be an argument in our favour. When people say “races are only 1% genetically different from each other and so we are all practically the same” then we can say “that small percentage makes a huge difference; even twins who are genetically identical still manifest differently”

    But if it is the case that twins are not genetically identical, then how does that help us?

  • highduke

    It’s just assumed that schizophrenia is genetic bc it runs in families rather than it being the product of inter-generational bad parenting (just like autism, assburgers, personality disorders) in the form of playing favorites between children &/or covertly scapegoating a child from birth. In the 50s they blamed the parents. That was very bad for business. Then psychiatry woke up, stopped blaming anyone and got in bed with pharmaceutical industry, got the West medicated and made billions.

  • Seneca The Younger

    So race is a social construct, but twins are genetically different? That makes sense.

  • TomSwift

    Although it is true that identical twins are not identical, I find it hard to believe that the genes that cause disease would keep appearing or disappearing thru mutation this rapidly.

    If I remember correctly everyone is born with about 100 random genetic mutations, mostly in the junk DNA. Very rarely in the useful stuff, as most mutations stop the fetus from developing correctly.

  • len

    The concept of Junk DNA went out some time ago. There is only useful DNA. It has not all been mapped yet. ( Re: Tom Swift.)

  • Reg

    This is Dr Rushton’s school. Indeed, it’s his department. I’d like to see his take on this in a future AR.

  • Mike H.

    We share 96-98.5% of our DNA with chimps. It should be clear to everyone that even a 0.1% change can make quite a large difference.

  • Anonymous

    7 — Mike H. wrote at 10:51 PM on April 3:

    We share 96-98.5% of our DNA with chimps. It should be clear to everyone that even a 0.1% change can make quite a large difference.

    Exactly my thoughts. I read where there are certain Africans that actually share some genetic markers with chimps that are not shared by other Africans or non-Africans. I find this interesting especially now that we know Caucasoid and mongoloids have 2-4% Neanderthal genes.

    All this new DNA data exploding in the news is so awesome. It all seems to bear out many of my theories.

  • Anonymous

    >>

    “Cells are dividing as we develop and differentiate. More importantly, these cells may lose or acquire additional DNA. The genome is not static.”

    >>

    And…

    >

    A team of scientists at Johns Hopkins University have just announced that susceptibility to a certain complex birth defect is not related to normal gene inheritance. Instead of occuring within a section of gene that codes for a protein molecule, the anomoly occurs in a section of gene that regulates the expression of other genes. This type of interaction, where one gene influences the activity of another, is known as epigenetic interaction. Ways that one gene can influence another include sequences that determine the probability that a gene is turned on (making protein) or off, how much of the protein product it makes, and with what frequency.

    “Our finding really underscores the fact that health and disease can be affected by all regions of a gene,” says study leader Aravinda Chakravarti, Ph.D., director of the McKusick-Nathans Institute of Genetic Medicine. “For diseases like diabetes and heart disease, just as for Hirschsprung disease, multiple inherited factors contribute to the disease, and these factors are not just going to be in protein-coding regions.”

    Epigenetic interactions may be a place to look for schizophrenia or bipolar genetic susceptibility as well. It is well-known that while a family history increases one’s risk for developing serious psychiatric diseases (see http://www.schizophrenia.com/research/hereditygen.htm), the genetic heritability is not a simple, single-gene affair. It is not a matter of gene-X coding for schizophrenia traits, and the presence of gene-X determines the presence or absence of that disease trait. Monozygotic identical twin studies have shown us that even if two people have the exact same genotype, one may still develop schizophrenia or bipolar disorder while the other will not.

    Searching for epigenetic factors in schizophrenia and other heritable psychiatric disorders can provide both new hypotheses for causes, and new targets for treatment. For example, valproic acid – a mood stabilizer used to treat bipolar disorder – seems to have an effect on the epigenetics of gene expression, in that it affects the chromatin structure (proteins that DNA is wrapped around when it is not being expressed) that determines which genes are being expressed and when (source: Schizophr Res. 2005 Jan 1;72(2-3):79-90).

    Epigenetic factors that affect gene regulation may partially explain why there is such a wide variability in symptom severity, disease course, and family heritability. There are also many environmental factors to consider (see http://www.schizophrenia.com/hypo.html)

    >

    http://goo.gl/7uefA

    Anytime you hear a geneticist using the term ‘development’ or ‘developmental’ you should first and foremost think epigenetics and transcriptor factors by which a gene cues the activated function of other gene groups rather than forming a protein of its own.

    The clue-in seems to be that chromatin encapsulations are not going on in certain areas which should be turned ‘off’ to prevent expression of unnecessary genetic functions.

    As a personal guess, I’m going to go with a biochemical agent (something like a follic acid) which activates specific genetic sequences and which, competed for by each twin at similar times in the development process, the mother only provides to one twin in sufficient quantity or of a sufficiently -controlled- amount, to induce or suppress regulatory function.

    Resulting in expression of specific abnormal trait behaviors which the other twin does not suffer from.

    Of course, treatments which end up nullifying some of the victim’s latent (expanded, schizoids are often highly intelligent) mental functions may end up robbing us of a few genius’ as it appears that new ‘ligand’ based therapies are specifically (ionized metals) designed to trade up electron covalencies between chemical states (i.e. change the function of the protein by changing it’s nature) and while these can be used reliably to ‘associate’ with specific cell types as neural processes in given brain centers, their binding with a given receptor protein can also permanently alter it’s function.

    The next generation of behavior modification drugs could very well be ‘mind altering’ in ways we won’t appreciate…

  • Jack

    All dogs are 99.8 % genetically identical.

    .2% is enough to make the difference between a chihuahua and a Mastiff.

    It matters not if it is 1,2,3 percent or even if it’s only 10 genes.

    What matters is the difference.