Unfit To Fly: Andreas Lubitz

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Newly released book, 4th April, 2015.

I believe genetic profiling should be conducted on pilots, to uncover the potential of detached retina and major depressive illness – both were suffered by Andreas Lubitz, and this combination can be traced to the gene TNF (tumor necrosis factor). Preventative surgery could have been done to avoid a detached retina in this young man. Furthermore, his major depressive illness would have been kept under scrutiny if this kind of profiling had been carried out. In my opinion, DNA profiling should be introduced wherever lives are at stake and the responsibility for them falls on the shoulders of one man.

New book release- UNFIT TO FLY: ANDREAS LUBITZ – forensic numerological criminal profile:

Unfit to Fly: Andeas Lubitz

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One thought on “Unfit To Fly: Andreas Lubitz

  1. Hello. I’m a medical student in Australia – I studied chemistry previously (as an undergrad) and I’m working on a research Masters as well. I stumbled upon your blog via a TED talk link. I’m interested in mathematics and genetics too, but my mathematics is pretty bad.

    So I have to admit from what I’ve read I don’t quite understand all of the mathematical methods you’re applying – some of them seem quite unique and interesting, but I only wish I was able to understand them with more clarity. No matter, though- this is obviously a field you’ve worked in for quite some time and it would be impudent of me, I think, to pretend to understand it after only having read your blog for an hour. I find it fascinating, though, and will continue to try to interpret the methods you’ve used, as they are immensely interesting.

    Is there a part of your blog where you have examples of your mathematical analyses ? I’m very interested to read them, for instance the ones about Ted Bundy and so on. (As a poor student I have little money, unfortunately, to spend on e-books, as much as I would like to support you and your efforts.) Thanks for putting this blog up though, again, just a really great site.

    But I wanted to comment briefly on the idea of genetic profiling. It is an area I’ve thought about a great deal. If you’re interested, please do read on. I apologise in advance for the length of this post. If anything (or everything) is unclear, let me know and I’ll be only too happy to help clarify anything at all.

    The thing about medicine, and particularly psychology and psychiatry currently is, they rely so heavily on behaviour, instead of neurophysiology. To my knowledge, nobody outside of a research lab has ever been diagnosed with, say, bipolar disorder because of a neurological biomarker – some physical indication of altered brain function, like a PET scan, an fMRI scan, or the identification of a gene associated with bipolar.

    Now, this is a huge problem. We don’t even have biomarkers for Alzheimer’s disease, Parkinson’s disease, and a range of other very harmful degenerative illnesses. In the next 20 years, the number of these illnesses will skyrocket – in Australia, where I live, by the year 2030, 1 in 10 people will have Alzheimer’s disease or attendant dementia. 1 in 4 people will spend at least 1 hour per wee caring for somebody with Alzheimer’s disease or dementia.

    The onset of Alzheimer’s disease in our aging population is going to hit us like a tidal wave – and it will overwhelm healthcare systems worldwide, but particularly in rural and regional areas where resources are fewer. This is a big part of why I want to practice rural and regional medicine when I finish school.

    Before I drone on too long, though, I’m not trying to write up a scare piece, though it seems like it. Actually, I just wanted to tell you about the field of ‘molecular psychiatry’, closely related to the field of biological psychiatry – there are excellent journals in both these areas.

    My dream is, one day, and one day soon, to have diagnostic compounds available for all neurological disorders. I spent my Honours year working on developing a PET diagnostic for Alzhemer’s disease, but unfortunately, while our compounds showed some promise, by the time our results came back, my Honours year was over.

    What does this have to do with genetic profiling ? Well, as you probably know, genes are organic molecular ‘monomers’ – subunits of DNA. Genes, in fact, are just segments of DNA, and they are converted, via RNA, to proteins. These latter compounds are the building blocks of our organs, our tissues, our cells.

    Very important to neurological function – for instance, depression – are ‘channel proteins’. Basically, they sit within neurons (nerve cells), and allow or prevent the movement of certain ions and neurotransmitters (these latter being molecules that aid or affect brain functioning by altering the channel pores, either stimulating or inhibiting them).

    For instance, the GABA receptor is a family/subtype of channel protein, and it is responsible for the movement of chloride ions, which, as a function of their negative charges, tend to send ‘inhibitory’ impulses along nerves. Essentially, GABA receptors are responsible for regulating anxiety, depression and sleep (in a complex and intricate concert with multiple other receptors and transporters, particularly the VMAT transporters, and the dopamine and serotonin receptors).

    So these tiny, complex pathways that control our behaviours and moods have, in recent years, been studied as part of long term analyses into why certain people are more anxious than others. One study published in the Journal of Molecular Psychiatry showed that children who, in their first 5 years of life, were exposed to unstable, aggressive, or overtly hostile parents/caregivers on a regular basis, developed certain genetic mutations. These mutations were in the genes responsible for the development of those GABA channels – and actually, the GABA receptors are composed of ‘subunits’.

    The researchers demonstrated that the genetic mutations resulted in growth of GABA receptors with different amino-acid residues facing the pores (so the receptors as I said are like channels from the inside of the nerve to the outside – the ‘pores’ of the channels are made up of charged portions of amino acids, which are the building-blocks of proteins – these charged portions of the amino acids allow ‘selection’ of what ions enter, and what ions do not enter the synapse (the space between one nerve cell and the next, integral to the conduction of an excitatory or inhibitory impulse).

    If you have a channel with negative charged interior pores, then negatively charged particles will be blocked from moving through those pores. And vice-versa. By blocking movement of certain ions, and allowing movement of others, the receptors govern anxiety, depression, behavioural impulses and an array of phsyiological stimuli.

    So, in the study, by demonstrating the genetic mutation had altered the makeup of the GABA subunit pore in children exposed to abusive/hostile/unstable environments, the researchers were able to, for the first time that I’ve read, actually physically link poor childgood caregiving, to anxiety, via certain genetic mutations.

    The study was intensely beautiful to read, amazingly elegant science. If all neurological disorders could be diagnosed this way, we would have a much greater knowledge of the brain, the human condition, and as you’ve suggested, a greater ability to possibly prevent tragedies such as the one your blog post mentioned.

    The problem, though, is actually identifying the genetic (and subsequent protein) mutations. Because, the question is, how do we do that ? There are a number of ways, but as of now, there is no single genes (nor are there even, to my knowledge, a set of genes) which we can screen for, to identify a particular mutation that would be associated with depression.

    For instance, certain mutations in the BRCAx genes are associated with certain types of unrestrained cellular growth leading to cancerous tissue.

    But for depression, there is no single gene – or a single gene product – that could be screened for, to rule the disorder in or out. Another problem is, who would we screen ? The goal of an effective screen would be to test people without having to analyse them behaviourally. What I mean is, sometimes people with depression conceal this from caregivers and healthcarers – it is often seen as a social stigma, and so understandably, people with depression are not keen to let others know about it. This is sad and troublesome as it may prevent them being helped. (Obviously consent is a huge issue here – even if we had a screening method, would it be ethically right to use it on those who claimed they did not have depression and who did not give consent to be screened ? In my honest opinion, a patient who does not consent to a procedure should not be forced to have that procedure; this is how I feel and this is what my medical school teaches me, and teaches all other students).

    Another problem is, how would a screen actually work ? We’d need a genetic target – and we don’t have one right now, unfortunately. We’d need a protein target – and again, we don’t have one. Screening for millions of genes is okay, but if we don’t know what they do, then we’re wasting time. Screening for thousands of proteins or microRNAs (via, for instance, arrays) again, might provide thousands of results – but if we don’t know what the proteins do, the results are meaningless.

    Sadly, even for a disease like Alzheimer’s, we actually have to wait until the patient has passed on to confirm the physical presence of the amyloidogenesis in their brains. Diagnosis is always made by interview with the patient/their family, i.e. on behaviour and observation.

    Depression is much harder to diagnose with respect to behavioural observation, and as of this writing (July 2015), there is no way to genetically screen for depression, or, in fact, reliably determine the genetic profile behind almost any mental illness. The best way doctors have, at this point, to determine your genetic profile, is to ask if your parents or grandparents had a particular disease or disorder. That is actually quite reliable in many respects and for many health problems.

    I don’t want to be a bringer of bad news by any means, though. I am just one of many, many people interested in molecular psychiatry, and interested in developing tools for helping those across the world (in my own case, tending to a focus on those in regional and rural Australia) who are suffering from health problems. Whatever those problems are, I’d like to be able to effectively and accurately diagnose them, and to treat those patients so that their quality of life improves, so that they and their loved ones are able to lived full, happy and satisfied lives. That is my goal – and I’m particularly interested in research into biomarkers for dementia, since as a chemist that is where I spent my Honours year, and as a human being, this affected me strongly. As a doctor my primary goal will obviously to improve health without harm, to relieve suffering, and to improve lives. That is, as a medical student, what I focus on every day. I hope I’m able to continue research in the areas I’ve mentioned, and if you’re interested I’d be happy to send you more information about the Alzheimer’s diagnostics we aimed to develop, or anything else you’d like to know.

    Sorry for swamping you with text by the way ! I’m keen to read more about your own interests, especially your mathematical methods and proofs, and I’m going off to do that now. Thanks for the interesting and insightful blog.

    All the best,
    Pete

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