Jo Cameron needs blood or the smell of her own burning flesh to know that something is very wrong. As the 71-year-old Scottish woman reported at The New York Times earlier this week, she has lived a life without pain, fear, and fear, thanks to a lack of DNA stretches. The doctors found that Cameron had something else when she came to surgery for a surgery and refused painkillers after the nerve blocker had stopped her surgery. After years of investigation, they identified the never-before-seen mutation that is believed to be responsible for their almost supernatural pain tolerance. Strangely, every wound she gets heals faster than other people, and she can not remember ever being afraid, depressed, or frightened. Their results were published Tuesday in the British Journal of Anesthesia .
In human biology, it is uncommon but not unsurpassed that a complex sense of pain is controlled by a single gene. For decades, scientists have been looking for rare families whose members are similarly insensitive to pain, and have found in their DNA at least one more genetic coding that acts as a volume control for human suffering. Pharmaceutical companies are currently in clinical trials for a drug that can mimic these effects. And the advent of Crispr offers an even more appealing option. What if you could repair not just pain but existential anxiety and fear of the human condition as a whole?
Megan Molteni deals with gene technology, medicine and sharks for WIRED.
This question feels particularly important The US is struggling to free itself from the depths of an opioid epidemic that costs five lives per hour. Drugs that help people escape the body parts and thoughts that hurt them today kill as many Americans every year as weapons or car accidents. Some medical researchers predict that Crispr and other gene editing tools could lead to a completely new method of pain relief without pills. But revelations in the last year of rogue Crispr experiments with people in China open up the ugly prospect of what might follow; This genetic insensitivity to pain might one day become the main designer menu, or worse, armed as a 21
This may be far-fetched if it were not something Vladimir Putin proposed in a Russian science event for students who describe the future of gene editing in 2017. A man who could fight without fear, compassion, regret or pain, he said, "could be worse than a nuclear bomb." You have to give it to the man who knows how to break down a Crispr party (for kids) no less!). Super-soldiers may be just a sparkle to the eyes of the authorities, but former US intelligence chief James Clapper has called gene-editing a potential weapon of mass destruction in his 2016 National Security Threat Report. In the study of intelligence, special mention was made of the possibility of using the technology for processing the DNA of human embryos.
The WIRED Guide to Crispr
A push to change the genes of the next generation forever has changed so far, both through an intense ethical debate about whether man has sufficient knowledge to control the species' own evolution as well as constrained by practical challenges. This DNA rarely works in a straightforward way. "We do not really understand how complicated biology is," said co-inventor of Crispr, Feng Zhang 60 minutes last spring in a segment. Suggest a gene here or add code to it and you could cause other problems. For example, removing a gene called PCSK9 significantly reduces the risk of heart attack. Great, right? But it also increases the likelihood of diabetes. Compromises against other less well-studied genes may be even more unpredictable. (For Cameron, the Scottish patient, the drawbacks of her unique DNA appear to have been just forgetfulness and the "adrenaline rush" she heard about so much, and she does not have an internal alarm system that signals her break degenerated joints and wounds.)
James Cox, a molecular geneticist at University College London who identified Cameron's genetic anomaly, says his group is now using Crispr in human cell lines to try to mimic their microdeletion and its effects to understand better. This helps them to find the best strategy for potential therapeutics. Because the mutation occurs in a pseudogen called FAAH-OUT – a gene that forms a long RNA chain that does not code for a protein but acts as a regulator elsewhere in the genome – they have several options. Some of these include designing and injecting a complementary RNA sequence that suppresses the production of FAAH-OUT. This could possibly provide temporary local relief. However, the treatment of chronic pain would require frequent shots or infusions. Therefore, they are also looking for a more permanent solution: to process DNA directly in the cells to replicate Cameron's analgesic microdeletion. "It's the beginning, so there's a lot to think about," says Cox. "However, we can imagine that a broad group of patients could possibly be helped."
The ability to experience pain while an unpleasant part of life developed for a reason developed for a reason. That way your body can tell you when something bad happens. To completely lose this sense of protection may sound great, but it can also be dangerous. This is one reason why some early explorations in the emerging field of gene-based pain therapy are not yet using Crispr (the other is the murky state of who owns the gene-editing IP). "The question with Crispr is that you only have to target the cells you want, in this case, the nerve cells that build up and down the spinal cord and send out axons throughout the body to feel pain," says Joseph C. Glorioso III, a microbiologist at the University of Pittsburgh who is studying both gene therapy and pain management. "If you could just do some editing in these cells, you can make them more resistant to pain signals, but then this is a permanent thing and you do not want to be in a situation where you can never feel that emotion."
In 2014, Glorioso Coda founded Biotherapeutics to develop a gene therapy approach to the treatment of chronic pain. The South San Francisco based Coda has so far raised $ 19 million to develop receptors in the sensory neurons of people who can be controlled by a small molecule drug. The idea is to use a virus that has evolved in nature to infiltrate the overexcitable nerves responsible for many types of neuropathic pain – from arthritic joints to thrown back and nerve damage caused by many cancer treatments become. A single injection into the skin sends the virus to the nerve cells and gives instructions on how to make this adjustable on / off switch. When a patient experiences pain, he or she takes the drug, reducing nerve cell electrical activity and preventing the onset of pain, with minimal body side effects and addictive dangers. Glorioso expects that it will take 18 to 24 months for experimental therapy to be ready for human testing. Coda starts with so much pain that it is virtually untreatable, but the same approach could be applied to other neurological conditions, including anxiety, says Glorioso.
What if you were one of the people who saw Cameron's story and thought to yourself saying, "Crispr me some of it!" The possibility of genetic control of pain is not as far away as you might think.
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