Bioelectronic medicine: a very brief overview
Drugs that affect the nervous system get administered systemically. It’s easy to imagine that we could do much more if we could stimulate one nerve at a time, and in patterns designed to have particular effects on the body.
“Neural coding” can detect the nerve impulses that indicate that a paralyzed person intends to move a limb, and build prosthetics that respond to the mind the way a real limb would. A company called BrainGate is already making these. You can see a paralyzed person using a robotic arm with her mind here.
A fair number of diseases that don’t seem “neurological”, like rheumatoid arthritis and ulcerative colitis, can actually be treated by stimulating the vagus nerve. The nervous system is tightly associated with the immune and endocrine systems, which is probably why autoimmune diseases are so associated with psychiatric comorbidities; it also means that the nervous system might be an angle towards treating autoimmune diseases. There is a “cholinergic anti-inflammatory pathway”, involving the vagus nerve, which inactivates macrophages when they’re exposed to the neurotransmitter acetylcholine, and thus lessens the immune response. Turning this pathway on electronically is thus a prospective treatment for autoimmune or inflammatory diseases. Vagus nerve stimulation has been tested and found successful in rheumatoid arthritis patients, in rat models of inflammatory bowel disease, and in dog experiments on chronic heart failure; vagus nerve activity mediates pancreatitis in mice; and vagus nerve stimulation attenuates the inflammatory response (cytokine release and shock) to the bacterial poison endotoxin.
Here is a detailed roadmap from this Nature article about the research that would need to be done to make bioelectronic medicine a reality.
We’d need much more detailed maps of where exactly nerves innervate various organs and which neurotransmitters they use; we’d need to record patterns of neural activity to detect which nerve signals modulate which diseases and experimentally determine causal relationships between neural signals and organ functions; we’d need to build small electronic interfaces (cuffs and chips) for use on peripheral nerves; we’d need lots of improvements in small-scale and non-invasive sensor technology (optogenetics, neural dust, ultrasound and electromagnetic imaging); and we’d need better tools for real-time, quantitative measurements of hormone and neurotransmitter release from nerves and organs.
A lot of this seems to clearly need hardware and software engineers, and signal-processing/image-processing/machine-learning people, in addition to traditional biologists and doctors. In the general case, neural modulation of organ function is Big Science in the way brain mapping or genomics is. You need to know where the nerves are, and what they’re doing, in real time. This is likely going to need specialized software which outpaces what labs are currently capable of.
Google is already on this; they recently announced a partnership with GlaxoSmithKline called Galvani Bioelectronics and they seem to be hiring.
Theodore Berger, the scientist who created the first neural memory implant , has cofounded a company, Kernel, to develop neural prostheses for cognitive function.
Bioelectronics seems potentially important not just for disease treatment today, but for more speculative goals like brain uploads or intelligence enhancement. It’s a locally useful step along the path of understanding what the brain is actually doing, at a finer-grained level than the connectome alone can indicate, which may very well be relevant to AI.
It’s tricky for non-academic software people (like myself and many LessWrong readers) to get involved in biomedical technology, but I predict that this is going to be one of the opportunities that needs us most, and if you’re interested, it’s worth watching this space to see when it gets out of the stage of university labs and DARPA projects and into commercialization.
Possibly of interest: The Second Brain—it’s about the neurology of the digestive tract. It’s harder than I thoughf for a body to manage having meat-digesting stomach acid in the middle of an organ. The author suggests that a lot of digestive problems are actually neurological rather than something wrong with specific organs.
It’s from 1998, but I don’t know of more recent books on the subject.
i know there was a paper last year that pointed out that 60% ? of serotonin receptors are in the gut, a lot more neuro down there than gets studied well.
A surprising number of ‘spiritual practices’ have turned out to stimulate the vagus nerve/affect its baseline tone. This is also probably one of the pathways by which cardiovascular conditioning affects health (vagus nerve innervates the heart). I had thought that the vagus nerve also innervates the diaphragm, which would explain how breathing exercises could affect it, but it turns out that’s the phrenic nerve.
Deep breathing does stimulate the vagus nerve though, if I understand correctly. How much the heart rate changes after a period of deep breathing is a standard test of vagal nerve function. People with autonomic dysfunction can’t slow their heart rate through deep breathing.
There was also a paper late 2015 that showed that the apicomplexans (toxo,malaria, chagas) were using the myelin sheath to get access to the brain and other major nerve bundles. There was another one that showed maltose or lactose could open the blood/brain barrier for up to 20 min., and there is some evidence that the plaques are actually to isolate and reduce the interference of the api spores that had burrowed into the nerve sheaths on the brain surfaces.
And more on the BBB and the gut barrier.
the recent paper published by Maria Fiorentino and colleagues\
“After that little rant, the paper from Fiorentino is an interesting one in that the goal was to “investigate whether an altered BBB and gut permeability is part of the pathophysiology of ASD.” To do this, tissue from both brain and gastrointestinal (GI) tract donated by a small number of deceased and non-deceased participants who were diagnosed with autism, schizophrenia or nothing related (not-autism controls) were analysed “for gene and protein expression profiles.” This work was undertaken on the basis of “the interconnectivity of the gut–brain axis, [that] suggests that inappropriate antigen trafficking through an impaired intestinal barrier, followed by passage of antigens or activated immune complexes through a permissive blood–brain barrier (BBB), can be part of the chain of events leading to neuroinflammation and thereby subsequent disease.” I might add that the use of the word ‘disease’ in that sentence is, I think, aiming to describe the physiological effects of ‘leaky barriers’ not the diagnosis of autism.”