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When it comes to caffeine and sleep, most experts would say the duo has a rocky relationship, at best. Of course, everyone responds to caffeine differently (some can tolerate an afternoon java; others will surely be up all night), but generally, the stimulant is associated with a poor circadian rhythm and disruptive sleep cycle.
So why, then, does clinical psychologist and board-certified sleep specialist Michael J. Breus, Ph.D., also known as “The Sleep Doctor,” claim that the secret to the perfect nap is, in fact, coffee? “I call it the ‘nap-a-latte,’” he says on the mindbodygreen podcast. “This is a caffeine-induced nap.”
Do tell, Dr. B.
How caffeine helps you nap.
To be clear, Breus is completely on board with how caffeine can hinder sleep. “Caffeine is arguably one of the biggest offenders in our sleep,” he says. The thing is, there’s a difference between regular, restorative sleep and a quick, 30-minute-long cat nap. For the latter, caffeine may be more friend than foe.
“It turns out that a buildup of something called adenosine in your brain is what makes you feel sleepy,” notes Breus, as the compound slows down nerve cell activity in your brain (which causes drowsiness). What caffeine does is binds to those adenosine receptors and effectively speeds the nerve cell activity back up, which provides a jolt of energy. But here’s the thing: To your nerve cells, caffeine and adenosine look the same. “If you look at the molecular structure of adenosine and the molecular structure of caffeine, they’re off by one molecule,” notes Breus (here’s a diagram, the structural similarities highlighted in red). “The thing that makes us wake up and the thing that makes us go to sleep is literally off by one molecule.”
So how does this relate to your midday nap? Well, says Breus, caffeine can actually fool your nerve cells for a time, as “those receptor sites will accept caffeine,” and allow you to sleep before the stimulant actually kicks in. It won’t last long (about 25 minutes before your sleep burns through the adenosine, he notes) but he says it can work for a little cat nap. ADVERTISEMENT
How to create Breus’ “nap-a-latte.”
If you’re itching to try Breus’ nap hack, here’s what he recommends:
Chuck in three ice cubes. “Merely to cool it down,” he says.
At around one o’clock in the afternoon (he advises against drinking caffeine too late in the day), slug it.
Immediately set an alarm for 25 minutes and close your eyes. Sweet dreams.
The takeaway.
Generally, caffeine and sleep do not go hand in hand. But for a quick, 30-minute nap, the stimulant might not be so terrible—it can even help you drift off for a bit. That certainly doesn’t mean you should chug cold brew right before bed (this hack only works for short sleep spurts, as your nerve cells will recognize the caffeine once your adenosine burns out), but the science behind it is pretty cool.
Jamie Schneidermbg Editorial AssistantJamie Schneider is the Editorial Assistant at mindbodygreen. She has a B.A. in Organizational Studies and English from the University of Michigan
Smartwatches and fitness wearables may be able to play a valuable role in the early detection of COVID-19, according to recent studies. Researchers from Mount Sinai have found that the Apple Watch can detect small changes to a user’s heartbeat that may indicate they have the coronavirus, a full week before they feel sick, as CBS News reported. One company is even developing a custom wearable to detect COVID-19 — all of which could help stop the spread of the disease by keeping asymptomatic folks at home.
In a study titled called “Warrior Watch,” the Mount Sinai researchers followed a group of 297 health care workers between April 29 and September 29. The participants wore Apple Watches equipped with special apps that measured changes in their heart rate variability (HRV). “The watch showed significant changes in HRV metrics up to seven days before individuals had a positive nasal swab confirming COVID-19 infection,” said study author Robert P. Hirten, MD.
A similar study done by Stanford University found that participants wearing a variety of trackers from Garmin, Fitbit, Apple and others found that 81 percent of patients testing positive for coronavirus had changes in their resting heart rate up to nine and half days prior to the onset of symptoms.
One of the challenging things about COVID-19 is that many people are asymptomatic, meaning they have no symptoms but are still contagious. This makes it difficult to contain this infection by using the traditional method of identifying someone who is sick and quarantining them.
The ramifications of the studies are clear. “Developing a way to identify people who might be sick even before they know they are infected would really be a breakthrough in the management of COVID-19,” Dr. Hirten said. “This technology allows us not only to track and predict health outcomes, but also to intervene in a timely and remote manner, which is essential during a pandemic that requires people to stay apart.”
The researchers aren’t the only ones to notice that early COVID-19 symptoms that can be picked up by a smartwatch. A company called NeuTigers, born out of research from Princeton University, has developed an artificial intelligence product called CovidDeep that can help identify people with the virus in clinical situations or care homes.
The company used a clinical-grade patient monitoring wearable, the Empatica E4, to take a variety of skin, heart-rate and blood pressure readings. Feeding that information into CovidDeep, they found they could detect the virus at a rate of 90 percent — more accurately than typical temperature screenings. They eventually plan to produce their own app that could work with Fitbit, Withings, Apple, Samsung and other smartwatches.
Even without custom algorithms, a smartwatch or wearable could still be useful. The PGA Tour started using Whoop health trackers recently, and that may have helped player Nick Watney realize he was positive. “They’ve done studies where, if your respiratory rate goes up during the night… that’s sort of a telltale sign that you might have something,” said major champ Rory McIlroy back in June. “It was actually his Whoop that told [Watney] his respiratory rate went up, and that’s why he thought maybe he could have it.”
Amazon wants brands to create their own voice assistants using Alexa’s tech.
Building a smart voice assistant like Alexa is hard, according to Amazon, and we can probably take its word for it. However, that doesn’t mean that voice assistants are out of reach for companies like car manufacturers, for example. Amazon wants car manufacturers to make their own voice assistants, using Alexa’s technology, of course, and the company has already found its first customer: Fiat Chrysler.Amazon’s Alexa Can Now Ask You Follow-Up Questions
Responding to demands from consumers for “an Alexa, but make it talk even more,” Amazon announced…Read more
Amazon unveiled its Alexa Custom Assistant in a blog post on Friday, a new solution that allows device makers and service providers build their own smart voice assistants for their brands using Alexa technology. Alexa Custom Assistant allows companies to create an assistant with its own unique wake word, voice, skills, and capabilities. You also don’t have to worry about fights between the brand’s assistant and Alexa, Amazon said, as they will coexist “seamlessly” and cooperate with each other to carry out requests.
Per the companies, the Alexa Custom Assistant relies on advanced AI to route each request to the relevant assistant. In Fiat Chrysler’s case, the custom assistant will act as the “product specialist with features and capabilities specific to the vehicle.”
“[I]f a customer asks Alexa to roll down a car window, or how to troubleshoot a device, the request will be routed to the brand’s assistant. If a customer asks the brand’s assistant to play an audio book, the request will b
It added that having Alexa in the equation also gives the brand access to tens of thousands of Alexa skills and integrations related to smart homes, entertainment, and shopping, among others. Amazon also mentioned that Alexa Custom Assistant was designed with “privacy in mind,” and that it will manage user data associated with it. Take that as you will. Just a reminder, neither Alexa or Amazon have the best track record on privacy.
The way Amazon sells it, Alexa Custom Assistant allows companies to innovate without putting in the investment, long-term continuous development, and resources required to build a voice assistant from square one. Yet, as noted by the Verge, it’s not clear whether Amazon is letting car manufacturers use its custom assistant for free or charging them to license it.
In a statement, Fiat Chrysler said it has already begun working on developing its own branded voice assistant for future vehicles. The company already has Alexa integrated into some of its vehicles around the world.
“Our customers expect to easily connect with their digital lifestyles wherever they go and today we responded with plans to offer new intelligent experiences built on Alexa’s world-class voice AI technology,” Mark Stewart, COO of the company’s North American operations, said in a statement.
To get a better idea of what a branded assistant could look like, Amazon made a video of a car assistant named “Brandon” for an unnamed brand, which you all can see below. It’s pretty interesting and ambitious, although I do wonder if all of the custom assistant’s skills, as well as Alexa’s, will go off without a hitch as in the video. I mean, the Alexa on my Echo Dot sometimes confuses Spotify playlists, which is a relatively simple task.https://gizmodo.com/ajax/inset/iframe?id=youtube-video-tmuGQjZcn2w&start=0
That doesn’t mean I don’t think it could get to the level showcased in the video. It’s just that it might take a while, which is also normal.
If you’re going to put a smart speaker in your home that disregards your privacy and functions onlyRead more
David Limp, Amazon senior vice president for devices and services, told CNBC that users are only going to want to interact with a voice assistant in their cars is if it’s built in. He added that the company has envisioned many possible uses for Alexa.Subscribe to our newsletter!Type your emailSign me upBy subscribing you agree to our Terms of Use and Privacy Policy.
“Obviously we started with smart speakers, we’ve extended to smart displays, we announced at CES this year with PCs,” Limp said, per CNBC. “We think this idea of ambient computing, and Alexa powering that, it has a lot of breadth and it can be in a lot of different places.”
Targeted neuromodulation tailored to individual patients’ distinctive symptoms is an increasingly common way of correcting misfiring brain circuits in people with epilepsy or Parkinson’s disease. Now, scientists at UC San Francisco’s Dolby Family Center for Mood Disorders have demonstrated a novel personalized neuromodulation approach that—at least in one patient—was able to provide relief from symptoms of severe treatment-resistant depression within minutes.
The approach is being developed specifically as a potential treatment for the significant fraction of people with debilitating depression who do not respond to existing therapies and are at high risk of suicide.
“The brain, like the heart, is an electrical organ, and there is a growing acceptance in the field that the faulty brain networks that cause depression—just like epilepsy or Parkinson’s disease—could be shifted into a healthier state by targeted stimulation,” said Katherine Scangos, MD, Ph.D., an assistant professor in the Department of Psychiatry and Behavioral Sciences and corresponding author of the new study. “Prior attempts to develop neuromodulation for depression have always applied stimulation in the same site in all patients, and on a regular schedule that fails to specifically target the pathological brain state. We know depression affects different people in very different ways, but the idea of mapping out individualized sites for neuromodulation that match a patient’s particular symptoms had not been well explored.”
In a case study published January 18, 2021 in Nature Medicine, Scangos and colleagues mapped the effects of mild stimulation of several mood-related brain sites in a patient with severe treatment-resistant depression. They found that stimulation at different sites could alleviate distinct symptoms of the brain disease—reducing anxiety, boosting energy levels, or restoring pleasure in everyday activities—and, notably, that the benefits of different stimulation sites depended on the patient’s mental state at the time.
“We’ve developed a framework for how to go about personalizing treatment in a single individual, showing that the distinctive effects of stimulating different brain areas are reproducible, long-lasting and state-dependent,” said Andrew Krystal, MD, director of UCSF’s Dolby Center and co-senior author on the new study. “Our trial is going to be groundbreaking in that every person in the study is potentially going to get a different, personalized treatment, and we will be delivering treatment only when personalized brain signatures of a depressed brain state indicate treatment is needed.”
Epilepsy studies laid groundwork for depression neuromodulation trial
Depression is among the most common psychiatric disorders, affecting as many as 264 million people worldwide and leading to hundreds of thousands of deaths per year. But as many as 30 percent of patients do not respond to standard treatments such as medication or psychotherapy. Some of these individuals respond positively to electroconvulsive therapy (ECT), but stigma and side effects make ECT undesirable for many, and one in ten patients experience little benefit even from ECT.
Previous research by Edward Chang, MD, co-senior author of the new study, has demonstrated the potential of brain mapping to identify promising sites for mood-boosting brain stimulation. These studies were conducted at UCSF Epilepsy Center in patients with and without clinical depression who already had electrode arrays implanted in their brains to map seizures ahead of epilepsy surgery.
“Our prior work showed a proof of principle for targeted stimulation across brain areas to treat mood symptoms, but an outstanding question has been whether the same approach would hold true for patients with depression alone,” said Chang, who is the Joan and Sanford I. Weill Chair of the UCSF Department of Neurological Surgery and Jeanne Robertson Distinguished Professor.
Brain mapping case study illustrates personalized neuromodulation and symptom relief
In the new study, the UCSF team demonstrated the use of a similar brain-mapping approach to identify patient-specific therapeutic stimulation sites as the first phase of the PRESIDIO trial.
The team used a minimally invasive approach called stereo-EEG to place 10 intracranial electrode leads into the brain of the first patient enrolled in the trial—a 36-year-old woman who has experienced multiple episodes of severe treatment-resistant depression since childhood. The patient then spent 10 days at the UCSF Helen Diller Medical Center at Parnassus Heights while researchers systematically mapped effects of mild stimulation across a number of brain regions that prior research had shown were likely to have an effect on mood.
The researchers found that 90-second stimulation of a several different brain sites could reliably produce an array of distinctive positive emotional states, as measured by a set of clinical scales that were used to assess the patient’s mood and depression severity throughout the study. For example, after stimulation of one region, the patient reported “tingles of pleasure,” while stimulation of a second area resulted in a feeling of “neutral alertness … less cotton and cobwebs.” Stimulation of a third area—a region called orbitofrontal cortex (OFC) that had been identified in Chang’s earlier studies—produced a sensation of calm pleasure “like … reading a good book.”
The team then tested more prolonged (three- to 10-minute) stimulation of these three areas to attempt longer-lasting relief of the patient’s depression symptoms. To their surprise, they found that stimulation of each of the three sites improved her symptoms in different ways, depending on the patient’s mental state at the time of stimulation. For example, when she was experiencing anxiety, the patient reported stimulation of the OFC as positive and calming, but if the same stimulation was delivered when she was experiencing decreased energy, it worsened her mood and made her feel excessively drowsy. The opposite pattern was observed in the other two regions, where stimulation increased the patient’s arousal and energy level.
“I’ve tried literally everything, and for the first few days I was a little worried that this wasn’t going to work,” the patient recalled. “But then when they found the right spot, it was like the Pillsbury Doughboy when he gets poked in the tummy and has that involuntary giggle. I hadn’t really laughed at anything for maybe five years, but I suddenly felt a genuine sense of glee and happiness, and the world went from shades of dark gray to just—grinning.”
The researchers focused in on an area known as the ventral capsule/ventral striatum, which seemed to best address this particular patient’s primary symptoms of low energy and loss of pleasure in everyday activities.
“As they kept playing with that area, I gradually looked down at the needlework I had been doing as a way to keep my mind off negative thoughts and realized I enjoyed doing it, which was a feeling I haven’t felt for years,” she said. “It struck me so clearly in that moment that my depression wasn’t something I was doing wrong or just needed to try harder to snap out of—it really was a problem in my brain that this stimulation was able to fix. Every time they’d stimulate, I felt like, ‘I’m my old self, I could go back to work, I could do the things I want to do with my life.'”
The researchers found that the effects of stimulation could be tailored to the patient’s mood, and that positive effects lasted for hours, well beyond the 40-minute window designed into the study protocol. The patient’s symptoms also got significantly better over the course of the 10-day study, leading to a temporary remission lasting 6 weeks.
“The fact that we could eliminate this patient’s symptoms for hours with just a few minutes of targeted stimulation was remarkable to see,” Krystal said. “It emphasizes that even the most severe depression is a brain circuit disease that may just need a targeted nudge back into a healthy state. Unlike antidepressant drugs, which might not have an effect for one to three months, probably by altering brain circuits in ways we don’t understand, our hope is that this approach will be effective precisely because it only requires brief, mild stimulation when the undesired brain state we want to change is present.”
Promising initial results of real-time, targeted neuromodulation seen in ongoing trial
When the patient’s symptoms returned after her initial remission, the researchers proceeded to the next phase of the PRESIDIO trial—implanting a responsive neuromodulatory device called the NeuroPace RNS System. This device is widely used for seizure control in epilepsy patients, in whom it can detect signs of oncoming seizures in real time and initiate brief, targeted stimulation that cancels them out. In the PRESIDIO trial, the device instead detects signature patterns of brain activity that indicate that a participant is moving towards a highly depressed state, and then provides mild, undetectable levels of stimulation to a targeted brain region to counteract this downswing.
“We hope that providing gentle neuromodulation throughout each day will be able to prevent patients from falling into long-lasting depressive episodes,” said Scangos, who was recently awarded a 1907 Research Trailblazer Award for her work to understand depression’s neural circuitry. “The idea is that keeping neural circuit activity functioning along the correct track, the pathways that support pathological negative thought processes in depression can be unlearned.”
The NeuroPace device was implanted in June of 2020 and activated in August, and so far, the study participant has reported that her symptoms—which in the past seven years had made it impossible for her to hold a job or even drive—have almost completely vanished, despite significant life stressors like a COVID exposure, helping her parents move out of state, and caring for her mother after a fall.
“2020 was terrible for everyone, and I’ve had some particularly stressful life events, but for the first time in a long time, I feel like I can bob back up again,” she said. “I can’t tell exactly when the device turns on, but I generally feel more of a sense of clarity, an ability to look at my emotions rationally and apply the tools that I’ve worked on through psychotherapy, and that is so far from where I was before.”
In the trial’s next phase, the patient will switch between six weeks with the device turned on and six weeks with it off, without being aware of which is which, in order to assess possible placebo effects.
Scientists studying the body’s natural defenses against bacterial infection have identified a nutrient–taurine–that helps the gut recall prior infections and kill invading bacteria, such as Klebsiella pneumoniae (Kpn). The finding, published in the journal Cell by scientists from five institutes of the National Institutes of Health, could aid efforts seeking alternatives to antibiotics.
Scientists know that microbiota–the trillions of beneficial microbes living harmoniously inside our gut–can protect people from bacterial infections, but little is known about how they provide protection. Scientists are studying the microbiota with an eye to finding or enhancing natural treatments to replace antibiotics, which harm microbiota and become less effective as bacteria develop drug resistance.
The scientists observed that microbiota that had experienced prior infection and transferred to germ-free mice helped prevent infection with Kpn. They identified a class of bacteria–Deltaproteobacteria–involved in fighting these infections, and further analysis led them to identify taurine as the trigger for Deltaproteobacteria activity.
Taurine helps the body digest fats and oils and is found naturally in bile acids in the gut. The poisonous gas hydrogen sulfide is a byproduct of taurine. The scientists believe that low levels of taurine allow pathogens to colonize the gut, but high levels produce enough hydrogen sulfide to prevent colonization. During the study, the researchers realized that a single mild infection is sufficient to prepare the microbiota to resist subsequent infection, and that the liver and gallbladder–which synthesize and store bile acids containing taurine–can develop long-term infection protection.
The study found that taurine given to mice as a supplement in drinking water also prepared the microbiota to prevent infection. However, when mice drank water containing bismuth subsalicylate–a common over-the-counter drug used to treat diarrhea and upset stomach–infection protection waned because bismuth inhibits hydrogen sulfide production.
Scientists from NIH’s National Institute of Allergy and Infectious Diseases led the project in collaboration with researchers from the National Institute of General Medical Sciences; the National Cancer Institute; the National Institute of Diabetes and Digestive and Kidney Diseases; and the National Human Genome Research Institute.Source:
It has been almost a year since I decided to write up my story on how I came to be injured by transcranial magnetic stimulation (TMS). In all honesty, at that time I was convinced that my injury was some sort of mystery that I would never solve. I could have never known how much I would be able to learn on my own, just having the willingness to search for answers.
In the past year I have spoken to approximately a hundred people injured by TMS, countless doctors, and quite a few medical researchers and scientists. What I was able to learn and put together about the nature of TMS injury and the culture surrounding it yields an incredible insight into the treatment itself and into the nature of the medical model in its current form.
This article is devoted to the analysis of the harm currently being caused by TMS. It is not intended to provide a balanced view of the therapy or its practice.
The Injury
First, I consider it important to identify the very clear set of symptoms that are emerging in the group of people harmed by TMS. After speaking with and reading the testimony of hundreds of people, the most common symptoms are:
Significantly worsening depression and anxiety (which may also be newly “treatment-resistant”)
Cognitive impairment such as short-term memory or functional memory loss and decreased ability to multitask
Irritability
Fatigue
Panic attacks
Increased suicidal ideation
Chronic headaches
Loss of balance,
Dizziness
Almost every person I’ve spoken with experienced at least one of these, if not all of them.
Additional symptoms that are somewhat less common include:
Environmental sensitivities to temperature, light, smell, and sound
Sensitivity to medications and supplements
Psychosis has also been observed in a few rare cases, but at least half of those specifically involve overuse of TMS (as described in this article).
It also became obvious to me that these symptoms manifest themselves in a very specific way. For instance, the worsening anxiety and/or depression is unrelenting and does not respond to treatment. As an example, before my TMS injury, when I was extremely anxious or depressed I would run longer and start eating really well, and this would always improve my symptoms to some degree. Typically, the harder I worked out, the better I felt, and the better I ate, the better I felt.
But after TMS, when I became depressed and anxious, exercise and eating did not help. I immediately began working out harder and harder and put myself on a stricter diet, which became stricter because I never got any relief from my symptoms. Every day I woke up feeling the same intense depths of despair, and I would become very anxious during the day. If I tried to meditate or run or use the CBT methods I had developed in the past, none of them made ANY difference at all. I found this to be remarkable and deeply disconcerting, which only compounded my situation.
Another characteristic of my TMS injury was that instead of improving in the months following TMS, I actually got worse. Immediately after TMS, I did not feel nearly as bad as I began to feel as time went on. Immediately after TMS, I still had my depression and anxiety, and I may have even felt slightly better due to the placebo effect and the hope that it was helping me.
However, about a month after TMS, I felt my symptoms were slowly intensifying until, about three months after TMS, they had become far more severe. The level of depression I felt was at least ten times what it was before. Also, instead of having anxiety occasionally bother me, I now had it all day, and panic attacks that I had only experienced once or twice in my whole life became a daily occurrence.
I concluded that this is what led to the subsequent increased, intense suicidal ideation that I experienced, which is what most others have mentioned to me when discussing their TMS injury as well. When you are extremely depressed and frequently panicking, suicidal ideation naturally follows; you come to believe you will never get any relief from the suffering and you begin to doubt if you can live with it.
To me, this is a normal human response to the trauma that TMS causes in the brain and on the nervous system. If we take a step back here and look at how these symptoms are manifesting, we can see this is “delayed onset.” New symptoms are continually manifesting after the initial injury has occurred.
This happens with most of the other symptoms as well. I developed constant muscle fasciculations in my legs about three to six months after TMS. These were part of a larger muscular issue that began developing a few months after treatment: cramps, burning, numbness, and tingling in my legs, as well as sciatica. The symptoms slowly evolved over that period into what I am experiencing at present.
TMS appears to create a dysregulation of electrolytes in the body. I believe it to be sodium ion channelopathy acquired from the electrical injury. While this may be controversial, it is my suspicion that it is what is causing the muscle spasms along with the pain, numbness, weakness and tingling. While those symptoms are very common, we are seeing also some less common symptoms that appear to be a more severe form of this condition.
For instance, I am aware of people who have had episodes of syncope from hyponatremia after drinking too much water due to excess thirst or at the direction of their physicians because of muscle cramping. They have also experienced trouble breathing.
Before TMS, I would occasionally become dehydrated after paying too little attention to my water intake for a week or two. Now, if I drink less than 80 oz of water in a day, I will experience serious dehydration, intense muscle cramping, and increased cognitive impairment the following day.
Additionally, it appears that people are experiencing more instances of tinnitus when they had hearing protection properly in place for the duration of the TMS treatments than those that did not have hearing protection at the time of injury. This seems to suggest that the tinnitus is being caused by damage to the auditory cortex and not from external sounds. In fact, TMS treatment did not seem excessively loud to me or to others, although I do know that loud, repetitive noises can cause hearing loss. The auditory cortex of the brain is located close to the typical treatment site in TMS.
As I began to experience these symptoms and struggle to understand the reason, I began to think about similarities with each person I was speaking to. They all told me the details of their experience with TMS and, typically, any theories they had about medical injury—specifically (and most often) psychiatric injury.
This led me to an interesting discovery. I began reading about the injuries that occurred with electroconvulsive therapy (ECT). My mind was almost instantly blown. I had been searching for a very long time to find some sort of cohesive explanation, a similarity to another type of injury or pattern that would give me some insight into what had happened to me. What I saw with ECT was that the types of injuries, the symptomology and the general fallout was very similar—almost exact.
Both injuries showed signs of traumatic/chronic brain injury, cognitive impairment, and neuromuscular and central nervous system (CNS) problems/agitation. I began searching the literature and found a community that was well-read in the evidence of the damage caused by ECT and the nature of diffuse electrical injury.
The Evidence
I realized it is important to understand not just the physiology of the damage caused by the injury, but also the kind of recovery people injured by TMS might expect.
The first important piece I read was an article by Jennifer Berg and Michael Morse. It is incredibly important because it describes both the diffuse electrical injury symptomatology and the difficulty some doctors have in addressing it because of the subjectivity of the symptoms. It describes the reasons for delayed onset of symptoms and damage, the psychological and physiological symptoms, and why the injury so rarely shows up on imaging and other diagnostics.
In summation, this article validates the theory of electrical injury and the difficulty doctors have verifying it. It is extremely important to point out that the problems with diagnosing and treating this injury are not the lack of evidence of injury but that doctors simply are not diligent enough in seeking the right conclusions to diagnose the injury.
The next important step is tying this electrical shock injury to TMS injury. You may think that since TMS does not use direct electrical current it is not shocking the brain or inducing electrical current into the brain, but that is not correct.
In fact, according to the manufacturer’s websites, you will typically find a statement that TMS is not the same as ECT. While this is true, it does not mean that TMS does not shock the brain and cause the same type of electrical trauma that ECT does. I think the fact that manufacturers overtly deny being an ECT treatment is very telling. TMS is obviously not ECT, just as it is obviously not an SSRI or talk therapy treatment. But unlike those, it does induce electricity into the brain.
I think the direct statement of difference is to try and diffuse an inherent connection people may make about having their brains shocked, the associated discomfort and obvious risks of such a treatment. TMS treatment is considered “benign” because it is less invasive (and less dramatic), but it is not.
Expert evidence presented in recent ECT litigation by Kenneth Castleman demonstrates that ECT causes damage by both heat and electroporation (that is, tearing holes in individual cell membranes so that they fail and cause cell death). Both heat and electroporation are generated by rapidly alternating electrical fields and are not exclusive to the physical manifestation of the electrical current itself. With TMS, electrical current is still being generated inside the skull by means of electromagnetic induction, as well.
Therefore, the same damage and impact on the brain is being exerted by the electromagnetic coil used in TMS. If you Google how TMS works, you will get the same answer: it works by generating rapidly alternating electrical fields, which we now know generate both heat and electroporation inside the human skull. In this way it is similar to ECT, simply without the direct electrical current applied to the temples. One could even say it is an evolution of ECT.
As if these similarities with ECT were not enough, we learn something else from the Castleman document: ECT practitioners go through a process of initially determining a patient’s seizure threshold. Clinicians have a testing session where they shock their patients with varying levels of electrical current to see what level of current is required to induce a seizure in the patient. After they have this data, they can produce a seizure at the lowest level of electrical current needed to avoid additional electrical damage to the patient.
In TMS, every patient is given an initial session where the clinician measures or maps the patients “motor threshold.” The patient is hooked up to the TMS machine and the clinician activates the machine and directs it at different parts of the brain to see if the patient’s hand twitches or not. To my knowledge, this is done so that the treatment will not induce a seizure.
However, the clinician has to specifically manipulate the machine to avoid inducing a seizure the way ECT does. This is further evidence that TMS is generating an electrical current inside the brain in a strikingly similar manner to ECT, and that it uses a similar methodology to measure its effects on a patient.
Some Science
To understand the dangers of TMS, we need to understand the basics of the energy it uses. Electromagnetic waves such as the ones created by TMS are made up of two simultaneous types of energy: magnetic and electric—hence the term electromagnetic wave or field.
TMS devices generate a minimum of a 1 to 1.5 tesla electromagnetic field. The electrical component of the field generated, based on this energy conversion table, is up to 797,700 to 1,196,550 milliamperes (mA) per square millimeter. In a study by Leo Alexander and Hans Löwenbach on specific damage done by ECT, they found that just 20 mA per square millimeter of brain tissue would cause irreversible damage to the tissue. TMS is far beyond the threshold established by the study.
The magnetic component of the field generates up to 10,000 to 15,000 gauss. The earth naturally generates a magnetic field of about .25 to .65 gauss, and the generally accepted safe occupational levels of gauss are generally set at 5 to 10 gauss. That means TMS could be generating anywhere from 1,000 to 1,500 times the amount of magnetic energy that is generally considered safe.
While electromagnetic fields do dissipate the further you are away from them, in TMS the coil is often held just millimeters away from the patient’s skull. This is causing damage to patients’ brains, and while the brain is a resilient organ, we cannot expect it to mitigate damage from that amount of force. The question is not why people are harmed by TMS but, rather, how is it that some are not harmed by TMS.
Those Who Were Not Harmed
I have spoken to quite a few people who were not harmed, but claim they were helped by TMS therapy. One such person told me they felt better after TMS treatment and were not harmed in any way.
When I asked further questions about how long they felt good and if they still felt better today, they replied that the positive effect had lasted for a few months after their last treatment, but they slowly reverted back to their previous state. They also told me they were currently battling some significant depression and a bit of anxiety. That was very interesting but, sadly, not a surprise.
The surprise came next, when I asked if they had any suspicion of being harmed by TMS. They said they did not feel they had been harmed in any way. I then asked if they were sure and I listed all of the aforementioned symptoms associated with TMS and electrical injury. This is where things became very interesting: a few months after TMS, this person had a severe and long-lasting bout of sciatica with no apparent physiological cause. That is, this person had never had sciatica before and they found no explanation for the occurrence.
I asked some probing questions about how the sciatica could have come on and they simply had no explanation. This opened up a discussion about the sensations experienced during TMS, particularly the “dip” in which the patient becomes more depressed during TMS and then has to stick with treatment in order to come out of the dip. This person had experienced such a dip and had concerns about their health during treatment. They expressed a tremendous amount of concern and emotional discomfort in association with their treatment when speaking about it with me as well.
Coming away from this interview, both of us felt that maybe TMS was not as beneficial as they had originally thought. In fact, the conversation raised a few new concerns. This depressive dip that occurs during TMS could be a neurological response to acute brain trauma. Furthermore, ignoring that dip causes so much trauma within the brain that the patient begins to experience anosognosia—becoming unaware of their condition because they are in a kind of shock and no longer possess the faculties to properly understand their condition.
I experienced this same thing. I was having so much cognitive dysfunction I could no longer recognize the disoriented state TMS had induced in me. Additionally, I think the delayed onset of symptoms is due to a similar phenomenon. The nervous system is in a dysfunctional state for several months after the injury caused by TMS.
When it starts to recover, it now has injuries and impairments to its ability to function, and we see the long-term symptoms begin to emerge—such as the sciatica in this case. In other cases, such as mine, we see a more severe set of symptoms, such as cognitive impairment and neuromuscular issues. It is also possible that cognitive impairment accounts for some of the indifference to and lack of reporting of serious side effects. Physicians are often well aware of this possibility and choose to ignore it in many cases.
For those who follow TMS testimony closely, a typical objection to the existence of injuries is “What about all the people it has helped?” The truth of the matter is that we see the same thing with ECT. People claim real relief from the treatment, and it does have some amount of temporary efficacy.
This may occur because electricity always follows the path of least resistance. Everyone’s brain physiology and the variables involved in the treatment are different. Also, the brain is made up of at least seventy percent water, so the electrical current and fields generated inside the brain will follow a different path every time. This means that while one treatment could prove harmless, the next one could have devastating effects.
We see the same variability with lightning strikes. While one person can walk away perfectly fine, the next will be killed instantly or have severe neurological problems like we see in TMS or ECT. There is actually a very interesting article on its effects on a group of children that also corresponds to what we see in ECT and TMS.
Another trend I am now seeing is that, as with ECT, people who were at first successful with TMS are going back for subsequent treatments when the benefits wear off. They will have a relapse of symptoms and then become injured in subsequent treatments. I fear patients undergoing TMS will be pulled into the same debilitating loop as those given ECT.
The initial treatment may prove beneficial, but its efficacy will fade, as the therapeutic effect seems to be simply some kind of endocrine response to the trauma itself. Traumatic injury causes the body to release hormones that promote healing and reduce pain. But subsequent TMS treatments will lead to additional sensitization of the CNS to electrical injury, inevitably causing serious, life-altering harm to the patient.
The Clinics
As if all the aforementioned problems with TMS were not enough, I have seen another pattern emerge from the people I have spoken with. Many of the clinics administering TMS know very little about the treatment, the science of its effects, and even less about the brain, CNS, and human body. The staff is made up of trained technicians, not educated scientists.
The person who administered my treatments was newly trained and had no other medical training or knowledge. Their only knowledge of TMS was given to them by the manufacturer’s training personnel shortly before my visit. I did not learn of this until well after my treatments had started.
Furthermore, during my treatments, the intensity of the machine was increased, creating a more intense feeling of drunkenness, lightheadedness, and impairment. When I described this to my technician and her manager, they both told me that they had to increase the intensity to reach the therapeutic effect. At this point, I was so desperate to make it work, I agreed. They did not know why, but they had been taught to do this.
Day after day, I made the same complaint, and they said it was “normal.” When I pressed them about it, they specifically told me that the manufacturer instructed them in training to turn up the intensity of the treatment regardless of patient complaints. The manufacturer told them to ignore patient complaints and turn up the intensity because there was “no chance of harm” during the process.
At this point, given all I have learned, experienced, and witnessed about TMS, I would disagree with that. It is bad enough that this happened to me, but worse knowing that those who came after me into that TMS clinic have experienced the same thing. I heard the same story from people injured by TMS all over the US, Canada, the UK, Australia, New Zealand, and Singapore—virtually all over the world.
Another disturbing pattern I identified was the use of TMS for off-label use. One gentleman I spoke with described severe anxiety, insomnia, and several other life altering problems after just one treatment. He could no longer work. He told me he was administered TMS for Irritable Bowel Syndrome (IBS).
I was in disbelief. I said, “Do you have any history of mental health issues?” He said, “No, never.” He had a very severe reaction to TMS; he could barely stand still and his voice was racing and disjointed—obviously in rough condition. In his case the treatment was much worse that the disease.
This was not the only such story I heard. People have described TMS being used to treat their addiction problems, dementia, Alzheimer’s disease, pain, or to simply “to improve brain function” as well. The cases of Alzheimer’s and dementia are particularly troubling because these patients were already suffering from cognitive impairment. We risk making things much worse for patients who may not possess the awareness or ability to report further harms.
I have also heard from many people that they had relatively minor anxiety or depression and were asked by the office staff to exaggerate their responses to the PHQ-9 questionnaire so that TMS would be approved by insurance. People who go in for TMS are usually desperate for help and have been convinced that this is a no-risk miracle cure. This is a massive contributor to both these clinics’ bank accounts and to inappropriate levels of risk and harm to their patients.
The Recovery
All of this has a huge impact on a person’s physical and emotional health for many reasons. So, what happens when they go to a doctor for help with the harm done? Typically, and almost exclusively, the patient is invalidated, with doctors denying the possibility of any harm having been done to them from this treatment. This is simply because these experiences are not listed as a side effect in the common literature or on the manufacturer’s website.
This is a fierce, fierce tragedy. Not only is someone harmed seriously despite being told they wouldn’t be, but now all the physicians they see deny the harm and sometimes even try to add an additional mental illness to their diagnosis simply because they were harmed by TMS.
It does not help that there is so little knowledge out there about electrical injuries. Once I learned that the injury is electrical in nature, I asked my doctors about it, but they had no insight nor any inclination to try to treat that type of injury, which is “outside their specialty.”
Interestingly enough, after I had queried all the usual medical resources, I called a large and reputable electrical injury rehabilitation institute and described my injury to them without using the word TMS. Instead, I told them that I had my head next to a 1 to 1.5 tesla electromagnetic coil for 20 minutes a day for two months—after which they replied that they do commonly treat those types of injuries and they gave me the rundown on what they did and how much it would cost, which would not be covered by my insurance.
I found this to be very interesting. Once the buzzword “TMS” was removed from the situation, physicians told me several times, and in subsequent follow up emails, that this is indeed an injury they could attempt to rehabilitate me from.
As for the injury itself, the next problematic point is that it is very difficult to show brain injuries diagnostically. TMS is no different. Electroporation affects each cell individually as it expands and contracts the cell walls; therefore, each cell has its tipping point where it cannot recover its form and fails altogether, causing cell death. That, combined with the fact that the current and electromagnetic fields being generated fluctuate based on the conductivity of the matter they are interacting with, means there is no way to predict which cells will be affected and which will not.
So, what we have is microscopic damage taking place throughout different, very small, particular areas of the brain which will not show on any kind of imaging test like an MRI, CT, or PET scan. I had several myself and have talked to countless others that have had the same, and so far we cannot see, nor have our technicians’ reports shown, any damage.
This makes it that much harder for doctors to believe their patients—although they do not have any reason to disbelieve them, either. It is very important to be aware that these scans also do not show damage caused by other means—even those which are now well-established—such as the brain damaging effects of psychiatric medications or chronic traumatic encephalopathy (brain damage caused by repetitive head injuries, typically in professional sports players).
These diagnostic techniques simply do not work as well in this area, even though there is very clearly significant damage to the brain’s function. In order for patients harmed by TMS to even begin to hope to recover, generally speaking, physicians need to start by acknowledging the injury. This is unlikely, however, due to the professional and financial pressure they are under to defend its highly profitable industry.
I do believe recovery is possible. Because of the way TMS injures the CNS, I believe that CNS sensitization is the primary issue to recover from. When our systems are overwhelmed enough or we come into contact with stimuli to which we are particularly sensitive, we experience panic attacks or sometimes other catastrophic symptoms like tachycardia, syncope, or seizures. On top of this our general sensitivity to anxiety and depression seems to be heightened.
So far, the best approach I have found is to provide as much of a neutral environment for the CNS to recover as possible. This means, psychologically, as little stress and negativity as possible. This will give the CNS a safe space to repair itself and use whatever bandwidth it has freed up for that. I have also found diet to be essential: I really only eat organic food with no preservatives. Essentially, I eat like our ancestors do: primarily organic and free-range vegetables, fruit, fish, and poultry.
Healthy activity is incredibly important to keep our bodies functioning optimally. I shoot for at least 45 minutes of cardio per day. For some people, that is not realistic and they have to start small—there is nothing wrong with that and it is actually the right move. Just keep active and engaged in your physical environment in ways that are not overly strenuous.
If we keep ourselves in a stimuli-neutral environment we can then introduce things that will help the brain recover cognitively as well. Playing games, listening to positive music, doing puzzles of all different kinds (like Legos, crosswords, etc.), and engaging in artwork to stimulate brain activity and create new neural networks that can build around our injuries and compensate for our losses.
It is key to focus on experiences you see as positive. Positive experiences are the building blocks of healthy brain activity and healing. This approach is the long-haul approach and with time, I think real recovery is possible and there is very little risk involved.
Recovering from injury caused by TMS demands respect and a healthy attitude toward healing just like all mental health challenges do. We cannot expect to solve these problems with more medications and therapies that have significant risks just so we can live the unhealthy lives that may be expected of us. It is time to focus on being human again, accepting and embracing the reality that comes with that, with all of our hearts and minds.
Lastly, I would like to express my sincere thanks to Sarah Price Hancock who has offered her indispensable brilliance in my endeavors to understand my injury and everything that comes with it.
***
Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.Previous articleWhat You Need to Know About Psychiatric Drugs, with Psychiatrist Joanna MoncrieffNext articleEyewitness to Psychiatry Functioning as a Conspiracy Theory-Based CultJames HallJames originally hails from the Pacific Northwest and enjoys spending his time eating well, exercising, and exploring the outdoors with his family. After years battling with his own mental health, James is passionate about having open and honest discussions about the realities of mental health treatments in America.
For example, if you have more than one Google Home speaker in your house, I’m sure it’s happened where the speaker you’re talking to ignores you while a different one in another room entirely tries to respond, right? That’s fixable. So is the worst smart speaker communication issue of all — when Google Home says, “Sorry, I don’t understand.”
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Next time you’re frustrated with your smart speaker not understanding you and you’re ready to break things off, one of these five Google Home fixes usually works for me.
If you’ve got Google Home speakers in close proximity to each other, you may have to adjust the “Hey Google” sensitivity setting to make sure the correct one responds to you.Dale Smith/CNET
How to right the Wrong Room, Wrong Speaker problem
It used to baffle me, but for the longest time it wasn’t unusual for the Google Home speaker I was in front of to ignore me while another one somewhere else in the house tried to do my bidding. That’s a problem when, for example, the command is to “turn on the lights.” Don’t get left in the dark, just open the Google Home app and modify a setting called “sensitivity.” Here’s how:
1. Open the Google Home app and tap the device icon for the speaker that’s giving you grief (if it’s more than one, simply repeat this process until you’ve got everything dialed in perfectly).
2. Tap the gear icon for settings in the upper right corner, then scroll down to Device features and tap Audio, then, at the very bottom of that screen, tap “Hey Google” sensitivity.
3. Now, drag the slider higher to make Google Home more likely to hear your voice and lower to make it less likely.
If your Google Home has become a glorified paperweight, try resetting to factory settings to clear it up.Dale Smith/CNET
What to do when Google Home says, ‘I don’t understand’
When Google Home says, “Sorry, I don’t understand,” the good news is that it heard you. The bad news is, of course, it doesn’t know what to do in response to whatever you said. There’s always a chance Google Home simply didn’t catch your command, so you’d be wise to repeat yourself at least one time just to be sure. If that doesn’t work, try these other tips:
When all else fails, try the nuclear option: a full factory reset (follow the link for detailed instructions for your specific device).
If Google Home has trouble moving music from one room to another, try using only lower-case letters when naming your devices. People on Reddit have reported success with this method.Dale Smith/CNET
When Google Home doesn’t know its own speaker names
Although you’d think the one thing Google Home would consistently get right would be its own name, it’s actually a fairly common problem for Google Home to misunderstand when asked to move something to — or do something with — a speaker in another room. Like when you’re listening to music, say, and you want to fling your tunes from the kitchen to the living room.
For the solution to this particular enigma, I turned to the always delightful repository of Google Home admiration and knowledge over at the r/googlehome subreddit. In response to a posted video illustrating this particular problem, one Redditor suggested using only lower-case letters when naming your Google Home speakers in the app, and based on the string of “holy crap” responses that followed, it appears to be a game-changer.
If your Google Home is tucked away in a corner, perhaps moving it closer to the center of the action will help it hear you better.Dale Smith/CNET
Perhaps the problem is physical
This may seem obvious, but if the cloth surrounding your speaker is dirty — especially if it’s clogged with visible gunk — that could be making it harder for Google Home to understand you. Try cleaning off your speakers so your commands aren’t muffled on their way to the device’s microphone.
Another possibility, however, is that you just haven’t placed your Google Home speakers ideally. Acoustics are a tricky science, and all kinds of weird things — echoes, sound-dampeners, the joyous shrieks of toddlers — can interfere with the sound of your voice. Try repositioning your speakers closer to or farther away from where you normally talk to them and see if that helps.
Give your smart home devices like smart bulbs unique names that both you and Google Home can easily remember.Chris Monroe/CNET
If your device names all sound the same, you’re asking for trouble
I know it’s hard to get creative when giving names to things like smart outlets or color-changing bulbs, but if everything in your smart home is called “Living room lamp 1” or “Philips Hue color bulb 4,” your digital assistant could have almost as much trouble keeping track of them as you do. For a while I tried naming my devices based on their locations relative to a compass, but I could never remember whether the living room lights were north and south or east and west.
Instead of cardinal directions or plain, boring ordinal numbers, now I name my smart home gadgets based on their physical characteristics or the landmarks surrounding them: “couch lights,” “tiny lamp,” “white credenza lights” and so on. If you want to get real creative, you could always give them actual names you won’t forget, like Agnes, Sylvester or Romulus.
Once you’ve ironed out all your communication woes, here are five things you need to be asking your Google Home smart speaker (probably every day). Also, it just got a little easier to avoid mentioning your speakers by name, since Google Home improved the app’s media controls. Make sure you’ve downloaded all the necessary apps to get the most out of Google Home, too.
Can artificial intelligence (AI) machine learning provide clinicians with predictions of patients who will develop psychosis? In a new European study released last month in Jama Psychiatry led by Dr. Nikolaos Koutsouleris at the Max-Planck Institute of Psychiatry in Munich, Germany, researchers used AI machine learning and human intelligence to predict mental illness.
“Our study showed for the first time, to our knowledge, that the augmentation of human prognostic abilities with algorithmic pattern recognition improves prognostic accuracy to margins that likely justify the clinical implementation of cybernetic decision-support tools,” wrote the researchers.
Psychosis is a treatable condition with many causes that affects how the brain processes information. It is characterized by a loss of connection with reality. Psychosis is a symptom of health issues such as schizophrenia and bipolar disorder, which are considered primary psychotic illnesses. Secondary psychosis is the term used to describe when a person experiences a disconnect from reality for triggers other than primary psychotic illnesses.
Roughly three out of 100 Americans will experience psychosis during their lives, and each year 100,000 young American adults and adolescents experience their first psychotic episode according to the National Institute of Mental Health (NIH).
The global antipsychotic drugs market will grow at a CAGR of 4.1 percent between 2020 and 2027 and is projected to reach USD 21.8 billion by 2027, according to a September 2020 report by Research and Markets. Last year, the U.S. had more than 28.8 percent market share of the global antipsychotic drug market, per the same report.
For this study, the researchers used NeuroMiner, a machine learning software available on GitHub, to develop “a sequential prognostic algorithm that identified the optimal sequence of predictive components to be combined into a stacked model.”
To find the optimal set of predict features for the risk calculators, the researchers used the Support Vector Machine (SVM) provided by the Liblinear library in NeuroMiner.
Support Vector Machines are supervised machine learning models that are used to find discernible patterns in complex datasets. It is a machine learning method that has a relatively reduced risk of overfitting high-dimensional imaging data such as neuroimaging. With its flexible method for handling classification, Support Vector Machines is an AI machine learning method particularly well-suited for neuroscience research for precision psychiatry for AI prediction of depression, Alzheimer’s disease, and schizophrenia.article continues after advertisement
“In this prognostic study of 334 patients and 334 control individuals, machine learning models sequentially combining clinical and biological data with clinicians’ estimates correctly predicted disease transitions in 85.9 percent of cases across geographically distinct patient populations,” reported the researchers.
The intent of the researchers was to provide an early intervention tool to help medical professionals in determining which patients require therapeutic interventions. Now there is a proof-of-concept for a potential new AI-assisted method for early detection of patient psychosis that may one day lead to improved mental health treatment in the future.
Cannabidiol (CBD), a compound derived from the cannabis plant, does not impair cognitive functioning when used in the treatment of children with intractable epilepsy, according to new research published in the journal Epilepsy & Behavior.
Previous research has found that CBD can reduce the number of seizures in patients with epilepsy. But the potential cognitive side-effects of long-term CBD use had not been examined in pediatric populations.
“Also, most of these children were not good candidates for surgical intervention, so CBD had the potential to offer some relief in terms of seizure control for many children. But we wanted to make sure there were no adverse cognitive consequences of this new medication.”
The study examined 38 participants between the ages of 3 and 19 years with treatment-resistant epilepsy who were enrolled in an open-label study of a pharmaceutical CBD formulation.
“The CBD product we used (Epidiolex) was a pharmaceutical-grade product that is available only by prescription. It is important for readers to know that this wasn’t the product you might purchase over the counter; instead, it is produced by a regulated pharmaceutical company, such that we know the precise concentration of CBD,” Thompson explained.
Prior to initiating CBD and one year later, 14 participants completed a computerized test of cognitive abilities that assessed attention/working memory, executive function, episodic memory, and language. A primary caregiver completed a behavior assessment instrument for the other 24 participants, who were not capable of completing computerized testing because of the magnitude of their impairment.
After one year of continuous CBD use, the researchers observed no significant changes in the cognitive performance or functional adaptive status of the participants.
“I believe the most important take away from this study is that CBD does not appear to cause any adverse cognitive changes in most children who have this medication prescribed for intractable epilepsy,” Thompson told PsyPost.
“We still need more information on a larger group of higher functioning children. Many of the children in this study were very impaired from a cognitive perspective, and this level of impairment made it difficult to detect changes in cognitive function; thus we had to rely on parent report of daily functioning, which has limitations.”
Gardner’s 11-day experiment didn’t kill him, but anyone who’s experienced total sleep deprivation can likely vouch that the end feels near.
Symptoms of sleep deprivation are progressive: The more sleep debt you rack up, the worse you feel. After a night or two of poor sleep, you feel irritable, cranky, unmotivated and sluggish.
After a week of short slumbers, you may find yourself snapping at people, crying over nothing, battling headaches, losing focus, overeating or under-eating and scraping by on stimulants. Go without sleep longer than that, and you may begin to experience hallucinations, paranoia, delusions and other scary symptoms.
How long will your body allow you to survive on short sleep? And what about complete lack of sleep — can it really kill you? CNET talked to sleep specialists to find out.
Can you die from not sleeping?
Sleep deprivation won’t kill you — directly, anyway.Matt Henry Gunther/Getty Images
“There is no evidence that a lack of sleep can directly kill you,” deadpans Annie Miller, sleep specialist and psychotherapist at DC Metro Sleep and Psychotherapy.
One extremely rare, hereditary disease seems to cause death via sleep deprivation. Fatal familial insomnia (FFI) starts with mild insomnia but progresses quickly, eventually leading to a complete inability to sleep. FFI patients also exhibit symptoms of dementia, difficulty controlling the body and degeneration of autonomic functions, such as digestion and temperature regulation.
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Still, this is a neurodegenerative disease that affects the brain, Miller says, and “it’s more likely that FFI patients die from neural degeneration, as opposed to lack of sleep.”
Interestingly, Miller encourages people not to be afraid of sleep deprivation, despite the known ill effects. “I think people are afraid of not sleeping and it contributes to the worsening of insomnia,” she says. “Think about parents of newborns. We are built to withstand a certain degree of sleep deprivation.”
Miller has a good point. Humans seem to be relatively capable during periods of sleep deprivation, complete or partial, although daily tasks feel more difficult and mundane. Randy Gardner would certainly say so.
How lack of sleep can kill you
Sleep deprivation increases your chances of accidents, including car crashes.BraunS/Getty Images
Yes, you just read that sleep deprivation can’t kill you, except in the case of the rare genetic disease FFI. Although it’s true there’s no hard evidence that people die directly from sleep deprivation, people can (and do) die from events related to sleep deprivation.
Lack of sleep can kill you indirectly by increasing your overall morbidity risk, says Dr. Shelby Harris, licensed psychologist, board-certified behavioral sleep medicine specialist and neurology professor. Medically, chronic sleep inadequacy can increase morbidity in a number of ways, she says, including:
Impaired immune functioning
Weight gain, which increases your risk for cardiovascular disease, stroke, some cancers, type 2 diabetes, sleep apnea and high blood pressure
Increased risk of depression, which increases the risk of suicide
Psychosis, which may lead to self-harm
Complete and partial sleep deprivation also heavily affect your risk of accidents, falls and injuries. For example, operating heavy machinery (including driving a car) becomes extremely dangerous when you’re running on little to no sleep.
Sleep deprivation may also increase your chances of dying from an underlying health issue that already exists. For example, people have died during video gaming marathons which, on the surface, seems due to sleep deprivation. However, autopsies reveal the true cause is likely a combination of exhaustion and heart failure, heart attack or stroke.
Symptoms of severe sleep deprivation
Severe sleep deprivation can make you feel like you’re in an alternate reality.Iuliia Isaieva/Getty Images
Though lack of sleep won’t kill you directly, you might feel like you’re on your way out if you’re experiencing severe sleep deprivation. If you stay up for more than 48 hours on end, you’ll likely battle intense physical and mental symptoms, including:
Memory loss
Inability to focus on normal daily tasks
Muscle weakness
Tremors
Heightened anxiety
Paranoia
Hallucinations
Delusions (believing false information)
Rapid heart rate
Inability to make decisions
Poor reaction time
Getting tongue-tied
Physical illness (due to impaired immune function)
If you can’t fall asleep and are experiencing symptoms similar to the above, contact a doctor right away. By that point, your risk of accidents is high and it’s best to stay safe by having someone else drive you to a medical facility.
How long can you go without sleeping?
There’s no solid answer to the question of how long humans can survive without sleeping. Apparently, people can live a rather long time with zero sleep, as proved by Randy Gardner and other people who intentionally deprived themselves of sleep for record-breaking purposes.
It’s clear that ill effects start to set in after just one day of total sleep deprivation and after a couple of nights of partial sleep deprivation, so it’s best to always strive to get as much sleep as possible.
Are you getting enough sleep?
“Enough sleep” is a highly individual concept — and the eight-hour rule comes from wishy-washy origins. You’ll know if you don’t get enough sleep.
A healthy, rested person should feel alert, have a healthy appetite, and have enough motivation and discipline to complete daily obligations. If you’re experiencing heightened irritability, cravings for unhealthy food or other appetite changes, lack of motivation, depression or anxiety, physical fatigue or an inability to focus, you probably need more sleep.
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