M1: From Kerkow media coming up on the show, you can't
M1: not move, you have to move the legs.
M2: I can't convey in simple words the experience is beyond
M2: anything any of us can imagine unless you actually have
M2: had the disease. And I can tell you, you become so,
M2: so desperate to get rid of the sensation that.
M21: Do you have any of these issues, daytime drowsiness can't
M21: fall asleep, can't stay asleep, you don't wake up refreshed
M21: in the morning snoring, she says you stop breathing. You
M21: may even be one of those people who joke around
M21: about how you haven't had a good night's sleep in years.
M21: So if you were anyone, you know, one of the
M21: hundred million people who don't get a proper night's sleep.
M21: This is your episode of Medicine. We're still practicing. I'm
M21: Bill Kurtis.
M8: Johns Hopkins is one of the highest regarded health care
M8: institutions in the country. There seems to be no end
M8: to the roster of specialists who bring us the edge
M8: of the art in research, medicine and patient care. Today,
M8: we continue our Johns Hopkins series with the issues that
M8: keep you up at night or have us yawning our
M8: way through the day. First, of course, my co-host, Doctor
M8: Stephen Tayback. He's the quadruple board certified doctor of internal medicine,
M8: pulmonary disease, critical care and neuro critical care. And he's
M8: also my very best friend, Dr. Tayback. How are you
M8: holding up these days?
M1: Hayesville actually doing a lot better. Things are looking up.
M8: Oh, that's good to hear. I look forward to getting
M8: into that a little bit. Dr. Christopher Lee joined Johns
M8: Hopkins almost three decades ago. He's board certified in internal
M8: medicine and psychiatry and neurology. He's also a professor of
M8: neurology at Johns Hopkins and he specializes in sleep or
M8: the lack thereof.
M3: Welcome. Nice to have you, Doctor early. Thank you for
M3: having me. I wonder, Chris, can you just help us
M3: define the phases of sleep? What are those?
M17: The sleep studies are published on the grounds that we
M17: have more or less broken step up into two big bits,
M17: which is what's called non REM sleep and REM sleep.
M17: And REM stands for Rapid Eye Movement. And in about
M17: a quarter of your sleep is involved in this REM state,
M17: which is the dreaming state. The non REM state can
M17: be partitioned into what's called stage one, stage two, three
M17: and four with stage three and four is really called
M17: slow wave sleep. Stage one would be drowsiness. We spend
M17: most of our time in stage two sleep the deeper
M17: sleep so-called stage three four tends to be of a
M17: larger proportion of sleep when you're younger. And so when
M17: you're in your teens and twenties, that's about 20 percent
M17: of your sleep. If you're in the 50s and 60s,
M17: that's about three or four percent, obviously.
M3: Did you say that the really quality sleep goes down
M3: to like three percent when you're old?
M17: Well, well, the deeper sleep our ability to maintain sleep
M17: in general from an age point of view is a
M17: little complex. But essentially the elements of sleep when we
M17: talk about stage three for sleep, that is much higher
M17: in the younger and gets less and less as we
M17: get older, fertility gets down to a few percentage, as
M17: I mentioned, after the age of 50.
M1: So for the lay public, what's the significance of those
M1: stages and and what should they be targeting and what
M1: do we do on a day to day basis that
M1: is either helpful or harmful to the stages that we
M1: actually require?
M17: The biggest element of sleep is consolidation of sleep, whether
M17: you're in stage two, stage three, stage four, it's how
M17: consolidate your sleep is. What is what does that mean? Consolidated.
M17: So humans, unlike cats and dogs, really need a continuous
M17: period of sleep. Now, we might be able to break
M17: that up into two sections, a four hour and a
M17: four hours. But generally most people need between seven and
M17: eight hours of sleep. And it needs to be fairly
M17: consistent from start to finish if you're awakening frequently at night,
M17: that sleep fragmentation. So the first and foremost thing is
M17: trying to get a consolidated amount of sleep. That is
M17: from the time your head hits the pillow to the
M17: time you wake up in the morning. That period of
M17: time should be seven to eight hours and basically you
M17: should be able to have slept through that full duration
M17: of the night. The second issue is that it's not
M17: clear if the different stages of sleep are relevant to
M17: you experiencing a certain good quality of sleep as much
M17: as it may be involved in memory and memory consolidation.
M17: So the deeper sleep is in stage three four might
M17: be relevant to how you hold on to certain memory. Generally,
M17: if you're spending most of your time in stage two,
M17: three or four sleep, that's good. If you're spending too
M17: much time in what's called stage one sleep, that's bad
M17: because stage one sleep would be drowsy. You're sort of
M17: in sleep, but you're never really you're not quite into
M17: sleep yet. And so if you have a disproportionate amount
M17: of stage one sleep, then you're more likely to experience
M17: a sense of not feeling rested, tired, memory problems, things
M17: like that.
M1: Now, is this in our control at all? Can the
M1: layperson do something so that they make sure that they
M1: don't linger in stage one and can optimise their stage
M1: three and stage four sleep?
M17: We talk about the brain resting and the importance of
M17: the brain and sleep. The truth is, sleep is really
M17: a total biological rest and your sleep is looking to
M17: the metabolic demands you put on your body during the day.
M17: As much as it's looking at the metabolic demands you
M17: put on its brain each day, a significant amount of
M17: physical activity during the day, we're. Well, to improve the
M17: quality of sleep, the timing of sleep is equally important,
M17: not all of us are designed to be going to
M17: bed at 10:00, getting up at 6:00. Some of us
M17: are called night owls. So our biological clock doesn't make
M17: us ready for sleep until 1:00 in the morning or
M17: two in the morning or three in the morning.
M3: Have you helped people to adjust that? Yes. How do
M3: you do that?
M7: There are two basic ways. The use of lights in
M7: the morning, particularly if you're getting up early. So you
M7: have a large urban society which gets up at whatever time,
M7: four or five, six in the morning in order to
M7: get to work. You spend an hour or two driving,
M7: so you've got to get up work. You have to
M7: be in work by 8:00, then you've got to be
M7: up at six, five or six. So using artificial lights,
M7: high intensity looks, lights to mimic the sunlight can help
M7: what's called phase advance. Move your clock back to something
M7: that's more socially acceptable.
M17: That's one thing. Melatonin appears to have some value. I
M17: know people use melatonin at high doses to try to
M17: get them to sleep.
M7: But the purpose of melatonin really is a biological marker
M7: to sort of indicate that sleep is about to happen
M7: in three or four hours. And you take it one
M7: to three milligrams, three or four hours before bedtime. That
M7: also might help the brain.
M17: Your phase delayed biological clock back to something that's a
M17: little bit more in line with your early bird tendency
M17: to get what is melatonin do and don't we make
M17: that naturally into the melatonin is tied to what you're
M17: called your circadian rhythm based on your circadian rhythm is
M17: your internal biological clock, which is ticking away over a
M17: twenty four hour period. That's sort of in the beginning
M17: decides to activate everything so you can be busy, inactive,
M17: ready to go and then start slowing things down as
M17: you approach sleep within that curve. There was a period
M17: of time in which it triggers this melatonin to be
M17: produced and have a peak. And that peak basically should
M17: appear three to four hours before you're actually ready for
M17: your brain to hit the go to sleep.
M7: So the purpose of the melatonin is to let the
M7: rest of the body. So when the melatonin goes up,
M7: your your heart rate starts going down, your metabolism, your liver,
M7: your muscle, those all start going down in terms of
M7: their metabolic need long before your head hits the pillow.
M7: The brain's the last organ on board about three or
M7: four hours later to get the sleep. So the purpose
M7: of that melatonin really is a biological signal to set
M7: that into motion for that given period of time.
M1: What about people who chronically have trouble falling asleep? Is
M1: it helpful to use sleep AIDS? Is it counterproductive? Is
M1: it better to only use natural means or no sleep aids?
M1: What's your perspective on sleeping pills and other sleeping AIDS?
M7: I'm not completely anti sleeping pill. I just think there
M7: are a lot of really good alternatives that will work
M7: for like 90 percent of people. I just think that
M7: the sleeping pill is a quick answer. You walk into
M7: a doctor's office, I can't fall asleep. I can enhance
M7: a prescription for a pill. There are a couple fairly
M7: straightforward approaches. Again, some really good data demonstrating the value
M7: of what's called sleep hygiene.
M3: What sleep hygiene.
M18: Sleep hygiene is trying to get the person to think
M18: in terms of what they need to do behaviorally in
M18: efforts to prepare for sleep. The simple things are about caffeine.
M18: There are some people that are very, very sensitive to caffeine.
M18: If they take a cup of coffee at 1:00 in
M18: the afternoon, it still affects them at night. So I
M18: understand how sensitive you are, but basically you shouldn't be
M18: drinking caffeine four or five hours before sleep onset time.
M18: That straightforward exercise exercise is something that you should be
M18: doing as a product of your arousal state, your awake state.
M18: What do you want to do in the morning or
M18: the afternoon? But you shouldn't be doing significant aerobic exercise
M18: for hours before bedtime or otherwise. You're just activating your system.
M4: The other issues and the most common problem and it
M4: has been very successful is what I call blue screen habits, iPhones, iPads, computers.
M4: People live in their bedrooms with these devices and they
M4: don't know how to disconnect. My general is no blue
M4: screens three hours before bedtime, no TV. The last hour
M4: before bedtime, people said, what do I do? I said,
M4: I'll read, listen to music. If you have a bit
M4: of a hobby, do something that relaxes. And they said, well,
M4: I'm going to get bored. So that's perfect. That's exactly
M4: what you you want to get bored and tired and
M4: ready to go to sleep. So sleep hygiene is really
M4: effective for the majority of people because I think many
M4: people have difficulty getting to sleep because they've developed bad
M4: habits around using their iPhones up until the last minute
M4: and things like that.
M1: What are the long term ramifications, then, of sleep fragmentation?
M1: Is it going to shorten your life expectancy or is
M1: it just a nuisance?
M4: There are three major consequences that come as a consequence
M4: of any sleep loss. The first and foremost is attention
M4: and concentration, and most of us attention. Concentration might not
M4: be a big deal. If you're in a job that's
M4: fairly routine, it's reflexive. It will impact learning significantly in
M4: the younger age groups because that's what kids are trying
M4: to do, is learn multitasking is probably the biggest consequence
M4: for the more working individual. The second element is moved
M4: off the state and increased problems with decreased interest, decreased drive,
M4: lack of motivation. It can aggravate or cause an anxiety
M4: or depression. And both those elements are pretty early in
M4: the process within weeks, if not months, of you having
M4: chronic sleep loss. The third element is sleepiness, which, interestingly enough,
M4: is really poor as a measure of one's sleep quality.
M4: It is the least reliable. There are plenty of people
M4: out there who are not getting quality sleep, who don't
M4: feel tired.
M3: Let's talk about sleep aids like Restoril and Ambien and
M3: challenges that people have had with that. And just to
M3: be straightforward, many years ago I pulverized my ankle on
M3: a ski slope and had trouble sleeping, was prescribed sleeping pills.
M3: I was told that you don't really get the same
M3: quality of sleep on something like Ambien, a Restoril. Is
M3: that so?
M4: Yes and no. There really there to suppress arousal. They
M4: don't necessarily induce sleep. We go back to my original
M4: discussion about the difference between sleep is not just the
M4: absence of arousal sleep. It's its own biological state. It
M4: has to exist.
M5: That biological phenomena has to exist for you to enter
M5: it just by knocking yourself out. I mean, I could
M5: I could knock myself out with a fifth of whiskey.
M5: Does that mean I'm sleepy?
M4: So the issue is the sleeping pills in general with
M4: respect to which one you choose, are there to suppress
M4: arousal such that if sleep is sitting there waiting, you
M4: can enter sleep. So I think the sleeping pills work
M4: well if you have a certain type of person, just
M4: can't turn it off, you know, sleep is there. Their
M4: the biology sitting there waiting for them. They're just waiting
M4: for them to finally turn off that arousal mechanism.
M18: Sleeping pills may be a value in that situation, but
M18: believe me, that's a very, very small number of people
M18: for which it has some value.
M3: Do you actually convince yourself, is it a psychological thing?
M3: You convince yourself that you're going to sleep well or
M3: you convince yourself, well, I'm not going to sleep well,
M3: and then you wake up at whatever time you think
M3: you're going to wake up?
M6: Yes, I think that there's a lot of cognitive machinations
M6: that go on to create an environment. I mean, the
M6: very nature that you go to your doctor for an
M6: answer and they give you an answer, you'll come to
M6: believe that that's the right answer. And therefore, you believe
M6: if I stop this, I won't be able to sleep.
M6: And unfortunately, what happens is if you try to stop,
M6: you'll get a rebound that is coming off the medications.
M6: There'll be a period of time which you will go
M6: back to some degree of insomnia. Thus it's sort of
M6: fulfilling your belief that I can't get off this medication.
M3: I wonder, could you talk to us a little bit about, well,
M3: that noise that you hear from your partner, that snoring
M3: kind of. So I understand that that falls into two categories.
M3: There's the snoring and there's sleep apnea. Can you explain
M3: the difference dynamically?
M7: The snoring really comes from the upper part, the soft palate.
M7: It's basically air rushing through your nasal passages versus your
M7: mouth at different pressure differences. So you get this flap,
M7: that's the the snore. Any time you have to pull
M7: the air fast across the soft palate, you're likely to
M7: get the snoring. So if you have a little bit
M7: of nasal congestion, you open your mouth a little bit
M7: to breathe and you're going to snore. If you have
M7: obstruction farther down in the upper part of the airway. Again,
M7: if there some resistance, you can breathe harder. And again,
M7: the air is going to rush across the soft power
M7: and cause you to snore. Sleep apnea, persay really involved
M7: in that upper part of our weight, sort of below
M7: the tonsils for want of a better word. That's basically
M7: a muscular tube. And essentially, when you have sleep apnea,
M7: that muscular tube is very collapsible. There's nothing to support it.
M7: So when you breathe in, that tube starts to collapse.
M7: The example I give is when we were kids, we
M7: used to have paper straws. And if you left the
M7: paper straw in the soda long enough, you want to
M7: suck it. What would happen? The straw would collapse in
M7: the middle. The same, too. If you have a tube
M7: going down to your lungs and that tube is relatively
M7: flabby and you take a breath in, it's going to
M7: collapse and cause obstruction. Thus the term obstructive sleep apnea.
M7: And so sleep apnea really has to deal with that
M7: lower part for want of a better anatomical term. Blow
M7: your where your tonsils are. The snoring is more or
M7: less above where the tonsils are into that soft part
M7: of your tissue.
M8: So other than divorce court, what are the other ramifications
M8: of snoring?
M4: There's a lot of associations and I will point out
M4: to people listening in an association doesn't mean it's causally related.
M4: That means there's some relationship. We just don't know what
M4: that relationship is. So there's an association between snoring and
M4: risk of high blood pressure, snoring and risk of stroke.
M4: But in general, most studies don't tie any specific health
M4: concerns to snoring persay. If it is not associated with
M4: sleep apnea, what if it wakes you up?
M9: You are not aware of your own snoring. If it
M9: wakes you up, it's because you have.
M8: Yeah, I keep telling her I don't snore. That's right.
M6: It is a problem to degree that you're awake in
M6: your bed partner up. So that's the critical Mexia. When
M6: people come to me from the snoring point of view,
M6: it's usually he comes to me, he's snoring and the
M6: answer is, I can't wake my wife. I, I keep
M6: getting nudged in the middle of the night. If you
M6: share a bed with someone, someone's going to have a
M6: consequence on the other bed partner unless the other bed
M6: partners are really good sleep as well.
M3: So, OK, so let's go to the more difficult one.
M3: Sleep apnea, the act of actually stopping breathing often many
M3: times a minute is that destructive.
M7: So when we talk about sleep apnea, even though the
M7: term apnea means to stop breathing, most of the events
M7: are partial obstructions and not always complete obstructions. So what
M7: we refer to as Hypponen is so the airway partially collapsed,
M7: doesn't completely collapse. So it's a range between the partial
M7: all the way up to 100 percent collapse. So when
M7: you talk about obstructive sleep apnea, we talk about some
M7: degree of collapse, maybe 40, 50 percent collapse, up to
M7: 100 percent collapse.
M18: And so sleep apnea by the numbers. So we can
M18: talk about having 20 events per hour, 30 events per
M18: our normal is considered less than five events per hour.
M18: So we all have a little bit during the night.
M18: The data is fairly strong for suggesting that untreated obstructive
M18: sleep apnea, if your rate is above 30 per hour,
M18: probably has risk of at least hypertension, stroke. And it's
M18: also about the heart disease at rates less than 15
M18: per hour. It's probably not a long term health risk
M18: between 15 and 30. It's unclear.
M1: What about position in sleep? Are there things that that
M1: an individual can do without using mechanical devices that might
M1: improve their sleep apnea and their quality of sleep?
M18: So obstructive sleep apnea tends to be worse on your
M18: back versus side versus your stomach. If you have a
M18: tendency to be a backslapper trying to recondition yourself to
M18: your side, there are wedge pillows and things like that
M18: that people can buy online. There are these special shirts
M18: that have a sort of rubber ball in the back
M18: of it that makes it very uncomfortable for you to
M18: roll over on your back. So those are positional things
M18: that you can do. A few people for whom they've
M18: never been able to tolerate PAP and I think their
M18: apnea is bad. I tell them to get a lounge
M18: chair and to start sleeping. So the more upright you sleep,
M18: the more the jaw and the tongue comes forward, basically
M18: reduces the degree of obstruction. So.
M12: We're going to take about a 30 second break. I'm
M12: going to go grab a coffee. We'll be right back
M12: with Dr. Christopher Lee from Johns Hopkins.
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F4: OK, we're back, Dr. Christopher, let's talk about kind of
F4: the opposite side of the coin, I'm going to tell
F4: you a quick story.
M8: I once sold advertising for a career, and I was
M8: in a very important meeting for probably the largest advertising
M8: contract that I had ever even imagined. And the CEO
M8: of the company was all excited and actually took out
M8: the contract, took out a pen, was prepared to sign
M8: that contract. The salesperson and I were all excited.
M3: He put the pen to the paper and fell asleep.
M3: And he was he was gone. What happened, Chris?
M6: Given the acute nature of it, I sort of does
M6: raise the question of whether or not he had narcolepsy.
M9: He did have that narcolepsy. He later talked about that.
M9: But what is that?
M16: Narcolepsy actually has some really nice, good understanding of the pathophysiology.
M16: It is now within the category of what's called autoimmune diseases,
M16: type one diabetes, narcolepsy. Basically, you develop antibodies for whatever reason.
M16: There are a couple concerns that certain viruses may trigger this,
M16: but basically develop an antibody to a very, very specific
M16: set of cells in your brain. The cells produce a
M16: peptide called Eareckson. What happens is this destroys those cells
M16: either completely or to a significant degree diminishes them. And therefore,
M16: you don't have enough of this peptide Orexigen to maintain alertness.
M16: And as I mentioned earlier, one of the parts of
M16: the brain that's relevant to wakefulness is this posterior hypothalamus
M16: and these cells sit in that posterior part and that
M16: erection is an important factor in maintaining alertness.
M8: So it wasn't contract avoidance, it was actually something more specific.
M8: So let's move from there and talk about some of
M8: your other specialties. One of the things I understand you've
M8: been researching and working on for some time is RLC know.
M8: Some of us didn't know anything about our last till
M8: we saw a commercial, the Restless Leg Syndrome. What exactly
M8: is that? And is it prevalent or just we see
M8: a lot of commercials for it on CNN.
M10: So the the estimated prevalence for the US is about
M10: five percent of the population, with about half of them having,
M10: I think, clinically relevant symptoms requiring some treatment. Basically, it
M10: is a motor sensory disorder. It's associated with this often
M10: hard to describe, very irritating, uncomfortable sensation in your legs
M10: that almost compulsives you. You can't not move. You have
M10: to move the legs. The reward is as soon as
M10: you move the legs, the sensation drops off and disappears,
M10: but may crescendo and Amanor start to increase again. So people,
M10: after moving the legs a couple times, often get out
M10: of bed and actually just walk for a while to
M10: get enough relief to get back in bed again. So.
M3: So you've been studying it quite a bit. What are
M3: some of the things that you found out about it?
M3: What causes it, who has it, who doesn't have it?
M3: And what are you guys doing about it?
M4: Well, essentially, it's about three to four times more common
M4: in women than men.
M10: It basically increases in prevalence over the age group, probably
M10: coming to a plateau at about 50 to 60 years
M10: of age. But there is a progressive increase through childhood,
M10: adolescence and up through the younger adult ages. Most of
M10: our research for the last 30 years has been trying
M10: to understand the pathophysiology of this disease. And what we
M10: know is that there is a association and what we
M10: believe is part of the primary pathology is that the
M10: brains of patients with restless syndrome have lower levels of
M10: iron in certain regions of the brain. So it's an
M10: insufficient state of brain and insufficient state, despite the fact
M10: that their blood levels of iron are normal. So it's
M10: very organ specific phenomena. And this iron insufficiency leads to
M10: a couple of changes in your brain, one of which
M10: is an alteration in this chemical called dopamine. By altering,
M10: it doesn't specifically decrease the overall amount of dopamine. It
M10: basically changes its circadian change in dopamine. So don't levels
M10: are right in the morning and low at night. And
M10: it seems to make that nater the lower point at night,
M10: lower or decreased, so that you start having symptoms of
M10: that lower level of dopamine at night that triggers the symptoms.
M10: And therefore, some of the first treatments that we had
M10: available back 30 years ago was the use of some
M10: of the agents commonly used in Parkinson's disease, generate RAPEX,
M10: reequip the agonists. The symptoms are somewhat different in the
M10: younger age group, particularly men whose symptoms start before the
M10: age of thirty five have a very vicious form of disease.
M10: I mean, it will come on basically affect the whole
M10: life within a year or two. I mean, I mean,
M10: it was not just happen at night or during the
M10: evening and eventually they'll have it 24/7. It is. It's
M10: in women at a younger age under 40. It starts
M10: to be an intermittent. So the symptoms come and go
M10: in coming and going, but becoming a nightly problem by
M10: the time they reach somewhere between 40 and 50.
M1: So early on, you alluded to the earliest reported sleep
M1: aid and I'd like to know where that fits in
M1: to all of these syndromes, that being alcohol, how does
M1: that impact our sleep, our restless legs, our sleep apnea, good, bad, indifferent,
M1: chronic use of alcohol will actually make your sleep worse.
M10: The usual scenario is you're using to get the sleep
M10: and it may work months, years, but then you start
M10: having problems with awakening from having a difficult time getting
M10: back sleep as regards to restless leg syndrome. About a
M10: third of patients, even a few sips of alcohol, would
M10: drive their legs nuts. In fact, seven is one that
M10: came out with the value of the Parkinson drug Sinemet
M10: being a significant value in treating Arless patients. Part of
M10: that time there were people who were suffering with our
M10: loss for 20, 30, 40 years who were getting no
M10: more than two or three hours sleep a night, and
M10: some of them used alcohol and the way they did.
M18: So if you take alcohol and it makes it worse,
M18: what you have to do is drink it fast enough
M18: and get enough down you to learn to become an anesthetic.
M18: But to clarify, you're not advising that? No, I'm not advising, no.
M18: It's a very unfortunate situation.
M16: That's how desperate I mean, I can't convey in simple
M16: words the experience is beyond anything any of us can
M16: imagine unless you actually have had the disease. And I
M16: can tell you, you become so, so desperate to get
M16: rid of the sensation. And obviously during the day you
M16: can walk. That's fine, but you can't walk and sleep
M16: at the same time. And so when you've missed night
M16: after night for years on end, you will do what
M16: you need to do. And some people have resorted to
M16: the use of figured out, if I drink this half
M16: this year, the whiskey straight down, I can get some sleep.
M3: How are you affecting treatment here?
M18: So one of the outcomes of that research I talked
M18: about was to see if I raised your body iron stores,
M18: whether a certain percentage of that could get over into
M18: the brain or your brain probably only constitutes about five
M18: percent of your total body in stores. But if I increase,
M18: the total amount, even of that fraction may not change
M18: the amount obviously would. We started with some simple studies,
M18: mostly Open-Ended designs, demonstrating the value of iron, initially oral iron.
M18: Then we went to intravenous iron and there's been several,
M18: essentially three randomized placebo controlled trials of intravenous iron in
M18: patients who were not anemic, who did not necessarily have
M18: an iron deficiency, and demonstrated that you can get about
M18: 45 percent of patients who are going to demonstrate a
M18: much greater improvement in symptoms with intravenous iron. And so
M18: that's one of the things I think, as was an
M18: outcome of all of our basic research, that we can
M18: improve symptoms.
M8: But that sounds kind of temporary because you're not going
M8: to have intravenous iron permanently.
M18: It's a one off experience. And then I usually evaluate
M18: the patient at eight weeks after the infusion. If they've
M18: had improvement in symptoms, I will check their current iron
M18: status and then I will follow. And it may be
M18: six months, it may be two years before they contact
M18: me and say my symptoms have worsened. I will repeat
M18: a set of iron labs and if it has dropped
M18: in a reasonable degree, I will give them another iron infusion.
M18: I have a patient who developed a bad gastritis and
M18: for whatever reason developed severe inefficiency, developed our and he
M18: calls me every 22 to 24 months, say they are
M18: less back time for our infusion. Check his blood guarantee.
M18: I know where it's going to be is iron is
M18: going to be a certain level given the iron infusion
M18: four or five weeks later, it's gone. And I don't
M18: hear from another two years.
M8: So I'm not trying to lead the witness here, Chris.
M8: But one of the things that we try to do
M8: on this show is debunk and misinformation that is often
M8: presented to our listeners. So these commercials that you're seeing
M8: all over the place for some prescribed pill for RLC,
M8: what is that? How does it work and does it work?
M8: And is that something that our listeners should be paying
M8: attention to?
M18: There are pills or creams there, devices out there. There's
M18: no shortage of information about our less about things that
M18: will work at the current time. I am not comfortable
M18: with any device. Is there are PADDs vibrators, there's leg sleeves.
M18: So far, none of my patients have ever found any
M18: success with any of them. There are numerous different creams
M18: out there which again, in general I don't see any
M18: harm in use them, but I don't have anyone for
M18: whom it's worked. There's a whole thing about magnesium pills.
M18: There's one clinical trial demonstrates the value of magnesium. I
M18: generally have no problems with my patients trying standard magnesium
M18: Oxlade or something like that, four 800 milligrams. Again, I
M18: have one person out of my experience for whom she
M18: swears by it. That's why the treatments that are out
M18: there that are value include those medications that are used
M18: for the Parkinson's disease, which are called dopamine agonist. They
M18: they mimic or they are both mean, they are valuable
M18: and some of them have been approved. Actually, all three
M18: have been approved by the FDA for us. Like, so
M18: do you have what's called the Alpha to. Delta agents,
M18: these are medications which bind to the protein called Alpha
M18: to Delta, which is calcium channel and modifies calcium and
M18: thus the intensity or discharge of the sensory nerves. And
M18: they fall into the categories of what's called gabapentin pregabalin.
M18: Many people have heard about them from they're used often
M18: used for pain, are often used for neuropathy, nerve pain.
M18: So those are value.
M1: There are so many patients who are awakened by troubling
M1: leg cramps, foot cramps, and the folklore is all your
M1: low in potassium. And yet when you checked people's potassium level,
M1: it turns out to be normal. What are these cramps
M1: and how do you avoid them?
M18: So leg cramps. Some people refer to them as Charlie Horace's.
M17: They are not exclusively but almost consistently in the lower
M17: extremities of a few of my patients. Get them in
M17: their upper extremities.
M6: Things like overly exercising, particularly if you're not really used
M6: to exercising, may cause some dehydration and dehydration may be
M6: relevant to the salt question about potassium, sodium, potassium, maybe low.
M6: There's a big family history. Family history plays into it
M6: in a big way. You know, I used to be
M6: for years used as the treatment option, but you can't
M6: get quinine over the counter anymore. So you can get tonic,
M6: you know, the sorts of stuff, the tonic that has
M6: quinine in it. Some people will take that. It's interesting
M6: because actually when you look at the data for treatment options,
M6: there's been a couple good, though not perfectly great studies
M6: that looked at the various treatments. And the only one
M6: that has consistently demonstrated some value in reducing the cramps
M6: is doing about five, six minutes of stretching exercises before
M6: you go to bed at night of that muscle group
M6: that's involved.
M14: So across a couple of different, smaller studies, that's the
M14: one that has been at least the most consistent and interesting. So, Chris,
M14: are you online? How can people follow you?
M10: We have a website, AAPA Less at Hopkins's, our primary website.
M19: Great. And how do they contact you for care? If
M19: you go through the Hopkins Sleep Disorder Clinic, they have
M19: a website for Hopkins' Sleep Disorders Medicine, which has the
M19: appointment number of things like that.
M12: Dr. Christopher, earlier, we want to thank you for joining
M12: us today. And Dr. Tayback, thank you for joining us
M12: as well. And we're still practicing is produced and edited
M12: by A.J. Mosley, mastering his by Steve Rickey Bird Music
M12: for We're Still Practicing is composed and performed by Celeste Anorectic.
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M12: get a good night's sleep.
M20: Bye bye from Kerkow Media Media for your mind.