Restless Limbs Sensorimotor Disorder

The purpose of this webpage is to provide an overview of my observations and etiological hypotheses for the single disorder which underlies the two diagnostic categories Restless Legs Syndrome (RLS) and Periodic Limb Movement Disorder / Syndrome (PLMD/S).  In addition to this, I discuss a variety of non-drug measures for combating this disorder.

If you are doctor, nurse, neurologist, neuroscientist, medical specialist or student, you might like to read the shortest possible summary of my observations and hypotheses which I wrote for a neurologist in August 2012 and updated in February 2015.  This contains some updates, most recently in November 2017, which I have not yet made to the page you are reading now.


2020-05-30 update:

I haven't worked on RLSD for some years, nor tried to keep up with the literature,  This was primarily because I found little new research concerning the spinal cord - which is obviously where the pathology is located.  It is as if many neuroscientists are uninterested in the lowly spinal cord when they could be working on the brain.

However, please see this 2019 article, which reviews and discusses all RLS/PLM work on spinal since the excellent 2000 article linked to below: #bara_jimenez Periodic limb movements in sleep - State-dependent excitability of the spinal flexor reflex

The 2019 review article is:

Restless legs syndrome: Clinical changes in nervous system excitability at the spinal cord level
Chloe Dafkin, Warrick McKinon and Samantha Kerr
Sleep Medicine Reviews Volume 47, October 2019, Pages 9-17 (Paywalled)

Much of what follows is novel and therefore likely to be controversial, such as where in the body I believe the problem occurs (the spinal cord); the biological processes which are involved; and the substances or environmental conditions which I believe are likely to aggravate or diminish symptoms.  Other statements are in agreement with the widely-held views of medical researchers and practitioners in this field, such as there being a single underlying disorder to which the symptoms of both RLS and PLMD can be traced, and the involvement of iron and dopamine in this disorder.  Doctors prescribe the same treatments for both RLS and PLMD.  When these treatments are effective, they invariably alleviate both sets of symptoms in the many patients who suffer both types of symptoms.

These new observations, etiological hypotheses and non-drug approaches I am discussing have not yet been published in a peer-reviewed journal, nor have they yet been the subject of widespread discussion by established researchers and clinicians.  However, it is only since September 2011 that I sent a paper (a 32-page PDF) documenting my ideas and observations to 25 or so researchers in the RLS/PLMD field.  I am hoping to receive feedback from them.

If you are interested in RLS/PLMD research, please let me know and I will send you a copy of the September 2011 document.

I suggest that the term Restless Limbs Sensorimotor Disorder (RLSD) be used to refer to the single disorder which underlies these two diagnostic categories.  However, below, I use the acronyms RLS and PLMD, because these are the currently accepted medical terms that are familiar to people researching, treating, or suffering from this disorder.  Below, "RLS/PLMD" is my shorthand for this single underlying condition.  I hope that in the future, this will be known as "RLSD".

This is a work in progress.  The update history is: updates/   Please let me know any corrections or suggestions. 

Please be sure to read the DISCLAIMER regarding health information at this site.  I have no formal qualifications and I am not a doctor.  Even if I was a doctor, I have not examined you!

To the index page of this site: ../
Contact details and copyright information: ../contact/
© 2011 to 2018 Robin Whittle   Melbourne Australia 

Last update except as noted above 6 November 2018. 


#intro                 Introduction.
Links to other sites.
#summary Summary of my new observations and etiological hypotheses.
Help for sufferers and their carers - Non-drug techniques for combating RLS/PLMD.

01 - Self-diagnosis, with videos.
02 - Other patterns of movement which are not RLS/PLMD.
03 - Ensure your iron levels are good.
04 - Do not drink coffee of any kind, including decaf.
05 - Reduce or ideally eliminate your consumption of caffeine.
06 - Dark chocolate and cocoa seems to worsen or cause RLS/PLMD.
07 - Excessive salt seems to worsen or cause RLS/PLMD.
08 - General nutrition, including Magnesium and Calcium.
09 - Avoiding drugs which worsen the condition.
10 - Sleeping position and keeping warm.
11 - Unusually high or low levels of exercise.
12 - Protein meals and snacks.
13 - Tyrosine capsules or tablets.
14 - Percussive massage.
15 - Other factors and techniques.
How opioid receptor antagonists in all types of coffee might be expected to increase the severity of, or cause, RLS/PLMD symptoms.  Also, some historical notes on coffee, Thomas Willis writing in 1672 about coffee and about what we now know as RLS. 

Also how some coffee drinkers find a cup of coffee stops symptoms and helps them sleep - for an hour or so.
#ownresearch The nature of RLS/PLMD varies considerably between individuals.  By conducting your own research you can determine which treatments work best for you.

On separate web pages:


The DSM-5, Diagnostic Criteria and a new name for Restless Legs Syndrome

Please see this page for my arguments for adopting Restless Limbs Sensorimotor Disorder in place of both RLS and PLMD, and to encompass less severe, but still more widespread, symptoms concerning sleep disturbance.  I also argue against using family names to identify any pathological condition.

The Restless Legs Foundation ( and the International Restless Legs Syndrome Study Group ( have decided to change the name of "Restless Legs Syndrome" to "Willis-Ekbom Disease".  Meanwhile, the American Psychiatric Association are finalizing the DSM-5 to include diagnostic criteria of "Restless Legs Syndrome", which was not in the DSM-IV.  However, the DSM does not cover movement disorders.  RLS/PLMD is a movement disorder.  It is not a sleep disorder, but it invariably disrupts sleep.  It is not a psychological or psychiatric disorder.  Sufferers are treated by their family doctor or neurologists - not by psychiatrists or psychotherapists.


Explanations of some neurological terms to help people understand the summary below of my etiological hypotheses.


List of updates to the pages in this RLSD section of the website.



This section of the website outlines new etiological hypotheses which I believe provide a good explanation of the processes which underly the diagnostic categories Restless Legs Syndrome (RLS) and Periodic Limb Movement Disorder (PLMD).  It also contains a list of non-drug measures which I believe will help many people reduce or eliminate the symptoms of the common - and for some people terribly disruptive - neurological disorder which underlies these two diagnostic categories. 

The novel material here is based on observations and experiments with myself and my wife Tina, together with reports from friends who have had some success with one or two of our suggested techniques.  Other RLS/PLMD sufferers with whom I have corresponded or who have reported their experiences in web forums have independently discovered some of these techniques.

The observations and hypotheses which I bring to this field have not been published in peer-reviewed journals and are not part of the accepted understanding researchers and medical professionals have of RLS/PLMD. 

In September 2011, I sent a detailed 32 page account of my observations and hypotheses to about 25 RLS researchers, including those who have contributed most to this field in the last decade or so.  As of now, (August 2012), I haven't received any feedback on the observations or hypotheses, but I am sure I will.  Many of these researchers are medical doctors, neurologists or have PhDs in neuroscience.  I have no medical or scientific qualifications and had only corresponded with one of these people before.  However, my experience in electronics since 1968 (I am a 1955 model) helped me fault-find the disruption of the spinal cord's sensory and reflex circuits. 

In May 2012, I received some encouraging feedback from an Australian medical doctor who is a sleep specialist and who sees many RLS patients: "Enjoyed your paper very much.  Welcome to the long haul of trying to improve the medical world, a lifetime is needed.  . . . You need to be patient and resilient in this business, and success never guaranteed." 

I also received a message from a 24 year old UK man who found that both both ordinary and decaf coffee, but not tea, when drunk late in the day or in the evening, caused him to have RLS/PLMD: #2012_06_08c.

In July 2012 I received an appreciative response from a US-based neurologist who read my material.

This disorder is unusual in many ways.  It is a movement disorder which is worsened by, or only occurs due to, periods of physical inactivity such as sitting or lying down for an hour or more. It is not a sleep disorder, but it invariably disrupts sleep.  It is the only disorder I know of in which either of these two processes play a role:

Localized depletion of a precursor chemical (the amino acid tyrosine).

Low levels of random depolarization (firing) of skin sensory neurons, even when the skin in which their input terminals are located is not being touched. 

These two situations have close parallels in electronics: power supply problems and noise - meaning random fluctuations of electrons, such as those which give rise to hiss in an audio amplifier.  So it was probably easier for an electronic technician such as me to identify these problems than for someone whose training is in medicine or neuroscience. 

I have been researching RLS/PLMD since 2004, when my wife Tina and I were married.  Tina has had RLS/PLMD in her legs, arms and torso since she was about 12.  The symptoms were random, occasional and annoying, but got worse over time.  Her doctors in Texas and New York City listened to her reports but did not mention RLS.  Neither Tina nor I had heard of "Restless Legs Syndrome" before 2004, when her symptoms became more serious.  I found out about this diagnostic category via a web search.  In the USA in the late 2000s, RLS became widely known - probably due to TV advertising of prescription drugs which in recent years have been approved to treat the condition.  RLS is now better known in Australia too.  The Internet has facilitated much greater awareness of many previously little-known health conditions.

Nowadays (2011 and beyond), for a person with such symptoms as strong as Tina was suffering in 2004, I think doctors would have no hesitation in prescribing dopamine receptor agonist drugs - which are routinely given to RLS/PLMD sufferers.  These drugs have serious potential side-effects, including compulsive behaviour, such as pathological gambling, and augmentation - after a few years they make symptoms worse.  Another class of drugs used to combat RLS/PLMD are  opioid receptor agonists ("opioids") such as Methadone and Oxycodone.  These are  indefinitely and are also frequently prescribed for RLS/PLMD.  However, opioids are addictive and potentially debilitating, commonly causing drowsiness, constipation and nausea.

Tina has never used any such prescription medications.  I devised non-drug techniques for reducing her symptoms.  In recent years we determined that the causes of her worst symptoms were primarily coffee (including decaf) and low iron levels.  (In 2014 we found that potassium supplements significantly reduced symptoms, but I am yet to update this page to report on this fully.)

I believe that most people's RLS/PLMD problems result from low iron, interference from opioid receptor antagonists in coffee; and interference other drugs.  (In 2011 I included caffeine as one of these drugs, but in 2015 I am not convinced that it is directly involved in RLS/PLMD, despite the generally accepted notion that it is.)  I propose that the common susceptibility to these deficiencies and forms of interference is due to a recently-evolved adaptation to the human nervous system, which is triggered by soft touch to the arches of the feet and which is not always deactivated when it should be. 

Tina may have some genetic proclivity to RLS/PLMD - I think quite a few people do.  Several research studies have identified genetic variants which can affect the susceptibility to RLS/PLMD - though in most cases it is not clear exactly which gene is involved; what the gene normally does; or what it does differently in the variations which worsen RLS/PLMD. 

Some people may have suffered spinal injuries and infections - or their nervous system may have developed (in-utero and shortly after birth) in ways which make the symptoms more likely.  Pregnancy and end-stage renal disease are also well-known for contributing to the risk of RLS/PLMD.

With good nutrition - including working with her doctor to ensure her iron levels are good - Tina now typically has most nights free of RLS/PLMD symptoms.  She does not drink coffee (including decaf) or anything else which contains caffeine - apart from chocolate, which contains a little caffeine.  We like chocolate but we find that more than small amounts of dark chocolate or cocoa in the evening or perhaps late afternoon is likely to cause RLS/PLMD symptoms.  Having some in the early afternoon and then going for a 4km walk does not seem to contribute to the risk of symptoms that evening. Consuming excessive salt is another risk factor we have not entirely eliminated. 

Around 2009, I started getting occasional mild RLS/PLMD symptoms too.  This is mainly a curiosity to me - to experience what I have been researching.  My iron levels are OK.  I stopped drinking coffee and all other caffeinated drinks in 2004.

Now, if either Tina or I get any more than minor RLS/PLMD symptoms it is usually because we ate too much chocolate or cocoa, had too much salt, and/or have not eaten enough protein in recent hours.  Tina remains more susceptible than I do, and her susceptibility is affected by her menstrual cycle. 

In November 2011, we only get RLS/PLMD symptoms going to bed if we have overdone salt or chocolate.  Tina often gets symptoms a few hours before we wake up - such as on about 50% of mornings.  For me, this happens every week or two.  I attribute this to a combination of innate proclivity to this condition - presumably genetic for Tina and age-related for me, since I am 56 - the influence of salt and/or chocolate and generally low levels of amino acids (including tyrosine) in the bloodstream, since it is 12 hours or more since our generally moderate- or high-protein evening meal.  These symptoms are mild, but disrupt the sleep of one or both of us.  They are typically one foot doing a set of ankle dorsiflexions every 40 seconds or so, as depicted in the videos of Tina's foot below.  We can make these go away for a few hours - long enough to complete our night's sleep, by using either percussive massage of the mid-lower spinal region and/or taking two 500mg tyrosine capsules.  Either approach seems to work reliably - our symptoms are not so strong as to require both.

One RLS-suffering friend of ours, in her 50s, who drank one plunger coffee and a few instants a day reports that her symptoms (1/3 nights, while sitting still and while in bed) have greatly diminished now she only drinks one or perhaps two espresso coffees a week (when out for the evening).  She now drinks more tea, which generally has less caffeine than coffee, and which is not known to contain opioid receptor antagonists.

This friend and another in her 60s, who doesn't drink significant quantities of coffee, both find that percussive massage of their mid-lower spine area prevents or reduces their RLS/PLMD symptoms.  Both our friends pummel either side of their mid-lower spine with their own fists.  The benefits are apparent within a minute or so and last for hours or for the rest of the evening.

Our first friend mentioned above is experimenting with tyrosine tablets, but now that she drinks significantly less coffee than in the past, she has not had enough RLS/PLMD symptoms to try the tyrosine with. 

Other sufferers have independently discovered the benefits of tyrosine and percussive massage of the lower spinal region.  Additionally they have also discovered exercises which help them, such as inverting the body by standing on the shoulders and elbows - perhaps with upside-down bicycling motions of the legs.  These exercises are likely to cause physical movement and diffusion of cerebro-spinal fluid in the lower part of the spinal cord, which I believe is the main beneficial effect of percussive massage.  When I told our second RLS/PLMD suffering friend about this extreme form of pre-bedtime bicycling exercise that some people had discovered, she nodded quietly, saying yes, she had done this too.


Feedback and discussion forums

If you are suffering from RLS or are caring for someone who is, and are interested in comparing notes, please email me (../contact/). 

There's an Australian RLS forum which I have not yet written to.  It seems to support of detailed messages, and in the first 4 weeks of Nov 2011 had about 20 messages: Forum (A subgroup of Sleep Disorders Australia)
No registration is required to read this forum.  Registration is required to contribute.

I wrote to this forum, but there is little activity: 12 or so messages in the first 4 weeks of Nov 2011:

The Non-Pharmaceutical Therapies section of the Restless Legs Foundation forum:
Registration is required to read these forums and to contribute to the discussions. 

The RLS Support forum has searchable archives of 53708+ messages.  There were some discussions about my observations, hypotheses and suggested techniques in this forum in November 2011, but the Moderator does not want messages longer than a few paragraphs.  Health is complex and important, so this forum is not a good place to be discussing my new observations and hypotheses.  There were 230 messages in the first 4 weeks of Nov 2011, so it is a  lively forum.

RLS Support forum at Yahoo Groups (est. 1998)
Registration is required to read and contribute. 

I wrote to the RLS forum too, but it has little activity in general.  There were about 10 messages in the first 4 weeks of Nov 2011.

The Movement Disorder Society's RLS Forum:
No registration is required to read these forums.  Registration is required to contribute.  (If you want to mention a commercial website of any kind, including any page here at, please delete "http://" and any "www." so the forum software does not make convert the text into a hyperlink.'s policies prohibit hyperlinks to commercial sites from their site, including in forum messages.)

Please remember this website, and my hypotheses, are not well known and involve considerable differences from the mainstream understanding of RLS.  That understanding involves little or no idea about the etiology (underlying mechanisms), other than a frequent assumption that the pathology is in the brain.  Please don't assume that anyone on these forums knows about this site, or that they would agree with this material if they read it.  Also, my suggestion that "Restless Limbs Sensorimotor Disorder" (RLSD) replace "RLS" and "PLMD/S" is likely to be controversial.

Spinal injuries and infections

Some people suffer RLS/PLMD primarily or solely because they have a spinal injury, including one which resulted from a surgical procedure.  I suggest that anyone who suddenly developed RLS/PLMD which continued indefinitely should discuss with their doctor the possibility that they suffered a spinal injury or infection at that time.  I understand that vitamin B12 deficiency can lead to neurological damage - which includes potentially permanent damage to the brain and/or the spinal cord. 

What I write below is directed mainly at people who do not have spinal cord damage.  While percussive massage near the spine, to shake up the fluid in the spinal cord, might reduce or eliminate symptoms for people with spinal injuries, I suggest that the dangers of compounding the injury are so great that they should not do this without their neurologist's approval. 

Spinal and spinal cord damage resulting from injury or infection might involve circulatory problems, or damage directly to the lower spinal cord circuitry, which sense the skin of the foot arch.  In my hypotheses, RLS/PLMD involves this circuitry becoming hypersensitive, and being triggered continually, to produce the sensory symptoms of RLS and the motor symptoms of PLMD (involuntary toe-lifting, foot withdrawal and leg withdrawal movements).  Spinal damage may also reduce the effectiveness of the pathway of neurons in the spinal cord from the brain or brain-stem to the lower spinal cord, which I propose exists to inhibit this highly sensitive mode of operation.

People with spinal damage may still have very serious RLS/PLMD symptoms, even if they use every non-drug preventative measure and remedy described below, and whatever other such measures there are. 

Genetic or developmental difficulties

Similarly, to people with spinal injuries and infections some people may have a genetic or developmental abnormality which makes them unusually prone to RLS/PLMD symptoms despite all the right nutrition, exercise, avoidance of disruptive drugs etc.  I don't know of any research suggesting that developmental difficulties may contribute to or cause RLS/PLMD symptomatology, but it would not be surprising if this occurred as a result of a person's nervous system building itself incorrectly. 

Perhaps some people have a genetic variation which reduces the level of iron in their neurons. Perhaps some people have a genetic problem with Tyrosine Hydroxylase or with some of the regulatory mechanisms for this enzyme, which catalyzes the first step in converting tyrosine into dopamine and which requires an atom of iron to function.

Neurologists working with RLS/PLMD patients who have any of these underlying problems - spinal damage, genetic predisposition, or some kind of developmental abnormality - are at a serious disadvantage at present, because there is no conventionally accepted etiology for RLS/PLMD.  I hope this material - or better still the longer not-for-publication PDF document I sent to RLS researchers - will be of interest to such doctors, neurologists and other specialists. 

In 2012 or 2013 I plan to revise that PDF document and make it publicly available on this website.  This will be primarily for medical professionals and researchers - including people such as myself who have no formal qualifications.  So I am keen for people who are up-to-speed with neuroscience and RLS/PLMD to read the current version and provide constructive feedback.

Your own research and comparing notes with others

Its strange that RLS/PLMD has resisted explanation for so long.  Perhaps the research has been less vigorous than for other disorders because no-one has ever died from the condition.  However, it is so widespread and disrupts so much sleep that surely some sufferers have fallen asleep or made mistakes while driving, leading to serious injuries and deaths. Chronic sleep disruption is also widely recognised as leading to other health problems. 

RLS/PLMD symptoms depend on a number of nutritional and other everyday factors which are amenable to change.  Experiments can produce results within minutes or days - and no special equipment or chemicals are required.  Percussive massage of the lower spine region, by hand or with a motorized massager, typically (in our experience, the experience of our friends and according to occasional reports by other people on RLS websites, forums etc.) reduces or eliminates symptoms in the legs in less than a minute, but not affect symptoms in the arms.  Percussive massage of the upper spinal region can reduce or eliminate symptoms in the arms, without affecting symptoms in the legs.  (We have only observed this arm-leg specificity ourselves.  We can't reproduce this now since Tina no longer has symptoms in her arms, and I have never had symptoms in my arms.)  These observations provide strong support for the hypothesis that the pathology is in the spinal cord. 

Below (#ownresearch) I encourage people with sufficient time and interest to research their own, or their spouse's, condition - with due care and caution about safety.  Doing so carefully and systematically, and reporting the findings to other researchers, enables people to contribute to the scientific process in ways which are more flexible and hands-on than is possible with most formal research projects.

Such reports may also motivate professional researchers - who have the required skills and access to  funding and large numbers of experimental subjects - to conduct larger trials.

Please don't try to become an amateur doctor or neurologist.  Doctors and other specialists undergo a decade or so of intensive training so they can make good judgments about safety and so they can reliably apply a huge wealth of knowledge to medical problems.  They are continually striving to keep up with research in many aspects of human health. 

Doctors, medical specialists and nurses are usually not researchers.  They generally don't base their clinical decisions on hypotheses or observations which have not been widely debated and accepted by other clinicians in their field.  However, this leaves them in a tricky position with conditions like RLS/PLMD where no etiological theory has been widely debated and accepted.

While your doctor can advise you in general - particularly regarding safety - he or she can't be making house-calls at 3AM when the RLS/PLMD monster is ravaging you or your loved-one.  Nurses in hospitals spend all day or night caring for patients, so they are perhaps in a better position to understand the impact of this condition, and to experiment with ways of reducing its occurrence.  Assuming you are not being cared for by a nurse, and your contact with you doctor and other specialists is at their offices, during the day, you (and your spouse) are in the best position to observe the problem and experiment with methods of combating it, provided you so so safely.  I can't tell you for sure what is safe or not.  You need to decide this yourself, ideally in consultation with your doctor or nurse.

RLS/PLMD will be somewhat different for different sufferers.  With care and thought, it is possible to research it yourself - yielding information which is more helpful specifically to you than anything you can read about other people in a book, website or journal article.

About us

I work with electronic musical instruments, computer programming and technical writing.  Tina helps me with electronics, looks after me really well, and works on her own creative projects.  Tina's blog with her friend Sandra involves creative writing and photography:

Tina was born in Texas and I was born in England.  We live in Melbourne, Australia.  Here we are at a flower show in Ballarat, in April 2011:

My other websites are  - Devil Fish electronic musical instruments, show-and-tell, many other things - and, which concerns physics and astrophysics research projects, including the mystery of the heating of the solar corona.



Here are some links:


Brief summary of my etiological hypotheses and some new observations

Please be sure to read the DISCLAIMER regarding health information at this site.

This section concerns scientific observations and hypotheses.  It is not intended as guidance for anyone seeking to treat RLS/PLMD.  (A more technically detailed and up-to-date summary is on a separate page: briefsumm/ .)

This brief summary lacks all the references, further discussion and qualifications which a proper account of any pathological condition should have.  For brevity, the hypotheses are stated as if they were facts - but please remember that these hypotheses and new observations have not been published in a peer-reviewed journal.  Nor have they been widely discussed or accepted by mainstream RLS researchers.

My not-for-publication 32 page PDF document (which I sent to about 25 RLS researchers at the start of September 2011) contains more references, discussion and qualifications.

Please don't copy and paste this into blogs and other websites.  Please link to this section of the page: . I will update this text and later replace it with a much fuller body of material.  So I don't want other copies of it floating around on other websites. 

The terminology/ page explains some of the terms used here.

Summary of new observations

[A] Percussive massage of the mid-lower back, around the level of the navel, on either side of the spine (but not touching the bony protrusions of spine itself) reduces or eliminates symptoms in the legs.  The effects begin within seconds or minutes and typically last for a few hours.  This does not affect any symptoms in the arms. Ordinary non-percussive massage - smoothly rubbing, kneading and pressing firmly - has no effect.

[B] Percussive massage of the upper spinal region, below the neck, between the shoulder blades (again, don't touch the spine itself, or its bony protrusions, just the ribs and muscles on either side) reduces or eliminates symptoms in the arms.  The effects begin within seconds or minutes and typically last for a few hours.  This does not affect symptoms in the legs.  Ordinary non-percussive massage - smoothly rubbing, kneading and pressing firmly - has no effect.

[C] If there are also symptoms in the torso (usually the pattern is legs, arms and then torso, as overall severity rises) these may be relieved to some extent at least by overall percussive massage of the whole area of the back , including close to the spine, but again, not actually contacting the spine itself.  (For more details of these three types of massage, see below: #help14_comprehensive_massage.)

[D] Oral tyrosine, such as 1, 2 or 3 x 500mg tablets or capsules (tyrosine, AKA L-tyrosine - we haven't tried N-acetyl-tyrosine) reduces or eliminates symptoms in the legs, arms and torso.  Effects begin within five to ten minutes and typically last for two hours or so, depending on dose and severity of the symptoms.  

The above four observations are consistent with the hypothesis that RLS/PLMD symptoms result (in the context of other precipitating factors such as low iron and/or opioid receptor antagonism and/or dopamine receptor antagonism) largely or entirely due to a localized depletion of tyrosine in the nociceptive (pain sensing) reflex generating circuitry in the spinal cord.  It is also consistent with reports by other people on RLS forums and the like that exercises which stretch, exercise, vibrate or invert the lower spinal area are helpful for reducing or preventing symptoms.

[E] While caffeine is generally (over many hours and days) disruptive of sleep and may contribute directly to RLS/PLMD symptoms and while acute doses of caffeine or at least of caffeinated coffee may for some people reduce symptoms and induce sleep for an hour or so (as some report, this is not our experience), Tina and one of our RLS/PLMD-suffering friends have discovered a link between coffee and RLS/PLMD symptoms which does not seem to be related to its caffeine content.  (Our other RLS/PLMD-suffering friend hardly drinks coffee.)   We observe that coffee of any kind, including decaf (which has about 5% the ordinary caffeine content) consistently worsens or causes RLS/PLMD symptoms.  Some other compounds in coffee appear to be responsible for the great majority of what we previously thought were naturally occurring symptoms due to some fundamental disorder in the body. 

This is consistent with the well researched, but little known, 1983 discovery that coffee of all kinds contains significant quantities of mu opioid receptor antagonists.  Researchers have identified the major substances and shown that they are created in the roasting process.  (See another page on this site: ../coffee.)

[F] With regret, we must report that we find sufficient quantities of dark chocolate or organic raw cacao powder (as mixed into a drink) precipitate RLS/PLMD symptoms.  Presumably ordinary cocoa (which is made from roasted cacao beans) does the same.  This only appears to be the case if we have the chocolate or cacao in the evening, or perhaps late afternoon, regarding symptoms appearing when we go to bed, which is typically after midnight.  Having some in the early afternoon, followed by a 4km walk, does not seem to cause much trouble.

The effect of raw cacao seems to indicate that whatever is causing this is not due to the roasting process or whatever else goes into chocolate.  There is presumably some caffeine and a lot of theobromine in these foods.  The researchers who discovered mu opioid receptor antagonists in coffee found no such activity in chocolate or any other foods or drinks they tested.  The mechanism behind this is unknown, but it might involve dopaminergic antagonism, some effect on blood flow, transport of amino acids, effects on Tyrosine Hydroxylase or some as-yet undocumented opioidic disturbance.  (Perhaps raw cacao has a stronger effect in causing or worsening RLS/PLMD than the same quantity of cocoa.)

[G] When symptoms are present in the legs, applying a very light touch, (a gram or a fraction of a gram as force) such as with a pencil-tip or matchstick, to the arch of the foot elicits an instant and powerful foot - and perhaps leg - withdrawal actionThis only occurs when the arch of the foot is touched in this way, not the heel, ball or toes and not the top of the foot or anywhere else in the leg.   It does not occur when there are no RLS/PLMD symptoms.  Nor, when there are symptoms, does the reflex response occur if this area is rubbed firmly, deeply and smoothly.

[H] Similarly, only when symptoms are present in the arms, a very light touch to the centre of the palm of the hand (the softer skin, somewhat equivalent to the softer skin of the arch of the foot) - elicits an instant and powerful hand and perhaps arm withdrawal action.  The hand lifts backwards, away from where the palm is, with the fingers becoming outstretched (the opposite of gripping or pushing the palm down) when a very light touch sensation occurs in the centre of the palm of the hand.  Similar light touch anywhere else on the hands does not elicit this sharp hand withdrawal and perhaps arm withdrawal response.  Again, firm, deep, smooth rubbing does not elicit any such response.

These withdrawal reactions are clearly spinal reflexes, but they are not triggered by a noxious stimulus - just a very light touch which would ordinarily be consciously perceptible, perhaps in a ticklish way.  [G] and [H] are entirely consistent with my hypothesis that disorder underlying RLS/PLMD symptoms involves a special (I suggest human-specific) reflex response which is ordinarily inhibited, but which becomes extremely sensitive when symptoms are present, due to inadequate activation of dopamine receptors and/or opioid receptors, in the spinal nociceptive/reflex circuits concerning the foot arch.  Similar circuits evidently exist for the hands and the torso, but these are either less sensitive to start with, and/or are less susceptible to disruption, so symptoms typically occur first and worst in the feet/legs, then in the hands/arms and finally in the torso. 

[I] Applying a local anesthetic such as EMLA (prilocaine and lidocaine to the arches of both feet reduces or eliminates symptoms in the feet and legs.  (We haven't tried this with the hands, since Tina no longer has symptoms there.) 

[G], [H] and [I] are consistent with my hypotheses regarding the pathological disinhibition of a foot arch protective reflex triggered by non-noxious soft touch, with the RLS/PLMD symptoms being generated even in the absence of any such touch by what I argue is the low but normally constant, level of random depolarizations of cutaneous mechanoreceptor neurons in the foot arch.  These observations are consistent with the hypothesis that partially anesthetizing these neuron's sensory terminals reduces this low level of random depolarizations to the point where symptoms are reduced or eliminated, despite the spinal nociceptive/reflex circuitry being pathologically hypersensitive to input from these neurons. 

We haven't tried anesthetizing the hands, or just one foot.  A prediction of these hypotheses is that anesthetizing just the palms of the hands would diminish or eliminate symptoms in the arms, but not the legs, and likewise anesthetizing the foot arches would reduce or eliminate symptoms in the legs, without affecting any symptoms which may be in the arms.  A further prediction is that if the symptoms were in both legs, anesthetizing just one foot arch should reduce or eliminate symptoms largely or entirely in that leg alone.  Likewise for anesthetizing a single palm when there are symptoms in both arms.

We find the following mixture better than EMLA in that its benefits seem to last for hours or perhaps the rest of the night in the case of milder symptoms:  40% Clove Bud Oil, 40% food-grade cold-pressed coconut oil and 30% isopropyl alcohol.  We have found this very effective when applied to the whole foot: heel, arch, ball and toes. 

I am not convinced that this idea of anesthetizing the foot arches will be acceptably safe on a regular basis, so it is not one of the suggestions I make below.  It does involve drugs, albeit applied to the skin.  But they go into general circulation through the skin and I cannot advise on the long-term side effects of this.  Nonetheless, this is a  powerful and instructive research technique - and I think the results we have observed will be easily replicated and provide strong support for my hypotheses.

[J] We have also observed what I regard as "crosstalk" within the spinal nociceptive/reflex circuits where cool skin on the lower back, upper back, shoulders or even the arms will precipitate periodic foot movements.  This appears to be consistent with my hypotheses in the context of the research into in-utero and/or post-natal developmental pruning of sensory input to these circuits, and how it may be imperfect, along the lines suggested by Chapter 12 of "The Science of Pain" ( Appropriate/Inappropriate Developed Pain Paths by Jens Schouenborg website see #help10 and #ownresearch below).

Summary of my new etiological hypotheses

For brevity, the hypotheses are stated as if they were facts - but please remember that these hypotheses and new observations have not been published in a peer-reviewed journal.

[1]  Humans have a recently evolved (~3 million years or so) soft-touch foot arch reflex response which lifts the toes and the foot, in response to a light touch sensation in the soft skin of the foot arches - not the heel, the ball of the foot, or the toes. This response is ordinarily enabled when walking on potentially spiky ground, or in swamps, to avoid puncturing the soft skin of the foot arch.  Humans are the only surviving species to have foot arches. The foot arch is a necessary consequence of a flexible foot which concentrates most weight on the heel and the distant ball and toes, in order to gain the greatest purchase on the ground, to facilitate the forwards-backwards balance which is so important for a bipedal species.  With only two feet for locomotion, our bi-pedal ancestors could not afford to have even one foot punctured and infected, so there would have been strong selection pressure to develop protection for the arches of the foot.

[2]  This reflex response is extremely sensitive, and is normally turned off by a population of so-far unidentified dopamine-producing (dopaminergic) neuron output terminals in the spinal cord.  These would be close to some dopamine receptors which inhibit the interneurons which give rise to the reflex response.  The brain or brainstem evidently activates these descending dopaminergic neurons most of the time, including when we are sitting still or sleeping, to prevent false triggering of the foot withdrawal reflex response.  Whatever part of the brain or brainstem (I assume) turns on this descending dopaminergic pathway evidently turns it off when we are walking on dangerous ground.

[3]  This is a modification of the standard foot withdrawal reflex which is common to mammals in general and to primates and apes in particular.  The genetic instructions which create this recently evolved soft-touch sensitive system and its descending dopaminergic inhibitory system also creates, as a probably non-functional side effect, similar arrangements for the hands, the torso and perhaps the face. (To do - find the paper which reports RLS-like symptoms and movements in the face.)  This system in the hands would help prevent the palm of the hand being punctured if we grip a spiny tree-branch, so it may be adaptive for the same pattern to be repeated in the hands. 

[4] RLS sensory symptoms and PLM (Periodic Limb Movement) movement symptoms result primarily from some combination of the following three processes.  These may be caused or aggravated by spinal injuries or infections and/or by genetic or developmental problems.

(4a) - Inadequate dopaminergic inhibition of these foot-withdrawal reflex circuits in the spinal cord.  This is likely to be due to lack of iron in the dopaminergic output terminals, and/or lack of tyrosine near these output terminals, and/or due to partial blockade of the dopamine receptors, due to dopamine receptor antagonists, such as the drug Phenergan (promethazine).  Please see point [5] below for a more detailed explanation of localized depletion of tyrosine resulting from long (typically hours) periods of physical inactivity (sitting or lying down, rather than walking, running, stretching or exerting a lot of physical effort).

(4b) - These and other nociceptive (pain sensing) circuits in the spinal cord being more than usually sensitive due to inadequate activation of their opioid receptors, such as due to ingestion of opioid antagonists in coffee, or the use of drugs such as naloxone.

(4c) - A sufficiently high level of "noise-driven" - random - firing of the soft-touch foot-arch sensory neurons, in the absence of any of the point-contact very light touch sensations which normally stimulate them. This is "noise" in the electrical engineering sense - random events caused by thermal motion of electrons.  The same process in an audio amplifier creates audible "hiss".  This low level random firing is probably normal and would not result in a conscious perception of touch, or in the foot withdrawal reflex.  However, if the reflex system was being properly inhibited by the descending dopaminergic pathway and by sufficient activation of opioid receptors, this random low level of sensory neuron depolarization can be sufficient to trigger RLS sensations and PLM reflex movements.

[5] RLS and PLMD are diagnostic categories which arise from a common disorder which I suggest be called Restless Limbs Sensorimotor Disorder (RLSD).  This is a  movement disorder which occurs after (or is worsened by) periods of stillness - lack of movement.  This has perplexed researchers for decades.  The most likely explanation for this is that the constant need for tyrosine in a narrow (say 1mm diameter, a few cm high) column of the dorsal horn of the lower spinal cord, in order to produce the constant supply of dopamine to inhibit the newly evolved highly-sensitive, foot arch soft-touch-driven foot withdrawal reflex response, leads to a localized depletion of tyrosine in this narrow column.  I propose that during active movement such as walking, running, etc., the cerebro-spinal fluid (CSF) in the spinal cord is constantly agitated, causing it to diffuse several mm over a period of seconds or minutes.  So even if the capillaries in this ~1mm diameter (my guess) column can't supply tyrosine from the blood to the CSF at the required rate, the dopaminergic output terminals in this column will receive fresh tyrosine-rich CSF from nearby parts of the spinal cord, via ordinary physical activity driving movement and diffusion of the CSF.  When we sit still, or lie down, for long periods, this diffusion is reduced, and it seems that - at least for RLS/PLMD sufferers - the dopaminergic output terminals deplete the CSF in their column of tyrosine, to the point of being unable to produce enough dopamine to inhibit the touch-sensitive foot-arch reflex response.

[6] From the above, it follows that we can reduce or eliminate RLS/PLMD symptoms by one or more of the following:

(6a) - Increasing the activation of the dopaminergic receptors in  these spinal circuits. The best way would be by ensuring there is sufficient iron and tyrosine in these parts of the spinal cord. (See above regarding percussive massage, and the section below regarding non-drug measures to combat RLS/PLMD.) Dopamine agonist drugs (compounds which activate dopamine receptors) will work too, but these affect the entire nervous system, including many parts of the brain, and can lead to augmentation and side-effects including compulsive behavior (punding 1999-paper) and pathological gambling.

(6b) - Reducing the level of opioid receptor antagonists, such as by reducing or eliminating the use of any kind of coffee. (Similarly reducing or eliminating caffeine or any other drugs which disrupt sleep or in some other way contributes to RLS/PLMD.)

(6c) - Increasing the levels of opioid receptor agonists, such as by increasing endorphins (such as through exercise or perhaps as one of the consequences of percussive massage of many parts of the body) or by taking opioid drugs such as methadone (which are potentially addictive and have serious ill-effects).

(6d) - Reducing the level of "noise" firings of the sensory neurons which can activate this foot-arch protective reflex system, to a lower level than normal, even if this means these sensors are not able to properly sense the lightest touch.  See observation [I] above regarding anesthetizing the skin of the foot arch. 


Help for sufferers - non-drug techniques for combating RLS/PLMD

Before considering this material, be sure to read and accept the DISCLAIMER.

Apart from the advice on iron, which is entirely conventional and accepted by all RLS/PLMD doctors and researchers - and probably the material on Folate and Magnesium - everything in this section is novel and not supported by research published in peer-reviewed journals.  The research I cite on opioid receptor antagonists in coffee is the work of conventional researchers and is published in peer-reviewed journals.  (../coffee/)  This research seems to have flown under the radar of pain and RLS/PLMD researchers.  However, its easy to see that opioid receptor antagonists are likely to cause or worsen RLS/PLMD and pain disorders such as fibromyalgia.

This is free information from an electronic technician with no medical qualifications.  Please let me know of your experiences - positive, negative or neutral (../contact/).  

Please consider these suggestions in the context of the conventional view of Restless Legs Syndrome and check your own symptoms against the conventional Diagnostic Criteria.  The best documents for these are from the Restless Legs Syndrome Foundation website's publications section (
You don't need to understand or accept the hypotheses in the above #summary section in order to consider accepting the following suggestions.  You do need to ensure that whatever you do or stop doing is safe.  I can't tell you for sure what is safe for you.  Your doctor is the best source of advice on the safety and appropriateness of various treatment options.

The subsections below are:

help01 - Self-diagnosis, with videos

Please be sure to read the Diagnostic Criteria on pages 2, 3 and 4 of the RLS Medical Bulletin linked to above #rlsorgpubs. 

Here are some further notes:

If your symptoms are "restlessness" (hard to describe feelings of creepy-crawlies, twitchiness etc.) in the legs, arms or torso AND these symptoms typically only arise, or get much worse, following periods of physical inactivity, then you would probably meet the RLS diagnostic criteria.  "Periods of inactivity" means sitting still or lying down, with little or no movement or exertion, for periods such as an hour or more.  Some sufferers may develop the symptoms with shorter periods of inactivity.

Some sufferers report their sensations as painful, but I recall a research paper which indicates that they meant a low-order pain, rather than something acute.

Tina never describes her RLS sensations as painful.  By contrast, I have sometimes felt the whole soles of both my feet, including the toes, to be sore.  In these instances, it has been my impression that reducing or stopping the underlying RLS/PLMD mechanism with percussive massage near the mid-lower spine, and/or taking 2 x 500mg tyrosine tablets with half a glass of water, reduced the RLS urge to rub my feet together and reduced the soreness.  This would be consistent with what I understand about the operation of the spinal cord's nociceptive (pain-sensing) circuits - they can become more sensitive when another nearby pain-sensing system is moderately activated.

An intense case of RLS foot-rubbing interrupted by involuntary movements can be seen in the video Restless Leg Syndrome? (BF109) in the Links section above.

If your feet or legs - or hands, arms or torso muscles - make involuntary movements AND this is associated with periods of physical inactivity AND if the movements were numerous enough per hour AND occurred with suitable timing (such as 20 to 40 seconds or so apart), you would probably meet the PLMD diagnostic criteria.  These movements can happen when awake or asleep. 

The underlying mechanism which gives rise to both the RLS and PLMD sets of diagnostic criteria is is a movement disorder, which disrupts sleep.  The mechanisms are the same when asleep or awake.  My hypotheses (summarized above) locate all the problems in the spinal cord.  I know of no evidence that there's anything wrong with sufferer's brains, legs or arms.  Please read these hypotheses so you can at least partially understand my viewpoint on this disorder, and how it differs from the viewpoint of many conventional researchers, who tend to assume it is a brain disorder and whose treatment options (after sorting out iron levels and perhaps magnesium) are largely based on prescription drugs with serious side effects. 

Here are two 15 second videos of Tina's right foot doing a single typical Periodic Limb Movement while she is asleep. 

These are not streaming videos like from YouTube servers.  Your browser will download the whole file - which may take a minute or two - and will pass it to an MPEG viewer program in your computer.  Each file is 5 Megabytes and plays for 15 seconds.  I suggest right-clicking the link or image and opening the video file in a separate browser window.

Click the image to see a 15 second 5 Megabyte video of a typical RLS / PLMS foot movement


This pink sock video above and the barefoot one below depict typical RLS/PLMD foot movements while Tina is sleeping. 

Click the image to see a 15 second 5 Megabyte video of a typical RLS / PLMS foot movement


These occur with intervals typically in the 20 to 40 second range.  My right foot occasionally does much the same thing, when I am awake - but usually only due to excessive chocolate, salt or perhaps inadequate protein in recent hours. 

Click the image to see a 15 second 5 Megabyte video of a typical RLS / PLMS foot movement


This one shows a common foot stretching response, which may be semi-voluntary, since Tina is being partially awoken by the sensory disturbance and is, by habit, stretching or rubbing her feet to try to reduce the problem.

If Tina pulls her feet towards herself, so the soles of her feet are pressed against the bed and her knees are elevated, this is a good sign that the RLS/PLMD monster is at work; likewise foot rubbing or shaking.  Tina's feet can also do a gentle but quite rapid (~3 cycles a second, like a pure sine-wave) ankle twisting motion where the toes are not pulled upwards.  Neither she nor I can do this consciously ourselves except in a coarse and jerky manner.

help02 - Other patterns of movements which are not RLS/PLMD

If you have muscle spasms in the legs arms and torso, while falling asleep (you may not notice this, but your bed-partner will) and you recently consumed a lot of caffeine - say a cup of coffee, or an "energy drink" earlier in the evening or that day, then I suggest that this is probably not related to RLS/PLMD.  I think it is more likely a direct result of the caffeine.  These spasms are random, rough and sudden, perhaps with the hand being drawn in and the foot going down.  Many muscles fire suddenly within a second or less, in ways which would not be possible to elicit by conscious commands from the brain.  RLS/PLMD movements are characteristically of the toes and foot moving upwards, and the fingers pulling back, with the hand and arm pulling away from what the palm might be touching.  The RLS/PLMD movements tend to repeat every 20 to 40 seconds.  The caffeine-caused spasms are more erratic and random - and it is my impression they only occur at the threshold of falling asleep.

One common night-time movement pattern which has nothing to do with RLS/PLMD is the Hypnic Jerk: also known as Hypnagogic Jerk.  This occurs when falling asleep, without warning.  It involves a sudden, surprising, sensation of falling for a split second.  It is my impression that these do not usually repeat themselves more than once a night.  I guess I have one or two a year. 

A serious and fortunately rare movement disorder which may affect the legs is RSD/CPRS - which is apparently usually a result of injury.  The leg spasms depicted in this YouTube video qE_OwuilOew do not resemble those of  RLS/PLMD since they involve lots of muscles being activated erratically at once. 

There is a separately recognized leg movement disorder called "Nocturnal Quiescegenic Dyskinesia": .  The movements in this YouTube video:  QOiRmXh4CA4 are quite unlike RLS/PLMD.  The movements in this video are centered in the thighs and hips, with none of the pulling back of the toes, or foot withdrawal motions which are characteristic of RLS/PLMD.

In June 2012 I had an interesting discussion with one of our electronic musical instrument clients about foot tapping.  He is a 37 year-old musician and computer programmer who is bristling with creative energy and enthusiasm.

With his foot on the floor while sitting in a chair, his toes push downwards, lifting the ankle, calf and knee, several times a second in a resonant bouncy fashion.  This pattern may continue for seconds to tens of minutes.  Since he was a child he has frequently tapped his foot.  This is when he is sitting in a chair - never while lying in bed - so his foot must be on the ground or a footrest.  It tends to happen when he is more tired, and not so much in the morning or after sleep.  It happens more when he is concentrating on technical matters such as computer programming, but not so much when painting or making music.  He is observant and is interested in health, so he has noticed and thought about this tendency for many years.  He does not consider it a disorder or a disability.  It is, nonetheless, a pattern of movement which might be considered "Restless Legs". 

He finds many factors make it occur more strongly, including especially sugar.  He used to drink large quantities of fruit juice; but now has minimal intake.  He speaks highly of Australian author David Gillespie's Sweet Poison - the Quit Plan .  He reports that these factors seem to increase his foot tapping: coffee (both ordinary and decaf); tea (caffeinated, not herbal); Coca Cola, including sugarless, caffeinated Coke Zero; tobacco; bad posture when sitting in a chair, such as leaning forward; placing weight on the leg; intense thoughts.  Typically he taps with his left foot, without really thinking about it, but his right one can do it too.  I think it tends to be one or the other, not both.  He can stop the movements if he thinks about it, which is totally different from the movements of PLMD.  Opioid drugs reduce it, I guess due to opioid receptor activation causing drowsiness, and generally relaxing muscles.  This may explain why decaf coffee - with ~5% the ordinary amount of caffeine, but with coffee's usual amount of mu opioid receptor antagonists - makes it worse.  These antagonists would reduce the ordinary level of activation due to the body's own mu opiate receptor agonists, as mentioned in the section below on coffee.

This pattern of foot tapping is common - I do it myself at times.  It seems unrelated to the movements of RLS/PLMD because it does not occur when lying down in bed, because it is continual and rhythmic, because it can be consciously inhibited and because (according to this fellow) he can easily and happily synchronize it with music, especially around 140 beats-per-minute.  There are foot-tapping movement disorders, but I am not convinced that what this fellow reports is one of them. 

help03 - Ensure your iron levels are good

Many people are at risk of low iron levels, particularly menstruating women and people (such as me) who don't eat meat.  There are various oral iron supplements, but you should work with your doctor on this. 

Your doctor can organize a blood test to assess the levels of iron in your blood, and perhaps most importantly the levels of iron stored in your blood in ferritin.  He or she can advise you on the need for supplementation and on the best type to use.  Your doctor will also test whether you have any iron regulation problems.

The body has other storage mechanisms for iron, but ferritin in the blood is the one which is most easily measured.  There is a little iron in solution in the blood plasma, but this is kept to a safe level, since iron ions (iron atoms missing some electrons) in solution are highly reactive and destructive. 

A ferritin molecule is a cage for containing iron atoms bound to other atoms in a way which protects the rest of the body from these highly reactive and potentially destructive atoms.  Details: Compared to the digital nature of DNA, and the subtle chain-based folding of  protein, ferritin strikes me as being like a robust piece of Victorian-era mechanical engineering!

Iron is needed for many functions in the body.  Its importance for RLS/PLMD is that the complex enzyme Tyrosine Hydroxylase (TH) requires an atom of iron in order for its catalytic site to function.  TH catalyzes the conversion of the amino acid Tyrosine into L-DOPA in the output terminal of dopaminergic (dopamine-producing) neurons.  The L-DOPA is converted into dopamine by a second enzyme which never gives any trouble.  Inadequate iron levels will reduce the efficiency of TH, so leading to the reduced dopamine production which is well recognized as a causative factor in RLS/PLMD.

While iron deficiency is a common cause of ill-health, iron poisoning of children who take iron supplements is a leading cause of death.  Please heed the advice in this University of Maryland Medical Center article:

Iron poisoning is the most common accidental poisoning in children. Keep iron supplements in childproof bottles and out of the reach of children.

help04 - Do not drink coffee of any kind, including decaf *

There are many health reasons for avoiding caffeine, including the fact that it disrupts sleep, and causes tiredness, irritability and anxiety.  I also think it stunts creativity, reduces our ability to relax, and drives people to use other harmful drugs, such as alcohol and tobacco, in an effort to calm their anxiety.

It is commonly stated, assumed and understood that caffeine, or excessive caffeine (whatever that might be) contributes to or causes Restless Legs Syndrome.  I don't recall reading any research which supports this assumption, and I have read a lot of RLS research!

Since one of the major impacts of RLS/PLMD is to disrupt sleep, and since caffeine (and alcohol) are commonly used drugs which disrupt sleep, it makes sense to cut down on these or eliminate them, in general, especially if RLS/PLMD is disrupting sleep.

However, if you feel you must use caffeine, I suggest you drink tea instead. (Caffeinated soda drinks and high-caffeine "energy drinks" contain more caffeine and are much less friendly to teeth.) 

Coffee contains opioid receptor antagonists.
  These opioid receptor antagonists are unrelated to caffeine - decaf coffee contains about 5% of the usual amount of caffeine, but the same levels of opioid receptor antagonists.  Please see a separate section of this website concerning this, with links to the peer reviewed journal research papers:


* However, please see the above page which has a note near the start of the likely protective effects of coffee, decaf or not, against both Parkinson's disease and Alzheimer's disease.

These were discovered in 1983 and more recent research has identified the major mu opioid receptor antagonists, which are not present in raw coffee beans but which are created by the breakup of some of the molecules during the roasting process.

These compounds, such as 4-Caffeoyl-1, 5-quinide:

Coffee contains opioid receptor antagonists including 4-Caffeoyl-1,5-quinide - AKA 4-Caffeoylquinide or 4-CQL
are unrelated to caffeine and have a high affinity for opioid receptors.  They occupy opioid receptors but do not active them.  This reduces the number of receptors which are open to being activated by the natural levels of endogenous (produced in our bodies) opioid receptor agonists, such as endorphins and enkephalins.  These are known collectively as "endogenous opioids". 

Normally, the activation of opioid receptors in the spinal cord by these endogenous opioids reduces our sensitivity to pain, and to the reflex reactions which the spinal cord generates to move limbs away from noxious stimuli. (The same spinal cord circuits produce both the pain signals to the brain and the muscle activation signals to withdraw limbs from noxious stimuli.)  Opioid receptor antagonists block these receptors and so make the spinal circuits more sensitive to pain and to creating reflex limb withdrawal motions .  I propose that when RLS/PLMD sufferers are having symptoms, these circuits are become hypersensitive in RLS/PLMD - so any antagonism of these receptors will make symptoms worse.

Tina and one of our RLS/PLMD-suffering friends have found that reducing or eliminating coffee of all kinds significantly reduces the incidence of RLS/PLMD. 

In June 2012 I received a message from a 24 year-old man from the UK who found that both ordinary and decaf coffee seemed to cause RLS/PLMD.  He wrote:

I've suffered (albeit lightly) with RLS during and shortly before sleep after drinking coffee. It's a bad habit of mine and I decided to move onto decaf to solve the problem of my RLS during sleep.

I soon discovered this wasn't the case. I can directly link drinking decaf coffee and RLS during sleep as I've tested it upon many occasions.  Drinking no decaf coffee in the evenings I experienced no RLS for several nights in a row.
Drinking decaf in the evenings even a few hours before sleep I suffer RLS.

The brand of coffee was Nescafe, though I've experienced it with other brands. I'm a 24 year old male, if that helps.

I'm no scientist, nor a doctor. I just wanted to do some quick Googling and found your page

I hope my experiences help or at least add another number to the statistics.

I hope to find more details of his observations, such as his symptoms and what other caffeinated drinks, including coffee, he may be drinking earlier in the day.

I suspect that these opioid receptor antagonists in coffee are also highly likely to disrupt sleep and cause, or worsen, pain disorders such as fibromyalgia.

I would not be surprised if a great deal, perhaps the majority, of the total symptomatology of RLS/PLMD is caused by these opioid receptor antagonists in coffee.  (Though some of the most severe sufferers who have spinal injuries, nutritional disorders or strong genetic predisposition will no-doubt suffer bad symptoms without any coffee or caffeine consumption.)

Vintagelifelover on YouTube has a 2 minute video of her squirming legs. 

"You gotta keep stretching, moving . . . and stretching, your legs . . . Driving you nuts, because something inside makes them want to go.  I fell off the raw food truck . . . I started to drink coffee, eat meat and processed food. What happens?  You feel terrible!   There were cookies this morning, yes there were - Nilla Wafers (link)- and now I can't stop with my silly legs!" 

She blames the unhealthy food - but I think it was the coffee.  Tina and I occasionally have Nilla Wafers sent by a friend from the USA, and there's no sign that they contribute to RLS/PLMD.

Many people drink coffee every day and think it helps them, overall.  I used to think this about tea and coffee.

A few people finding that coffee of any kind makes RLS/PLMS much worse does not establish beyond reasonable doubt that this is the case for all other people.  But it does point to something which is easy to try, and may provide significant benefits for many people.

Anyone reading the above will be able to consider that perhaps coffee, for whatever reasons, is causing them long-term difficulties which they may not have realized, thinking that RLS and other problems, such as tiredness, anxiety etc. are just part of life, or part of getting older.

Caffeine generally perks us up, which would be great if that was all that happens.  But after a few hours the positive effects wear off and we are left more tired for a day or two than if we had not used it.  This might be a good deal if we achieve something great in the few hours and don't have to worry about the impact of the tiredness, anxiety etc.  To call caffeine a "stimulant" is to describe only its short-term effects.

Please see a section below for more details regarding coffee and RLS/PLMD, including the history of coffee and how the RLS sufferers Thomas Willis observed in 1672 may have been coffee drinkers:  #coffee

In March 2015, I mentioned these opioid antagonists and RLS/PLMD in a letter:

Beyond Caffeine: Coffee Contains Opioid Antagonists
Robin Whttle. Journal of Caffeine Research. March 2015, 5(1): 1-2. doi:10.1089/jcr.2014.0024.

See an update to this regarding caffeine and restless legs syndrome: ../briefsumm/#ccc .

help05 - Reduce or ideally eliminate your consumption of caffeine

Caffeine, as found in tea, coffee, soft-drinks / soda-pop and high-caffeine "energy drinks" is an addictive drug which, amongst other things, disrupts sleep.

RLS/PLMD disrupts sleep, and I think caffeine probably contributes to the RLS/PLMD processes, though I am not sure how.

More information below in the #coffee section.  Please remember that decaf coffee contains, very approximately 5% of the caffeine of ordinary coffee, which I think is quite enough to keep people addicted and to disrupt sleep.  But if you feel you must use caffeine, I suggest you avoid coffee of any kind for the reasons noted above.

Perhaps if the caffeine or coffee is drunk just before vigorous exercise, such as a long, fast walk or a bike ride, the ill-effects my be diminished significantly due to the compounds being metabolized and excreted quickly, rather then remaining in the nervous system at high concentrations for many hours or a day or so.  Short-term use of caffeine after not using any for a few days can certainly boost physical endurance and perhaps mental performance for a few hours. 

However, I think that using it continually - as most people do - does not improve mental or physical performance.  One of the ways caffeine interferes with neurons is as an adenosine receptor antagonist.  If humans had better overall performance with less activation of adenosine receptors, evolution would have quickly lead to most or all of us having less sensitive adenosine receptors. 

help06 - Dark chocolate and cocoa seems to worsen or cause RLS/PLMD

This heading should be preceded by "UNFORTUNATELY . . . ". 

Lacking X-ray vision, I can't know for sure how chocolate will affect other people, but Tina and I have recently discovered (October-November 2011) a causal link between dark chocolate - or sufficient quantities of cocoa (including organic raw cacao) - and RLS/PLMD.

Please let me know your experiences with this.

Most people can consume chocolate without getting RLS/PLMD, but if you are predisposed to it for some reason, such as low iron, some inherited genetic factors or whatever, you may find, as we did, that dark chocolate or cocoa increases your chances of having RLS/PLMD.

These effects would diminish with time, in part related to the level of metabolic activity affecting the breakdown and excretion of whatever it is in chocolate which causes the trouble.  I think that having dark chocolate late at night is likely to be more of a problem than having it in the afternoon, or morning.

In early November 2011, we went for a 4km walk in the late afternoon and shared a 100 gram bar of Lindt dark chocolate with roasted almonds.  That night Tina had unusually bad RLS/PLMD.  Without coffee or any other source of caffeine, on days with little or no chocolate, she typically has no symptoms at all.

One night she made two chocolate drinks, each with a "tablespoonful" (actually a desert-spoon) of raw organic cacao powder .  (Cocoa powder is prepared from roasted cacao beans.)  Bad RLS/PLMD followed that evening.  The only other potential contributing factors were salt, but I think that was not enough to explain what happened.  There have been several other occasions on which raw cacao at night was followed by unusually bad RLS/PLMD.

Tina's experience with raw cacao makes me think the RLS/PLMD-increasing effects must be due to something intrinsic to cocoa - not the fats and other things which are added to it to create chocolate.  I assume it is not the same mechanism as the opioid receptor antagonists in coffee, because the 1983 researchers who found these only found them in coffee, not in chocolate or other common foodstuffs they tested.  (See the coffee section of this website for more information: ../coffee/ .)  These opioid receptor antagonists were not in raw coffee beans, but were created by the roasting process breaking up molecules which occur naturally in the beans .  Raw cacao hasn't been roasted, and my impression is that it induces RLS/PLMD symptoms more strongly than the same quantity of cocoa powder.

Cocoa contains some caffeine and a lot more theobromine, which is like a caffeine molecule but with a CH3 group in place of one of the hydrogens.  Theobromine is generally considered to be less disruptive to the central nervous system (the brain, brain-stem and spinal cord) than caffeine.  Maybe there's something else in cocoa and chocolate which is causing this RLS/PLMD trouble.  I would be surprised if this amount of trouble was caused just by chocolate's relatively low caffeine content.

I am much happier without tea, coffee or other forms of caffeine.  I know more than a little dark chocolate will make me anxious and irritable for a day or two afterwards, and will make me tired and perhaps give me a headache if I have quite a lot of it for a day or two and then stop.  However, I like chocolate and think its benefits and pleasures in moderation, or occasional immoderation, outweigh its ill-effects.  I ate a little while writing the Help section, and didn't get RLS/PLMD that night.

I was surprised to find that dark chocolate and cocoa contributes to the RLS/PLMD that Tina and I experience, but that's what we found.  I am becoming more wary of dark chocolate, especially later in the evening.

help07 - Excessive salt seems to worsen or cause RLS/PLMD

Tina and I have repeatedly observed that if we eat salty foods, we are more likely to get some RLS/PLMD symptoms that night.  Pizza, salty corn chips and the like, olives . . . there are quite a few foods and snacks with higher than average levels of salt.  Vegemite (Australia's black axle-grease-like yeast extract spread) is notoriously salty.  I eat the new half-salt version, which is supposedly for children - My First Vegemite.  Tina takes her chances with the original full-salt version.

On 16 November 2011 I ate some salted cashews before going to bed - this was a bad idea.  I had a few foot movements and some vaguely restless feet when trying to get to sleep.  I used the Homedics massager (#help14) on either side of my spine, from my mid-lower back up to my shoulders.  For good measure I took two 500mg tyrosine capsules too (#help13).  That fixed the problem.

Google finds lots of pages mentioning salt and RLS.  I don't know what the mechanisms are but sodium chloride affects blood pressure, kidney function and many other bodily systems, so it would not be surprising if it affected something in the spinal cord, especially to do with circulation or with the transport of amino acids such as tyrosine across cell membranes. The concentrations of sodium and chloride ions inside and outside neurons are primary mechanisms driving their electrical operation. Amino-acid transporter proteins which span the cell membrane are also affected by these concentrations.

help08 - General nutrition, including Magnesium and Calcium:

Avoiding pernicious drugs - tobacco, non-prescription opioids, cocaine, amphatemines, cannabis, etc. is obviously necessary for maintaining good health. 

Alcohol may bring temporary benefits of aiding sleep and perhaps (via some indirect generation of opioid receptor agonists) direct dampening of spinal pain receptor circuitry.  However, it is a carcinogenic (American Cancer Society) depressant (Mayo Clinic) which in the long-term disrupts sleep ( - and it has a long history of causing damage and addiction. 

I used to drink wine etc. like most other people, but when I stopped using caffeine in 2004, I found I generally didn't feel the need to use it to relax - which seems to be the primary attraction of drinking for me and many other people.  I might occasionally be tempted by a little wine or a beer on a really hot day.

Folate ( has many references) deficiency is sometimes linked to RLS, particularly in pregnant women who may also be short of iron.

Restless Legs Syndrome and Sleep Disturbance during Pregnancy: The Role of Folate and Iron
Kathryn A. Lee et al. Journal of Women's Health & Gender-Based Medicine  Volume: 10 Issue 4: July 7, 2004:

Compared with those without complaints of restless legs, those with restless legs had low serum ferritin at preconception and significantly lower folate levels during preconception and at each trimester. In addition, time to sleep onset was significantly delayed and depressed mood was significantly higher in the RLS group. Rather than indicators of iron deficiency anemia (serum ferritin, serum iron, and hemoglobin) or pernicious anemia (vitamin B12), it was reduced serum folate level that was associated with RLS in this sample of pregnant women.

Perhaps most of the folate goes to the developing baby, since it is so vital for the body building itself.  Best to consult your doctor about supplements.  There's plenty of folate in leafy vegetables.  Folate is vital for may other cellular processes.

(Note added 2012-04-08.) There's a hypothesis that high levels of folate in pregnant mothers causes more children to be born with a genetic disposition to autism. .

There's considerable debate about vitamin supplements.  It seems that Vitamin E is no longer well regarded.  It is an anti-oxidant with some possible benefits, but it also disrupts the body's own oxidative processes for getting rid of pathogens and errant cells.  A 2010 open-access paper in the British Medical Journal concerning Vitamin E and stroke: .

The US National Institutes of Health has information Zinc. They state that for most adults, 8mg and 40mg are the daily minimum and maximum allowances, and that vegetarians may need more than the minimum.  Not eating meat (I eat plenty of fish and other seafood), I take a 25mg Zinc tablet each day, because there is only a small amount in the multivitamin tablets we take.  A single Zinc atom is essential to the operation a hundred or so enzymes:

There are numerous benefits of Vitamin D, including reducing the incidence and progression of many forms of cancer.  These benefits are now being recognised, along with the need for higher levels than those previously chosen, which were merely sufficient to prevent the extreme deficiency condition of rickets.  I don't have any evidence for Vitamin D's involvement in RLS/PLMD, but I mention it because many people are deficient in it (according to the standards set by recent research, in part due to people being careful not to expose their skin to the sun), because it affects many systems within the body, and because RLS/PLMD symptoms are evidently affected by many aspects of the body's functioning.

The Vitamin D Council has guidance on dosage and having a doctor organize a blood test.  They recommend at least "5,000 IU" for adults.  This may sound like a lot, but "1,000" IU of Vitamin D3 is 25 micrograms: 1/40,000 of a gram.  If we took 5,000 IU this for 80 years, it would total 3.65 grams, which is a not-too-heaped teaspoon full.

Many countries still officially adhere to much smaller minimum and maximum doses which are out of step with recent research.  In Australia, the biggest Vitamin D3 tablet which can be sold is 2,000 IU.  Tina and I buy small 50,000 IU capsules from the USA:
which is less expensive and more convenient than using several locally available 2,000 IU tablets a day, since we only need one every ten days or so. ProHealth ( sell 50,000 and 25,000 IU capsules.  A continually updated compendium of Vitamin D information is: .

I understand that a great deal of research indicates that the Omega 3 fatty acids are very important for physical and mental health.  We take the equivalent of four 1 gram fish oil capsules a day (two double-strength capsules: Nature's Way and Swisse) and eat plenty of fish and other seafood. 

Some people find that their RLS problems are reduced or resolved by taking Magnesium supplements.  Magnesium and Calcium are generally taken together, and I understand that proper levels of Vitamin D are essential for metabolizing Calcium.  A number of US manufacturers produce "Cal Mag Citrate" tablets, for instance: .  I haven't researched the arguments for the various forms of Calcium and Magnesium supplementation.  I understand that these supplements and sufficient Vitamin D are well regarded in terms of reducing the risk of osteoporosis, but the quantities of Vitamin D in these tablets may be much lower than the Vitamin D Council recommended daily intake.  This analysis and summary of various documents: includes material on low levels of magnesium being common in the USA, and that these may impact Vitamin D metabolism. 

Further thoughts on nutrition and light exposure to avoid seasonal affective disorder are on another page: ../coffee/#proper  Light exposure in the morning helps synchronize the circadian rhythm, which is important for being alert during the day and falling asleep without trouble in the evening.

I understand that the sugar addiction work of Kathleen DesMaisons in New Mexico is highly regarded by many people who have tried it.  I read the first five chapters of the 2008 edition of her memorably named 1998 bestseller Potatoes not Prozac. (Amazon link)  She cites the work of Elliot Blass (Google Scholar search) who researched the pain-reducing activation of opioid receptors in rats due to ingestion of sucrose increasing the production of beta endorphins.  (Interactions between sucrose, pain and isolation distress, 1987 PubMed abstract.)  These are the same mu opioid receptors which are antagonized by compounds in coffee. 

Some more recent research supports the concept of sugar addiction, such as this freely available, extensively referenced, 2007 paper: Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake,  NM Aveda, 2008 PubMed abstract and full article. "The evidence supports the hypothesis that under certain circumstances rats can become sugar dependent. This may translate to some human conditions as suggested by the literature on eating disorders and obesity."

In #help12 suggest a high-protein snack before bed may help reduce RLS/PLMD symptoms, but this is contrary to Kathleen DesMaisons' advice to avoid protein, and instead to consume complex carbohydrates, such as a potato. 

help09 - Avoiding drugs which worsen the condition

In addition to caffeine, there are a variety of prescription and non-prescription drugs which may worsen RLS/PLMD symptoms. 

Various SSRIs (Selective Serotonin Re-uptake Inhibitor) and other antidepressant drugs are reputed to worsen symptoms.  Drugs may have different effects on different people, and it is possible that some prescription and non-prescription drugs may reduce the symptoms, at least for some people.

One drug I suggest all sufferers steer well clear of is Phenergan.  The chemical name is Promethazine and the drug is sold under a variety of brand names, and as an antihistamine in cough syrups.

Amongst other effects, Promethazine is a dopamine antagonist: it occupies dopamine receptors but does not activate them.  This occupation prevents those receptors from being occupied and activated by dopamine itself, or by drugs which also occupy and activate the receptor (dopamine receptor agonists, such as those frequently used to treat RLS/PLMD).

Phenergan is a CNS (Central Nervous System) depressant, which is intended to make people drowsy.  I understand some parents give it to their children to calm them down . . . which sounds horrible to me.  (Maybe the children are acting up because they are fed Coca Cola, Pepsi and excessive sugar and chocolate.)

Tina once took some to help her sleep on the 14 hour flight from Sydney to Los Angeles.  Not only did it make her less sleepy, it set her RLS/PLMD symptoms on fire for the next two days.  In the Yahoo Groups RLS Support forum (linked to above #intro) on 2011-11-11 (message 53522), there is a report of an injection containing Phenergan leading to pacing all night with RLS.

I won't try to develop a list of medications to avoid.  Please refer to the  Word file RLS Medical Alert Card at which is compiled by  RLS-specialist  Mark J. Buchfuhrer M.D .  This lists dozens of drugs to avoid, with alternatives which cause fewer problems.  (If you don't have Microsoft Word, you can save the file and upload it to - which will convert and display it in your browser.)

The 2010 RLS Medical Bulletin (see #rlsorgpubs above) mentions some medications to avoid (pages 4 and 5), but this is not as extensive as the RLS Medical Alert Card.

Medications are, ideally, prescribed or suggested for good medical reasons.  So any decision not to take such medications should be taken in consultation with your doctor or nurse.

help10 - Sleeping position and keeping warm

RLS/PLMD sufferers have probably figured out the sleeping positions which worsen or reduce their symptoms.  Tina and I generally find that lying on our backs worsens symptoms. 

There's a fascinating chapter (12 Appropriate/Inappropriate Developed Pain Paths) in the  2009 book "The Science of Pain" (see #ownresearch below), which I think is the best reference on spinal nociceptive (pain perception and reflex generation) circuitry.  The author of this chapter, Jens Schouenborg (website) describes how the spinal circuitry for a particular function (in the case of RLS/PLMD, the foot-withdrawal reflex action and pain perception in the dole of the foot) is initially driven by inputs from sensory neurons all over the body.  A pruning process occurs in-utero or shortly after birth, which would ideally remove all the inputs apart from those in the particular area of the body which matters.

I propose that these pruning arrangements are imperfect and that different individuals may have their foot-arch spinal cord circuitry also driven by sensory neurons from other parts of the body.  This is the best explanation I can give for the observations I am about to relate.

We have recently discovered some surprising things regarding sleep position and coolness.  I have no idea to what extent this applies to other people - please let me know your thoughts and experiences: ../contact/ .

At first I thought that the RLS/PLMD-increasing effects we observe of sleeping on our backs could be due to pressure on the lower back reducing circulation in the spinal cord.  However, I think the effects of lying on our backs or on our sides are too immediate for this to be the primary mechanism.  Also one of our RLS/PLMD-suffering friends finds that her symptoms get worse if she sleeps on her back. 

I now think a more likely explanation is that sensory neurons in the skin or flesh of the back are driving the foot-arch spinal circuitry, due to some imperfect pruning of neuron axons (output terminals) during the development of the nervous system, before or shortly after birth.  So lying on our back adds input to these circuits, making them more prone to being triggered by (what I hypothesize is) the low level of random depolarizations (firing) of sensory neurons from the skin of the foot arch, even when nothing is touching the skin there.

Several chapters in "The Science of Pain" note that it is not just noxious stimuli, such as acute puncturing pressure or heat, which stimulates the spinal nociceptive circuits.  Coldness or even coolness on some areas of skin can stimulate them as well.

If we consider this in combination with a possibly imperfectly pruned set of input sensors for the foot-arch protective section of the spinal cord, then the following observations we have made are more understandable:

help11 - Unusually high or low levels of exercise

I don't have a specific reference, but I recall multiple instances in the RLS literature and forum discussion of researchers and sufferers observing a complex relationship between exercise and symptoms.  Generally, I think, the view is that some exercise reduces symptoms but too much makes the symptoms worse.

One one or two occasions we have observed a high level of exercise apparently contributing to RLS/PLMD symptoms that night.  An explanation can be found if we consider that a shortage of tyrosine will reduce the ability of the spinal cord to make dopamine, especially (or perhaps only, depending on how deficient the blood tyrosine levels are) when only some of the Tyrosine Hydroxylase enzyme molecules are working due to a shortage of iron.

When we eat protein, it is broken down into its constituent amino acids by enzymes in the intestine.  The individual amino acid molecules are transported into the bloodstream.  Tyrosine is one of the larger amino acids.  Different food proteins have different amino acid compositions.  The amino acids are transported around the body in the blood and can be assembled (by huge enzymes called ribosomes, according to genetic instructions in messenger RNA) into new proteins.  Some amino acids are also used as precursors for neurotransmitters.  Tyrosine is a precursor for dopamine, noradrenaline and adrenaline (AKA norepinephrine and epinephrine).  Another large neutral amino acid, tryptophan, is the precursor for the neurotransmitter serotonin.

If we have an unusually high level of exercise during the day, I would expect the body to be synthesizing more protein to repair damaged muscles and perhaps tendons during the night and perhaps for the next few days - and also to make them bigger and stronger in readiness for any exercise of this type in the future.

It is not hard to imagine this increased level of protein synthesis reducing the levels of tyrosine in the blood, so leading to reduced levels in the Cerebro-Spinal Fluid in the spinal cord, and so to reduced levels in the dopaminergic output terminals where tyrosine is needed to produce dopamine.  (These "dopaminergic output terminals" are  parts of the dopamine-producing neurons which release dopamine to reduce the sensitivity of the soft-touch foot arch reflexes.  Dopamine must be produced in these output terminals on a continual basis.)  This lack of tyrosine my reduce the dopamine production in these output terminals to the point where they release so little dopamine that it causes, or contributes to the RLS/PLMD symptoms by failing to sufficiently inhibit the soft-touch foot arch reflex.

Having too little exercise may constitute "prolonged physical inactivity" - so during the day the descending dopaminergic output terminals, which inhibit the foot withdrawal reflex, are depleting their narrow region of the spinal cord, due to there being insufficient physical agitation of the cerebro-spinal fluid.  This would apply to many elderly and unwell people, especially anyone confined to bed, or to a wheelchair.

Also, perhaps excessive inactivity during the day, with consistently low heart rate and blood flow, may allow fatty deposits to build up, blocking the capillaries in the spinal cord where the blood exchanges its nutrients with the cerebro-spinal fluid.  This would reduce the amount of tyrosine which could be delivered by the blood capillaries to the Cerebro Spinal Fluid in the spinal cord.

Our bodies are optimized for operation with exercise every day, so it is not surprising if things go wrong if we don't get out and walk a kilometer or two most days.

help12 - Protein meals and snacks

Tina and I have observed a greater incidence of RLS/PLMD symptoms if we had a low-protein evening meal, or the meal was many hours in the past.  This would reduce the levels of tyrosine in the blood.  Our biggest fish meals are typically Tasmanian salmon, and we have observed less RLS/PLMD symptoms on the night of such meals.  The high protein (and therefore tyrosine) content of the fish is a likely explanation.  However, perhaps there are other factors at work, including the large amount of fish oil.

This points to a simple method of combating RLS/PLMD: high-protein snacks late at night.  Nuts, maybe cheese, or whatever might be helpful.  However, I suggest avoiding foods which are too salty or hard to digest.  There are various protein powders produced for body-builders and other people keen to improve their muscle strength.  Many of these are based on whey protein, but soy, peas and rice protein powders are also available.  Some of these list the amount of tyrosine and other amino acids which are contained in a single serve.

We often read in bed for a while and an a few occasions Tina has requested scrambled eggs in bed.  On the nights I served her this, she had no RLS/PLMD symptoms.

I understand that tyrosine can also be synthesized in the liver, from another similar amino acid: phenylalanine.  So perhaps foods with high levels of these amino acids would be helpful. 

While I believe this principle of high protein evening meals and late-night snacks reducing RLS/PLMD symptoms has a good theoretical basis and may well be useful for some people, this is at odds with the principle of avoiding high protein meals late at night, because of the time they take to digest and the negative impact this can have on sleep. 

The next suggestion - taking tyrosine capsules or tablets before bed, or during the night if symptoms occur - directly targets the tyrosine depletion problem without involving proteins or any significant digestive effort. 

help13 - Tyrosine capsules or tablets

The previous section suggested tackling the tyrosine depletion problem by eating proteins, which are broken down into their constituent amino acids, one of which is tyrosine.  However, high protein snacks can disrupt sleep.

An alternative, more direct, approach to the problem is to take tyrosine capsules or tablets before bed, or during the night if symptoms occur, with half a glass of water. 

There is no digestion required, since there are no proteins to be broken down.  The tyrosine goes straight into the bloodstream within minutes.  We have never noticed any excitatory or sleep-disturbing effects after ingesting tyrosine.  However, this approach has not been properly researched, and it is possible that some people may have an adverse reaction to it.

Tyrosine can reduce the symptoms of RLS - Restless Legs Syndrome
500mg Tyrosine capsules or tablets are readily available in health-food shops in Australia.  As far as I know, they are a non-prescription nutritional supplement in all countries.  The US chain GNC sells 500mg and 1000mg Tyrosine capsules or tablets.  GNC stores are in many Australian shopping malls, and Nutralife tyrosine capsules are available in many healthfood shops.  Walmart in the USA carries the Twinlab tyrosine capsules:

Tyrosine powder can also be purchased, for 10 cents a gram or less. 

The formal name for the compound is Levo-Tyrosine (L-Tyrosine) meaning the left-hand stereoisomer of the molecule.  Living things use the left-hand version of tyrosine and other amino-acids..

We discovered very quickly in 2004 that taking one, two or three tablets (0.5 to 1.5 grams) would reduce or eliminate RLS/PLMD symptoms, typically for a few hours - unless the symptoms were particularly severe (as was sometimes the case then, primarily due to coffee and/or low iron levels).  Other people have discovered the benefits of oral tyrosine - for instance from 2002:

l-tyrosine is solving my restless legs.   I just wanted to get a message to other sufferers.

I have been suffering from RLS for over 20 years and have tried all sorts of cures with no release. Recently I found some info regarding a natural amino acid called L-tyrosine which I have been trying with great success for the past months.

It is truly amazing to stumble upon the answer. Perhaps other RLS sufferers can find similar relief.

to which Dr Buchfuhrer replied:

Various natural remedies such as L-tyrosine seem to help a small minority of RLS sufferers, but we will put your information on our web site to see if others may benefit.

As far as I know, no-one has formally researched the use of tyrosine regarding RLS/PLMD.  As far as I know, it would only be helpful to take it at the time the symptoms occurred, rather than taking it during the day in the hope of cutting down symptoms at night.  I imagine that most people who used 500, 1000 or 1500mg of tyrosine at the time of the symptoms would found it helpful - but without more reports from people who try this, there's no way of knowing.

I searched the archives of the RLS Support Yahoo Group (see #forums above) for "tyrosine", which was mentioned as early as 1999 (msg 4756).  One message from late 2000 (15054) reports success using tyrosine to treat RLS with the effects being apparent within minutes.

Around 2001 it appears some people were trying it, perhaps based on a recommendation for tyrosine for depression in a 2001 book by Gabriel Cousens "Depression Free for Life".  I haven't seen a copy of this, but on (2011-11-20) I found an apparent paraphrase of part of the book here .

If your mild depression and anxiety symptoms during menopause are related to tyrosine or dopamine imbalance, you may experience relief in as little as two days, says Cousens.

Some people on the RLS Support forum reported trying tyrosine without success, but they didn't report their dosage or when they were taking it.  Perhaps some  people were taking it during the day, expecting an overall longer-term positive impact.  My understanding is that oral tyrosine helps reduce RLS/PLMD symptoms for a few hours, and so needs to be taken when RLS/PLMD symptoms are active or likely to become active.  In some other messages, such as 15559, there are reports of tyrosine being helpful, such as with one 500mg tablet before bed, another during the night and another after waking up.

In 2004 I couldn't find any safety warnings about oral tyrosine, so I took ten (5 grams) with a glass of water, and didn't notice any effects.  A paper from 1980

Tyrosine for the Treatment of Depression
American Journal of Psychiatry May 1980, 137:5 pages 622-623
Gelenberg, A.J., Wojcik, J.D., Growdon, J.H., Sved, A.F., and Wurtman, R.J.. Tyrosine for the Treatment of Depression ...

describes researchers giving a 60kg woman 6 grams (6,000mg) of tyrosine a day.  This simple treatment consistently resolved her severe unipolar depression.

On 2011-11-20 I found an excellent resource on the use of tyrosine supplements for neurological conditions:

This is Chapter 21 of the 2005 book "Nutritional Neuroscience"  (Amazon link).  The chapter is written by Jan Berend Deijen, of University of Amsterdam  (his page)

The chapter concludes:

Amino acids used as dietary supplements can interact with prescription drugs such as monoamine oxidase inhibitors and other antidepressants, sympathomimetic amines, and opioids (Food and Drug Administration, 1992).

I also understand that tyrosine supplements may interfere with the absorption of L-DOPA (Levodopa AKA Sinemet), and that they should not be taken by anyone with hyperthyroidism - an over-active thyroid gland.  Tyrosine is commonly recommended as a supplement for those with hypothyroidism (an underactive thyroid gland).  Tyrosine supplements are not suitable for anyone with one of the  relatively rare disorders known as Tyrosinemia.

This chapter states that tyrosine supplementation should not be considered for pregnant women, babies or children.  Also from this chapter:

The usual daily L-tyrosine intake from the diet is about 2.2 g for an individual consuming 100 g protein per day. In one study in which the extremely high dose of 500 mg/kg body weight (35 g for a 70-kg individual) was given, no side effects were reported.  Thus, from the information of one subject, L-tyrosine given  at ca. 15 times the
daily intake does not seem to induce side effects.  However, as noted previously, the occurrence of more severe effects of high doses of L-tyrosine is found in animals receiving low-protein diets.  Therefore, humans with low intakes of protein may be more susceptible to possible adverse effects of chronic consumption of L-tyrosine as a dietary supplement.

Most of the tyrosine supplementation trials this chapter mentions use daily doses - either divided or as a single dose - of 100mg/kg body weight.  So for a 70 kg (154lb) person, this is 7 grams - the equivalent of 14 500mg tablets or capsules.

It is also possible to buy "N-acetyl-tyrosine" supplements.  This has less actual tyrosine per milligram, but is much more soluble in water.  This chapter states that ordinary tyrosine (L-tyrosine) has very limited solubility in water:  435mg per liter (four cups) at 25C (room temperature).  The research studies mentioned in this chapter used ordinary tyrosine (L-tyrosine), not N-acetyl-tyrosine.

So as far as I know, two or three 500mg tyrosine tablets with a glass of water should be generally safe for most healthy adults - but not for children, pregnant women, or anyone whose health is frail or who has hyperthyroidism.  I suspect it is probably safe to do this two or even three times a night.  However, I am not a doctor and I can't advise on the real safety of this, or of any other drug or nutritional supplement.

We find that 2 or 3 capsules is very helpful in reducing or eliminating RLS/PLMD symptoms.  This can be combined with percussive massage, as described below, with the two methods helping each other. 

We find that the tyrosine's effects take five to ten minutes to start and are probably fully established after 20 minutes or so.

This chapter also mentions research which indicates that high levels of tyrosine in the blood plasma are limited by an upregulation (increased production or activation) in the liver enzyme tyrosine aminotransferase (TAT), which breaks it down.

It would be great if someone created a sustained release tyrosine capsule, to release tyrosine into the intestine, and so the blood, over a period such as 6 to 8 hours.  This would provide a sustained supply of tyrosine all night long.  I suspect that only a small amount is needed per hour, and that taking a gram or so results in a sharp peak in the concentration, which diminishes rapidly, such as within two hours or so.

I think that taking one or two capsules in the event that RLS/PLMD symptoms wakes the sufferer up may be quite a useful and sustainable approach, with each such capsule providing an hour or two's respite.

While we find oral tyrosine and percussive massage very effective, I am not suggesting them in place of any of the foregoing techniques.  This is why percussive massage and tyrosine supplements are near the end of this list.  While I think they are likely to be effective and safe for most people, it will generally be better to avoid direct causes of the problem, such low iron or opioid receptor antagonists on coffee, than to continue with such unhealthy arrangements and then try to cope with their impact with tyrosine and percussive massage. 

I hope that by following the suggestions on this list that people will be able to generally eliminate their symptoms or at least reduce them to a level which is manageable with tyrosine and percussive massage (assuming this is actually safe, which I can't say for sure) - rather than having to use prescription medications such as dopamine agonists and opioids.

However, Tina and I are not entirely rigid about the above suggestions, since we sometimes eat salty meals or enough dark chocolate to put us at risk of RLS/PLMD symptoms. 

help14 - Percussive massage

First, a caution:

I cannot assure you that it is safe to use percussive massage on anyone, especially with a motorized massager.  While these devices are widely used, and may be safe for many people, please make your own well-informed decisions about how safe this would be for you, such as by checking first with your doctor or nurse.

In particular I caution against percussive massage for children, the elderly or infirm, anyone with a back weakness or injury - and pregnant women.

If you have symptoms in the legs, try performing percussive massage on your mid-lower back, about level with your navel.

Use your fists or a motorized massager to pummel either side of this part of your spine for a minute or so.  Don't pummel or press against the bony protrusions of the spine itself - just the ribs and muscles on either side.  This is only for fit and healthy adults, not for children, pregnant women, the elderly or anyone with back problems.  I can't assure you that percussive massage is safe for you - you or your doctor need to decide whether it is or not. 

We find that doing so reduces or eliminates RLS/PLMD symptoms in the legs, within seconds or a minute or so.  We find that the benefits typically last for hours.  I argue that this is most likely due to the vibration causing renewed diffusion of tyrosine-rich Cerebro Spinal Fluid into the presumably narrow zone where the descending dopaminergic output terminals have, over the previous hours, depleted most of the tyrosine.  Within a minute or two, these output terminals produce more dopamine, typically enough to reduce or eliminate the disinhibition of the soft-touch foot arch sensitive circuits, which gave rise to RLS/PLMD symptoms.

If you have symptoms in the upper body (arms) as well, have someone give you similar percussive massage around your upper spine - below your neck and between your shoulder blades.  As with the lower back, this needs to be pretty firm to shake the body around a bit.  However, it should not be so hard as to be painful.  Don't pummel or press against the bony protrusions of the spine itself - just the ribs and muscles on either side.  I suggest lying face down with your arms lifted forward, so the neck, upper spinal area and mid spinal area can be massaged without hitting the shoulder blades.

Tina no longer gets symptoms in the upper body - she only got symptoms this bad when drinking coffee.  (I suspect several teaspoons of raw cacao just before bedtime might be enough to induce symptoms so strongly that her arms would be affected.)  When she did have RLS sensations and PLMD movements in her hands and arms, we found that this massage of the upper spine would reduce or eliminate symptoms in the hands and arms, but not the feet and legs.  We found that percussive massage of the lower spine (around the level of the navel) would reduce or eliminate symptoms in the feet and legs but not the hands and arms.  I am confident that the same observations could be made with any RLS/PLMD sufferer whose symptoms affect both arms and legs.  Any successful etiological hypothesis needs to explain these observations.

In November 2011, we have two friends who reduce or prevent their RLS/PLMD symptoms by using their own fists on their lower backs.  These women are in their fifties and sixties and are in good general health.  You may find this technique helpful, but I can't assure anyone that percussive massage anywhere on the body is safe. Please consult your doctor if you have any doubts about the safety of percussive massage.  A forum post in which a husband does karate-chop-style percussive massage on his wife's lower back is here:  Ginny from Tampa (2011-09-12) at: (We have not yet tried her idea of menthol cream on the lower back.  See the help subsection above on sleep position and coolness of the skin.)

The most likely explanation for the dramatic and localized effectiveness of percussive massage vibrating the spinal region is that it quickly diffuses tyrosine-rich Cerebro Spinal Fluid into the tyrosine-depleted region.  However, this massage may also improve circulation in general, which would help the blood capillaries deliver more tyrosine in the hours which follow.

If you decide that this is safe for you, you may like to try it and let me know what transpires.  ../contact/.

For any extensive or regular such massage, I suggest using a motorized massager with care, if only to avoid Repetitive Strain Injury RSI in the wrists and arms of the person who would otherwise be doing it manually.  However, the massager body vibrates, so if you use it a lot, watch out for the vibration affecting sensitive hands and wrists.

We have been happily using this "PA MA" Homedics model since 2005, illustrated below.  In early 2012 I found the exact same model at a Shaver Shop in a nearby shopping mall, though it is not at their website.  We use the rubber domes, rather than the hard plastic ones.  This model has two speeds and heaters, but the heaters are only for particular hard plastic plastic domes. 

Homedics motorized percussive massager we find helpful for Restless Legs Syndrome (RLS)

The domes are 84mm (3.3") apart. At high speed they vibrate at 45 to 48 Hz with a displacement of about 3.3mm (1/8"). The domes alternate in their movement.  This is ideal for straddling the spine and strongly vibrating the ribs and muscles on either side of the spine.

Around 2004 Homedics used to make a massager like this where the business end was in the middle of a large, wide, "U" shaped handle.  It seemed purpose-built for a person to hold it behind their waist, so the rubber knobs could percussively massage their mid-lower spinal region.  I can't find any such product now.

The above approaches to percussive massage - of the upper spinal and lower-mid spinal regions - make sense to me in terms of physically agitating the spinal cord to redistribute the Cerebro Spinal Fluid, replenishing small parts of the spinal cord where the tyrosine has been largely depleted by pushing in fresh fluid from a few millimetres away.  This is a very direct method of reversing the lack of vibration and general physical agitation which results from the "periods of inactivity" which tend to cause or contribute to the occurrence of RLS/PLMD symptoms.

(Added 2012-05-12.)  Here is an extended form of percussive massage - in addition to massaging the areas close to the upper and lower spine as just described.  I call this a Comprehensive Percussive Massage, although it doesn't concern the front of the body, the hands, lower arms or the head. 

We find this even more effective at combating RLS/PLMD than just massaging the upper and lower spinal areas as described above. 

I think this Comprehensive Percussive Massage must help by other mechanisms than redistributing tyrosine-rich Cerebro Spinal Fluid in particular parts of the spinal cord.  Perhaps it works by generally increasing circulation - but it does not seem to increase Tina's heart rate.  Perhaps it releases endorphins (and other related substances): the body's own (endogenous) opioid receptor agonists. These would activate opioid receptors, making sleep more likely and reducing the sensitivity of all the spinal cord's nociceptive (pain sensing) neurons, including those which drive the soft-touch foot arch (and palm of the hand) foot (and hand) withdrawal reflexes. 

Perhaps it released endocannabinoids, which are now widely believed to be the mechanism behind "runner's high", which was previously believed to result from release of endorphins in response to the pain of over-exercise.  Perhaps this form of massage works by other mechanisms which are not yet understood.

I can't say for sure that this Comprehensive Percussive Massage of most of the body will help anyone get to sleep or overcome RLS/PLMD.  Nor can I advise whether it is safe for anyone.  However we find it very helpful.  Here is how I do it, using the above-illustrated motorized massager.
  1. I start by using the massager on either side of the mid-lower spine, not touching the bony spines of the spine itself which are very close to the skin.  One ball of the massager is to the left of the spine and the other to the right.  I begin at about the level of the navel.  I press quite firmly, such as with a force equivalent to 3 to 5 kilograms (7 to 13 pounds).  The instantaneous pressure of the percussive massage would be greater than this.  This is quite a lot of force, and it is on the borderline of being uncomfortable.  I want to shake the muscles and bones in this area to shake up the spinal cord, which is fully enclosed by the spine itself.  I press in one pair of spots for five to ten seconds, and then move up or down to a different pair of spots, in a zone about 15 cm (6 inches) top to bottom.  I do this for 60 to 90 seconds.  This action alone will be quite effective at reducing RLS/PLMD symptoms in Tina's feet and legs, or on the rare occasions when I have symptoms in my feet.  I do not attempt to move the massager across the skin when I am pressing so hard.  While using the massager on her lower back with my right hand, I usually smoothly rub Tina's neck and shoulders with my left hand.

  2. I then move to the upper spinal region at the base of the neck.  I press quite gently here, moving slowly left and right, and up and down.  I press more firmly on either side of the spine at the top of the shoulders, but probably only 2 kg or less.  I want to shake up this area as well, just as for the mid-lower spine.  I do this for 60 to 90 seconds too.  I use my right hand for the massager, which leaves my left hand free to smoothly but firmly rub her lower spinal area.  The following steps are the "comprehensive" extension to this basic percussive massage. 

  3. Next, I move the massager gently from the upper shoulders area, down the mid-spinal area towards the mid-lower spinal area of step 1.  I press gently and move the massager in a slightly circular fashion as I move it downwards.  I work on this area for a minute or two, quite gently.  I speculate that this improves general circulation in the lower spinal cord.

  4. For a second time I work on the mid-lower spine, as for step 1, with firm pressure, for a minute or so.

  5. Now I work on the upper arms.  The two-ball massager is not a good match for this part of the body.  I press gently and keep the massager moving smoothly, from the shoulder end of the upper arm towards the elbow.  I work on one arm and then the other, avoiding all bony parts.  This is purely massaging the muscle - I am not attempting to vibrate any bones.  I don't know why vibrating the muscle helps, but we find that all these steps seem to help Tina sleep and avoid RLS/PLMD symptoms, typically for quite a few hours.

  6. Next I work on the back and sides of the rib cage in the mid back.  I usually start by moving the massager very lightly over the shoulder blades.  Then I press reasonably firmly on the left side of the spine, below the shoulder blades and down to the bottom of the rib cage.  I move the massager outwards and down the side of the rib cage.  This is really massaging the muscles in this area, rather than trying to shake up the ribs themselves.  When Tina's RLS/PLMD symptoms were really bad, this part of the massage would invariably be accompanied by a lot of involuntary kicking!  As far as I can tell, there was no correlation between which side I was massaging - both legs kicked about as much.  This was a perplexing experience for Tina, but she found it helpful.  It is almost as if I am chasing the heebie-jeebies out of her body with this part of the massage.  The degree of kicking was always in direct proportion to the severity of her symptoms before the massage began. The kicking did not resemble the foot withdrawal reflex motion. After a few minutes of this, the kicking would subside.  I do this for a minute or so for each half of the back, though when her symptoms were so strong as to elicit kicking, I would spend more time on this part of the massage - until the kicking subsided.

  7. I return briefly to the mid-lower spine and then work on the waist and the upper parts of the hips.  I press quite firmly and move the massager in various ways, reaching around to the sides of her body.

  8. Next I massage her bottom and thighs.  Firm pressure and constant movement is the technique here.  I am careful not to get to close to the tendons behind the knees.  This may take several minutes.

  9. Likewise I massage her calves for a minute or so.

  10. Before massaging her feet, I return for a final firm session with her mid-lower back.  I may also revisit her neck and shoulder area.  Finally, I massage the bottom of her feet.  This is tricky with the two-ball massager.  I press moderately on the heels, the arch, the ball and the toes.  This takes a few minutes for both feet, and it seems to be well worth spending some time here.  Finally, I turn off the massager and smoothly massage her calves, feet and each individual toe, two toes at a time.
This takes 10 or 15 minutes.  Typically, just before the massage, Tina would have taken two or so 500mg tyrosine tablets with half a glass of water. 

We find this combination very effective at repelling the RLS monster and helping her sleep, with the benefits lasting for two or more hours. 

It seems that once she gets enough sleep, perhaps getting enough REM sleep (which only tends to happen later in the evening once the body's needs for non-REM sleep are satisfied) that this somehow reduces the RLS/PLMD mechanisms for the rest of our time in bed.  So if the RLS/PLMD symptoms flare up at 3AM, two tyrosine capsules and a Comprehensive Full Body Massage will frequently solve the problem for the rest of the night.

help15 - Other factors and techniques

As some people have written on RLS forums, we observe that the menstrual cycle affects the likelihood and severity of RLS/PLMD symptoms.  Trying to research this rigorously would involve controlling all other factors.  I think this would be unethical to the woman involved and hazardous for the experimenter - who would need to stand between his or her premenstrual experimental subject and the chocolate stash!

Suffice to say that:
  1. The spinal circuitry can be affected by many aspects of the body's operation, including the circulatory system and levels of tyrosine and other amino acids in the blood.

  2. The menstrual cycle affects and is affected by many bodily systems.

  3. It may take only a moderate and otherwise unnoticeable change in one or more bodily systems to make the difference between no RLS/PLMD symptoms and mild symptoms, or between mild symptoms and more severe symptoms.

  4. Many women towards the end of their menstrual cycle (and perhaps just after ovulation) typically crave chocolate - and we find that chocolate can drive RLS/PLMD symptoms.
No doubt menopause has its effects as well. 

Some sufferers have devised exercises which they find reduce or prevent their symptoms for a significant period of time.  This is quite different from simply walking, or rubbing the soles of the feet - which brings temporary relief for a few minutes at most.

One fellow did intense push-ups.  This would have raised his heart-rate and probably given his lower back a work-out - both of which might increase he distribution of tyrosine to the dopaminergic output terminals in the lower spinal cord.

Other people discovered inverted bicycling helped - hoisting yourself up on shoulders and elbows, legs in the air, and then moving them as if pedaling a push-bike.  This would be a great way of shaking up the cerebro-spinal fluid in the spinal cord.

However, this is not the sort of thing most people want to be doing - or be capable of doing - before going to bed.


It is best to avoid coffee, including decaf coffee

Further to the sections #help04 and #help05 above, please see another section of this website, which is not related to RLS/PLMD, but concerns the opioid receptor antagonists in coffee:


This links to all the research papers.  As of 2018-11-06 it also contains a note pointing to research which indicates that coffee, decaf or not, is likely to be protective against both Parkinsons disease and Alzheimer's disease, which would constitute a good argument for drinking it regularly.
2011-10-20 update on coffee:

A friend of ours also found that reducing her coffee consumption resulted in a significant decrease in her RLS symptoms.  She was suffering RLS about every third evening, sometimes in the evening when sitting still, and also when going to bed or during the night.  She has been using percussive massage on either side of her lower-mid spine (with her own fists) with considerable success.  This would reduce or eliminate the RLS/PLMD symptoms for hours or for the rest of the night

She was drinking one not-too-strong plunger coffee in the morning, with one or two not-too-strong instant coffees later in they day.  She also typically had an espresso coffee when she went out, such as once or twice a week.

In the last few weeks she stopped having these coffees at home and drank tea instead.  She still has one or two coffees a week when she and her husband go out.  She reports that this has significantly reduced the incidence of RLS/PLMD symptoms.

The history of coffee in England - and Thomas Willis' observations of RLS/PLMD and on the effects of coffee

Sir Thomas Willis (Wikipedia page) is regarded as the father of clinical neuroscience.  He wrote, in 1672 (English translation from the original Latin) what is now regarded as the earliest known description of Restless Legs Syndrome.  The following text, or some version of it with different spellings and typos, is widely quoted:

wherefore to some, when being a Bed they betake themselves to sleep, presently in the Arms and Legg Leapings and Contractions of the Tendons, and so great a Restlessness and Tossings of their Members ensue, that the diseased are no more able to sleep, than if they were in a Place of the greatest Torture.

This is my transcription from The London Practice of Physick, Thomas Willis  which can be viewed for free by anyone with a Google Account, at:

Google digitized this copy from the University of Madrid on 1 October 2010.  A fuller quote appears below.

According to this history of coffee:

"In the UK, the first coffee house opened in 1650 in Oxford.  The
first London coffee house opened in 1652 in St Michael’s Alley,
Cornhill.  Lloyds of London was originally a Coffee Shop called
“Edward Lloyds Coffee House”.  London coffee houses were
nicknamed “Penny Universities” because for the price of a cup of
coffee you could sit and join in the stimulating conversation with
the great thinkers of the day.  Jonathon’s Coffee House in Change
Alley was frequented by entrepreneurs and merchant venturers,
and was the beginning of the London Stock Exchange. By 1675
there were nearly 3,000 coffee houses in England."

The page states that the population of England was about 4 million in 1600 and about 5.5 million in 1700.  Interpolating these figures gives a population of 5.125 million in 1675.  If there were in fact 3000 coffee houses, that would be one for every 1708 people.

So it seems that the unfortunate, "tortured", RLS sufferers Willis observed in 1672 could have been coffee drinkers.  Below I quote Willis writing on coffee, from the same volume.

In the 2006 book Restless Legs Syndrome by Mark J. Buchfuhrer, Wayne A. Hening and Clete A. Kushida. (Google books link.) the authors (p14) state that Cicero (106BC - 43BC) had the disorder.  They also mention as potential RLS sufferers an earlier and un-named Indian sage, and that French writer Michel de Montaigne (1533 - 1592) wrote about the restlessness of his legs. 

Robert Yoakum's 2006 book of the same name (Amazon Kindle version with part of the first chapter link) has an English translation of the text from Montaigne's final essay Of Experience, (1587 to 1588, English translation at ) in which he mentions his inability to keep his legs still even during the most interesting church sermons.  The passage ends with:

. . . it may have been said of me from my infancy that I had either folly or quicksilver in my feet, so much stirring and unsettledness there is in them, wherever they are placed.

As far as I know, Thomas Willis's report is the earliest recognised account of RLS/PLMD.  What Willis reports is far more intense than Montaigne's account.  His description of torture, leapings and contractions of tendons, makes me think of one of the videos linked to above:  k2eGoHk9AAc Restless Leg Syndrome? (BF109) .   I know of no suggestion that the disorder was reported by the physicians of ancient Egypt, India, Greece or Rome.  The above history of coffee begins with:

It is known that coffee was being cultivated in the Yemen in the 6th Century AD, though some say it was drunk as early as 900BC. . . .

Around 900 AD, coffee was well established in Arabia.

so perhaps these ancient civilizations had little or no really severe RLS/PLMD because coffee was not used.

My guess is that the symptoms such as reported by Montaigne, from infancy - inability to keep his legs still while sitting (implicitly for extended periods of time) - occurs in a small proportion of people without any involvement of coffee or any other source of caffeine.  There may be genetic, nutritional, developmental or spinal injury reasons for this.  I doubt if the dysfunction which occurs in these ways reaches the intensity described by Willis and depicted in the abovementioned video, except perhaps for people with serious spinal cord damage or other spinal problems.

Willis successfully treated one of his patients with laudanum - a drink of alcohol with ~10% opium.   This is not just my interpretation of Willis's text - Dr Mark Buchfuhrer and co-authors note on page 15 that he used "laudanum, a preparation of opium".  They also wrote that "we do not know whether a single dose, a short course, or continued treatment was necessary to control his patient's symptoms".  I guess that at the time they wrote this, there was no freely available copy of Thomas Willis's book.

Here is my transcription of the relevant passage from Willis, page 404, concerning what I will refer to as the RLS/PLMD-style Watching-Evil.  This is from Chapter IV, Instructions and Prescripts for curing the Watching Evil and the Watching Coma.  "Watching Evil" means disruption to falling asleep or lack of interest in doing so, while "Watching Coma" (p406) means being always inclined to sleep but not being able to do so properly.  I think "Spirits being called from their Watchings" means that the person falls asleep, at least temporarily.

Thomas Willis in 1672 describing what is now widely regarded as Restless Legs Syndrome

... or secondly the Spirits being called from their Watchings, and converted to the Genus Nervosum, sometimes transfer their Sallies into the spinal Marrow: and thence into the Nerves that pass into all the outward Members: wherefore to some, when being a Bed they betake themselves to sleep, presently in the Arms and Legg Leapings and Contractions of the Tendons, and so great a Restlessness and Tossings of their Members ensue, that the diseased are no more able to sleep, than if they were in a Place of the greatest Torture.

Sometime since I was advised with for a Lady of Quality, who in the day time was wont to be afflicted with a Cardialgia, and a Vomiting, and in the Night was hindred from Sleep by reason of these spasmodick affects which came upon her as now and then she was upon the point of rest: nor was she able to sleep all Night, unless she took first a pretty good dose of Laudanum:  Wherefore of this Medicine, which at first was allowed her only twice a Week, she took afterward daily for about three Months, receiving no injury thereby, either in the Brain, or about any other function, and when in the mean while by the use of other Remedies, the discraises of the Blood and Nervous Juice being corrected, the animal Spirits became more benign and mild, she afterward leaving off wholly the Opium, was able to sleep indifferently well.

So it seems that opium stopped the spasmodic RLS-style Watching-Evil and enabled her to sleep.  Perhaps the symptoms were caused largely by coffee, and/or some acute iron deficiency, and went away a few months after the Lady of Quality stopped drinking so much coffee and/or improved her nutrition.

The next paragraph, spanning pages 404 and 405, lists various drinks and preparations for treating the above "RLS/PLMD-style" of Watching-Evil.  Techniques include bleeding ("opening a vein"), vesicatories (something to do with blistering - Google Books link) and opiates.  Diacodium is a syrup made from (opium) poppies.

... moreover let Diacodium and Laudanum, in case they agree well, be frequently taken; and mean while that the Opiats give truce from the violence of the Disease, let the cause of it be eradicated by the use of other Remedies, as much as may be : Wherefore day after day, at Physical hours, let things be given that take away the sharpness of the Blood and Nervous Juice, and restore them to sweetness: In which rank we account Testaceous Powders (link), Apozemes and altering distilled waters of temperate Antiscorbuticks, gentle preparations of Steel, spirit of Harts-horn, of Soot, and above all things, tincture of Antimony.

The paragraph which spans pages 405 and 406 concerns a different kind of Watching-Evil (difficulty attaining or maintaining sleep) than the presumably RLS kind just mentioned.  Sufferers of this kind, which I will call the "lack of desire to sleep" Watching-Evil:

perceive no drowsiness or heaviness of the Sinciput, no appulse or desire to sleep.  I have known some affected after this manner, who when they had past many Nights one after the other wholly with out Sleep, yet being still cheerful and brisk, having a good Stomack, and ready at business, seemed not as yet to have wanted Sleep.

He likens this to the effects of coffee:

We may observe that Coffee also on the same account keeps Persons from Sleeping.

Willis also notes that opiates are unsuitable for inducing sleep (p 406):

Opiats will not do; for being given in a good large quantity they seldom cause Sleep, and render the affected more faint and weak.  It often succeeds better if going to bed they take some gentle and pleasant drink, as especially our being clear and mild, or also posset drink [hot drink of milk curdled with wine or ale] with Cowslip Flowers boyled in it, or an emulsion of the Seeds of Melons and Almonds in great quantity, viz. to two or three pounds.

By the magick of Google Book Search, I was able to find a small dissertation by Willis on coffee (pp 68-69) - all this is an English translation of his Latin.  The boldface is mine.  Willis identifies two classes of people - one for which he finds coffee beneficial and the other for which he finds it harmful.

I shall now say something concerning the Effects of the great Anti-Hypnotick Coffee

Coffee, though in some cafes it be very profitable and Physical, in others it is hurtful and unwholesome ; for we see that the great Coffee-drinkers become lean, and are very often subject to be Parylitick, and grow impotent for generation.

Yet as to the Affects of the Brain, and of the Genus Nervosum, I very often prescribe this Drink for them.

For indeed in the very many Cephalick Diseases and Infirmaties, viz. in Head-aches, Giddiness, the Lethargy, Catarrhs, and the like, where the full habit of Body ; and a cold temperament, or one that is not hot, and a watery Blood, there is a moist Brain with a sluggishness and dullness of the Animal Spirits, Coffee often has a very good effect, for being daily drank, it wonderfully clears and enlightens each part of the Soul, and disperses all the Clouds of every function. 

But on the contrary, those who being thin, and of a Bilious, or Melancholick temperament, have a sharp or burnt Blood, a hot Brain, and the Animal Spirits too much stirred and restless, ought to forbear this Drink altogether, as being apt to pervert both the Spirits and humours in a greater measure, and to render them wholly unfit, and unable to perform any functions :  For I have  obvserv'd many, not having a sufficient plenty of Spirits, and also being subject to Head-ache, Vertigo, Palpitation of the Heart, and a trembling or numbness of the Limbs, who presently after drinking Coffee became worse as to those Affects, and suddenly found unusual Langour in their whole Body.

On pages 415, 418 and 426 he prescribes "a draught of tea or coffee", which indicates he recognizes a commonality between these two drinks which we know know as caffeine.

Here are some highly speculative thoughts, hopefully of interest to history fusspots and the like:

Coffee puts some people to sleep, and stops RLS/PLMD symptoms - for an hour or so

Some people find a cup of coffee stops RLS symptoms and puts them to sleep

On 2011-11-20 two people wrote to the RLS Support forum (#forums) in messages 53615 and 53617 that they don't drink much coffee but sometimes drink a cup of coffee (they did not mention decaf, so I assume it was full-caffeine coffee) when they have RLS symptoms, with the effect that the symptoms stop for an hour or so, enabling them to get some sleep.  I don't know how much coffee or other sources of caffeine they use. 

This very short-term (minutes to an hour or so) beneficial effect does not preclude the possibility that these people are still suffering a longer-term (days) increase in RLS/PLMD symptoms and sleep difficulties due to both the caffeine and the opioid receptor antagonists in coffee.

Perhaps this very short term benefit from coffee is due to the symptoms being worsened by caffeine withdrawal, and the cup of coffee reversing those symptoms. (Tina suggested this hypothesis.) 

Perhaps the very short-term benefit is caused by the intense caffeine or some other compounds in the coffee causing a temporary cessation of symptoms for some reason which is unrelated to withdrawal.

It would be possible to test these two competing hypotheses by having RLS sufferers who have reported this very short-term benefit from a cup of coffee having no coffee at all, or any other sources of caffeine, for a few weeks.  Then if similar RLS symptoms appeared, testing to see if the single cup of coffee stopped the symptoms and helped them sleep for an hour or so.  Assuming the RLS symptoms appeared, then if the single cup diminished them, this could not be due to reversing any caffeine withdrawal symptoms which might have been causing or worsening the RLS symptoms.  Another line of research would involve these people, with they usual level of caffeine and coffee usage, taking a caffeine tablet instead of the cup of coffee.

However, I suspect that anyone who drinks coffee and who as RLS/PLMD symptoms will have less symptoms overall, perhaps no symptoms, when they stop drinking all coffee, even if they consume the same amount of caffeine in other ways.  The logic is simple:
  1. It is well known that activation of particular spinal opioid receptors reduces or eliminates RLS/PLMD. (The 32 page PDF version of my hypotheses explains where these receptors are and why this is the case.)

  2. Researchers have established beyond reasonable doubt that coffee of all kinds contains compounds which antagonize the mu opioid receptors, which are the primary ones involved in pain/reflex (the same circuits do both) regulation in the spinal cord.

  3. Endogenous opioids such as endorphins and enkephalins normally activate some of these opioid receptors - and so presumably reduce the levels of RLS/PLMD symptoms below what would occur without this activation, but the compounds in coffee are known to block such activation.
The full impact of coffee's opioid receptor antagonists has not been researched.  There may be all sorts of complexities concerning the various compounds, whose concentrations may vary with different types of coffee.  Different compounds may have different half-lives and patterns of diffusion in the bloodstream and the CSF in which the brain and spinal neurons are bathed.  Different compounds will have different affinities for different types of opioid receptor (mu 1, 2 & 3; delta 1 & 2; kappa 1, 2 and 3 and the nociceptin receptor).  Perhaps some of these compounds activate some of these receptors, at least for some people, since there can be genetic differences which affect the structure and behavior of all these receptors.  Perhaps some patterns of intermittent or continual activation and/or antagonism will cause more of some classes of receptor to be expressed, at least in some parts of the nervous system.  Perhaps these actions would cause greater generation of endogenous opioids, such as due to antagonism of auto-receptors which provide negative feedback to the neurons which release endogenous opioids.

Reducing or halting the ingestion of opioid receptor antagonists might have a variety of effects.  In the long term, we would expect the previously reduced level of mu receptor activation to return to normal levels.  In the short term, such as days after stopping the ingestion, it is possible that the levels of activation of mu opioid receptors would rise above the long-term normal levels, before falling back to those levels.  This could be due to the body readjusting in various ways.

For instance, exogenous opioid receptor antagonists might be expected to cause three kinds of short-term adjustments.  Sorry I don't have references handy for any of these - this is from memory from my neuroscience reading.
  1. Increase in production of endogenous opioids due to the antagonists reducing the activity of the autoreceptors on the cells which produce (or control the production of) the endogenous opioids. (Autoreceptors in this instance would be activated by opioids and inhibit the output of the cell - thereby forming a local negative feedback circuit which would tend to stabilize the production of opioids, if there were no interference from antagonists.)

  2. Up-regulation in the number of opioid receptors due to the antagonists generally reducing their level of activation.  I understand this is a common pattern of adaptation in neuronal systems in general. 

  3. Perhaps some increase in the sensitivity of individual opioid receptors, again due to the antagonists reducing their overall level of activation.
If the antagonists is cleared out of the body (more particularly, out of the bloodstream and then, with some delays from the CSF in various parts of the CNS) faster than any of these three adaptive responses just mentioned, then we might expect a short term increase in opioid receptor activation, until these adaptive responses were reduced over the days, weeks or perhaps months which follow.

So any conclusions regarding the impact of drugs or foods in general, especially regarding caffeine and opioid antagonists such as those in coffee, should be based on long-term research, no just on what happens in the days or week after cessation of the ingestion of the substances.

The full impact of these compounds in coffee will take decades to research.  I think they will prove to be important for mood, pain perception and pain disorders such as fibromyalgia, and for RLS/PLMD.


Conducting your own research

Even if you don't understand anything about the spinal cord, neurons and neurotransmitters, you can still experiment with foods, sleeping positions and - if you, or ideally your doctor, decide it is safe - with oral tyrosine and percussive massage.

If you report your experiences on one of the forums, and/or let me know about it, then this will help other sufferers and their carers.  It will also help people who are researching this disorder.

RLS/PLMD is a neurological disorder.  There's nothing wrong with the skin, muscles or bones in the affected limbs - the problem is that their sensing and control circuits in the spinal cord are malfunctioning.  Food, sleep position and other potential treatments, including avoidance of disruptive drugs, all achieve their positive or negative benefits by altering the function of neurons.  So if you experiment with something which might affect RLS/PLMD and you analyse and report your observations to others in a clear, scientific, fashion, I would say you are an amateur, unqualified, neuroscientist, like me!

Science is an activity.  It is not necessary to have formal training or a degree to do good scientific work.

The scientific process involves carefully observing phenomena, carefully devising and conducting experiments, and carefully devising and arguing for and against hypotheses which attempt to elegantly explain all the known observations.  It also involves  imagination, good luck and making the most of mistakes and chance discoveries.

None of this requires qualifications or academic tenure.  However, it does require patience, education (including self-education) and a passion for discovering and elegantly explaining Nature.

Even if you don't understand the hypotheses I present, any other alternative hypotheses, or much about neuroscience, by carefully observing and experimenting with conditions, foods etc. which affect RLS/PLMD symptoms - and by sharing these results with others - you can contribute to neuroscience.

If you have a thirst for knowledge and are familiar with basic chemistry and biology, you can pursue this in greater depth by learning more about the nervous system and about RLS/PLMD research.  Unfortunately, many of the research papers are only available via purchase or access via the library of a university which subscribes to the publication. 

Hands-on research with RLS/PLMD is one of the forefronts of medical science - it is probably quite easy to make novel and significant observations, or devise and conduct new experiments.  It is easy to experiment with foods, sleep position,  massage, coolness of different parts of the body.  The results may show up in less than a day, or even within a minute.  Please let me know what you find or write about it on the forums listed above #intro.

I believe that most conventional RLS/PLMD researchers have taken far too little interest in exactly what is happening with sufferers and the discoveries sufferers have made which prevent or reduce their symptoms. 

Its obvious when you look at the limb movements that they resemble reflex responses.  A few researchers have noted this, and correctly argued that these responses are of a purely spinal origin - so it makes sense to look at the spinal cord, rather than the brain.  The most significant paper in this regard is from 2000:

Periodic limb movements in sleep - State-dependent excitability of the spinal flexor reflex
W. Bara-Jimenez, M. Aksu, B. Graham, S. Sato, and M. Hallett.
Neurology (American Academy of Neurology)
April 25, 2000 vol. 54 no. 8 1609-1616 
This is behind a paywall, but is available via SciHub:

Also, for background on the particular reflex responses which are being erroneously triggered in RLS/PLMD, I believe the following article is a crucial reference for all RLS/PLMD researchers. Other than citing the above paper, it does not mention RLS/PLMD.

The lower limb flexion reflex in humans
Giorgio Sandrini, Mariano Serrao, Paolo Rossi, Antonietta Romaniello, Giorgio Cruccu and Jean Claude Willer.
Progress in Neurobiology. Vol 77, Issue 6, Dec 2005, pp353-395
(Freely available.)

Yet I don't recall any RLS/PLMD research papers citing this paper.

Pharmaceutical companies are primarily interested in funding drug trials - and there have been dozens of expensive drug trials for RLS.  Tens or hundreds of millions of dollars are spent each year on prescription medications for RLS, all of them with potentially serious side effects.  Yet despite all this effort, none of these researchers have proposed a comprehensive etiological theory or figured out that the opioid receptor antagonists which were discovered in coffee in 1983 cause or worsen RLS/PLMD via an easily understandable mechanism.

There is plenty of scope for amateur neuroscientists to do significant new work.  Your observations, experiments and hypotheses may get little or no recognition from mainstream researchers - but keen researchers can still compare notes and inspire each other's efforts via Internet communications.  If there's a call for it, I will establish a mailing list for RLS/PLMD researchers - with and without formal training.

Neurology or neuroscience students looking for experiments to do as part of their education may also be interested in conducting research.  It is easy to find experimental subjects.  Of the last three electronic clients who I worked for in Melbourne (November 2011), one suffered RLS/PLMD himself and the other two had a parent who suffered from it badly.

In 2012 or 2013, when I have updated my current researcher-only PDF document to be released publicly, I plan to have a section of this site for researchers, with a sub-section suggesting experiments for people studying neurology, neuroscience and sleep medicine.

Assuming you have a basic understanding of chemistry and biology, it is pretty easy to pick up some extra neuroscience knowledge from various Internet sources.  Google Scholar and PubMed are particularly useful:

If you want to develop a broader and deeper understanding of neuroscience, without spending the next four years at university, I suggest you buy a textbook and either dip into it, or read it from one end to the other.  It is my impression that neuroscience is the most complex science of all.  The most voluminous textbooks seem to be neuroscience texts - and a good neuroscience textbook is beautifully illustrated.  In 2004/5 I read what is perhaps the most prominent of the neuroscience textbooks:

Principles of Neural Science 4th Edition

Kandel ER, Schwartz JH, Jessell TM 2000.
Principles of Neural Science, 4th ed.
McGraw-Hill, New York.
Amazon page.

At 1414 pages and 7.4 pounds (over 3kg) this is way too heavy to read in bed.  I cut mine into five comb-bound sections.  It is possible to buy used copies of the 4th edition at for $60 or so including postage.

I found this a truly fascinating book - but I would not want to be examined on the vast amount of information it contains.  Anyone looking for insights into higher cognitive or emotional functions is likely to be disappointed, because most of the brain and most of this book concerns sensory, motor, visual and auditory processing.  The starting point is neurons and the proteins and other molecules which make them work, especially the receptor molecules which sit in the cell membrane of neurons, accepting molecules which fit into their outside sections and activating a process which changes the internal voltage and so increases or decreases the chance of it depolarizing (firing) or in some other way alters the function of the neuron. 

There are no-doubt other good neuroscience textbooks which are more up-to-date.  In November 2011, the 5th edition is due in 2013.  I suggest not waiting for this, since this date has been repeatedly pushed back.  The Wikipedia article history shows that in 2006, the 5th edition was due for release in 2007.

Neuroscience textbooks cover the the brain, spinal cord, muscles and sensory neurons, such as in the skin.  For RLS/PLMD we need more detailed information on the spinal nociceptive (pain sensing) circuits, which are the same circuits which drive reflex muscle movements.  As far as I know, the best source of up-to-date information in this field is this 1088 page 2008 reference, which is nearly as hefty as Principles of Neural Science 4th ed. 

Alan Basbaum and M. Bushnell eds
The Science of Pain
Elsevier Academic Press Aug 2008
ISBN 978-0-12-374625-2
Amazon page.

I read chapters 12, 23, 24, 25, 49 (I read to page 731 and page 734) and 50.  I photocopied the chapters from a library copy.  Reading this formidable volume intently in a train or tram would give your fellow travelers a fright!

I do not suggest attempting to become an amateur neurologist.  Neurologists are medical doctors with extensive further training.  They work hard to maintain their  knowledge of a vast array of research and of the clinical experience of their colleagues.  They bring this to bear on your medical problems in ways which no-one else can.  Medical doctors and neurologists are the only people who can professionally advise you on the safety or appropriateness of the various treatment options for RLS/PLMD. 

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