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An Evidence and Experience based Mechanism for Narcolepsy


Fifty years of symptoms and a decade searching PubMed compels me to share my conclusions.






Narcolepsy is a debilitating sleep disorder resulting in persistent fatigue and an inability to control sleep onset.  The symptoms of narcolepsy are caused by the depletion of the neurotransmitter orexin in the body and the brain.  Orexin increases wakefulness.


If your orexin levels are high, you are alert.

If your levels are low, you fall asleep. 


People with narcolepsy have been shown to have undetectable levels of orexin in their systems.

And blocking orexin receptors causes a rapid descent into sleep.


Orexin is involved with a lot of other things beside sleep though-

It helps control your digestive system

It is affected by the immune system

And triggered by the light-dark sensing circadian system.


At its most basic level orexin stimulates you to find food.

When people are hungry orexin levels are high. They are awake and alert and mobile.

After they eat, their orexin levels go down and they become less active.

And when they sleep, orexin levels are very low.


Consciousness- is pretty vital to food acquisition. Cells in the eyes are connected to the orexin cells. When light hits the retina they send impulses to the orexin cells and they begin firing. This is what wakes you up in the morning. (And puts you to sleep at night, and in movie theaters.)


Cognitive function- orexin stimulates the prefrontal cortex which is responsible for attention and calculation.


Digestion/Metabolism-  Orexin regulates stomach mucous and gastric acid secretion, insulin release, and intestinal movement. Orexin receptors are found in fat tissue. Orexin also modulates alcohol craving and tolerance.



When your orexin cells aren't working properly, a whole lot of other things can go wrong.





There are three primary things that lower orexin levels naturally.


Darkness-  as I said before, we produce more orexin in the light.   And therefore more in the summer and less in winter.


Diet-  the orexin system is a basic regulator of digestion and metabolism.
Orexin cells sense glucose in blood and alter their output based on that information. When blood sugar rises, orexin cells produce less orexin. That's why people get sleepy after eating.

Infection- in addition, orexin is critically involved in the immune response.
When there is bacteria in the bloodstream, orexin production is drastically curtailed. This shifts metabolic resources to fighting the infection. That's why people get tired when they are sick.









Occult Infection:

An infection first recognized by secondary manifestations as opposed to visible observation or palpation.   For example, secondary symptoms include fever or increased white blood cell counts.

Occult infections are often caused by a bacterial infection in an hidden site, the intestines, for example.


Occult bacteremia:

The presence of bacteria in the bloodstream of a patient who has a fever but who may not appear particularly sick and who has no apparent other source of infection.


I propose UltraOccult bacteremia as the presence of bacteria in the bloodstream without abscess or fever or the other standard indicators...






Despite what you have been led to believe, narcolepsy is not a mysterious disease.  


All the data support the conclusion that the orexin deficiency and orexin cell loss inherent in narcolepsy are a predictable complication of a common infection.  Most of the pathology and resulting symptoms can be explained by well documented immune reactions.


The evidence is accumulating that numerous respiratory and oral infections can trigger narcolepsy.

My experience conforms with those observations, and convinces me that narcolepsy is a rheumatic disease. Specifically, it's an immune complication to certain strep infections, similar to rheumatoid arthritis and rheumatic heart disease.


Post-streptococcal complications commonly cause neurological symptoms, and strep infections have been associated with the onset of narcolepsy.  1   Encephalitis Lethargica was a post 1918 flu complication with symptoms similar to narcolepsy, and has also been associated with recent exposure to strep. 2  3


The post infection complications of strep infections have historically been an enormous public health concern. Rheumatic fever, scarlet fever, rheumatoid arthritis, kidney nephritis- all were common illnesses. Before antibiotics, there were entire hospitals of people just recovering from the post infection complications. They had to rest for weeks or months until they healed from kidney or heart disease.

Those commonly recognized streptococcal autoimmune disorders are triggered by Strep pyogenes. This is the species which causes "strep throat" .
Although antibodies to S. pyogenes are commonly found in narcoleptics- and associated with the sudden onset of symptoms- I get the feeling Strep B also causes symptoms, and S pneumoniae is the most persistent trigger.  I also believe that instead of attacking the joints or heart valves, the critical immune reaction affects the digestive system.   4






The other major infectious illness associated with narcolepsy is H1N1 flu. Although no direct causation has been proven, an increased incidence of narcolepsy after the 2009 pandemic has been documented. That this result occurred after both vaccination and natural infection provides strong evidence this is a real and specific effect. The 1918 influenza epidemic was also a strain of H1N1 and there was a similar occurrence of a post-infection sleeping sickness called Encephalitis Lethargica. 5

My preferred explanation is that H1N1 flu does not directly trigger narcolepsy- it facilitates a secondary strep infection that does.  There are more studies than I can reference showing that infection with the flu virus lowers immunity to strep pneumoniae and that it is the most common complication.

I have covered most of that here...

Other researchers reasoned that if H1N1 was the actual trigger, there would have been many more cases.  So they looked for a comorbid illness.


Recently an experiment has shown that post-vaccination narcolepsy patients in Sweden show a marked increase in strep antibodies.    6


This supports the hypothesis that the incidence of narcolepsy after H1N1 is not evidence of a viral cause of narcolepsy, it is further evidence that strep is the primary trigger.


 7  8  9  10  11  12  13




These are the species you report to me most often:


Strep pyogenes (strep A) likes the tonsils.   It will live there forever if you let it.   If the tonsils are removed, it seems to take up residence in the tooth sockets.  Impetigo and cellulitis are strep A infections of the skin.   Infection with strep A also facilitates infection by pneumococcus.

Strep pneumoniae (pneumococcus) infects the nose and lungs.   It does cause bacterial pneumonia, but also many less well known infections.   Low levels are found in asthma, and nasal or middle ear colonization is extremely common.  I had childhood meningitis, infection of the brain with fever, and it occurs in many of your reports to me.

Strep Galacticae (strep B)-  resides in the urogenital tracts.   Causes urinary tract infections.  Is transmitted sexually.   And flares up predictably during pregnancy.


The association between these illnesses and your symptoms is obscured and difficult to recognize because


-These are common illnesses. They are sort of "expected" parts of life.  Your doctor certainly isn't concerned.

-Different species colonize in different areas of the body.  And they tend to cycle. You think of them as independent events.

- Over time, the symptoms of the infections become suppressed.


One thing they all do have in common- all of these species produce the lysin molecule which punctures (lyses) cell membranes. One of their most prominent features is that they destroy epithelial tissues.   So they are all also capable of creating lesions and getting into the bloodstream.


 (Epithelial tissues are environmental interface tissues, so that not only includes your skin, but your intestine and lung surfaces too.  The interior spaces are wrinkled and branched and much more expansive than you might think...the old saying is your lungs have as much surface area as a tennis court.)





When bacteria is present in the bloodstream, the condition is known as bacteremia.

Sepsis is a constellation of symptoms secondary to infection that manifest as disruptions in heart rate, respiratory rate, temperature and white blood cell count. If sepsis worsens to the point of end-organ dysfunction (renal failure, liver dysfunction, altered mental status, or heart damage), then the condition is called severe sepsis. Once severe sepsis worsens to the point where blood pressure can no longer be maintained with intravenous fluids alone, then the criteria have been met for septic shock.   14





Orexin is intimately involved in the immune response to infection.


Acute systemic infection curtails orexin production directly and drastically.


When there is bacteria in the bloodstream, there is an immediate cascade of neurological and hormonal and immune effects and orexin is a key factor.

When animals are inoculated with microbes into their tissues, abdomens or bloodstreams, orexin production is rapidly curtailed. It seems to happen with anything they've tried.

Orexin production is rapidly reduced to about one-sixth of normal.    15
  16  17
You also become insulin resistant almost immediately. That's why you don't feel like eating.

Anorexia is a symptom of acute infection. Bacteremia. Sepsis.
That applies to most animals and has been documented since the beginning of civilization.

You shouldn't be eating because the energy ordinarily used for digestion is needed to fight off the infection. Your whole metabolism shifts to accomplish that. Tries to knock you out so you don't interfere.

Pharmaceuticals have changed all that. Interfere is exactly what we do.
They dull the pain, shrink the inflammation, shut down your immune system, give you energy and keep you going even though you are actually still sick...they address the symptoms and create chronic illness.

But The Really Interesting Thing About Bacteremia- it has so many causes.
Including inadvertent ones.
It can be caused by traumatic injury, or acute ulcerative infections, or a chronic infection that progresses to abscess. In addition, the bacteria are spread into the tissues and circulation by dentistry or the surgical procedures used to repair injuries or excise fetid infections.

Read that again. It is crucial to understanding our predicament.

Not only is trauma or infection or neglect able to cause this acute systemic response- many of the treatments actually trigger and compound the pathology.    








Chronic infection involves persistent low level microbial activity.     Insufficient immune response can result in persistent colonization.  If the immune response is too low, bacterial populations persist...




My research indicates most of the damage to the orexin system comes from endotoxin.   Endotoxin is a molecule bound into the cell membranes of gram negative bacteria. 

Long term endotoxemia is well documented to cause most of the metabolic and neurological effects associated with narcolepsy.   It's the logical suspect.


The problem is-  Strep is a gram positive bacteria-  it makes a lot of noxious molecules, but doesn't produce endotoxin...




So, there is clearly more than one underlying trigger.

That has been obvious from the beginning though- the spectrum of narcolepsy symptoms across ages and sexes clearly indicates at least two factors interacting creating an array of effects..
I have been thinking for years that it was an infection interacting with food. But now I'm sure it's an interaction between these two different kinds of infection. And those then mess up our digestive tract and metabolism.

(and then the drugs we are given to solve the problem create an immune system clusterfuck... but I'm getting ahead of the story...)




Here's the fundamental insidious feedback loop.

-Strep bacteria (gram positive)  release a molecule called lysin which creates holes in epithelium.  

Strep then gets through these pores and trigger the septic shock response- which pretty much starts with intestinal permeability.  The first step in sepsis is epithelial dysfunction: the cells of the intestine literally spread out and lose their barrier ability.

-The enterobacteria that live in your guts (gram negative), then get in your bloodstream and interior tissues too. 

Now you would think that having two systemic infections would make everything spiral out of control.
But that's not what really happens.

The difference between gram positive and negative is the structure of the cell membrane.  Gram negative bacteria have a molecule called Lipopolysaccharide (LPS) or endotoxin on their cell membranes.  Endotoxin is bad stuff, it has a lot of adverse effects.... but one positive trait that trumps all of them:    LPS actually lowers the immune response to strep infections. Dampens it down.  If you have endotoxin in your system, you are much less likely to have an extreme acute respiratory illness or septic event.  Most respiratory infections kill you by producing too strong of an immune response- not because of too many germs in your system. Most of the damage is done by the cascade of immune molecules.

Acute strep infection triggers suppression by endotoxin.
LPS suppresses the strep infection, but only a few strep bacteria are required to induce the septic response, so the cycle continues.  18  19 

Recurring acute strep infections lead to two chronic low level systemic infections instead.

Historically, this has been an advantageous trait.
In certain circumstances- crowded conditions for example, it is better to consistently have a low level infection than to risk an overwhelming episode of a novel strain.  20   21   22   23   24

However the long term effects of this process are insidious.
All kinds of sleep and memory problems are associated with endotoxemia.



It's complicated, but it all progresses  naturally if we just follow the effects of strep infection.


·         Strep bacteria create epithelial permeability.

·         Intestinal permeability facilitates systemic gram negative bacteria infection.

·         Systemic gram negative bacteria release endotoxin.

·         Endotoxemia then facilitates Strep bacteria colonization.

·         Lather rinse repeat.



Abracadabra.  It's an infection roller coaster with a half twist.  A freakin Möbius strip of misery.








Anyhow...  that's just the beginning of the wicked twists and vicious circles, my friends...



Alcohol increases intestinal permeability and regular dosing stimulates the immune suppressing effect of endotoxin.

Contrary to popular knowledge, it doesn't "kill the germs", it indirectly reduces the immune response.


This particular effect seems to have been very advantageous for a lot of neolithic northern Europeans who were stuck inside with each others' coughs and runny noses all winter...

Alcohol was an easily available, effective form of infection control.   Not to mention social lubricant.
It's probably been advantageous through the industrial revolution too.   Crowded conditions, poor air and light quality, inadequate nutrition and medical care all contribute to respiratory and contagious illness.  And crankiness.

The medium term benefits have historically exceeded the long term consequences... Alcohol is the reason most of us are alive.

Unfortunately, antibiotics change everything   Antibiotics turbocharge this process.


Most antibiotics kill bacteria by degrading their cell membranes.  Strep bacteria then release all their lysin molecules destroying tissues all over the body.  Antibiotics kill your gram negative bacteria too - rupturing their cell walls not only frees the endotoxin, it makes it more bioactive.   Like fifty times more bioactive.   25   26   27


And they increase intestinal permeability while they're at it.   Yeah you read that right.

They put out the fire on your boat by drilling holes in the bottom.

Antibiotics do not "cure" or "clear" your infection.  They do not eliminate the germs.

They suppress the excess bacterial activity while increasing the amount of chronic colonization you can tolerate.

Specifically, they kill off susceptible bacteria and increase levels of resistant strains.  28  29 


Antibiotics ultimately accelerate the carriage rate and  increase bacterial load of chronic strep infection.


Not only that...

·      They directly disable mitochondria.  Because mitochondria are descended from bacteria, their membranes are also destroyed.   Mitochondria produce the energy for your body- without them, your entire metabolism starts to fail.  30  31


See the source of your Vortex.
Antibiotics as treatment for strep bacteremia is probably the source of most modern narcolepsy cases.








A single dose of endotoxin increases intestinal permeability in healthy humans.  32.

Could that vicious circle be any more obvious??





LPS effects are tested by injecting it into animals.   Usually into the abdomen.


Endotoxin is associated with both short and long term neurological and behavioral effects.


Short term LPS increases alertness via cortisol and histamine.   33  34


Endotoxin induced adrenal changes were accompanied by dose-related decreases in mood and increased anxiety levels. Research suggests the existence of at least two counter-acting mechanisms, one promoting and one inhibiting cognitive performance during acute systemic inflammation. 35


LPS has been shown to drastically reduce the number of dopamine neurons in the brain.  36


It also specifically affects the Orexin System-


LPS innoculation  significantly reduced hypothalamic orexin-A activity.  37   38 


In addition, chronic LPS administration produced a dramatic loss in orexin neurons in rats over a period of 30 days.  (29.7% reduction) 39



Polymicrobial Sepsis is tested by stabbing the animals and emptying their intestinal contents into the gut space.


Septic encephalopathy is a severe brain dysfunction caused by systemic inflammation in the absence of direct brain infection. Changes in cerebral blood flow, release of inflammatory molecules and metabolic alterations contribute to neuronal dysfunction and cell death. 40


Cognitive and functional decline often follow severe sepsis in both humans and experimental animals.  41  42


Survivor rats show learning and memory impairment and depression after complete physical recovery from sepsis    43  44


REM and EEG results are dramatically altered during sepsis, and sleep is fragmented, indicating that the quality of sleep is diminished. Effects on sleep persisted for at least 84 h after sepsis induction, the duration of the testing period.  45









Check this out:  it very much looks like energy production is increased while the cells are being killed.

Endotoxin quickly raises cortisol and histamine levels.

Endotoxin eventually kills orexin cells.

This also creates a vicious circle that masks itself.
Since high cortisol and histamine improve glucose sensitivity and energy levels, and orexin deficiency lowers them.... together they create an effect that mimics normalcy even though it is sickness squared.


The pathology masks the perception of the pathology.



That's the source of most of our symptoms- endotoxin amps up our stress while killing our orexin cells.

But from the very beginning, the effects in women seem to diverge from men.  A significant difference between males and female response to sepsis is a well documented phenomenon. 46   47


Estrogen affects the septic response and insulin production, and women seem to get fat and tired and depressed right away.    Estrogen also increases the tolerance for endotoxin. 

Women's immune response to bacteremia is fundamentally lower and our overall bacterial carriage rate is higher.

(this is probably to facilitate survival through a pregnancy, but prenatal endotoxin exposure has other significant adverse effects.)    48  49   50


Males have much more cortisol production and I think they just burn out their adrenal system and hair follicles while the orexin cells are being killed.   Men report less food triggers. less cataplexy, and more insomnia and debilitating fatigue.  51  52


Decreased pituitary adrenal responsiveness a documented effect of repeated LPS inoculation  .53  54


Converse to the females, male gender is significantly associated with an increased incidence of postinjury pneumonia.   55










The orexin system in fundamentally involved in regulating numerous feeding and digestive activities including blood glucose control. 

Orexin depletion leads to changes in glucose metabolism.  



Orexin is directly involved in gastrointestinal function.

·         It signals the increase in gastric acid secretion and intestinal movements involved in feeding and digestion.  Low orexin levels lead to slower digestion.    56  57  58  59


Orexin is also quite involved in fat metabolism.

·      Orexin receptors are found in human adipose tissue and low circulating orexin-A concentrations have been shown to be associated significantly with severe obesity (overproduction of white fat). 60  61

·      It has also been shown that orexin stimulates the production of brown fat. Orexin deficient animals produce less brown fat (which burns energy) and have lower basal metabolisms. This results in individuals who actually eat less but weigh more than the normal population. 62  63



Insulin Resistance

Orexin also controls how well your body uses insulin.   When your orexin levels drop, your insulin resistance goes up.  (like in sepsis.)  64


When insulin resistance rises, your pancreas creates more insulin to compensate.

Insulin combines with glucose to create fat.

If you eat a lot of carbohydrates, most of your food gets made into (white) fat...

And then your blood sugar crashes and you get hungry again. 

Instant blood sugar swings and food cravings are the result.




GABA sensitivity,

High insulin levels also amplify the effect of GABA. So if you have high insulin levels you will be extra sensitive to it's effects.  GABA strongly suppresses the central nervous system. Puts you right to sleep. It definitely contributes to central apnea, daytime sleepiness, and negative affect.   65





We become hyperinsulinemic.  We make too much insulin. And too much fat.

And that causes Hypoglycemia- Low Blood Sugar

It's a snowball effect.

We get fat on the outside while we starve on the inside.


Estrogen increases the production of insulin, so women get even fatter.  66


...aaaaaaand just in case all that irony isn't quite enough...


Leptin is produced by fat cells, so the heavier you get the higher your leptin load is.  And the more leptin we have, the less orexin we make.  It also seems to preferentially kill orexin cells in females.   Seriously, the fatter we get, the faster we gain.  It's a freaking black hole of flab. 67




 Now Listen Up.   Infection isn't the only thing that messes with your orexin levels.


Orexin cells aren't ordinary.

All cells are sensitive to their own internal glucose levels and moderate their activity to compensate.

Unlike most brain cells, orexin neurons are sensitive to external glucose levels.


·      As blood sugar rises orexin cells lower their activity.

·      As blood sugar lowers they increase production of orexin.


So every time you eat, you alter your orexin system and everything it regulates.

You can shut them down just by spiking your blood sugar.  68





If you have low orexin levels, you cannot tolerate as much glucose before you fall asleep.
Ingestion of glucose increases symptom severity in narcoleptics. 69

And lowering serum glucose levels improves orexin function.
More specifically-
Orexin expression is increased by fasting and insulin-induced hypoglycemia.  70

Read that again. It explains a lot.

There are two "ingestive behaviors" that lower blood glucose and increase orexin levels- fasting and bingeing.


Sound familiar?

Unfortunately both of those are unsustainable.
Intermittent fasting has been shown to increase insulin resistance over the long term.
And bingeing increases it over the short term.
An overall long term carb restriction diet seems to work better.




And just for thoroughness.

LPS increases the transport of insulin to the brain. 71

And type 2 diabetes is associated with increased endotoxemia in humans.   72   73


Sepsis explains the sudden onset or worsening of symptoms.
Chronic infection and dietary dysfunction explains the persistence and cumulative effects.


One reason all of this gets worse is because of the glucose problems.
We eat lots of carbs, it suppresses our immune system, and we never recover properly from the infections.
(We crave them and we are told to, so go figure.)

Sugar directly promotes infections too.
Mouth bacteria for sure.
Also predictable- urinary tract infections. Kidneys excrete excess glucose and bacteria take advantage of that.







There are a number of overlapping factors that contribute to the symptoms of narcolepsy. The combination you have determines your combination of symptoms.





Sleep attacks- a combination of rising blood sugar and immune response lowers orexin levels after a meal.  The sugar and endotoxin gang up on your neurons and your orexin levels drop faster and go lower than other people.



Cataplexy- I tend to think  a sudden spike in blood sugar due to stress causes orexin levels to crash.

I very much think this is associated with endotoxemia though.   It makes us twitchy.  And is associated with hypotensive attacks.   74


·         Stimulating the locus coeruleus at certain high frequencies causes episodes that resemble cataplexy .75 

·         And endotoxin speeds up the firing rate of the LC. 76


I would guess that endotoxin is one thing that primes the locus coeruleus for total shutdown during a panic attack.


But I think it is confounded by the fact that hypoglycemia also causes syncope.  77



Excessive Fatigue-  Narcoleptics produce much less epinephrine (adrenaline) than other people.
This results in mitochondrial dysfunction which causes the brown fat cells to deteriorate.
It also results in less energy in skeletal muscles.
This gives us less overall energy. Really, truly, it does.

Insomnia/Fragmented Sleep

This is an indication that you have so much stress hormones that it's overwhelming your lack of orexin. 

Fitful sleep and vivid dreaming are signs of infection.


And lucid dreaming is a sign of severe illness- if you were awake it would be called delirium.


(Are you paying attention, Dr. Dreamy?  Lucid dreaming is not entertainment or therapy, and definitely not something you should be promoting to your patients.)



The number one cause of apnea is surely infection. Viruses and bacteria proliferate in the nose and throat. Infected tissues become inflamed, infected nerves don't function properly, and the hypotonia of the airways leads to breathing difficulties.


Impaired nasal breathing leads to obligate mouth breathing.

·         Which dries out the tissues, And leads to increased bacterial growth.

·         Which leads to more mouth breathing.  And more inhalation of the bacteria.



Bruxism- tooth grinding is surely caused by apical periodontitis, infection of the tooth sockets.





People with narcolepsy are documented to have altered core and skin temperatures, but persistent fever is not a reported symptom. 78


I believe this is because the long term effects of the pathology suppress hyperthermic activity.


First of all, brown fat is neccessary to run a fever.  79

And narcoleptics lose their brown fat cells.    80


Secondly, narcoleptics have much more histamine production in their brains. 

Endotoxin increases hypothalamic histamine activity.    81 

And histamine lowers fever.  82 


Thermic response also seems to be dependent on metabolic status:

Fed rabbits responded to endotoxin with fever, starved animals became hypothermic.   83  84


We don't have fevers, we have fever dreams.





While we're finding ways to disguise an infection...

Reducing  discomfort is a good strategy.   If colonized individuals can't see OR feel the infection... well they are much more likely to just carry on, aren't they?


Pain insensitivity seems to be a completely unrecognized symptom of our illness.
(We don't complain about it, so go figure.)


Strep not only pokes holes in our epithelium, it dehydrates the skin and kills the nerve endings along the way.   85  86

Endotoxin reduces gut pain sensation more than morphine.   87

Insulin reduces skin pain sensitivity.  88


Also relevant-  lower respiratory system and enteric nerves are wired to the emotional, not sensory part of the brain.   Irritating them makes us moody.  89

All this stuff combines to totally mess up our sensory input. We cannot feel our mouths or noses or guts or lungs.  We are not aware of our own chronic illness. It just doesn't ever even occur to us. Everyone expects a toothache or stomachache to hurt...

And just for another wicked twist-
The insensitivity probably occurs first where the most infectious activity is.
It isn't uniform. We do have some sensation in healthier spots. But we can't feel the bad spots.
And the more infected we are, the less able we are to feel pain in general.


This is what seems to happen:

We have some pain symptoms when the infection first flares up, but it subsides, so we assume we're better, rather than the nerves have been shut down.



This is so fundamental. We are not stupid. We are not crazy. The pathology masks the perception of the pathology.


And the longer it goes on, the less aware we are of our symptoms.   Our infection level gets higher.   And we inevitably cross the event horizon into sepsis and delirium.








People with narcolepsy often experience spontaneous auditory or visual activity.  We see lights or patterns or shadows when we close our eyes, and we hear tones and noises in our heads.  These often occur with sleep onset or waking, but can also manifest while fully awake.


My experience convinces me that trigeminal neuralgia from oral and nasal infection causes the visual and auditory phenomena, depending on the site of the neuralgia. The trigeminal nerve is the major sensory nerve of the face. It innervates all around the main sensory organs up there.  And it's easily accessed by microbes via the nose or mouth.

The primary symptom of trigeminal neuralgia is described as sharp intense pain.
I would like to dispute that. I think the ultimate symptom of trigeminal neuralgia due to bacterial toxins is actually loss of sensation.

Although the surface small nerves are damaged, the underlying large fibers are usually still functioning. These evoke a more diffuse and aching sort of pain. That's why we have headaches a lot.
The infectious and immune activity also creates spontaneous nerve activity.

So this is the result:

Sensory paralysis- we can't feel real input
Spontaneous nerve activity- we experience erroneous input

This is how I think most of the hallucinations are generated. Your nerve is "pinched" or "poisoned", but you don't feel the pain, you experience the associated sensation- vision or hearing or odors or whatever.

·      If the neuralgia is in your ophthalmic branch, your eyelids don't hurt (they will probably droop), but you will experience visual phenomena.

·      If it's in your lower jaw or mastoid process, not only do you lose hearing function, you also generate false auditory signals. You won't have an earache but you will have tinnitus or auditory hallucinations.

·      If it's in your sinuses, you will be prone to puffy eyes, droopy cheeks and uncontrolled weeping. I actually think that spontaneous crying often results in chronic rhinitis. And I think runny noses are a major cause of depression. I think crying actually causes depression.


This is how Botox works for depression and migraines, they paralyze the nerves around the nose and eyes.

I think a lot of the other phenomena are similar, but are triggered by other nerves somehow.
Crawling sensations must be peripheral neuropathy of the skin.



The obvious corollary to all this also needs to be made explicit-
We do have symptoms of our infections. It's just not what we think.
If you are having visual or auditory hallucinations-
Or are lying on the floor crying your eyes out-
Or spend your nights lucid dreaming-
You probably have an oral or nasal abscess you can't feel.








Narcolepsy affects our thinking in all kinds of ways.  

Like making us crave sugar, for instance.





 Antisocial behavior


This the source of most of our symptoms- endotoxin amps up our stress while killing our orexin cells.


Low orexin levels cause depression and moodiness.

And the high cortisol makes us anxious and impatient.

One of the earliest and most annoying symptoms is irritability.  90

We're sick.  Go figure.


Severe hypoglycemia also causes belligerence, combativeness and rage... just ask my husband.   91




Brain Fog/ Memory Loss


Orexin stimulates the prefrontal cortex which is responsible for attention and calculation. 

If your orexin levels are low, you just flat out have less neural bandwidth to think with.


Insulin resistance is correlated with impaired cognition.   92


Acute septic illness can impair post recovery cognitive abilities pretty substantially.   Memory loss and learning impairment are common results after sepsis.  93


Chronic endotoxemia increases Beta amyloid levels in the brains of mice.  94

Beta amyloid accumulation is associated with the dementive effects of Alzheimers disease. 





We also have fascinating complex behavioral changes. 

We instinctively choose behaviors that lower our immune response.  Because if we don't, the strep flares up, and we get really sick.


Sugar causes depressive/sleep symptoms.
Infection causes the hyper symptoms- anxiety, nightmares, obsession.
We seem to navigate between the highs and lows and approximate a sort of normalcy.


As our orexin levels decrease, we have less cortisol production and less activity in our frontal cortex. 95

We get brain fog... 

Altering blood sugar levels and endotoxin load are easy methods to affect our neurotransmitters... so somehow we intuitively gravitate to behaviors that increase our cortisol or histamine production.  Like self medicating or eating a bunch of junk and letting our intestines leak endotoxin.


Alcohol does not lower orexin levels the way sugar does, so as we get older, we prefer it to candy.  96

... until we can't metabolize it at all anymore...


Steroids and Opiates reduce the immune response and pain sensation.   Like almost everything else we enjoy, they make us "feel better" but our underlying infection level actually gets higher.


Most people call this addiction.   We experience it as survival...








The basic knowledge of the functions of orexin  allows us to understand the action of the drugs we use to treat our condition.
Most of the pharmaceutical drugs for narcolepsy improve sleep propensity by altering glucose metabolism. They are fundamentally weight loss medications. In a few different ways, they alter insulin production or insulin resistance, and stabilize blood glucose levels. I have a paper about that here...


The important thing to realize about that strategy is it addresses one of the effects of the illness, not the cause.

By not addressing the cause, it allows the illness to progress.




Benzodiazepines (for anxiety and mania)  seem to be the exact WRONG drug for us.

They are shown to increase insulin resistance and diabetes incidence.

They also  increase mortality from pneumonia.   97

This includes Diazepam, Alprazolam, Clonazepam, Lorazepam.


Amphetemines are fun, but the reason they make you psychotic after a while is they ruin your blood-brain-barrier and facilitate infection in your brain.   98  99

Not to mention they dry out and destroy your mouth so those infections don't have to go very far.



Xyrem  (GHB) works in a couple ways.


-It reduces insulin resistance and induces ketone bodies.  Ketosis causes the rapid weight loss.  And more slow wave sleep.  This the same metabolic effect that occurs when you reduce your carbohydrate intake drastically.  100

-It reduces cellular damage during sepsis.  And seemed to increase survival of surgical patients with severe sepsis. 101  102  103


Those are beneficial outcomes.

The problem is, Jazz doesn't seem to know these things.   They are still saying their drug works by "consolidating sleep architecture" or some such blather while signing you up for government subsidized financial assistance...


Like some other general anesthetics, it probably is a viable alternative for acute septic episodes.   It would probably be a good option for certain people, IF it were temporary, and combined with some real infection and metabolic care.

Long term use is problematic.   And not just because it's obscenely expensive.

It doesn't really address the underlying problem.  You're still infected.  And eating sugar and crap.

By the time it stops working, you're much sicker, and cessation crashes your metabolism and commonly increases infection and causes sepsis and delirium.


But they "don't know" that, so they don't have to inform you of it.  They just call it "withdrawal symptoms".  Clever, that.








I once wrote-


Experiments generally assume a one to one relationship between factors. Unless they are specifically designed for an interaction- they do not detect multiple causes. If x or y cause z, and you're only testing for x, well you're half right, but your results will not register statistically.

Conversely, this is also true if your illness has multiple or variable effects. If you are only looking for a subset of the possibilities, your experiment will not show a relationship.


Likewise, most experiments do not account for less than threshold activity. If your illness is extremely mild or intermittent, it will never be statistically relevant in a study.  They just won't even see it.


Narcolepsy seems to be a result of all of these sources of obscurity.





For those of you keeping score-


The assortment of strep infections.
Their interactions with endotoxin.

The suppression of "indicator" symptoms.

The lack of distinct pain.

The paradoxical effect of antibiotics.

The variety of dietary triggers
The different effects in men and women.

This is why the overall syndrome has been so hard to detect.


All these factors seem to combine to make narcolepsy diagnosis difficult, and apparently nearly impossible in females.

85% of men were likely to be diagnosed 16 years after symptom onset, while it took about 28 years for women.    That's half a lifetime.  There's many, many more of us out there.  104




Yes, narcolepsy is an immune problem.   But it's  not an autoimmune problem.  This does not require an aberrant gene or antibody response to our own tissues.  Narcolepsy is a  long term consequence of mild strep infection and low grade bacteremia.    We are exhibiting the expected symptoms of chronic infection exacerbated by inappropriate treatment.

Yes, many of us probably have inherited genes that accelerate this effect,  but they do not appear to be necessary to experience the orexin depleting effects of endotoxin.



It's this simple:

We are infected.   But we can't tell that we're sick. 


First of all, our number one symptom is sleeping.   We're unconscious for craps sake.  I didn't actually consciously experience grinding my teeth until my late twenties, and only because I was lucid dreaming all night long by that point.


Secondly, the symptoms of the actual infections are really mild:  asthma, headache, rhinitis or sinusitis, constipation, depression...

And they are usually residual after a much more acute illness.   We don't notice that we don't recover fully, because we feel so much better than we did... and well...  we're usually cognitively impaired afterward too.


Thirdly we do not feel the pain.   We get cranky instead.



Since the illnesses which actually trigger our problems seem insignificant and unrelated to our really debilitating symptoms-  We tend to ignore them.

We become desperately ill because we don't have alarming sores or feel the discomfort of our infections.



We are infected.   But our doctors don't notice we're sick.

Because we don't present the "standard" array of symptoms, infection is dismissed from consideration.  Even though it's a documented risk factor.

They shuttle us off to specialists who measure all kinds of other things instead, because if they don't do something, they don't get paid.

And then they give us drugs that alter our minds and mask our symptoms so we can never figure it out.





I think this puts us somewhere around (DoublePlus)(UltraOccult)(Bacteremia)² .






This is so incredibly crucial to understand. We are not stupid. We are not crazy. The pathology masks the perception of the pathology in almost every conceivable way.


Which sort of makes my argument difficult to prove...

But these processes are so basic, so predictable, it would be highly unlikely that this is not the primary mechanism.


I have been trying to figure this out for decades.

In the last ten years I have talked to and observed hundreds of us.

And this is what we all have in common:


Recurrent Strep Infections.  Multiple Rounds of Antibiotics.  




Why this matters.


Ummmm, because this contagion carousel makes us weird.  And miserable.  And unpredictable.   And unemployable.  And poor.  We can't afford our own health care.

And it never seems to get better.


Sepsis is a predictable outcome of these processes.
Sepsis explains the sudden onset of acute symptoms.
Especially suicidality.

Low orexin levels cause depression. Sometimes perpetual debilitating melancholia. But it's really not the worst feeling in the world. Most of the time we usually don't actively consider suicide. It's a lot of effort, and we're too tired. So we just lie in bed and get sicker.

On the other hand, the eventual crossing of the event horizon into sepsis causes an immediate spike in histamine and cortisol and other stress hormones, while further lowering orexin levels. Not only are we miserable, we start to panic. And that's when things get really bad. We get self-destructive.
And we suddenly have the motivation and energy to follow through...

That's absolutely terrifying.
That's what I call a nightmare.



Why this matters right the hell now.


Because the current Narcolepsy protocols address none of this.   It's all a mystery to them.

Sleep doctors just rake in the testing bucks and prescribe CPAP and stimulant drugs as fast as they can.   The only criteria for the success of their protocols is if they get us to shut up and go away.

They are actually going to test GHB on elementary school children.  That's how desperate and greedy they are.   

That is absolutely unacceptable.   Those kids would probably fully recover if their doctors had half a  clue.   Short term endotoxin exposure does not kill orexin cells...



And even more urgent:


Some sleep researchers actually are figuring out that the underlying trigger of Narcolepsy is a strep infection.  

However, they probably won't figure out the endotoxin twist right away. 


And as noted earlier....sleep doctors are extremely frivolous about pumping drugs into us.   It's the path of least resistance and most revenue.  They realize we're more desperate than they are, we'll try anything.

So the first thing they are likely to do is put a bunch of sleepy kids on long term antibiotics and destroy their immune and digestive systems.  Create some more chronically ill perma-patients...


All the medical history I have ever read says that's exactly what will happen next.

It's the primary lesson of the past.


Narcolepsy is already caused by the cumulative effects of inappropriate medical information, treatment, and advice. 

Left to themselves, doctors are going to create even more of it.   Not less.









Pneumonia patients nearly twice as likely to suffer from depression, impairments
Pneumonia is the second most common hospital-acquired infection
Cognitive and Functional Decline Often Follow Severe Sepsis





If you start looking for people with walking bacteremia, you will find them.

If you tell people they might have suppressed infections and to look for secondary symptoms, they will notice them.




It has become evident that we can't just stop eating sugar or just "eradicate the strep infection"  we have to interrupt and address this whole cycle. 

I believe the key is suppressing the strep infection without rupturing millions of bacteria to do it, and restoring epithelial integrity in the mouth, nose, lungs and guts. At the same time.


Healing your guts won't be effective without suppressing your infections.

And suppressing your infections won't work without healing your digestive system.


We have to rebuild our whole immune system.

And do preventative maintenance over the long term.


It seems we can recover decent functionality, if we don't make it worse...






Infection Control:



Most antibiotics kill bacteria by rupturing their cell membranes...  they are bacteriolytic. 

The amounts of total endotoxin released, free endotoxin, and the rate of release of endotoxin varies with the antibiotic used.

Beta Lactam antibiotics seem to cause the most problems.    

Those include penicillin, ampicillin, amoxycillin and keflex, which surely are familiar to my readers.


 Pre-treatment with a bacterial protein synthesis inhibitor reducea the strong release of bacterial products usually observed during treatment with a beta-lactam antibiotic.  105  106


Ciprofloxacin kills bacteria by interrupting cell division.   It has shown some anti-endotoxin effects.  But it still results in some bacterial bursting and endotoxin release.  107 108  109



Macrolide antibiotics do not puncture the cells to kill them.

They have been shown to reduce the amount of endotoxemia after use.  110


Macrolide antibiotics appropriate for strep include:  azithromycin, clarithromycin. erythromycin. fidaxomicin. and telithromycin.


Clarithromycin has been tested on narcoleptics and had some positive results.  

111  112







Strep vaccines look promising for the long term.

Flu vaccines, not so much.


The relatively new conjugate vaccine against Streptococcus pneumoniae, given to infants, has greatly reduced the incidence of occult pneumococcal bacteremia.

However, it doesn't seem to work nearly as well on older kids who are already colonized...

A significant percentage of children with recurrent infections fail to produce adequate antibodies following pneumococcal immunization.    113


Similarly, Flu shots are not effective in preventing flu-related hospitalizations in asthmatic children. 114 

Live virus influenza vaccine has been shown to induce the same immune changes and promote strep pneumonia the same as natural infection.  115

And flu vaccine seems to be especially vulnerable to endotoxin contamination. 116    117   118

Vaccines are not required to adhere to endotoxin levels as outlined in the United States Pharmacopoeia.


Sialidase-based anti-influenza virus therapy has been shown to be protective against secondary pneumococcal infection, though.   119





Vitamin D3


Vitamin D3 is crucial to intestinal immune function.   It should be on the checklist when the doctor first talks to us.


There are tons of studies showing vitamin D deficiency is associated with illness.

Tonsillitis, upper respiratory infection, sepsis, obesity...  the list is very long.


And that supplementing with vitamin D improves illness parameters.

tonsillitis, respiratory infections, depression.   

120  121  122  123  124  125 126


Current studies show the established recommended levels are far too low.   You should be taking between 2000-5000 IU per day.


Getting out in the sun is important though.  It activates your immune system and increases orexin production.

(Bonus twist:  Vitamin D deficiency makes your eyes more sensitive so you don't want to go outside.)




There are a few other existing drugs that might be promising:



Metformin  improves intestinal barrier function.  It alleviates fructose induced liver damage.  It has been used for decades in Type 2 diabetes.  It has been proven safe and well tolerated.  The fact that this drug has not been tested on us is a travesty. 127


Lithium chloride induces partial responsiveness to LPS in nonresponder B cells, which may account for some of lithium's efficacy in mania and depression.  128


Ketamine seems like it might be a viable candidate for crisis intervention.

Large dose ketamine halts the progression of sepsis, and inhibits lipopolysaccharide induced acute lung injury in rats.  129  130

And it also provides rapid relief to depressed and suicidal individuals...131


It looks like Lidocaine might be another possible antiseptic anesthetic.   132   133 


Nicotine - is anti-inflammatory and tightens up intestinal epithelium.   134 135

It has been shown to relieve numerous neurological and digestive disorders.  136  137


Marijuana- also increases intestinal integrity via cannabinoid type 1 receptor activation   138

And cannabidiol has been shown to reduce cognitive impairment after pneumococcal meningitis. 139





NSAIDS  increase intestinal permeability.  this includes ibuprophen and naproxen, but not aspirin.  140  141  142


Statins have been shown to reduce septic pneumonia complications, but it may be due to suppression of the immune response by endotoxin or other means.  They also strongly increase the incidence of Type 2 diabetes over the long term, an indicator they may just be facilitating chronic colonization.










This particular research obsession started for me when I observed that a gluten free diet drastically reduced my symptoms.  And then learning that other narcoleptics reported the same thing.  I have been searching for the reason ever since.


This mechanism explains it.  These processes destroy our intestines and ruin our metabolism.


That is why certain dietary interventions ameliorate our symptoms.   They reduce intestinal permeability.   And thereby lower systemic bacteria levels.


Gluten increases intestinal permeability.

It increases permeability even in people who don't have an allergy or "intolerance."   Gluten binds to the intestines directly and increases intestinal permeability though the release of zonulin.   Zonulin not only disassembles intestinal tight junctions, but all tight junctions, including your blood-brain barrier.


And the reason a wheat free diet is not sufficient to alleviate symptoms in a lot of people...

Other foods and other things trigger the same response.




We could really use some appropriate diet protocols.

The standard recommendations to "lower fat" and "eat fruits and vegetables" drastically worsen our condition.

We all need to be told to lower our carbohydrate intake and eat more protein and fat. It just doesn't get any more basic than that.

·         The orexin suppressing properties of sugar require that you restrict it from your diet.

·         That includes eliminating almost all carbs if you are a woman.

·         Protein increases orexin production.  143

·         And the gut healing properties of fats are crucial to your complete recovery.



I don't have a lot of advice to give yet.  These are the things I have found so far.   I'm sure y'all will figure out more.




A ketogenic diet (very low-carb) improves narcoleptic symptoms.   144


Patients with Chronic fatigue syndrome showed indications of endotoxin and increased gut permeability.   And their symptoms were ameliorated with improvement of intestinal integrity.

Patients with major depressive disorder also exhibited intestinal permeability and endotoxemia.

145  146  147  148





Things to avoid.   Things that cause intestinal/mouth permeability.


Alcohol- once you are as sick as us, it's not helping anymore.  149


Fructose- fruit juice is not an appropriate substitute.  You may not give up drinking and take up smoothies.   Just like alcohol,  it induces endotoxemia and liver injury in every test they do.  That's why it's correlated with obesity.   150


Gluten (gliadin).  Uh huh.    151


Special shout out to beer here.  A potent concoction of alcohol and gluten that disintegrates your intestines and allows toxins to accumulate in your belly and liver...


Dietary fructooligosaccharides increase intestinal permeability in rats and humans.   152  153
FOS is mildly sweet and is founds in fruits and vegetables and some grains and cereals, such as wheat and barley.


Corn oil increases gut permeability, in a mouse model of alcoholic liver disease.   154


Green and unripe tomatoes, cherry tomatoes contain the glycoalkyloid alpha tomatine.

Potatoes -- are concentrated sources of two glycoalkyloids which also degrade the gut lining and increase leakage of LPS from gut into circulation.

Dairy -- in allergic people casein increases intestinal permeability.


The following all have saponins, which increase gut permeability

Peppers- Hot peppers, cayenne, paprika, green peppers etc.

Legumes- Soy beans (including soy products: tempeh, tofu, soy sauce, soy oil etc) lentils, peas, beans, and peanuts
Oats , Quinoa, and Amaranth
Alfalfa sprouts contain some of the highest concentrations of saponins in any plant substance and dramatically alter intestinal physiology.




Things to include:


Green or White Tea- has been documented to reverse many of the effects of endotoxin: 

pain, fatigue, immobility, sickness behavior, liver damage.    155  156  157  158  159  160


Coffee, coffee, coffee.   Reduces insulin resistance.  Improves glucose metabolism  161


Omega 3- high dose fish oil reduced inflammation in endotoxin induced sepsis.   162

Saturated fat- also reduces intestinal permeability and alcoholic liver disease. 163


Glutamine administration improves the prognosis of critically ill patients presumably by maintaining the intestinal barrier and by reducing the frequency of infections.  164   165


l-Arginine-  reduces inflammation and stimulates growth and prevents endotoxin-induced death of intestinal cells.    166  167


Butyrate- enhances the intestinal barrier in tissue tests, and  improves insulin sensitivity and increases energy expenditure in mice.  168  169

Butyric acid is found in milk, butter, parmesan cheese.




Antibiotics kill off a lot of the bacteria that live in your intestine.  Some of them are beneficial.

We must restore our intestinal microbial populations.


Speaking of butyrate:

Butyric acid decreases intestinal epithelial permeability by increasing the expression of tight junction proteins.  Butyric acid-producing bacteria have been proposed as a  probiotic treatment  for inflammatory bowel disease  170

Lactobacillus bacterial strains have been shown to alleviate almost all of these factors.

pneumonia, endotoxemia, alcoholic liver disease, intestinal permeability... 171  172


Prebiotics are usually fructooligosaccharides which increase permeability.

One study concludes that the adverse effects of FOS on the resistance to intestinal infections in their studies do not support the concept that stimulating the intestinal microflora with prebiotics is beneficial to humans.173








These infections tend to run in families.   And persist in our households.

We reinfect ourselves and each other all the time.  But don't panic...

We can improve our own immunity so we don't have to worry so much about contact with microbes.


Cleaning your hair, mouth, nose, and skin is crucial for infection control.   You must also moisturize your skin and mucous membranes.   You are probably breathing lysin all over yourself.   Dried out tissues promote bacterial growth. 


Avoid Sodium Laurel Sulfate.  It's a detergent used in beauty products and it removes the oil from your skin.   Ruins your epithelial integrity.  Skin is your first defense against microbes.

It's in your soap and shampoo and toothpaste.  You need to switch products.


I now use castille soap.

And "extra mild flavor" olive oil, because it doesn't make me smell like salad. 

The oleic acid in olive oil suppresses strep bacteria. It is safe for use on the skin and in the ears, nose, mouth and nether regions.

If your skin is very problematic, I suggest epsom salt or baking soda baths too. 


Don't forget your hands.   Ripped fingernails and ordinary cuts and injuries all contribute to bacteremia.    I find gardening or painting will dry them out, cause cracks,  and trigger my obsessive and arthritic symptoms.


Hydration of the nose, mouth, and skin is crucial.

However, when we are acutely ill, this seems like the last thing we want to do.  And that accelerates the infections. You must clean every day to avoid getting too sick to do it at all.

You must take a shower and wash out your nose and mouth every day. Because that's where the microbes are.  The less you feel like doing it, the more necessary it is.


If you are eating clean and lying in bed wondering why you are miserable,

This is what you should be thinking:

It's because I'm sick.  I need to get up and clean my head.

Repeat it until you do it.





Aerobic exercise is quite beneficial for long term fitness, and it lowers insulin resistance and raises orexin levels too.   174   However- the muscle in obese individuals produces a high amount of a protein called myostatin which suppresses muscle growth. Strenuous exercise is not recommended if you are too heavy.    And too much strenuous exercise is not recommended at all.  (Compulsive exercising is a sign of endotoxin induced mania. Have some white tea instead.)


Low impact movement is required, though

Even mild activity improves blood circulation and digestion.

But more importantly:

Exercise stimulates and drains the lymphatic system.  It has vessels running through your body to clear immune debris, and we have a lot of that.   It's a passive system though, it doesn’t have a pump like your blood circulation.   You have to move your muscles around so your lymph nodes will drain.


I especially recommend walking and shoulder exercises-

The regular rhythm of walking allows gravity to move the toxins down from your head and neck and into your chest cavity where they can be cleared.

But you have to work out your arms and shoulders too, or everything backs up in your stiff neck...


I believe head and neck massages fit in here too.

(If you crave face massages, you have trigeminal neuralgia.)




The medical/dental solution to apnea is mechanical. Mouth guards and CPAP.

Both of those breed bacteria, and CPAP  is associated with increased incidence of pneumonia.  175  176


Conversely, simple and inexpensive cleaning methods are highly effective in controlling oral and nasal colonization.

Here is my link to nasal care.







All the triggers and effects of orexin depletion point to periodontal disease as a practically inevitable outcome of narcolepsy.

Strep pyogenes is a bacteria that creates lesions in your mouth and throat.

And people with Strep pneumonia get that into their mouths too.

We breathe and swallow lysin all the time.   It destroys our gums.

And guess what, periodontal lesions and abscesses are the Number One Cause of bacteremia and endotoxemia... there are gram negative bacteria in your gum pockets too...



·         A propensity for sleeping after eating facilitates bacterial growth in the mouth.

·         Inflammation of the tissues promotes crevices and impairs salivary drainage, especially behind the molars.

·         I believe orthodontia greatly contributes to chronic oral infection. The appliances tear up the oral tissues, and the traction damages the bony structure.  Gum recission is documented to increase after braces.

·         Low orexin levels curtail osteoblast production. Your bone production is lower than normal.

·         We tend to have smaller jaws from reduced human growth hormone production. that causes poor saliva drainage.

·         Strep bacteria also deposit calcium in your salivary ducts clogging them up, Low saliva allows more bacteria to grow and more calcium to accumulate.

·         Stimulants reduce saliva production further.

·         This fundamentally alters carbohydrate digestion as amylase is in saliva.

Crowded and impacted wisdom teeth are probably the number one cause of symptoms in young adults. 

They often rot even before eruption, and even if not, they crush the surrounding tissues and promote infection. The symptoms are usually ignored until no longer possible. And then there is some pretty traumatic surgery.


Interestingly- chlorhexedine rinse does not seem to affect LPS activity.  177  178


Speaking of treatments that make it worse- Toothpaste is going to kill you.

My recommendations for dental care.




Pre and post surgical care.


The protocols involving tonsillectomy have shifted radically back and forth in my lifetime.  When I was young, doctors cut them out and pumped you full of penicillin practically without thinking.


These days they don't seem to want to do it at all.    I have numerous reports from young people describing yearly tonsillitis and antibiotic treatment without even a concern from their doctors, much less the recommendation of surgery.


Both of those practices are unacceptable.  There has to be a better way.

I'm pretty sure this dire outcome is fueled by bacteriolytic antibiotic use in the first place, and the real solution involves treating the infection more appropriately before it gets critical, but that's not going to help a lot of people right now...


So an intermediate strategy would be to reduce the immune response before surgery and minimizing the trauma during the process.  

Vitamin D and some mouth rinses sound like a good start.

Using appropriate antibiotics only if necessary. 

No opiates for pain because they suppress the immune system.

And not eating sugary ice cream afterward.  Yeah.



Tooth Extraction

Ditto for getting teeth pulled.  

Especially. Wisdom. Teeth.

You need to prepare and plan for that.   It's major trauma.


Halothane gas pretreatment drastically increases bacterial load in Strep pneumonia.  179

They don't use this very much anymore, but I have vivid memories of the terrifying effects.


For the record:

If you are under the age of 30, I will pretty much assume you have either tonsillitis or wisdom teeth problems.







Women with narcolepsy are extra vulnerable to the immune and metabolic changes during pregnancy.

Strep B has a strong tendency to flare up.  

Insulin resistance is higher.

Periodontitis increases.

Sleep decreases.


Autism spectrum disorders seem to be common in our offspring too.

For you ladies who have been trying to figure this out with me...

Yeah, prenatal endotoxin affects neurodevelopment.   And messes with our children's glucose metabolism too.   It's surely a major contributor to their problems.

Antibiotic treatment during pregnancy needs to be reassessed immediately.









The strep infection is connected to the sepsis response

The sepsis response is connected to the antibiotics

The antibiotics are connected to the endotoxemia
The endotoxin is connected to the cortisol
It's also connected to the orexin cells
Orexin cells are connected to the insulin resistance
The insulin resistance is connected to the obesity
The obesity is connected to the brain fog.
And it all just makes us tired.





You doctors might want to look into this:

Limulus amebocyte lysate (LAL) testing has been shown to be a quick and practical method, with a high sensitivity and specificity for endotoxin.

The Lactulose/mannitol test  is for intestinal permeability.

Those sound like a better use of resources than the MSLT.



Oh, and you researchers really need to start segregating all your narcolepsy experimental results by sex.

Get some accurate metabolic data, please.




The major lesson we need to take away from this scenario is that our illness is concealed.

We need to be really creative in looking for more sources of feedback cancellation in the mechanism.



I have so far described what happens once a person has been infected by strep.

We need to look at why it happens in the first place.

A susceptibility to recurrent strep infection seems like a good way to cause this outcome.

We need to start looking for things that cause that.   Like the flu virus...



C reactive protein deficiency


C reactive protein (CRP) is an immune molecule that is produced in reaction to the C polysaccharide of the strep Pneumonia bacteria. and binds to it and activates the immune system.

C reactive protein is one of the things they test as an indication of "inflammation'.  that's code for immune response.


·         C-reactive protein is essential for innate resistance to pneumococcal infection  180

·         CRP-deficient mice are remarkably susceptible to Streptococcus pneumoniae infection

·         C-reactive protein has several potentially antibacterial effects, and variation in the CRP gene is known to influence CRP levels in humans.   181

·         A common CRP genetic variant has been associated with susceptibility to invasive pneumococcal disease.  182 

·         Mutations of the C-reactive protein gene are associated with mortality in strep pneumoniae bacteremia. 183


CRP deficiency is a real interesting concept in our scenario-


If CRP fights off strep infections

And we happen to produce low levels of CRP,

Then we will get more strep infections.

And we will test negative.


That is just the right amount of irony to make me think it must be true.


Strep antibody deficiency would result in something very similar...




I am now assuming that the DQB1-0602 gene contributes to either strep susceptibility or intestinal permeability, not gluten sensitivity in specific.     Somebody should look into that.  Maybe.  Someday.   


I am getting a lot of reports of MTHFR gene mutations.   MTHFR mutations cause problems with folic acid metabolism.

Folic acid reduced the severity of complications from pneumococcal meningitis.  184



The  R620W version of the PTPN22 gene is associated with invasive pneumococcal disease, and seems to be sourced in Northern Europe...    185  186




Toll-like receptor 2–deficient mice are highly susceptible to streptococcus pneumoniae meningitis.  That might be a clue.  187






Somebody. Please. Investigate. Pain. Suppression.


Substance P- is an important element in pain perception. The sensory function of substance P is thought to be related to the transmission of pain information into the central nervous system.

Substance P and other sensory neuropeptides can be released from the peripheral terminals of sensory nerve fibers in the skin, muscle and joints.


Substance P seems to be a multifunctional molecule in this scenario.


·         Pain behaviors induced by mechanical, thermal, and chemical stimulation of peripheral and internal tissues were reduced in mutant mice lacking substance P receptors.  It also increased aggression....   188

·         It also seems to trigger the immune system.  Substance P reduces pneumonia rates after traumatic brain injury.  189

·         Substance P also contributes to fever pathology.  190

·         And very interestingly, Orexin axons and substance P neurons, share a common interface neuron in the spinal cord.    191



I wonder if that could be related to this...

Children with intractable constipation show a deficiency of intestinal substance P nerve fibers.  192





For further inspiration,   I recommend this book:

Rheumatic Fever in America and Britain: A Biological, Epidemiological, and Medical History by Peter C. English M.D.


You probably aren't interested in the 900 page volume on endotoxin...  193





Thank you for reading my rambling.









I told you that your days were numbered.

Tick Tock.  Time's Up.


You are already obsolete and just don't know it yet.

Narcolepsy just *poof* disappeared before your eyes.   It's not a rare incurable disease, it's a symptom of infection.  And a big fat indicator of medical malpractice...

Ditto insomnia and apnea, darlings.  Sucks to be you.


Plausible deniability is no longer an option.

There is boatloads of literature on Pneumonia and Sepsis and Endotoxin. 

Sepsis is the number one problem in emergency care.  Always has been...

Post-antibiotic endotoxin release has been documented since antibiotics were discovered.

And LPS is the molecule they use to "model" chronic disease for crap's sake.   All those experiments about "inflammation"?  That's induced with endotoxin.     They inject animals with LPS and they get all our symptoms dammit.

Almost all the research we need has already been done.   It's just not filed under Narcolepsy.  You can be sure we will find it anyway, though-  we're actually extremely motivated under these droopy eyelids.   Not that you would notice...


We no longer want to play Suppress the Symptoms and Microbial Whak-a-Mole with you.

We are just getting worse while you are out shopping for another house.


I am guessing, that given the available options, none of us would choose to treat our bleeding gums or runny nose with a powerful central nervous system depressant that costs thousands of dollars.

Just sayin.

And I bet we would also reassess the option to take more antibiotics if we knew it might make us fat or bald or freaking-out-on-the-floor miserable...


We are sick and tired of being sick and tired.


And we do understand the Germ Theory of Disease.  

It is now very apparent that we don't need your "sleep experts" or your whiz-bang brain scanners, breathing machines and Schedule I drugs, they are merely a waste of our time, money and brain cells.

Some competently educated community care nurses should be able to handle this.


Here's the reality:  

You are merely diverting our attention and prolonging our progression.

·         For decades, you have somehow managed not to diagnose some of the most common illnesses on the planet.

·         Your current protocols insure we will never be accurately diagnosed...

·         Even though these infections are already notated somewhere in our charts.  


It's time to stop measuring irrelevant sleep parameters and start swabbing noses and throats.

Then pony up some real solutions or get the hell out of our way. 






This document was posted by Heidi Lindborg on July 7, 2015.  

but I am surely still tweaking on it.   I have a few more citations to insert...





1              Narcolepsy and Streptococcal Infections


2            Elevated Anti-Streptococcal Antibodies in Patients with Recent Narcolepsy Onset


5          Influenza and Bacterial Pathogen Coinfections in the 20th Century


10          Invasive Bacterial Infections in Relation to Influenza Outbreaks, 2006–2010


13 Seriously, I have at least 50 citations... email me if you want them.

14       Septic shock


17      Inflammation-induced lethargy is mediated by suppression of orexin neuron activity


18     Endotoxin tolerance impairs antimicrobial capacity in bacterial pneumonia and decreases murine lung inflammation


23     Bacterial Endotoxin in Human Disease


24     Translocation of gut flora and its role in sepsis


25        Antibiotic induced endotoxin release and clinical sepsis: a review.


26     Clinical relevance of antibiotic-induced endotoxin release.


30      Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells


31     Tetracyclines Disturb Mitochondrial Function across Eukaryotic Models: A Call for Caution in Biomedical Research


32    A single dose of endotoxin increases intestinal permeability in healthy humans.


33   Endotoxemia-induced Inflammation and the Effect on the Human Brain


34   Lipopolysaccharide increases plasma levels of corticotropin-releasing hormone in rats.


35    Dose-Dependent Effects of Endotoxin on Neurobehavioral Functions in Humans


36   Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration.


40         Sepsis causes neuroinflammation and concomitant decrease of cerebral metabolism.


43      Cognitive impairment in sepsis survivors from cecal ligation and perforation.


44      Behavioral deficits in sepsis-surviving rats induced by cecal ligation and perforation.


45       Sepsis-induced alterations in sleep of rats.


46        Gender Differences in Human Sepsis


47     Incidence of Septic Complications and Multiple Organ Failure in Severely Injured Patients Is Sex Specific

48    Gender differences in the inflammatory response and survival following haemorrhage and subsequent sepsis


55         Male gender is associated with increased risk for postinjury pneumonia.


56        The effect of orexins on intestinal motility in vitro in fed and fasted rats.


59        Central and local (enteric) action of orexins.


60         Orexin receptor expression in human adipose tissue: effects of orexin-A and orexin-B


61        Plasma orexin A, orexin B, leptin, neuropeptide Y (NPY) and insulin in obese women.


63      Orexin Is Required for Brown Adipose Tissue Development, Differentiation, and Function


65       Insulin Increases Sensitivity to GABA


66      Pancreatic Insulin Content Regulation by the Estrogen Receptor ERα


67     Leptin modulates orexin-mediated functions at the behavioral and cellular level in mice


68    Metabolism-Independent Sugar Sensing in Central Orexin Neurons


69      Sleepiness after glucose in narcolepsy.


70       Hypothalamic orexin expression: modulation by blood glucose and feeding


71      Effect of LPS on the permeability of the blood–brain barrier to insulin


73    Endotoxemia Is Associated With an Increased Risk of Incident Diabetes


74    A role for abdominal vagal afferents in lipopolysaccharide-induced hypotension.


75     Tuning arousal with optogenetic modulation of locus coeruleus neurons


77      Hypoglycemia


78  Altered skin-temperature regulation in narcolepsy relates to sleep propensity.


79    Involvement of sympathetic nervous system and brown fat in endotoxin-induced fever in rats


80     Orexin Is Required for Brown Adipose Tissue Development, Differentiation, and Function


81    Greatly increased numbers of histamine cells in human narcolepsy with cataplexy.


83  Metabolic and Hormonal Response to Endotoxin Fever in Fed and Starved One-Week Rabbits


85   Bacterial Pore-Forming Cytolysins Induce Neuronal Damage in a Rat Model of Neonatal Meningitis


87 The effect of endotoxin on nociception in mice.


88              Insulin Attenuates Formalin-Induced Nociceptive Response in Mice through a Mechanism that Is Deranged by Diabetes Mellitus


91         Hypoglycemia


92      Insulin, cognition, and dementia.


96     Orexin receptor 1 signaling contributes to ethanol binge-like drinking: Pharmacological and molecular evidence


97    Benzodiazepines and related drugs: pneumonia.


100          Central and peripheral metabolic changes induced by gamma-hydroxybutyrate.


103       Effect of sodium oxybutyrate on the development of a staphylococcal intoxication.


104       The impact of gender on timeliness of narcolepsy diagnosis.


112      Clarithromycin in GABA-related Hypersomnolence: A Randomized, Crossover Trial.


113        Response to pneumococcal immunization in children with and without recurrent infections.


114     Flu shots are not effective in preventing flu-related hospitalizations in asthmatic children


116     Clinical implications of endotoxin concentrations in vaccines.


117    Acceptable levels of endotoxin in vaccine formulations during preclinical research.


118   GSK confident despite ongoing endotoxin problems at Canadian flu vaccine plant


120      The role of vitamin D in children with recurrent tonsillopharyngitis.


121     Vitamin D levels in children with recurrent tonsillitis.


122    Vitamin D and mucosal immune function.


125    Prevalence of Vitamin D Deficiency Among Overweight and Obese US Children


126   Association of low serum vitamin D levels and sepsis in the critically ill.


127  Metformin protects against the development of fructose-induced steatosis in mice by improving intestinal barrier function


128 Lithium chloride induces partial responsiveness to LPS in nonresponder B cells


129   Mechanisms of ketamine-induced immunosuppression.


130    Large dose ketamine inhibits lipopolysaccharide-induced acute lung injury in rats.


135  Nicotine and inflammatory neurological disorders


142     Intestinal permeability and inflammation in patients on NSAIDs


143    Activation of Central Orexin/Hypocretin Neurons by Dietary Amino Acids


144    Diet therapy for narcolepsy.


148  The gut-brain barrier in major depression


150         Dietary fructose induces endotoxemia and liver injury in calorically controlled primates.


152       Dietary Fructooligosaccharides Increase Intestinal Permeability in Rats


153      Dietary Fructooligosaccharides Affect Intestinal Barrier Function in Healthy Men


156      Reversal of LPS-induced central and peripheral hyperalgesia by green tea extract.


158    Green tea extract and catechin ameliorate chronic fatigue-induced oxidative stress in mice.


159      Green tea (Camellia sinensis) extract ameliorates endotoxin induced sickness behavior and liver damage in rats.


162     Omega-3 PUFA supplementation and the response to evoked endotoxemia in healthy volunteers.


166    l-Arginine stimulates proliferation and prevents endotoxin-induced death of intestinal cells


167   Arginine Cools the Inflamed Gut


169    Butyrate Improves Insulin Sensitivity and Increases Energy Expenditure in Mice


172      Lactobacillus Feeding Reduces Endotoxemia and Severity of Experimental Alcoholic Liver (Disease).


173  Dietary Fructooligosaccharides Affect Intestinal Barrier Function in Healthy Men


175   Influence of sport mouthguards on the ecological factors of the children oral cavity.


176  Sleep apnea and risk of pneumonia: a nationwide population-based study.


177 The Role of Chlorhexidine on Endotoxin Penetration to the Implant-Abutment Interface (IAI).


179  Effect of anesthetics on pathogenesis of experimentally induced murine pneumococcal pneumonia.


180   C-reactive protein is essential for innate resistance to pneumococcal infection


181  CRP gene variation and risk of community-acquired pneumonia.


182 Association of common CRP genetic variant with susceptibility to invasive pneumococcal disease.


185 Why is PTPN22 a good candidate susceptibility gene for autoimmune disease?


186            PTPN22 and invasive bacterial disease


189            Substance P mediated reduced pneumonia rates after traumatic brain injury.


190      Role of Substance P (SP) in the Mediation of Endotoxin (LPS) Fever in Rats


191     Orexin A and orexin receptor 1 axonal traffic in dorsal roots at the CNS/PNS interface.


193   Endotoxin in Health and Disease by Helmut Brade