Epilepsy and Migraines: a theory

James Howard phis at sprynet.com
Wed Jan 1 20:33:52 EST 1997

My theory suggests all tissues of the body depend on 
the "melatonin-DHEA cycle."  I think this cycle is 
necessary for growth, development, and function 
during childhood and adolescence and maintenance 
and function of the adult.  I look for disturbances of 
this cycle to help explain pathology.  Migraine 
headaches and epilepsy may result from malfunctions 
in melatonin (MLT) and DHEA.  Prior to my 
explanation, increased MLT in epilepsy and reduced 
MLT in migraines has been discovered.  However, 
according to a medical literature search (medline), no 
one has addressed any connection of DHEA with 
migraines or epilepsy.  

The main connection of low MLT in migraines is 
found in the female cycle.  MLT "increases 
significantly from the follicular to the luteal phase" in 
normal women’s cycles (Cephalalgia 1995; 15: 136); 
another study found that MLT is significantly 
reduced throughout the cycle in women with 
migraines.  This second study also found that MLT is 
decreased during headaches (Caphalalgia 1994; 14: 
205).  I have read anecdotal remarks on the internet 
that some women have increased migraines during 
the second part of their cycles (luteal phase).  MLT 
begins a steep decrease just prior to puberty, and 
declines rapidly thereafter.  Since, "migraine occurs 
most commonly in men and women aged 25-55 
years" (Neurology 1994; 34 Suppl. 2: 6), I suggest 
that this is a time when MLT reaches critically low 
levels in susceptible people.  Low MLT is somehow 
connected to migraines, but, I suggest, the levels of 
DHEA have to be examined to fully explain it.

I suggest migraines result from low MLT and 
increased DHEA.  Women produce more DHEA 
from birth than men.  This extra DHEA should have 
most effect on migraines prior to the onset of 
interfering sex hormones, before puberty.  It has been 
found that "when the onset [of migraines] is below 
the age of puberty there is a striking predominance of 
women over men in a ratio of 3:1," (Headache 1994; 
34: S8).  It is part of my theory that the hormone, 
testosterone, causes DHEA to be used for 
"testosterone target tissues."  This use of DHEA by 
these tissues should reduce the availability of DHEA, 
i.e., increased testosterone should decrease 
migraines.  This can be seen in the fact that, 
following puberty, women still have more migraines 
and that whites have more migraines than blacks.  
Blacks produce more testosterone than whites.  "In 
women, migraine prevalence was significantly higher 
in Caucasians (20.4%) than in African (16.2%)...  A 
similar pattern was observed among men (8.6%, 
7.2%, ...)." (Neurology 1996; 47: 52).  Interestingly, 
my theory suggests that people of higher testosterone 
congregate together, as in cities, and higher 
DHEA/lower testosterone types tend to live apart 
from cities.  The prevalence of migraines also follows 
this pattern.  "Females, whites, and individuals 
residing in rural counties were more likely to suffer 
migraine headache than their respective comparison 
groups." (Clinical Therapeutics 1994; 16: 855).

I have read that headaches occur when blood vessels 
in the brain constrict.  Since I have suggested 
elsewhere that I think DHEA stimulates constriction 
of blood vessels and increases blood pressure, I 
suggest increased DHEA causes the constriction of 
blood vessels in migraine headaches.  Constricting 
blood vessels and reduced blood flow is 
characteristic in migraines.  "The transient neuronal 
excitatory wave is followed by a longer lasting 
‘depressive’ wave, which involves a substantial 
reduction in cortical blood flow (with an active 
constriction of resistance vessels) and ionic changes 
and transmitter release into the extracellular fluid 
compartment." (Cephalalgia 1992; 12: 75). 

I have produced a theory of sleep that explains the 
connection of MLT and DHEA.  It can be found in 
detail at http://www.naples.net/~nfn03605 on the 
internet.  At its most basic, I suggest melatonin binds 
to neurons and shut them down.  The connection 
with DHEA is that MLT shuts down the nerves that 
release the hormone, prolactin (PRL).  It is also 
known that PRL specifically and powerfully 
stimulates DHEA.  When MLT shuts down PRL, 
DHEA production is reduced and its stimulating 
effects on the brain are reduced.  This is sleep.  Now, 
to keep this from killing us, PRL is released in 
rebound to the negative effects of MLT.  This cycles 
slowly until a large release of PRL occurs in the early 
morning.  This large release of PRL then starts a large 
morning release of DHEA, which awakens us.  In the 
quotation just above, I suggest the "excitatory wave" 
represents the effects of MLT, i.e., the shutdown of 
MLT causes nerves to rebound in response.  I 
suggest the "depressive wave" represents the 
restabilization caused by a subsequent response of 
secreted DHEA.  The increased DHEA causes the 
blood vessel constriction that causes the migraine 

With the foregoing in mind, it should be easier to 
explain epilepsy with the MLT - DHEA cycle.  MLT 
is high in epileptic people.  "Melatonin production in 
untreated patients with active epilepsy is increased 
and had a circadian pattern with a phase difference as 
compared with that of normal subjects." (Epilepsia 
1995; 36: 75).  In the paragraph, just above, I 
demonstrated how MLT can induce the production of 
DHEA.  During the day, my sleep mechanism 
suggests that the larger production of DHEA is 
involved in inhibiting synthesis of MLT from the 
pineal gland (where MLT is made).  This means that 
once DHEA is "used up" during the day, there is not 
enough DHEA to keep the pineal from making MLT.  
When MLT production occurs, the shut down of PRL 
occurs and DHEA is reduced to even lower levels.  
This is how the sleep - wake cycle occurs.

Sleep deprivation keeps MLT from being released.  
This has been determined.  "It was found that the 
melatonin levels were increased after sleep 
deprivation..." (Sleep 1988; 11: 362).  A much later 
study found that MLT was not increased by sleep 
deprivation, but that "Prolactin was higher on the 
post-sleep deprivation and control nights but did not 
rise on the deprivation night." (Journal of Pineal 
Research 1996; 20: 7).  Sleep deprivation increases 
the build up of the thing that stimulates DHEA, i.e., 
prolactin.  Since increased sleep is a consequence of 
sleep deprivation, I suggest MLT increases.  Since it 
is the PRL that stimulates DHEA production, both of 
these studies say, essentially, the same.

There is another way of seeing this.  I have suggested 
that DHEA stimulates the nerves that inhibit synthesis 
of MLT.  I suggest that electroconvulsive shock 
exerts its effects by stimulating DHEA.  In the 
following quotation, I suggest the reduced production 
of MLT is due to increased DHEA, inhibiting the 
pineal gland.  "In ECS [chronic elctroconvulsive 
shock]-treated rats, both pineal and serum melatonin 
levels after isoproterenol administration were 
significantly lower than those in sham-treated animals 
and in rats receiving subconvulsive shock." 
(Psychiatry Research 1994: 53: 185).  

I suggest that the opposite mechanism explains 
epilepsy.  I suggest the increased melatonin found in 
untreated epileptics builds up and is released so that 
nerves are shut down.  Individuals susceptible to 
epilepsy must have entire sections of the brain shut 
down so much that they "rebound" and call up a 
large response of DHEA.  It is this rebound response 
that is the large area of stimulated nerves that cause 
the seizures.  Once the brain has stimulated sufficient 
DHEA, then the seizure stops.
James Howard

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