I fully understand how you lost all faith in your doctor. You asked him which one had the fewest side effects and he gave you the antidepressant most likely to cause withdrawal and side effects. Doctors have nicknamed the drug sideEffexor.

How ever, switching to Prozac can be useful for many people.

See James's story
theeffexoractivist.org/forum/...pic.php

Prozac has a very long half-life, which helps to minimise withdrawal
problems. Effexor has the shortest half-life which is why so many people have such a hard time with withdrawal. The liquid form of Prozac permits the dose to be reduced more slowly than can be done with
pills.

www.ssri-uksupport.com/files/...RIs.pdf
_________________
One of the important things to know about withdrawal is that for people who are very sensitive to withdrawal, 10% per week can be much to fast.

This is Morse's advice from www.network54.com/Forum/281849/

Try a craft knife, shave slivers off each tablet or indeed consider using a nail file.

The idea of using scales and weighing each part tablet is an excellent idea.

Cutting by a quarter is very ambitious, many folks can only manage cuts of 10%, some only 5%

Wait at least a week, sometimes 2, stabilese before cutting further

Remember it's a cut of 5 or 10% of the last dose you were on, not 10% of the original dose

As u get towards the end of the taper the doses and hence dose reduction is minimal

Remember u taper dose like a reverse exponential curve .........visualise an aeroplane landing

Glide yourself down
____________________________________________________________

We prefer a compounding pharmacist for cutting the dose down but this can be expensive and a pain to find. The analogy of a plane gliding in to land is perfect. Slow and gentle is best.

The following is from a taper plan for getting off Paxil (known as Seroxat in Britain) It can be used with effexor as well.

www.network54.com/Forum/281...Lustral%29

.........If there are difficulties at any particular stage the answer is to wait at that stage for a longer period of time before reducing further........

In some cases people need to stay at each stage for a month or more. Some need to make smaller cuts.

Some people are extremely sensitive to withdrawal effects. If there are problems....., return to the original dose and from there reduce as tolerated...............

Each person is different and each persons tapering program needs to be tailored for the individual. This is why we recommend reading “The Antidepressant Solution” By Joseph Glenmullen M.D.

As well as contacting one of the Professional Practitioners from the National Database for help withdrawing.

You may have been better off, if you had been working with a doctor who is an expert, at dealing with a bad withdrawal.

But the fact is, there is no way to know. I keep thinking that we have found some pattern, such as long term use or high doses or a too quick withdrawal. But then some one like you comes along and proves me wrong.

Anyway, why I posted this... What dose did you take, how long did you take it, how fast did you withdraw, what symptoms did you have, when did they appear, how well have you recovered, how long did it take, and what other drugs (prescription or recreational) were co-administered?

I was on effexor for seven years. I was also on celexa for a good part of that time as effexor was not working for me. I sure do admire your brain power and mental stamina. I am mentally fogged up today and cannot attempt the long drawn out story that constitutes my antidepressant use. I took my first ad 18 years ago - was given prozac for back pain. At the time the label named it differently I only recently clued into the fact that it was prozac. I had a terrible reaction to it halucinated the whole nine yards yet it didn't happen immediately and the connection was never made. As I was told the med was for my back I was not expecting any reaction thought it was like tylenol. After a long time trying to recover and not know what was wrong with me I was diagnosed with chronic fatigue sent to a pain clinic and given amitrityline. which is laughable considering amitriptyline inhibits serotonin[1] and noradrenaline reuptake almost equally. I had severe insomnia and it did help me sleep but led to years of ad use and several cold turkeys. It has been one hell of a ride.
I will continue this another time in the mean time for you information you may want to read this. I find helpful.
I have thought this too long to post but I think mentally you are up to it.
"All Truth passes through Three Stages: First, it is Ridiculed...
Second, it is Violently Opposed...
Third, it is Accepted as being Self-Evident." - Arthur Schopenhauer (1778-1860)

The Serotonergic System, the Pineal Gland and SSRI-AntiDepressant Side-Effects
-Part 1-


1. Introduction: Neurons & Neurotransmitters
The billions of working cells in our brain are called Neurons. There is a great variety in the kind of brain cells or neurons in the brain. Each group of neurons represent a specific cluster of functions. A neuron is communicating with another neuron (of the same kind), by firing molecules from it's nerve endings to the receiving nerve endings of the other neuron. The nerve endings of the firing part of the neuron are called axon terminals and the nerve endings of the receiving part of the neuron are called dendrites. The end of the axon terminals are called synapses. The space where synapses and dendrites meet each other -and where all the activity takes place- is called the synaptic cleft. Each neuron is able to receive and to fire molecules simultaniously. The molecules which are fired in the synaptic cleft are called neurotransmitters. Situated at the end of the axon terminals of the firing part of the neuron, the synapses work like "ball throwers." The dendrites of the receiving part of the other neuron, work like "catcher's mitts." They use receptor-molecules, or receptors, to capture the "thrown" neurotransmitters. (See Picture)
Re-Uptake
Once one neuron is firing neurotransmitters from it's synapse to the receiving dendrite of the other neuron, it is critically important that the "mis-fired" neurotransmitter left overs must be removed from the synaptic cleft. Any neurotransmitter which is not removed from the synaptic cleft, prevents further neurotransmitters from getting through. Re-uptake, the process of removing neurotransmitters after firing or release, allow these neurotransmitter left overs to be recycled for further use. Re-uptake is carried out by "transporter proteins" which bind to the mis-fired neurotransmitter and carry it across the plasma membrane back into the synapse of the firing neuron.
Medication classified "Re-Uptake Inhibitors" act on these transporter proteins and thereby inhibit the re-uptake of neurotransmitters back into the synapse of the firing neuron. SSRI-AntiDepressants or Selective Serotonin Re-uptake Inhibitors, belong to this class of medication. Each group of neurons fire specific neurotransmitter-molecules. The neurotransmitter Serotonin, also known as 5-Hydroxy-Tryptamine (5-HT) is such a molecule. SSRI-AntiDepressants inhibit the re-uptake of serotonin what means that more serotonin will be fired from synapse to dendrite in the synaptic cleft of every communicating serotonergic neuron in the brain.
2. The neurotransmitter "Serotonin"
In the brain, serotonin is synthesized from the amino acid precursor "Tryptophan". By enzymatic interaction, tryptophan converts into 5-HTP and eventually into serotonin. (see image) This neurotransmitter belongs to the group of serotonergic neurons which make the Serotonergic System in the brain. Levels of serotonin are highly concentrated in the Raphe Nuclei. Raphe Nuclei are present in the Medulla and Pons, 2 structures which are part of the Brainstem. From the Raphe Nuclei in the pons of the brainstem, also called "Rostral Raphe Nuclei", serotonin pathways project through parts of the Limbic System (like the Thalamus and Hypothalamus) into the Forebrain. (See Picture)
2.a. Serotonergic functioning
If you would believe the overwhelming advertisements of the pharmaceutical companies, you would think that serotonin primarily regulates mood. In fact, serotonin regulates a lot of other activities in the brain and body. In 1948, Maurice Rapport, a hematologist, found that serotonin tended to make blood form clots, and it tended to be a muscle- as well as a vasoconstrictor. Next to be a muscle- and vasoconstrictor, serotonin plays an important role in sleep, appetite, memory, sexual behavior, respiratory activity, aggression, motor output, sensory and neuroendocrine function, but most important, perception! Since 1988 the serotonin hype brought us several SSRI-AntiDepressants all stimulating this neurotransmitter. For about 11 years now, Dr. Ann Blake Tracy (Prozac: Panacea or Pandora?), persistently warns the public against raising serotonin levels. Doctor Tracy has tought us that an increase in serotonin produces rushes of insulin dropping sugar levels and chemically inducing hypoglycaemia (low blood sugar) in this way. Other sources have learned us that too much serotonin damages blood vessels, particularly in the lungs, and may also harm heart valves. This would be due to the fact that serotonin is a powerful vasoconstrictor.
Affecting mood or mind?
But most alarming is the serotonin and perception connection. Doctor Tracy and other sources described how the hallucinogenic drug LSD strongly acts on this neurotransmitter serotonin. The numurous examples of human LSD experiences have learned us that serotonin plays a major part in perception, our sense of reality, how we experience our in- and outside world! Other examples of drugs acting on the serotonergic system are PCP and MDMA (Ecstasy). Most of the readers will recognize also these serotonergic drugs for their capability to produce "an altered state of consciousness" in human beings. In the way that the serotonergic system responds to serotonergic drugs, we may conclude that this system is heavily involved in the determination of ones perception and therefore ones thought processes and emotions. The advertisements from the pharmaceutical companies, promoting elevated serotonin levels as were they purely mood lifting, therefore seem to be rather misleading then informative. SSRI-AntiDepressants are to be considered mind-altering drugs and not primarily mood-altering.
In all these years since 1988, scientists are still not shure why serotonin boosters seem to "alleviate" depression. They assume that low serotonin levels could be a possible cause of endogenous depression, but it's still just a theory and not a proven fact! New research present us a different view on serotonin, which may not even have that connection with mood as previously thought. By experimental research, scientists discovered that a new drug, code-named MK-869, blocked a neuropeptide called " Substance P." By blocking this neuropeptide, people became less depressed. An interesting fact was, that blocking substance P did not affect the function of serotonin! This raises new concerns about the involvement of serotonin in mood and/or depression.
But how come that I hear people talking about benefits from these SSRI-AntiDepressants?, you might want to ask. They surely must work somehow don't they? The answer is yes, they "work" somehow, but not in a very proper way. What actually happens when you elevate your serotonin levels is this: the stress hormones "Cortisol" and "Adrenaline" (Epinephrine) in the brain and body are triggered by elevated serotonin levels. It is a natural reaction from the body to combat the excessive serotonin levels. These released hormones, cortisol and adrenaline, are secreted from the "Adrenal Glands." They give the human personality a boost, producing a euphoric state, which can last for a prolonged period of time! In this manner SSRI-AntiDepressants initially produce the deceptive results the doctor and "patient" are both expecting. Unfortunately when the bodies Adrenal Glands lose their efficiency, then "Adrenal Exhaustion Syndrome" will be the end result. Adrenal Exhaustion causes levels of adrenaline initially to fall and levels of cortisol to rise. Ultimately, also cortisol levels fall. When untreated, Adrenal Exhaustion will lead to seriously declining physical health. Many (former) SSRI-AntiDepressant users reported fatigue as a long term side-effect or were diagnosed with "Chronigue Fatigue Syndrome." People suffering from stress are generally diagnosed with this disorder. Symptoms range from simple exhaustion to much more complex problems that are secondary to excessive output of adrenal hormones in the bloodstream, leading to Adrenal Exhaustion. Unlike the other hormones, it takes a long time before the Adrenal Glands have their adrenaline levels restored. Could we say that the SSRI-AntiDepressant "works" by slowly excavating the body's Adrenal Glands?
The Serotonin-Cycle: beaconing of conscious awareness and dream sleep?
One of the first significant discoveries about the serotonergic system in the brain was that it's activity was dramatically altered across the sleep-wake cycle. Serotonergic activity gradually decreases as one becomes drowsy and enter slow-wave sleep. An overall slowing of serotonergic activity is observed during slow-wave sleep known as non-REM sleep. During REM sleep (Rapid Eye Movement-the original dream sleep), serotonergic activity falls completely silent. Serotonergic activity returns to it's basic level several seconds prior to the end of REM sleep. REM sleep occurs in roughly 90-100 minute cycles, alternating with non-REM sleep (around 4 to 5 times during sleep). During non-REM sleep, there is lots of movement, but during REM sleep, only the eye muscles move. REM-dreaming turns on neurons in the medulla of the brainstem that inhibit all other motor activity. In this way it prevents the dreamer from sleepwalking and to act out his/her dreams in real time.
Another significant discovery was that, when during REM sleep the serotonergic neurons in the brainstem were "off" (silent), cholinergic neurons in the brainstem were "on" (firing)! Cholinergic neurons fire the neurotransmitter "Acetylcholine." Acetylcholine not only plays an important role in dreaming, but also in long-term memory processes. In the brainstem, the cholinergic "REM-on" neurons can only trigger REM sleep (and thus dreaming) when the serotonergic "REM-off" neurons are inactive. This happens because, in the brainstem, the serotonergic neurons inhibit the cholinergic neurons whilst we are awake. When, in the brainstem, the serotonergic neurons release their inhibitory constraint, only then, the cholinergic brainstem neurons will be able to get active, triggering the REM-dream sleep. Both the REM-on and the REM-off cells are localized in the brainstem. These brainstem mechanisms work as an "oscillator", which controls the transitions from waking to sleeping and further controls the REM/non-REM cycle, which occurs 4 to 5 times during sleep.
Now at this moment you might ask yourself, how it is possible that so many individuals report bizarre vivid lifelike dreams whilst on serotonin boosters, when an active serotonergic system suppresses REM sleep, and thereby dreaming? Serotonergic suppression of REM sleep in humans by acute dosage of SSRI-AntiDepressants was indeed confirmed. (see article) This is what Dr. Tracy is also been telling us for many years in her book. The PubMed article discusses rebound of REM sleep after abrupt withdrawal from an SSRI-AntiDepressant, but it still doesn't answer the question how it is possible that individuals are experiencing disturbing dreams and nightmares whilst they are taking an SSRI-AntiDepressant over a prolonged period of time. When I delved deeper into this matter I discovered some interesting facts. Although there is an important link between REM sleep and dreaming, they are in fact doubly dissociable states. That is, REM can occur without dreaming and dreaming can occur without REM. Although REM is triggered from the brainstem, it alone will not result in dream states. Dreams require input from the forebrain and structures in the limbic system. The forebrain mechanisms are the final common path to dreaming. The brainstem is just one of the many arousal triggers that can activate these forebrain mechanisms. Although REM sleep is controlled by the brainstem, dreaming seems to be controlled by these forebrain mechanisms. It is now acknowledged that REM sleep is not necessary for dreaming, that dreaming can also occur during non-REM sleep, and that dream-like experiences can even be elicited during quiet wakefulness! The controversial human reports of very vivid lifelike dreams whilst taking an SSRI-AntiDepressant could therefore be explained as existing outside and independent of the REM (dream) sleep! But, -now that we know that the forebrain is the final common path to dreaming, and SSRI-AntiDepressants suppress the brainstem's REM arousal system (which normaly activates forebrain dreaming)- what kind of arousal triggers are then responsable for the activation of forebrain dreams during use of SSRI-AntiDepressants?
Serotonergic Forebrain Seizures?
An even more exciting discovery was that dreaming can also be induced by focal forebrain stimulation and by complex partial forebrain seizures during non-REM sleep, whithout the involvement of the brainstem's REM mechanism! There is a causal link between epileptic activity and recurring nightmares during non-REM sleep. This was demonstrated by the famous neurosurgeon and researcher Wilder Penfield, who was able to reproduce these anxious experiences artificially in the form of waking "dreamy state" seizures. The causal link between forebrain seizures and recurring nightmares was confirmed by the fact that both the underlying seizure disorder and the nightmares responded to anticonvulsant therapy.
Here is an example of a recurring nightmare, caused by epileptic activity in the forebrain:
The patient [35 year old woman with idiopathic complex-partial seizures] reported a recurrent dream about her [dead] brother ... which has reappeared several times. The dream is as follows: "I am walking down the street. I meet him. He is with a group of people whom I know now. I feel that I will be so happy to see him. I say to him, `I'm glad you're alive,' but he'll deny that he is my brother and he'll say so, and I'll wake up crying and trying to convince him."' Electroencephalography revealed a poorly defined right anterior temporal / right temporal spike focus which appeared with the onset of drowsiness and light sleep (Epstein & Ervin 1957, p. 45).
Could it be that the bizarre vivid lifelike dreams, reported by SSRI-AntiDepressant users are epileptiform of nature? Notice the "poorly defined spike focus." Could it be that this is epileptic activity which remains undiscovered because it is bearly detectable? Standard tests for epilepsy included?
3. The Pineal Gland
The Pineal Gland -also called the epiphysis- looks like a miniature pine cone and is situated in the middle of the brain beneath the two brain halves, surrounded by the ventricles, under the roof of the corpus callosum (cross-beam connecting the 2 brain halves). (see picture) This active organ has, together with the Pituitary Gland (see picture), the next highest blood circulation after the kidneys. It is not protected by the blood-brain barrier and therefore makes this gland fragile to any substance entering the bloodstream. It is, for instance, very sensitive to fluoride.
Another factor involved in affecting the Pineal Gland can be excessive high or toxic levels of an SSRI-AntiDepressant in the bloodstream. Certain individuals have a metabolic deficiency in the metabolism of SSRI-AntiDepressants. In the liver, cytochrome P-450 enzymes, also called CYP2D6 enzymes, metabolize SSRI-AntiDepressants. When not properly metabolized, because one has a metabolic deficiency, an SSRI-AntiDepressant can build to excessive high or toxic levels in the bloodstream. Hence, the Pineal Gland would be an easy target, since it is not protected by the blood-brain barrier. It is it's connection to serotonin what makes this organ so very interesting.
3.a. The Pineal Gland-Serotonin connection
Nicholas Giarmin, a professor of pharmacology and Daniel Freedman, a professor of psychiatry, confirmed that the human brain manufactures serotonin at various sites in the brain. For example, in the Thalamus, they discovered 61 nanograms of serotonin per gram of tissue; in the Hippocampus, 56 ng.; in the Central Gray Section of the Midbrain, they found 482 ng. But in the Pineal Gland, they found 3140 ng. of serotonin per gram of tissue. The Pineal Gland was unmistakably the richest site of serotonin in the brain! This discovery implicates the Pineal Gland as an important site of serotonergic activity.
The neurohormone Melatonin & the Endocrine System
One of the neurotransmitters secreted by the Pineal Gland is Melatonin, also known as N-Acetyl-5-Methoxy-Tryptamine (NA-5-MT). In the Pineal Gland, serotonin converts into melatonin by enzymatic interaction. Melatonin is also an important hormone to the body, that's why it is called a neurohormone. It is necessary to regulate the function of all organs of the Endocrine System in the body. The organs or glands of the endocrine system are: the Pituitary Gland, situated in the brain; the Thyroid + Parathyroid Glands; the Thymus; the Pancreas; the Ovaries/Testes (see image). All of these endocrine organs/glands secrete their hormones to the blood. The Pituitary Gland stimulates the secretion of these hormones, while the Pineal Gland apply the brakes on them through it's neurohormone melatonin. If the endocrine organs/glands release too much of their hormones, for instance when we are stressed, then the Pineal Gland releases melatonin to counteract these hormones. Also serotonin gets released when stress is involved. The increased serotonin triggers the release of adrenaline, which allows the body to work through the stress.
The Pineal Gland is a magnetosensitive organ, what means that it is sensitive to electromagnetic fields (EMF). It is sensitive to electromagnetic waves from computer monitors, cellular phones, microwave ovens, high voltage lines, etc.. Electromagnetic fields suppress the activity of the Pineal Gland and reduce melatonin production. EMF also affect serotonin.
The neurohormone Melatonin & the Eye-SCN-Pineal Gland Axis
The Pineal Gland is also a photosensitive organ, what means that it is sensitive to light. It normally releases melatonin when it no longer receives light impulses. Just like serotonin, also melatonin has it's own day & night cycle (circadian rhythm) which begins where the cycle of serotonin normally ends. When serotonin reaches it's lowest level at night (in the dark) during slow wave sleep, the Pineal Gland starts to convert it's store of serotonin into melatonin to be released prior to REM sleep. Melatonin has it's peak around 02:00 AM. During daytime, the daylight inhibits the release of melatonin. This works as follows: when, during daytime, light reaches the eyes, then it's presence gets translated into nerve impulses, which travel through the optic nerve between the eyes and a region of the Hypothalamus called the "Suprachiasmatic Nucleus" (SCN). (see picture) The SCN in it's turn sends it's nerve impulses to the Pineal Gland. These impulses inhibit the Pineal Gland's production of melatonin until it gets dark, when it's to be released again.
Melatonin is not only present in the brain and body but also in the eye! One has speculated whether or not high melatonin levels in the eyes during daylight exposure, may bring damage to them over time. Visual/eye problems (lightsensitivity, spots, blurred vision) are other symptoms, frequently reported by (former) SSRI-AntiDepressant users. I questioned myself if these problems could be related to elevated melatonin levels in the eye. When serotonin accumulates in the Pineal Gland, on account of an SSRI-AntiDepressant, then it would come under pressure to produce more melatonin out of the excessive amounts of serotonin. Hence, during daytime, melatonin levels in the eyes would be significantly higher then normally would occur...
But, I had to revise this hypothesis. In a PubMed study, SSRI-AntiDepressants were found not to elevate melatonin levels in humans. Although "Luvox" and "Paxil" increases melatonin to a more or lesser amount, apparently this seemed not to be the case for the other SSRI-AntiDepressants. However, since the Pineal Gland does contain a complete map of the visual field of the eyes, could there be a correlation between visual/eye problems and a disfunctional Pineal Gland?
A case, noted by Dr. Berman, could give us some more insight into this matter:
A child was brought to a German clinic suffering from eye trouble and headaches. He was five years old and very mature, and apparently had reached the age of adolescence. He was abnormally bright mentally, discussing metaphysical and spiritual subjects. He was strongly group-conscious and only happy when sharing what he had with others. After his arrival at the clinic, he rapidly grew worse and died in a month. An autopsy showed a tumor of the pineal gland. - Berman, Louis, M.D., The Glands Regulating Personality, p. 89.
Could it be that the visual/eye problems (lightsensitivity, spots, blurred vision), frequently reported by (former) SSRI-AntiDepressant users, are caused by some element of Pineal Gland disfunction?
-CONTINUE PART 2-

-Part 2-


Psychoactive substances, Serotonin and the Pineal Gland
Melatonin is not the only neurotransmitter made out of serotonin. Other serotonin derivatives which are psychoactive or mind altering are thought to be produced by the Pineal Gland. The necessary enzymes for the formation of these molecules exist in high concentrations in the Pineal Gland. By acute administration -either smoked or injected into the bloodstream- of one of these serotonin derivatives, also known as tryptamines, humans will experience an altered state of consciousness, which can differ from "hypnogogic dream-like states" to full blown "hallucinatory psychosis." It is recently thought that these molecules are responsible for our dream imagery. They are, just like melatonin, released at night, prior to REM-sleep and interact within the central nervous system. DMT (Di-Methoxy-Tryptamine) and 5-MeO-DMT (5-Methoxy-Tryptamine) are such tryptamines and serotonin derivatives. They can produce color imagery, out of body(like) experiences, lucid dreams, visions of beings and/or animals, mystical states, subjective "other realities" as well as experiences of "being somewhere else." DMT and 5-MeO-DMT can be extremely frightening when smoked or injected for the first time.
Another psychoactive serotonin derivative produced by the Pineal Gland is called Pinoline, also known as 6-Methoxy-Tetra-Hydro-Beta-Carboline (6-Methoxy-THBC). Pinoline is not a tryptamine but a beta-carboline. It is similar to harmaline, an extract from the psychoactive plants Banisteriopsi Caapi and Psycotria Viridis in the Amazonian Rain Forest. Harmaline is the active ingredient in a psychadelic cocktail called "Ayahuasca." It is used by Indian tribes and shamans to communicate with the spirits telepathically while they "dream awake."
Also a very interesting molecule is Bufotenine, also known as 5-Hydroxy-Dimethyl-Tryptamine (5-HDT). Although bufotenine is both a serotonin derivative and a tryptamine it is not established yet if it is produced by the Pineal Gland. It also occurs naturally in humans but in very small amounts. In higher amounts it becomes highly toxic. Bufotenine also derives from the dermal substance of a toad. The Shamans of the ancient Maya ingested bufotenine on special ceremonies. It would turn the user into a "mouthpiece for the gods." The effects seem as being possessed by an evil spirit.
3.b. The Disrupted Serotonin Cycle & The Malfunctioning Pineal Gland
SSRI-AntiDepressants inhibit the re-uptake of serotonin into the firing synapse of the serotonergic neuron. As a result, more serotonin is fired continuously to the receiving dendrite which results in more serotonin in the synaptic cleft. Because of this continuous action, the natural cycle of serotonergic activity during daytime and serotonergic inactivity at night gets disrupted! Under the influence of the SSRI-AntiDepressant, the serotonergic system now works overtime, 24 hours a day. The implications of a disrupted serotonin cycle could be as follows:
What can happen, when the serotonergic system isn't cycling anymore, in a natural circadian rhythm, is that daily consciousness will shift closer and closer to the "dream state". The verge between reality and dreaming will gradually become blurred. The lack of rhythm is the cause. Under the influence of an SSRI-AntiDepressant, serotonin levels won't fluctuate anymore, but remain continiously high. Many SSRI-AntiDepressant users reported that they had problems to distinguish reality from dreaming when they woke up from a dream and that it took quiet some time to realize that they had been dreaming instead of experiencing something real.
Consciousness on the verge of Dreaming and Reality
We already know that an active serotonergic system suppressess REM sleep and thereby REM related dreaming. Our brains need to dream. Although we do not always remember our dreams, we are dreaming around 4 to 5 times every night. Only a few days of sleep deprivation (and thus dreaming) will cause the brain to hallucinate. To counteract the SSRI-AntiDepressant induced suppression of REM related dreaming, the brain litterly forces it's dreams upon us. This doesn't necessarily has to be a rebound of REM related dreaming triggered by the brainstem mechanisms (since an active serotonergic system suppresses these mechanisms), but could as well be induced by epileptic activity in the forebrain, triggering forebrain dreams or nightmares, as previously discussed. Most critical, when the normal brainstem REM mechanisms are not included in these forebrain dreams or nightmares, then they won't turn on the cells in the medulla that inhibit all motor activity. The implications of this contradictional dream sleep could be quiet dramatic.
Next to experiencing hallucinations, suppression of REM sleep can lead to an other serious disorder. On page 45 of her brilliant book "Prozac: Pancea or Pandora?", Doctor Ann Blake Tracy introduced us to the violent REM Sleep Behavior Disorder, caused by psychoactive drugs such as SSRI-AntiDepressants. This condition means a sleepwalk nightmare wherein the patient acts out violent dreams while sleepwalking. The violent REM Sleep Behavior Disorder is further discussed in chapter 7: "Sleepdisorders, serotonin and the SSRI's" on page 182.
From SSRI-AntiDepressant induced "consciousness on the verge of dreaming and reality", it will be a very close step to SSRI-AntiDepressant induced "psychosis" or "hallucinatory psychosis", in which extremely lifelike dreams/nightmares become hallucinations and will be experienced for real! Many (former) SSRI-AntiDepressant users reported major perception changes, altered states of consciousness, a disturbed sense of reality and out of character behavior. The symptoms vary from urges to spend money excessively, flamboyant/provocative behavior, indifference and mania, till abnormal dream and thought patterns, racing thoughts, hearing voices or telepathic like thoughts and akathisia (an extreme mental state of inner restlessness). Also frequently reported is the feeling of living in a bubble, feeling possessed or living in a dream.
I questioned myself if it could be possible that the psychoactive serotonin derivatives, which are thought to be secreted by the Pineal Gland, could play a (secondary) role in these reported altered states of consciousness and behavior. Under the influence of an SSRI-AntiDepressant, serotonin levels in the Pineal Gland could increase to excessive, possibly even toxic amounts. Although I had to revise my previous hypothesis regarding increased melatonin levels in the eyes (melatonin levels didn't increase under the influence of an SSRI-AntiDepressant), this time I found more support for the hypothesis that certain serotonin derivatives, like the psychoactive tryptamines DMT, 5-MeO-DMT and Bufotenine, could very well increase on account of an SSRI-AntiDepressant.
In an article published on the internet, Dr. Callaway states that the natural re-uptake of serotonin account for most of the inactivation of these psychoactive tryptamines. Blocking the re-uptake of serotonin, like SSRI-AntiDepressants do, could not only increase serotonin levels but also the levels of the other psychoactive tryptamines, whether or not secreted by the Pineal Gland. Furthermore, Dr. Callaway discusses the possible correlation between tryptamines and our dream imagery: "Since these same Psychoactive tryptamines occur in humans, it is possible that their activity may be promoted by the actions of endogenous beta-carbolines for normal psychological processes; e.g. the production of visual / emotive imagery in sleep. The periodic altering of consciousness in sleep may even be necessary for the maintenance of normal mental health, since only a few days of sleep deprivation will result in a seepage of hallucinatory phenomena into the waking state." -Tryptamines, Beta-carbolines and You. Dr J.C. Callaway, Dept. of Pharmaceutical Chemistry, University of Kuopio, Finland
An absolutely shocking discovery was the correlation between high serotonin levels in the Pineal Gland and certain mental disorders! During autopsy on recently dead mental patients, Giarmin and Freedman (see chapter 3.a.) discovered that the Pineal Glands of those who had suffered from specified mental disorders, showed a considerable excess of serotonin in their Pineal Glands. The average amount of serotonin found in the Pineal Glands of normal persons is about 3.14 to 3.52 micrograms per gram of tissue. One schizophrenic was found to have a Pineal Gland containing 10 micrograms of serotonin, around 3 times higher, while another patient, a sufferer from delirium tremens, had a Pineal Gland containing 22.82 micrograms of serotonin, around 10 times higher then the avarage amount!
This is a most interesting research contemplating the similarities between symptoms of schizophrenia or schizophrenic psychosis and SSRI-AntiDepressant induced perception changes, altered states of consciousness, disturbed sense of reality and out of character behavior in severe cases. As a direct result from the actions of the SSRI-AntiDepressant (disruption of the natural serotonin cycle), serotonin levels in the Pineal Gland could gradually increase to excessive amounts comparable to the excessive amounts of serotonin in the Pineal Glands of recently dead mental patients. Hence, the production of psychoactive serotonin derivatives increases, which can lead to excessive amounts of these molecules in the brain. The combined effects of suppression of REM sleep, excessive amounts of serotonin in the Pineal Gland, as well as elevated levels of psychoactive serotonin derivatives, could make an individual experience hypnogogic dream-like states (which depersonalize an individual from their own emotions) to full blown "hallucinatory psychosis." ( A; B; C)
Tardive Dyskinesia & Parkinsonism
Other frequently reported neurological side-effects from SSRI-AntiDepressants, involving loss of motor control, are called Tardive Dyskinesia/Dystonia and Parkinsonism. Tardive Dyskinesia/Dystonia is the collective noun for various abnormal involuntary body movements like: tics and twitches in the face or/and around the eye, muscle spasms, muscle contractions in the neck, jaw, tongue, or/and shoulders and irregular jerking movements in body parts. Parkinsonism is a term used to indicate symptoms similar to those seen in Parkinson's disease like: apathy or indifference, tremors and muscle stiffness.
Dr. Joseph Glenmullen (Prozac Backlash) introduced us to these terms and defined them as related to damaged dopaminergic neurons in the limbic system. The SSRI-AntiDepressant induced increased serotonin would cause a downregulation of the neurotransmitter dopamine and therefore cause the same damage at dopaminergic neurons as observed with neuroleptic (anti-psychotic) treatment.
However, in 4 PubMed articles (1; 2; 3; 4), Tardive Dyskinesia and Parkinsonism are associated with disturbances of serotonin and melatonin secretion and a malfunctioning Pineal Gland. The represented cases involve neuroleptic-induced movement disorders related to Pineal Gland calcification. There were "significant differences between the severity of dystonic movements in patients with no Pineal Gland calcification and those with pathologically enlarged Pineal Gland calcification."
Could there be a similar existing pattern in (former) SSRI-AntiDepressant users? Further research will be needed to establish if (former) SSRI-AntiDepressant users who have more or less severe Tardive Dyskinesia/Dystonia and Parkinsonism, are actually suffering from a malfunctioning Pineal Gland, whether or not calcified. This research could involve measurements of plasma melatonin levels.
The Endocrine System
A malfunctioning Pineal Gland and disturbances in serotonin and melatonin secretion could also lead to excessively secreted hormones of the Endocrine System. Women who are experiencing side-effects after discontinuing their SSRI-AntiDepressant, mentioned a worsening of their problems around their ovulation period. Normally, the Pineal Gland releases melatonin to sedate the Endocrine Organs/Glands when they are too active or stressed. When this doesn't happen, because of the disturbed natural melatonin cycle, then the hormones of the Endocrine System which usually are released every period, could now cause problems.
-CONTINUE PART 3-


4. Side-Effects: withdrawal or brain-damage?
SSRI-AntiDepressants certainly don't raise your serotonin levels in a gentle manner. They prevent serotonin from being removed from the synaptic cleft. As a result, a lot of excess firing takes place and therefore more serotonin remains in the synaptic cleft. In this manner, the (receiving) post-synaptic receptors get bombarded with serotonin. According to Gary Null, Ph.D., all this overstimulation causes a decrease in the number of post-synaptic receptors. Depending on the intensity and duration of blocking re-uptake, around 30% to 40% of the post-synaptic receptors will be eliminated (Eli Lilly, the manufacturer of Prozac, would knew about the disappearance of receptors from their laboratory experiments). It is not established whether or not receptors ever come back after discontinuing an SSRI-AntiDepressant. The damage may be permanent or not.
Apparently this is not the only neuro damage caused by SSRI-AntiDepressants. In a recent study, researchers saw marked changes in the axon terminals (nerve endings) of serotonergic neurons in rats, treated with SSRI-AntiDepressants. The terminals shriveled or took on corkscrew shapes. These changes were similar to those observed with the serotonin booster drug "Ecstasy" (MDMA). In studies with baboons who were treated with Ecstasy, researchers used Positron Emission Tomography (PET) to take brain scans of them. The researchers found that Ecstasy was toxic to the brain and damaged the axon terminals (nerve endings) of serotonergic neurons. This damage was still present in the baboons 7 years after discontinuing the drug. Later studies in humans who had used Ecstasy, documented the same damage at serotonergic neurons as observed with the baboons. Likewise, the SSRI-AntiDepressant induced brain damage observed in the rats, could be present in humans as well.
Previously we discussed that an SSRI-AntiDepressant induced hyperactive serotonergic system, could lead to disruption of the circadian (daily) serotonin cycle and excessive amounts of serotonin in the Pineal Gland. Another dangerous situation occurs when a hyperactive serotonergic system causes a condition called the "Serotonin Syndrome." This is a serious life threatening condition which needs immediate and adequate treatment.
An underactive serotonergic system will be a result of (1)the damaged axon terminals at the firing part of the serotonergic neuron and/or (2)the eliminated receptors at the dendrites of the receiving part of the serotonergic neuron. When discontinuing an SSRI-AntiDepressant, serotonergic activity dramatically decreases because the neurons aren't able to communicate properly with eachother anymore. As a result of this decreased serotonergic activity, side-effects occur, which are falsely defined as "withdrawal side-effects." p> Sensory Disturbances
Some of these side-effects are the frequently reported electrical shocks, zaps or shivers through the head (brain) and/or body, lightflickering in the head, "falling into walls" along with "pinns and needles" in the skin. Sometimes these phenomena are so severe that the individual who's experiencing them, feels very confused or like being on the verge of blacking out, losing consciousness.
It's striking how consciousness seem to be involved in these "sensory disturbances." I was thinking about an indirect neuronal mechanism, responsible for these phenomena. Serotonin is an inhibitory neurotransmitter. An underactive serotonergic system would not inhibit other neurotransmitters anymore, like dopamine, or acetylcholine released by the cholinergic neurons in the brainstem (which are responsible for the extreme rebound of REM dreams when discontinuing an SSRI-AntiDepressant). Hence, these neurons would start to fire excessively, causing the side-effects as described above.
Another explanation could be that the serotonergic neurons are excessively firing their impulses through the axon to the axon terminals and synapses, as a compensatory mechanism for the loss of electrochemical activity in the synaptic cleft. In this manner, serotonergic electrochemical bursts of discharges would take place in the brain. Both examples of excessive electrochemical activity in the brain could be defined as epileptic activity. (see chapter 2.a. (3)Forebrain Nightmares and Forebrain Seizures)
Epileptic Activity
One reason why these "sensory disturbances" side-effects are not recognized as epileptic activity, could be because they are not the full blown epileptic seizures that we know of and which are visible to others. As a matter of fact, epileptic activity can occur as petit mal seizures called "absences." Absences are blanks in the short-term memory that remain invisible to the observer. Researchers Hutt and Gilbert of the University of Keele in England, performed tests on children with epilepsy, in which they were using stroboscope flashlights. It occured that 18 flashlights per second induced these absences in epileptic children.
This reminded me of the problems which some former SSRI-AntiDepressant users reported that they had with flashing sunrays through the trees when passing them in a car, or that they were forgatten that they were doing something in the midst of the process of doing it. Could these problems, as well as the other side-effects, be related to epileptic activity, possibly in the forebrain? Some SSRI-Antidepressant users were even more less fortunate, they developed full blown epileptic seizures whilst taking the drug, which remained after discontinuation.
Another factor in epileptic activity could be a malfunctioning Pineal Gland. In 3 PubMed articles the Pineal Gland, as well as it's neurohormone melatonin are discussed in relation to epileptic seizures. Significant changes were found in "day-night melatonin levels during convulsions, consistent with the hypothesis that melatonin has an inhibitory function on central nervous system activity." (1) Patients with epileptic seizures had "a significantly lower urinary secretion of melatonin, which may indicate that melatonin has a protective effect on seizures" (2) and the Pineal Gland and melatonin "exert a major influence in the control of brain electrical activity and have been shown to be involved in seizure and sleep mechanisms." (3)
My particular attention got attracted by the Pineal Gland as a magnetosensitive organ. Former SSRI-AntiDepressant users reported that the electrical shocks, zaps or shivers through the head (brain) and/or body, as well as the lightflickering in the head, increased in severity when working behind a computer monitor. Computer monitors are known to radiate low frequency electromagnetic waves. Knowing that electromagnetic fields (EMF) affect serotonin, melatonin and the Pineal Gland, these electromagnetic waves could therefore trigger epileptic activity by altering the functions of the Pineal Gland. Here is a field of research to establish if these post-SSRI-Antidepressant side-effects are indeed epileptiform of nature and if forebrain seizures -whether serotonergic, dopaminergic or cholinergic- as well as the Pineal Gland are involved.
Hypoglycaemia (Low Blood Sugar)
Ramo Kabbani, the Director of the Prozac Survivors Support Group (PSSG) in England, developed seizures within a month of going on Prozac. She had four EEGs, three of which proved abnormal but inconclusive. This means that there was some minor abnormality there, but they did not know what was causing it and they didn't bother investigating it further. Remember the case of Epstein and Ervin (see chapter 2.a. (3)Forebrain Nightmares and Forebrain Seizures) in which EEG also revealed a poorly defined spike focus in a woman who was experiencing seizures.
An interesting fact that Ramo discovered was, that everytime when she had a seizure or a zap, her sugar levels plummeted to extremely low levels. Other (former) Prozac users that have been having seizures and zaps, who contacted the help line of the PSSG in England, have all found that they have low blood sugar levels. Low blood sugar, or low blood glucose, occurs when blood levels of glucose drop too low to fuel the body's activity. This condition is called "Hypoglycaemia," when the body isn't able anymore to maintain normal levels of glucose in the bloodstream. Glucose levels are determined by how fast glucose enters and leaves the bloodstream. When glucose leaves the bloodstream it enters the brain, which needs a constant supply of it to function properly.
In other PubMed articles the involvement of the Pineal Gland was discussed in the regulation of glucose metabolism in the brain (1; 2). In animal studies the Pineal Gland's neurohormone melatonin was found to significantly increase both brain and blood levels of glucose i.e. by enhancing carbohydrate metabolism into glucose (1; 2). Previously I mentioned that Doctor Tracy has tought us that an increase in serotonin, produces rushes of insulin, dropping sugar levels and chemically inducing hypoglycaemia (low blood glucose) in this way. In another animal study published at PubMed it was found that insulin-induced hypoglycaemia also affected the Adrenal Glands and caused a dramatic decrease of serotonin in the Pineal Gland. (1) This could lead to disturbances in melatonin secretion after which blood glucose levels can fall even lower.
Epilogue...
Whether or not the function of the Pineal Gland gets affected by SSRI-AntiDepressants, either owing to a metabolic deficiency, or damaged serotonergic nerve terminals and receptors, or as a result of a hyperactive serotonergic system, needs to be established. A malfunctioning Pineal Gland could lead to disturbances in the natural circadian rhythm of melatonin secretion, as well as disturbances in glucose metabolism in the brain and an overall decrease of brain and blood levels of glucose. Hence, the natural defense to epileptic activity in the brain will fall off, as well as the natural defense to a hyperactive Endocrine System.
>>>to be continued...>>>
October 2001, Charles Groenendijk, The Netherlands.
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Blessed are the cracked for they are the one who let in the light.
Life is what happens when your busy making other plans.

I think you are right. there have been test on rats that show the receptors in the brain were shaped like a corkscrew after antidepressant use there is a lot more to this for sure. I wish we could force some accountability but doubt that will ever happen.

Although I acknowledge that abrupt withdrawal is potentially torturous and life-threatening, I have this hypothesis that it makes little difference how fast someone withdraws, for the long-term outcome. I am curious if we can detect a trend, since many have told me that I withdrew too fast and that is why I got sick. I am skeptical of this claim, as I am of other claims. I suspect that it is the dose, length of treatment, individual susceptibility, and interactions with other drugs that determine the long-term outcome... not how fast one withdraws.

The above is a quote from you cheryle and I am tempted to agree with you as I have watched on withdrawal boards as many sufferred thru withdrawal and some had horrible effects that never left even with a slow taper. Seems they refuse to study or collect the information that is readily available. Part of the fraud I would say.

Another crazy thing that hit my head. You were sueing when you were given antidepressants and guess what so was I. Both of us were given drugs we didn't need. What does that say to you anything or is it my paranoid brain. Us and them get on the wrong side of them they will debilitate you with drugs hmmm what a thought. So much for first do no harm.