For a long time now (a year hiatus), I have wanted to delve back into the world of changa. However, I am concerned about the possible risk of serotonin syndrome posed by MAOI inhibitors...And every informed member on the nexus of course knows that the caapi leaf component of changa contains MAOIs.

While I've never experienced adverse effects with changa during the brief time that I used it in the past, Lately I have been concerned that some unforseen factor might interact negatively with the MAOIs in changa.

So, my question is, what are the initial "warning signs" that one is on the precipice of serotonin syndrome due to too much MAO inhibition? If I am going to try changa again, I will start with extremely low dosages and work my way up. Are there certain ill-effects I can look for that would be indicative of an adverse reaction (e.g., nausea, headache, etc)?

This information was pulled from Wikipedia; take it as it is.

Serotonin Syndrome:

Signs and symptoms

Symptom onset is usually rapid, often occurring within minutes. Serotonin syndrome encompasses a wide range of clinical findings. Mild symptoms may only consist of increased heart rate, shivering, sweating, dilated pupils, myoclonus (intermittent tremor or twitching), as well as overresponsive reflexes.[1] Moderate intoxication includes additional abnormalities such as hyperactive bowel sounds, high blood pressure and hyperthermia; a temperature as high as 40 °C (104 °F) is common in moderate intoxication. The overactive reflexes and clonus in moderate cases may be greater in the lower limbs than in the upper limbs. Mental status changes include hypervigilance and agitation.[1] Severe symptoms include severe increases in heart rate and blood pressure that may lead to shock. Temperature may rise to above 41.1 °C (106.0 °F) in life-threatening cases. Other abnormalities include metabolic acidosis, rhabdomyolysis, seizures, renal failure, and disseminated intravascular coagulation; these effects usually arise as a consequence of hyperthermia.[1][3]
The symptoms are often described as a clinical triad of abnormalities:[1][5]
Cognitive effects: headache, agitation, hypomania, mental confusion, hallucinations, coma
Autonomic effects: shivering, sweating, hyperthermia, hypertension, tachycardia, nausea, diarrhea.
Somatic effects: myoclonus (muscle twitching), hyperreflexia (manifested by clonus), tremor.

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Hypertensive Crisis


The eyes may show retinal hemorrhage or an exudate. Papilledema must be present before a diagnosis of malignant hypertension can be made.
The brain shows manifestations of increased intracranial pressure, such as headache, vomiting, and/or subarachnoid or cerebral hemorrhage.
Patients will usually suffer from left ventricular dysfunction.
The kidneys will be affected, resulting in hematuria, proteinuria, and acute renal failure.
It differs from other complications of hypertension in that it is accompanied by papilledema.[2] This can be associated with hypertensive retinopathy.
Other signs and symptoms can include:
Chest pain
Arrhythmias
Headache
Epistaxis
Dyspnea
Faintness or vertigo
Severe anxiety
Agitation
Altered mental status
Paresthesias
Vomiting
Chest pain requires immediate lowering of blood pressure (such as with sodium nitroprusside infusions), while urgencies can be treated with oral agents, with the goal of lowering the mean arterial pressure (MAP) by 20% in 1–2 days with further reduction to "normal" levels in weeks or months. The former use of oral nifedipine, a calcium channel blocker, has been strongly discouraged because it is not absorbed in a controlled and reproducible fashion and has led to serious and fatal hypotensive problems.
Sometimes, the term hypertensive emergency is also used as a generic term, comprising both hypertensive emergency, as a specific term for a serious and urgent condition of elevated blood pressure, and hypertensive urgency, as a specific term of a less serious and less urgent condition (the terminology hypertensive crisis is usually used in this sense).

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Worthy links:


http://en.wikipedia.org/...oamine_oxidase_inhibitor

http://en.wikipedia.org/wiki/Serotonin_syndrome

http://en.wikipedia.org/...tensive_crisis#Treatment

http://en.wikipedia.org/wiki/Antihypertensive

http://en.wikipedia.org/...r_of_monoamine_oxidase_A

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Hope something from these links can help you feel safer.

well..why are you worried about this? Forgive me but I just dont really understand why you are worried about this.

The risk of seratonin syndrom presents itself when you take beta carbolines in the presense of SSRI's or other seratonin upregulators like MDMA etc..there is no reason to be worried at all about seratonin syndrom otherwise.

A headache after you smoke changa is hardly reason to assume it is a symptom of seratonin syndrom comming on..unless you had already taken SSRI's or seratonin upregulators..eating tyramine foods is nothing to worry about either, btw..especially when you are just smoking changa.

The term 'malignant hpertension' is a little out-dated but the wikipedia article rightly defines a hypertensive crisis as a BP of >/= 180/120 with the subdivision into hypertensive urgencies and hypertensive emergencies with the latter having clear signs of cardiovascular/renal/neurological end-organ dysfunction/damage.

The rate of evolution of the uncontrolled hypertension has a major bearing on the development of some of the end-organ damage which can be detected clinically.Papilledema (swelling of the optic nerve head as seen in the retina with an opthalmoscope) can be seen given enough time, and quite often the patient can present before sufficient time has passed for this to be apparent;one may simply see other changes such as retinal hemorrhages and no discernible optic nerve swelling.Also, if one has optic atrophy for whatever reason then papilledema may not develop at all because theres not enough viable nerve fibres in the optic nerve to get the axpolasmic swelling which cumulatively results in the appearance known as papilledema. I personally would not regard papilledema as being an indispensable feature of these types of hypertension; other features in the history and examination may still allow such diagnoses to be made.