_This Kratom FAQ has been compiled to help people gain a better understanding of Kratom and how it can work in the body and also help debunk false myths about Kratom. Some of the Questions and subsequent answers are quite technical, so we have attempted to define some of the more important keywords for you. If you get confused, feel free to shoot us an email with further questions._
> KRATOM TREES (MITRAGYNA SPECIOSA) TREES USUALLY GROW TO A HEIGHT OF 12–30 FT (3.7–9.1 M) TALL AND 15 FT (4.6 M) WIDE, ALTHOUGH SOME SPECIES CAN REACH 40–100 FT (12–30 M) IN HEIGHT.
**Q: What is Kratom?** A: Kratom is a tree native to Southeast Asia in the Indochina and Malaysia floristic regions. Its botanical name is Mitragyna Speciosa [mih-tr-ah-jin-yah | spee-see-OH-sah]. Kratom is in the same family as the coffee tree Rubiaceae. The leaves of Kratom have been used as an herbal drug for centuries by peoples of Southeast Asia.
**Q: What are the effects of Kratom?** A: At lower doses, it is used in folk medicine as a stimulant, reducing stress, anxiety and depression*, and at higher doses acts as a sedative for painkiller, recreational and medicinal use. Finally, Kratom is reported as being used for withdrawal treatment for opiate addiction and recovery*. For more details about this topic, please visit our kratom effects.
**Q: What’s in Kratom?** A: Chemistry Make up of Kratom: There are 40 compounds in M. speciosa leaves, including many alkaloids such as mitragynine (once thought to be the primary active constituent), mitraphylline, and 7-hydroxymitragynine (which is currently the most likely candidate for the primary active chemical in the plant). Other active chemicals in M. speciosa include raubasine (best known from Rauwolfia serpentina) and some Yohimbe alkaloids such as corynantheidine. Mitragyna speciosa also contains at least one alkaloid (rhynchophylline) that is a calcium channel blocker and reduces NMDA-induced current. There is considerable research as to the role of NMDA receptor activity in the formation of dependence, and the symptoms of withdrawal.
**Q: What are Alkaloids?** A: Alkaloids are a group of naturally occurring chemical compounds, that contain mostly basic nitrogen atoms.
**Q: I hear the use of the term ANALGESIC. What does that term mean and how is it relevant to Kratom?** A: An analgesic, or painkiller, is any member of the group of drugs used to achieve analgesia — relief from pain. The word analgesic derives from Greek αν – (“without”) and άλγος – (“pain”). There are many types of analgesic drugs from anesthesia to opiates such as oxycontin, oxycodone, Percocet, and Vicodin. It is relevant to Kratom since Kratom is considered analgesic in nature.
**Q: What’s the best way to use Kratom?** A: This is mostly about personal preference. Using kratom capsules provides convenience and a tasteless/odorless experience. Using kratom powder, while more involved, generally produces quicker effects. So, it’s really up to you.
**Q: Is Kratom safe?** A: When used in moderation, kratom is safe.
**Q: Can you overdose on Kratom?** A: No reports from overdose on kratom alone are documented. Unlike other drugs such as Oxycontin or Vicodin which are synthetic, Kratom is unique due to the fact that if you take a dose stronger than your body needs it will expel it naturally. Taking Kratom by itself has not been found to result in overdose.
**Q: Can I get sick from using too much Kratom?** A: Every pro can have a con. Here it is: Yes, it is possible to get minor hot flashes and a tummy ache. This effect will generally last 30-60 minutes. Please keep in mind, this effect only occurs if you have used more than the body needs. If this occurs, drink a cool glass of water and lay down in a dimly lit room.
**Q: I have heard about Hypoventilation and it being associated with overdoses. What is Hypoventilation and can this happen with using Kratom?** A: No, Hypoventilation has not been reported to occur when you use Kratom independently, without any other substance. _Read more below about hypoventilation._ _Hypoventilation:_ In medicine, hypoventilation (also known as respiratory depression) occurs when ventilation is inadequate (hypo meaning “below”) to perform the needed gas exchange. By definition, it causes an increased concentration of carbon dioxide (hypercapnia) and respiratory acidosis.
_Causes:_ It can be caused by medical conditions, such as stroke affecting the brainstem, by holding one’s breath, or by drugs, typically when taken in overdose. Hypoventilation may also occur in chronic mountain sickness to conserve energy. 
_Effects:_ As a side effect of prescription medicines or illicit recreational drugs, hypoventilation may become potentially life-threatening. Many different CNS depressant drugs such as alcohol, benzodiazepines, barbiturates, GHB, sedatives, and opiates produce respiratory depression when taken in large or excessive doses; however, this is most commonly seen as a cause of death with opiates or opioids, particularly when they are combined with sedatives such as alcohol or benzodiazepines. This has NOT however been reported as a possible side effect of using Kratom.
**Q: How is Kratom said to work in the brain?** A: As of late 2011, no controlled, clinical studies have been performed on humans. Therefore, its metabolic half-life, protein binding, and elimination characteristics are all unknown within the scientific world. We do know that Kratom behaves as a μ-opioid receptor agonist, similar to opiates like morphine, although its effects differ significantly from those of opiates.Kratom does not appear to have significant adverse effects, and in particular appears NOT to cause the hypoventilation typical of other opioids.
**Q: What is a μ- Opioid Receptor (MOR) and why is it important to talk about?** _(see reference Section 2 for notations)_ A: μ-(pronounced MU) opioid receptors are the receptors in your brain associated with pain. Kratom is said to be an agonist of these receptors; theory suggests it activates the receptors and aids the body to block the reception of pain signals, similar in nature to an opiate but without the negatives. We feel individuals should be knowledgeable about the theories on how kratom interacts with the brain and body in order to be fully cognizant of what is going on when using kratom and to combat the myths about Kratom use. _So, read below!_
Active and inactive μ-opioid receptors. The μ-opioid receptors (MOR) are a class of opioid receptors with high affinity for enkephalins and beta-endorphin but low affinity for dynorphins. They are also referred to as μ opioid peptide or (MOP) receptors. The prototypical μ receptor agonist is the opium alkaloid morphine; μ (mu) refers to morphine.
**_SUBQUESTION:_ Wait a minute, this is complicated….What’s an Agonist?** A: An agonist is a chemical that binds to some receptor of a cell within the body and triggers a response by that cell. Agonists often mimic the action of a naturally occurring substance. So, an agonist causes an action, and an antagonist blocks the action of the agonist and an inverse agonist causes an action opposite to that of the agonist.
_TYPES of μ Receptors :_ Three variants of the μ opioid receptor are well-characterized, though reverse-transcriptase PCR has identified up to 10 total splice variants in humans (we have complicated brains eh?).
* μ1 –More is known about the μ1 opioid receptor than is known about the other types. * μ2 –TRIMU 5 is a selective agonist of the μ2 receptor. * μ3 –In 2003, a μ3 variant was described, which was responsive to opiate alkaloids but not opioid peptides.
**Q: Where are these receptors located?** A: In layman’s terms, they are within the brain and in the spinal cord.
_Here’s the technical science behind them:_ They can exist either presynaptically or postsynaptically depending upon cell types. The μ-receptors exist mostly presynaptically in the periaqueductal gray region, and in the superficial dorsal horn of the spinal cord (specifically the substantia gelatinosa of Rolando). Other areas where μ-receptors have been located include the external plexiform layer of the olfactory bulb, the nucleus accumbens, in several layers of the cerebral cortex and in some of the nuclei of the amygdala, as well as the nucleus of the solitary tract.
μ receptors are also found in the intestinal tract. This causes constipation, a major side effect of μ agonists, due to inhibition of peristaltic action.
**Q: Ok, I think I understand a bit more about all of this. Now, what about Activating all of this?** A: MOR can mediate acute changes in neuronal excitability via “disinhibition” of presynaptic release of GABA (see works from “Charles Chavkin, PhD.;”. and “Roger Nicoll, M.D.;”. ). Activation of the MOR leads to different effects on dendritic spines depending upon the agonist and may be an example of functional selectivity at the μ receptor.
Activation of the μ receptor by an agonist causes analgesia, sedation, slightly reduced blood pressure, itching(with certain agonists like morphine), euphoria, decreased respiration (again, no fear of HYPOVENTILATION using Kratom!), miosis (constricted pupils) and decreased bowel motility. Some of these effects, such as analgesia, sedation, euphoria and decreased respiration, tend to lessen with continued use as tolerance develops.
_We hope the Kratom FAQ section has helped you learn more about this special herb._
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**_REFERENCE SECTION 2:_** **1. **“hypoventilation” at _Dorland’s Medical Dictionary_
**2. **Zubieta-Calleja, GR; Paulev, PE; Zubieta-Calleja, L; Zubieta-Calleja, N; Zubieta-Castillo, G (September 2006). “Hypoventilation in chronic mountain sickness: a mechanism to preserve energy.”. _Journal of Physiology and Pharmacology: An Official Journal of the Polish Physiological Society_. 57 Suppl 4: 425–30\. PMID 17072073\. Cite uses deprecated parameters (help)
**3. **Harper,D. (2001). “Online Etymology Dictionary: Analgesia”. Retrieved December 3, 2012.
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**13. **Microgram Bulletin – Department of Justice
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