Tag Archives: Monoamine neurotransmitter

Why medical detox is necessary to addicts

Good neurotransmitters and moods for addiction healing

October 21, 2016
Good Neurotransmitters

Good Neurotransmitters and moods for addiction healing as away of containing substance abuse

Good neurotransmitters and moods for addiction healing: Feeding on good nutrition

In the process of seeking for solutions when it comes to overcoming drug addiction, people often go for very big things, big rehabilitation institutions and expensive and elaborate addiction professionals. I certainly don’t have any problem with that for it is very much in order since the most important thing is the reclaiming of one’s health and freedom from the scourge of addiction. However what many may not know or if they do, then they don’t care about is the avenue of nutrition as a tool of fighting and eliminating all sorts of addictions you may be privy to. For quite a while now we have been posting articles touching on the use of healthy nutrition in the fight against substance abuse and we are not about to stop. We want all of us to have the knowledge so that the work of dealing with drug addiction can be made easier and much lighter to both the direct and indirect victims. From the expert’s point of view, correcting addiction by good neurotransmitters and moods is one very important avenue available for containing the problem.

According to doctor Dalal Akoury (MD) a well-respected expert in addiction, it is important to note that psychoactive substances may lead to psychiatric problems because in many cases the substances can have toxic effects on brain chemistry. She adds that before detoxification is done, neurotransmitters are reduced due to poor nutrition which then alters the amino acid absorption and utilization. The implication of this is that the victims (addicts) are left feeling depressed, agitated and unregulated early in recovery. From the various studies conducted so far, it is believed that these imbalances will disappear over a couple of weeks but then again, they may also last as long as one year after an addict becomes sober further necessitating normalizing neurotransmitters and moods for the perfection in addiction healing process.

Good neurotransmitters and moods for addiction healing: Moods and behavior abnormalities

As we progress into the discussion, it is worth noting that for some, moods and behavior abnormalities may have been present before the substance abuse. With proper diagnosis of any possible underlying mental health disorders, a healthy diet and education on how nutrition influences mood and brain chemistry, recovery can be enhanced. An understanding of how food affects mood and the risk of substance abuse begins with macronutrients. And with carbohydrates being the body’s main source of energy it therefore means that without this macronutrient, the brain can’t function properly, blood sugar becomes unstable, and neurotransmitters become disrupted. Unstable blood sugar can lead to feelings of frustration, anxiety, and cravings. You can however avoid this by scheduling for an appointment with doctor Dalal Akoury today for a more professional input that will help you effectively in the normalizing neurotransmitters and moods for addiction healing.

Good neurotransmitters and moods for addiction healing: Feeding on good nutrition

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Neurotransmission and substance abuse

July 12, 2016
Neurotransmission

Neurotransmission and substance abuse needs immediate treatment

Neurotransmission and substance abuse: Why immediate solution is necessary?

Neurotransmission is a recurring process that emerges in several steps utilizing specialized components of the sending and receiving cells. Through this, it will then identifies the exact step that the specific substance disrupts, and how it does that by providing very vital insight into its effect on the victim. It is also very essential in the identification of medical and behavioral interventions that inhibits, counter, or reverse the disruption. And from the experts point of view at AWAREmed Health and Wellness Resource Center under the able leadership of doctor Dalal Akoury, MD so many substances that re being abused today actually imitates the functions of neurotransmitters. Doctor Akoury reiterates that a number of opioid drugs like heroin and OxyContin chemically resembles the brain’s natural opioids sufficiently to engage and stimulate their specialized receptors. And being a strong stimulant, heroin therefore stimulates so many receptors beyond what the brain is able to use in the normal cycle of endorphin. The consequences of that will be a massive amplification of opioid activities.

Neurotransmission and substance abuse: Molecular components

If you are abusing any drug, it is very important that you seek for immediate treatment from the experts. Doctor Akoury and her team of experts will be very helpful to you if only you can schedule for an appointment with her today. Treatment is very important because majority of these drugs normally alters the neurotransmission by interacting with molecular components of the sending and receiving process other than receptors. Like for instance cocaine normally attaches to the dopamine transporter, the molecular conduit that draws free-floating dopamine out of the synapse and back into the sending cell.

Neurotransmission and substance abuse: Cocaine dopamine connection

It must be noted that as long as cocaine still occupies the transporter (neurotransmission), the dopamine cannot re-enter the cell using this route says doctor Akoury. It builds up in the synapse, stimulating receiving cell receptors more abundantly and producing much greater dopamine impact on the receiving cells than occurs naturally. The Cocaine’s Dopamine Connections will then tallies some of cocaine’s interactions with the mechanisms of dopamine signaling, and how they motivate abuse and contribute to dependence and addiction.

Finally, doctor Akoury registers that, under normal circumstances, some drugs will alter the neurotransmission using other means besides increasing or decreasing the quantity of receptors stimulated. Benzodiazepines, such as diazepam or lorazepam, enhance receiving cells’ responses when the neurotransmitter gamma-aminobutyric acid (GABA) attaches to their receptors. Benzodiazepines’ relaxation effects result from this increased sensitivity to GABA’s inhibitory impact on cellular activity. Therefore it will not matter how it happens, the best you can do for yourself is to seek for lasting solutions today. The establishment of AWAREmed Health and Wellness Resource Center gives you an opportunity of regaining your health today if only you can schedule for an appointment with doctor Akoury today for the commencement of your recovery process.

Neurotransmission and substance abuse: Why immediate solution is necessary?

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Striatum Methamphetamine Toxicity

March 22, 2015

Methamphetamine Toxicity in the Striatum

The striatum is a crucial part of the brain. This part of the brain plays very important roles but it can be adversely affected by the use of stimulants and other drugs of leisure. Substances such as cocaine and methamphetamine produce their primary effects inside the brain by boosting the presence of dopamine which is a neurotransmitting chemical that activates the pleasure-producing neurons contained within the limbic system. As stated above the limbic system includes the hippocampus, along with several other brain structures. According to the results of two separate studies published in 2008 in the Journal of Neuroscience and Biological Psychiatry, the presence of either cocaine or methamphetamine alters normal adult neurogenesis inside the hippocampus and damages this region’s ability replenish its neuron supply.  It is no longer news that methamphetamine intoxication causes long-lasting damage to dopamine nerve endings in the striatum. However the mechanisms underlying this neurotoxicity are not yet known but oxidative stress has been linked to it.

methamphetamine

 

Microglia are the major antigen-presenting cells in brain and when activated, they secrete an array of factors that cause neuronal damage. Astoundingly, very little work has been directed at the study of microglial activation as part of the methamphetamine neurotoxic cascade. It has been report that methamphetamine activates microglia in a dose-related manner and along a time course that is coincident with dopamine nerve ending damage. Through tests done on mice scientists have discovered that prevention of methamphetamine toxicity by maintaining treated mice at low ambient temperature prevents drug-induced microglial activation. MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) not only damages dopamine nerve endings and cell bodies but also  causes extensive microglial activation in striatum as well as in the substantia nigra. Contrastingly, methamphetamine causes neither microglial activation in the substantia nigra nor dopamine cell body damage.

Dopamine transporter antagonists do not mimic the effect of methamphetamine on microglia. Hyperthermia, a prominent and dangerous clinical response to methamphetamine intoxication, has been also ruled out as the cause of microglial activation. Together, these data suggest that microglial activation represents an early step in methamphetamine-induced neurotoxicity. Other neurochemical effects resulting from methamphetamine-induced overflow of dopamine into the synapse, but which are not neurotoxic, do not play a role in this response.

Methamphetamine use on the rise despite effects

The use of methamphetamine has been on the rise despite the fact that it is a powerful stimulant drug that has adverse effects when abused as most people do. According to the UN Office on Drugs and Crime reported recently that abuse of amphetamines, including designer drugs such as methamphetamine and 3, 4-methylenedioxymethamphetamine, now exceeds that of cocaine and heroin on a global scale. This presents no sign that its use will decline any soon. Past researchers were able to establish a fact that methamphetamine causes persistent reductions of function in dopamine nerve endings of animals and humans. Methamphetamine neurotoxicity has been under intense study for over 20 years, but still there is much that still remains to be learned about how this dangerous drug causes damage to dopamine nerve endings. The theory that revolves around oxidative stress has been at the top of the speculations. Drug-induced oxidative stress is an attractive construct that can account for many of the effects of methamphetamine on the dopamine nerve ending such as inhibition of tyrosine hydroxylase activity as well as reductions in the dopamine transporter and the vesicle monoamine transporter. This may even be an early event that leads eventually to methamphetamine-induced apoptosis. However, the source of the reactant species that mediate methamphetamine-induced damage is not known.

methamphetamine

Due to their crucial roles they play in mediating the mediating damage to the nervous system, Microglia has attracted considerable attention. Immune like in many ways  these interesting cells become activated by damage and then transmigrate to sites of injury where they can secrete an array of factors  like cytokines, prostaglandins, nitric oxide, and superoxide that are known to have detrimental effects on neurons. However, the role of microglia in methamphetamine-induced damage to the dopamine system has received little attention. In 1994 a researcher, Bowyer and his colleagues noted for the first time that methamphetamine resulted in activation of microglia in striatum of treated rats. These investigators concluded that microglia were increased in response to nerve ending damage and were not apparently a cause of it.  Recently, another research was conducted to give an in-depth analysis of the effect of methamphetamine on striatal gene expression. Numerous genes linked to microglia were activated significantly within hours of methamphetamine intoxication, suggesting the possibility that microglial activation occurs earlier in the methamphetamine toxic cascade than previously thought.

Today there are researchers who are building on the initial analysis of methamphetamine and report the pharmacological characterization of microglial activation by methamphetamine in striatum. As mentioned before, striatum is an area dense in dopamine nerve endings and is known to be targeted for damage by methamphetamine. Microglial activation coincides with the onset of methamphetamine-induced damage in striatum and the extent of this effect is related to the degree of damage to dopamine nerve endings. Numerous nontoxic effects exerted by methamphetamine, such as inhibition of the DAT, increases in synaptic levels of dopamine, activation of D1 and/or D2 DA receptors, and hyperthermia, cannot explain methamphetamine-induced microglial activation.

Finally, this is still a dark area and there is need for more literature so as to establish the mechanism of methamphetamine toxicity on the striatum. Needless to say, Drug abuse, addiction and independence are problems that people grapple with every day. These problems need to be treated effectively through integrative medicine. Dr. Dalal Akoury (MD) is an expert at this.  Call her on (843) 213-1480 for help.

Methamphetamine Toxicity in the Striatum

 

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