Tag Archives: Neurotransmitter

Methamphetamine Use May Risk Development of Parkinson’s Disease

March 25, 2015

Methamphetamine Use May Predispose Consumers to Future Development of Parkinson’s Disease

There are several neurodegenerative disorders but it will still not be right for anybody to talk about neurodegenerative disorders without mentioning the Parkinson’s disease. This disorder is the second most common after Alzheimer’s disease and it is affecting approximately ten million people worldwide. The probability of a person suffering from this disease increases with age with most people being diagnosed after the age of 50. Early in the course of the disease, the most obvious symptoms are movement-related. These include shaking, rigidity, slowness of movement, and difficulty with walking and gait. However, the symptoms worsens as time passes by, these may include cognitive and behavioral problems with dementia commonly occurring in the advanced stages of the disease. Other symptoms include sensory, sleep, and emotional problems. PD is caused by degeneration of midbrain dopaminergic neurons that project to the striatum. The loss of striatal dopamine is responsible for the major symptoms of the disease. Although a small proportion of cases can be attributed to known genetic factors, most cases of PD are idiopathic. While the etiology of dopaminergic neuronal demise is mysterious, a combination of genetic susceptibilities, age, and environmental factors seems to play a critical role. Dopamine degeneration process in PD involves abnormal protein handling, oxidative stress, mitochondrial dysfunction, excitotoxicity, apoptotic processes, and microglial activation or neuroinflammation.

methamphetamine

Studies on animals on methamphetamine toxicity

Studies done on animals have shown that methamphetamine can cause long-term dopamine terminal damage as well as dopamine neuronal body loss. In rodents, repeated administration of methamphetamine causes a decrease in dopaminergic markers such as tyrosine hydroxylase (TH) and dopamine transporter. Accompanied by a reduction in TH activity, reduced levels of dopamine and its metabolites and decreased levels of vesicular monoamine transporter 2 (VMAT2). These effects occur primarily in the striatum but also in the cortex, thalamus, hypothalamus and hippocampus. Methamphetamine induces neurotoxicity in a dose-dependent manner as do other amphetamine-derivatives like MDMA. Although partial recovery of TH and dopamine transport fibers occurs after methamphetamine administration, methamphetamine-induced neurotoxicity is persistent. In mice, the greatest dopaminergic fiber loss is seen 24 hours after methamphetamine administration. Neurotoxic effects persist for more than seven days after methamphetamine exposure and one month after MDMA exposure. Drugs that induce PD symptoms and TH loss such as MPTP in mice also show a partial recovery with time in nonhuman monkeys and mice. The time courses and degrees of TH and dopamine transport fiber recovery after methamphetamine or after MDMA exposure are similar, suggesting terminal regrowth, as these two proteins are independently regulated. Researchers have also noted that there is partial recovery of dopamine levels in the striatum strongly suggesting that the regrown terminals are functional. However the mechanisms responsible for partial recovery are not known, but it is speculated that it might involve compensatory sprouting and branching as has been reported for regrowth following MPTP-induced damage. Dopamine terminal recovery has also been described in rhesus monkeys and velvet monkeys, although it appears to occur on a slower timescale than in mice. Methamphetamine-induced dopaminergic damage persists for more than 12 weeks in velvet monkeys and more than 3 years in rhesus monkeys, demonstrating the persistence of methamphetamine-induced brain damage.

Methamphetamine Toxicity in the Substantia Nigra

This drug doesn’t only cause fiber loss in TH but also produces dopamine cell body loss in the substantia nigra as shown in tests in mice that were treated with 3 methamphetamine injections (5 mg/kg) at 3-hour intervals. From the counts it is evident that 20 to 25% dopaminergic cell loss, measured at different time are linked to exposure to methamphetamine. The observed pattern of TH-stained neuron loss is very similar to the pattern of Nissl-stained neuron loss, indicating that neuronal loss is specific to dopaminergic neurons. Dopamine cell body loss was confirmed via staining with Fluoro-Jade, a general marker of neuronal degeneration that fluoresces after administration of known dopaminergic toxins such as 6-OHDA and MPTP. Fluoro-Jade stains scattered neurons degenerated in the substantia nigra after methamphetamine treatment. there is a possibility that the lack of complete recovery of TH fibers in the striatum is related to the loss of dopaminergic neurons in the Substantia nigra similar to what occurs in Parkinson’s disease.

methamphetamine

Increased Risk of Parkinson’s Disease in Methamphetamine Abusers

There are literatures that have linked the abuse of amphetamine to the later development of PD. In a report of a study done by Callaghan and his colleagues, there is an increase in of PD in methamphetamine users in an epidemiological investigation based on data from California statewide hospital discharge records. The researchers identified 1,863 methamphetamine users, 9,315 patients hospitalized for appendicitis as a nondrug control group, and 1,720 cocaine users as a drug control group. All subjects were aged at least 50 years, had been hospitalized in California between 1990 and 2000, and had been followed for up to 10 years after discharge. The methamphetamine user group showed an elevated incidence of PD, with a 165% higher risk for development of PD than the patients from the control group. the results have been confirmed by the same group after doing the same research but in a much broader scope; 40,000 people hospitalized for methamphetamine versus 200,000 for appendicitis and 35,000 for cocaine and a 16-year follow-up period. From these two studies it is evident that methamphetamine use increases the chances of PD development in adulthood.

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 Use May Predispose Consumers to Future Development of Parkinson’s Disease

 

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Dopamine and Norepinephrine Contributing to Addiction?

March 20, 2015

Dopamine and Norepinephrine and Their Contribution to Addiction

Dopamine and norepinephrine are very crucial neurotransmitters whose functions can never be underestimated. These are some of the most crucial neurotransmitters in the body. In particular, dopamine has very many functions in the body but to many people it is famous for its good feeling effects that it is always identified with but this should not be the case as it has functions beyond the mesolimbic pathway. In the brain dopamine plays such roles as: It plays a big role in starting movement, and the destruction of dopamine neurons in an area of the brain called the substantia nigra is what produces the symptoms of Parkinson’s disease. Dopamine is involved in the frontal cortex in executive functions like attention and feelings among others. In the rest of the body, dopamine is involved in nausea, in kidney function, and in heart function. Though only relevant to most people when it comes to such aspects as motivation, addiction, attention or lust, dopamine is a crucial neurotransmitter that also does vital functions in different pathways. Therefore dopamine should not only be limited to the mesolimbic pathway. A pathway which starts with cells in the ventral tegmental area, buried deep in the middle of the brain, which send their projections out to places like the nucleus accumbens and the cortex.  the levels of dopamine is naturally controlled by the brain, for example when a person engages  in pleasurable activities the brain will increase the level of dopamine in the nucleus accumbens, however during addiction the dopamine signaling in this area is changed. For any drug to have any pleasurable feeling to the user then the level of dopamine must be increased and this is what causes euphoric feelings that drug users will do anything to achieve.

Dopamine

Dopamine depletion and cocaine addiction

Despite one of the most dangerous drugs of pleasure, cocaine has remained to be one of the drugs that are highly abused worldwide. Cocaine works in such a way that it targets the dopamine which is a neurotransmitter related with euphoric feelings. When taken cocaine will cause a surge of dopamine extracellular in limbic areas, specifically, nucleus accumbens it is this surge that causes euphoric effects cocaine is known for. It is the euphoric properties of cocaine that lead to the development of chronic abuse, and appear to involve the acute activation of central dopamine neuronal systems. Dopamine plays a key role in reward system and stimulation behavior. However, when a person uses cocaine for a long time his neurotransmitter and neuroendocrine alterations will eventually occur. Dopamine depletion is hypothesized to result from overstimulation of these neurons and excessive synaptic metabolism of the neurotransmitter. It is this depletion of dopamine that may underlie dysphoric aspects of cocaine abstinence, and cocaine cravings.  With many research findings on cocaine relations with dopamine, it is clear that cocaine addiction stems from the depletion of synaptic dopamine in the mesolimbic dopamine reward system, leading to a dysphoric withdrawal state that drives cocaine seeking to restore dopamine to normal, drug-dependence level.

After using cocaine for a long time, your brain will be conditioned to use cocaine in order to raise cocaine to the required levels and this result in addicted brain that can’t function without taking cocaine. At this stage it will be hard for an addict to quit using this drug as every time you try to quit all the withdrawal symptoms will set in thereby causing addiction and dependence thereafter. These cravings contribute not only to addiction but to relapse after a hard-won sobriety especially when the addict encounters triggers.

Norepinephrine and Drug Addiction

Norepinephrine is a very vital neurotransmitter in the brain that is also one of the most abundant in the brain. It is important for such roles as selective attention, general arousal, and stress reactions in challenging environments. Norepinephrine has been implicated by several studies as a key mediator of drug reward for three primary reasons. First, the noradrenergic pathways support intracranial self-stimulation (ICSS) and modulate drug-induced changes in ICSS threshold. Secondly, the biochemical activity of psychostimulant drugs includes blockade of Norepinephrine reuptake and enhancement of Norepinephrine release and thirdly, compounds that interfere with Norepinephrine synthesis or signaling influence drug self-administration. The idea that drugs of abuse act via the endogenous reward systems in the brain first arose when psychostimulants such as amphetamine and cocaine have been found to alter support intracranial self-stimulation thresholds. One interpretation of these results was that Norepinephrine mediates the effect of psychostimulants on support intracranial self-stimulation, because these drugs cause Norepinephrine release, block Norepinephrine reuptake or do both.

Dopamine

In a 1970s research done by Davis WM and Smith SG in a study titled: Catecholaminergic mechanisms of reinforcement: direct assessment by drug-self-administration, it was found that catecholamines were important in the mediation of opiate self-administration. in this research, a series of experiments showed that depletion of Norepinephrine and dopamine with amphetamine , a drug which is known to inhibit tyrosine hydroxylase prevents or attenuates the self-administration of morphine in rodents and in nonhuman primates as was shown earlier by Pozuelo and Kerr in 1972.

Finally, Drug addiction is a vice that should be fought by all means that is why we at AWAREmed Health and Wellness Resource Center are committed to availing help to addicts and offering them a place to call home. We offer NER Treatment and Amino acid therapy that are the most effective approaches to addiction treatment and recovery. You call on Dr. Dalal Akoury (MD) today and begin your journey to victory against addiction.

Dopamine and Norepinephrine and Their Roles in Causing Addiction

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Reward Deficiency Syndrome In Addiction

March 19, 2015

Reward Deficieny syndromeReward Deficiency Syndrome and Its Role in Addiction and Treatment

The first people to come up with the term Reward deficiency syndrome were Blum K, Sheridan PJ, Wood RC, Braverman ER, Chen TJ, Cull JG and  Comings DE in a research titled; The D2 dopamine receptor gene as a determinant of reward deficiency syndrome in 1996. This term refers to an insufficiency of usual feelings of satisfaction. Reward deficiency syndrome results from a dysfunction in the brain reward system which is a complex interaction among neurotransmitters primarily dopaminergic and opiodergic neurotransmitters. Those who have a family history of alcohol and other drugs addictions may be born with a deficiency in the ability to produce or utilize these neurotransmitters which are known to play crucial in etiology of addiction to substances. This problem can also be caused by corruption of brain reward system that may be caused by exposure to long periods of stress or use of alcohol and other substance for a long time. When the neurotransmitters are low or are blocked from reaching the intended brain receptors, individuals often feel discomfort or pain. Behaviors resulting from a failure of the system that normally confers satisfaction include drug and alcohol abuse, overeating, heavy cigarette smoking, gambling, and hyperactivity. These problems have been linked to genetic defects especially to dysfunction of the dopamine receptors.

A dysfunction in the dopamine receptors obviously leads to myriads of health complications since it is the brain neurotransmitter that controls feelings of well-being and is mostly targeted by drugs of abuse. However powerful dopamine doesn’t work alone, it interacts with other neurotransmitters like serotonin and other neurotransmitters to control moods and cravings. When these neurotransmitters bind on the neural receptors, they trigger a reaction in the reward system, therefore any interference with this coordination will result in abnormal behavior in Reward deficiency syndrome, including addictions, impulsivity, and excessive risk taking. This is the reason why people who have a defect in the DRD2 dopamine receptor gene lack a sufficient number of dopamine receptors in their brains to produce the brain reward cascade. In turn, this leads to Reward deficiency syndrome, including abnormal cravings and resultant strange conduct.

 

Reward deficiency syndrome and Drug Abuse

The reward circuitry consists of an in-series circuit linking the ventral tegmental area, nucleus accumbens and ventral pallidum via the medial forebrain bundle. In the past the reward circuitry was believed to encode only the set point of hedonic tone but have since been found to be functionally far more complex, also encoding attention, expectancy of reward, disconfirmation of reward expectancy, and incentive motivation. Here have been speculations that hedonic dysregulation within the reward circuits may lead to addiction. A second-stage dopaminergic component in this reward circuitry is the crucial addictive-drug-sensitive component. All drugs that are addictive are known to enhance the dopaminergic reward synaptic function in the nucleus accumbens. as for most of addictive drugs like cocaine the tolerance to the euphoric effects will develop after a long term use after which a post use dysphoria then comes to dominate reward circuit hedonic tone, and addicts no longer use drugs to get high, but simply to get back to normal. Reward deficiency syndrome as seen here may make an addict chained to the drug of use since the addict will need to feel normal but that will not possible since the dopamine receptors and parts of the reward circuit will have been affected adversely and so the drug use will be continued as a result of Reward deficiency syndrome and not for euphoric purposes.

It is also important to note that the brain circuits that mediates pleasurable effects of addictive drugs are anatomically, neurophysiologically, and neurochemically different from those mediating physical dependence, and from those mediating craving and relapse. Apart from Reward deficiency syndrome other factors that also come to play in addiction include gene variations that may increase vulnerability to drug addiction. Environmental factors also have an input for example prolonged stress and social defeat may also increase a person’s vulnerability to drug addiction as they alter the brain reward system. However dopaminergic dysfunction within the reward circuitry is the biggest contribution to addiction-prone personality effects.

Treating Reward deficiency syndrome

Reward Deficieny syndromeReward deficiency syndrome has influence in drug addiction and therefore any drug addiction treatment must incorporate strategies to treat Reward deficiency syndrome in order to avoid reoccurrence of the addiction after a hard won fight. In fact when the problem in the reward circuitry isn’t addressed then treatment of addiction will have very narrow chances of success. To help in this pursuit, treatment of cocaine addiction should have in part a dopamine agonist agonistic therapy to heal the dopaminergic system.

When an agonist therapy is to be used, it’s crucial to note that the baseline amount of dopamine receptors has predictability as to differential clinical outcomes in reward deficiency syndrome. In a study of 10 subjects with an allele on the Taq1A DRD2 gene, which is associated with reduced dopamine receptor concentration and decreased neural responses to rewards (A1+ subjects). The 10 subjects were scanned twice, once on placebo and once on cabergoline which is D2 receptor agonist. Consistent with an inverted-U relationship between the DRD2 polymorphism and drug effects, cabergoline increased neural reward responses in the medial orbitofrontal cortex, cingulate cortex, and striatum for A1+ subjects, but decreased reward responses in these regions for A1− subjects.  Drug addiction treatment should therefore put in place measures to ensure that reward deficiency syndrome is treated. Dr. Dalal Akoury of AWAREmed Health and Wellness Center has dedicated her life to helping patients restore their lives by use of integrative medicine. She also holds many conferences in which she offers training on how integrative medicine can be used to fight addiction among other conditions.  Call her on (843) 213-1480 for help.

Reward Deficiency Syndrome and Its Role in Addiction and Addiction Treatment

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Foods That Help Boost Serotonin Level

March 17, 2015

Foods That Raise Serotonin Level

Serotonin is one of the most important neurotransmitters in the brain. Serotonin helps in regulation of mood and sleep. According to recent research findings, when the level of serotonin is below optimum it can cause increased incidences  of aggressive behavior. Low serotonin levels have also been linked to anxiety and depression. If the recent research findings have to be believed which of course they are, then low serotonin levels are dangerous as it may lead to suicidal acts. In terms of dieting, making sure you’re not serotonin deficient is vital because serotonin triggers satiety after eating. Depressed serotonin levels is the likely reason why the vast majority of people cannot stay on a very low carbohydrate diet for the long term without feeling an unavoidable need to binge which may lead to more complex disorders. In the brain the production of neurotransmitter happens naturally without intervention of any other drug, however when you have used the drugs of abuse for some time they will lead to depletion in the levels of the brain chemicals such as serotonin and dopamine. This therefore means that for healthy levels of serotonin to be achieved after use of drugs, there is need for replenishing and supplementing serotonin through diet. There are foods that are very helpful in raising the levels of serotonin . Here are some of them.

Serotonin

Fresh Vegetables

Fresh vegetables work in myriad ways to ensure good health. the greens are rich in various minerals and vitamins that go along way in boosting the levels of serotonin. some of the fresh vegetables that are actually beneficial in increasing the level of serotonin include Spinach which contains a substantial dose of folic acid. it  is also a wonderful source of the mineral magnesium, a natural anxiety combatant. Without enough magnesium in your diet, you may find it hard to concentrate in addition to being fatigued and irritable. other foods that are rich in magnesium and hence helpful in boosting levels of serotonin include; cacao, seaweed, bananas, orange, tree nuts, peanuts, whole grains, corn, cheese, eggs, milk, and white fish.

Fresh Fruit

Fresh fruits are rich in nutritional content. The fresh fruits are rich in vitamins that serve the purpose of rejuvenating the body and giving it a healing approach as well as protecting the body and restoring crucial neurotransmitters like the serotonin which therefore helps in ensuring good moods. fruits are rich in B3 vitamins. these fruits may include watermelon, peaches, bananas, cantaloupe, and avocado. Generally, the B vitamins are very essential in restoration of neurotransmitters especially after a period of long term use of drugs of pleasure that are known to disrupt the functions of the neurotransmitters.

 Apples

An apple a day keeps the devil away is a common adage. The health benefits of apples are many and this explains why it is always recommended for patients. A compound found in apples called “quercetin’ is an antioxidant that studies have shown may not only help in the prevention of cancer but may also play an important role in the prevention of neurodegenerative disorders. the medicinal abilities of this compound is confounding. It also helps in boosting serotonin as well as dopamine levels.

 Herbs that Boost Serotonin Levels:

SerotoninSt. John’s wort -St. John’s wort is effective against mild to moderate depression, alleviates anxiety, insomnia, and irritability and eases pain. It increases the level of serotonin in the brain as well.

Dandelion– This herb is widely used in Europe as an excellent liver detoxifier and mild diuretic. It increases the flow of bile and encourages both the transformation and transportation of nutrients. It has been used historically to treat liver disorders, arthritis and gout. In the addict it will ease the transportation of nutrients in the body and restore energy in the cells as well as boost the level of serotonin.

Cannabis- though known for all the wrong reasons, cannabis has very high medicinal content, however it is highly addictive and that dictates that it be used in moderation as unregulated use can cause addiction. It works in a way that it increases the levels of excitatory neurotransmitters like dopamine and serotonin.

Burdock– burdock has been used to treat other conditions ranging from arthritis to diabetes to hair loss, and it’s an active ingredient in some cancer treatments this herb is also good in resoring the levels of serotonin.

Ginseng–  contrary to what many people believe , ginseng does not only increase the level of serotonin in the body but also works in rejuvenating, restorative, boosts energy and vitality and is tonic to the brain. Ginseng is often prescribed for patients fighting depression which is a common symptom of withdrawal from drug use. This herb is a better therapy for those who are under physical, emotional, mental or spiritual stress as it is a very strong antidepressant and adaptogenic. Ginseng promotes strong nerves, sound sleep, improves memory, clear thinking and enhances concentration.

Use of drugs for along time causes damage to the neurotransmitters. apart from the foods and the herbs, you can also increase the level of serotonin by sunlight. Bright light increases the production of Serotonin in the body.  Basking in the sunlight can absolutely improve your mood and also soothe muscle aches. It is good to note that by increasing the level of serotonin in your body, you are setting good grounds for addiction treatment and recovery. However, 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.

Foods That Raise Serotonin Level

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Correcting Neurotransmitter Imbalances with IV Amino Acids

March 14, 2015

Correcting Neurotransmitter Imbalances with IV Amino Acids

When taken, drugs will alter the normal the bodily functions. That is no news to even those who use drugs of abuse, in fact the basic definition of a drug is; any substance that when taken will interfere with the normal functions of the body. However some drugs do not only alter minor body functions but go a step further in inhibiting the functions of neurotransmitters to a greater extent.  Most of the drugs that can mimic or interfere with the functions of the neurotransmitters in any way are mostly drugs of pleasure that are prone to abuse and are hence illegal in many parts of the world. The brain and the entire nervous system functions in a way that the entire body needs them to work properly, you can’t imagine how fast the coordination between the central nervous system and the peripheral nervous system is but most important fact to note is that any interference within the nervous system even only to a neurotransmitter goes a long way in affecting the entire body. The brain has various mechanisms through which it accomplishes all the functions of the body. The effect of drugs on the neurotransmitters can be underestimated by those who haven’t known how the neurotransmitters work, here is how the neurotransmitters work.

Neurotransmitters

How Neurotransmitters Work

Neurotransmitters are very crucial in the nervous system. They are the chemicals that transmit messages from one nerve cell to another. Nerve cells are known as neurons. The nerve impulse travels from the first nerve cell through the axon, a single smooth body arising from the nerve cell to the axon terminal and the synaptic knobs. Each synaptic knob communicates with a dendrite or cell body of another neuron, and the synaptic knobs contain neurovesicles that store and release neurotransmitters. The synapse lies between the synaptic knob and the next cell. For the impulse to continue traveling across the synapse to reach the next cell, the synaptic knobs release the neurotransmitter into that space, and the next nerve cell is stimulated to pick up the impulse and continue it. An interference with the neurotransmitters can adversely affect the flow of message within the nervous system. This is what most drugs of abuse do. They affect the harmonious flow of information from the brain to the rest of the body maiming its normal functions. Let’s look at how drugs affect specific neurotransmitters in the nervous system.

How Drugs affect Dopamine and GABA

One of the neurotransmitters that are highly targeted by drugs of pleasure is Dopamine. To some people it is known as the ‘bliss neurotransmitter’. It is responsible for good feeling, the euphoric feelings that drug addicts seek from various drugs of abuse. Dopamine has great influence on well-being, alertness, learning, creativity, attention and concentration. Levels of dopamine should be optimal in the brain since when the level of dopamine is low it can leave us craving food, sex or stimulation. When the dopamine level is too high it can cause addictive behaviors. It has been observed that patients who are put on medications to boost dopamine level especially the Parkinson’s patient, they will form an addictive behavior like gambling when the levels of dopamine shoots beyond the optimal level. Dopamine boosts the feelings of pleasure but when the levels are too high it may result in Paranoia or a suspicious personality. Dopamine is also released when there is high stress. Therefore the level of dopamine should be regulated to ensure sound health. This is where the functions of inhibitory neurotransmitters set in, however with influence of drugs this coordination between excitatory neurotransmitters and inhibitory neurotransmitters is maimed.

Nicotine influences mood, cognition, and body function by binding to and activating nicotinic acetylcholine receptors (nAChRs) located on neurons in the brain. When activated by either nicotine or the endogenous neurotransmitter acetylcholine, the nAChR opens a channel that allows ions to pass through the neuron’s membrane from the exterior to the interior of the cell and trigger changes that activate the cell. When you take tobacco or other drug with nicotine the nicotine will have interactions with nAChRs and therefore any nicotine dependence treatment should focus on altering these interactions.

Nicotine produces rewarding effects by interacting with nAChRs on neurons in the brain’s mesolimbic reward system. This system comprises dopaminergic neurons that originate in the ventral tegmental area often shortened as VTA and release the neurotransmitter dopamine in regions involved in information processing, memory, and emotions, such as the nucleus accumbens (NAc), hippocampus, amygdala, and prefrontal cortex (PFC). Increases in dopamine levels within the mesolimbic system give rise to rewarding effects. Nicotine directly enhances dopamine levels in the mesolimbic system by interacting with nAChRs on the dopaminergic neurons and causing them to release more of the neurotransmitter. Nicotine also modulates dopamine release indirectly by binding to nAChRs located on excitatory glutamatergic and inhibitory gamma aminobutyric acid (GABAergic) neurons in the ventral tegmental area. These glutamatergic and GABAergic neurons originate from a number of brain areas, such as the NAc, hippocampus, PFC, amygdala, ventral pallidum, and pedunculopontine tegmental nucleus, and regulate the activity of dopaminergic neurons.

Neurotransmitters

Restoring nicotine addiction can’t be done with IV amino acid to restore NER balance

Nicotine is one of the most available addictive substances. You can find it in tea but it can be found in greater proportions. Unfortunately, Nicotine addiction is never easy to fight. And the bitter truth is that nicotine addiction can’t be fought successfully without IV amino acid to restore NER balance. IV amino acids are the best in restoring the balances in the neuroendocrine system. The IV amino acids are the best in detoxification and getting rid of the effects of nicotine and curbing nicotine addiction by ensuring the balance of neuroendocrine chemicals.  With IV amino acid, dopamine has been noted to be the major cause of addiction can be regulated. IV amino acids is used as an  outpatient program which focuses on biochemical detoxification of the body and brain hence perfect treatment for nicotine addiction.

Any addiction treatment must focus on restoring the general well-being of the patient that can only be achieved by restoring the neurotransmitters affected. This is why we at AWAREmed are dedicated to ensuring that we offer the best neuroendocrine restoration. Dr. Dalal Akoury (MD) is one of the few doctors that have embraced the benefits of NER in fighting addiction. Call on her and be helped in finding the best solution for nicotine and other substances addiction.

Neurochemical and Imbalances Involved In With Nicotine & Smoking

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