Ethanol ingestive behavior as a function of central neurotransmission

Blum, Kenneth; Briggs, Arthur H.; Trachtenberg, Michael C.

doi:10.1007/bf01952026

Cited by 38 publications

(9 citation statements)

References 64 publications

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“…Certainly, you can never get patients into recovery if you cannot keep them in treatment. The importance here is that NAAT reduces the need for benzodiazepines, reduces withdrawal tremors, reduces building up to drink scores (BUD) and increases recovery scores [28,61,63,64–66]. …”

Section: Neuroimaging Evidence Of Naat Effects At the Neurological Simentioning

confidence: 99%

Neurogenetics and Nutrigenomics of Neuro-Nutrient Therapy for Reward Deficiency Syndrome (RDS): Clinical Ramifications as a Function of Molecular Neurobiological Mechanisms

Blum¹

2013

J Addict Res Ther

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In accord with the new definition of addiction published by American Society of Addiction Medicine (ASAM) it is well-known that individuals who present to a treatment center involved in chemical dependency or other documented reward dependence behaviors have impaired brain reward circuitry. They have hypodopaminergic function due to genetic and/or environmental negative pressures upon the reward neuro-circuitry. This impairment leads to aberrant craving behavior and other behaviors such as Substance Use Disorder (SUD). Neurogenetic research in both animal and humans revealed that there is a well-defined cascade in the reward site of the brain that leads to normal dopamine release. This cascade has been termed the “Brain Reward Cascade” (BRC). Any impairment due to either genetics or environmental influences on this cascade will result in a reduced amount of dopamine release in the brain reward site. Manipulation of the BRC has been successfully achieved with neuro-nutrient therapy utilizing nutrigenomic principles. After over four decades of development, neuro-nutrient therapy has provided important clinical benefits when appropriately utilized. This is a review, with some illustrative case histories from a number of addiction professionals, of certain molecular neurobiological mechanisms which if ignored may lead to clinical complications.

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Section: Neuroimaging Evidence Of Naat Effects At the Neurological Simentioning

confidence: 99%

Neurogenetics and Nutrigenomics of Neuro-Nutrient Therapy for Reward Deficiency Syndrome (RDS): Clinical Ramifications as a Function of Molecular Neurobiological Mechanisms

Blum¹

2013

J Addict Res Ther

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“…THE RELATIONSHIP between alcohol consumption, abuse, and dependence, and the endogenous opioid system (EOS) has been investigated frequently (7,8,10,24,28,34). Although the findings have been contradictory, it nonetheless appears clear that the effects of alcohol may become manifest via the EOS.…”

mentioning

confidence: 99%

Plasma concentrations of β-endorphin, adrenocorticotropic hormone, and cortisol in drinking and abstinent chronic alcoholics

Arbol

Aguirre

Raya

et al. 1995

Alcohol

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“…For example, previous research has shown that the endorphinergic system [27] and GABA (Gamma-AminoButyric Acid) [28] are intimately involved in the actions of alcohol. The sedative, tranquilizing and/or anaesthetic properties of alcohol have been related to the enhancement of the flow of chlorine ions across neural membranes due to GABA [28].…”

Section: Discussionmentioning

confidence: 99%

Even low alcohol concentrations affect obstacle avoidance reactions in healthy senior individuals

et al. 2010

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BackgroundAlcohol is a commonly used social drug and driving under influence is a well-established risk factor for traffic accidents[1]. To improve road safety, legal limits are set for blood alcohol concentration (BAC) and driving, usually at 0.05% (most European countries) or 0.08% (most US states, Canada and UK). In contrast, for walking there are no legal limits, yet there are numerous accounts of people stumbling and falling after drinking. Alcohol, even at these low concentrations, affects brain function and increases fall risk. An increased fall risk has been associated with impaired obstacle avoidance skills. Low level BACs are likely to affect obstacle avoidance reactions during gait, since the brain areas that are presumably involved in these reactions have been shown to be influenced by alcohol. Therefore we investigated the effect of low to moderate alcohol consumption on such reactions.Thirteen healthy senior individuals (mean(SD) age: 61.5(4.4) years, 9 male) were subjected to an obstacle avoidance task on a treadmill after low alcohol consumption. Fast stepping adjustments were required to successfully avoid suddenly appearing obstacles. Response times and amplitudes of the m. biceps femoris, a prime mover, as well as avoidance failure rates were assessed.FindingsAfter the first alcoholic drink, 12 of the 13 participants already had slower responses. Without exception, all participants' biceps femoris response times were delayed after the final alcoholic drink (avg ± sd:180 ± 20 ms; p < 0.001) compared to when participants were sober (156 ± 16 ms). Biceps femoris response times were significantly delayed from BACs of 0.035% onwards and were strongly associated with increasing levels of BAC (r = 0.6; p < 0.001). These delays had important behavioural consequences. Chances of hitting the obstacle were doubled with increased BACs.ConclusionsThe present results clearly show that even with BACs considered to be safe for driving, obstacle avoidance reactions are inadequate, late, and too small. This is likely to contribute to an increased fall risk. Therefore we suggest that many of the alcohol-related falls are the result of the disruptive effects of alcohol on the online corrections of the ongoing gait pattern when walking under challenging conditions.

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Ethanol ingestive behavior as a function of central neurotransmission

Cited by 38 publications

References 64 publications

Neurogenetics and Nutrigenomics of Neuro-Nutrient Therapy for Reward Deficiency Syndrome (RDS): Clinical Ramifications as a Function of Molecular Neurobiological Mechanisms

Neurogenetics and Nutrigenomics of Neuro-Nutrient Therapy for Reward Deficiency Syndrome (RDS): Clinical Ramifications as a Function of Molecular Neurobiological Mechanisms

Plasma concentrations of β-endorphin, adrenocorticotropic hormone, and cortisol in drinking and abstinent chronic alcoholics

Even low alcohol concentrations affect obstacle avoidance reactions in healthy senior individuals

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