Alcohol, Adolescents, and Young Adults – A Neurological Disaster Waiting to Happen

Monday, September 15, 2014
By: Linda J Dobberstein, DC, DACBN, DCBCN

Adolescence and young adulthood bring a time of many changes, challenges, and explorations. Alcohol intake is a common area of exploration that our teenage children and young adults engage in during high school and college. It is considered a natural rite of passage with the consequences of “losing just a few brain cells” or being sick for a weekend. It is not that harmless. Real evidence exists that this rite of passage is linked to severe brain health consequences. It is not just a simple hangover that occurs. Adolescent alcohol intake can have profound, long-term, neurological consequences for the young adult brain.

Statistics from the National Institute of Drug Abuse provide some eye opening statistics on underage drinking. Nearly 40% of 8th graders have tried alcohol. The number jumps to 72% of 12th graders as having consumed alcohol. It identified that nearly 50% of the high school seniors were currently consuming alcohol with half of the drinkers classifying themselves as heavy drinkers, i.e. 5 or more drinks in one sitting in the last two weeks. Another study shows that 60-70% of adolescents, who report alcohol use, are binge drinkers. Adolescents who begin drinking around 13 years of age double the risk, regardless of family history, of developing Alcohol Use Disorder.

The Adolescent Brain and Alcohol

The adolescent brain is unique. It is physically not the same as an adult brain. It responds differently to alcohol than an adult brain. The brain’s structural foundation has been laid by adolescence, but the fine tuning of nerve connections is a substantial work in progress. The nerve connections are being made and remodeled, neurotransmitters receptors and transporters are evolving, and hormonal changes all occur during adolescence. This is especially important to understand in the context of underage drinking. Significant mounting evidence from human and animal research shows that adolescents are much more susceptible to neurological toxicity of alcohol than adults. This occurs both in cognitive performance and the brain’s structural integrity. 

In animal studies, adolescents showed greater impairment in learning and memory tasks than adults as a result of excessive alcohol consumption. These memory impairments or deficits were considerably more challenging or difficult with long-term persistent effects compared to adults. Adult impairments tended to be more short-lived.

Adolescent human studies with binge type alcoholic consumption showed several things. Neurodegenerative cognitive changes such as verbal and spatial working memory, poor memory recall of visual and non-visual stimuli, and attention deficits were evident more so in adolescents with binge type drinking than adults. Underage alcohol usage with heavy binge drinking was clearly shown to impair study habits and erode skills necessary for adulthood. In essence, it caused brain damage and impaired intellectual development.

MRI studies show altered brain structure and a decrease in the size of the hippocampus in adolescents who drank. This is more evidence of alcohol based neurodegeneration. The hippocampus is part of the old brain, or limbic system, that is involved with learning, memory, and mood. It also influences neurotransmitter regulation and balance including GABA, glutamate, and substance P, and compounds like BDNF (brain derived neurotrophic factor) which is involved with brain repair and neuroplasticity. It is known that chronic dysfunction or damage to the hippocampus may be found with depression, anxiety, schizophrenia, seizure disorders, diabetes (both type 1 and type 2), Alzheimer’s, Parkinson’s, ALS, and other neurodegenerative disorders. It is not yet known to what extent underage drinking may affect the development of these disorders decades later, but gene expression studies are beginning to see connections.

New animal research is studying the effects of adolescent alcohol drinking on the gene expression changes in the deep “old brain” structures. Results showed that underage drinking affected the limbic system’s hypothalamus. This caused changes in a number of genetic expressions that may lead to disease development. Animal research published in the journal Alcohol showed a link with adolescent drinking with adult onset dilated cardiomyopathy – a type of heart failure. The changes that occurred in the adolescent animal brain, with drinking into adulthood, provoked enough stress and inflammation that cardiac gene signals and sympathetic autonomic nervous system changes took place. The end result was a very distressed heart. Another animal study showed that underage drinking caused changes in the hypothalamic gene signals that led to the development of type 2 diabetes and changes in insulin signaling pathways. Human and animal studies also indicate that the adolescent binge drinking, especially between the ages of 13-15, caused up-regulation of the Advanced Glycation End Units receptor sites that contributes to the development of alcoholism and neurodegenerative brain diseases.

Recent research shows that adolescent binge drinking provokes high levels of oxidative stress that can turn on abnormal neurological gene signals that persist with neurodegeneration. The results of underage binge drinking and neurodegeneration have been shown to persist for years after the behavior occurred. The increased oxidative stress from the alcohol toxicity causes a higher level of activity and number of microglial cells in the brain. This over-activity and increased number of microglial cells release more pro-inflammatory chemicals that stress nearby neurons and interfere with communications between cells. Essentially, it creates a snow-ball effect. The binge headache and hangover translates into a type of war with the bullets ricocheting. The initial barrage of bullets hit. They ricochet and the damage escalates as the receiving end (microglial cells) scrambles and creates a flurry of activity to fight the attack. If it is an intense battle, the damage is not easily repaired and leads to neurodegeneration. 

Frat parties, homecoming games, school breaks, weekends, and adolescent poor judgment and experimental behavior happen. Research demonstrates very clearly that what our adolescents and young adults choose to do with alcohol consumption during their times of exploration and experimenting has serious neurological consequences. It’s not just the hangover, the amnesia of the previous night, or a weekend spent recovering. It has real, long-term consequences. Because the adolescent brain is still developing, the consequences are more destructive immediately and last longer than in cases with adult drinking.

Clearly abstinence in adolescence is vital to prevent the needless tidal waves of damage from occurring. Prevention is worth a pound of cure. This is true in any circumstance, but certainly it has profound applications in adolescent brain health and intoxication. It becomes even more evident when looking at the potential gene expression associated with hypothalamus and hippocampal breakdown from adolescent alcohol intake leading to not only neurodegeneration but potentially loss of organ function outside of the brain years later. This has potentially profound implications.

Brain Repair Support

If you are dealing with this concern personally or with a family member, there is good news. The brain has remarkable plasticity, i.e. the ability to make new pathways and regain function when inflammation and stress sources are removed. Reducing microglial cell activation and inflammation while also improving BDNF production for nerve tissue repair provide powerful tools for helping the brain to heal from insults and injury. The brain repair compound BDNF and microglial cell inflammation has been shown to respond quite favorably to foods like blueberries, strawberries, etc. or the compound fisetin. Fisetin has been shown to provide outstanding neuroprotection and reduces neurological oxidative stress. It helps with the production of the most important brain antioxidant glutathione, which protects against oxidative inflammatory stress and is fundamentally important for detoxification. Alcohol exposure causes depletion of glutathione stores not only in the liver but also in the brain because of the detoxification process and also the inflammatory injury. Glutathione is particularly important if the adolescent consumes alcohol, uses tobacco, and has underlying concerns such as bipolar disorder. Research using advanced spectroscopy brain imaging published just weeks ago shows that adolescents who drank, used tobacco, and had bipolar disorder had significantly reduced levels of glutathione in the hippocampus. The hippocampus was damaged, smaller, and depleted of its protective glutathione. Additional compounds that protect the activated brain microglial cells and reduce neurological inflammation include grape seed extract, DHA, and lipoic acid.

Supporting underlying neurotransmitter imbalances can also be very helpful. Animal research published last month demonstrates that adolescents who consumed alcohol altered the brain’s dopamine pleasure response site. It caused the brain to become more sensitive and responsive to alcohol and possibly created the basis for alcoholism in adulthood. Genetic dopamine imbalances have long been implicated in those with a predisposition for addictive behaviors and chronic alcohol use. The mechanics of the dopamine imbalances and how it is present in those with chronic alcohol use are still being debated. Dopamine helps with focus, pain (all types) tolerance, and reward or gratification responses. Compromised dopamine production and function increase risk for addictive behaviors and addictions. Dopamine is made from the amino acid L-phenylalanine, which then converts into tyrosine and then eventually converts into dopamine. In order to make this happen, the protein building blocks, i.e. amino acids, must be present along with co-factors that help the conversion process. The co-factors are adequate oxygen, iron, copper, folate, vitamins C, B3, and B6 and S-Adenosyl-Methionine (SAMe). If any one of these cofactors are not present, dopamine production is compromised and risk behaviors increase. Pantethine may also be used to help support dopamine in the brain. Pantethine has been shown to protect dopamine nerves in the brain. Acetyl-L-Carnitine has been shown to be highly beneficial in protecting nerves and the blood brain barrier from alcohol damage. Music also supports dopamine in the brain.

Alcohol use also affects GABA production and function in the brain, especially with continuing or high dose consumption. Long-term alcohol use leads to GABA depletion and causes excess glutamate or too much neurostimulation. Last week’s newsletter, GABA: Managing Brain Stimulation, Anxiety, and Other Consequences discussed this topic.

If the statistics presented at the beginning of this article are correct, then nearly one in two adolescents at some point in their young life have used alcohol and frequently to excess. Our youth are our pride and joy. We cannot ignore this issue as parents, relatives, and friends of this generation. Knowledge and understanding is fundamental to inspiring and making changes. Having resources to repair damage and rebuild are equally vital to change. What road are you or your young adult taking?

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