Biological Photography in November (North Carolina)

Dieting vs. Biochemistry

During Biochemistry lecture today, my professor displayed this figure depicting the body's biochemical response whenever an organism is undergoing starvation. As shown, there are five main phases which occur over a forty day period before expiration. Whenever the body intakes glucose, the exogenous supply  is depleted after four hours. After two days, the body isn't able to pull glucose from glycogen anymore, therefore gluconeogenesis begins.  As the body enters starvation, the body begins to shut down to maintain heart and brain function. Interestingly enough, the Atkins diet places patients in stage four.

Reference:
Dr. James Knopp
Lecture 11/18/2011

The Physiological Effects of Alcohol on Adolescents and Young Adults

During the adolescent years in Western societies, countless juveniles become inquisitive about the depressive and euphoric effects of ethanol, commonly found in distilled and fermented beverages. Despite the alluring persona of alcohol advertised by the media, many individuals do not consider the devastating physiological imbalances intoxication causes. A Homo sapiens internal physiology is intricately connected to maintain homeostasis, therefore the toxic effects of alcohol has a cumulative domino effect on numerous organ systems. Although adolescents rarely exhibit severe chronic disorders commonly associated with alcohol consumption, adolescent exposure to alcohol does result in long-term medical consequences due to disruptions in homeostatic physiology.

Ethanol is a toxic drug with a broad range of side effects that are dependent upon the individuals blood alcohol concentration and their genetic disposition. Research studies have shown that adolescents are less sensitive to the unpleasant effects of intoxication (Spear 115). Despite a short-term sensation of euphoria, ethanol poisoning will adversely cause ataxia, garrulousness, belligerence, bradycardia, hypotension, purging, respiratory depression, respiratory acidosis, and pulmonary aspiration. Rapid increases in the adolescent’s blood alcohol concentrations can cause an acute dysfunction of the hippocampus resulting in a blackout. Between six and twelve hours after ingesting the toxin, adolescents are prone to experiencing withdrawal symptoms such as tachycardia, nausea, tremors, and headache (Dickins 26). After the withdrawal symptoms degrade, and the adolescent no longer feels symptomatic from the ethanol poisoning, the body physiologically still hasn’t recovered from the ingested toxin. Repeated ethanol abuse has been documented to have subsequent long-term physiological effects on cell proliferation, enzyme activity, hormone release, development, and cognition.

Both acute and chronic consumption of ethanol can have detrimental metabolic changes within the liver. Ethanol is a non-ionized, lipid-soluble compound, which is readily absorbed in the stomach, small intestine, and colon. Approximately 98% of ingested ethanol is oxidized by alcohol dehydrogenase into acetaldehyde, and a smaller percentage is oxidized by cytochrome p450 isoform in the liver (Dickinson 25). Acetaldehyde, a toxic metabolite, is subsequently oxidized into acetate and further metabolized into carbon dioxide and water. The oxidation of acetaldehyde in the liver is rate limiting, therefore toxicity can be determined by the concentration of acetaldehyde in the blood (Thompson 751). The body is capable of metabolizing 120 mg/kg*h^-1 and is kinetically saturated at this amount despite the individual’s blood alcohol concentration (Dickinson 25). Exposure of ethanol and acetaldehyde to the liver causes subsequent liver tissue damage, resulting in metabolic changes in the liver. Adolescents who repeatedly abuse ethanol, compared to nondrinkers, will develop increased triglyceride levels, which is correlated with fatty liver disease (Thompson 751). Early indicators, such as increased gamma-glutamyl-transpeptidase and alanine aminotransferase levels, can detect the onset of hepatitis and liver failure (Anonymous 126).

Figure 1: The effects of ethanol exposure

on the mechanism of cellular growth and

development in the hippocampus (Smith 600)

The brain constantly matures during the adolescent years, and studies have shown that adolescent alcohol consumption adversely affects neuropsychological function, physical development, and performance (Burke 206). After ingestion, ethanol stimulates endorphin and dopamine release, resulting in the adolescent to experience brief euphoria. As the adolescent’s blood alcohol concentration increases, so does the ethanol concentration in the brain, since ethanol can readily cross the blood-brain barrier (Anonymous 127). Due to ethanol’s properties, it readily penetrates the central nervous system and interacts with multiple neurotransmitter pathways. Ethanol causes an increase in gamma-aminobutyric acid, which is an inhibitory neurotransmitter, and decreases the excitatory neurotransmitter glutamate. Under normal conditions, glutamate binds to N-methyl-D-aspartate receptors causing a neuronal response to a neurochemical signal. During ethanol withdrawal, synaptic potentials are inhibited by N-methyl-D-aspartate receptors and calcium channels are regulated in a way  that calcium-induced excitotoxicity occurs, leading to neurodegeneration in the hippocampus (Dickinson 25). Figure 1 exemplifies an adolescent whose hippocampus has been exposed to ethanol, versus a control subject with no prior history of drug abuse. Ethanol exposure decreases proliferation, differentiation, and migration of cells within the brain leading to neurodegeneration (Smith 600). Brain abnormalities, involving the degeneration of neural tissue, have been associated with adolescent alcohol use. In addition to reduced hippocampal volumes, neurophysiological change has been observed in the frontal-anterior cortical region, and the corpus callosum (Anonymous 127).

 A research study completed in 2000 used magnetic resonance imaging to visualize the volume of brain structures in adolescents who consumed ethanol. The study also provided supporting evidence of imperilment of the integrity of white matter in the corpus callosum and hypothalamus. Under normal conditions, the hypothalamus is responsible for learning new information and forming memories (Burke 207). In individuals who abuse ethanol, chemical and electrical responses to brain stimuli are decreased, meaning the amount of time it takes for a brain wave to occur after a stimulus is dampened. Using brain waves as indicators of information processing, researchers were able to conclude that regardless of gender, education level, or socioeconomic status, that adolescents who abused alcohol compared to nondrinkers had decreased neurophysiological function. These adolescents performed poorly on examinations that tested memory, attention, visuospatial skills, and executive functioning (Burke 206). One hypothesis stated that repetitive ethanol exposure decreases the concentration of oxygen in the brain, which is important for nerve cell activity. Figure 2 exemplifies the specific regions of the brain, of adolescents who consumed alcohol, and had decreased oxygen concentrations. The frontal, cerebellar, and cerebral cortex regions had the most significant reductions (Burke 208). With decreased oxygen supply, neural impulses between neurons subsequently decrease which causes an impairment of the ability to learn tasks that require spatial skills (Anonymous 125).

Figure 2: Locations of the brain that have

documented physical irregularities 

or decreased oxygen levels (Burke 208)

In addition to the hepatic and nervous systems, ethanol has an extensive impact on the endocrine system. Under normal circumstances, the hypothalamus secretes gonadotropin-releasing hormone, which stimulates the pituitary to secrete follicle-stimulating hormone and luteinizing hormone. This sequence then activates the release of estrogen and testosterone, which subsequently increases the production of growth hormone and insulin-like growth factor. Since the hypothalamus is largely affected by ethanol, it decreases the release of gonadotropin-releasing hormone, which disrupts the hormone release of subsequent organ structures. Decreased levels in testosterone and estrogen from the endocrine system will adversely influence target organs in different systems. Indicators of decreased hormone levels include delayed puberty, decreased maturation of the gonads, muscle development, and mineralization of the skeleton. As testosterone levels decrease, osteoblast formation decreases, leading to an irreversible reduction in bone growth (Anonymous 126). The hypothalamus has various functions and is not only in control of the gonadotropin-releasing hormone pathway. Osmoreceptors found in the hypothalamus monitor solute concentrations of the blood, and send excitatory impulses to hypothalamic neurons whenever solute concentrations are high. These hypothalamic neurons synthesize and release antidiuretic hormone, which normally keeps homeostasis by preventing fluctuations in water balance. Whenever antidiuretic hormone is released through the posterior pituitary into the blood, it normally targets the kidney tubule cells via cyclic 3’5’-adenosine monophosphate. This sequence of events causes the kidney tubule cells to reabsorb water into the bloodstream and prevent its excretion as urine. This process results in decreased urine output and decrease solute levels in the bloodstream. Whenever antidiuretic hormone is inhibited by ethanol, copious urine output results. Since the tubule cells were not signaled to increase water intake, the adolescent becomes dehydrated and disrupts the homeostatic water balance the body needs for proper physiological function (Widmaier 223)

            In conclusion, adolescent use of ethanol as a brief euphoric depressant is not worth the risk of developing long-term physiological abnormalities. Homeostatic imbalances caused by ethanol intoxication long outlast the ephemeral sensations which many adolescents desire. The long-term side effects not only affect cognition and function, but also dangerously alter the body’s chemistry and the metabolic pathways that allow it to sustain existence. Overall, the body treats ethanol as a toxin on the molecular level; therefore, individuals should be aware of their consumption and consciously treat alcohol as if they were ingesting a metabolic poison.

Bibliography

Anonymous (09/01/2004). "The Effects of Alcohol on Physiological Processes and Biological Development". Alcohol research & health (1535-7414), p. 125.

Burke, Christina (12/31/2004). "Alcohol and the Adolescent Brain: Human Studies". Alcohol research & health (1535-7414), 28 (4), p. 205.

Dickinson, Barry D (01/01/2004). " The neurocognitive effects of alcohol on adolescents and college students". Preventive medicine (0091-7435), 40 (1), p. 23.

Smith Aleksander R (05/01/2010). "Alcohol inhibition of neurgenesis: a mechanism of hippocampal neurodegeneration in an adolescent alcohol abuse model". Hippocampus (1050-9631), 20 (5), p. 596.

Spear, L (06/01/2000). "Modeling adolescent development and alcohol use in animals". Alcohol research & health (1535-7414), 24 (2), p. 115.

Thompson, R P (07/01/1986). "Measuring the damage-ethanol and the liver". Gut (0017-5749), 27(7), p. 751.

Tuma, D J 07/01/1996). "Betaine, ethanol, and the liver: A review". Alcohol (Fayetteville, N.Y.)(0741-8329), 13 (4), p. 395.

Widmaier, Eric P. Vander's Human Physiology: The Mechanisms of Body Function. 10/e/McGraw-Hill Higher Education, 2006. 1 Nov. 2011.