"Alcohol and the Heart" is a wonderful example of a paper on addiction. The abstract described in a fairly accurate manner the purpose of the study, methods that were used, the results, and the corresponding conclusions. The study is concerned with the possible effect or link of alcohol toxicity from either binge drinking or chronic alcoholism to heart damage. In particular, this study investigated the possible relationship between massive alcohol intake to observed myocardial (heart muscle) malfunctions such as myocardial contractile dysfunction, cardiomyocyte enlargement, mitochondrial damage and apoptosis (or cell death).
The suspected toxin (poison) is acetaldehyde, which is an ethanol metabolite, that is, a by-product when alcohol (ethanol) is metabolized by the body upon intake. The abstract had contained more than enough information as it was very detailed. Introduction: 1. The purpose of the study was to find a possible linkage between acetaldehyde to several symptoms of alcoholic cardiomyopathy, as previous studies had tentatively pointed to this metabolite as responsible for the myocardial excitation-contraction coupling, release of endoplasmic reticulum, and cardiac contractile functions. 2. The background information was extensive enough but the results of previous research studies on the exact role of acetaldehyde in causing myocardial functional damage and changes to morphology were not very conclusive. So the authors in this study went further than that by investigating the role that a chronic or an acute ethanol challenge play in causing mitochondrial damage and apoptosis (cell death). Methods: 1.
The study authors used transgenic mice, using VFB (Friend Virus-B type) and an experimental group of mice injected with ADH (alcohol dehydrogenase) and the two groups were later on compared using bio-metric criteria or parameters as shown in Table 1. Overall, the methods were detailed enough for others similarly interested to be able to repeat the same experiment or for them to extend the study further.
Essentially, the mice were then killed by the use of anesthesia (euthanized), their heart cells were subjected to histological examination by use of staining to easily contrast the cells (using red fluorescence to see mitochondrial O2) and the mitochondrial membrane potential was likewise measured. TUNEL staining was used for measuring any myonuclei positive for DNA strand breaks and lastly, a Western blot analysis was utilized to assess the fractions of certain proteins within the heart cells.
2. The reasons for certain procedures were clearly indicated; for example, the cDNA for murine class I ADH was used because of its cardiac-specific over-expression qualities, being the most efficient in terms of ethanol oxidation (Guo 2). 3. No potential problems were indicated by the study authors on the use of their chosen methods of analysis and there was no need for such at all. 4. A variety of statistical methods were used such as repeated ANOVA and Turkey's post hoc analysis to further determine the validity and reliability of the data gathered in their study. Results: 1.
The results were as expected, which means it would be logical to find anomalies in the mice cardiac cells, such as the changed cardiac morphology and compromised myocardial contractility (ibid. 6) as this study was merely a repetition of some previous studies already. A good job was done regarding presenting the data in graphical format with the legends in text. All the accompanying explanations were more than adequate, given their technical language and its intrinsic complexity in terms of biological, anatomical, and chemical terminologies. Discussion: 1.
The aim of the study was not met, because the results were not conclusive. The results were contradictory, as what the authors pointed out, that the present study did not give or produce any significant change in the gross weight of the heart, contrary to previous studies in which there were observed overt cardiac hypertrophy (enlargement) which used the same ADH transgenic mice (ibid. ) However, what the study proved was to provide evidence that ethanol exposure causes mitochondrial damage and apoptosis, worsened by the presence of ADH. 2.
The authors had discussed extensively their results with the results of previous studies, and this produced some contradictory conclusions. 3. The authors interpreted their data relatively quite accurately and extensively but the causal link between ADH and myocardial anomalies like myocardial dysfunction, histological alterations (changes in size and morphology), and apoptosis was not conclusively established. What the authors have is more in the nature of the circumstantial evidence only.
A possible explanation is a confounding factor that authors had postulated or put forward, such as the possible hypertrophy and apoptosis of the murine cardiomyocytes. What the study found was ADH causes mitochondrial damage, which may or may not lead to myocardial malfunctions. It would be a big jump to conclude otherwise but it can be conceded that mitochondrial damage has been linked to several ailments or diseases; it causes neurodegenerative disorders, ischemia, and even diabetes. 4. Surprisingly, the authors did not discuss any limitations to their study; this is a critical omission that can impact the study's validity and reliability, such as allowing the mice to drink water freely at any time.
Water can dilute the effects of alcohol in the bloodstream and may have altered the results somewhat. In a complex study like this one, it is very hard to isolate one factor from another, that is how the independent variable affects the dependent variables. 5. The “ take-home” or a very sensible message of this research article is that excessive drinking is certainly harmful to the heart. It is common sense that anything done in excess is not conducive to good health, whether it is the binge drinking or chronic alcoholism.
The lesson is to drink in moderation. 6. A perhaps good potential future experiment is to do the same study using higher mammals, such as monkeys, for example. This species most closely resembles humans and the results may have more than passing relevance in terms of how heavy drinking can lead to heart damage. Using people or humans as subjects for the same experiment would be unethical, as it might lead to deaths in some cases when some people have prior health ailments or those who were previously quite healthy might suffer some damage to their heart if subjected to heavy drinking experiments.
ReferencesGuo, Ren. “Alcohol Dehydrogenase Accentuates Ethanol-Induced Myocardial Dysfunction and Mitochondrial Damage in Mice: Role of Mitochondrial Pathway.” PloS One 5.1 (2010): 1-10. Print.