Have you ever indulged in a beer or two on a late Friday evening out with friends? You may have woken up feeling quite bad the next morning if you may have overindulged. But what if I told you that drinking beer may actually be beneficial?
In a new study published by the American Chemical Society, they have found that the hops in beer may actually protect against developing Alzheimer’s disease. Alzheimer’s disease is a neurodegenerative disease that is characterized by memory loss and personality changes (Palmioli et al. 2022). The hop flowers used to flavor beer are considered a “neutraceutical” or a food that can function with medicinal benefits (Palmioli et al. 2022).
Extraction of certain chemicals from the flowers include feruloyl and p-coumaroylquinic acids, flavan-3-ol glycosides, and procyanidins (Palmioli et al. 2022). The main target of the chemical extracted from various hop flowers is amyloid beta peptides, oxidative stress, and accumulation of misfolded proteins (Palmioli et al. 2022). They do so by inhibiting the target ligand, preventing amyloid beta aggregation, and preventing cell death from oxidative stress by inducing autophagic pathways (Palmioli et al. 2022).
While research has not gone past nematodes in this study, it would be interesting to see if this makes it to clinical trials. This article was posted on an online news platform and while interesting, can pose some ethical issues. Publication of this article to the general public may cause false hope and can lead to people drinking more beer than they need to, thinking that it may be beneficial to them. The health benefits have not been researched enough and therefore the risks of drinking beer may outweigh the benefits. According to alzheimers.org, excessive alcohol consumption may lead to an increased risk of brain damage and the development of dementia. This brings up another issue. Should we be reporting on scientific discoveries to the general public without full knowledge of the benefits vs. risks?
Palmioli A., Mazzoni, V., De Luigi A., Bruzzone C., Sala G., Colombo L., Bazzini C., Zoia C., Inserra M., Salmona M., De Noni I., Ferrarese C., Diomede L., Airoldi C., Alzheimer's Disease Prevention through Natural Compounds: Cell-Free, In Vitro, and In Vivo Dissection of Hop (Humulus lupulus L.) Multitarget Activity, ACS Chemical Neuroscience (2022). DOI: 10.1021/acschemneuro.2c00444
This is a very interesting topic to discuss when considering therapeutic approaches to Alzheimer’s Disease (AD). Due to the progressive nature of AD, researchers have sought methods to intervene at the very early stages of AD before the cascade gets too far. As such, understanding the biomarkers associated with this cascade is crucial in AD research (Briggs et al., 2016). The most prevalent biomarkers associated with progression of AD include beta amyloid, tau, Apolipoprotein-E, structural changes, and functional changs (Weller & Budson, 2018). As you mentioned, amyloid aggregation can lead to plaques. If enough plaques build-up, the cells become toxic which can lead to cell death. With regards to Tau, hyperphosphorylation leads to the build-up of neurofibrillary tangles, also resulting in neurotoxic environments and cell death (Briggs et al., 2016). I think the utilization of chemicals/agents like that of what is in hops is super interesting when discussing its effects on biomarkers like beta-amyloid. AD is a massive heath crisis and finding a means to disrupt its progression is critical when discussing a solution to the crisis. Furthermore, if scientists can utilize the chemicals in hops to disrupt beta-amyloid aggregation, would this also have effects downstream such as preventing hyperphosphorylation of tau?
ReplyDeleteReferences
Briggs, R., Kennelly, S. P., & O’Neill, D. (2016). Drug treatments in Alzheimer’s disease. Clinical Medicine, 16(3), 247–253. https://doi.org/10.7861/clinmedicine.16-3-247
Weller, J., & Budson, A. (2018). Current understanding of Alzheimer’s disease diagnosis and treatment. F1000Research, 7, F1000 Faculty Rev-1161. https://doi.org/10.12688/f1000research.14506.1
You make a great point at the end... should we be reporting these benefits even though we really don't the full extent of benefits vs. risks? I would probably have to say no! It could be limiting patient autonomy by providing half of the story. We see a lot of this type of information being shared on television with "doctors" behind the story. Legally, is there any problem with doctors reporting half of the story, or only what has been researched so far? Probably not... but if they would have gone to Regis University, they would understand that this information limits their patient's autonomy and could also hinder beneficence by causing more harm than good.
ReplyDeleteThis was a terrific article to read on such a popular topic...alcohol consumption. My first thought when reading this article was to look at the acknowledgements of the study cited to see the conflict of interest and who funded the study. I was relieved to find that I did not see any competing financial interests or funding from any brewing companies. Knowing that alcohol reduces long-term potentiation of neurons, the use of non-alcoholic beer would seem to be a more logical solution, but alcoholic beer contains a much greater quantity of phenols than non-alcoholic beer indicating greater health benefits (Boronat et al., 2020).
ReplyDeleteBoronat, A., Soldevila-Domenech, N., Rodríguez-Morató, J., Martínez-Huélamo, M., Lamuela-Raventós, R. M., & de la Torre, R. (2020). Beer Phenolic Composition of Simple Phenols, Prenylated Flavonoids and Alkylresorcinols. Molecules (Basel, Switzerland), 25(11), 2582. https://doi.org/10.3390/molecules25112582
I really enjoyed your article; I think this is a very interesting topic. As much as we all would love to see that drinking a beer with friends isn’t bad for our brains, it sounds like it is very controversial whether it weighs out the risks. This study I found was looking at a few neurological diseases including Alzheimer’s (AD), Parkinson’s (PD), and Amyotrophic Lateral Sclerosis (ALS), and the impact of alcohol consumption it has. It shows the epidemiological studies that have reported a reduction of Alzheimer’s disease in patients who drink low or moderate concentrations of ethanol (Peng 2020). They are reporting that the little amounts of ethanol protect against Beta-amyloid toxicity in the hippocampal neurons; however, an excessive amount of ethanol increases the accumulation of Beta-amyloid and Tau (Peng 2020). As for PD excessive alcohol consumption have dopamine neurotoxic effects by the induction of Cytochrome P450 2E1 and this increases the amount of alpha-Synuclein (Pend 2020).
ReplyDeleteAlthough there are studies working to prove that some ethanol consumption could be beneficial, it is still under study, and hard to say if it will outweigh the risks of drinking.
Peng B, Yang Q, B Joshi R, Liu Y, Akbar M, Song BJ, Zhou S, Wang X. Role of Alcohol Drinking in Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis. Int J Mol Sci. 2020 Mar 27;21(7):2316. doi: 10.3390/ijms21072316. PMID: 32230811; PMCID: PMC7177420.
Thank you for this Arielle. As a very big fan of drinking beer, I am happy to hear that my new belly might come with some benefits attached to it.
ReplyDeleteCuriously, this is the second time I hear this in a period of two months. I have a friend that goes to medical school in Yakima, WA. Yakima is the biggest producer of Hops in the United States. She mentioned this exact information since there is a 'beer tour' in her town and they used this to promote the drinking of beer.
I found this really cool article about why beer could help the microbiota as well as many other body processes such as aging. I really enjoyed your post, and the discussion it opened in the comments.
Marco, M. L., Heeney, D., Binda, S., Cifelli, C. J., Cotter, P. D., Foligné, B., Gänzle, M., Kort, R., Pasin, G., Pihlanto, A., Smid, E. J., & Hutkins, R. (2017). Health benefits of fermented foods: microbiota and beyond. Current opinion in biotechnology, 44, 94–102. https://doi-org.dml.regis.edu/10.1016/j.copbio.2016.11.010