First off, what exactly is in fish oil? Fish oil contains omega-3 fatty acids. There are two types of omega-3 fatty acids found in fish oil: docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) (LeWine 2013). Our body cannot make these fatty acids, therefore we must rely on getting them from our food. DHA is an important structural component of our brain. Deficiencies in DHA have been linked to a decline in mental function (Yurko-Mauro K 2010).
Dementia according to Alzheimer's Association is "a general term for a decline in mental ability severe enough to interfere with daily life". Dementia is caused by damage to the brain. One very common way of damaging the brain is through alcohol abuse. Alcohol related dementia is caused by excessive, long-term alcohol use that results in damage to the brain cells thus mental impairment. Many of us know, the things we do to our bodies now may have long term effects. Risk factors for developing dementia include "having a close family member who suffers from dementia, low cognitive function and alcohol abuse" (Lappato 2013).
I have a grandfather currently suffering from dementia which puts me at a greater risk of developing the disease myself. What can I do now to help prevent myself from developing dementia? The answer may be fish oil.
Researchers at Loyola University Chicago Stritch School of Medicine have been studying the effects of alcohol on brain cells with the addition of fish oil compounds. Using adult rat brain cells, they exposed the cells to alcohol concentrations equal to the equivalent of four times the legal driving limit. They then compared these cells to brain cells exposed to the same high alcohol content plus DHA. The researchers found that there was 90% less neuroinflammation and cell damage in the cells that were exposed to both high alcohol and DHA compared to the cell only exposed to alcohol. They concluded that fish oil may help prevent alcohol related dementia in current alcohol abusers (Lees 2013).
However the researchers greatly discourage popping fish oil capsules and continue to binge drink. The best way to prevent alcohol abuse and alcohol related dementia is to "quit drinking or drink in moderation" (Lees 2013).
Engler N. 2003. Marathon Dilemma: How Much Water is Too Much? Reuters Health. The American Medical Athletic Association.
Lees K. 2013. Omega-3 fish oil may help prevent alcohol related dementia. Science World Report. Available from: http://www.scienceworldreport.com/articles/9338/20130908/omega-3-fish-oil-help-prevent-alcohol-related-dementia.htm
LeWine H. 2013. Fish-oil friend or foe. Harvard Health Publications. Harvard Medical School. Available from: http://www.health.harvard.edu/blog/fish-oil-friend-or-foe-201307126467
Yurko-Mauro K, McCarthy D, Rom D, Nelson EB, Ryan AS, Blackwell A, Salem N, Stedman M. 2010. Beneficial effects of docosahexaenoic acid on cognition in age-related cognitive decline. Alzheimer's & Dementia: The Journal of the Alzheimer's Association. 6. 6. 456-464. Available at:
http://www.alzheimersanddementia.com/article/S1552-5260%2810%2900040-3/abstract
Loppato E. 2013. Study: teenage drinking can increase risk of dementia. Salon. Avaliable from:
http://www.salon.com/2013/08/13/study_teenage_boys_who_drink_excessively_at_risk_of_developing_early_dementia_newscred/
This is very interesting, and thank you for sharing your personal experiences with dementia.
ReplyDeleteYour blog sparked an interest, so I started looking up other ways we may be able to prevent dementia/other supplements we can take to reduce our risk of developing dementia.
More specifically, I looked up ways to prevent Alzheimer's disease (AD), and I found this really cool article about the role of cannabinoids in AD. AD, the most common form of dementia, is marked by amyloid plaques (for those of you who don't know what amyloid plaques are, basically the amyloid proteins in cells tangle, preventing the neuron from functioning). Researchers found that activated microglia are associated with these plaques, directly relate to the ongoing inflammatory processes in Alzheimer's Disease, and cause neurodegeneration in vivo and in vitro (Ramirez, Blazquez, Gomez del Pulgar, Guzman, & Ceballos, 2005)--probably because activated microglia are energetically taxing for cells, causing them to die sooner than non-activated cells (Streit, 2006). Consequently, researchers are investigating ways to inhibit microglial activation to prevent AD.
Many receptors are named after the pharmacological agents that activate them, and cannabinoid receptors are no exception. Two types of cannabinoid receptors have been well-documented, CB1 and CB2. The CB1 receptors are expressed in all types of neural cells, as well as in astrocytes, microglia, and oligodendrocytes. The CB2 receptors are found in microglial cells in vitro. Based on these factors, in addition to the findings that cannabinoids have neuroprotective effects in vivo by inhibiting glutamate transmission, reducing calcium influx, and preventing oxidative stress, Rameriz et al. studied the effects of cannabinoids on AD brains in mice.
Ramirez et al. found that AD brains had less CB1 density and increased protein nitration of CB1 and CB2. However, administration of a synthetic cannabinoid prevented microglial activation, cognitive impairment, and loss of neuronal markers in the mice. They then proposed that cannabinoids can prevent the neurodegenerative processes of AD.
This is all fun information, and it aligns well with the psychopharmacology course many of us are taking. However, as a disclaimer, I am NOT suggesting that everyone (or anyone) consume cannabinoids (synthetic or otherwise--but be especially weary of the synthetic ones that have been killing people) to prevent Alzheimer's disease. In fact, one of the beneficial effects of the cannabinoids used (namely, preventing the increased TNF-alpha release that regulates inflammation) was found for both the CB-1 agonist, which had psychoactive effects, and the CB-2 agonist, which did not have psychoactive effects. Thus, it may be possible to manufacture a cannabinoid-based pharmacological agent that would give people the neuroprotective benefits without the high. Therefore, again, I am NOT suggesting doing cannabinoids. However, this study could have interesting effects in terms of future pharmacological developments (i.e. of CB2 agonists that are as readily available as fish oil to those predisposed to AD) and politics (i.e. in legalization of certain cannabinoids).
References:
Ramirez, B. G., Blazquez, C., Gomez del Pulgar, T., Guzman, M., & de Ceballos, M. L. (2005). Prevention of Alzheimer's disease pathology by cannabinoids: Neuroprotection mediated by blockade of microglial activation. The Journal of Neuroscience, 25, 1904-1913. doi:10.1523/JNEUROSCI.4540-04.2005
Streit, W. J. (2006). Microglial senescence: Does the brain's immune system have an expiration date? Trends in Neurosciences, 29, 506-510. Doi: 10.1016/j.tins.2006.07.001
Most of the people I know, especially my girl friends, find babies absolutely adorable. I on the other hand, find elderly people adorable. This is why I chose to work at a retirement center this summer. At Lincoln Meadows there was independent living, assisted living, and memory care available for all residents. In general, the resident’s memory and independence declined with each living assignment to the extent that memory care is a lockdown facility that has 24/7 nurses available. Lincoln Meadows also had the Resident’s Club, which is a transitional group between assisted living and memory care. The club is designed to keep the residents’ minds, bodies, and spirits engaged and active. Over this summer, I was fortunate to help lead this club and plan activities. One of the activities was eating smoothies in memory care. My boss said that smoothies help improve memory and slows the progress of dementia. So maybe fish oil and smoothies reduce your risk of memory disorders such as dementia and Alzheimer’s disease.
ReplyDeleteIf the brain is made of tissue and needs electrical stimulation to operate like the rest of our body, wouldn’t it also be affected by toxins, stress and a poor diet like our bodies? M.D. Mark Hyman suggests that we need to take care of our brain like we take care of our body (Hyman, n.d.). Six out of the nine ways Hyman suggests to reverse dementia are diet oriented. Smoothies are a great way to get the vitamins that Hyman encourages us to take.
Barberger-Gateau et al. examined Alzheimer’s disease and other memory related disorders through the lenses of genetics and dietetics. Healthy diets such as the Mediterranean diet with an abundance of omega 3 fatty acids found in fish, and antioxidants found in fruits and veggies decrease the risk for AD. However, the preventative effect of omega 3 fatty acids is limited to APOE4 non-carriers (Barberger-Gateau et al., 2013).
I also found an interesting article where researchers used the Swedish Twin Registry and had 3,779 twins complete a diet questionnaire before cognitive screening and a full clinical evaluation 30 years later. In general, eating a medium to a large amount of fruits and vegetables were associated with a decreased risk of dementia and AD (Hughes et al., 2010).
So, we have many preventative options to decrease our risk of getting dementia or AD. Hughes et al. and Hyman draw attention to the dietary procedures of decreasing your risk. But, Barberger-Gateau et al. argues that we cannot completely guarantee that a healthy diet with the right vitamins can prevent dementia or AD because we might carry the APOE4 gene. Although a diet cannot make us “immune” to the disorder, this research motivates me to take care of myself so I can have a better future.
Stevensen, S. (2013, February 21). [Web log message]. Retrieved from http://www.aplaceformom.com/blog/2013-2-21healthy-smoothies-for-seniors/
Hyman, M. (n.d.). 9 steps to reverse dementia and memory loss after you age. Retrieved from http://www.danielplan.com/healthyhabits/9stepstoreversedementia/
Barberger-Gateau, P., Lambert, J., Féart, C., Pérès, K., Ritchie, K., Dartigues, J., & Alpérovitch, A. (2013). From genetics to dietetics: The contribution of epidemiology to understanding alzheimer's disease. Journal of Alzheimer's Disease, 33, S457-S463. doi: 1875-8908
Hughes, T., Andel, R., Small, B., Borenstein, A., Mortimer, J., Johansson, B., Fratiglioni, L., & Pedersen, N. (2010). Midlife fruit and vegetable consumption and risk of dementia in later life in swedish twins. The American Journal of Geriatric Psychiatry, 18(5), 413-420. doi: 10.1097/JGP.0b013e3181c65250