Fish oil is an extract of fish and seafood rich in n-3 omega fatty acids. But fish oil is not equal to omega 3 fatty acids, because the content of ordinary fish oil is about 30% omega 3 fatty acids, and the rest is other fatty acids.
The human body does not have the ability to synthesize omega 3 fatty acid on its own. Instead, it needs to get these fatty acids from food.
Fish oil contains two essential omega-3 acids for the body: eicosapentenoic acid (EPA) and dihydroxyapatenoic acid (DHA).
Eating more fish has been shown to reduce the risk of developing depression by a factor of 0.58.
According to a study conducted in a Greek island in 2009, eating an additional serving of fish each week was linked to a lower rate of depression.
Hibbeln (1998) found an association between higher fish consumption and lower annual rates of major depressive disorder in many countries around the world. [2]
A 2014 meta-analysis [3] showed that fish oil containing omega 3 can help treat patients with major depressive disorder.
A meta-analysis in 2019 [4] showed that omega 3 fish oil containing more than 60% EPA, with a dose of less than 1g per day, is helpful in treating depression patients.
The effectiveness of fish oil in promoting human health is a subject of ongoing debate. A clinical study conducted in 2016 [5] examined the use of fish oil in the treatment of depression but failed to provide substantial evidence that either EPA (Eicosapentaenoic Acid) or DHA (Docosahexaenoic Acid) alone could deliver significant therapeutic benefits. This lack of efficacy might be attributed to the purity of the fish oil and its EPA content.
In a 2012 meta-analysis, researchers made certain adjustments to an earlier omega-3 fats meta-analysis [6], which included 13 clinical studies conducted by other researchers prior to their own investigation. Notably, this meta-analysis excluded non-clinical definitions of depression.
According to a study carried out in the United States, supplementing omega-3 fats with fish oil indeed has a substantial impact on the treatment of depression.
Furthermore, this study categorized the findings of previous clinical studies and arrived at the conclusion that individuals who consumed fish oil with an EPA content exceeding 60% experienced significantly better results in managing depression compared to those who consumed fish oil with less than 60% EPA content. In the end, the consensus is that both EPA (Eicosapentaenoic Acid) and DHA (Docosahexaenoic Acid) hold equal importance for human health. Nevertheless, when it comes to treating depression, EPA (Eicosapentaenoic Acid) proves to be more effective than DHA (Docosahexaenoic Acid).
In 2014, a meta-analysis, encompassing 19 clinical studies on depression, also arrived at the same verdict [7]. The consensus drawn was that supplementing omega-3 fatty acids proved effective in managing depression. However, the key factor influencing this effectiveness was the EPA content in fish oil. Consequently, among the omega-3 fatty acids, EPA demonstrated greater effectiveness than DHA in treating depression.
In 2015, a significant animal experiment provided answers to most of our inquiries regarding the connection between omega-3 fatty acids and Endotoxin LPS [8]. Endotoxin LPS can induce inflammation in brain and in body. The study's design was remarkably clever, involving the use of genetically modified mice known as "Fat-1 Mice," These unique rodents distinguished themselves from regular mice by their ability to transform n-6 fatty acids (considered bad fat) from their diet, such as corn oil, into n-3 fatty acids(EPA,DHA,ALA)
The
researchers then fed both Fat Mouse No. 1 and the control group of
ordinary mice a diet rich in n-6 fatty acids. Remarkably, the
n-6 fatty acids in the blood of Fat Mouse No. 1 did not see a
significant increase because they were efficiently converted into n-3
fatty acids. What's more, the LPS levels in the blood of Fat
Mouse No. 1 remained stable, whereas ordinary mice experienced a
considerable increase in LPS.
Further analysis of the
feces from these two groups of mice revealed that Fat Mouse No. 1
hosted a substantial population of beneficial probiotics, including
Bifidobacterium and Lactobacillus, which were notably absent in the
regular mice.
The researchers then applied three methods to mice that produced substantial amounts of LPS: broad-spectrum antibiotics, exposing normal mice to the feces of Fat Mouse No. 1, and supplementing with omega-3 fatty acids. All three approaches successfully reduced LPS levels in the blood of regular mice.
This outcome
underscores the connection between LPS in the blood and the
composition of intestinal flora, as well as the ability of n-3 fatty
acids to mitigate LPS production. But the question remained: by
what mechanism did this occur? To answer that, the researchers
utilized sterile feces from Fat Mouse No. 1 and found that regular
mice could also reduce LPS in their blood. This is when the star
of the study emerged: IAP (Intestinal alkaline phosphatase). IAP
is a protein secreted by intestinal parietal cells, equipped with the
capability to combat bacteria and reduce LPS toxins. N-3 fatty
acids stimulate the secretion of IAP by intestinal parietal cells,
while n-6 fatty acids inhibit it.
Returning to the
experiment, the researchers fed regular mice IAP supplements, which
also resulted in a reduction of LPS in their blood. Therefore, the
balance between n-3 and n-6 fatty acids affects the behavior of
intestinal wall cells, influencing the secretion of IAP, modifying
the composition of intestinal
flora, and concurrently impacting the quantity of LPS in the blood.
Regrettably, there is currently no readily available health
product for direct IAP supplementation.
Therefore, the most effective steps we can take at present involve supplementing with fish oil rich in n-3 and reducing the consumption of n-6 vegetable oil.
The sole dietary and nutritional supplement capable of simultaneously treating symptoms (reducing inflammation) and tackling the root issue (reducing LPS) is fish oil. It's essential that the fish oil comprises pure omega-3. If the content is only 30%, the remaining 70% might consist of detrimental omega-6 fatty acids. One of the primary goals of using fish oil is to balance the n-3/n-6 ratio. Naturally, the higher the content of n-3 in the fish oil, the more effective it is.
Benefits of Fish Oil for anxiety and depression
Regarding the potential of fish oil to alleviate anxiety and depression, based on the properties of fish oil and existing research, the potential reasons for fish oil's capacity to alleviate anxiety and depression are as follows:
1. Anti-inflammatory effect
Symptoms of depression are associated with the ongoing inflammatory response within the body. The antidepressant properties of Omega-3 are attributed to their role in regulating oxidative reactions in nerve cells and curbing the generation of inflammatory cytokines like TNF-a or IL-6. Omega-3 also binds with the building blocks of these inflammatory cytokines (such as arachidonic acid) to diminish inflammation. Furthermore, EPA hinders the enzyme responsible for arachidonic acid production (A5 unsaturase).[9]
2. Promote the transmission of information in the nerves.
Omega-3 has the potential to influence neurotransmission by altering the flexibility of cell membranes and boosting the transmission of information through G protein and PKC (protein kinase C). This results in heightened sensitivity of serotonin and dopamine receptors. EPA, in particular, has the capability to enhance the transmission of dopamine and serotonin, consequently amplifying neurotransmission associated with feelings of happiness.
In animal experiments, the supplementation of Omega-3 in test mice was shown to increase the brain's dopamine by 40% and elevate the proportion of dopamine receptors binding to it. This, in turn, allows more dopamine, responsible for transmitting joyous information, to reach the brain.[10]
3. Relieve endocrine system disorders
Depression is linked to elevated cortisone levels in the body. This occurs when excessive stress triggers the overactivation of the HPA axis, leading to the excessive secretion of corticotropin-releasing hormone (CRH). CRH plays a pivotal role as the primary switch in the hormonal system for stress regulation, and heightened CRH levels stimulate the amygdala in the brain, resulting in increased feelings of anxiety and fear.
EPA has the capacity to inhibit the excessive activation of the HPA axis and reduce the secretion of CRH. Additionally, it can curb the protein responsible for transporting cortisone, thereby limiting the entry of cortisone into the brain. This helps maintain a balance in cortisone levels within the brain and stabilizes the overexcited endocrine system.[11]
4. Stabilize brain balance
Research has revealed that following the supplementation of EPA, there is an increase in N-acetyl-aspartate in the brain. N-acetyl-aspartate is known for its neuroprotective properties, and this rise can contribute to stabilizing brain nerves. Furthermore, Omega-3 is capable of enhancing the fluidity of brain cell membranes and reinforcing the integrity of the tight junctions within the blood-brain barrier (BBB). Ultimately, Omega-3 can diminish the likelihood of brain atrophy caused by depression by reducing cortisone levels.[12]
Which fish oil to choose for anti-depression and anxiety?
It is recommended to choose "pure EPA" or "EPA-based" fish oil, which will be more effective than DHA-based fish oil. But in fact, compared with DHA, EPA is not concentrated in the brain. EPA is more effective than DHA because EPA can quickly enter the brain as a free fatty acid and has a better anti-inflammatory effect. [13]
We can choose "Concentration", "Ratio", and "Quality" respectively:
► Concentration: In fish oil, the recommended concentration is EPA+DHA>60%, or >80%. In studies that recommend using EPA+DHA more than 80%, it is indicated that >80% content is better than <80%.
► Ratio: EPA and DHA are synergistic. The recommended ratio is EPA/DHA>2.
►Quality: Quality has a great influence on the effect. When selecting fish oil, you need to pay attention to the absorption, extraction method, heavy gold plaque and the content of pollutants.
How much fish oil do you need to eat to effectively fight anxiety and depression?
In recent clinical studies, EPA mostly uses "720-1000mg" per day, which is more effective than DHA-based. And the use of EPA fish oil alone, or with anti-anxiety and depression drugs are effective. If you want to improve your memory at the same time, you can choose 1 or 2g of DHA per day, which is more effective than a high dose of 4g/day.
Ref:
[1]Long-term fish intake is associated with less severe depressive symptoms among elderly men and women: the MEDIS (MEDiterranean ISlands Elderly) epidemiological study Vassiliki Bountziouka, Evangelos Polychronopoulos, Akis Zeimbekis, Eftichia Papavenetiou, Evaggelia Ladoukaki, Natassa Papairakleous, Efthimios Gotsis, George Metallinos, Christos Lionis, Demosthenes Panagiotakos PMID: 19587361 https://doi.org/10.1177/0898264309340693
[2] Fish consumption and major depression Joseph Hibbeln Published:April 18, 1998 https://doi.org/10.1016/S0140-6736(05)79168-6
[3] Grosso, Giuseppe & Pajak, Andrzej & Marventano, Stefano & Castellano, Sabrina & Galvano, Fabio & Bucolo, Claudio & Drago, Filippo & Caraci, Filippo. (2014). Role of Omega-3 Fatty Acids in the Treatment of Depressive Disorders: A Comprehensive Meta-Analysis of Randomized Clinical Trials. PloS one. 9. e96905. 10.1371/journal.pone.0096905. http://dx.doi.org/10.1371/journal.pone.0096905
[4] Liao, Yuhua & Xie, Bo & Zhang, Huimin & He, Qian & Guo, Lan & Subramaniapillai, Mehala & Fan, Beifang & Ciyong, Lu & Mclntyer, R.. (2019). Efficacy of omega-3 PUFAs in depression: A meta-analysis. Translational Psychiatry. 9. 10.1038/s41398-019-0515-5. https://doi.org/10.1038/s41398-019-0515-5
[5] Mischoulon, D., Nierenberg, A. A., Schettler, P. J., Kinkead, B. L., Fehling, K., Martinson, M. A., & Hyman Rapaport, M. (2015). A double-blind, randomized controlled clinical trial comparing eicosapentaenoic acid versus docosahexaenoic acid for depression. The Journal of clinical psychiatry, 76(1), 54–61.https://doi.org/10.4088/jcp.14m08986
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