Food for Mood: Relevance of Nutritional Omega-3 Fatty Acids for Depression and Anxiety
Front. Physiol., 06 August 2018 | https://doi.org/10.3389/fphys.2018.01047
Thomas Larrieu*† and Sophie Layé*
UMR 1286, NutriNeuro: Laboratoire Nutrition et Neurobiologie Intégrée, Institut National de la Recherche Agronomique, Université de Bordeaux, Bordeaux, France
Vitamin D and Omega-3 category starts with
Omega-3 and Vitamin D separately & together help with Autism, Depression, Cardiovascular, Cognition, Pregnancy, Infant, Obesity, Mortality, Breast Cancer, Smoking, Sleep, Stroke, Surgery, Longevity, Trauma, Inflammation, MS, etc
See also - Overview: Omega-3 many benefits include helping vitamin D
Items in both categories Omega-3 and Depression:
- Depression treatments: diet, exercise, bright light, Vitamin D, B12, Omega-3, Zinc, Music, etc. – May 2019
- Omega-3 helps treat Major Depression – International Consensus Sept 2019
- Mental disorders fought by Omega-3 etc. - meta-meta-analysis Oct 2019
- Omega-3 reduces Depression. Anxiety, Stress, PTSD, etc. – Aug 2018
- Depression treated by Omega-3 (again) – meta-analysis Aug 2019
- Depression after childbirth 5 X less likely if good Omega-3 index – April 2019
- Occupational burnout reduced after 8 weeks of Omega-3 – RCT July 2019
- Anxiety severity reduced if more than 2 grams of Omega-3 – meta-analysis Sept 2018
- Psychotic disorders not treated by Omega-3 when patents take anti-depressants and get therapy – June 2018
- Happy Nurses Project gave Omega-3 for 3 months – reduced depression, insomnia, anxiety, etc for a year – RCT July 2018
- Depression – is it reduced by Vitamin D and or Omega-3 – RCT 2019
- Benefits of Omega-3 beyond heart health - LEF Feb 2018
- Omega-3 improves gut bacteria, reduces inflammation and depression – Dec 2017
- Unipolar depression treated by Omega-3, Zinc, and probably Vitamin D – meta-analysis Oct 2017
- Omega-3 reduces many psychiatric disorders – 2 reviews 2016
- Omega-3 does not consistently treat depression if use small amounts for short time period – review Oct 2016
- How Omega-3 Fights Depression – LEF July 2016
- Depression due to inflammation reduced by Omega-3 (children and pregnant) – Nov 2015
- Depression treated somewhat by Omega-3 (St. John's Wort better) – RAND org reviews 2015
- Depression substantially decreased with Omega-3 – Sept 2015
- Omega-3 for just 3 months greatly reduced psychosis for 80 months – RCT Aug 2015
- Omega-3 prevents PTSD and some mood disorders - Aug 2015
- Omega-3, Vitamin D, and other nutrients decrease mental health problems – March 2015
- Serotonin regulated by Vitamin D – part 1 autism – Feb 2014
Anxiety studies include
- Anxiety severity reduced if more than 2 grams of Omega-3 – meta-analysis Sept 2018
- Omega-3 reduces Depression. Anxiety, Stress, PTSD, etc. – Aug 2018
- Why is teen anxiety increasing so much (no mention of Magnesium, Vitamin D nor Omega-3) – Oct 2017
- Happy Nurses Project gave Omega-3 for 3 months – reduced depression, insomnia, anxiety, etc for a year – RCT July 2018
- Salmon intervention (vitamin D and Omega-3) improved heart rate variability and reduced anxiety – Nov 2014
- Search Vitamin D Life for ANXIETY 207 items as of Dec 2019 (not including PDFs)
 Download the PDF from Vitamin D Life
The central nervous system (CNS) has the highest concentration of lipids in the organism after adipose tissue. Among these lipids, the brain is particularly enriched with polyunsaturated fatty acids (PUFAs) represented by the omega-6 (ω6) and omega-3 (ω3) series. These PUFAs include arachidonic acid (AA) and docosahexaenoic acid (DHA), respectively. PUFAs have received substantial attention as being relevant to many brain diseases, including anxiety and depression. This review addresses an important question in the area of nutritional neuroscience regarding the importance of ω3 PUFAs in the prevention and/or treatment of neuropsychiatric diseases, mainly depression and anxiety. In particular, it focuses on clinical and experimental data linking dietary intake of ω3 PUFAs and depression or anxiety. In particular, we will discuss recent experimental data highlighting how ω3 PUFAs can modulate neurobiological processes involved in the pathophysiology of anxiety and depression. Potential mechanisms involved in the neuroprotective and corrective activity of ω3 PUFAs in the brain are discussed, in particular the sensing activity of free fatty acid receptors and the activity of the PUFAs-derived endocannabinoid system and the hypothalamic–pituitary–adrenal axis.
Introduction
Since the discovery of omega-3 (ω3) PUFAs in 1929 by George Burr and Mildred Burr (Burr and Burr, 1929; Spector and Kim, 2015), research on ω3 PUFAs became an appealing topic ranging from their role in cardiovascular risk to more recently neuropsychiatric pathologies such as depression and anxiety, cognitive decline or neurodegenerative diseases (Bazinet and Layé, 2014; Joffre et al., 2014; Coulombe et al., 2017). The relevance of lipids in brain function is illustrated by the fact that the CNS has the highest concentration of lipids in the organism after the adipose tissue (50–60% of the dry weight of the brain; Sastry, 1985). Among these lipids, the brain is particularly greedy for PUFAs from the ω6 and ω3 PUFAs families, in particular the LC PUFA (AA, 20:4n-6) and (DHA, 22:6n-3), respectively (Sastry, 1985). In the Human brain, DHA accounts for 10 to 15% of the total fatty acids (saturated, monounsaturated and PUFAs) in both males and females (McNamara et al., 2007, 2008b). This makes PUFAs indispensable to the normal development and function of the CNS (Makrides and Gibson, 2000; Innis, 2007; Bazinet and Layé, 2014). One hypothesis explaining this abundance in brain tissue is that Homo sapiens in Paleolithic settled around the lakes and seas where access to foods rich in ω3 PUFAs is easy (Bradbury, 2011). It is generally considered that humans evolved on a diet with a ratio of ω6 to ω3 PUFAs equal approximately to 1. During the industrial era, the rapid expansion of Western countries has been associated with drastic changes in the ω6/ω3 PUFAs content of the diet. This is reflected in large quantities of ω6 PUFA-containing foods and smaller amounts of ω3 PUFA-rich foods leading to Western diet being typically poor in ω3 PUFAs. In addition, the intake of saturated fats from lard and butter has been replaced by plant-based PUFAs based on recommendations from health agencies (Gibson et al., 2011). As a result, the use of oils such as sunflower oil which are mostly high in (LA, the precursor of AA) and low in a-linolenic acid (ALA, the precursor of DHA) leads to a marked increase in LA intake. In mammals, LA and ALA cannot be synthesized de novo and need to be provided through the diet (Simopoulos, 1991; Gibson and Makrides, 2001). These essential PUFAs are metabolized into LC PUFAs using the same enzymatic pathway, meaning that LA and ALA are in competition for endogenous conversion to their respective LC forms AA, and DHA (Figure 1) but also for their entry into the brain (Bazinet and Layé, 2014). Of importance, ALA bioconversion into DHA through several cycles of elongation (ELOVLs) and desaturation (Δ5 and Δ6 desaturases) is in the range of 0.05% (Burdge et al., 2003) to 4% (Emken et al., 1994) and might not be sufficient to cover brain needs. This led to the recommendation of dietary intake of oily fish rich in the LC ω3 PUFAs DHA and EPA (Tejera et al., 2016). Overall, western diets which are rich in LA (coming from vegetable oils rich in LA) and poor in ALA and DHA (coming from fat fish, sea food or certain algae) have created “a conditional essentiality for ω3 PUFAs” as previously described by Cunnane (2003) and Gibson et al. (2011). Indeed, the amount of LC ω3 PUFAs needed to compensate this lack in western diet is likely to increase, which is not sustainable in the actual context of fish stock decline (Fernandes and Cook, 2013). . . .
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