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Unhealthy dietary habits have been identified as a risk factor for the development and progression of cancer. Therefore, adopting a healthy eating pattern is currently recommended to prevent the onset of different types of cancers, including breast carcinoma. In particular, the Mediterranean diet, based on high consumption of omega-3 polyunsaturated fatty acids (N-3 PUFAs), such as those found in cold-water fish and other seafood, nuts, and seeds, is recommended to reduce the incidence of several chronic-degenerative diseases. Indeed, the consumption of N-3 PUFAs, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), reduced the risk of different types of cancer, including breast cancer. Moreover, they can counteract breast cancer progression and reduce the side effects of chemotherapy in breast cancer survival. Studies have demonstrated that DHA, exhibiting greater antitumor activity than EPA in breast cancer, can be attributed to its direct impact on breast cancer cells and also due to its conversion into various metabolites. N-docosahexaenoyl ethanolamine, DHEA, is the most studied DHA derivative for its therapeutic potential in breast cancer. In this review, we emphasize the significance of dietary habits and the consumption of N-3 polyunsaturated fatty acids, particularly DHA, and we describe the current knowledge on the antitumoral action of DHA and its derivative DHEA in the treatment of breast cancer.

Long-term dietary habits play a crucial role in creating a host-specific gut microbiota community in humans. Despite the many publications about the effects of carbohydrates (prebiotic fibers), the impact of dietary fats, such as omega-3 polyunsaturated fatty acids (PUFAs), on the gut microbiota is less well defined. The few studies completed in adults showed some common changes in the gut microbiota after omega-3 PUFA supplementation. In particular, a decrease in Faecalibacterium, often associated with an increase in the Bacteroidetes and butyrate-producing bacteria belonging to the Lachnospiraceae family, has been observed. Coincidentally, a dysbiosis of these taxa is found in patients with inflammatory bowel disease. Omega-3 PUFAs can exert a positive action by reverting the microbiota composition in these diseases, and increase the production of anti-inflammatory compounds, like short-chain fatty acids. In addition, accumulating evidence in animal model studies indicates that the interplay between gut microbiota, omega-3 fatty acids, and immunity helps to maintain the intestinal wall integrity and interacts with host immune cells. Finally, human and animal studies have highlighted the ability of omega-3 PUFAs to influence the gut–brain axis, acting through gut microbiota composition. From these findings, the importance of the omega-3 connection to the microbiota emerges, encouraging further studies.

DHA is an important component of neural lipids accumulating in neural tissue during development. Inadequate DHA in gestation may compromise infant development, but it is unknown whether there are lasting effects. We sought to determine whether the observed effects of fetal DHA inadequacy on infant development persist into early childhood. This follow-up study assessed children (5–6 years) whose mothers received 400 mg/d DHA or a placebo during pregnancy. Child neurodevelopment was assessed with several age-appropriate tests including the Kaufman Assessment Battery for Children. A risk-reduction model was used whereby the odds that a child from the maternal placebo group would fail to achieve a test score in the top quartile was calculated. The association of maternal DHA intake and status in gestation with child test scores, as well as with child DHA intake and status, was also determined. No differences were detected in children (n 98) from the maternal placebo and DHA groups achieving a high neurodevelopment test score (P>0·05). However, maternal DHA status was positively related to child performance on some tests including language and short-term memory. Furthermore, child DHA intake and status were related to the mother’s intake and status in gestation. The neurodevelopment effects of fetal DHA inadequacy may have been lost or masked by other variables in the children. Although we provide evidence that maternal DHA status is related to child cognitive performance, the association of maternal and child DHA intake and status limits the interpretation of whether DHA before or after birth is important.

Background Neuroinflammatory processes are considered a double-edged sword, having both protective and detrimental effects in the brain. Microglia, the brain’s resident innate immune cells, are a key component of neuroinflammatory response. There is a growing interest in developing drugs to target microglia and control neuroinflammatory processes. In this regard, docosahexaenoic acid (DHA), the brain’s n-3 polyunsaturated fatty acid, is a promising molecule to regulate pro-inflammatory microglia and cytokine production. Several works reported that the bioavailability of DHA to the brain is higher when DHA is acylated to phospholipid. In this work, we analyzed the anti-inflammatory activity of DHA-phospholipid, either acetylated at the sn-1 position (AceDoPC, a stable form thought to have superior access to the brain) or acylated with palmitic acid at the sn-1 position (PC-DHA) using a lipopolysaccharide (LPS)-induced neuroinflammation model both in vitro and in vivo. Methods In vivo, adult C57Bl6/J mice were injected intravenously (i.v.) with either AceDoPC or PC-DHA 24 h prior to LPS (i.p.). For in vitro studies, immortalized murine microglia cells BV-2 were co-incubated with DHA forms and LPS. AceDoPC and PC-DHA effect on brain or BV-2 PUFA content was assessed by gas chromatography. LPS-induced pro-inflammatory cytokines interleukin IL-1β, IL-6, and tumor necrosis factor (TNF) α production were measured by quantitative PCR (qPCR) or multiplex. IL-6 receptors and associated signaling pathway STAT3 were assessed by FACS analysis and western-blot in vitro. Results In vivo, a single injection of AceDoPC or PC-DHA decreased LPS-induced IL-6 production in the hippocampus of mice. This effect could be linked to their direct effect on microglia, as revealed in vitro. In addition, AceDoPC or PC-DHA reduced IL-6 receptor while only AceDoPC decreased IL-6-induced STAT3 phosphorylation. Conclusions These results highlight the potency of administered DHA—acetylated to phospholipids—to rapidly regulate LPS-induced neuroinflammatory processes through their effect on microglia. In particular, both IL-6 production and signaling are targeted by AceDoPC in microglia.

The present study evaluated the effects of increasing the dietary levels of EPA and DHA in Atlantic salmon (Salmo salar) reared in sea cages, in terms of growth performance, welfare, robustness and overall quality. Fish with an average starting weight of 275 g were fed one of four different diets containing 10, 13, 16 and 35 g/kg of EPA and DHA (designated as 1·0, 1·3, 1·6 and 3·5 % EPA and DHA) until they reached approximately 5 kg. The 3·5 % EPA and DHA diet showed a significantly beneficial effect on growth performance and fillet quality compared with all other diets, particularly the 1 % EPA and DHA diet. Fish fed the diet containing 3·5 % EPA and DHA showed 400–600 g higher final weights, improved internal organ health scores and external welfare indicators, better fillet quality in terms of higher visual colour score and lower occurrence of dark spots and higher EPA and DHA content in tissues at the end of the feeding trial. Moreover, fish fed the 3·5 % EPA and DHA diet showed lower mortality during a naturally occurring cardiomyopathy syndrome outbreak, although this did not reach statistical significance. Altogether, our findings emphasise the importance of dietary EPA and DHA to maintain good growth, robustness, welfare and fillet quality of Atlantic salmon reared in sea cages.

The digitization of health care led to a steady increase in the adoption and use of mobile health (mHealth) apps. Germany is the first country in the world to cover the costs of mHealth apps through statutory health insurance. Although the benefits of mHealth apps are discussed in detail, aspects of problems and barriers are rarely studied. This scoping review aimed to map and categorize the evidence on problems and barriers related to the use of mHealth apps. Systematic searches were conducted in the MEDLINE, Embase, and PsycINFO databases. Additional searches were conducted on JMIR Publications and on websites of relevant international organizations. The inclusion criteria were publications dealing with apps similar to those approved in the German health care system, publications addressing problems and barriers related to the use of mHealth apps, and articles published between January 1, 2015, and June 8, 2021. Study selection was performed by 2 reviewers. The manuscript was drafted according to the PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews) checklist. The analysis of the included publications and categorization of problems and hurdles were performed using MAXQDA (VERBI Software GmbH). The database search identified 1479 publications. Of the 1479 publications, 21 (1.42%) met the inclusion criteria. A further 8 publications were included from citation searching and searching in JMIR Publications. The identified publications were analyzed for problems and barriers. Problems and barriers were classified into 10 categories (\"validity,\" \"usability,\" \"technology,\" \"use and adherence,\" \"data privacy and security,\" \"patient-physician relationship,\" \"knowledge and skills,\" \"individuality,\" \"implementation,\" and \"costs\"). The most frequently mentioned categories were use and adherence (eg, incorporating the app into daily life or dropouts from use; n=22) and usability (eg, ease of use and design; n=19). The search identified various problems and barriers in the context of mHealth apps. Although problems at the app level (such as usability) are studied frequently, problems at the system level are addressed rather vaguely. To ensure optimal use of and care with mHealth apps, it is essential to consider all types of problems and barriers. Therefore, researchers and policy makers should have a special focus on this issue to identify the needs for quality assurance. RR2-10.2196/32702.

Compared with APOE3 , APOE4 is associated with greater age-related cognitive decline and higher risk of neurodegenerative disorders. Therefore, development of supplements that target APOE genotype-modulated processes could provide a great benefit for the aging population. Evidence suggests a link between APOE genotype and docosahexaenoic acid (DHA); however, clinical studies with current DHA supplements have produced negative results in dementia. The lack of beneficial effects with current DHA supplements may be related to limited bioavailability, as the optimal form of DHA for brain uptake is lysophosphatidylcholine (LPC)-DHA. We previously developed a method to enrich the LPC-DHA content of krill oil through lipase treatment (LT-krill oil), which resulted in fivefold higher enrichment in brain DHA levels in wild-type mice compared with untreated krill oil. Here, we evaluated the effect of a control diet, diet containing krill oil, or a diet containing LT-krill oil in APOE3 - and APOE4- targeted replacement mice ( APOE -TR mice; treated from 4 to 12 months of age). We found that DHA levels in the plasma and hippocampus are lower in APOE4 -TR mice and that LT-krill oil increased DHA levels in the plasma and hippocampus of both APOE3 - and APOE4 -TR mice. In APOE4 -TR mice, LT-krill oil treatment resulted in higher levels of the synaptic vesicle protein SV2A and improved performance on the novel object recognition test. In conclusion, our data demonstrate that LPC-DHA/EPA-enriched krill oil can increase brain DHA and improve memory-relevant behavior in mice that express APOE4 . Therefore, long-term use of LT-krill oil supplements may on some level protect against age-related neurodegeneration.

This research focused on obtaining eicosapentaenoic acid (EPA, 20:5 n-3) and docosahexaenoic acid (DHA, 22:6 n-3) (EPA+DHA) concentrates from refined commercial salmon oil (RCSO). Independent variables of the complexation process were optimized by means of the application of response surface methodology (RSM) in order to obtain the maximum content of such fatty acids (FAs). As a result of employing the optimized conditions for all the variables (6.0, urea:FA content ratio; −18.0 °C, crystallization temperature; 14.80 h, crystallization time; 500 rpm, stirring speed), high contents of EPA and DHA could be obtained from RCSO, achieving increases of 4.1 and 7.9 times in the concentrate, with values of 31.20 and 49.31 g/100 g total FA, respectively. Furthermore, a 5.8-time increase was observed for the EPA + DHA content, which increased from 13.78 to 80.51 g/100 g total FA. It is concluded that RCSO can be transformed into a profitable source of EPA and DHA (EPA+DHA), thus leading to a product with higher commercial value.

Artemisinin resistance, first reported on the Thai-Cambodian border in 2009, has spread across Southeast Asia, characterized by delayed parasite clearance. Extended artemisinin-based combination therapy (ACT) regimens have shown efficacy where standard 3-day treatments failure. In Indonesia, dihydroartemisinin-piperaquine (DHA-PPQ) has been the first-line treatment for uncomplicated Plasmodium falciparum malaria since 2010. This study evaluates the efficacy, safety, and parasite clearance times of DHA-PPQ in West Sumba and Kupang Districts, East Nusa Tenggara, while assessing single-nucleotide polymorphisms (SNPs) in the Pfk13 and Pfcrt genes, which are linked to artemisinin and piperaquine resistance, respectively. Following WHO guidelines, 382 cases were screened, with 41 eligible for 42-day clinical and parasitological monitoring. Molecular analyses utilized PCR and real-time PCR. All cases demonstrated adequate clinical and parasitological response (100% APCR). No mutations were detected in 21 Pfk13 SNPs associated with artemisinin resistance or in Pfcrt codons M343L, C350R, G353V, and I356L linked to piperaquine resistance. However, 10 of 41 samples (24.39%) exhibited Pfpm2 gene amplification, indicating early piperaquine selection pressure. DHA-PPQ remains effective, but Pfpm2 amplification underscores the need for continuous molecular surveillance and exploration of extended ACT regimens to sustain malaria control.

Clinical evidence indicated that eicosapentaenoic acid (EPA) was more effective than docosahexaenoic acid (DHA) in depression treatment. However, possible mechanisms remain unclear. Here, a chronic unpredictable mild stress (CUMS)-induced model of depression was used to compare EPA and DHA anti-depressant effects. After EPA or DHA feeding, depression-like behavior, brain n-3/n-6 PUFAs profile, serum corticosterone and cholesterol concentration, hippocampal neurotransmitters, microglial and astrocyte related function, as well as neuronal apoptosis and survival signaling pathways were studied. EPA was more effective than DHA to ameliorate CUMS-induced body weight loss, and depression-like behaviors, such as increasing sucrose preference, shortening immobility time and increasing locomotor activity. CUMS-induced corticosterone elevation was reversed by bother fatty acids, while increased cholesterol was only reduced by EPA supplement. Lower hippocampal noradrenaline and 5-hydroxytryptamine concentrations in CUMS rats were also reversed by both EPA and DHA supplement. However, even though CUMS-induced microglial activation and associated increased IL-1β were inhibited by both EPA and DHA supplement, increased IL-6 and TNF-α levels were only reduced by EPA. Compared to DHA, EPA could improve CUMS-induced suppressive astrocyte biomarkers and associated BDNF-TrkB signaling. Moreover, EPA was more effective than DHA to attenuate CUMS-induced higher hippocampal NGF, GDNF, NF-κB, p38, p75, and bax expressions, but reversed bcl-2 reduction. This study for the first time revealed the mechanisms by which EPA was more powerful than DHA in anti-inflammation, normalizing astrocyte and neurotrophin function and regulating NF-κB, p38 and apoptosis signaling. These findings reveal the different mechanisms of EPA and DHA in clinical depression treatment.