Nordic diet and its benefits in neurological function: a systematic review of observational and intervention studies (2024)

Table 1

Characteristics of observational and intervention studies.

FFQ, Food frequency questionnaire; ND, Nordic diet; NDD, New Nordic diet; LCPUFA, Long-chain polyunsaturated fatty acids; Hb, Hemoglobin.

4.1. Observational studies

4.2. Intervention studies

5.1. Vegetables and fruits

The ND is rich in vegetables and fruits which are the main sources of nutritious components such as minerals, natural antioxidants, vitamins, and dietary fibers (58, 59). These components have multiple beneficial effects in preventing and improving several chronic disorders. Their benefits for health are mediated by polyphenolic compounds to provide antioxidant, anticarcinogenic, antimicrobial, antiviral, and anti-inflammatory effects (58, 60–62). Thus, daily consumption of foods rich in plant-derived polyphenols has been encouraged, especially in the Western world (61, 63).

Berries are important and abundant wild fruits in the Nordic countries with significant health-promoting outcomes, attributed mainly to a special class of polyphenols known as anthocyanins (64). Anthocyanins are organic water-soluble glycosidic pigments widely found in dark-colored vegetables, fruits, and grains with considerable inherent antioxidant properties (65). It has been reported that anthocyanins have a wide and various range of beneficial impacts such as anti-inflammatory, immunomodulatory, cardioprotective, hepatoprotective, neuroprotective, anticancer, antidiabetic, anti-obesity, and antioxidant effects, which make them promising factors for the prevention and treatment of pathological circ*mstances including neurological disorders (66, 67). Multiple lines of evidence suggest that anthocyanins may have neuroprotective and anti-neuroinflammatory activities that result in improving neural function (68). Neuroinflammation defines specific processes related to the trafficking of immune cells in the central nervous system, which leads to a pathological condition by affecting certain pathways. During the neuroinflammatory process, activation of microglia and astrocytes can cause proinflammatory cytokines to be released and, in turn, activate a second level of inflammatory signaling pathways like nuclear factor-kappa B (NF-κB) (69, 70). Thus, oxidative stress and neuroinflammation can disrupt normal brain function (71). It is suggested that increased generation of reactive oxygen species (ROS) may trigger oxidative injury, cellular damage, mitochondrial dysfunction, and impaired deoxyribonucleic acid repair system which are detrimental factors for neurological function (72, 73). Polyphenols, including anthocyanins, can prevent neuroinflammation, protect neurons against neurotoxin-induced damage, and promote cognitive performance, learning, memory, and neuron survival through their anti-inflammatory and antioxidant activities (74–76). In this regard, Poulose et al. demonstrated that anthocyanins protect the microglial cells subjected to lipopolysaccharide (LPS), a bacterial endotoxin, against neuroinflammation by preventing the activation of p38 and NF-κB and reducing proinflammatory factors such as cyclooxygenase-2 (COX-2) and tumor necrosis factor-α (TNF-α) (77). These findings are consistent with another study in which anthocyanins prevented the up-regulation of inflammatory pathways including Phosphoinositide 3-kinase (PI3K)/AKT, NF-κB, and mitogen-activated protein kinases (MAPKs) in microglial cells, decreasing the generation of pro-inflammatory factors, such as TNF-α, nitric oxide (NO), interleukin (IL)-1β, and prostaglandin E2 (PGE2) (78).

It is noteworthy that the relatively low bioavailability of anthocyanins in the brain may limit their efficacy. Indeed, low concentrations of circulating anthocyanins are considered to be due to the metabolism by gut microbiota to produce different phenolic acid and aldehyde metabolites (79). Some studies indicated that protocatechuic acid (PA), a key anthocyanin metabolite, is a neuroprotective factor through anti-inflammatory and antioxidant features (79, 80).

Cruciferous vegetables including kale, cabbage, Brussels sprouts, horseradish, cauliflower, radish, turnips, and broccoli sprouts are also identified as one of the main components in the ND (81). These vegetables contain a wide variety of nutrients such as protein, carbohydrate, vitamins, minerals, phytochemicals (Tannins, flavonoids, anthocyanins, and carotenoids), phytosterols, and non-nutritive metabolites such as nitrogen-containing compounds and sulfur compounds (glucosinolates and S-methyl cysteine sulfoxide) (82). Several studies have examined the health-promoting effects of cruciferous vegetables in humans and showed that higher consumption of these vegetables is related to a reduced risk of several chronic disorders (83). Besides phytochemicals, the beneficial health characteristics of these vegetables are mainly related to the functions of glucosinolates. In case of plant tissue damage, glucosinolates are hydrolyzed by enzymatic activity, and metabolites such as isothiocyanate, nitriles, and thiocyanates are formed. Also, glucosinolates hydrolysis can occur by intestinal microbiota (84, 85). Cruciferous vegetables, due to their glucosinolates and other metabolites, exhibit several biological properties related to neurological and psychiatric conditions (86, 87). Several studies have provided mechanistic insight into the advantageous effects of glucosinolates on brain health through modulating the hypothalamic–pituitary–adrenal axis, reducing neuroinflammation, oxidative stress, beta-amyloid, and tau production, inhibiting DNA methyltransferases, and increasing brain-derived neurotrophic factor and cellular lifespan (88–90). In a clinical study, daily oral administration of isothiocyanate sulforaphane increased peripheral and brain glutathione, an antioxidant, in healthy human subjects (91). In addition, Ghazizadeh-Hashemi et al. showed that a 6-week sulforaphane administration safely decreased depressive symptoms in patients with a history of cardiac interventions and presence of mild to moderate depression (92). Although, a variety of animal model studies has reported a good effectiveness of sulforaphane interventions for psychiatric and neurodegenerative disorders such as depression, anxiety, schizophrenia, cognitive function, learning and memory, multiple sclerosis, and AD (86, 93–96). Therefore, considering that the positive impacts of cruciferous vegetables and their metabolites are mainly associated with antioxidant and anti-inflammatory mechanisms, the ND may also have beneficial outcomes on neurological function.

Apples and pears are widely consumed in the Nordic regions and are generally recognized as healthy food sources (97). Some studies demonstrated that apples are a good source of antioxidants with various phytochemical compounds. The main phytochemicals in apples are flavonoids (including quercetins, catechin, epicatechin, and proanthocyanidins) and phenolic acids (including p-coumaric acid, chlorogenic acid, and caffeic acid) (97). Quercetin, (3,5,7,3′,4′-pentahydroxyflavone), plays a principal neuroprotective role by inhibiting the proinflammatory mediators that are released by glial cells. Indeed, it is a strong scavenger of free radicals such as ROS and reactive nitrogen species (98). It has been proposed that quercetin prevents neuroinflammation by inhibiting the production of NO in glial cells, which further inhibits the NF-κB signaling pathway and prevents inflammation-related neuronal damage (99). Similarly, it ameliorated activated astrocytes which mediate the generation of ROS and cytokines and further influence neuronal cells and degeneration (100). Most importantly, quercetin may protect the neuronal cells against amyloid beta peptide toxicity by activating the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)- antioxidant response elements (ARE) pathway (101). Activation of the Nrf2-ARE signaling pathway promotes neuroprotection against oxidative injury and cell death (102). Another area of interest regarding the neuroprotective mechanisms provided by quercetin is sirtuins. Quercetin has been shown to activate sirtuin-1, which leads to the protection of cells from apoptosis (101).

5.2. Whole grains

The ND is characterized by a high content in whole grain cereals versus refined grains. Whole wheat, oat, rye, and barley are among the main food sources of carbohydrates and other nutrients such as dietary fibers, minerals, and vitamins in the Scandinavian nations. It has been reported that whole-grain cereals are high in phytochemicals such as phytosterols, phenolic acid, and β-glucans which are responsible for the high antioxidant properties (103). A Finnish study revealed that whole-grain consumption was very high among the subjects in Finland with the lowest quartile median consumption (79 g/day), which was higher than the highest quintile mean consumption (45.6 g/day) found in the US population (32). There is ample evidence to support that whole grain cereals have health-benefits effects (30). Mounting evidence demonstrated that whole-grain cereals are good sources of fermentable carbohydrates, including resistant starch, dietary fibers, and oligosaccharides, that cannot usually be broken down by the digestive enzymes of humans. However, the gut microflora selectively breaks down and ferments them into gases and short-chain fatty acids (SCFAs) (104). SCFAs are absorbed and utilized by the gastrointestinal epithelial cells, as well as beneficial bacteria such as lactobacilli and bifidobacterial; therefore improving the gut microbial community, decreasing the gut pH, and enhancing the immunity of the body (105). Extensive research efforts have indicated that an appropriate increase in whole-grain intake (barley and oats) can enhance the growth of probiotics and enhance intestinal and distal organ functions (106, 107). On the other hand, evidence is emerging supporting the role of intestinal microbiota in the brain function by the gut-brain axis, thereby regulating neurological activities such as behavior, cognitive function, and mood (108, 109). Gut-brain axis involves a complex structure of immunological, neural, and endocrinological factors, that can be an important target for manipulating brain health (109). A cross-sectional study demonstrated an inverse relationship between fiber supplementation and depressive symptoms (110). However, there was no significant association in Gopinath et al. study (111). Overall, there are complex mechanistic processes involved in the impacts of dietary fiber-derived whole grains on brain health. Metabolites from bacterial fermentation, such as SCFAs, may play a variety of regulatory roles including histone acetylation, signaling through G protein-coupled receptors, and affect the host’s immune system by altering the circulating levels of inflammatory mediators and reducing neuroinflammation (112). In animal models of endotoxin-induced sickness behavior, pectin as the only source of fiber decreased brain TNF-α and IL-1β (113).

Moreover, gut microbiota modulates serotonin concentration, a neurotransmitter, and the metabolism of tryptophan, which is often targeted by anti-depressant medications in the central nervous system (114). Butyrate, one of the SCFAs, can increase the transcripts of brain-derived neurotrophic factor (BDNF), an important molecule for maintaining the integrity of neurons and cognitive function, in the brain (115). It is worth noting that the gut microbiome may directly or indirectly affect the generation of neurotransmitters, such as dopamine, γ-aminobutyric acid (GABA), and acetylcholine which modulate cognition and mood status (109). The potential action mechanisms of the ND on the gut-brain axis are shown in Figure 3.

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Figure 3

Summary of the effects of the ND on the gut-brain axis. One of the components of the Nordic diet is whole grains, which are a good source of fermentable carbohydrates. The intestinal microbial flora selectively ferments them into gases and SCFAs, which in several ways lead to the improvement of the gut barrier function and effect on the central nervous system (gut-brain-axis). (1) Modulating histone through GPR, (2) reducing cytokines such as TNF-α, IL-6, and IL-1β, (3) modulating neurotransmitters and neuroactive (tryptophan, serotonin, GABA, dopamine, and acetylcholine), (4) increasing BDNF. GABA, Gamma-Aminobutyric Acid; BDNF, Brain-derived neurotrophic factor; TNF-α, Tumor necrosis factor-alpha; IL-6, Interleukin-6; IL-1β, Interleukin-1beta; SCFAs, Short chain fatty acids; GPR, G protein-coupled receptor.

Besides fibers, a growing body of evidence has revealed that whole-grain cereals are rich in a variety of phytochemicals, including phytic acid, flavonoids, terpenes, coumarins, and phenolic compounds, which have various physiological activities, including hypotensive, antibacterial, anti-hyperglycemia, immunomodulation, antioxidant, anti-tumor, anti-inflammation, and anti-aging (103). These compounds are documented to exert antioxidant and anti-inflammatory activities, resulting in a neuroprotective effect (103). It is worth noting that studies on animals have shown that diets high in carbohydrates and low in protein could lead to the longest lifespan and improved cognition. It may be concluded that the quality of dietary carbohydrates is more important than its quantity on nerve function and brain health (116, 117).

5.3. Legumes

Legumes are nutritionally valuable, providing several nutritious components including proteins with essential amino acids, minerals, vitamins, dietary fibers, complex carbohydrates, unsaturated fats, and non-nutritional compounds such as alkaloids, isoflavone, phytic acid, phenolic compounds (tannins), and saponins (113). Dietary isoflavones derived from legumes may have beneficial effects on brain health, receiving new attention regarding neuroprotective properties (118). These compounds are classified as phytoestrogens which are most extensively investigated. Isoflavones can mimic the transcriptional effects of estrogen via binding to estrogen-receptor beta (ERβ), mediating estrogen action, and thereby inhibiting apoptotic cell death (119). Estrogen and its mimics modulate synaptic plasticity, neuronal survival and growth, and brain function through an estrogen receptor-mediated pathway, and subsequently regulation of gene transcription and second messenger systems (120).

Moreover, the antioxidant action of isoflavones has been suggested to be involved in the presumed effect of legumes on brain health. These compounds afford protection against neuroinflammation by ameliorating oxidative damage, upregulating endogenous antioxidant signaling pathways, and protecting the integrity of the mitochondria (119, 121). These antioxidant activities may be attributed to the inhibition of the NF-κB signaling pathway (121). In this regard, some studies demonstrated that isoflavones prevent microglial activation and inflammation (122, 123). In vitro studies have shown that isoflavone treatment exhibited protection against apoptosis via regulating the antiapoptotic bcl-2 protein suppression and modulating cell survival signaling (120, 121). Other protective effects of dietary isoflavones on brain health can mediate by reductions in proapoptotic proteins such as Bax and Bad, and modulation of kinase signaling (119).

5.4. Fish/seafood

Fish, especially fatty fish, and seafood are one of the natural components in the ND, with high amounts of polyunsaturated fatty acids (PUFAs) containing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). In addition, these food sources contain many other valuable nutrients such as vitamins and minerals (30). It was commonly suggested that the major dietary components of fish are DHA and EPA, which are the main building blocks for nerve cell membranes and play a crucial role in proper brain development and function, neurotransmission, and ion channel modulation, and thus are effective in neuroprotection. Some studies reported that there is a relationship between the reduction of omega-3 PUFA concentration in the blood serum and erythrocyte membranes with several neuropsychiatric disorders such as depression, schizophrenia and also dyspraxia, dyslexia, autism, and attention-deficit hyperactivity disorder (ADHD) (124–126). Omega-3 PUFAs have several mechanisms of action in the cerebral vascular system and brain that could improve brain function (127). First, they seem to attenuate inflammation by reducing the production of pro-inflammatory cytokines from arachidonic acid. Omega-3 PUFAs compete with arachidonic acid for incorporation into phospholipid membranes in the cyclooxygenase pathway by preventing the generation of proinflammatory eicosanoids, including prostaglandin E2 and thromboxane B2. EPA and DHA can also prevent the secretion of other pro-inflammatory mediators including interleukins (IL-1, IL-1β, IL-2, IL-6), TNF-α, and interferon-gamma (IFN-γ). Other anti-inflammatory mechanisms are the reduction of T-cell proliferation and inhibition of leukocyte migration. Considering that inflammation is involved in the pathophysiology of neurological disorders, these fatty acids might exert neuroprotective properties through their anti-inflammatory effects (127–129). Second, long-chain omega-3 fatty acids decrease cardiovascular risk factors, including hypertriglyceridemia, and enhance the blood flow in the brain, thus reducing cerebrovascular disease by modulating risk factors (127).

Moreover, a growing body of evidence suggests that omega-3 fatty acids affect the receptor function, the neurotransmitter level, and its metabolism. In this regard, some studies indicated that these fatty acids are related to the activity of the serotoninergic system. There is a relationship between low DHA levels and low concentrations of 5-hydroxyindolacetic acid (5-HIAA), the main metabolite of serotonin, in the cerebrospinal fluid, observed in people suffering from depression and schizophrenia. This can imply that low levels of omega-3 fatty acids are associated with impaired serotonergic neurotransmission (130, 131). DHA induces BDNF synthesis, thus sustaining the life of neurons. In addition, PUFAs deficiency may impair the release and uptake of neurotransmitters, enzymatic processes, and function of ion and receptor channels such as dopaminergic, GABAergic, and cholinergic in nervous system cells, contributing to the development of psychiatric disorders including depression, anxiety, and aggression (126, 132). Some studies suggest that low consumption of fish is associated with increased prevalence of depression (129).

It is also known that the consumption of omega-3 PUFAs is recommended for the prevention of AD. Consuming fish once a week decreases the risk of AD by 60%. EPA and DHA can reduce amyloid-β production and its accumulation in plaques, and improve its clearance (127). In the Cardiovascular Health and Cognition study, consumption of fatty fish (≥ 2 servings per week) reduced the incidence of dementia by 28% and reduced the risk of AD by 41% (133).

5.5. Rapeseed oil

Rapeseed oil is regarded to be a key oilseed product in Nordic countries. It is characterized by a low level of saturated fatty acids (7%), and substantial amounts of mono- and polyunsaturated fatty acids such as alpha-linolenic acid, linoleic acid, and oleic acid (134). These fatty acids are known as neuroactive molecules (135). Oleic acid (18:1ω9 monounsaturated fatty acid) is critical for the survival of neural stem cells, which are the source of newborn neurons in the brain and are involved in mood, memory, learning, and stress response. In a rodent model study, oleic acid bound to the orphan nuclear receptor TLX/NR2E1 (nuclear receptor subfamily 2, group E, member 1), converted it from a transcriptional repressor to a transcriptional activator of cell-cycle and neurogenesis genes and induced neurogenesis and brain development (136). Similar beneficial effects were also shown in another animal study, in which oleic acid administration demonstrated its neuroprotective effects in transient and permanent focal cerebral ischemia (137). It is believed that oleic acid is associated with the onset of neurodegeneration disease through anti-inflammatory and vascular activities (138).

Moreover, multiple regression analysis of cohort study data revealed that daily consumption of oleic acid has a significantly positive effect on cognitive decline in community-dwelling Japanese elderly subjects (139). Certain dietary patterns, such as MD which contains high amounts of oleic acid, have been strongly associated with protection against age-related cognitive decline (140–142). Therefore, it is highly likely that rapeseed oil, as a source of oleic acid and PUFAs, may be a beneficial food that is closely related to neurological disorders.

7.1. Future directions

Future directions should focus on precise dietary patterns and their applications in brain health. The neurological benefits of ND are not very well investigated. On the other hand, considering the different designs of studies and limitations in the number of studies, we chose the narrative approach for the present review. There is a need to investigate the randomized trial in placebo versus Nordic diet group in different populations. Overall, more and long-term human studies are needed to confirm the neuroprotective effects of the ND.

1. Godos J, Currenti W, Angelino D, Mena P, Castellano S, Caraci F, et al.. Diet and mental health: review of the recent updates on molecular mechanisms. Antioxidants. (2020) 9:346. doi: 10.3390/antiox9040346, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

2. Friedrich MJ. Depression is the leading cause of disability around the world. JAMA. (2017) 317:1517. doi: 10.1001/jama.2017.3828, PMID: [PubMed] [CrossRef] [Google Scholar]

3. James SL, Abate D, Abate KH, Abay SM, Abbafati C, Abbasi N, et al.. Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. The Lancet. (2018) 392:1789–858. [PMC free article] [PubMed] [Google Scholar]

4. Riccò M, Vezzosi L, Balzarini F, Gualerzi G, Ranzieri S, Signorelli C, et al.. Prevalence of Parkinson disease in Italy: a systematic review and meta-analysis. Acta Bio Medica. (2020) 91:e2020088. doi: 10.23750/abm.v91i3.9443, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

5. Jack CR, Therneau TM, Weigand SD, Wiste HJ, Knopman DS, Vemuri P, et al.. Prevalence of biologically vs clinically defined Alzheimer spectrum entities using the National Institute on Aging–Alzheimer’s association research framework. JAMA Neurol. (2019) 76:1174–83. doi: 10.1001/jamaneurol.2019.1971, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

6. Austen W. An approach on the biological disease of psychiatric and neurological disorders in young patients. J Mult Scler. (2021) 8:1–2. [Google Scholar]

7. Pavón S, Lázaro E, Martínez O, Amayra I, López-Paz J, Caballero P, et al.. Ketogenic diet and cognition in neurological diseases: a systematic review. Nutr Rev. (2021) 79:802–13. doi: 10.1093/nutrit/nuaa113, PMID: [PubMed] [CrossRef] [Google Scholar]

8. Mayeux R, Stern Y. Epidemiology of Alzheimer disease. Cold Spring Harb Perspect Med. (2012) 2:a006239. doi: 10.1101/cshperspect.a006239, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

9. Francis HM, Mirzaei M, Pardey MC, Haynes PA, Cornish JL. Proteomic analysis of the dorsal and ventral hippocampus of rats maintained on a high fat and refined sugar diet. Proteomics. (2013) 13:3076–91. doi: 10.1002/pmic.201300124, PMID: [PubMed] [CrossRef] [Google Scholar]

10. Pistell PJ, Morrison CD, Gupta S, Knight AG, Keller JN, Ingram DK, et al.. Cognitive impairment following high fat diet consumption is associated with brain inflammation. J Neuroimmunol. (2010) 219:25–32. doi: 10.1016/j.jneuroim.2009.11.010, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

11. Yoon J-H, Baek SJ. Molecular targets of dietary polyphenols with anti-inflammatory properties. Yonsei Med J. (2005) 46:585–96. doi: 10.3349/ymj.2005.46.5.585, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

12. Estruch R. Anti-inflammatory effects of the Mediterranean diet: the experience of the PREDIMED study. Proc Nutr Soc. (2010) 69:333–40. doi: 10.1017/S0029665110001539, PMID: [PubMed] [CrossRef] [Google Scholar]

13. Dominguez LJ, Veronese N, Vernuccio L, Catanese G, Inzerillo F, Salemi G, et al.. Nutrition, physical activity, and other lifestyle factors in the prevention of cognitive decline and dementia. Nutrients. (2021) 13:4080. doi: 10.3390/nu13114080, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

14. Pagliai G, Sofi F, Vannetti F, Caiani S, Pasquini G, Molino Lova R, et al.. Mediterranean diet, food consumption and risk of late-life depression: the Mugello study. J Nutr Health Aging. (2018) 22:569–74. doi: 10.1007/s12603-018-1019-3, PMID: [PubMed] [CrossRef] [Google Scholar]

15. Nouripour F, Hejazi N. Nordic diet and cardio-metabolic diseases: a review. Int J Nutr Sci. (2019) 4:105–8. doi: 10.30476/IJNS.2019.82686.1025 [CrossRef] [Google Scholar]

16. Ramezani-Jolfaie N, Mohammadi M, Salehi-Abargouei A. The effect of healthy Nordic diet on cardio-metabolic markers: a systematic review and meta-analysis of randomized controlled clinical trials. Eur J Nutr. (2019) 58:2159–74. doi: 10.1007/s00394-018-1804-0, PMID: [PubMed] [CrossRef] [Google Scholar]

17. Adamsson V, Reumark A, Fredriksson IB, Hammarström E, Vessby B, Johansson G, et al.. Effects of a healthy Nordic diet on cardiovascular risk factors in hypercholesterolaemic subjects: a randomized controlled trial (NORDIET). J Intern Med. (2011) 269:150–9. doi: 10.1111/j.1365-2796.2010.02290.x, PMID: [PubMed] [CrossRef] [Google Scholar]

18. Olsen A, Egeberg R, Halkjær J, Christensen J, Overvad K, Tjønneland A. Healthy aspects of the Nordic diet are related to lower total mortality. J Nutr. (2011) 141:639–44. doi: 10.3945/jn.110.131375, PMID: [PubMed] [CrossRef] [Google Scholar]

19. Kanerva N, Kaartinen NE, Schwab U, Lahti-Koski M, Männistö S. Adherence to the Baltic Sea diet consumed in the Nordic countries is associated with lower abdominal obesity. Br J Nutr. (2013) 109:520–8. doi: 10.1017/S0007114512001262, PMID: [PubMed] [CrossRef] [Google Scholar]

20. Kanerva N, Loo B-M, Eriksson JG, Leiviskä J, Kaartinen NE, Jula A, et al.. Associations of the Baltic Sea diet with obesity-related markers of inflammation. Ann Med. (2014) 46:90–6. doi: 10.3109/07853890.2013.870020, PMID: [PubMed] [CrossRef] [Google Scholar]

21. Gunge V, Andersen I, Kyrø C, Hansen C, Dahm C, Christensen J, et al.. Adherence to a healthy Nordic food index and risk of myocardial infarction in middle-aged Danes: the diet, cancer and health cohort study. Eur J Clin Nutr. (2017) 71:652–8. doi: 10.1038/ejcn.2017.1, PMID: [PubMed] [CrossRef] [Google Scholar]

22. Hansen CP, Overvad K, Kyrø C, Olsen A, Tjønneland A, Johnsen SP, et al.. Adherence to a healthy Nordic diet and risk of stroke: a Danish cohort study. Stroke. (2017) 48:259–64. doi: 10.1161/STROKEAHA.116.015019, PMID: [PubMed] [CrossRef] [Google Scholar]

23. Gorelick PB, Scuteri A, Black SE, DeCarli C, Greenberg SM, Iadecola C, et al.. Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. (2011) 42:2672–713. doi: 10.1161/STR.0b013e3182299496, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

24. Männikkö R, Komulainen P, Schwab U, Heikkilä HM, Savonen K, Hassinen M, et al.. The Nordic diet and cognition–the DR's EXTRA study. Br J Nutr. (2015) 114:231–9. doi: 10.1017/S0007114515001890, PMID: [PubMed] [CrossRef] [Google Scholar]

25. Eskelinen MH, Solomon A, Ngandu T, Antikainen R, Hänninen T, Laatikainen T, et al.. Effect of berries and fruits on cognitive change during a 2-year multi-domain lifestyle intervention: the Finnish geriatric intervention study to prevent cognitive impairment and disability (FINGER) prevention (nonpharmacological)/nutrition. Alzheimers Dement. (2020) 16:e042431. doi: 10.1002/alz.042431 [CrossRef] [Google Scholar]

26. Mithril C, Dragsted LO, Meyer C, Blauert E, Holt MK, Astrup A. Guidelines for the new Nordic diet. Public Health Nutr. (2012) 15:1941–7. doi: 10.1017/S136898001100351X, PMID: [PubMed] [CrossRef] [Google Scholar]

27. Flight I, Clifton P. Cereal grains and legumes in the prevention of coronary heart disease and stroke: a review of the literature. Eur J Clin Nutr. (2006) 60:1145–59. doi: 10.1038/sj.ejcn.1602435, PMID: [PubMed] [CrossRef] [Google Scholar]

28. Kanerva N, Kaartinen NE, Schwab U, Lahti-Koski M, Männistö S. The Baltic Sea diet score: a tool for assessing healthy eating in Nordic countries. Public Health Nutr. (2014) 17:1697–705. doi: 10.1017/S1368980013002395, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

29. Neuman N, Leer J. Nordic Cuisine but National Identities. “New Nordic Cuisine” and the gastronationalist projects of Denmark and Sweden. Anthropol Food. (2018) 13 doi: 10.4000/aof.8723 [CrossRef] [Google Scholar]

30. Mithril C, Dragsted LO, Meyer C, Tetens I, Biltoft-Jensen A, Astrup A. Dietary composition and nutrient content of the new Nordic diet. Public Health Nutr. (2013) 16:777–85. doi: 10.1017/S1368980012004521, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

31. Perälä M-M, von Bonsdorff M, Männistö S, Salonen MK, Simonen M, Kanerva N, et al.. A healthy Nordic diet and physical performance in old age: findings from the longitudinal Helsinki birth cohort study. Br J Nutr. (2016) 115:878–86. doi: 10.1017/S0007114515005309, PMID: [PubMed] [CrossRef] [Google Scholar]

32. Åkesson A, Andersen LF, Kristjánsdottir AG, Roos E, Trolle E, Voutilainen E, et al.. Health effects associated with foods characteristic of the Nordic diet: a systematic literature review. Food Nutr Res. (2013) 57:22790. doi: 10.3402/fnr.v57i0.22790 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

33. Bere E, Brug J. Towards health-promoting and environmentally friendly regional diets–a Nordic example. Public Health Nutr. (2009) 12:91–6. doi: 10.1017/S1368980008001985, PMID: [PubMed] [CrossRef] [Google Scholar]

34. Krznarić Ž, Karas I, Ljubas Kelečić D, Vranešić BD. The Mediterranean and Nordic diet: a review of differences and similarities of two sustainable, health-promoting dietary patterns. Front Nutr. (2021):339. doi: 10.3389/fnut.2021.683678 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

35. Bechthold A, Boeing H, Tetens I, Schwingshackl L, Nöthlings U. Perspective: food-based dietary guidelines in Europe—scientific concepts, current status, and perspectives. Advances in nutrition. (2018) 9:544–60. [PMC free article] [PubMed] [Google Scholar]

36. Magnusdottir OK, Gunnarsdottir I, Birgisdóttir BE. Dietary guidelines in type 2 diabetes: the Nordic diet or the ketogenic diet?Curr Opin Endocrinol Diabetes Obes. (2017) 24:315–9. doi: 10.1097/MED.0000000000000361, PMID: [PubMed] [CrossRef] [Google Scholar]

37. Recommendations NN . Nordic Nutrition Recommendations 2012: Integrating nutrition and physical activity. Copenhagen, Denmark: Nordic Council of Ministers; (2014). 627 p. [Google Scholar]

38. Fogelholm M. New Nordic nutrition recommendations are here. New York: Taylor & Francis; (2013). 22903 p. [PMC free article] [PubMed] [Google Scholar]

39. Hemler EC, Hu FB. Plant-based diets for personal, population, and planetary health. Adv Nutr. (2019) 10:S275–83. doi: 10.1093/advances/nmy117 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

40. Ngandu T, Lehtisalo J, Solomon A, Levälahti E, Ahtiluoto S, Antikainen R, et al.. A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial. Lancet. (2015) 385:2255–63. doi: 10.1016/S0140-6736(15)60461-5, PMID: [PubMed] [CrossRef] [Google Scholar]

41. Lehtisalo J, Levälahti E, Lindström J, Hänninen T, Paajanen T, Peltonen M, et al.. Dietary changes and cognition over 2 years within a multidomain intervention trial—the Finnish geriatric intervention study to prevent cognitive impairment and disability (FINGER). Alzheimers Dement. (2019) 15:410–7. doi: 10.1016/j.jalz.2018.10.001, PMID: [PubMed] [CrossRef] [Google Scholar]

42. Stephen R, Solomon A, Ngandu T, Levälahti E, Rinne JO, Kemppainen N, et al.. White matter changes on diffusion tensor imaging in the FINGER randomized controlled trial. J Alzheimers Dis. (2020) 78:75–86. doi: 10.3233/JAD-200423, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

43. Lankinen M, Schwab U, Kolehmainen M, Paananen J, Poutanen K, Mykkänen H, et al.. Whole grain products, fish and bilberries alter glucose and lipid metabolism in a randomized, controlled trial: the Sysdimet study. PLoS One. (2011) 6:e22646. doi: 10.1371/journal.pone.0022646, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

44. Brader L, Uusitupa M, Dragsted LO, Hermansen K. Effects of an isocaloric healthy Nordic diet on ambulatory blood pressure in metabolic syndrome: a randomized SYSDIET sub-study. Eur J Clin Nutr. (2014) 68:57–63. doi: 10.1038/ejcn.2013.192, PMID: [PubMed] [CrossRef] [Google Scholar]

45. Adamsson V, Reumark A, Cederholm T, Vessby B, Risérus U, Johansson G. What is a healthy Nordic diet? Foods and nutrients in the NORDIET study. Food Nutr Res. (2012) 56:18189. doi: 10.3402/fnr.v56i0.18189 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

46. Uusitupa M, Hermansen K, Savolainen MJ, Schwab U, Kolehmainen M, Brader L, et al.. Effects of an isocaloric healthy N ordic diet on insulin sensitivity, lipid profile and inflammation markers in metabolic syndrome–a randomized study (SYSDIET). J Intern Med. (2013) 274:52–66. doi: 10.1111/joim.12044, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

47. Lacoppidan SA, Kyrø C, Loft S, Helnæs A, Christensen J, Hansen CP, et al.. Adherence to a healthy Nordic food index is associated with a lower risk of type-2 diabetes—the Danish diet, cancer and health cohort study. Nutrients. (2015) 7:8633–44. doi: 10.3390/nu7105418, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

48. Roswall N, Sandin S, Löf M, Skeie G, Olsen A, Adami H-O, et al.. Adherence to the healthy Nordic food index and total and cause-specific mortality among Swedish women. Eur J Epidemiol. (2015) 30:509–17. doi: 10.1007/s10654-015-0021-x, PMID: [PubMed] [CrossRef] [Google Scholar]

49. Kyrø C, Skeie G, Loft S, Overvad K, Christensen J, Tjønneland A, et al.. Adherence to a healthy Nordic food index is associated with a lower incidence of colorectal cancer in women: the diet, Cancer and health cohort study. Br J Nutr. (2013) 109:920–7. doi: 10.1017/S0007114512002085, PMID: [PubMed] [CrossRef] [Google Scholar]

50. Kanerva N, Rissanen H, Knekt P, Havulinna A, Eriksson J, Männistö S. The healthy Nordic diet and incidence of type 2 diabetes—10-year follow-up. Diabetes Res Clin Pract. (2014) 106:e34–7. doi: 10.1016/j.diabres.2014.08.016, PMID: [PubMed] [CrossRef] [Google Scholar]

51. Kolehmainen M, Ulven SM, Paananen J, de Mello V, Schwab U, Carlberg C, et al.. Healthy Nordic diet downregulates the expression of genes involved in inflammation in subcutaneous adipose tissue in individuals with features of the metabolic syndrome. Am J Clin Nutr. (2015) 101:228–39. doi: 10.3945/ajcn.114.092783, PMID: [PubMed] [CrossRef] [Google Scholar]

52. Haapala EA, Eloranta A-M, Venäläinen T, Schwab U, Lindi V, Lakka TA. Associations of diet quality with cognition in children–the physical activity and nutrition in children study. Br J Nutr. (2015) 114:1080–7. doi: 10.1017/S0007114515001634, PMID: [PubMed] [CrossRef] [Google Scholar]

53. Sørensen LB, Damsgaard CT, Dalskov S-M, Petersen RA, Egelund N, Dyssegaard CB, et al.. Diet-induced changes in iron and n-3 fatty acid status and associations with cognitive performance in 8–11-year-old Danish children: secondary analyses of the optimal well-being, development and health for Danish children through a healthy new Nordic diet school meal study. Br J Nutr. (2015) 114:1623–37. doi: 10.1017/S0007114515003323 [PubMed] [CrossRef] [Google Scholar]

54. Sørensen LB, Dyssegaard CB, Damsgaard CT, Petersen RA, Dalskov S-M, Hjorth MF, et al.. The effects of Nordic school meals on concentration and school performance in 8-to 11-year-old children in the OPUS school meal study: a cluster-randomised, controlled, cross-over trial. Br J Nutr. (2015) 113:1280–91. doi: 10.1017/S0007114515000033, PMID: [PubMed] [CrossRef] [Google Scholar]

55. Sabet JA, Ekman MS, Lundvall AS, Risérus U, Johansson U, Öström Å, et al.. Feasibility and acceptability of a healthy Nordic diet intervention for the treatment of depression: a randomized controlled pilot trial. Nutrients. (2021) 13:902. doi: 10.3390/nu13030902, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

56. Abbaszadeh A, Saharkhiz M, Khorasanchi Z, Karbasi S, Askari M, Hoseini ZS, et al.. Impact of a Nordic diet on psychological function in young students. Nutr Health. (2021) 27:97–104. doi: 10.1177/0260106020964981, PMID: [PubMed] [CrossRef] [Google Scholar]

57. Shakersain B, Rizzuto D, Larsson SC, Faxén-Irving G, Fratiglioni L, Xu W-L. The Nordic prudent diet reduces risk of cognitive decline in the Swedish older adults: a population-based cohort study. Nutrients. (2018) 10:229. doi: 10.3390/nu10020229, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

58. Serafini M, Peluso I. Functional foods for health: the interrelated antioxidant and anti-inflammatory role of fruits, vegetables, herbs, spices and cocoa in humans. Curr Pharm Des. (2016) 22:6701–15. doi: 10.2174/1381612823666161123094235, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

59. Bourre J-M. Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. J Nutr Health Aging. (2006) 10:377. PMID: [PubMed] [Google Scholar]

60. Tardy A-L, Pouteau E, Marquez D, Yilmaz C, Scholey A. Vitamins and minerals for energy, fatigue and cognition: a narrative review of the biochemical and clinical evidence. Nutrients. (2020) 12:228. doi: 10.3390/nu12010228, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

61. Heber D. Vegetables, fruits and phytoestrogens in the prevention of diseases. J Postgrad Med. (2004) 50:145. PMID: [PubMed] [Google Scholar]

62. Liu RH. Health-promoting components of fruits and vegetables in the diet. Adv Nutr. (2013) 4:384S–92S. doi: 10.3945/an.112.003517, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

63. Rodriguez-Casado A. The health potential of fruits and vegetables phytochemicals: notable examples. Crit Rev Food Sci Nutr. (2016) 56:1097–107. doi: 10.1080/10408398.2012.755149 [PubMed] [CrossRef] [Google Scholar]

65. Li D, Wang P, Luo Y, Zhao M, Chen F. Health benefits of anthocyanins and molecular mechanisms: update from recent decade. Crit Rev Food Sci Nutr. (2017) 57:1729–41. doi: 10.1080/10408398.2015.1030064 [PubMed] [CrossRef] [Google Scholar]

66. Wang Y, Zhao L, Lu F, Yang X, Deng Q, Ji B, et al.. Retinoprotective effects of bilberry anthocyanins via antioxidant, anti-inflammatory, and anti-apoptotic mechanisms in a visible light-induced retinal degeneration model in pigmented rabbits. Molecules. (2015) 20:22395–410. doi: 10.3390/molecules201219785, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

67. Tsakiroglou P, VandenAkker NE, Del Bo’ C, Riso P, Klimis-Zacas D. Role of berry anthocyanins and phenolic acids on cell migration and angiogenesis: an updated overview. Nutrients. (2019) 11:1075. doi: 10.3390/nu11051075, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

68. Henriques JF, Serra D, Dinis TC, Almeida LM. The anti-neuroinflammatory role of anthocyanins and their metabolites for the prevention and treatment of brain disorders. Int J Mol Sci. (2020) 21:8653. doi: 10.3390/ijms21228653, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

69. Kim WI, Ryu HJ, Kim J-E, Seo CH, Lee BC, Choi I-G, et al.. Differential nuclear factor-kappa B phosphorylation induced by lipopolysaccharide in the hippocampus of P2X7 receptor knockout mouse. Neurol Res. (2013) 35:369–81. doi: 10.1179/1743132812Y.0000000137, PMID: [PubMed] [CrossRef] [Google Scholar]

70. Sahin C, Dursun S, Cetin M, Aricioglu F. The neuroinflammation perspective of depression: reuniting the outstanding mechanisms of the pathophysiology. Klinik Psikofarmakoloji Bülteni. (2016) 26:196–206. doi: 10.5455/bcp.20160520092044 [CrossRef] [Google Scholar]

71. Uddin M, Kabir M, Jakaria M, Mamun AA, Niaz K, Amran M, et al.. Endothelial PPARγ is crucial for averting age-related vascular dysfunction by stalling oxidative stress and ROCK. Neurotox Res. (2019) 36:583–601. doi: 10.1007/s12640-019-00047-5, PMID: [PubMed] [CrossRef] [Google Scholar]

72. Van Houten B, Santa-Gonzalez GA, Camargo M. DNA repair after oxidative stress: current challenges. Curr Opin Toxicol. (2018) 7:9–16. doi: 10.1016/j.cotox.2017.10.009, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

73. Liguori I, Russo G, Curcio F, Bulli G, Aran L, Della-Morte D, et al.. Oxidative stress, aging, and diseases. Clin Interv Aging. (2018) 13:757. doi: 10.2147/CIA.S158513 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

74. Vauzour D. Dietary polyphenols as modulators of brain functions: biological actions and molecular mechanisms underpinning their beneficial effects. Oxidative Med Cell Longev. (2012) 2012:914273. doi: 10.1155/2012/914273, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

75. Choi D-Y, Lee Y-J, Hong JT, Lee H-J. Antioxidant properties of natural polyphenols and their therapeutic potentials for Alzheimer's disease. Brain Res Bull. (2012) 87:144–53. doi: 10.1016/j.brainresbull.2011.11.014, PMID: [PubMed] [CrossRef] [Google Scholar]

76. Uttara B, Singh AV, Zamboni P, Mahajan R. Oxidative stress and neurodegenerative diseases: a review of upstream and downstream antioxidant therapeutic options. Curr Neuropharmacol. (2009) 7:65–74. doi: 10.2174/157015909787602823, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

77. Poulose SM, Fisher DR, Larson J, Bielinski DF, Rimando AM, Carey AN, et al.. Anthocyanin-rich açai (Euterpe oleracea Mart.) fruit pulp fractions attenuate inflammatory stress signaling in mouse brain BV-2 microglial cells. J Agric Food Chem. (2012) 60:1084–93. doi: 10.1021/jf203989k, PMID: [PubMed] [CrossRef] [Google Scholar]

78. Jeong J-W, Lee WS, Shin SC, Kim G-Y, Choi BT, Choi YH. Anthocyanins downregulate lipopolysaccharide-induced inflammatory responses in BV2 microglial cells by suppressing the NF-κB and Akt/MAPKs signaling pathways. Int J Mol Sci. (2013) 14:1502–15. doi: 10.3390/ijms14011502, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

79. Winter AN, Brenner MC, Punessen N, Snodgrass M, Byars C, Arora Y, et al.. Comparison of the neuroprotective and anti-inflammatory effects of the anthocyanin metabolites, protocatechuic acid and 4-hydroxybenzoic acid. Oxidative Med Cell Longev. (2017) 2017:6297080. doi: 10.1155/2017/6297080, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

80. Wang H-y, Wang H, Wang J-h, Wang Q, Ma Q-f, Chen Y-y. Protocatechuic acid inhibits inflammatory responses in LPS-stimulated BV2 microglia via NF-κB and MAPKs signaling pathways. Neurochem Res. (2015) 40:1655–60. doi: 10.1007/s11064-015-1646-6, PMID: [PubMed] [CrossRef] [Google Scholar]

81. Galbete C, Kröger J, Jannasch F, Iqbal K, Schwingshackl L, Schwedhelm C, et al.. Nordic diet, Mediterranean diet, and the risk of chronic diseases: the EPIC-Potsdam study. BMC Med. (2018) 16:1–13. doi: 10.1186/s12916-018-1082-y [PMC free article] [PubMed] [CrossRef] [Google Scholar]

82. Manchali S, Murthy KNC, Patil BS. Crucial facts about health benefits of popular cruciferous vegetables. J Funct Foods. (2012) 4:94–106. doi: 10.1016/j.jff.2011.08.004 [CrossRef] [Google Scholar]

83. Connolly EL, Sim M, Travica N, Marx W, Beasy G, Lynch GS, et al.. Glucosinolates from cruciferous vegetables and their potential role in chronic disease: investigating the preclinical and clinical evidence. Front Pharmacol. (2021) 12:2964. doi: 10.3389/fphar.2021.767975 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

84. Kissen R, Rossiter JT, Bones AM. The ‘mustard oil bomb’: not so easy to assemble?! Localization, expression and distribution of the components of the myrosinase enzyme system. Phytochem Rev. (2009) 8:69–86. doi: 10.1007/s11101-008-9109-1, PMID: [CrossRef] [Google Scholar]

85. Luang-In V, Narbad A, Nueno-Palop C, Mithen R, Bennett M, Rossiter JT. The metabolism of methylsulfinylalkyl-and methylthioalkyl-glucosinolates by a selection of human gut bacteria. Mol Nutr Food Res. (2014) 58:875–83. doi: 10.1002/mnfr.201300377, PMID: [PubMed] [CrossRef] [Google Scholar]

86. Wu S, Gao Q, Zhao P, Gao Y, Xi Y, Wang X, et al.. Sulforaphane produces antidepressant-and anxiolytic-like effects in adult mice. Behav Brain Res. (2016) 301:55–62. doi: 10.1016/j.bbr.2015.12.030, PMID: [PubMed] [CrossRef] [Google Scholar]

87. Panjwani AA, Liu H, Fahey JW. Crucifers and related vegetables and supplements for neurologic disorders: what is the evidence?Curr Opin Clin Nutr Metabolic Care. (2018) 21:451–7. doi: 10.1097/MCO.0000000000000511, PMID: [PubMed] [CrossRef] [Google Scholar]

88. Folkard DL, Melchini A, Traka MH, Aa A-B, Saha S, Mulholland F, et al.. Suppression of LPS-induced transcription and cytokine secretion by the dietary isothiocyanate sulforaphane. Mol Nutr Food Res. (2014) 58:2286–96. doi: 10.1002/mnfr.201400550, PMID: [PubMed] [CrossRef] [Google Scholar]

89. Kim J, Lee S, Choi BR, Yang H, Hwang Y, Park JHY, et al.. Sulforaphane epigenetically enhances neuronal BDNF expression and TrkB signaling pathways. Mol Nutr Food Res. (2017) 61:1600194. doi: 10.1002/mnfr.201600194, PMID: [PubMed] [CrossRef] [Google Scholar]

90. Kim J. Pre-clinical neuroprotective evidences and plausible mechanisms of sulforaphane in Alzheimer’s disease. Int J Mol Sci. (2021) 22:2929. doi: 10.3390/ijms22062929, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

91. Sedlak TW, Nucifora LG, Koga M, Shaffer LS, Higgs C, Tanaka T, et al.. Sulforaphane augments glutathione and influences brain metabolites in human subjects: a clinical pilot study. Complex Psychiatry. (2017) 3:214–22. doi: 10.1159/000487639 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

92. Ghazizadeh-Hashemi F, Bagheri S, Ashraf-Ganjouei A, Moradi K, Shahmansouri N, Mehrpooya M, et al.. Efficacy and safety of sulforaphane for treatment of mild to moderate depression in patients with history of cardiac interventions: a randomized, double-blind, placebo-controlled clinical trial. Psychiatry Clin Neurosci. (2021) 75:250–5. doi: 10.1111/pcn.13276, PMID: [PubMed] [CrossRef] [Google Scholar]

93. Zhang J-c, Yao W, Dong C, Yang C, Ren Q, Ma M, et al.. Prophylactic effects of sulforaphane on depression-like behavior and dendritic changes in mice after inflammation. J Nutr Biochem. (2017) 39:134–44. doi: 10.1016/j.jnutbio.2016.10.004, PMID: [PubMed] [CrossRef] [Google Scholar]

94. Kim HV, Kim HY, Ehrlich HY, Choi SY, Kim DJ, Kim Y. Amelioration of Alzheimer’s disease by neuroprotective effect of sulforaphane in animal model. Amyloid. (2013) 20:7–12. doi: 10.3109/13506129.2012.751367 [PubMed] [CrossRef] [Google Scholar]

95. Sunkaria A, Bhardwaj S, Yadav A, Halder A, Sandhir R. Sulforaphane attenuates postnatal proteasome inhibition and improves spatial learning in adult mice. J Nutr Biochem. (2018) 51:69–79. doi: 10.1016/j.jnutbio.2017.09.016, PMID: [PubMed] [CrossRef] [Google Scholar]

96. Lim JL, van der Pol SM, Baron W, McCord JM, de Vries HE, van Horssen J. Protandim protects oligodendrocytes against an oxidative insult. Antioxidants. (2016) 5:30. doi: 10.3390/antiox5030030, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

97. Soler C, Soriano JM, Mañes J. Apple-products phytochemicals and processing: a review. Nat Prod Commun. (2009) 4:1934578X0900400504. [PubMed] [Google Scholar]

98. Boots AW, Haenen GR, Bast A. Health effects of quercetin: from antioxidant to nutraceutical. Eur J Pharmacol. (2008) 585:325–37. doi: 10.1016/j.ejphar.2008.03.008, PMID: [PubMed] [CrossRef] [Google Scholar]

99. Khan A, Ali T, Rehman SU, Khan MS, Alam SI, Ikram M, et al.. Neuroprotective effect of quercetin against the detrimental effects of LPS in the adult mouse brain. Front Pharmacol. (2018) 9:1383. doi: 10.3389/fphar.2018.01383, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

100. Yang Y, Liu X, Wu T, Zhang W, Shu J, He Y, et al.. Quercetin attenuates AZT-induced neuroinflammation in the CNS. Sci Rep. (2018) 8:1–8. doi: 10.1038/s41598-018-24618-2 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

101. Costa LG, Garrick JM, Roquè PJ, Pellacani C. Mechanisms of neuroprotection by quercetin: counteracting oxidative stress and more. Oxidative Med Cell Longev. (2016) 2016:2986796. doi: 10.1155/2016/2986796, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

102. Gan L, Johnson JA. Oxidative damage and the Nrf2-ARE pathway in neurodegenerative diseases. Biochimica et Biophysica Acta. (2014) 1842:1208–18. doi: 10.1016/j.bbadis.2013.12.011, PMID: [PubMed] [CrossRef] [Google Scholar]

103. Guo H, Wu H, Sajid A, Li Z. Whole grain cereals: the potential roles of functional components in human health. Crit Rev Food Sci Nutr. (2022) 62:8388–402. doi: 10.1080/10408398.2021.1928596, PMID: [PubMed] [CrossRef] [Google Scholar]

104. Slavin J. Whole grains and human health. Nutr Res Rev. (2004) 17:99–110. doi: 10.1079/NRR200374, PMID: [PubMed] [CrossRef] [Google Scholar]

105. Gill SK, Rossi M, Bajka B, Whelan K. Dietary fibre in gastrointestinal health and disease. Nat Rev Gastroenterol Hepatol. (2021) 18:101–16. doi: 10.1038/s41575-020-00375-4, PMID: [PubMed] [CrossRef] [Google Scholar]

106. Dvoncova D, Havrlentova M, Hlinkova A, Hozlar P. Effect of fertilization and variety on the beta-glucan content in the grain of oats. Żywność Nauka Technologia Jakość. (2010) 17:108–16. [Google Scholar]

107. Peterson DM, Wesenberg DM, Burrup DE. β-Glucan content and its relationship to agronomic characteristics in elite oat germplasm. Crop Sci. (1995) 35:965–70. doi: 10.2135/cropsci1995.0011183X003500040005x [CrossRef] [Google Scholar]

108. Mayer EA. Gut feelings: the emerging biology of gut–brain communication. Nat Rev Neurosci. (2011) 12:453–66. doi: 10.1038/nrn3071, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

109. Kim C-S, Cha L, Sim M, Jung S, Chun WY, Baik HW, et al.. Probiotic supplementation improves cognitive function and mood with changes in gut microbiota in community-dwelling older adults: a randomized, double-blind, placebo-controlled, multicenter trial. J Gerontol. (2021) 76:32–40. doi: 10.1093/gerona/glaa090, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

110. Xu H, Li S, Song X, Li Z, Zhang D. Exploration of the association between dietary fiber intake and depressive symptoms in adults. Nutrition. (2018) 54:48–53. doi: 10.1016/j.nut.2018.03.009, PMID: [PubMed] [CrossRef] [Google Scholar]

111. Gopinath B, Flood VM, Burlutksy G, Louie JC, Mitchell P. Association between carbohydrate nutrition and prevalence of depressive symptoms in older adults. Br J Nutr. (2016) 116:2109–14. doi: 10.1017/S0007114516004311, PMID: [PubMed] [CrossRef] [Google Scholar]

112. Kim C-S, Byeon S, Shin D-M. Sources of dietary fiber are differently associated with prevalence of depression. Nutrients. (2020) 12:2813. doi: 10.3390/nu12092813, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

113. Sherry CL, Kim SS, Dilger RN, Bauer LL, Moon ML, Tapping RI, et al.. Sickness behavior induced by endotoxin can be mitigated by the dietary soluble fiber, pectin, through up-regulation of IL-4 and Th2 polarization. Brain Behav Immun. (2010) 24:631–40. doi: 10.1016/j.bbi.2010.01.015, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

114. O’Mahony SM, Clarke G, Borre Y, Dinan TG, Cryan J. Serotonin, tryptophan metabolism and the brain-gut-microbiome axis. Behav Brain Res. (2015) 277:32–48. doi: 10.1016/j.bbr.2014.07.027, PMID: [PubMed] [CrossRef] [Google Scholar]

115. Schroeder FA, Lin CL, Crusio WE, Akbarian S. Antidepressant-like effects of the histone deacetylase inhibitor, sodium butyrate, in the mouse. Biol Psychiatry. (2007) 62:55–64. doi: 10.1016/j.biopsych.2006.06.036, PMID: [PubMed] [CrossRef] [Google Scholar]

116. Le Couteur DG, Solon-Biet S, Cogger VC, Mitchell SJ, Senior A, de Cabo R, et al.. The impact of low-protein high-carbohydrate diets on aging and lifespan. Cell Mol Life Sci. (2016) 73:1237–52. doi: 10.1007/s00018-015-2120-y, PMID: [PubMed] [CrossRef] [Google Scholar]

117. Wahl D, Solon-Biet SM, Wang Q-P, Wali JA, Pulpitel T, Clark X, et al.. Comparing the effects of low-protein and high-carbohydrate diets and caloric restriction on brain aging in mice. Cell Rep. (2018) 25:2234–43. e6. doi: 10.1016/j.celrep.2018.10.070, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

118. Gorzkiewicz J, Bartosz G, Sadowska-Bartosz I. The potential effects of phytoestrogens: the role in neuroprotection. Molecules. (2021) 26:2954. doi: 10.3390/molecules26102954, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

119. Schreihofer DA. Neuroprotection by dietary isoflavones and their role in cerebral ischemia In: Bioactive nutraceuticals and dietary supplements in neurological and brain disease. Amsterdam: Elsevier; (2015). 385–94. [Google Scholar]

120. Lee Y-B, Lee HJ, Sohn HS. Soy isoflavones and cognitive function. J Nutr Biochem. (2005) 16:641–9. doi: 10.1016/j.jnutbio.2005.06.010, PMID: [PubMed] [CrossRef] [Google Scholar]

121. Qian Y, Guan T, Huang M, Cao L, Li Y, Cheng H, et al.. Neuroprotection by the soy isoflavone, genistein, via inhibition of mitochondria-dependent apoptosis pathways and reactive oxygen induced-NF-κB activation in a cerebral ischemia mouse model. Neurochem Int. (2012) 60:759–67. doi: 10.1016/j.neuint.2012.03.011, PMID: [PubMed] [CrossRef] [Google Scholar]

122. Jantaratnotai N, Utaisincharoen P, Sanvarinda P, Thampithak A, Sanvarinda Y. Phytoestrogens mediated anti-inflammatory effect through suppression of IRF-1 and pSTAT1 expressions in lipopolysaccharide-activated microglia. Int Immunopharmacol. (2013) 17:483–8. doi: 10.1016/j.intimp.2013.07.013, PMID: [PubMed] [CrossRef] [Google Scholar]

123. Wang X, Chen S, Ma G, Ye M, Lu G. Genistein protects dopaminergic neurons by inhibiting microglial activation. Neuroreport. (2005) 16:267–70. doi: 10.1097/00001756-200502280-00013, PMID: [PubMed] [CrossRef] [Google Scholar]

124. Astorg P, Couthouis A, Bertrais S, Arnault N, Meneton P, Guesnet P, et al.. Association of fish and long-chain n-3 polyunsaturated fatty acid intakes with the occurrence of depressive episodes in middle-aged French men and women. Prostaglandins Leukot Essent Fat Acids. (2008) 78:171–82. doi: 10.1016/j.plefa.2008.01.003, PMID: [PubMed] [CrossRef] [Google Scholar]

125. Murakami K, Miyake Y, Sasaki S, Tanaka K, Arakawa M. Fish and n-3 polyunsaturated fatty acid intake and depressive symptoms: Ryukyus child health study. Pediatrics. (2010) 126:e623–30. doi: 10.1542/peds.2009-3277, PMID: [PubMed] [CrossRef] [Google Scholar]

126. Pawełczyk T. The role of omega-3 polyunsaturated fatty acids in the etiopathogenesis and treatment of psychiatric disorders. Farmakoterapia w Psychiatrii i Neurologii. (2010) 26:71–7. [Google Scholar]

127. Fotuhi M, Mohassel P, Yaffe K. Fish consumption, long-chain omega-3 fatty acids and risk of cognitive decline or Alzheimer disease: a complex association. Nat Rev Neurol. (2009) 5:140–52. doi: 10.1038/ncpneuro1044, PMID: [PubMed] [CrossRef] [Google Scholar]

128. Cardoso C, Afonso C, Bandarra NM. Dietary DHA and health: cognitive function ageing. Nutr Res Rev. (2016) 29:281–94. doi: 10.1017/S0954422416000184, PMID: [PubMed] [CrossRef] [Google Scholar]

129. Wendolowicz A, Stefanska E, Ostrowska L. Influence of selected dietary components on the functioning of the human nervous system. Rocz Panstw Zakl Hig. (2018) 69:15–21. [PubMed] [Google Scholar]

130. Morris G, Berk M, Carvalho A, Caso JR, Sanz Y, Walder K, et al.. The role of the microbial metabolites including tryptophan catabolites and short chain fatty acids in the pathophysiology of immune-inflammatory and neuroimmune disease. Mol Neurobiol. (2017) 54:4432–51. doi: 10.1007/s12035-016-0004-2, PMID: [PubMed] [CrossRef] [Google Scholar]

131. Kennedy DO. B vitamins and the brain: mechanisms, dose and efficacy—a review. Nutrients. (2016) 8:68. doi: 10.3390/nu8020068, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

132. Rao TS, Asha M, Ramesh B, Rao KJ. Understanding nutrition, depression and mental illnesses. Indian J Psychiatry. (2008) 50:77. doi: 10.4103/0019-5545.42391, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

133. Huang TL, Zandi P, Tucker K, Fitzpatrick A, Kuller L, Fried L, et al.. Benefits of fatty fish on dementia risk are stronger for those without APOE ε4. Neurology. (2005) 65:1409–14. doi: 10.1212/01.wnl.0000183148.34197.2e, PMID: [PubMed] [CrossRef] [Google Scholar]

134. Lin L, Allemekinders H, Dansby A, Campbell L, Durance-Tod S, Berger A, et al.. Evidence of health benefits of canola oil. Nutr Rev. (2013) 71:370–85. doi: 10.1111/nure.12033, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

135. Galán-Arriero I, Serrano-Muñoz D, Gómez-Soriano J, Goicoechea C, Taylor J, Velasco A, et al.. The role of Omega-3 and Omega-9 fatty acids for the treatment of neuropathic pain after neurotrauma. Biochimica et Biophysica Acta. (2017) 1859:1629–35. doi: 10.1016/j.bbamem.2017.05.003, PMID: [PubMed] [CrossRef] [Google Scholar]

136. Kandel P, Semerci F, Mishra R, Choi W, Bajic A, Baluya D, et al.. Oleic acid is an endogenous ligand of TLX/NR2E1 that triggers hippocampal neurogenesis. Proc Natl Acad Sci. (2022) 119:e2023784119. doi: 10.1073/pnas.2023784119, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

137. Song J, Kim Y-S, Lee DH, Lee SH, Park HJ, Lee D, et al.. Neuroprotective effects of oleic acid in rodent models of cerebral ischaemia. Sci Rep. (2019) 9:10732. doi: 10.1038/s41598-019-47057-z [PMC free article] [PubMed] [CrossRef] [Google Scholar]

138. López-Miranda J, Pérez-Jiménez F, Ros E, De Caterina R, Badimón L, Covas MI, et al.. Olive oil and health: summary of the II international conference on olive oil and health consensus report, Jaén and Córdoba (Spain) 2008. Nutr Metab Cardiovasc Dis. (2010) 20:284–94. doi: 10.1016/j.numecd.2009.12.007, PMID: [PubMed] [CrossRef] [Google Scholar]

139. Sakurai K, Shen C, Shiraishi I, Inamura N, Hisatsune T. Consumption of oleic acid on the preservation of cognitive functions in Japanese elderly individuals. Nutrients. (2021) 13:284. doi: 10.3390/nu13020284, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

140. Willcox DC, Scapagnini G, Willcox BJ. Healthy aging diets other than the Mediterranean: a focus on the Okinawan diet. Mech Ageing Dev. (2014) 136:148–62. doi: 10.1016/j.mad.2014.01.002 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

141. Omar SH. Mediterranean and MIND diets containing olive biophenols reduces the prevalence of Alzheimer’s disease. Int J Mol Sci. (2019) 20:2797. doi: 10.3390/ijms20112797, PMID: [PMC free article] [PubMed] [CrossRef] [Google Scholar]

142. Panza F, Solfrizzi V, Colacicco A, Dintrono A, Capurso C, Torres F, et al.. Mediterranean diet and cognitive decline. Public Health Nutr. (2004) 7:959–63. doi: 10.1079/PHN2004561, PMID: [PubMed] [CrossRef] [Google Scholar]