Depression is a mental disorder triggered by the interaction of social, psychological and biological factors that have an important impact on an individual’s life. Despite being a well-studied disease with several established forms of treatment, its prevalence is increasing, especially among older adults. New forms of treatment and prevention are encouraged, and some researchers have been discussing the effects of vitamin D (VitD) on depression; however, the exact mechanism by which VitD exerts its effects is not yet conclusive. In this study, we aimed to discuss the possible mechanisms underlying the association between VitD and depression in older adults. Therefore, we conducted a systematic search of databases for indexed articles published until 30 April 2021. The primary focus was on both observational studies documenting the association between VitD and depression/depressive symptoms, and clinical trials documenting the effects of VitD supplementation on depression/depressive symptoms, especially in older adults. Based on pre-clinical, clinical and observational studies, it is suggested that the maintenance of adequate VitD concentrations is an important issue, especially in older adults, which are a risk population for both VitD deficiency and depression. Nevertheless, it is necessary to carry out more studies using longitudinal approaches in low- and middle-income countries to develop a strong source of evidence to formulate guidelines and interventions.

Vitamin D insufficiency is associated with various disease processes. We determined whether consumption of a diet supplemented with HyD®, a 25-hydroxycholecalciferol (25(OH)D3) source, would safely increase plasma 25(OH)D3 concentrations in Golden Retrievers with low vitamin D status. We hypothesised that dietary supplementation with HyD® would rapidly increase and sustain plasma 25(OH)D3 levels in healthy Golden Retrievers with low vitamin D status compared with supplementation with vitamin D3. Of fifty-seven privately owned dogs recruited with written owner consent, eighteen dogs with low vitamin D status were identified and sorted between two groups to have similar initial plasma 25(OH)D3 concentrations, sex distributions, ages and body weights. Dogs of each group were fed a dry dog food supplemented with either 16 μg/kg of 25(OH)D3 as HyD® (n 10) or 81 μg/kg of cholecalciferol (D3) (n 8) for 4 months. Plasma 25(OH)D3 concentrations were determined monthly. A significant time effect (P < 0⋅001) and time by group interaction (P = 0⋅0045) were found for monthly determined plasma 25(OH)D3 concentrations. Dogs fed the HyD®-supplemented diet experienced a 40⋅5 % rise in plasma 25(OH)D3 values after 1 month (P < 0⋅001) and no change thereafter. Plasma 25(OH)D3 values of dogs supplemented with vitamin D3 did not increase (P > 0⋅05) and were less than values of dogs supplemented with HyD® (P = 0⋅044). With few exceptions, average haematologic, biochemical and urinalyses results remained within the reference range for both groups. Dietary supplementation with HyD® is sufficient to safely increase and sustain plasma 25(OH)D3 levels in healthy dogs.

Coccidial infections reduce fat-soluble vitamin status and bone mineralisation in broiler chickens. We hypothesised that broilers infected with Eimeria maxima would benefit from increased dietary supplementation with vitamin D (vitD) or with 25-hydroxycholecalciferol (25(OH)D3 or 25D3). Broilers were assigned to diets with low (L) or commercial (M) vitD levels (25 v. 100 μg/kg) supplemented as cholecalciferol (D3) or 25D3. At day 11 of age, birds were inoculated with water or 7000 E. maxima oocysts. Pen performance was calculated over the early (days 1–6), acute (days 7–10) and recovery periods (days 11–14) post-infection (pi). At the end of each period, six birds per treatment were dissected to assess long bone mineralisation, plasma levels of 25D3, Ca and P, and intestinal histomorphometry. Parasite replication and transcription of cytokines IL-10 and interferon-γ (IFN-γ) were assessed at day 6 pi using quantitative PCR. Performance, bone mineralisation and plasma 25D3 levels were significantly reduced during infection (P < 0·05). M diets or diets with 25D3 raised plasma 25D3, improved performance and mineralisation (P < 0·05). Offering L diets compromised feed efficiency pi, reduced femur breaking strength and plasma P levels at day 10 pi in infected birds (P < 0·05). Contrastingly, offering M diets or diets with 25D3 resulted in higher parasite loads (P < 0·001) and reduced jejunal villi length at day 10 pi (P < 0·01), with no effect on IL-10 or IFN-γ transcription. Diets with M levels or 25D3 improved performance and mineralisation, irrespective of infection, while M levels further improved feed efficiency and mineralisation in the presence of coccidiosis.

The present study was carried out to evaluate the effect of dietary supplemental vitamin D3 (VD3) on P absorption and utilisation as well as its related mechanisms in the small intestine of broilers. A total of 384 1-d-old Arbor Acres male broilers were assigned randomly into four treatments following a completely randomised design with a 2 (dietary non-phytate P (NPP) contents: 0·43 and 0·22 %)×2 (dietary VD3 supplemental levels: 0 and 87·5 μg/kg) factorial arrangement. The experiment lasted for 22 d. The results showed that P contents in serum from the hepatic portal vein and tibia ash of broilers were higher (P<0·05) for 0·43 % NPP than for 0·22 % NPP. The type IIb Na-dependent phosphate cotransporter (NaP-IIb) protein expressions in the duodenum and ileum were higher (P<0·05) also for 0·43 % NPP than 0·22 % NPP. Supplementation of VD3 enhanced (P<0·05) tibia P retention rate and type III Na-dependent phosphate cotransporter (PiT)-1 protein expression in the duodenum of all broilers. Moreover, VD3 supplementation decreased (P<0·002) mortality and increased (P<0·02) serum P content from the hepatic portal vein after 4 h of feeding, tibia ash content, tibia ash P content and protein expressions of NaP-IIb and PiT-1 in the jejunum of broilers fed diet with 0·22 % NPP. Thus, dietary supplemental VD3 promoted intestinal P absorption and bone P utilisation, and this effect might be associated with enhanced PiT-1 levels in the duodenum and PiT-1 and NaP-IIb levels in the jejunum respectively when dietary NPP is limiting.

Vitamin D deficiency (plasma 25-hydroxycholecalciferol (25(OH)D)<50 nmol/l) is highly prevalent, increases risk of non-communicable diseases (NCD) and associates with increased oxidative stress in obese subjects, the elderly and patients suffering from NCD. If confirmed as an independent driver of oxidative stress, nutritional and other public health strategies to improve vitamin D status would be strongly supported. We investigated vitamin D/oxidative stress links without the confounding effects of advanced age, obesity, smoking or pre-existing disease. Plasma 25(OH)D and biomarkers of oxidative stress and antioxidant status (plasma allantoin, oxidised LDL, ferric reducing antioxidant power (FRAP), ascorbic acid, urine 8-oxo-7,8-dihydro-2'-deoxyguanosine) were measured in fasting samples from 196 consenting, healthy adults aged 18–26 years. Correlation between 25(OH)D and each biomarker as well as biomarker differences across 25(OH)D quartiles and groups (<25/25–49/≥50 nmol/l) were investigated. Median 25(OH)D was 40 nmol/l; >70 % of participants were vitamin D deficient. No significant correlations and no biomarker differences across 25(OH)D quartiles or groups were seen except for total antioxidant status. A weak direct association (r 0·252, P<0·05) was observed between 25(OH)D and FRAP, and those in the lowest 25(OH)D quartile and group had significantly lower FRAP values. Results did not reveal a clear link between vitamin D status and oxidative stress biomarkers in the absence of advanced age, obesity and disease, though some evidence of depleted antioxidant status in those with vitamin D deficiency was seen. Poor antioxidant status may pre-date increased oxidative stress. Study of effects of correction of deficiency on antioxidant status and oxidative stress in vitamin D-deficient but otherwise healthy subjects is needed.

We previously found a weak response in serum 25-hydroxyvitamin D3 (25(OH)D3) concentrations when dogs were supplemented with oral vitamin D3 (D3). In the present study, we determined the relative potency of oral 25(OH)D3 compared with D3 for increasing vitamin D status in dogs with low serum 25(OH)D concentrations. Four male and three female, 4-year-old, intact, lean, genetically related, Chinese-crested/beagle dogs were studied in a randomised, single cross-over trial. After feeding a low-vitamin D diet (<4 IU/100 g) for 30 d, four dogs received daily D3 supplementation at 2·3 µg/kg body weight0·75, while three dogs received a molar equivalency as 25(OH)D3. The supplements, dissolved in ethanol, were applied to a commercial treat for consumption. Serum 25(OH)D3 and 24R,25-dihydroxyvitamin D3 (24R,25(OH)2D3) were analysed weekly using a validated HPLC method. Both supplementations increased (P ≤ 0·01) serum 25(OH)D3 concentrations. However, oral 25(OH)D3 resulted in greater (P < 0·0001) concentrations than D3 by week 1, with a difference of 173 % (P < 0·0001) by week 2. The supplementation period was limited to 14 d after serum 25(OH)D3 concentrations were not appearing to plateau. Thereafter, a washout period of 1 month separated the cross-over. Following 25(OH)D3, but not D3 supplementation, serum 24R,25(OH)2D3 concentrations increased (P ≤ 0·02), 3 to 5 weeks after initiating supplementation. Vitamin D status, as indicated by serum 25(OH)D3 and 24R,25(OH)2D3 concentrations, is more rapidly and efficiently increased in adult dogs by oral supplementation of 25(OH)D3 than D3.

Little is known regarding optimal vitamin D status in adult dogs. To date no studies on vitamin D supplementation for improving vitamin D status have been reported for adult dogs. The aims of this study were to identify dogs with low vitamin D status and evaluate an oral dosage of cholecalciferol (D3) for effectiveness in increasing vitamin D status. For this, forty-six privately owned dogs were evaluated. Of the dogs, thirty-three (or 71·7 %) had serum 25-hydroxyvitamin D (25(OH)D) concentrations less than 100 ng/ml, a minimum previously suggested for vitamin D sufficiency in dogs. Subsequently, thirteen dogs were enrolled in a supplementation trial. Dogs were given either a D3 supplement (n 7; 2·3 µg/kg0·75) or olive oil placebo (n 6) daily with food. Serum concentrations of 25(OH)D were determined at weeks 1, 3 and 6, and at the trial end. Only at the trial end (weeks 9–10) was 25(OH)D significantly greater (P = 0·05) in supplemented v. placebo dogs. Serum concentrations of 24R,25-dihydroxycholecalciferol determined at the trial end were about 40 % of that of 25(OH)D3 and not significantly different between the groups. Concentrations of parathyroid hormone, ionised Ca, P and creatinine measured in initial and final serum samples indicated supplementation caused no toxicity. We conclude that vitamin D3 supplementation at a dosage near the National Research Council recommended safe-upper limit was not effective for rapidly raising serum 25(OH)D concentrations in healthy, adult dogs. Further work is needed in evaluating the metabolism of orally administered D3 in dogs before dosing recommendations can be made.

A sufficient but balanced vitamin supplementation is a prerequisite for a satisfactory growth pattern and an effective immune system in mink and all other species. The fat-soluble vitamins are very sensitive to over- or under-supply because they interact with each other with respect to dose–response and chemical form. The purpose of the present study was to investigate the effect of increasing the amount of retinol in combination with RRR-α-tocopherol or all-rac-α-tocopherol in the feed given to growing mink on their retinol, cholecalciferol and α-tocopherol concentrations in plasma and selected organs. The results showed that the mink met their retinol requirements from the basal diet, but there were no negative effects of supplying various amounts of retinol on their plasma α-tocopherol concentrations. On the other hand, the study showed that the cholecalciferol status in plasma, assessed as the 25-hydroxycholecalciferol concentration, was low when retinol was supplemented in the feed at high levels. In addition, supplementation with RRR-α-tocopherol in the feed negatively affected the plasma concentration of 25-hydroxycholecalciferol compared with supplementation with all-rac-α-tocopherol. In general, female mink had higher concentrations of fat-soluble vitamins in plasma than male mink.

In vitro studies with skin samples or pure precursors of cholecalciferol indicated that cholecalciferol synthesis during UV light exposure is a non-linear process. However, in vitro studies indicate nothing about the relationship between sunlight exposure and physiological cholecalciferol status of living organisms. Due to the lack of cholecalciferol in plant material, this relationship is important for herbivores including domestic cattle, particularly in organic agriculture, because the use of synthetic additives, like cholecalciferol, is restricted in order to fulfil the principles of sustainable organic production. The major physiological metabolite of cholecalciferol is the liver-derived 25-hydroxycholecalciferol (25(OH)D3). The purpose of the present study was to determine the relationship between sunlight exposure and 25(OH)D3 status in vivo in large herbivores during mid-summer at 56°N. Five groups of cows were given access to pasture during 15, 30, 75, 150 or 300 min daily for 28 d in June and plasma analysed for 25(OH)D3. Animals allowed 15, 30 or 75 min of daily access to pasture showed a declining linear relationship between plasma 25(OH)D3 and sampling day in contrast to animals allowed 150 or 300 min of pasture access which showed linear increasing plasma 25(OH)D3 status. Determined from the slopes of 25(OH)D3 concentration curves within treatments, breakeven for maintaining the initial 25(OH)D3 status of 45 nmol/l was 90 min pasture access per d during summer at 56°N.

There is increasing epidemiological evidence linking sub-optimal vitamin D status with overweight and obesity. Although increasing BMI and adiposity have also been negatively associated with the change in vitamin D status following supplementation, results have been equivocal. The aim of this randomised, placebo-controlled study was to investigate the associations between anthropometric measures of adiposity and the wintertime serum 25-hydroxycholecalciferol (25(OH)D) response to 15 μg cholecalciferol per d in healthy young and older Irish adults. A total of 110 young adults (20–40 years) and 102 older adults ( ≥ 64 years) completed the 22-week intervention with >85 % compliance. The change in 25(OH)D from baseline was calculated. Anthropometric measures of adiposity taken at baseline included height, weight and waist circumference (WC), along with skinfold thickness measurements to estimate fat mass (FM). FM was subsequently expressed as FM (kg), FM (%), FM index (FMI (FM kg/height m2)) and as a percentage ratio to fat-free mass (FFM). In older adults, vitamin D status was inversely associated with BMI (kg/m2), WC (cm), FM (kg and %), FMI (kg/m2) and FM:FFM (%) at baseline (r − 0·33, − 0·36, − 0·33, − 0·30, − 0·33 and − 0·27, respectively, all P values < 0·01). BMI in older adults was also negatively associated with the change in 25(OH)D following supplementation (β − 1·27, CI − 2·37, − 0·16, P = 0·026); however, no such associations were apparent in younger adults. Results suggest that adiposity may need to be taken into account when determining an adequate wintertime dietary vitamin D intake for healthy older adults residing at higher latitudes.