Vitamin D deficiency along with long chain n-3 PUFA deficiency is common in both adults and children and particularly in the obese 
. This secondary analysis aimed to investigate whether n-3 PUFA could have deleterious effects on vitamin D status in obese individuals. Accordingly, most patients from our study population exhibited vitamin D deficiency. All patients had normal serum levels of VDBP. Under physiologic conditions, serum PTH concentrations tend to correlate negatively with serum 25(OH)D concentration in case of severe vitamin D deficiency 
, but no such correlation was found in our study, a finding which has been also reported by others 
. There is no consensus on the threshold of 25(OH)D values below which PTH levels starts to increase. Furthermore it seems that the inverse relationship between serum PTH and 25(OH)D is not causative, but reflects biochemical abnormalities associated to obesity, as multiple linear regression analyses from other studies have demonstrated that BMI itself accounts for the decreased serum vitamin D and increased PTH concentration 
Vitamin D and n-3 PUFA are found together in cod liver oil, known for its unpleasant taste. Since purified re-esterified n-3 PUFA have become available, cod liver oil supplementation has further lost in appeal. Thus, concerns have arisen that supplementation with n-3 PUFA derived from fish-oil might, as a side effect, cause a diminished supplementation with vitamin D. There is scarce evidence from animal models receiving combined therapy with n-3 PUFA and vitamin D, so it is difficult to speculate on their combined effect. A large trial investigating the concomitant effect of n-3 PUFA and vitamin D supplementation on the prevention of cancer and cardio-vascular disease is set to be finished by 2017 
. In addition, Niramitmahapanya et al.
found that dietary PUFA intake negatively correlated with the vitamin D status of elderly patients, receiving supplemental vitamin D3
and suggested that n-3 PUFA treatment affects vitamin D absorption 
. We could show here that a considerable daily n-3 PUFA dose of 3.36 g did not impact the overall vitamin D status, irrespective of the season. VDBP concentration was also unaffected by the treatment. However, we cannot rule out that a higher n-3 PUFA dose affects vitamin D status. Inuits who consume high doses of n-3 PUFA and vitamin D from free-living fish and sea mammals have high circulating vitamin D concentrations 
. In a cross-sectional analysis where serum 25(OH)D concentration and dietary intake of n-3 PUFA was assessed, the group with the highest vitamin D concentration had also the higher n-3 PUFA intake (1.5 g/d) 
. These epidemiological data further argue against a significant impact of n-3 PUFA on vitamin D status. Moreover, baseline vitamin D concentrations in the obese middle aged cohort investigated here positively correlated with plasma phospholipid EPA and total n-3 PUFA content, strongly arguing against a negative effect of n-3 PUFA in the regular diet on vitamin D uptake. The duration of our study can be considered long enough to detect an interaction between n-3 PUFA and vitamin D as the half-life of vitamin D is reported at circa 1 month in humans and serum 25(OH)D is essentially at the plateau concentration by 1 month 
. It is hence rather unlikely that a longer duration of treatment would significantly impact vitamin D status. Another factor which could clearly influence a possible interaction between n-3 PUFA and vitamin D is the type of patient. In this case, pathologies affecting vitamin D absorption and metabolism, such as intestinal, severe liver or kidney disease have to be considered. However, the existence of these conditions was excluded in our study.
Inflammation considerably contributes to obesity-associated complications such as insulin resistance, type 2 diabetes and cardiovascular disease 
. In this regard, anti-inflammatory therapies are currently under investigation as novel preventive and therapeutic strategies. We have shown that long chain n-3 PUFA reduce the concentration of inflammatory markers such as IL-6 in severely obese subjects 
. IL-6 regulates hsCRP production in the liver, thus a reduction in hsCRP concentration might also occur with longer treatment. Vitamin D is negatively associated with both BMI and inflammatory markers, such as IL-6 and hsCRP in healthy lean and obese subjects 
. We and others have shown that n-3 PUFA reduce systemic and adipose tissue inflammation, induce anti-inflammatory gene expression in circulating mononuclear cells and improve metabolic control in severely obese, overweight and elderly subjects 
. The data presented here indicate that the anti-inflammatory action of n-3 PUFA occurs even in vitamin D deficiency. Particularly noteworthy is the finding, that n-3 PUFA but not control treatment abolished the negative association of vitamin D concentration and inflammatory parameters. Hence it could be speculated that the anti-inflammatory action of n-3 PUFA may in part compensate for the detrimental outcome of vitamin D deficiency. Clearly, causalities of these interrelations need to be investigated in future studies.
In conclusion, treatment with n-3 PUFA does not compromise the overall vitamin D status of obese patients, many of whom were vitamin D deficient, but abrogates the inverse association of vitamin D deficiency with inflammation. The fact that n-3 PUFA treatment reduces inflammation indicates that adequate n-3 PUFA intake could compensate for some detrimental outcomes of vitamin D deficiency. Cumulative effects of n-3 PUFA and vitamin D on unfavorable obesity-related complications remain to be evaluated.