Krill oil attenuates left ventricular dilatation after myocardial infarction in rats

Background: In the western world, heart failure (HF) is one of the most important causes of cardiovascular mortality. Supplement with n-3 polyunsaturated fatty acids (PUFA) has been shown to improve cardiac function in HF and to decrease mortality after myocardial infarction (MI). The molecular structure and composition of n-3 PUFA varies between different marine sources and this may be of importance for their biological effects. Krill oil, unlike fish oil supplements, contains the major part of the n-3 PUFA in the form of phospholipids. This study investigated effects of krill oil on cardiac remodeling after experimental MI. Rats were randomised to pre-treatment with krill oil or control feed 14 days before induction of MI. Seven days post-MI, the rats were examined with echocardiography and rats in the control group were further randomised to continued control feed or krill oil feed for 7 weeks before re-examination with echocardiography and euthanization. Results: The echocardiographic evaluation showed significant attenuation of LV dilatation in the group pretreated with krill oil compared to controls. Attenuated heart weight, lung weight, and levels of mRNA encoding classical markers of LV stress, matrix remodeling and inflammation reflected these findings. The total composition of fatty acids were examined in the left ventricular (LV) tissue and all rats treated with krill oil showed a significantly higher proportion of n-3 PUFA in the LV tissue, although no difference was seen between the two krill oil groups. Conclusions: Supplement with krill oil leads to a proportional increase of n-3 PUFA in myocardial tissue and supplement given before induction of MI attenuates LV remodeling

Krill oil significantly decreases 2-arachidonoylglycerol plasma levels in obese subjects

We have previously shown that krill oil (KO), more efficiently than fish oil, was able to downregulate the endocannabinoid system in different tissues of obese zucker rats

Benzodiazepines and antidepressants: Effects on cognitive and functional decline in Alzheimer's disease and Lewy body dementia

Objectives We aim to study the effects of the prescription of benzodiazepines and antidepressants on cognitive and functional decline in older adults living with Alzheimer's disease (AD) and Lewy body dementia (LBD) over a 5-year follow-up. Methods This is a longitudinal analysis of a Norwegian cohort study entitled “The Dementia Study of Western Norway” (DemVest). We included 196 patients newly diagnosed with AD (n = 111) and LBD (n = 85), followed annually for 5 years. Three prescription groups were defined: only benzodiazepines (BZD), only antidepressants (ADep), and the combination of benzodiazepines and antidepressants (BZD-ADep). Linear mixed-effects models were conducted to analyze the effect of the defined groups on the outcomes. The outcomes were functional decline, measured by the Rapid Disability Rating Scale—2, and cognition measured with the Mini-Mental State Examination. Results Prescription of the combination of benzodiazepines and antidepressants in LBD was associated with faster functional decline. In AD, the prescription of BZD and BZD-ADep was associated with greater functional deterioration. ADep alone did not show positive or negative significant associations with the studied outcomes. Conclusions BZD and especially the combination of BZD and ADep are associated with functional decline in AD and LBD and should be used cautiously.publishedVersio

Effects of similar intakes of marine n-3 fatty acids from enriched food products and fish oil on cardiovascular risk markers in healthy human subjects

There is convincing evidence that consumption of fish and fish oil rich in long-chain (LC) n-3 PUFA (n-3 LCPUFA), EPA (20 : 5n-3) and DHA (22 : 6n-3) reduce the risk of CHD. The aim of the present study was to investigate whether n-3 LCPUFA-enriched food products provide similar beneficial effects as fish oil with regard to incorporation into plasma lipids and effects on cardiovascular risk markers. A parallel 7-week intervention trial was performed where 159 healthy men and women were randomised to consume either 34 g fish pâté (n 44), 500 ml fruit juice (n 38) or three capsules of concentrated fish oil (n 40), all contributing to a daily intake of approximately 1 g EPA and DHA. A fourth group did not receive any supplementation or food product and served as controls (n 37). Plasma fatty acid composition, serum lipids, and markers of inflammation and oxidative stress were measured. Compared with the control group, plasma n-3 LCPUFA and EPA:arachidonic acid ratio increased equally in all intervention groups. However, no significant changes in blood lipids and markers of inflammation and oxidative stress were observed. In conclusion, enriched fish pâté and fruit juice represent suitable delivery systems for n-3 LCPUFA. However, although the dose given is known to reduce the risk of CVD, no significant changes were observed on cardiovascular risk markers in this healthy populatio

Metabolic Effects of Krill Oil are Essentially Similar to Those of Fish Oil but at Lower Dose of EPA and DHA, in Healthy Volunteers

The purpose of the present study is to investigate the effects of krill oil and fish oil on serum lipids and markers of oxidative stress and inflammation and to evaluate if different molecular forms, triacylglycerol and phospholipids, of omega-3 polyunsaturated fatty acids (PUFAs) influence the plasma level of EPA and DHA differently. One hundred thirteen subjects with normal or slightly elevated total blood cholesterol and/or triglyceride levels were randomized into three groups and given either six capsules of krill oil (N = 36; 3.0 g/day, EPA + DHA = 543 mg) or three capsules of fish oil (N = 40; 1.8 g/day, EPA + DHA = 864 mg) daily for 7 weeks. A third group did not receive any supplementation and served as controls (N = 37). A significant increase in plasma EPA, DHA, and DPA was observed in the subjects supplemented with n-3 PUFAs as compared with the controls, but there were no significant differences in the changes in any of the n-3 PUFAs between the fish oil and the krill oil groups. No statistically significant differences in changes in any of the serum lipids or the markers of oxidative stress and inflammation between the study groups were observed. Krill oil and fish oil thus represent comparable dietary sources of n-3 PUFAs, even if the EPA + DHA dose in the krill oil was 62.8% of that in the fish oil

Frailty in Older Adults with Mild Dementia: Dementia with Lewy Bodies and Alzheimer’s Disease

Introduction: The aim of the study is to describe the frequency of frailty in people with a new diagnosis of mild dementia due to Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB). Methods: This is a secondary analysis of the Dementia Study of Western Norway (Demvest). For this study, we analysed a sample of 186 patients, 116 with AD and 70 with DLB. Subjects were included at a time in which mild dementia was diagnosed according to consensus criteria after comprehensive standardized assessment. Frailty was evaluated retrospectively using a frailty index generated from existing data. The cut-off value used to classify an older adult as frail was 0.25. Results: The prevalence of frailty was 25.81% (n = 48). In the DLB group, 37.14% (n = 26) were classified as frail, compared to 18.97% (n = 22) of those with AD (p < 0.001). The adjusted multivariate analysis revealed an OR of 2.45 (1.15–5.23) for being frail in those with DLB when using AD as the reference group. Conclusion: Frailty was higher than expected in both types of dementia. The prevalence of frailty was higher in those with DLB compared to AD. This new finding underscores the need for a multi-systems approach in both dementias, with a particular focus on DLB

Frailty in Older Adults with Mild Dementia: Dementia with Lewy Bodies and Alzheimer’s Disease

Introduction: The aim of the study is to describe the frequency of frailty in people with a new diagnosis of mild dementia due to Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB). Methods: This is a secondary analysis of the Dementia Study of Western Norway (Demvest). For this study, we analysed a sample of 186 patients, 116 with AD and 70 with DLB. Subjects were included at a time in which mild dementia was diagnosed according to consensus criteria after comprehensive standardized assessment. Frailty was evaluated retrospectively using a frailty index generated from existing data. The cut-off value used to classify an older adult as frail was 0.25. Results: The prevalence of frailty was 25.81% (n = 48). In the DLB group, 37.14% (n = 26) were classified as frail, compared to 18.97% (n = 22) of those with AD (p < 0.001). The adjusted multivariate analysis revealed an OR of 2.45 (1.15–5.23) for being frail in those with DLB when using AD as the reference group. Conclusion: Frailty was higher than expected in both types of dementia. The prevalence of frailty was higher in those with DLB compared to AD. This new finding underscores the need for a multi-systems approach in both dementias, with a particular focus on DLB

Neuropsychiatric symptoms and functional decline in alzheimerʼs disease and lewy body dementia

Background/objectives: Functional status is one of the most important markers of well-being in older adults, but the drivers of functional decline in dementia are not well known. The aim of our work was to study the association of neuropsychiatric symptoms (NPSs) with functional decline over 5 years in newly diagnosed people with Alzheimer´s disease (AD) and Lewy body dementia (LBD). Design: Secondary analysis of the Dementia Study of Western Norway longitudinal cohort study. Setting: Multicenter study conducted in memory clinics in western Norway. Participants: We included a total of 196 patients newly diagnosed with AD (n = 111) and LBD (n = 85), followed up annually for 5 years. Main Outcomes and Measures: The outcome was the rapid disability rating scale (items 1-13). Linear mixed-effects models were used for analysis with the total score of the Norwegian Neuropsychiatric Inventory (NPI) as a predictor measured either at baseline or longitudinally, adjusted for potential confounders, including cognition. Effect modification was checked by introducing interactions with NPI score and stratifying by diagnosis. Results: The total NPI score longitudinal course was associated with functional decline in both AD and LBD. At baseline, the total NPI score predicted functional decline in AD. Conclusion: NPSs were associated with the rate of functional decline in people with AD and LBD, independent of cognitive impairment. These results highlight the relevance of early detection and intervention of NPSs, which may also reduce functional decline