Diminished skeletal muscle strength and size, termed sarcopenia, contributes substantially to physical disability, falls, dependence and reduced quality of life among older people. Physical activity and nutrition are the cornerstones of sarcopenia prevention and treatment. The optimal daily protein intake required to preserve muscle mass and function among older adults is a topic of intense scientific debate. Older adults require protein intakes about 67 % higher than their younger counterparts to maximally stimulate postprandial muscle protein synthesis rates. In addition, evidence suggests a possible benefit of increasing protein intake above the population reference intake (0⋅83 g/kg/d) on lean mass and, when combined with exercise training, muscle strength. In addition to protein quantity, protein quality, the pattern of protein intake over the day and specific amino acids (i.e. leucine) represent key considerations. Long-chain n-3 PUFA (LC n-3 PUFA) supplementation has been shown to enhance muscle protein synthesis rates, increase muscle mass and function and augment adaptations to resistance training in older adults. Yet, these effects are not consistent across all studies. Emerging evidence indicates that an older person's dietary, phenotypic and behavioural characteristics may modulate the efficacy of protein and LC n-3 PUFA interventions for promoting improvements in muscle mass and function, highlighting the potential inadequacy of a ‘one-size-fits-all’ approach. The application of personalised or precision nutrition to sarcopenia represents an exciting and highly novel field of research with the potential to help resolve inconsistencies in the literature and improve the efficacy of dietary interventions for sarcopenia.

The precision nutrition paradigm is based on the premise that substantial variation exists between human subjects in terms of diet-related disease risk and response to dietary interventions. In terms of better defining, ‘the right diet for the right person at the right time’ may be more appropriate than ‘one-diet-fits-all’. This review will explore how systems biology and nutrigenomics approaches have advanced the precision nutrition paradigm. We will draw upon a number of elegant mechanistic studies that have enhanced our understanding with respect to the complex biology and inter-organ crosstalk, relating to inflammation and metabolism, that underpin cardio-metabolic health. Also, this review will explore the extent to which more targeted, precision nutrition approaches may attenuate adverse risk factors associated with cardio-metabolic disease. We will focus on the key characteristics or ‘metabotypes’ of high- v. low-risk individuals and response v. non-response to interventions, to generate greater insights with respect to risk stratification and therapeutic interventions to enhance disease prevention. The goal is to utilise systems biology to enhance understanding by underpinning more targeted nutritional approaches, which may improve efficacy of personalised nutrition interventions.

While discussion of eugenics and biopolitics during the Third Reich has largely focused upon the regime's most destructive and genocidal policies, this article concentrates on Nazi ‘special schools’ and ‘elite schools’ as a crucial sphere of quasi-eugenic thought and praxis, drawing attention to education as a previously under-researched category of intervention in the history of modern biopolitics. The article also sheds new light on the racialized nature of the Nazi ‘national community’ (the Volksgemeinschaft), and contributes to recent debates on the Third Reich's status as a ‘racial state’ which suggest that the National Socialist regime was driven less by fanatical adherence to racial ideology, and more by a mixture of anthropological and eugenic racism, combined with productivist pragmatism. The two case-studies draw attention to less familiar corners of the National Socialist pedagogical landscape, covering both extremes of the spectrum of biological selection in education, from the negative, eugenic policies applied to supposedly ‘abnormal’ pupils at the so-called ‘special schools’ (Hilfsschulen), to the ‘positive’ biological selection of elite-school applicants at the National Political Education Institutes (Nationalpolitische Erziehungsanstalten, NPEA), the regime's principal training institutions for the future elite of the Third Reich.

As COVID-19 continues to spread worldwide, severe disease and mortality have been observed in obese patients. We discuss how obesity and obesity-associated factors such as ‘meta-flammation’, dietary fat intake and paradoxical suppression of the innate immune response within the pulmonary compartment may be crucial determinants in the host response to a novel viral pathogen. Modulation of immune cell bioenergetics and metabolic potential plays a central role in the innate immune response to infection, and as we strive to combat this new global health threat, immunometabolism of the innate immune system warrants attention.

Reduced inflammatory signaling (IL-1RI-/-) alters metabolic responses to dietary challenges (1). Inflammasome deficiency (e.g. IL-18-/-, Asc-/-) can modify gut microbiota concomitant with hepatosteatosis; an effect that was transferable to wild-type (WT) mice by co-housing (2). Taken together, this evidence suggests that links between diet, microbiota and IL-1RI-signaling can influence metabolic health. Our aim was to determine whether IL-1RI-mediated signaling interacted with the gut microbiome to impact metabolic tissue functionality in a diet-specific fashion. Male WT (C57BL/J6) and IL-1RI-/- mice were fed either high-fat diet (HFD; 45% kcal) or low-fat diet (LFD; 10% kcal) for 24 weeks and were housed i) separately by genotype or ii) with genotypes co-housed together (i.e. isolated vs shared microbial environment; n = 8–10 mice per group). Glucose tolerance and insulin secretion response (1.5 g/kg i.p.), gut microbiota composition and caecal short-chain fatty acids (SCFA) were assessed. Liver and adipose tissue were harvested and examined for triacylglycerol (TAG) formation, cholesterol and metabolic markers (Fasn, Cpt1α, Pparg, Scd1, Dgat1/2), using histology, gas-chromatography and RT-PCR, respectively. Statistical analysis included 1-way or 2-way ANOVA, where appropriate, with Bonferroni post-hoc correction. Co-housing significantly affected gut microbiota composition, illustrated by clustering in PCoA (unweighted UniFrac distance) of co-housed mice but not their single-housed counterparts, on both HFD and LFD. The taxa driving these differences were primarily from Lachnospiraceae and Ruminococcaceae families. Single-housed WT had lower hepatic weight, TAG, cholesterol levels and Fasn despite HFD, an effect lost in their co-housed counterparts, who aligned more to IL-1RI-/- hepatic lipid status. Hepatic Cpt1α was lowest in co-housed WT. Adipose from IL-1RI-/- groups on HFD displayed increased adipocyte size and reduced adipocyte number compared to WT groups, but greater lipogenic potential (Pparg, Scd1, Dgat2) alongside a blunted IL-6 response to pro-inflammatory stimuli (~32%, P = 0.025). Whilst caecal SCFA concentrations were not different between groups, single-housed IL-1RI-/- adipocytes showed greatest sensitivity to SCFA-induced lipogenesis. Interestingly, differences in tissue functionality and gut microbiome occurred despite unaltered glucose tolerance; although there was a trend for phenotypic transfer of body weight via co-housing. For all endpoints examined, similar genotype/co-housing effects were observed for both HFD and LFD with the greatest impacts seen in HFD-fed mice. In conclusion, while the gut microbiome may be an important consideration in dietary interventions, these results question the magnitude of its impact in relation to the IL-1RI-dependent immunometabolism-glucose homeostasis axis.

Sarcopenia is a muscle disease rooted in adverse muscle changes that accrue across a lifetime. It is an independent risk factor for numerous adverse health outcomes. In 2010, the European Working Group on Sarcopenia in Older People (EWGSOP) published a definition for the identification of people with sarcopenia (EWGSOP1). In 2018, this definition was updated based on the newest evidence (EWGSOP2), with the focus now on low muscle strength rather than low muscle quantity as the key characteristic of sarcopenia. In addition, EWGSOP2 provides clear cut-off points for measurements of variables that identify sarcopenia. The aim of this study was to determine the prevalence of sarcopenia among community-dwelling older adults in Ireland for the first time and to assess agreement between the EWGSOP1 and EWGSOP2 definitions. In a cross-sectional analysis, 490 community-dwelling adults (age 78.4 ± 8.0 y, body mass index 27.6 ± 5.1 kg/m2) were assessed. Skeletal muscle mass was estimated using bioelectrical impedance analysis, muscle strength was measured via handgrip dynamometry and physical performance via the Short Physical Performance Battery. Sarcopenia was defined according to both the 2010 criteria (EWGSOP1) and the updated 2018 criteria (EWGSOP2). Using the EWGSOP1 criteria, the prevalence of sarcopenia was 7.1% (2.6% sarcopenia, 4.5% severe sarcopenia) and 3.6% were classified as pre-sarcopenic (low muscle mass without a decrement in strength or physical performance). Using the EWGSOP2 criteria, the prevalence of sarcopenia was 5.5% (1.6% sarcopenia, 3.9% severe sarcopenia) and 23.4 % were classified as having low strength but without a decrement in muscle mass. Five of the participants who were classified as sarcopenic (2 sarcopenia, 3 severe sarcopenia) by EWGSOP1 were classified as “normal” using the EWGSOP2 criteria. In conclusion, the prevalence of sarcopenia in community-dwelling older adults in Ireland is in line with the prevalence reported in other European countries using the EWGSOP1 criteria (3.3–11.4 %). To our knowledge this is the first study to compare the prevalence based on the EWGSOP1 and the EWGSOP2 criteria. We report a slightly lower prevalence using the EWGSOP2 definition compared to the EWGSOP1 definition. Importantly however, in contrast to EWGSOP1, the EWGSOP2 definition identified a substantial proportion of older adults with poor strength in the absence of overt sarcopenia (23.4%). These older adults represent a group who would benefit from further clinical investigation and intervention.

Preliminary evidence has suggested that high-fat diets (HFD) enriched with SFA, but not MUFA, promote hyperinsulinaemia and pancreatic hypertrophy with insulin resistance. The objective of this study was to determine whether the substitution of dietary MUFA within a HFD could attenuate the progression of pancreatic islet dysfunction seen with prolonged SFA-HFD. For 32 weeks, C57BL/6J mice were fed either: (1) low-fat diet, (2) SFA-HFD or (3) SFA-HFD for 16 weeks, then switched to MUFA-HFD for 16 weeks (SFA-to-MUFA-HFD). Fasting insulin was assessed throughout the study; islets were isolated following the intervention. Substituting SFA with MUFA-HFD prevented the progression of hyperinsulinaemia observed in SFA-HFD mice (P < 0·001). Glucose-stimulated insulin secretion from isolated islets was reduced by SFA-HFD, yet not fully affected by SFA-to-MUFA-HFD. Markers of β-cell identity (Ins2, Nkx6.1, Ngn3, Rfx6, Pdx1 and Pax6) were reduced, and islet inflammation was increased (IL-1β, 3·0-fold, P = 0·007; CD68, 2·9-fold, P = 0·001; Il-6, 1·1-fold, P = 0·437) in SFA-HFD – effects not seen with SFA-to-MUFA-HFD. Switching to MUFA-HFD can partly attenuate the progression of SFA-HFD-induced hyperinsulinaemia, pancreatic inflammation and impairments in β-cell function. While further work is required from a mechanistic perspective, dietary fat may mediate its effect in an IL-1β–AMP-activated protein kinase α1-dependent fashion. Future work should assess the potential translation of the modulation of metabolic inflammation in man.

Dietary intake and nutritional status is an important environmental factor which can modulate metabolic-inflammation. In recent years, research has made significant advances in terms of understanding the impact of dietary components on metabolic-inflammation, within the context of obesity, type-2 diabetes (T2D) and CVD risk. Our work demonstrated that different fatty acids differentially modulate metabolic-inflammation, initially focusing on Nod-like receptor family, pyrin domain-containing three protein (NLRP3) inflammasome mediated IL-1β biology and insulin signalling. However, the paradigm is more complex, wherein data from the immunology field clearly show that nature of cellular energy metabolism is a key determinant of inflammation. Whilst metabolic-inflammation is a critical biological interaction, there is a paucity of data in relation to the nature and the extent to which nutritional status affects metabolic-inflammation. The complex paradigm will be discussed within the context of if/how dietary components, in particular fatty acids, may modulate obesity, T2D and CVD risk, via inflammatory and metabolic processes.

SFA intakes have decreased in recent years, both in Ireland and across other European countries; however a large proportion of the population are still not meeting the SFA recommendation of <10% of total energy (TE). High SFA intakes have been associated with increased CVD and type-2 diabetes (T2D) risk, due to alterations in cholesterol homoeostasis and adipose tissue inflammation. PUFA, in particular EPA and DHA, have been associated with health benefits, including anti-inflammatory effects. It is well established that dietary fat composition plays an important role in biological processes. A recent review of evidence suggests that replacement of SFA with PUFA has potential to reduce risk of CVD and T2D. The public health and molecular impact of EPA and DHA have been well-characterised, while less is known of effects of α-linolenic acid (ALA). The current dietary guideline for ALA is 0·5% TE; however evidence from supplementation trials suggests that benefit is observed at levels greater than 2 g/d (0·6–1% TE). This review highlights the gap in the evidence base relating to effects of the replacement of SFA with ALA, identifying the need for randomised controlled trials to determine the optimal dose of ALA substitution to define the efficacy of dietary fat modification with ALA.

Studies of German philhellenism have often focused upon the idealization of Greece by German intellectuals, rather than considering the very real, at times reciprocal, at times ambivalent or even brutal, relationship which existed between contemporary Germans and the Greek state from the Greek War of Independence onwards. This review essay surveys historiographical developments in the literature on German philhellenism which have emerged in the past dozen years (2004–16), drawing on research in German studies, classical philology and reception studies, Modern Greek studies, intellectual history, philosophy, art history, and archaeology. The essay explores the extent to which recent research affirms or rebuts that notion of German cultural exceptionalism which posits a Hellenophile Sonderweg – culminating in the tyranny of Germany over Greece imposed by force of arms under the Third Reich – when interpreting the vicissitudes of the Graeco–German relationship. The discussion of new literature touches upon various themes, including Winckelmann reception at the fin-de-siècle and the anti-positivist aspects of twentieth-century philhellenism, the idealization of ‘Platonic’ homoeroticism in the Stefan George-Kreis, the reciprocal relationship between German idealist philhellenism and historicism, and the ways in which German perceptions of modern Greece's materiality have constantly been mediated through idealized visions of Greek antiquity.

FFQ, food diaries and 24 h recall methods represent the most commonly used dietary assessment tools in human studies on nutrition and health, but food intake biomarkers are assumed to provide a more objective reflection of intake. Unfortunately, very few of these biomarkers are sufficiently validated. This review provides an overview of food intake biomarker research and highlights present research efforts of the Joint Programming Initiative ‘A Healthy Diet for a Healthy Life’ (JPI-HDHL) Food Biomarkers Alliance (FoodBAll). In order to identify novel food intake biomarkers, the focus is on new food metabolomics techniques that allow the quantification of up to thousands of metabolites simultaneously, which may be applied in intervention and observational studies. As biomarkers are often influenced by various other factors than the food under investigation, FoodBAll developed a food intake biomarker quality and validity score aiming to assist the systematic evaluation of novel biomarkers. Moreover, to evaluate the applicability of nutritional biomarkers, studies are presently also focusing on associations between food intake biomarkers and diet-related disease risk. In order to be successful in these metabolomics studies, knowledge about available electronic metabolomics resources is necessary and further developments of these resources are essential. Ultimately, present efforts in this research area aim to advance quality control of traditional dietary assessment methods, advance compliance evaluation in nutritional intervention studies, and increase the significance of observational studies by investigating associations between nutrition and health.

Evidence suggests that processed red meat consumption is a risk factor for CVD and type 2 diabetes (T2D). This analysis investigates the association between dietary patterns, their processed red meat contributions, and association with blood biomarkers of CVD and T2D, in 786 Irish adults (18–90 years) using cross-sectional data from a 2011 national food consumption survey. All meat-containing foods consumed were assigned to four food groups (n 502) on the basis of whether they contained red or white meat and whether they were processed or unprocessed. The remaining foods (n 2050) were assigned to twenty-nine food groups. Two-step and k-means cluster analyses were applied to derive dietary patterns. Nutrient intakes, plasma fatty acids and biomarkers of CVD and T2D were assessed. A total of four dietary patterns were derived. In comparison with the pattern with lower contributions from processed red meat, the dietary pattern with greater processed red meat intakes presented a poorer Alternate Healthy Eating Index (21·2 (sd 7·7)), a greater proportion of smokers (29 %) and lower plasma EPA (1·34 (sd 0·72) %) and DHA (2·21 (sd 0·84) %) levels (P<0·001). There were no differences in classical biomarkers of CVD and T2D, including serum cholesterol and insulin, across dietary patterns. This suggests that the consideration of processed red meat consumption as a risk factor for CVD and T2D may need to be re-assessed.

Obesity-related metabolic conditions such as insulin resistance (IR), type 2 diabetes and CVD share a number of pathological features, one of which is metabolic-inflammation. Metabolic-inflammation results from the infiltration of immune cells into the adipose tissue, driving a pro-inflammatory environment, which can induce IR. Furthermore, resolution of inflammation, an active process wherein the immune system counteracts pro-inflammatory states, may be dysregulated in obesity. Anti-inflammatory nutritional interventions have focused on attenuating this pro-inflammatory environment. Furthermore, with inherent variability among individuals, establishing at-risk populations who respond favourably to nutritional intervention strategies is important. This review will focus on chronic low-grade metabolic-inflammation, resolution of inflammation and the putative role anti-inflammatory nutrients have as a potential therapy. Finally, in the context of personalised nutrition, the approaches used in defining individuals who respond favourably to nutritional interventions will be highlighted. With increasing prevalence of obesity in younger people, age-dependent biological processes, preventative strategies and therapeutic options are important to help protect against development of obesity-associated co-morbidities.