European Journal of Nutrition (v.54, #1)

A quality dietary supplement: before you start and after it’s marketed—a conference report by Mark A. LeDoux; Kristy R. Appelhans; Lesley A. Braun; Darren Dziedziczak; Sam Jennings; Laura Liu; Henry Osiecki; Edward Wyszumiala; James C. Griffiths (1-8).
Consumers worldwide are turning to dietary supplements as one part of their personal goal to lead healthier and more active lives. In truth, the quality of life now supersedes the length of life as no one would trade living to one hundred (the last forty with compromised physical abilities and decreased mental acuity) for 80 years of travel, time with family, and intellectual pursuits. If there is the possibility of preventing a disease or debilitating condition through efficient lifestyle changes (additions, subtractions, modifications) and to also avoid the costly and escalating medical and pharmaceutical treatments that accompany having the disease/condition, then a sensible individual would focus on their overall health and wellness…proactively, instead of reactively. However, an important caveat is that over-regulation or inappropriate application of current regulations can increase the price of dietary supplements and nutritional products and thus cause underutilization of the potentially beneficial physiological attributes of these products. Conversely, strict adherence to regulatory guidelines could result in safer dietary supplements and fewer adverse reactions requiring medical attention. If new regulations or stricter interpretation/application of existing regulations result in certain dietary supplements being taken off the market, will continued demand create a completely unregulated, underground economy that will create unforeseen problems? More research should be supported by government agencies to determine the effectiveness of dietary supplements, nutritional products and complementary medicine in reducing personal and societal medical costs and further contribution to the overall health of the population.

Dietary sugars: their detection by the gut–brain axis and their peripheral and central effects in health and diseases by Melissa Ochoa; Jean-Paul Lallès; Charles-Henri Malbert; David Val-Laillet (1-24).
Substantial increases in dietary sugar intake together with the increasing prevalence of obesity worldwide, as well as the parallels found between sugar overconsumption and drug abuse, have motivated research on the adverse effects of sugars on health and eating behaviour. Given that the gut–brain axis depends on multiple interactions between peripheral and central signals, and because these signals are interdependent, it is crucial to have a holistic view about dietary sugar effects on health.Recent data on the effects of dietary sugars (i.e. sucrose, glucose, and fructose) at both peripheral and central levels and their interactions will be critically discussed in order to improve our understanding of the effects of sugars on health and diseases. This will contribute to the development of more efficient strategies for the prevention and treatment for obesity and associated co-morbidities.This review highlights opposing effects of glucose and fructose on metabolism and eating behaviour. Peripheral glucose and fructose sensing may influence eating behaviour by sweet-tasting mechanisms in the mouth and gut, and by glucose-sensing mechanisms in the gut. Glucose may impact brain reward regions and eating behaviour directly by crossing the blood–brain barrier, and indirectly by peripheral neural input and by oral and intestinal sweet taste/sugar-sensing mechanisms, whereas those promoted by fructose orally ingested seem to rely only on these indirect mechanisms.Given the discrepancies between studies regarding the metabolic effects of sugars, more studies using physiological experimental conditions and in animal models closer to humans are needed. Additional studies directly comparing the effects of sucrose, glucose, and fructose should be performed to elucidate possible differences between these sugars on the reward circuitry.
Keywords: Dietary sugars; Gut–brain axis; Sugar sensing; Eating behaviour; Reward circuitry

The relation of diet with PAF and its metabolic enzymes in healthy volunteers by P. Detopoulou; E. Fragopoulou; T. Nomikos; M. Yannakoulia; G. Stamatakis; D. B. Panagiotakos; S. Antonopoulou (25-34).
Platelet-activating factor (PAF), a potent inflammatory mediator, is implicated in atherosclerosis. Its key biosynthetic enzymes are lyso-PAF acetyltransferases (lyso-PAF-AT), responsible for PAF synthesis through the remodeling route and a specific CDP-choline:1-alkyl-2-acetyl-sn-glycerol cholinephosphotransferase (PAF-CPT), responsible for its de novo biosynthesis. PAF acetylhydrolase (PAF-AH) and its extracellular isoform lipoprotein-associated phospholipase A2 catabolize PAF. The impact of diet on PAF metabolism is ill-defined. The aim was to investigate associations between PAF, its enzymes and dietary factors.One-hundred and six (n = 106) healthy volunteers were recruited. Food-frequency questionnaires, dietary recalls, lifestyle and biochemical variables were collected. Food groups, macronutrient intake, a priori (MedDietScore) and a posteriori defined food patterns with PCA analysis, dietary antioxidant capacity (DAC), glycemic index (GI) and glycemic load were assessed.PAF was inversely correlated with antioxidant-rich foods (herbal drinks and coffee), the DAC as well as a dietary pattern characterized by legumes, vegetables, poultry and fish (all Ps < 0.05). PAF was positively correlated to % fat intake. Lyso-PAF-AT was also negatively associated with healthy patterns (fruits, nuts and herbal drinks, and a pattern rich in olive oil and whole-wheat products), as well as the DAC and % monounsaturated fatty acids. PAF-CPT was negatively associated with GI and coffee intake and positively with dietary cholesterol. PAF-AH was negatively associated with coffee and positively associated with alcohol consumption (all Ps < 0.05).In conclusion, the DAC and healthy dietary patterns were inversely associated with PAF or its biosynthetic enzymes, suggesting potential new mechanisms of the diet–disease associations.
Keywords: Diet; PAF; Acetyl-CoA: lyso-PAF acetyltransferase; CDP-choline:1-alkyl-2-acetyl-sn-glycerol cholinephosphotransferase; PAF acetylhydrolase; Lp-PLA2

Exercise induces oxidative stress and causes adaptations in antioxidant defenses. The aim of the present study was to determine the effects of a 2-month diet supplementation with docosahexaenoic acid (DHA) on the pro-oxidant and antioxidant status of peripheral blood mononuclear cells (PBMCs) during football training and after acute exercise.Fifteen male football players, in a randomized double-blind trial, ingested a beverage enriched with DHA or a placebo for 8 weeks. Blood samples were collected in basal conditions before and after the training period and after an acute and intense exercise.The training season increased the carbonyl and nitrotyrosine index but decreased the malondialdehyde (MDA) levels. Basal catalase activity decreased in both groups after 8 weeks of training, whereas glutathione peroxidase activity increased mainly in the placebo group. Protein levels of uncoupling proteins (UCP2 and UCP3) and inducible nitric oxide synthase significantly increased after the training period. Acute exercise induced redistribution in the number of circulating cells, increased the MDA levels and nitrotyrosine index, and decreased the levels of nitrate. Acute exercise also increased PBMCs reactive oxygen species (ROS) production after immune stimulation. Diet supplementation with DHA significantly increased the UCP3 levels after training and the superoxide dismutase protein levels after acute exercise, and reduced the production of ROS after acute exercise.Docosahexaenoic acid increased the antioxidant capabilities while reducing the mitochondrial ROS production in a regular football training period and reduced the oxidative damage markers in response to acute exercise.
Keywords: DHA; PBMC; Oxidative stress; Exercise; ROS production

Hyperuricemia is a recognized risk factor for cardiovascular diseases. Soy foods contain a moderate amount of purine and may predispose to raised serum uric acid (UA). However, no study has examined the long-term effect of soy intake on UA levels. We examined whether consumption of soy foods and isoflavone extracts for 6 months altered serum UA.The analysis included two randomized controlled trials (soy protein trial and whole soy trial) among total 450 postmenopausal women with either prehypertension or prediabetes. We conducted a pooled analysis by combining participants from both the soy flour and soy protein groups (combined soy foods group), participants from both the isoflavone and daidzein groups (combined isoflavone group) and participants from both milk placebo groups. Fasting venous samples were obtained at baseline and the end of the trial for serum UA analysis.In the pooled data, 417 subjects completed the study according to protocol. The baseline serum UA levels were comparable among the three combined groups. There was a lower decrease in UA levels among women in the combined soy foods group compared with women in the other two groups (p = 0.028 and 0.026). The net decrease and % decrease in UA were 14.5 μmol/L (95 % CI 1.93–25.6, p = 0.023) or 4.9 % (95 % CI 1.3–8.5 %, p = 0.023) between the combined soy foods group and placebo group.Among Chinese postmenopausal women with either prehypertension or prediabetes, soy intake did not increase urate levels.
Keywords: Soy foods; Isoflavones; Uric acid

Dietary energy density is associated with obesity and other biomarkers of chronic disease in US adults by Jacqueline A. Vernarelli; Diane C. Mitchell; Barbara J. Rolls; Terryl J. Hartman (59-65).
Given the current prevalence of obesity, it is important to identify dietary factors that may aid in disease prevention. The objective of the present study was to evaluate the association between consumption of an energy-dense diet and established markers factors for chronic disease, including body weight and measures of body fatness. Data from a nationally representative sample of 9,551 adults ≥18 years who participated in the 2005–2008 National Health and Nutrition Examination Survey were analyzed. The association between dietary energy density (ED, energy per weight of food, kcal/g) and markers for obesity [including body mass index (BMI) and waist circumference (WC)], insulin insensitivity [including fasting glucose, insulin and homeostasis assessment model for insulin resistance (HOMA-IR)], and markers for inflammation was examined. Dietary ED was positively associated with obesity in both men and women in multivariate models. Overall, obese adults had a significantly higher dietary ED than lean adults (p < 0.0001). Current smokers had significantly higher ED than non-smokers (2.00 vs. 1.75, p < 0.01), and it was determined that smoking status modified the relationship between ED and weight status in women (p interaction 0.03). In both sexes, there was a positive linear relationship between BMI and ED (p trend 0.01 and 0.0002, respectively); a linear trend between WC and ED was also observed in women (p trend <0.001) after adjusting for relevant cofactors. In women, ED was positively associated with HOMA-IR and fasting insulin; though, this relationship was not observed in men. No significant associations between ED and C-reactive protein were observed in either sex.These findings support recent obesity and disease prevention recommendations to consume a diet low in ED.
Keywords: Energy density; NHANES; Waist circumference; BMI; Obesity

Long-term adherence to the New Nordic Diet and the effects on body weight, anthropometry and blood pressure: a 12-month follow-up study by Sanne Kellebjerg Poulsen; Charlotte Crone; Arne Astrup; Thomas Meinert Larsen (67-76).
The New Nordic Diet (NND) has induced weight loss in a 26-week controlled intervention. We aim to investigate whether high compliance and satisfaction can be maintained after the active intervention is discontinued thereby maintaining the health effects.After 26 weeks of intervention with NND or Average Danish Diet (ADD), 147 participants (mean age 43 years and mean BMI 29.1 kg/m2) were followed for further 52 weeks. All participants were encouraged to follow NND but without further guidance. The study is registered with ClinicalTrials.gov, study id NCT01195610.One hundred and ten participants (75 %) completed the follow-up. Among participants previously randomised to NND (NND group), dietary compliance and satisfaction decreased from 4.3 to 3.0 and from 4.8 to 4.0, respectively (both p < 0.0001) (1–5 point scale). Among those originally randomised to ADD (ADD group), satisfaction with NND was significantly higher than with ADD during follow-up (3.3 vs. 2.5, p = 0.026). Weight losses during intervention of −6.2 kg and −3.0 kg were followed by regains of 4.6 kg (SE 0.5) and 1.1 kg (SE 0.7) for the NND group and ADD group, respectively [adjusted difference; mean (95 % CI): 1.8 kg (0.1–3.4), p = 0.041]. Across diet groups, every 1 score higher in compliance with NND was associated with 0.90 kg less body weight regain (p = 0.026) and those who increased physical activity regained 3.4 kg less compared to those who did not (p < 0.0001).NND provides higher satisfaction, and body weight regain is reduced with higher compliance with NND and increased physical activity.
Keywords: New Nordic Diet; Dietary intervention; Weight loss maintenance; Follow-up; Compliance

Fermenting soybeans with Bacillus licheniformis potentiates their capacity to improve cognitive function and glucose homeostaisis in diabetic rats with experimental Alzheimer’s type dementia by Hye Jeong Yang; Dae Young Kwon; Hyun Jin Kim; Min Jung Kim; Do Yeon Jung; Hee Joo Kang; Da Sol Kim; Suna Kang; Na Rang Moon; Bae Keun Shin; Sunmin Park (77-88).
Brain insulin resistance is related to both diabetes and Alzheimer’s disease. We investigated whether both chungkookjangs, soybeans fermented in a traditional method (TFC) and with Bacillus lichenifomis (SFC), can protect against cognitive dysfunction and glucose dysregulation in rats with Alzheimer’s disease and type 2 diabetes.Partial pancreatectomy (Px) and ICV β-amyloid (25–35) infusion into the CA1 region were fed either control diet (AD–CON), 10 % cooked soybeans (CSB), 10 % TFC, or 10 % SFC in a high fat diet for 8 weeks. Px rats infused β-amyloid (35–25) as a normal-control group (Non-AD–CON).SFC increased isoflavonoid aglycones, DDMP soyasaponin βg, E soyasaponin Be and lysoposphatidylcholines in comparison to CSB. SFC markedly decreased its accumulation in β-amyloid deposition in AD rats and improved hippocampal insulin signaling (pAkt → pGSK → pTau) that exacerbated in AD–CON rats. AD rats markedly impaired cognitive function than Non-AD–CON rats as measured by a water maze and passive avoidance tests while the disturbance was prevented in an ascending order of CON < CSB and TFC < SFC. In comparison to Non-AD rats, AD–CON rats lowered whole body glucose infusion rates and increased hepatic glucose output at hyperinsulinemic state during euglycemic hyperinsulinemic clamp which SFC normalized in AD rats. Interestingly, insulin secretion, especially at the second phase during hyperglycemic clamp, was higher in AD–CON rats, compared to Non-AD rats while CSB, TFC, SFC lowered it in AD-rats. However, SFC restored β-cell mass in AD rats that reduced β-cell mass by increased β-cell apoptosis.β-Amyloid accumulation in the hippocampus exacerbated insulin resistance and decreased β-cell mass and SFC prevented their exacerbation in AD diabetic rats.
Keywords: Alzheimer’s disease; Cognitive function; Memory; Glucose homeostasis; Insulin secretion; β-Cell mass

Prebiotic effect during the first year of life in healthy infants fed formula containing GOS as the only prebiotic: a multicentre, randomised, double-blind and placebo-controlled trial by Carlos Sierra; María-José Bernal; Javier Blasco; Rosario Martínez; Jaime Dalmau; Inmaculada Ortuño; Beatriz Espín; María-Isabel Vasallo; David Gil; María-Luisa Vidal; Dámaso Infante; Rosaura Leis; José Maldonado; José-Manuel Moreno; Enriqueta Román (89-99).
Currently, there is no consensus concerning the possible beneficial colonic and systemic effects of prebiotic-containing infant formula. This study assesses whether the feeding of a galactooligosaccharides (GOS)-containing infant formula (0.44 g/dl of GOS) and the subsequent feeding of a GOS-containing follow-on formula (0.50 g/dl of GOS) have a prebiotic effect on intestinal microbiota that helps to decrease infections and allergy manifestations in healthy infants during the first year of life.A multicentre, randomised, double-blind and placebo-controlled trial was carried out on 365 healthy term infants enrolled before 8 weeks of age and randomly assigned to a formula with or without GOS, until 12 months of age. The incidence of infections and allergy manifestations, the antibiotics prescribed and faecal characteristics were recorded up to 12 months of age, while faecal samples were collected up to 4 months for the measurement of secretory immunoglobulin A, short-chain fatty acids and microbiota.A prebiotic effect on the faecal analysis was observed at 4 months of life. The GOS group showed a lower faecal pH (P = 0.019), a lower decreasing trend in secretory immunoglobulin A (P = 0.078), lower butyric acid concentration (P = 0.040) and an increase in Bifidobacterium counts (P = 0.010). Changes in faecal characteristics involved greater frequency (P < 0.001) and softer consistency (P < 0.05). The incidence of infections or allergic manifestations during the first year of life was similar in both groups, with no statistical differences (P > 0.05).The feeding of GOS-containing infant formula produced a definite prebiotic effect consisting of changes in faecal composition and microbiota, and in faecal consistency and the frequency of defaecation. No changes in the incidence of infection or allergic manifestation during the first year of life were observed.
Keywords: Clinical trial; Prebiotics; Infant nutrition; Infant formula; Randomised double-blind, placebo-controlled study

Recent data suggest that chronic low-grade inflammation, a characteristic of obesity, is associated with altered tryptophan (Trp) and tyrosine (Tyr) metabolism and plays a role in neuropsychiatric symptoms. The present study assessed the effect of an extreme short-term diet on Trp breakdown and inflammatory biomarkers in overweight adults.Thirty-eight overweight participants (16 women, 22 men; average body mass index: 29 kg/m2, mean age 52.8 years) were randomized into two diet groups: a very low kcal diet group (VLCD; Ø 600 kcal/day, n = 21) and a low kcal diet group (LCD; Ø 1,200 kcal/day, n = 17). Assays included the measurement of Trp, kynurenine (Kyn), and their ratio, neopterin, phenylalanine (Phe), Tyr, as biologic markers; leptin, plasma insulin, glucose, and homeostatic model assessment-insulin resistance; and interleukin 6, tumor necrosis factor alpha, and C-reactive protein, as biochemical and inflammatory markers at baseline and after 2 weeks of treatment.Weight loss diet lowered leptin levels in both groups by 46 %, although not reaching significance. Trp and Kyn decreased significantly by 21 and 16 % for VLCD and by 15 and 17 % for the LCD group, respectively. A significant reduction in Phe was only seen after VLCD. Inflammatory biomarkers, neopterin, and Tyr were not significantly altered during the study period. Leptin was significantly correlated with Trp breakdown before and after the intervention (P < 0.02).Since disturbed metabolism of Trp affects biosynthesis of serotonin and might be associated with increased susceptibility for mood disturbances and carbohydrate craving, strategies to supplement Trp while dieting could be highly useful in treating uncontrolled weight gain or in preventing neuropsychiatric symptoms.
Keywords: Diet; Leptin; Tryptophan; Inflammation; Mood

Protective effects of l-alpha-glycerylphosphorylcholine on ischaemia–reperfusion-induced inflammatory reactions by Tünde Tőkés; Eszter Tuboly; Gabriella Varga; László Major; Miklós Ghyczy; József Kaszaki; Mihály Boros (109-118).
Choline-containing dietary phospholipids, including phosphatidylcholine (PC), may function as anti-inflammatory substances, but the mechanism remains largely unknown. We investigated the effects of l-alpha-glycerylphosphorylcholine (GPC), a deacylated PC derivative, in a rodent model of small intestinal ischaemia–reperfusion (IR) injury.Anaesthetized Sprague-Dawley rats were divided into control, mesenteric IR (45 min mesenteric artery occlusion, followed by 180 min reperfusion), IR with GPC pretreatment (16.56 mg kg−1 GPC i.v., 5 min prior to ischaemia) or IR with GPC post-treatment (16.56 mg kg−1 GPC i.v., 5 min prior to reperfusion) groups. Macrohaemodynamics and microhaemodynamic parameters were measured; intestinal inflammatory markers (xanthine oxidoreductase activity, superoxide and nitrotyrosine levels) and liver ATP contents were determined.The IR challenge reduced the intestinal intramural red blood cell velocity, increased the mesenteric vascular resistance, the tissue xanthine oxidoreductase activity, the superoxide production, and the nitrotyrosine levels, and the ATP content of the liver was decreased. Exogenous GPC attenuated the macro- and microcirculatory dysfunction and provided significant protection against the radical production resulting from the IR stress. The GPC pretreatment alleviated the hepatic ATP depletion, the reductions in the mean arterial pressure and superior mesenteric artery flow, and similarly to the post-treatments with GPC, also decreased the xanthine oxidoreductase activity, the intestinal superoxide production, the nitrotyrosine level, and normalized the microcirculatory dysfunction.These data demonstrate the effectiveness of GPC therapies and provide indirect evidence that the anti-inflammatory effects of PC could be linked to a reaction involving the polar part of the molecule.
Keywords: Rat; Mesenteric ischaemia–reperfusion; Inflammatory mediators; Oxidative stress; Nitrosative stress; Microcirculation

Human milk composition differs in healthy mothers and mothers with celiac disease by Marta Olivares; Simone Albrecht; Giada De Palma; María Desamparados Ferrer; Gemma Castillejo; Henk A. Schols; Yolanda Sanz (119-128).
To investigate whether breast-milk composition and microbiota differ in healthy mothers and mothers with celiac disease (CD) to ultimately contribute to identify additional factors determining CD risk.Breast-milk samples from healthy mothers (n = 12) and mothers with CD (n = 12) were collected. Cytokines and secretory immunoglobulin A (sIgA) were analyzed by bead-arrays and flow cytometry and human milk oligosaccharides (HMOs) were assessed by capillary electrophoresis with laser-induced fluorescence (CE-LIF) detection. Breast-milk microbiota composition was analyzed by conventional and quantitative real-time PCR. Breast milk from CD mothers showed significantly lower levels of interleukin (IL) 12p70 (P < 0.042), transforming growth factor (TGF)-β1 (P < 0.018) and sIgA (P < 0.003) and almost significantly lower levels of interferon (IFN)-γ (P < 0.058). Six mothers in each group belonged to the secretor Le(a−b+) type, one to the secretor Le(a−b−) type and five to the non-secretor Le(a+b−) type. CD mothers of non-secretor Le(a+b−) type showed increased Lacto-N-tetraose content (P < 0.042) compared with healthy mothers. CD mothers’ milk showed reduced gene copy numbers of Bifidobacterium spp. (P < 0.026) and B. fragilis group (P < 0.044).CD mothers’ breast milk is characterized by a reduced abundance of immunoprotective compounds (TGF-β1 and sIgA) and bifidobacteria. The reduction in these components could theoretically diminish the protective effects of breast-feeding on the child’s future risk of developing CD.
Keywords: Celiac disease; Human milk; Immunity; Microbiota

Formula-feeding is associated with shift towards Th1 cytokines by Beate Winkler; Julia Aulenbach; Thomas Meyer; Armin Wiegering; Matthias Eyrich; Paul-Gerhardt Schlegel; Verena Wiegering (129-138).
Breast-feeding (BF) versus formula-feeding (FF) may be a factor for the development and differentiation of T-cell subsets and cytokine production in infancy and childhood. We therefore investigated T-cell subpopulations and their cytokine production by flow cytometry as well as cytokine levels in serum samples in breast-fed versus formula-fed infants and children.Heparinised blood was taken from 191 healthy infants and children. Peripheral blood mononuclear cells were stimulated with phorbol-mystriate-acetate and ionomycin in the presence of brefeldin. T-cell subsets and cytokines were determined by flow cytometry. Furthermore, serum concentrations of IFNγ and IL4 were measured using ELISA. An IFNγ/IL4 ratio was calculated to estimate the Th1/Th2 balance. Children who were formula-fed show higher numbers of memory T and T helper cells. After stimulation, the number of IFNγ-positive memory T-cells was increased up to the age of 6 years. Breast-fed infants show higher percentages of IL4-positive T helper cells. At ELISA determination, formula-fed children showed higher IFNγ levels than breast-fed children, while IL4 levels did not differ. The IFNγ/IL4 ratio (FACS and ELISA) was elevated in formula-fed infants and children.This systematic analysis of cytokine profiles during childhood in dependency of BF allows a better understanding of immune maturation and demonstrates the influence of early feeding on immune function throughout childhood, even after cessation of BF. FF induces a shift towards Th1 cytokines in children. This may have an influence on the development of autoimmune disease in later life.
Keywords: Breast-feeding; Cytokines; Th1/Th2; Flow cytometry

Mediterranean diet and mortality in Switzerland: an alpine paradox? by Kerstin Vormund; Julia Braun; Sabine Rohrmann; Matthias Bopp; Peter Ballmer; David Faeh (139-148).
Reports on the protective effect of a Mediterranean diet on mortality usually refer to populations from Mediterranean countries, leaving uncertain whether really diet is the fundamental cause. Our aim was to examine the effect of a Mediterranean diet on mortality in Switzerland, a country combining cultural influences from Mediterranean and Central European countries within a common national health and statistical registry.In this prospective investigation, we included 17,861 men and women aged ≥16 years who participated 1977–1993 in health studies and were followed up for survival until 2008 by anonymous record linkage with the Swiss National Cohort. A 9-point score Mediterranean Diet Score (MDS) was used to assess adherence to a Mediterranean diet. Mortality hazard ratios (HR) and 95 % confidence intervals (CIs) were calculated by using Cox regression models adjusted for age, sex, survey wave, marital status, smoking, body mass index, language region and nationality.In all language regions, MDS was inversely associated with mortality. Consumption of dairy products was also consistently associated with lower mortality. When categorizing dairy food consumption as beneficial instead of harmful, this association between MDS and mortality increased in strength and was partly statistically significant. For all causes of death combined (HR for a one-point increase in MDS 0.96, 95 % CI 0.94–0.98), in men (0.94, 0.92–0.97), in women (0.98, 0.95–1.02) for cardiovascular diseases (CVD, 0.96, 0.92–0.99; 0.95, 0.90–1.00; 0.98, 0.92–1.04) and for cancer (0.95, 0.92–0.99; 0.92, 0.88–0.97; 0.98, 0.93–1.04).Stronger adherence to a Mediterranean diet was associated with lower all-cause, CVD and cancer mortality, largely independently of cultural background. These associations were primary due to the effect in men. Our finding of a beneficial rather than a deleterious impact of dairy products consumption prompts at considering culturally adapted Mediterranean diet recommendations. However, results should be interpreted with caution since only a crude 1-day dietary estimate was available to assess individuals’ habitual dietary intake.
Keywords: Mediterranean diet; Alpine paradox; Dairy food; Mortality; Switzerland

Consumption of a dark roast coffee decreases the level of spontaneous DNA strand breaks: a randomized controlled trial by T. Bakuradze; R. Lang; T. Hofmann; G. Eisenbrand; D. Schipp; J. Galan; E. Richling (149-156).
Coffee consumption has been reported to decrease oxidative damage in peripheral white blood cells (WBC). However, effects on the level of spontaneous DNA strand breaks, a well established marker of health risk, have not been specifically reported yet. We analyzed the impact of consuming a dark roast coffee blend on the level of spontaneous DNA strand breaks.Healthy men (n = 84) were randomized to consume daily for 4 weeks either 750 ml of fresh coffee brew or 750 ml of water, subsequent to a run in washout phase of 4 weeks. The study coffee was a blend providing high amounts of both caffeoylquinic acids (10.18 ± 0.33 mg/g) and the roast product N-methylpyridinium (1.10 ± 0.05 mg/g). Before and after the coffee/water consumption phase, spontaneous strand breaks were determined by comet assay.At baseline, both groups exhibited a similar level of spontaneous DNA strand breaks. In the intervention phase, spontaneous DNA strand breaks slightly increased in the control (water only) group whereas they significantly decreased in the coffee group, leading to a 27 % difference within both arms (p = 0.0002). Food frequency questionnaires indicated no differences in the overall diet between groups, and mean body weight during the intervention phases remained stable. The consumption of the study coffee substantially lowered the level of spontaneous DNA strand breaks in WBC.We conclude that regular coffee consumption contributes to DNA integrity.
Keywords: Antioxidants; Coffee; Comet assay; Intervention study; DNA strand breaks

In his offered opinion piece, (Dietary glycaemic load and cognitive performance in elderly subjects) Dr. Kawada comments upon the statistical analysis and suggests that the conclusions of the study should be interpreted with caution. Having closely examined these comments, we believe that they are over-stated and we draw different conclusions. At first viewing, the statistical arguments put forward by Dr. Kawada look complicated, but one may summarize that he believes the analysis lacked statistical power. This argument is directed towards two sets of regression analyses, a Poisson analysis on which one of the messages of the paper hinges, and a second logistic analysis that was acknowledged as statistically underpowered in our publication. No statistical argument is provided as to why the Poisson regression model is underpowered; the critique contains no new scientific content but relies on a technical re-iteration of the limitations of the study (that were highlighted in the original manuscript) combined with quasi philosophical arguments on data set size and the need for biochemical markers in observational dietary studies.