This study evaluated the feasibility and safety of a telehealth delivered exercise plus plant-based protein diet in adults with non-alcoholic fatty liver disease (NAFLD). This was a 12-week, randomised controlled feasibility trial including twenty-eight adults aged > 45 years with NAFLD randomised to a home muscle strengthening program (3 d/week) with increased protein intake (target ∼1·2–1·5 g/kg/d) from predominately plant-based sources and behavioural change support (3–4 text messages/week) (Pro-Ex n 14) or usual care (UC, n 14). Feasibility was assessed via retention (≤ 10 % attrition), adherence (exercise ≥ 66 %; recommended daily protein serves ≥ 80 %) and safety (adverse events). Secondary outcomes included macronutrient intake (3 × 24-h records), weight, moderate-to-vigorous physical activity (MVPA) and 30 s sit-to-stand (STS) performance. Study retention was 89 %. Mean exercise adherence (Pro-Ex) was 52 % with one adverse event from 241 sessions. In Pro-Ex, mean daily plant protein serves increased (0·9 to 1·4/d) and animal protein decreased (1·5 to 1·2/d) after 12-weeks, but overall adherence (serves/day) was 32[RD1] % (plant) and 42 % (animal). Relative to UC, Pro-Ex experienced a mean 2·7 (95 % CI: 0·9, 4·4) increase in 30 s STS number, 46-minute (95 % CI: −153, 245) increase in MVPA, 1·7 kg (95 % CI: −3·5, 0·2) decrease in weight, 35·2 g (95 % CI: 11·0, 59·3) increase in protein. In adults with NAFLD a telehealth home exercise and dietary intervention was safe and improved habitual plant and animal protein intake, but overall adherence was modest suggesting more intensive healthcare support may be required.

Olive oil (OO) polyphenols have been shown to improve HDL anti-atherogenic function, thus demonstrating beneficial effects against cardiovascular risk factors. The aim of the present study was to investigate the effect of extra virgin high polyphenol olive oil (HPOO) v. low polyphenol olive oil (LPOO) on the capacity of HDL to promote cholesterol efflux in healthy adults. In a double-blind, randomised cross-over trial, fifty participants (aged 38·5 (sd 13·9) years, 66 % females) were supplemented with a daily dose (60 ml) of HPOO (320 mg/kg polyphenols) or LPOO (86 mg/kg polyphenols) for 3 weeks. Following a 2-week washout period, participants crossed over to the alternate treatment. Serum HDL-cholesterol efflux capacity, circulating lipids (i.e. total cholesterol, TAG, HDL, LDL) and anthropometrics were measured at baseline and follow-up. No significant between-group differences were observed. Furthermore, no significant changes in HDL-cholesterol efflux were found within either the LPOO and HPOO treatment arms; mean changes were 0·54 % (95 % CI (0·29, 1·37)) and 0·10 % (95 % CI (0·74, 0·94)), respectively. Serum HDL increased significantly after LPOO and HPOO intake by 0·13 mmol/l (95 % CI (0·04, 0·22)) and 0·10 mmol/l (95 % CI (0·02, 0·19)), respectively. A small but significant increase in LDL of 0·14 mmol/l (95 % CI (0·001, 0·28)) was observed following the HPOO intervention. Our results suggest that additional research is warranted to further understand the effect of OO with different phenolic content on mechanisms of cholesterol efflux via different pathways in multi-ethnic populations with diverse diets.

Individuals with discordantly high apoB to LDL-cholesterol levels carry a higher risk of atherosclerotic CVD compared with those with average or discordantly low apoB to LDL-cholesterol. We aimed to determine associations between apoB and LDL-cholesterol discordance in relation to nutrient patterns (NP) using National Health and Nutrition Examination Survey data. Participants were grouped by established LDL-cholesterol and apoB cut-offs (Group 1: low apoB/low LDL-cholesterol, Group 2: low apoB/high LDL-cholesterol, Group 3: high apoB/low LDL-cholesterol, Group 4: high apoB/high LDL-cholesterol). Principle component analysis was used to define NP. Machine learning (ML) and structural equation models were applied to assess associations of nutrient intake with apoB/LDL-cholesterol discordance using the combined effects of apoB and LDL-cholesterol. Three NP explained 63·2 % of variance in nutrient consumption. These consisted of NP1 rich in SFA, carbohydrate and vitamins, NP2 high in fibre, minerals, vitamins and PUFA and NP3 rich in dietary cholesterol, protein and Na. The discordantly high apoB to LDL-cholesterol group had the highest consumption of the NP1 and the lowest consumption of the NP2. ML showed nutrients that had the greatest unfavourable dietary contribution to individuals with discordantly high apoB to LDL-cholesterol were total fat, SFA and thiamine and the greatest favourable contributions were MUFA, folate, fibre and Se. Individuals with discordantly high apoB in relation to LDL-cholesterol had greater adherence to NP1, whereas those with lower levels of apoB, irrespective of LDL-cholesterol, were more likely to consume NP3.

We explored the role of lipid accumulation products and visceral adiposity on the association between red meat consumption (RMC) and markers of insulin resistance (IR) and inflammation in USA adults. Data on RMC and health outcome measurements were extracted from the 2005–2010 US National Health and Nutrition Examination Surveys. Overall 16 621 participants were included in the analysis (mean age = 47·1 years, 48·3 % men). ANCOVA and ‘conceptus causal mediation’ models were applied while accounting for survey design. In adjusted models, a lower RMC was significantly associated with a cardio-protective profile of IR and inflammation. BMI had significant mediation effects on the association between RMC and C-reactive protein (CRP), apo B, fasting blood glucose (FBG), insulin, homoeostatic model assessment of IR and β-cell function, glycated Hb (HbA1c), TAG:HDL ratio and TAG glucose (TyG) index (all Ps < 0·05). Both waist circumference and anthropometrically predicted visceral adipose tissue mediated the association between RMC and CRP, FBG, HbA1c, TAG:HDL ratio and TyG index (all Ps < 0·05). Our findings suggest that adiposity, particularly the accumulation of abdominal fat, accounts for a significant proportion of the associations between red meat consumption, IR and inflammation.

No data exist on the associations of dietary tomato and lycopene consumption with total and cause-specific mortality. Using the National Health and Nutrition Examination Surveys 1999–2010, we evaluted the long-term impact of tomato and lycopene intake on total and cause-specific (CHD and cerebrovascular disease) mortality. We also assessed the changes in cardio-metabolic risk factors according to tomato and lycopene intake. Vital status to 31 December 2011 was ascertained. Cox proportional hazard regression models (followed by propensity score matching) were used to investigate the link between tomato and lycopene consumption total, CHD and cerebrovascular mortality. Among the 23 935 participants included (mean age = 47·6 years, 48·8 % men), 3403 deaths occurred during 76·4 months of follow-up. Tomato intake was inversely associated with total (risk ratio (RR) 0·86, 95 % CI 0·81, 0·92), CHD (RR 0·76, 95 % CI 0·70, 0·85) and cerebrovascular (RR 0·70, 95 % CI 0·62, 0·81) mortality. Similar inverse associations were found between lycopene consumption, total (RR 0·76, 95 % CI 0·72, 0·81), CHD (RR 0·73, 95 % CI 0·65, 0·83) and cerebrovascular (RR 0·71, 95 % CI 0·65, 0·78) mortality; these associations were independent of anthropometric, clinical and nutritional parameters. Age and obesity did not affect the association of tomato and lycopene consumption with total, CHD and cerebrovascular mortality. C-reactive protein significantly moderated the link between lycopene and tomato intake with total, CHD and cerebrovascular mortality. ANCOVA showed that participants with a higher tomato and lycopene consumption had a more cardio-protective profile compared with those with a lower intake. Our results highlighted the favourable effect of tomato and lycopene intake on total and cause-specific mortality as well as on cardio-metabolic risk factors. These findings should be taken into consideration for public health strategies.