Repositioning of the global epicentre of non-optimal cholesterol

High blood cholesterol is typically considered a feature of wealthy western countries1,2. However, dietary and behavioural determinants of blood cholesterol are changing rapidly throughout the world3 and countries are using lipid-lowering medications at varying rates. These changes can have distinct effects on the levels of high-density lipoprotein (HDL) cholesterol and non-HDL cholesterol, which have different effects on human health4,5. However, the trends of HDL and non-HDL cholesterol levels over time have not been previously reported in a global analysis. Here we pooled 1,127 population-based studies that measured blood lipids in 102.6 million individuals aged 18 years and older to estimate trends from 1980 to 2018 in mean total, non-HDL and HDL cholesterol levels for 200 countries. Globally, there was little change in total or non-HDL cholesterol from 1980 to 2018. This was a net effect of increases in low- and middle-income countries, especially in east and southeast Asia, and decreases in high-income western countries, especially those in northwestern Europe, and in central and eastern Europe. As a result, countries with the highest level of non-HDL cholesterol—which is a marker of cardiovascular risk—changed from those in western Europe such as Belgium, Finland, Greenland, Iceland, Norway, Sweden, Switzerland and Malta in 1980 to those in Asia and the Pacific, such as Tokelau, Malaysia, The Philippines and Thailand. In 2017, high non-HDL cholesterol was responsible for an estimated 3.9 million (95% credible interval 3.7 million–4.2 million) worldwide deaths, half of which occurred in east, southeast and south Asia. The global repositioning of lipid-related risk, with non-optimal cholesterol shifting from a distinct feature of high-income countries in northwestern Europe, north America and Australasia to one that affects countries in east and southeast Asia and Oceania should motivate the use of population-based policies and personal interventions to improve nutrition and enhance access to treatment throughout the world.</p

Repositioning of the global epicentre of non-optimal cholesterol

High blood cholesterol is typically considered a feature of wealthy western countries1,2. However, dietary and behavioural determinants of blood cholesterol are changing rapidly throughout the world3 and countries are using lipid-lowering medications at varying rates. These changes can have distinct effects on the levels of high-density lipoprotein (HDL) cholesterol and non-HDL cholesterol, which have different effects on human health4,5. However, the trends of HDL and non-HDL cholesterol levels over time have not been previously reported in a global analysis. Here we pooled 1,127 population-based studies that measured blood lipids in 102.6 million individuals aged 18 years and older to estimate trends from 1980 to 2018 in mean total, non-HDL and HDL cholesterol levels for 200 countries. Globally, there was little change in total or non-HDL cholesterol from 1980 to 2018. This was a net effect of increases in low- and middle-income countries, especially in east and southeast Asia, and decreases in high-income western countries, especially those in northwestern Europe, and in central and eastern Europe. As a result, countries with the highest level of non-HDL cholesterol�which is a marker of cardiovascular risk�changed from those in western Europe such as Belgium, Finland, Greenland, Iceland, Norway, Sweden, Switzerland and Malta in 1980 to those in Asia and the Pacific, such as Tokelau, Malaysia, The Philippines and Thailand. In 2017, high non-HDL cholesterol was responsible for an estimated 3.9 million (95 credible interval 3.7 million�4.2 million) worldwide deaths, half of which occurred in east, southeast and south Asia. The global repositioning of lipid-related risk, with non-optimal cholesterol shifting from a distinct feature of high-income countries in northwestern Europe, north America and Australasia to one that affects countries in east and southeast Asia and Oceania should motivate the use of population-based policies and personal interventions to improve nutrition and enhance access to treatment throughout the world. © 2020, The Author(s), under exclusive licence to Springer Nature Limited

Rising rural body-mass index is the main driver of the global obesity epidemic in adults

Body-mass index (BMI) has increased steadily in most countries in parallel with a rise in the proportion of the population who live in cities 1,2 . This has led to a widely reported view that urbanization is one of the most important drivers of the global rise in obesity 3�6 . Here we use 2,009 population-based studies, with measurements of height and weight in more than 112 million adults, to report national, regional and global trends in mean BMI segregated by place of residence (a rural or urban area) from 1985 to 2017. We show that, contrary to the dominant paradigm, more than 55 of the global rise in mean BMI from 1985 to 2017�and more than 80 in some low- and middle-income regions�was due to increases in BMI in rural areas. This large contribution stems from the fact that, with the exception of women in sub-Saharan Africa, BMI is increasing at the same rate or faster in rural areas than in cities in low- and middle-income regions. These trends have in turn resulted in a closing�and in some countries reversal�of the gap in BMI between urban and rural areas in low- and middle-income countries, especially for women. In high-income and industrialized countries, we noted a persistently higher rural BMI, especially for women. There is an urgent need for an integrated approach to rural nutrition that enhances financial and physical access to healthy foods, to avoid replacing the rural undernutrition disadvantage in poor countries with a more general malnutrition disadvantage that entails excessive consumption of low-quality calories. © 2019, The Author(s)

Do unfavourable working conditions explain mental health inequalities between ethnic groups?: cross-sectional data of the HELIUS study

Contains fulltext : 155053.pdf (publisher's version ) (Open Access)BACKGROUND: Ethnic inequalities in mental health have been found in many high-income countries. The purpose of this study is to test whether mental health inequalities between ethnic groups are mediated by exposure to unfavourable working conditions. METHODS: Workers (n = 6278) were selected from baseline data of the multi-ethnic HELIUS study. Measures included two indices of unfavourable working conditions (lack of recovery opportunities, and perceived work stress), and two mental health outcomes (generic mental health: MCS-12 and depressive symptoms: PHQ-9). Mediation of the relationships between ethnicity and mental health by unfavourable working conditions was tested using the bias-corrected bootstrap confidence intervals technique. Linear models with and without the mediators included, and adjusted for gender and age. Attenuation was calculated as the change in B between the models with and without mediators. RESULTS: The sample comprised Dutch (1355), African Surinamese (1290), South-Asian Surinamese (1121), Turkish (1090), Ghanaian (729), and Moroccan (693) workers. After controlling for age and gender, all ethnic minorities had a higher risk of mental health problems as compared to the Dutch host population, with the exception of Ghanaians in the case of depressive symptoms, and African Surinamese workers with regard to both outcomes. The Turkish group stands out with the lowest mental health on both mental health indices, followed by Moroccan and South-Asian Surinamese workers. A lack of recovery opportunities mediated the relationship between ethnic group and a higher risk of mental health problems. Perceived work stress did not contribute to the explanation of ethnic inequalities. CONCLUSIONS: The higher risk of mental health problems in ethnic minority groups can be partly accounted for by a lack of recovery opportunities at work, but not by perceived work stress. This may imply that workplace prevention targeting recovery opportunities have the potential to reduce ethnic inequalities, but ethnic-specific experiences at the workplace need to be further explored

Hoe bereik je jongeren als het over groente gaat? : Communiceren over groente als ingrediënt met de 'digital natives'

In het zesde nummer van Voeding Nu vorig jaar werd beschreven hoe groenterijke snacks door jongeren gewaardeerd werden na introductie in schoolkantines (1). Een belangrijke vraag die hierbij naar boven kwam is: hoe communiceer je met jongeren over groente en groenterijke producten? Ook dit is onderzocht binnen het project Groente als Ingrediënt van Wageningen Food & Biobased Research en HAS Hogeschool Den Bosch (2)

Structural and kinetic studies on ligand binding in wild-type and active-site mutants of penicillin acylase

Penicillin acylase catalyses the condensation of Cα-substituted phenylacetic acids with β-lactam nucleophiles, producing semi-synthetic β-lactam antibiotics. For efficient synthesis a low affinity for phenylacetic acid and a high affinity for Cα-substituted phenylacetic acid derivatives is desirable. We made three active site mutants, αF146Y, βF24A and αF146Y/βF24A, which all had a 2- to 10-fold higher affinity for Cα-substituted compounds than wild-type enzyme. In addition, βF24A had a 20-fold reduced affinity for phenylacetic acid. The molecular basis of the improved properties was investigated by X-ray crystallography. These studies showed that the higher affinity of αF146Yfor (R)-α-methylphenylacetic acid can be explained by van der Waals interactions between αY146:OH and the Ca-substituent. The βF24A mutation causes an opening of the phenylacetic acid binding site. Only (R)-α-methylphenylacetic acid, but not phenylacetic acid, induces a conformation with the ligand tightly bound, explaining the weak binding of phenylacetic acid. A comparison of the βF24A structure with other open conformations of penicillin acylase showed that βF24 has a fixed position, whereas αF146 acts as a flexible lid on the binding site and reorients its position to achieve optimal substrate binding.

Socio-economic status and ethnicity are independently associated with dietary patterns: The HELIUS-Dietary Patterns study

10.3402/fnr.v59.26317Food and Nutrition Research592631

6 '-beta-fluoro-homoaristeromycin and 6 '-fluoro-homoneplanocin a are potent inhibitors of Chikungunya virus replication through their direct effect on viral nonstructural protein 1

Alphaviruses are arthropod-borne, positive-stranded RNA viruses capable of causing severe disease with high morbidity. Chikungunya virus (CHIKV) is an alphavirus that causes a febrile illness which can progress into chronic arthralgia. The current lack of vaccines and specific treatment for CHIKV infection underscores the need to develop new therapeutic interventions. To discover new antiviral agents, we performed a compound screen in cell culture-based infection models and identified two carbocyclic adenosine analogues, 6'beta-fluoro-homoaristeromycin (FHA) and 6'-fluoro-homoneplanocin A (FHNA), that displayed potent activity against CHIKV and Semliki Forest virus (SFV) with 50% effective concentrations in the nanomolar range at nontoxic concentrations. The compounds, designed as inhibitors of the host enzyme S-adenosylhomocysteine (SAH) hydrolase, impeded postentry steps in CHIKV and SFV replication. Selection of FHNA-resistant mutants and reverse genetics studies demonstrated that the combination of mutations G230R and K299E in CHIKV nonstructural protein 1 (nsP1) conferred resistance to the compounds. Enzymatic assays with purified wild-type (wt) SFV nsP1 suggested that an oxidized (3'-keto) form, rather than FHNA itself, directly inhibited the MTase activity, while a mutant protein with the K231R and K299E substitutions was insensitive to the compound. Both wt nsP1 and the resistant mutant were equally sensitive to the inhibitory effect of SAH. Our combined data suggest that FHA and FHNA inhibit CHIKV and SR/ replication by directly targeting the MTase activity of nsP1, rather than through an indirect effect on host SAH hydrolase. The high potency and selectivity of these novel alphavirus mRNA capping inhibitors warrant further preclinical investigation of these compounds