“Metabolic damage is a term that has been used in certain fitness and weight loss sectors, but it’s not a recognised medical condition or term used by healthcare professionals.”
Belgique Dernières Nouvelles, Belgique Actualités
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Body mass index and all-cause mortality in a 21st century U.S. population: A National Health Interview Survey analysisIntroduction Much of the data on BMI-mortality associations stem from 20th century U.S. cohorts. The purpose of this study was to determine the association between BMI and mortality in a contemporary, nationally representative, 21st century, U.S. adult population. Methods This was a retrospective cohort study of U.S. adults from the 1999–2018 National Health Interview Study (NHIS), linked to the National Death Index (NDI) through December 31st, 2019. BMI was calculated using self-reported height & weight and categorized into 9 groups. We estimated risk of all-cause mortality using multivariable Cox proportional hazards regression, adjusting for covariates, accounting for the survey design, and performing subgroup analyses to reduce analytic bias. Results The study sample included 554,332 adults (mean age 46 years [SD 15], 50% female, 69% non-Hispanic White). Over a median follow-up of 9 years (IQR 5–14) and maximum follow-up of 20 years, there were 75,807 deaths. The risk of all-cause mortality was similar across a wide range of BMI categories: compared to BMI of 22.5–24.9 kg/m2, the adjusted HR was 0.95 [95% CI 0.92, 0.98] for BMI of 25.0–27.4 and 0.93 [0.90, 0.96] for BMI of 27.5–29.9. These results persisted after restriction to healthy never-smokers and exclusion of subjects who died within the first two years of follow-up. A 21–108% increased mortality risk was seen for BMI ≥30. Older adults showed no significant increase in mortality between BMI of 22.5 and 34.9, while in younger adults this lack of increase was limited to the BMI range of 22.5 to 27.4. Conclusion The risk of all-cause mortality was elevated by 21–108% among participants with BMI ≥30. BMI may not necessarily increase mortality independently of other risk factors in adults, especially older adults, with overweight BMI. Further studies incorporating weight history, body composition, and morbidity outcomes are needed to fully characterize BMI-mortality associations.
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5 hacks for improving your metabolic health (and why it’s more important than BMI)Metabolic health is a very real, important part of our overall wellbeing, but the word ‘metabolism’ has a complicated history.
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5 hacks for improving your metabolic health (and why it’s more important than BMI)Writer Morgan Fargo calls time on the metabolism scaremongering once and for all…
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Frontiers | Glucose metabolism and its role in the maturation and migration of human CD1c+ dendritic cells following exposure to BCGTuberculosis (TB) still kills over 1 million people annually. The only approved vaccine, BCG, prevents disseminated disease in children but shows low efficacy at preventing pulmonary TB. Dendritic cells (DCs) are promising targets for vaccines and immunotherapies to combat infectious diseases due to their essential role in linking innate and adaptive immune responses. DCs undergo metabolic reprogramming following exposure to TLR agonists, which is thought to be a prerequisite for a successful host response to infection. We hypothesized that metabolic rewiring also plays a vital role in the maturation and migration of DCs stimulated with BCG. Consequently, we investigated the role of glycolysis in the activation of human primary myeloid CD1c+ DCs in response to BCG We show that CD1c+ mDC mature and acquire a more energetic phenotype upon challenge with BCG. Pharmacological inhibition of glycolysis with 2-deoxyglucose decreased cytokine secretion and altered cell surface expression of both CD40 and CCR7 on BCG-challenged, compared to untreated, mDCs. Furthermore, inhibition of glycolysis had differential effects on infected and uninfected bystander mDCs in BCG-challenged cultures. For example, CCR7 expression was increased by 2-deoxyglucose treatment following challenge with BCG and this increase in expression was seen only in BCG-infected mDCs. Moreover, although 2-DG treatment inhibited CCR7-mediated migration of bystander CD1C+ DCs in a transwell assay, migration of BCG-infected cells proceeded independently of glycolysis. Our results provide the first evidence that glycolysis plays divergent roles in the maturation and migration of human CD1c+ mDC exposed to BCG, segregating with infection status. Further investigation of cellular metabolism in DC subsets will be required to determine whether glycolysis can be targeted to elicit better protective immunity against Mtb.
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Effect of onset of type 2 diabetes on risks of cardiovascular disease and heart failure among new Zealanders with impaired glucose tolerance over 25 years: tapered-matched landmark analysis - Cardiovascular DiabetologyBackground This study aimed to examine the association between the incident onset of T2DM and 5- and 10-year risks of CVD and HF in people with IGT identified in primary care in South and West Auckland, New Zealand (NZ) between 1994 and 2019. Methods We compared CVD and HF risks in patients with IGT and with/without T2D newly diagnosed within the exposure window (1–5 years). Tapered matching and landmark analysis (to account for immortal bias) were used to control for potential effects of known confounders. Results Among 26,794 patients enrolled with IGT, 845 had T2D newly diagnosed within 5 years from enrolment (landmark date) and 15,452 did not have T2D diagnosed. Patients progressing to T2D (vs. those not progressing) had a similar 5-year risk for CVD (hazard ratio 1.19; 95% CI 0.61–2.32) but significantly higher 10-year risk of CVD (2.45(1.40–4.29)), 5-year risk of HF (1.94(1.20–3.12)) and 10-year risk of HF (2.84(1.83–4.39). The association between the onset of T2D and risk of 10-year risk of CVD, 5-year and 10-year risk of HF was more likely among men, the socioeconomically deprived, those currently smoking, patients with higher metabolic measures and/or those with lower renal function. Patients of NZ European ethnicity had a lower 10-year risk of CVD. Conclusions The study suggests that the diagnosis of T2D mediates the risk of CVD and HF in people with IGT. The development of risk scores to identify and better manage individuals with IGT at high risk of T2D is warranted.
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I tried out 8 hacks for a perfect pout without filler - chilli oil was a hot tipFILLERS were once all the rage but women are now turning to natural methods to achieve luscious lips. Social media is now full of ways to get a perfect pout without cosmetic help. The hashtag make…
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