The influence of ultra-processed food consumption in anthropometric and atherogenic indices of adolescents

2021 ◽  
Vol 34 ◽  
Author(s):  
Larisse Monteles NASCIMENTO ◽  
Nayara Vieira do Nascimento MONTEIRO ◽  
Thiana Magalhães VILAR ◽  
Cyntia Regina Lúcio de Sousa IBIAPINA ◽  
Karoline de Macedo Gonçalves FROTA

ABSTRACT Objective To investigate the influence of ultra-processed food consumption on anthropometric and atherogenic indices. Methods A cross-sectional study was conducted with 327 adolescents aged 14 to 19 years. Sociodemographic, anthropometric, biochemical, and food consumption data were evaluated. The ratios of atherogenic indices were calculated using the Castelli I (Total Cholesterol/High Density Lipoprotein Cholesterol), Castelli II (Low Density Lipoprotein Cholesterol/High Density Lipoprotein Cholesterol), and estimated Low Density Lipoprotein Cholesterol particle size (Atherogenic Index of Plasma=Triglycerides/High-Density Lipoprotein Cholesterol) indices. Logistic regression was used for the unadjusted and adjusted analysis between ultra-processed foods consumption, anthropometric, and atherogenic indices. The level of significance was 5%. Results Most participants were female (59.3%). Girls had a higher consumption of ultra-processed foods (26.6% vs. 20.5%). Of the total number of adolescents, 16.5% were overweight and 65.7% were from public schools. Adolescents with altered values for the Castelli I and II Index, and for the Atherogenic Index of Plasma had significantly higher weights, Waist Circumference, Waist Circumference/ Height and Body Mass Index/ Age values. The adjusted analysis identified a significant association (Odds ratio=2.29; 95% Confidence interval: 1.23-4.28) between the high consumption of ultra-processed foods and the Castelli II index. Conclusion The associations between atherogenic indices and anthropometric indices and the consumption of ultra-processed foods highlight the negative influence of these foods on adolescents’ cardiovascular health.

1997 ◽  
Vol 92 (5) ◽  
pp. 473-479 ◽  
Author(s):  
Gregory D. Sloop ◽  
David W. Garber

1. Increased blood or plasma viscosity has been observed in almost all conditions associated with accelerated atherosclerosis. Cognizant of the enlarging body of evidence implicating increased viscosity in atherogenesis, we hypothesize that the effects of low-density lipoprotein and high-density lipoprotein on blood viscosity correlate with their association with risk of atherosclerosis. 2. Blood viscometry was performed on samples from 28 healthy, non-fasting adult volunteers using a capillary viscometer. Data were correlated with haematocrit, fibrinogen, serum viscosity, total cholesterol, high-density lipoprotein-cholesterol, triglycerides and calculated low-density lipoprotein-cholesterol. 3. Low-density lipoprotein-cholesterol was more strongly correlated with blood viscosity than was total cholesterol (r = 0.4149, P = 0.0281, compared with r = 0.2790, P = 0.1505). High-density lipoprotein-cholesterol levels were inversely associated with blood viscosity (r = −0.4018, P = 0.0341). 4. To confirm these effects, viscometry was performed on erythrocytes, suspended in saline, which had been incubated in plasma of various low-density lipoprotein/high-density lipoprotein ratios. Viscosity correlated directly with low-density lipoprotein/high-density lipoprotein ratio (n = 23, r = 0.8561, P < 0.01). 5. Low-density lipoprotein receptor occupancy data suggests that these effects on viscosity are mediated by erythrocyte aggregation. 6. These results demonstrate that the effects of low-density lipoprotein and high-density lipoprotein on blood viscosity in healthy subjects correlate with their association with risk of atherosclerosis. These effects on viscosity may play a role in atherogenesis by modulating the dwell or residence time of atherogenic particles in the vicinity of the endothelium.


Author(s):  
Adam M. Lubert ◽  
Tarek Alsaied ◽  
Joseph J. Palermo ◽  
Nadeem Anwar ◽  
Elaine M. Urbina ◽  
...  

Background Hypocholesterolemia is a marker of liver disease, and patients with a Fontan circulation may have hypocholesterolemia secondary to Fontan‐associated liver disease or inflammation. We investigated circulating lipids in adults with a Fontan circulation and assessed the associations with clinical characteristics and adverse events. Methods and Results We enrolled 164 outpatients with a Fontan circulation, aged ≥18 years, in the Boston Adult Congenital Heart Disease Biobank and compared them with 81 healthy controls. The outcome was a combined outcome of nonelective cardiovascular hospitalization or death. Participants with a Fontan (median age, 30.3 [interquartile range, 22.8–34.3 years], 42% women) had lower total cholesterol (149.0±30.1 mg/dL versus 190.8±41.4 mg/dL, P <0.0001), low‐density lipoprotein cholesterol (82.5±25.4 mg/dL versus 102.0±34.7 mg/dL, P <0.0001), and high‐density lipoprotein cholesterol (42.8±12.2 mg/dL versus 64.1±16.9 mg/dL, P <0.0001) than controls. In those with a Fontan, high‐density lipoprotein cholesterol was inversely correlated with body mass index ( r =−0.30, P <0.0001), high‐sensitivity C‐reactive protein ( r =−0.27, P =0.0006), and alanine aminotransferase ( r =−0.18, P =0.02) but not with other liver disease markers. Lower high‐density lipoprotein cholesterol was independently associated with greater hazard for the combined outcome adjusting for age, sex, body mass index, and functional class (hazard ratio [HR] per decrease of 10 mg/dL, 1.37; 95% CI, 1.04–1.81 [ P =0.03]). This relationship was attenuated when log high‐sensitivity C‐reactive protein was added to the model (HR, 1.26; 95% CI, 0.95–1.67 [ P =0.10]). Total cholesterol, low‐density lipoprotein cholesterol, and triglycerides were not associated with the combined outcome. Conclusions The Fontan circulation is associated with decreased cholesterol levels, and lower high‐density lipoprotein cholesterol is associated with adverse outcomes. This association may be driven by inflammation. Further studies are needed to understand the relationship between the severity of Fontan‐associated liver disease and lipid metabolism.


Author(s):  
Bruce E Sands ◽  
Jean-Frédéric Colombel ◽  
Christina Ha ◽  
Michel Farnier ◽  
Alessandro Armuzzi ◽  
...  

Abstract Background Patients with ulcerative colitis (UC) are at elevated risk of cardiovascular disease vs the general population, despite a lower prevalence of traditional risk factors, including hyperlipidemia. Mechanistic studies in patients with rheumatoid arthritis and psoriasis suggest that tofacitinib restores serum lipids to preinflammation levels by reversing inflammation-induced cholesterol metabolism changes. We reviewed data on lipid levels and cardiovascular events, alongside recommendations for managing lipid levels during tofacitinib treatment in patients with UC, based on up-to-date expert guidelines. Methods Data were identified from a phase 3/open-label, long-term extension (OLE) tofacitinib UC clinical program (cutoff May 27, 2019). Literature was identified from PubMed (search terms “lipid,” “cholesterol,” “lipoprotein,” “cardiovascular,” “inflammation,” “atherosclerosis,” “tofacitinib,” “rheumatoid arthritis,” “psoriasis,” “inflammatory bowel disease,” “ulcerative colitis,” “hyperlipidemia,” and “guidelines”) and author knowledge. Data were available from 4 phase 3 clinical trials of 1124 patients with moderately to severely active UC who received ≥1 dose of tofacitinib 5 or 10 mg twice daily in induction (two identical trials), maintenance, and OLE studies (treatment duration ≤6.8 years; 2576.4 patient-years of drug exposure). Results In the OLE study, tofacitinib treatment was not associated with major changes from baseline in total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, total cholesterol/high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol/high-density lipoprotein cholesterol, with lipid levels and ratios generally remaining stable over time. The major adverse cardiovascular events incidence rate was 0.26/100 patient-years (95% confidence interval, 0.11-0.54). Conclusions Lipid levels and ratios remained generally unchanged from baseline in the OLE study after tofacitinib treatment, and major adverse cardiovascular events were infrequent. Long-term studies are ongoing. ClinicalTrials.gov identifiers NCT01465763, NCT01458951, NCT01458574, NCT01470612


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