Visceral adiposity and metabolic syndrome after very high-fat and low-fat isocaloric diets: a randomized controlled trial.
"Visceral adiposity and metabolic syndrome after very high-fat and low-fat isocaloric diets: a randomized controlled trial. VL Veum, J Laupsa-Borge, Ø Eng et al. American Journal of Clinical Nutrtion. 2017 Jan;105(1):85-99. Epub 2016 Nov 30. "
"Aspects of diet, including macronutrient and food proﬁles, may affect visceral fat mass and metabolic syndrome. Previous studies exploring the effects of high-fat diets often include E-dense diets with large amounts of processed carbohydrates and poor overall quality, confounding effects of a high fat intake per se Aim: to test the hypothesis that consuming energy primarily from carbohydrate or fat in diets with similar food proﬁles would differentially affect the ability to reverse visceral adiposity and metabolic syndrome"
"Primary: visceral adiposity and metabolic syndrome markers Visceral adiposity and other measures of body composition, including: - weight - BMI - waist size - body fat %, body fat mass - subcutaneous fat Measure of metabolic syndrome: - SBP, DBP - lipids - glucose control (FBG, HbA1c) - inflammation (HOMA)"
"Both diets similarly improved (WG SS, BG NSS): - weight - waist size - abdominal subcutaneous fat mass - visceral fat mass - liver fat and liver function markers - TG - fasting insulin - insulin C-peptide - HbA1c - HOMA Diets differed (BG SS) for: - HDL-C - increased only in VHFLC diet - LDL-C, total-C - lowered only in LFHC diet Values reported are all unadjusted. WG SS p values NR."
"HOMA2-IR & HOMA2-%S WG: Y BG: N HOMA2-IR At 12 wks VHFLC diet -0.48 LFHC -0.60BG NSS "
"All liver function markers improved or NSS change. "
" Our results are in line with systematic reviews and metaanalyses of epidemiologic and dietary intervention studies,which overall do not support a causal connection between SFA intake per se and risk of metabolic syndrome, fatty liver, or CVD, regardless of the effects on LDL cholesterol. ...Consuming E primarily as carbohydrate or fat for 3 mo did not differentially inﬂuence visceral fat and metabolic syndrome in a low-processed, lower-glycemic dietary context. Our data do not support the idea that dietary fat per se promotes ectopic [in abnormal place] adiposity and cardiometabolic syndrome in humans."
AHA - American Heart Association;
ALT - alanine aminotransferase;
AMDR - acceptable macronutrient distribution range;
AST - aspartate aminotransferase;
BG - between study groups;
BHOB - beta-hydroxybutyrate;
DBP - diastolic blood pressure;
E- energy, caloric intake;
eGFR - estimated glomerular filtration rate;
FBG - fasting blood glucose;
GGT - gamma-glutamyl transferase;
HDL-C - high-density lipoprotein cholesterol;
iGFR - isotope glomerurar filtration rate;
LDL-C - low-density lipoprotein cholesterol;
NAFLD - non-alcoholic fatty liver disease;
NR - not reported (or data needed for calculation not available);
N - no;
NA - not applicable;
NS - not specified;
NSS - not statistically significant;
SBP - systolic blood pressure;
SS - statistically significant;
TG - triglyceride;
total C - total cholesterol;
V - varied, mixed;
WG - within a study group;
WMD - weighted mean difference;
Y - yes
Number of People in Studies:
3,296 Enrolled in randomized controlled trials on 25% or less carbohydrates
2,626 Completed randomized controlled trials on 25% or less carbohydrates
79.67% 82% completion of studies
Duration of Trial
1 -2 years
# of Trials
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