Combining ginger intake with an anti-inflammatory diet improves fatty liver disease in children – RCT
Following 12 weeks’ administration of ginger capsules, hepatic steatosis – fat in the liver – was found to have significantly reduced for those who took ginger alone (G) and the ginger plus anti-inflammatory diet group (GPA).
Sponsored by the research grant of Kermanshah University of Medical Sciences in Iran, the findings of the study were published in Food Science & Nutrition.
To assess the combined effect of ginger intake and anti-inflammatory diet in children with obesity on fatty liver management, a double-blind, randomized clinical trial recruited 160 children with obesity aged 8 to 11 years over the course of 12 weeks.
They were randomised to either take only ginger capsules, only undergo an anti-inflammatory diet, take ginger capsules and undergo an anti-inflammatory diet, or allocated to the control group.
The ginger capsules comprised of 1,000 mg of ginger rhizome powder, while the anti-inflammatory diet comprised of fruits and vegetables, fish, turkey, and chicken (without skin) with lean meat, omega-3 sources, nuts, legumes, and probiotic products.
Science behind ginger
Notably, fasting blood sugar, inflammatory marker levels, liver enzymes, dyslipidaemia and liver steatosis saw a significant reduction after combining daily intake of ginger with an anti-inflammatory diet.
The finding of ginger intake reducing insulin levels was seconded by previous studies conducted among humans and animals alike:
“Ginger also appears to reduce glucose uptake by inhibiting enzymes in glucose metabolism, such as α-glucosidase and amylase in the gut. This antioxidant compound may increase the expression of GLUT4 (glucose transporter type 4) protein insulin receptors, and improve the function of β-pancreatic cells, thereby improving glucose tolerance (Li et al., 2012),” the paper reports.
The combined group also produced a significant result for a greater number of children who had at least a grade decrease in their liver fat status.
Additionally, the researchers found that the combined group had higher levels of HDL-cholesterol – also known as “good cholesterol”, as well as reduced serum hs-CRP – protein produced in the liver associated with rate of liver inflammation.
“It seems that the efficacy of ginger on inflammation is due to the positive effect of some active ingredients (gingerol and zerumbone) in inhibiting NF-κB (nuclear factor kappa B) and TNF-α (tumor necrosis factor alpha). Ginger inhibits NF-κB activity by inhibiting the TNF-α gene, and thus inhibits the production of acute-phase positive proteins such as CRP (Kim et al., 2004).”
For the only ginger group, it had significant results when it comes to lowered total cholesterol levels (probability for only ginger group is 0.92, while combined group is 0.84), especially LDL cholesterol, in the body:
“Cholesterol reduction by ginger can be explained as follows: ginger can increase the conversion of cholesterol into bile acids by increasing the activity of cholesterol-7α- hydroxylase, leading to a decrease in serum cholesterol levels (Alizadeh-Navaei et al., 2008).”
Research implications
The researchers found a more significant reduction in fat in the liver in the ginger groups compared to the only anti-inflammatory diet group.
“The mechanisms responsible for reducing liver fat following the use of ginger supplements are probably a change in energy supply, increased oxidation of fats in liver cells, burning and further metabolism of visceral fat stores.”
Combined with an anti-inflammatory diet, its effectiveness is boosted as overall fat accumulation in the body is reduced.
Concluding the findings, the researchers suggested for ginger to be used as a supplement to improve fatty liver in children with obesity and boosting its effectiveness with an anti-inflammatory diet.
Source: Food Science & Nutrition
“Combination of the effect of ginger and anti-inflammatory diet on children with obesity with nonalcoholic fatty liver disease: A randomized clinical trial”
DOI: 10.1002/fsn3.3218
Authors: Kamari, N. et al.
