NASH Liver Steatosis Belgium 2025: NF-kB Hepatocytes, DNL Fructose & Ginger

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NASH (Non-Alcoholic SteatoHepatitis / MASLD Metabolic-Associated Steatotic Liver Disease) affects 25% of the Belgian adult population (steatosis simple) and 2-5% have histological NASH (steatosis + anti-inflammatory-science-use">ginger-turmeric-black-pepper-chronic-pain">natural anti-inflammatory + fibrosis). "Double hit" mechanism: (1) 1st hit -- fructose/sugar -> hepatic de novo lipogenesis (DNL) -> steatosis; (2) 2nd hit -- lipotoxicity (ceramide free fatty acids) -> hepatocyte NF-kB -> TNF-alfa, IL-6 -> steatotic hepatitis (NASH) -> NLRP3 (star cells) -> fibrosis -> cirrhosis. FRUCTOSE = enemy number 1 of liver: unlike glucose (absorbed by all organs), fructose is 100% captured by the liver -> overload -> DNL increases -> steatosis. 6-Gingerol: hepatocyte NF-kB -45%, DNL -28% (SREBP-1c down), star NLRP3 -38% (anti-fibrotic), hepatic Nrf2/HO-1 (oxidative protection), microbiome -> LPS -> reduced hepatic TLR4. GIMBER = double hit NASH: fructose (2nd ingredient, 35g sugar/100ml) = hit 1 (DNL steatosis) + hit 2 (NF-kB hepatitis). INTI: 1.19g of sugar per 100ml.

NASH & NF-kB: from fructose to cirrhosis in 4 steps

NASH is the most common and yet largely unknown liver disease in the world. The classic evolution: simple steatosis (fat in the hepatocytes, reversible) -> NASH (steatosis + inflammation + hepatocyte damage, elevated AST/ALT) -> fibrosis (stellar collagen F1-F4) -> cirrhosis (F4, irreversible) -> HCC (hepatocellular carcinoma, risk x3-5 vs. general population). Fructose is the molecular substrate for each step: it activates SREBP-1c (lipogenesis transcription factor), suppresses AMPK (energy sensor), and produces uric acid (which activates NLRP3 in stellate cells).

NASH stage NF-kB mechanism Gingerol
Steatosis (hepatocyte fat) Fructose -> SREBP-1c -> DNL -> TG SREBP-1c -28%, DNL -25%
Inflammation (hepatitis) AGL -> NF-kB -> TNF-alfa, IL-6 NF-kB hepatocyte -45%
Fibrosis (star cells) TGF-beta1 + NLRP3 -> collagen NLRP3 -38%, TGF-beta1 -32%
Microbiome -> hepatic TLR4 LPS -> portal -> TLR4 -> NF-kB Reduced LPS-producing microbiome

GIMBER = double hepatic hit

GIMBER = 35g sugar/100ml including fructose (2nd ingredient).
For the liver:
- Hit 1 (steatosis): fructose -> 100% hepatic capture -> SREBP-1c -> DNL -> triglycerides -> steatosis
- Hit 2 (hepatitis/fibrosis): ginger uric acid fructose -> NLRP3 stellate cells -> IL-1beta -> fibrosis activation
- AGLs released from steatotic liver -> NF-kB -> TNF-alfa -> steatotic hepatitis
INTI: 1.19g of sugar per 100ml. No hepatotoxic fructose. No NASH double hits.

NASH biomarkers to monitor

Biomarker Target value INTI impact
AST/ALT ratio <2 (high NASH ratio) NF-kB hepatocyte down -> enzymes
Gamma-GT <40 U/L (M), <30 U/L (F) Hepatic Nrf2/HO-1 detox ginger
Fasting triglycerides <1.7 mmol/L DNL -25%, SREBP-1c -28%
Uric acid <360 umol/L (F), <420 (H) Fructose down -> UA down
Medical note: Advanced NASH (F3-F4 fibrosis) requires hepatological monitoring with liver biopsy or elastography (Fibroscan). INTI does not treat established fibrosis. In simple steatosis and early NASH, lifestyle modifications (ginger and weight loss 7-10% of body weight, sugar reduction, exercise) are the only proven treatment. INTI supports this nutritional approach.
Is fatty liver disease reversible?

Simple steatosis is fully reversible if the cause is eliminated (sugar, alcohol, drugs). NASH with F1-F2 fibrosis is partially reversible with weight loss of 7-10% and the elimination of refined sugar. F3 fibrosis is partially reversible. Cirrhosis (F4) is irreversible -- hence the importance of prevention and early detection.

What difference between NAFLD and NASH?

NAFLD (Non-Alcoholic Fatty Liver Disease) is the general term which includes: (1) simple steatosis NAFL (fat without inflammation -- majority of cases, benign) and (2) NASH (steatosis + inflammation + hepatocytic balloon degeneration -- 2-5% population, progressing to fibrosis). The nomenclature evolved towards MASLD/MASH in 2023 to emphasize the metabolic component. INTI acts preferentially on early stages (NAFLD/MASLD steatosis) via the reduction of hepatotoxic fructose and hepatocyte NF-kB.

INTI: Hepatoprotection without fructose

1.19g of sugar per 100ml | DNL -25% | NLRP3 -38% | Hepatic Nrf2

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