01
What is fatty liver - and how does it develop?
Non-alcoholic fatty liver disease (NAFLD) occurs when excess fat accumulates in liver cells - in people who drink little or no alcohol. It's driven primarily by excess caloric intake (particularly refined carbohydrates and fructose), insulin resistance, obesity, and physical inactivity. In early stages it's completely asymptomatic. If untreated, it can progress to NASH (non-alcoholic steatohepatitis, with inflammation), fibrosis, cirrhosis, and liver failure over decades.
- NAFLD affects 25–30% of adults globally - most don't know they have it
- Insulin resistance is the central driver - excess glucose is converted to fat in the liver
- Fructose is particularly harmful - metabolised almost entirely by the liver, unlike glucose
- Early NAFLD is completely reversible - even advanced fibrosis can improve with sustained lifestyle change
- Visceral obesity (belly fat) is the strongest clinical predictor of NAFLD severity
What Isabella tracks
Ziva tracks your weight trend, waist circumference (if logged), fasting glucose or CGM data, and caloric intake - the primary markers of NAFLD risk. Isabella shows how your numbers are trending and what's driving them.
02
Alcohol and the liver - what the evidence actually says.
The liver processes approximately 90% of ingested alcohol. It can metabolise about one unit per hour. Beyond this, alcohol and its toxic metabolite acetaldehyde accumulate, causing oxidative stress, fat accumulation (alcoholic fatty liver), and inflammation. Chronic heavy drinking leads to alcoholic hepatitis and eventually cirrhosis. But the effects begin well below "heavy drinking" thresholds - even moderate regular drinking accelerates NAFLD and raises liver enzyme levels.
- More than 14 units/week significantly raises liver enzyme levels and NAFLD risk
- Binge drinking (>6 units in one session) is particularly damaging regardless of weekly total
- The liver takes 48–72 hours to fully recover from a heavy drinking session
- Alcohol-free days are as important as weekly total - consecutive drinking days compound damage
- Coffee (3 cups/day) has one of the strongest protective effects against liver fibrosis in drinkers
What Isabella tracks
Ziva logs your weekly alcohol units and tracks alcohol-free days - flagging weeks above safe limits and showing the direct effect of alcohol on your overnight HRV and resting heart rate.
03
The diet that most reliably improves liver health.
The Mediterranean diet has the strongest and most consistent evidence for reducing liver fat and improving liver function. Its benefits come from multiple mechanisms: olive oil's oleocanthal reduces hepatic inflammation, omega-3 fatty acids from fish reduce hepatic lipogenesis, high polyphenol intake (vegetables, olive oil, nuts) reduces oxidative stress, and the low sugar and refined carbohydrate content directly reduces fructose-driven fat synthesis in the liver.
- Eliminate added fructose - soft drinks, fruit juice, and processed foods with HFCS are the primary driver
- Increase olive oil - reduces hepatic fat and inflammation in RCTs
- Eat oily fish 2–3×/week - omega-3 reduces liver fat by up to 20% in studies
- Increase coffee - 3 cups/day is associated with 40% lower fibrosis risk; one of the strongest liver-protective foods known
- Reduce refined carbohydrates - white bread, pasta, rice all drive insulin spikes that promote hepatic lipogenesis
- Eat adequate protein - prevents muscle loss during caloric restriction; targets 1.2–1.6g/kg body weight
What Isabella tracks
Ziva's nutrition logging tracks your macro breakdown, fructose and sugar intake, and meal quality - giving Isabella the data to show how your diet is affecting your glucose and metabolic markers over time.
04
The glucose-liver connection - more direct than most people know.
The liver is the primary regulator of blood glucose. After meals, it absorbs glucose from the portal vein and converts excess to glycogen (short-term storage) or fat (long-term storage). In insulin resistance, the liver fails to suppress glucose production appropriately - causing fasting hyperglycaemia and driving more hepatic fat accumulation. Continuous glucose monitoring reveals the direct relationship between meal choices, glucose spikes, and liver health markers.
- Fasting glucose above 100 mg/dL is associated with 2× higher NAFLD prevalence
- Post-meal glucose spikes above 180 mg/dL drive de novo lipogenesis in the liver
- Time-restricted eating reduces hepatic glucose production and liver fat in NAFLD
- Reducing glycaemic variability (fewer spikes) is more important than average glucose level
- Even moderate weight loss (5–7%) dramatically improves hepatic insulin sensitivity
What Isabella tracks
With CGM integration, Ziva tracks your fasting glucose, post-meal spikes, and glycaemic variability - the metrics most directly linked to hepatic fat accumulation and insulin resistance progression.
05
Exercise reduces liver fat - even without weight loss.
Exercise is one of the most powerful interventions for liver health - and its benefits are partially independent of weight loss. During aerobic exercise, the liver increases fat oxidation directly. Improved insulin sensitivity from regular exercise reduces hepatic fat synthesis. Both aerobic and resistance training are effective, though the combination is superior to either alone. The dose needed is achievable: 150 minutes per week of moderate-intensity activity.
- 150 min/week of moderate aerobic exercise reduces liver fat by 20–30% in NAFLD
- Even without weight loss, exercise reduces hepatic fat - fat is burned directly during activity
- Resistance training 2×/week adds independent benefits via improved insulin sensitivity
- High-intensity interval training (HIIT) produces the largest liver fat reduction per time invested
- Sedentary time between exercise sessions also matters - regular movement breaks help throughout the day
What Isabella tracks
Ziva tracks your weekly exercise minutes, Zone 2 time, and step count - and shows you when you've hit the 150-minute threshold that clinical evidence links to meaningful liver fat reduction.
06
Why sleep is an underrated liver health intervention.
Poor sleep is an independent risk factor for NAFLD - separate from its effects on weight and diet. Sleep deprivation increases cortisol and growth hormone dysregulation, drives insulin resistance, increases inflammatory cytokines, and promotes hepatic fat accumulation. People who sleep less than 6 hours per night have significantly higher rates of NAFLD even after controlling for diet, obesity, and physical activity.
- Less than 6 hours of sleep increases NAFLD risk by 50% independent of other factors
- Sleep apnea (nocturnal hypoxia) is one of the strongest predictors of NAFLD severity and fibrosis progression
- Poor sleep raises cortisol, which directly promotes hepatic gluconeogenesis and fat accumulation
- Treating sleep apnea with CPAP measurably reduces liver inflammation and fibrosis markers
- Deep sleep is when growth hormone peaks - essential for hepatic protein synthesis and repair
What Isabella tracks
Ziva tracks your nightly sleep duration, deep sleep %, and SpO2 (a key sleep apnea signal) - and correlates poor sleep nights with next-day glucose and HRV patterns that reflect liver metabolic stress.