Browse the evidence

Saturated fatty acids (SFAs) are more hepatotoxic than unsaturated fatty acids (UFAs) because they induce ER stress, oxidative stress, and apoptosis more effectively.

Not all fats affect the liver equally. Saturated fats are more likely to cause liver damage and inflammation than unsaturated fats. Reducing saturated fat intake may help mitigate liver stress in NAFLD patients.

M1 macrophage/Kupffer cell polarization drives insulin resistance and NASH progression, while M2 polarization protects against it.

Liver inflammation in NAFLD is driven by immune cells (Kupffer cells) shifting into a pro-inflammatory 'M1' state. Shifting these cells to an 'M2' state is protective. While lifestyle changes help, specific micronutrients like carotenoids are being studied for their ability to force this M2 shift.

Low dietary fiber intake increases the abundance of the gut bacterium Collinsella, which is positively correlated with circulating insulin levels in overweight and obese pregnant women.

If you are overweight or obese and pregnant, ensuring adequate dietary fiber intake (aiming for >28g/day as recommended) may help maintain a healthier gut microbiota balance by keeping Collinsella levels low. This is associated with lower circulating insulin levels, which may support better metabolic health during pregnancy. Focus on increasing fiber from whole food sources rather than supplements.

Dysbiosis, characterized by an imbalance in bacterial ratios (e.g., increased Firmicutes/Bacteroidetes ratio or decreased Akkermansia muciniphila), drives low-grade systemic inflammation and insulin resistance through the translocation of bacterial lipopolysaccharides (LPS) into the bloodstream.

Maintain gut barrier integrity to prevent metabolic inflammation. This involves avoiding factors that cause dysbiosis (like excessive antibiotics or poor diet) and supporting beneficial bacteria (like Akkermansia muciniphila) which are often depleted in obesity and diabetes.

Caloric restriction (CR) reprograms the single-cell transcriptional landscape of aging, altering gene expression patterns in specific tissues.

Caloric restriction changes how genes are expressed in cells, particularly in rats. This database allows researchers to see exactly which genes are affected, potentially leading to drugs that mimic these benefits without strict dieting.

The association between egg consumption and CVD/mortality is largely explained by the dietary cholesterol content within the eggs, as the association becomes non-significant when adjusting for total dietary cholesterol.

If you eat eggs, be mindful of your total dietary cholesterol intake. The risk associated with eggs appears to come from their cholesterol content, so balancing egg intake with other cholesterol-containing foods is key to managing CVD risk.

Enhancing autophagy through genetic or pharmacological means improves glucose tolerance, insulin sensitivity, and resistance to obesity in high-fat diet models.

Boosting your body's natural cleanup processes (autophagy) can help you stay lean and sensitive to insulin, even if you eat a high-fat diet. This suggests that maintaining cellular health through fasting or exercise is as important as the food you eat.

Reducing dietary protein intake (specifically BCAAs) improves insulin sensitivity in obese mice, whereas increasing BCAA intake exacerbates insulin resistance.

For obese individuals, reducing the intake of branched-chain amino acids (found in high-protein foods like meat, eggs, and dairy) may improve insulin sensitivity. Conversely, high BCAA intake can worsen insulin resistance. This suggests that the quality of protein (BCAA content) is as important as the quantity.

The protein content of microalgae varies significantly (6-71% of dry matter) and is heavily influenced by environmental factors such as light intensity, temperature, CO2 concentration, and nutrient availability.

When choosing microalgal products, be aware that protein content can vary widely depending on how the algae were grown. Look for products that specify their protein content, as this can range from 6% to over 70% of dry weight depending on cultivation conditions.

Age-related insulin resistance in older adults is primarily driven by increased visceral adiposity and central fat distribution rather than aging itself, as accounting for body fat and distribution eliminates age as a predictor of insulin action.

Focus on maintaining a healthy body weight and minimizing visceral fat through diet and exercise. This is more critical for metabolic health in older age than simply accepting 'aging' as the cause of metabolic issues.

Fructose ingestion acutely and robustly increases FGF21 blood levels in both mice and humans, whereas glucose causes only a modest and delayed increase, establishing a liver-brain feedback loop for sugar consumption regulation.

Eating fructose triggers a rapid spike in FGF21, a hormone that helps regulate sugar intake, while glucose has a much weaker effect. This suggests your body uses FGF21 to specifically manage fructose consumption.

Probiotic supplementation does not significantly reduce fat mass in overweight or obese subjects, despite reducing body weight and fat percentage.

Do not expect probiotics to reduce your body fat. While they might lower your total body weight slightly, the specific reduction in fat mass was not statistically significant in this review.

Commercial determinants of health (CDoH), including corporate political activity and marketing of unhealthy commodities, are primary structural drivers of non-communicable diseases (NCDs) and health inequalities, overriding individual behavioral factors.

To improve public health, focus on regulating corporate practices (marketing, lobbying, product formulation) rather than solely educating individuals. Support policies that limit the power of industries selling unhealthy commodities like ultra-processed foods, alcohol, and tobacco.

Sarcopenia diagnosis requires combining DXA-derived lean mass indices (specifically ASMMI) with functional strength tests; lean mass alone is insufficient for diagnosis.

If DXA shows low appendicular skeletal muscle mass index (ASMMI <7.0 kg/m2 men, <6.0 kg/m2 women), do not diagnose sarcopenia yet. Perform functional strength tests (grip strength, gait speed). Only diagnose sarcopenia if strength is also low.

In obesity and type 2 diabetes, adipose tissue macrophages undergo 'metabolic activation' characterized by high glycolysis and lipid internalization, which drives insulin resistance and chronic inflammation without exhibiting the classical M1 activation markers.

In obesity, fat tissue immune cells change their metabolism to fuel chronic inflammation and insulin resistance. This is not a standard immune response but a specific 'metabolic' adaptation. Understanding this helps explain why weight loss and metabolic health improvements are key to resolving this specific type of inflammation.

Obesity-induced infiltration of M1 macrophages into metabolic tissues (adipose, liver, muscle) drives chronic inflammation that directly causes insulin resistance by interfering with insulin signaling pathways.

For those with obesity, reducing the inflammatory burden on metabolic tissues is key. This involves strategies that reduce macrophage infiltration, such as weight loss and potentially anti-inflammatory dietary patterns, to improve insulin sensitivity.

Obese individuals exhibit altered glutamine metabolism, characterized by decreased serum glutamine and alpha-ketoglutarate, and increased succinate, which correlates with M1 macrophage accumulation.

Obesity is associated with lower levels of glutamine and alpha-ketoglutarate, and higher succinate. While this is a marker of disease, simply taking glutamine supplements may not fully reverse these changes in humans, as muscle mass and other factors also play a role. Focus on overall metabolic health.

Hunter-gatherer diets are not invariably low-carbohydrate; many populations consume diets rich in carbohydrates and simple sugars (e.g., from honey and tubers) while maintaining excellent metabolic health.

You do not need to avoid carbohydrates to be healthy. Many traditional populations thrive on high-carbohydrate diets rich in fiber and micronutrients (from tubers, fruits, and honey). Focus on the quality and source of carbohydrates rather than eliminating them.

As income and food system industrialization increase, per capita supply of animal-source foods increases, while supply of pulses and coarse grains decreases.

As your income rises, you may naturally gravitate towards more animal proteins and away from pulses and coarse grains. Be aware that this shift is a common economic trend, not necessarily a nutritional improvement. Pulses and coarse grains remain valuable, nutrient-dense components of a balanced diet.

There is a curvilinear (inverted-U) relationship between GDP per capita and BMI: weight gain increases with development in low-income countries but decreases or levels off in high-income countries.

In developing economies, rising wealth often leads to higher obesity rates due to dietary changes. However, as countries become wealthier, these rates tend to stabilize or decrease, suggesting that long-term development can improve health outcomes.

Women's empowerment is positively associated with increased BMI, particularly in high-income countries.

As women gain more social and economic empowerment, there may be an increase in obesity rates due to lifestyle changes. Policymakers should ensure that healthy food options are accessible and convenient for working women.

Ketogenic diets increase the risk of cardiovascular disease markers, specifically LDL-C elevation, which persists even with weight loss, and are associated with increased risks of kidney stones and chronic kidney disease.

Monitor your LDL cholesterol closely if you follow a ketogenic diet, especially if it is high in animal fats. The risk of kidney stones and chronic kidney disease also increases with high animal protein intake.

Elevated atmospheric CO2 concentrations (eCO2) significantly reduce the protein content of C3 staple crops (rice, wheat, barley, potato), leading to a global increase in the population at risk of protein deficiency by 2050.

This research highlights a systemic risk to global food security rather than an individual intervention. For individuals, the key takeaway is to support agricultural policies that promote crop diversification, particularly the breeding of crops resilient to high CO2, and to prioritize diets that include protein sources less affected by eCO2 (like C4 crops or legumes) where possible. For policymakers, it underscores the urgent need to incorporate crop nutrient decline into food security models.

Fructose consumption promotes hepatic de novo lipogenesis (DNL) and NAFLD development through both substrate provision and independent upregulation of lipogenic transcription factors (SREBP1c and ChREBP), even in the absence of insulin signaling.

High amounts of fructose (especially from added sugars or juices) directly stimulate your liver to make new fat, even if you aren't insulin resistant. This process is unique to fructose compared to glucose.