Browse the evidence

Between 1999 and 2007, French adults significantly decreased consumption of traditional starchy foods (bread, potatoes) and dairy products, while increasing consumption of rice, pasta, fruits, vegetables, and chocolate.

If you are in France or a similar Western European context, expect that traditional staples like bread and potatoes are being replaced by rice and pasta, and that dairy intake is dropping while fruit, vegetable, and chocolate consumption is rising. This shift represents a move toward a 'mixed' European diet rather than a purely Mediterranean one.

High-fat diets contribute to positive energy balance by increasing hunger levels and reducing 24-hour plasma leptin concentrations, unlike high-carbohydrate meals.

Be aware that high-fat meals can increase your hunger and reduce satiety hormones like leptin more than high-carb meals. This makes it harder to stop eating. Prioritize foods that support satiety signaling rather than just counting calories.

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.

Subcutaneous adipose tissue, particularly in the gluteal-femoral region, acts as a metabolically protective 'sink' for lipids, preventing ectopic deposition in vital organs.

Building lower-body muscle and promoting subcutaneous fat storage in the legs and hips can protect against metabolic disease by acting as a safe storage site for excess lipids, preventing them from damaging the liver and muscles.

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.

High-fat diet (HFD) feeding in mice leads to elevated LSD1 expression and reduced expression of energy-expenditure genes in white adipose tissue, which can be reversed by inhibiting LSD1.

In mice, a high-fat diet increases the levels of LSD1 in fat tissue, which in turn suppresses genes responsible for burning fat. This creates a biological state where the body is less efficient at energy expenditure. Inhibiting LSD1 can reverse this effect, suggesting that targeting this pathway might help counteract the metabolic adaptations caused by high-fat diets.

Ipragliflozin (an SGLT2 inhibitor) improves hepatic steatosis and liver dysfunction in patients with Type 2 Diabetes irrespective of body weight reduction.

If you have Type 2 Diabetes and fatty liver, taking Ipragliflozin (50mg daily) can improve your liver health markers (like ALT) even if you do not lose significant body weight. This suggests the drug helps move fat out of the liver into safer storage areas, offering a specific benefit for liver health independent of weight loss efforts.

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.

Eucaloric diets that are very low in fat and high in simple sugars markedly stimulate de novo fatty acid synthesis, leading to increased plasma triglycerides proportional to the amount of synthesis.

If you eat a diet that is very low in fat and high in simple sugars (like high sugar/starch ratios), your body will synthesize more fat from those carbohydrates, which raises your blood triglycerides. This happens regardless of whether you are lean or obese, and it is not driven by your insulin levels. To manage triglycerides, avoid extreme low-fat diets that are high in simple sugars.

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.

Substituting red meat or dairy products for carbohydrate-dense foods is associated with a significantly increased risk of coronary heart disease (CHD) mortality in postmenopausal women.

Avoid replacing carbohydrates with red meat or dairy if you want to protect your heart. This study found that doing so increases the risk of dying from heart disease by 41-44%. Instead, if you are reducing carbs, choose vegetable protein sources like legumes, nuts, and tofu, which were associated with a 30% lower risk of heart disease mortality.

Continuous administration of fat-free, eucaloric diets (via intravenous or nasogastric routes) induces biochemical essential fatty acid (EFA) deficiency in healthy adult humans within 2 weeks, characterized by decreased linoleic acid and appearance of eicosatrienoic acid in plasma lipids.

If you are receiving intravenous nutrition or a strictly fat-free diet for an extended period, you are at high risk for essential fatty acid deficiency. Medical protocols should include periodic fat emulsions or intermittent feeding to mobilize body stores and prevent biochemical deficiency, even if clinical symptoms like dermatitis are not immediately visible.

Subcutaneous fat, particularly in the limbs and gluteal regions, plays a protective metabolic role by safely storing lipids, whereas visceral fat accumulation is strongly associated with metabolic complications.

Preserve subcutaneous fat in limbs and glutes if possible, as it protects against metabolic disease, while minimizing visceral fat accumulation.

Moderate dietary fructose consumption (≤50g/day or ~10% of energy) does not have deleterious effects on lipid and glucose control, and consumption up to 100g/day does not influence body weight.

You do not need to fear moderate amounts of fructose (up to 50g/day, or about 10% of your calories). It does not inherently cause weight gain or metabolic issues at this level. The problem arises from excessive consumption and overall caloric surplus, not the fructose itself. Focus on total energy balance rather than demonizing specific sugars.

Protein restriction, specifically methionine restriction, increases maximum lifespan in rodents by approximately 20%, potentially accounting for half of the life-extending effects of caloric restriction.

While animal studies show that restricting protein, especially methionine, can extend lifespan, this is not yet recommended for humans. More research is needed to determine if this is safe or beneficial for people.

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.

In middle-aged men without prior cardiovascular disease or diabetes, total intake and specific types of dietary fat (saturated, monounsaturated, polyunsaturated, trans) and dietary cholesterol are not associated with the risk of ischaemic or haemorrhagic stroke.

For men without existing heart disease or diabetes, current evidence from this large study suggests that you do not need to strictly restrict total fat, saturated fat, or cholesterol intake specifically to prevent stroke. Focus on a balanced diet rather than fearing specific fat types for stroke prevention.

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.

Long-term consumption of dietary gluten is not associated with an increased risk of coronary heart disease in adults without celiac disease.

If you do not have celiac disease, there is no evidence that eating gluten harms your heart. In fact, avoiding gluten might lead you to eat fewer whole grains, which are good for your heart. You do not need to follow a gluten-free diet for cardiovascular health.