Browse the evidence

Pure protein-energy malnutrition (starvation) responds dramatically to nutritional support, unlike cachexia, because the primary mechanism is an energy deficit rather than active catabolic signaling.

If weight loss is due to not eating enough or not absorbing food (malnutrition), providing adequate nutrition will reverse the wasting.

Obesity impairs the efficacy of influenza vaccination, resulting in a higher incidence of influenza-like illness despite vaccination, suggesting similar immune evasion may occur with other vaccines.

Obesity can reduce how well your flu shot works, making you twice as likely to get sick compared to non-obese vaccinated people. Still get vaccinated, but be aware you may need extra precautions or discuss high-dose options with your doctor.

High-fat diet (HFD) consumption triggers rapid hypothalamic inflammation (within 24 hours) and neuronal injury, which causes leptin resistance and an upward resetting of the body fat set-point, thereby driving obesity pathogenesis.

If you struggle with weight regain after dieting, it is likely due to biological defenses (leptin resistance) triggered by high-fat diets, not just a lack of willpower. This suggests that long-term management may require addressing the underlying hypothalamic inflammation rather than just caloric restriction.

In humans with Type 2 diabetes, apM1 (adiponectin) mRNA expression is significantly reduced in both omental and subcutaneous adipose tissue compared to lean and obese non-diabetic controls.

This research highlights that low levels of the fat-derived hormone adiponectin (apM1) are a hallmark of Type 2 diabetes, distinct from obesity alone. While not a direct intervention, maintaining healthy adipose tissue function and managing blood glucose are critical for preserving normal adiponectin levels, which may help mitigate insulin resistance.

Obesity spreads through social networks via clustering, where individuals' BMIs converge toward the majority BMI of their social neighbors, creating self-sustaining clusters of weight status.

Your social circle significantly influences your weight. If your close friends are overweight, you are statistically more likely to gain weight, regardless of your personal efforts. Recognizing this social contagion is the first step to mitigating it.

Carriers of the preproghrelin Leu72Met polymorphism (specifically Met72 allele) exhibit lower body mass index, fat mass, and visceral adiposity compared to non-carriers, suggesting a protective effect against obesity.

If you have the Met72 variant, your body may naturally resist fat accumulation better than others. However, since this is a rare genetic variant, most people should focus on standard evidence-based weight management: caloric balance and physical activity. This finding highlights that individual biological responses to energy balance vary significantly.

The Arg51Gln mutation in the ghrelin gene is associated with significantly lower plasma ghrelin concentrations, but this reduction does not translate to a protective effect against obesity or altered obesity-related phenotypes.

Having lower ghrelin levels due to the Arg51Gln mutation does not appear to protect against obesity. Do not attempt to artificially lower ghrelin as a weight loss strategy, as this paper shows no benefit. Focus on overall energy balance.

Met72 allele carriers, particularly women, exhibit a lower prevalence of hypertension compared to non-carriers, suggesting a protective effect against cardiovascular comorbidities associated with obesity.

For obese women with the Met72 variant, there is an observed lower risk of hypertension. This does not replace blood pressure monitoring, but it suggests that genetic factors play a role in cardiovascular health independent of BMI. Regular monitoring is still essential.

Chronic low-level mercury exposure from fish consumption does not significantly increase coronary heart disease (CHD) risk in the general adult population, and may only lessen the magnitude of benefit from fish intake without causing net harm.

You do not need to avoid fish due to mercury concerns if you are an adult eating modest amounts. The mercury levels in typical fish do not significantly increase your risk of heart disease, and the heart benefits of eating fish remain intact.

Alternate day fasting does not significantly alter skeletal muscle genes involved in fatty acid transport/oxidation or mitochondrial biogenesis in nonobese humans.

Three weeks of alternate day fasting does not significantly change the expression of genes responsible for fat burning or mitochondrial growth in nonobese people. Your muscle's capacity to oxidize fat may not have increased measurably at the gene level.

SGLT2 inhibitors improve heart failure outcomes through mechanisms independent of glucose lowering, including natriuresis, osmotic diuresis, reduced plasma volume, and improved myocardial energetics via ketone utilization.

SGLT2 inhibitors help the heart by making it work more efficiently. They help remove excess fluid and sodium, reducing strain on the heart, and shift the heart's fuel source to ketones, which are more energy-efficient. This happens regardless of blood sugar levels.

Early-life chronic malnutrition (stunting) predisposes individuals to obesity in adolescence and adulthood, even within low-income populations with limited food supply.

In low-resource settings, preventing stunting in early childhood is critical to preventing obesity later in life. Simply providing enough calories for weight gain without addressing height/stunting may not prevent the shift to obesity; early nutritional quality and infection control are key to preventing the 'fat but stunted' phenotype.

Training to volitional failure, contraction velocity, set configuration, inter-set rest, periodization, time of day, and exercise order do not significantly influence skeletal muscle hypertrophy.

You do not need to obsess over training to failure, specific tempos, exercise order, or rest periods to build muscle. These variables have little to no impact on hypertrophy compared to the main drivers: load, frequency, and volume. Choose what is sustainable for you.

Excessive dietary intake of linoleic acid (LA) leads to the formation of oxidized linoleic acid metabolites (OXLAMs) and alters cardiolipin composition, causing mitochondrial dysfunction and contributing to chronic diseases such as cardiovascular disease, cancer, and Alzheimer's.

Reduce intake of seed oils (soybean, corn, canola, sunflower) to lower linoleic acid consumption. This may help reduce the production of harmful metabolites linked to chronic disease, though the process is slow due to LA's long half-life.

High dietary linoleic acid intake inhibits the conversion of short-chain omega-3 fatty acids (ALA) to long-chain omega-3 fatty acids (EPA/DHA) by inhibiting delta-desaturase enzyme activity.

If you consume high amounts of seed oils, your body's ability to convert plant-based omega-3s (ALA) into active forms (EPA/DHA) is reduced. Consider direct sources of EPA/DHA if you are not consuming fish.

Time-restricted eating (TRE) with a 9-hour window (10:00-19:00) does not significantly improve glycaemic control (HbA1c) or reduce body mass in individuals with Type 2 Diabetes compared to habitual eating patterns.

If you have Type 2 Diabetes, simply shifting your eating window to 9 hours (e.g., 10am-7pm) without changing *what* or *how much* you eat will not significantly improve your blood sugar levels or help you lose weight. TRE may be feasible to adhere to, but it is not an effective standalone metabolic intervention for T2D unless it leads to reduced caloric intake.

Greater dietary diversity (variety of foods) is associated with suboptimal eating patterns, higher energy intake, and increased risk of weight gain and obesity in adult populations.

Stop trying to eat a wide variety of foods as a strategy for weight loss. Instead, focus on eating a healthy pattern that emphasizes plant foods, protein, low-fat dairy, and limits sweets and processed foods. Variety in the context of a modern food environment often leads to consuming more calories and less healthy options.

Genetic variants associated with HbA1c levels are linked to an increased risk of coronary artery disease, although this association is attenuated when adjusting for other cardiovascular risk factors.

Higher HbA1c levels are associated with a higher risk of heart disease. While this link is strong, it may be partly explained by other risk factors like cholesterol and weight. Monitoring HbA1c is important for overall cardiovascular health.

Genetic variants associated with fasting glucose (FG) levels do not show a significant independent association with coronary artery disease risk in this Mendelian randomization analysis.

While fasting glucose is a standard test, this genetic study suggests it may not be the primary driver of heart disease risk compared to overall diabetes status or HbA1c. However, maintaining healthy glucose levels is still important.

Obesity prevalence has increased significantly in the US since 1980 despite a plateau or decline in national energy intake and stable or increasing physical activity levels since 2000.

Focus on the quality and processing of your food rather than just counting calories. Prioritize minimally processed foods with intact cellular structures (fiber, phytonutrients) and avoid highly processed 'acellular' nutrients. This supports a healthy gut microbiome and metabolic function, which may help regulate body weight more effectively than caloric restriction alone.

Using technology-based self-monitoring tools alone (without phone intervention) does not significantly improve weight loss or adherence compared to traditional self-monitoring tools in the short term.

Using a fitness tracker and calorie app alone may not lead to significantly better weight loss than using paper logs and a basic pedometer. To get the most benefit, consider adding brief phone check-ins with a health coach to help you stay consistent.

Exclusive soft drink pouring rights contracts in schools significantly increase children's consumption of sugar-sweetened beverages, leading to higher daily caloric intake and contributing to childhood obesity.

School districts should reject exclusive pouring rights contracts with soft drink companies. The financial incentives tied to sales volume encourage schools to actively promote soda consumption, which adds significant 'empty calories' to children's diets and undermines nutritional education and health goals.

Under conditions of oxidative stress, glucose is prioritized for the Pentose Phosphate Pathway (PPP) to generate NADPH for antioxidant defense, whereas glycolysis is suppressed.

When your body is under significant stress (like intense exercise or illness), glucose is used to protect your cells from damage rather than just for energy. This highlights the importance of maintaining adequate glucose availability during high-stress periods.

Chronic carbohydrate overload combined with a sedentary lifestyle causes redox dysregulation, contributing to metabolic syndrome and type 2 diabetes.

If you are sedentary, eating large amounts of carbohydrates can disrupt your body's antioxidant balance and increase the risk of metabolic syndrome. Reducing carbohydrate intake or increasing physical activity may help mitigate this risk.