Browse the evidence

The sugar industry successfully influenced the 1971 National Caries Program (NCP) to prioritize interventions that reduce the harm of sugar consumption (e.g., fluoride, dextranases, vaccines) over restricting sugar intake, thereby deflecting attention from the causal role of sucrose in dental caries.

Be skeptical of public health initiatives that focus on 'harm reduction' technologies (like additives or enzymes) while ignoring the need to limit sugar intake. If an industry group promotes a technical solution that allows continued high consumption of a product, scrutinize their motives, as they may be trying to avoid stricter regulations on consumption.

A bimodal GLP-1/MK-801 conjugate produces synergistic weight loss and metabolic improvements in diet-induced obese rodents by targeting NMDA receptors in GLP-1-expressing brain regions, while mitigating the adverse behavioral and physiological effects of MK-801 monotherapy.

This research describes a new experimental drug that combines two mechanisms to treat obesity in animals. It works by targeting specific brain cells to reduce food intake and increase energy expenditure without the side effects of older drugs. This is not yet available for humans.

Acute ingestion of capsinoids (1–12 mg) does not significantly increase resting metabolic rate or fat oxidation in healthy human subjects within a 2-hour window.

Taking capsinoids (1-12 mg) will not increase your calorie burn or fat oxidation in the short term (2 hours). Do not rely on this supplement for immediate weight loss or metabolic boosting effects.

Intentional, medically supervised weight loss in overweight patients with type 2 diabetes does not reduce all-cause mortality or cardiovascular morbidity and may be associated with increased mortality in obese subgroups (BMI ≥30).

For overweight patients with type 2 diabetes, aiming for significant weight loss under medical supervision does not guarantee a longer life and may not reduce heart disease risk. Focus on stable management of blood sugar, blood pressure, and lipids rather than prioritizing weight loss as the primary goal for longevity.

Hepatic overexpression of the enzyme ALOXE3 enhances whole-body insulin sensitivity and reduces weight gain by generating the PPARγ ligand 12-KETE.

This research identifies ALOXE3 as a key enzyme induced by fasting that improves insulin sensitivity by activating PPARγ. While direct supplementation with ALOXE3 is not currently available, the findings suggest that strategies inducing this enzyme, such as fasting or specific glucose transporter blockers (like trehalose), may offer metabolic benefits. Current clinical application is limited as genetic therapy is not yet optimized for polygenic diseases like obesity.

In real-world outpatient settings for Type 2 Diabetes, pharmacological management of blood pressure, HbA1c, and LDL cholesterol achieves target control in only a minority of patients, with combined adequate control of all three factors occurring in just 16.4% of cases.

If you have Type 2 Diabetes, having prescriptions for blood pressure, sugar, and cholesterol medication does not guarantee your body is responding correctly. In this study, only 16% of patients had all three numbers in the safe zone. You must actively monitor your HbA1c, LDL, and Blood Pressure, not just fill your prescriptions. If your numbers are not at target, discuss intensifying or changing your therapy with your doctor.

Peri-operative protein or amino acid supplementation does not significantly improve muscle strength (quadriceps or handgrip) or functional outcomes in total joint arthroplasty patients.

Do not expect protein supplements to restore your leg strength after surgery. The evidence shows they help keep muscle mass from shrinking, but they do not significantly improve strength or walking ability on their own. You must combine supplementation with physical therapy and exercise to regain strength.

Sibutramine increases the risk of nonfatal cardiovascular events (myocardial infarction and stroke) in patients with pre-existing cardiovascular disease or type 2 diabetes with additional risk factors, leading to its contraindication in these populations.

If you have heart disease, a history of stroke, or diabetes combined with other heart risks (like high blood pressure or smoking), sibutramine is not safe for you. It increases your chance of having a heart attack or stroke. Do not use this medication if you fall into these categories; consult your doctor for safer alternatives.

Higher dietary resistant starch intake is NOT significantly associated with reduced cardiovascular disease (CVD) mortality.

Do not rely on resistant starch alone to protect your heart. This study found no significant link between RS intake and reduced cardiovascular mortality. While RS may offer other benefits, managing overall cardiovascular risk requires a holistic approach including blood pressure, lipid management, and overall diet quality, not just increasing RS.

Traditional weight management strategies, including lifestyle interventions and metabolic and bariatric surgery (MBS), are generally ineffective for reducing hyperphagia in patients with rare MC4R pathway diseases because they do not address the underlying pathophysiology.

For patients with rare genetic obesity (POMC, LEPR, BBS, etc.), standard diets, exercise programs, and even weight-loss surgery often fail to control the insatiable hunger (hyperphagia). This is not a failure of willpower but a failure of the treatment to address the specific brain signaling defect. Recognizing this can reduce caregiver guilt and shift focus toward seeking targeted genetic therapies.

There is no statistically significant association between weight loss (amount or frequency) and cancer mortality in men or women.

Losing weight, whether once or repeatedly, does not appear to reduce your risk of dying from cancer based on this study. Focus on other aspects of health.

Selective activation of Gs signaling in enteroendocrine K cells increases endogenous GIP secretion, which improves glucose tolerance in obese and diabetic mouse models.

This research suggests that therapies targeting the specific signaling pathways (Gs) in gut K cells to boost natural GIP production could be a viable strategy for managing obesity and Type 2 Diabetes, potentially offering better glucose control than current approaches that rely on external hormone administration.

Reducing global obesity prevalence to 2019 levels could save an estimated US$2.2 trillion annually by 2060 through healthcare and productivity-related cost savings.

Addressing obesity at a population level saves massive amounts of money globally. Public health policies that reduce obesity prevalence have a high economic return on investment.

Other GLP-1 receptor agonists and SGLT2 inhibitors, including semaglutide, dulaglutide, and canagliflozin, did not demonstrate a statistically significant elevation in gynecologic tumor risk compared to controls.

If you are taking other GLP-1 receptor agonists (like semaglutide or dulaglutide) or SGLT2 inhibitors (like canagliflozin or empagliflozin), this network meta-analysis did not find a statistically significant increase in gynecologic tumor risk for these agents. However, the authors note that more data is needed to confirm whether the association with tirzepatide is causal.

GLP-1 receptor agonists (GLP-1 RAs) are not cost-effective at current prices, requiring significant price reductions to meet standard willingness-to-pay thresholds.

GLP-1 RAs are clinically effective but not cost-effective at current prices. They should be used selectively (e.g., for those who cannot undergo surgery) and only if pricing aligns with their health benefits.

Peripheral GLP-1 signaling is not essential for long-term energy balance or bodyweight regulation in humans or rodents, as evidenced by normal body weight in GLP-1R knockout mice and lack of effect from peripheral antagonism.

Your body's natural production of GLP-1 in the gut does not significantly control your long-term weight. This is why lifestyle changes alone often fail to sustain weight loss, and why pharmacologic doses that strongly activate brain receptors are needed for significant weight reduction.

Fecal Microbiota Transplantation (FMT) from lean donors does not result in significant weight loss or improved metabolic health in humans with obesity, despite showing benefits in some animal models.

Do not pursue FMT for weight loss at this time, as human trials have not shown benefit. Focus on dietary interventions which are more accessible and have stronger evidence for long-term health.

Feeding rats a cafeteria diet with low protein content (approx 7%) significantly increases energy expenditure and brown adipose tissue (BAT) activity compared to normal or high protein cafeteria diets, primarily through sympathetic activation of non-shivering thermogenesis.

This research suggests that when consuming highly palatable, energy-dense foods, a very low protein intake might trigger a specific metabolic defense mechanism (increased brown fat activity) that burns off excess calories. However, this comes at the cost of stunted growth and reduced fat-free mass in rats. For humans, this highlights that diet composition (specifically protein levels) significantly influences how the body handles excess energy, but it does not recommend low protein diets for general use due to the negative impact on lean mass.

Improvements in household technology (electrification and appliance diffusion) did not cause the mid-20th century baby boom; instead, evidence shows a negative correlation between technology access and fertility rates.

This paper refutes the economic theory that household technology drives fertility increases. It argues that the baby boom was not caused by appliances like washing machines or refrigerators, pointing to negative correlations between technology access and birth rates, and noting that the Amish, who limited technology use, still had a baby boom.

In low-latitude or semiarid snowpacks, evaposublimation accounts for 24-33% of total annual ablation, making it a dominant driver of hydrological balance.

This paper is about hydrology, not human fitness. However, the principle holds: in specific environments (like high altitude or dry climates), energy balance is driven by factors beyond simple heat transfer (melting). For fitness, this implies that environmental factors (humidity, wind, radiation) significantly impact energy expenditure and balance, not just caloric intake and exercise output.

The presence of muricholic acids (MCAs) in mice is critical for their high basal bile acid and cholesterol synthesis and low serum LDL levels; genetic elimination of MCAs in mice results in a human-like metabolic phenotype characterized by reduced synthesis and increased LDL cholesterol.

This research highlights that mice and humans regulate cholesterol and bile acids differently due to specific bile acid types (MCAs). For humans, this implies that therapies targeting bile acid metabolism must account for species-specific pathways, as mouse models lacking these pathways (KO mice) better mimic human metabolic responses.

Bile duct ligation (BDL) paradoxically stimulates bile acid synthesis in wild-type mice but not in mice lacking MCAs, indicating that MCAs are required for this paradoxical response.

This finding suggests that the body's response to bile flow obstruction (cholestasis) is heavily influenced by the type of bile acids present. In humans, where MCAs are not produced, this paradoxical response does not occur, highlighting a key difference in how we might treat cholestatic diseases compared to rodent models.

Gut-derived GLP-1 is not essential for the control of food intake or body weight in mice under normal conditions.

While gut health is important, the brain's response to GLP-1 is more critical for regulating food intake. GLP-1 medications work by acting on the brain, not just the gut.

Hypothalamic Glp1r-expressing cells are predominantly neuronal and localized to arterial vascular beds, whereas Gipr-expressing cells are predominantly non-neuronal (oligodendrocytes and pericytes) and localized to venous vascular beds.

This research suggests that GLP-1 and GIP drugs work through different pathways in the brain. GLP-1 primarily targets neurons and arterial blood vessels, while GIP targets support cells (oligodendrocytes) and venous blood vessels. This distinct localization may explain why combining them (dual agonism) is more effective for weight loss than using GLP-1 alone.