Browse the evidence

Higher circulating and tissue levels of arachidonic acid (AA) are not associated with an increased risk of cardiovascular disease, and may be associated with a lower risk of total CVD.

You do not need to worry about high levels of arachidonic acid (AA) in your blood as a risk factor for heart disease. This study shows that higher AA levels are not associated with increased CVD risk and may even be linked to lower risk.

Physiological adaptations to weight loss, including slowed resting metabolic rate (RMR) and increased hunger hormones, actively defend a higher body weight 'set-point' and promote weight regain.

After you lose weight, your body will fight to get it back by slowing your metabolism and increasing hunger. This is a biological 'set-point' defense, not a lack of willpower. To maintain weight loss, you must accept that you will need to be more vigilant about food intake and exercise than before, as your body is biologically programmed to regain the weight.

The carbohydrate-insulin model, which posits that high carbohydrate intake causes hyperinsulinemia leading to fat storage and weight gain, is experimentally falsified because low-carbohydrate diets fail to produce the expected fat loss or sustained increase in energy expenditure.

Do not rely on the carbohydrate-insulin model to explain weight loss. Low-carb diets do not inherently increase energy expenditure or fat loss compared to other diets when calories are matched. Focus on sustainable dietary patterns.

Intentional long-term weight loss in overweight or obese adults with type 2 diabetes increases the risk of frailty fractures (hip, pelvis, upper arm/shoulder) despite not increasing total or hip fracture rates overall.

If you have type 2 diabetes and are planning to lose weight, be aware that this specific intervention (intensive lifestyle change) has been linked to a higher risk of breaking bones in the hip, pelvis, or shoulder area, even if your overall fracture risk doesn't change. To mitigate this, focus on preserving muscle mass through resistance training and ensure adequate calcium and vitamin D intake, as bone loss is a key mechanism for this increased risk.

Global dietary intake data is highly available for fruits, non-starchy vegetables, and sugar-sweetened beverages, but critically sparse for iodine, vitamin A, plant protein, selenium, added sugar, and animal protein.

When evaluating global diet quality, recognize that data on fruits, vegetables, and sugary drinks is robust, but data on essential micronutrients (iodine, selenium, vitamin A) and specific protein sources is often missing. This limits our ability to assess diet-related health risks in many populations accurately.

Perioperative fish oil supplementation (EPA+DHA) does not increase the risk of major bleeding in cardiac surgery patients and may reduce blood transfusion requirements.

If you take fish oil for heart health, you likely do not need to stop it before heart surgery. This study of over 1,500 patients showed that continuing fish oil did not increase bleeding risk and actually reduced the amount of blood transfused. Consult your surgeon, but current evidence supports continuing supplementation.

A 10-year intensive lifestyle intervention for weight loss and increased physical activity does not improve overall or domain-specific cognitive function in middle-aged and older adults with type 2 diabetes compared to diabetes support and education.

For adults with type 2 diabetes, a 10-year intensive lifestyle program focused on weight loss and exercise did not improve cognitive function compared to standard diabetes education. While lifestyle changes are crucial for cardiovascular health, they should not be relied upon as a primary strategy to prevent cognitive decline in this specific population based on current evidence.

Mitochondrial dysfunction, characterized by ROS overproduction, Ca2+ overload, and structural changes, is a primary driver of cellular senescence and age-related diseases.

Maintaining mitochondrial health is crucial for longevity. This involves managing oxidative stress through a balanced diet, regular exercise, and potentially avoiding excessive ROS-producing activities. Understanding that mitochondria are central to aging helps prioritize interventions that support their function.

Metabolic surgery reduces the risk of microvascular and macrovascular complications, as well as all-cause mortality, compared to non-surgical treatment in T2D patients.

Beyond weight loss, metabolic surgery significantly lowers the risk of diabetes-related organ damage (eyes, kidneys, nerves) and reduces the risk of early death compared to managing diabetes with medication and lifestyle changes alone.

Leptin regulates glucose homeostasis through direct actions on POMC neurons, but does not regulate food intake or energy balance through direct actions on these same neurons.

Understanding that leptin's effect on blood sugar is distinct from its effect on hunger helps explain why leptin therapy fails for weight loss in most obese individuals (who are leptin resistant) but might still have metabolic benefits. It shifts focus from 'blocking hunger' to 'metabolic flexibility' and non-POMC pathways.

Obesity can result from an intrinsic metabolic disorder that shifts fuel partitioning toward storage and sequestration in adipose tissue, causing 'internal starvation' and compensatory hyperphagia, independent of excessive energy intake.

This paper argues that for some individuals, obesity is driven by a biological defect in how the body handles fuel (partitioning), not just by eating too much. This biological defect traps energy in fat cells, causing the body to feel starved and triggering hunger. While this explains specific pathological cases in animal models, it suggests that for some humans, treating obesity requires addressing these underlying metabolic shifts rather than just focusing on calorie restriction.

Resting energy expenditure (REE) is primarily determined by the mass and specific metabolic rates of organs and tissues, with fat-free mass (FFM) explaining the majority of variance in REE.

Your resting metabolic rate is largely dictated by your body composition, specifically your fat-free mass (muscle, organs, bone). Maintaining muscle mass is key to preserving metabolic rate.

Acute postexercise elevations in systemic anabolic hormones (testosterone, growth hormone, IGF-1) are neither necessary nor sufficient to stimulate muscle protein synthesis or drive resistance exercise training-induced hypertrophy.

Stop worrying about the exact time of day you train or trying to manipulate your hormones for better gains. Whether you train in the morning or evening, or whether your hormones fluctuate during your menstrual cycle, does not significantly change your ability to build muscle. Focus on consistent, progressive resistance training rather than trying to 'optimize' your hormonal environment.

Obesity is a biologic disorder caused by alterations in CNS pathways controlling energy balance, not a lifestyle failure remediable by willpower alone.

Stop blaming yourself for your weight. Your body is fighting you due to biological mechanisms, not just willpower. Seek medical treatment for obesity just as you would for high blood pressure.

GLP-1 therapy is associated with significant gastrointestinal side effects (nausea, vomiting, diarrhea, constipation) which are dose-dependent and can lead to discontinuation, although most side effects decrease with continued use.

You will likely experience some gastrointestinal side effects like nausea, diarrhea, or constipation, especially when you start the medication or increase the dose. These symptoms often improve over time. Talk to your doctor about managing these side effects through diet and slow dose titration.

Obesity is fundamentally driven by a disruption in energy balance, mediated by central nervous system resistance to leptin and insulin, and dysregulation of the reward system.

Obesity involves biological resistance to satiety signals (leptin/insulin) and reward dysregulation, meaning willpower alone is often insufficient. Medical interventions that bypass or enhance these signals are often necessary.

Obesity is not caused by a lack of willpower but is the result of complex interactions between individual biological factors and environmental determinants, requiring multifactorial prevention and treatment strategies.

Stop blaming yourself for your weight. Obesity is a complex disease influenced by biology and your environment, not just willpower. Effective management requires addressing both individual health behaviors and the broader environment, such as access to healthy food and safe spaces for activity.

Environmental-level factors, such as the food environment and socioeconomic status, interact with individual-level biological factors to drive obesity, and interventions focusing solely on the individual are suboptimal.

To manage weight effectively, you need to address both your personal habits and your environment. This might mean seeking out healthier food options, advocating for policy changes, and understanding how your biology interacts with your surroundings.

Obesity is a chronic, progressive, relapsing, and treatable multi-factorial neurobehavioral disease, not just a lifestyle choice.

Understand that obesity is a disease with biological drivers, not just a failure of will. This reduces self-blame and opens the door to effective medical and lifestyle interventions.

SGLT2 inhibitors provide consistent cardiovascular benefits (reduced mortality and morbidity) across all BMI classes in heart failure, with no mediating effect of obesity on their efficacy.

If you have heart failure, SGLT2 inhibitors (like Dapagliflozin or Empagliflozin) are a standard, highly effective treatment that works regardless of your weight. They reduce the risk of hospitalization and death. Discuss starting these with your doctor if you are not already on them.

Obesity is fundamentally a chronic metabolic disease characterized by disturbances in energy homeostasis and excessive fat accumulation, driven by a complex interplay of genetic, epigenetic, biological, psychological, and environmental factors.

Understand that obesity is a complex chronic disease, not a moral failing. Effective management requires addressing biological, genetic, and environmental factors, often necessitating medical interventions alongside lifestyle changes.

Genetic variants, particularly in the MC4R, FTO, and LEP/LEPR genes, significantly influence susceptibility to obesity, affecting appetite regulation, energy expenditure, and fat storage.

Genetics play a significant role in obesity risk. If you have a family history of obesity, you may have a higher predisposition. However, this does not mean weight management is impossible; tailored medical and lifestyle strategies can be highly effective.

BMI is an insufficient diagnostic tool for obesity because it fails to differentiate between fat mass and lean body mass, leading to misclassification.

Do not rely solely on BMI to determine your health status. It fails to distinguish between muscle and fat. Ask your doctor for more precise assessments like waist circumference or body composition analysis to get a true picture of your metabolic risk.

Higher genetically predicted lifelong BMI causally increases all-cause mortality, with the effect substantially mediated through diabetes.

In this population, higher lifelong BMI significantly increases the risk of premature death, largely by increasing the risk of diabetes. Managing weight and blood sugar are critical for longevity.