Browse the evidence

Global age-standardised mean BMI in children and adolescents increased significantly from 1975 to 2016, with obesity prevalence rising from 0.7% to 5.6% in girls and 0.9% to 7.8% in boys, while underweight prevalence decreased.

Track your child's growth using standard BMI percentiles for their age and sex, not just absolute weight. Recognize that both underweight and obesity carry significant health risks. In many regions, underweight remains a larger burden than obesity, so nutritional support should address both ends of the spectrum.

The trajectory of BMI increase in children and adolescents has decoupled from adults in many high-income countries, where childhood BMI trends have plateaued while adult BMI continues to rise.

In high-income countries, public health efforts for children may be showing results (plateauing BMI), but adult obesity continues to rise. This suggests that childhood interventions are working to some extent, but adult lifestyle factors remain unaddressed. Focus on maintaining childhood gains and addressing adult-specific barriers.

Underweight remains a more prevalent issue than obesity globally for children and adolescents, with the highest burden concentrated in South Asia and parts of Africa.

Do not assume that obesity is the only or main nutrition problem for children. In many parts of the world, underweight is far more common. Nutrition programs must be tailored to address both undernutrition and overnutrition, especially in South Asia and Africa.

Brown adipose tissue (BAT) thermogenesis is exclusively mediated by uncoupling protein-1 (UCP1) and requires lipolysis-derived fatty acids as the trigger; in the absence of UCP1, norepinephrine-induced thermogenesis does not occur.

Brown fat burns energy through a specific protein (UCP1) that uncouples heat from ATP production. This process is triggered by fatty acids released from fat stores when stimulated by the nervous system (norepinephrine). Without UCP1, this heat production cannot happen, regardless of other metabolic pathways.

Brown adipose tissue thermogenesis is strictly dependent on lipolysis; thermogenesis cannot be evoked without simultaneously evoking lipolysis, and fatty acids released from triglycerides act as the direct trigger for UCP1.

Brown fat burns energy by breaking down stored fats (lipolysis). The released fatty acids directly activate the UCP1 protein to generate heat. You cannot have brown fat heat production without first breaking down fat stores.

Prebiotics are defined as substrates selectively utilized by host microorganisms to confer a health benefit, distinguishing them from non-selective dietary fibers and non-microbial agents.

Not all gut-friendly foods are prebiotics. To be a prebiotic, a substance must be selectively eaten by beneficial bacteria to produce a specific health benefit. Common examples like inulin and FOS fit this, but general fibers like cellulose do not necessarily qualify.

Health benefits from prebiotics are mediated by the selective growth of specific microbial taxa and their metabolic products (e.g., SCFAs), rather than the substrate itself acting directly on host cells.

Prebiotics work by feeding specific gut bacteria. These bacteria then produce beneficial compounds (like short-chain fatty acids) that improve your health. You need a healthy gut microbiome for prebiotics to work.

Underweight prevalence has decreased globally but remains a significant public health problem in specific regions, particularly South Asia and parts of Africa.

In many parts of the world, being underweight is still a major health risk, particularly in South Asia and Africa. Public health efforts need to address both ends of the BMI spectrum, not just obesity.

The mortality risk associated with high BMI is significantly lower in Black individuals compared to White individuals, particularly in Black women.

For Black adults, the mortality risk associated with higher BMI is lower than for White adults, but it is not zero. Health monitoring should still be prioritized, as elevated BMI still carries some increased risk, especially in White populations.

Diabetes mellitus is an independent major risk factor for cardiovascular disease (CVD), and from a cardiovascular medicine perspective, it is appropriate to classify diabetes itself as a cardiovascular disease.

If you have diabetes, you must treat your cardiovascular health with the same urgency as your blood sugar. Diabetes is not just a metabolic issue; it is a direct cause of heart attacks, strokes, and heart failure. Aggressive management of blood pressure, cholesterol, and smoking cessation is mandatory because your baseline risk for heart disease is already significantly elevated by the diabetes itself.

In healthy aging men, serum total testosterone and free testosterone index decline at a constant, age-invariant rate regardless of chronic illness, medication use, or lifestyle factors, leading to a high prevalence of hypogonadal levels in older age.

If you are an older man, expect your testosterone to drop by about 3.2 ng/dL every year, regardless of how healthy you are. This is a biological fact, not just a result of being sick. By your 70s or 80s, a significant portion of men will have testosterone levels in the 'hypogonadal' range. If you experience symptoms like loss of muscle mass, low energy, or sexual dysfunction, discuss testing with your doctor, as replacement therapy may be beneficial for those with the lowest levels.

Sarcopenia diagnosis requires both low muscle mass and weakness; low muscle mass alone is weakly or not associated with functional disability.

To accurately diagnose sarcopenia in older adults, you must measure both muscle mass and muscle strength. Relying on muscle mass alone will miss many individuals at risk for disability. Use standardized cutpoints: grip strength <26 kg for men and <16 kg for women, and appendicular lean mass adjusted for BMI <0.789 for men and <0.512 for women.

High systolic blood pressure (SBP) is a leading metabolic risk factor globally, contributing to 7.8% of total disability-adjusted life-years (DALYs) in 2021, with an increasing annual exposure rate of 1.8%.

High blood pressure is a major driver of global disease burden. Regular monitoring and management are crucial for long-term health.

Obesity induces a chronic, low-grade inflammatory state termed 'metainflammation' characterized by the accumulation of proinflammatory M1 macrophages in adipose tissue, which directly impairs insulin signaling and contributes to systemic insulin resistance and type 2 diabetes.

Excess body fat, especially visceral fat, triggers an immune response that actively blocks your body's ability to use insulin efficiently. This isn't just 'being heavy'; it's a biological state of chronic low-grade inflammation. Addressing the underlying inflammation through weight management and metabolic health improvements is key to reversing insulin resistance.

Activation of Toll-like receptor 4 (TLR4) by saturated free fatty acids is a primary mechanism linking nutrient excess to inflammation and insulin resistance in metabolic tissues.

High intake of saturated fats can directly activate immune receptors (TLR4) in your cells, triggering inflammation that blocks insulin. Reducing saturated fat intake may help lower this specific inflammatory trigger.

Habitual sleep duration of 9 hours or more per night is associated with a 30% increased risk of all-cause mortality compared to the reference range of 7-8 hours.

Aim for 7-8 hours of sleep per night. Sleeping consistently 9 hours or more is associated with a 30% higher risk of death. If you consistently need this much sleep, it may be a sign of underlying health issues worth investigating with a doctor.

Causal inference between short sleep and obesity is difficult due to lack of control for important confounders and inconsistent evidence of temporal sequence in prospective studies.

While short sleep is linked to obesity, we cannot yet say it causes it. Other factors like diet, activity, and stress may explain the link. However, given the consistency of the association, improving sleep is still a prudent health strategy.

Prospective cohort studies are methodologically superior to case-control studies for investigating diet-disease relationships because they avoid recall bias and reverse causation bias inherent in case-control designs.

For long-term health research, tracking dietary habits over many years in large groups (prospective cohorts) provides more reliable evidence of cause-and-effect than comparing sick and healthy people after the fact (case-control). This is because it avoids the errors of remembering past diets and the influence of disease on current biological markers.

Women with polycystic ovary syndrome (PCO) exhibit profound peripheral insulin resistance that is independent of obesity, body composition, and glucose tolerance status.

If you have PCO, you likely have insulin resistance regardless of your weight. This is not just a 'weight problem' but a hormonal one. Focus on managing insulin sensitivity through diet and lifestyle, as standard weight-loss advice alone may not address the underlying resistance inherent to the syndrome.

Intensive glycemic therapy in Type 1 Diabetes produces a 'metabolic memory' effect, where the initial intensive treatment continues to reduce the risk of complications for years even after glycemic separation between treatment groups disappears.

Even if your blood sugar levels aren't perfect now, getting them under control early in your Type 1 Diabetes journey has long-lasting benefits. This 'metabolic memory' means that your body continues to benefit from early intensive treatment, reducing your risk of heart disease and other complications for decades, even if your glucose levels later become less distinct from those who had less intensive treatment.

Spending 9.5 or more hours per day sedentary is associated with a statistically significantly higher risk of death.

Avoid sitting for more than 9.5 hours a day. If you have a desk job, incorporate standing breaks and light movement throughout the day. The risk of death increases significantly once sedentary time exceeds this threshold, even if you exercise moderately.

Magnesium acts as a physiological calcium antagonist and is involved in over 600 enzymatic reactions, making it essential for cellular physiology.

Magnesium is not just a supplement; it is a critical mineral involved in hundreds of body processes, from energy production to muscle function. Ensuring adequate intake supports these fundamental biological functions.

Statins are the first-choice pharmacological treatment for lowering LDL-C, non-HDL-C, and apo B, but they only marginally lower triglycerides and do not fully correct the dyslipidemia characteristic of obesity.

Statins are the primary medication for lowering bad cholesterol (LDL) and are recommended for obese patients with high cardiovascular risk. However, they do not significantly lower triglycerides, which are often elevated in obesity, so lifestyle changes remain crucial.

Inflammation and disease burden are critical etiologic criteria for malnutrition, contributing to altered metabolism, increased muscle catabolism, and adverse outcomes.

Malnutrition isn't just about not eating enough; active disease and inflammation can cause muscle loss and metabolic changes even if food intake is normal. Diagnosis must account for these inflammatory drivers.