Browse the evidence

The term 'food addiction' is scientifically inaccurate and misleading; 'eating addiction' is the correct terminology for addictive-like eating behavior because it reflects a behavioral addiction rather than a substance-based one.

Stop using the term 'food addiction' when discussing your relationship with food. It is scientifically inaccurate and shifts blame to the food itself. Instead, recognize it as 'eating addiction,' which highlights that the issue lies with the behavior and psychological patterns of eating, not the chemical properties of the food. This shift empowers you to focus on changing behaviors and environmental cues rather than just avoiding specific nutrients.

Berberine activates AMPK and improves insulin sensitivity by inhibiting mitochondrial respiratory complex I, a mechanism shared with metformin and rosiglitazone.

Berberine improves insulin sensitivity by inhibiting mitochondrial complex I, similar to prescription drugs like metformin. However, standard berberine has very poor oral bioavailability, requiring high doses in animal models. A derivative, dihydroberberine, shows significantly improved efficacy and absorption in rodents, suggesting that formulation matters for clinical utility.

Dihydroberberine (dhBBR), a derivative of berberine, exhibits significantly improved in vivo efficacy, reduced adiposity, and improved insulin sensitivity compared to berberine at equivalent lower doses.

Dihydroberberine (dhBBR) is a derivative of berberine that is much better absorbed by the body. In rodent studies, dhBBR was significantly more effective at reducing fat and improving insulin sensitivity than standard berberine at the same dose. This suggests that for metabolic benefits, the form of berberine (bioavailability) is critical.

Population-wide restriction of dietary saturated fat intake below current levels does not reduce cardiovascular disease risk and may increase stroke risk, as evidenced by recent large-scale observational studies and meta-analyses of randomized trials.

Current evidence suggests that strictly limiting saturated fat intake for the general population does not lower heart disease risk and may even increase stroke risk. Focus on whole food sources of fat (like dairy and meat) within a balanced diet rather than aiming for a specific low-saturated-fat percentage, especially if you are replacing fats with refined carbohydrates.

Selenium is preferentially retained and redistributed to endocrine tissues (thyroid, adrenals, pituitary, testes, ovary) and the brain during nutritional depletion, prioritizing thyroid hormone homeostasis and cellular defense over other organs.

Ensure adequate dietary selenium intake to support thyroid and endocrine health. The body prioritizes these organs, so maintaining sufficient levels helps protect thyroid function and hormone regulation, especially if you live in a region with low soil selenium.

Selenium status modulates the expression and activity of selenoproteins that regulate transcription by redox-sensitive nuclear hormone receptors, linking selenium metabolism to broader endocrine signaling.

Maintain adequate selenium levels to support the body's redox balance, which influences how hormones interact with cells and regulate gene expression.

Excessive lipolysis from visceral adipose tissue drives lipotoxicity and insulin resistance by flooding the liver with free fatty acids, leading to ectopic fat accumulation and metabolic dysfunction.

Focus on improving insulin sensitivity rather than just cutting dietary fat. Visceral fat is metabolically active and releases fatty acids that clog up your liver and muscles, causing insulin resistance. Reducing visceral fat through exercise and metabolic health improvements can lower this harmful fatty acid overflow.

Visceral adipose tissue is more lipolytically active than subcutaneous fat, releasing fatty acids directly into the portal vein to the liver, thereby driving hepatic steatosis and insulin resistance more strongly than subcutaneous fat.

Waist circumference is a better health indicator than total weight. Reducing visceral fat through aerobic exercise and metabolic health improvements is crucial for preventing liver disease and type 2 diabetes, even if your total weight doesn't change drastically.

Estrogen deficiency during menopause leads to dysregulated lipid metabolism, characterized by increased LDL-C, increased triglycerides, and altered HDL subfractions, thereby increasing cardiovascular disease risk.

Understand that the drop in estrogen after menopause naturally raises your LDL cholesterol and triglycerides while lowering protective HDL. This increases your risk of heart disease. Managing this through diet (healthy fats, fiber) and potentially medical intervention is crucial for long-term heart health.

Poor social engagement (including poor social network and poor social support) is associated with a significantly increased risk of developing dementia.

Prioritize building and maintaining a reliable social network and seeking social support, as these structural aspects of socialization are linked to a lower risk of dementia. Focus on objective measures like having a close friend, regular contact, and support systems rather than just subjective feelings of loneliness, which showed less consistent protective effects in this analysis.

Obesity causes hypertension and chronic kidney disease through multiple mechanisms including increased renal tubular sodium reabsorption, sympathetic nervous system activation, RAAS activation, and physical compression of the kidneys by visceral fat.

Obesity is a direct cause of high blood pressure and kidney disease through specific physiological pathways like increased sodium retention and nerve system activation. Managing visceral fat is crucial for mitigating these risks.

RAAS blockade with ACE inhibitors or ARBs reduces proteinuria and slows the progression to end-stage renal disease in obese patients with proteinuria.

Obese patients with proteinuria benefit significantly from ACE inhibitors like ramipril, which can greatly reduce the risk of kidney failure.

Androgen excess drives metabolic dysfunction in PCOS by promoting visceral adiposity, inducing insulin resistance through adipocyte hypertrophy and reduced adiponectin, and suppressing brown adipose tissue thermogenesis.

For women with PCOS, metabolic issues like insulin resistance and visceral fat accumulation are strongly linked to high androgen levels, not just diet. Treating the hormonal imbalance (e.g., via anti-androgens or insulin-sensitizers) may be necessary to address metabolic health, as lifestyle changes alone may be insufficient if androgen excess persists.

Insulin resistance in PCOS is characterized by selective ovarian insulin resistance (hyper-sensitivity) alongside peripheral resistance, which exacerbates androgen production.

Standard insulin-sensitizing treatments (like metformin) can help lower androgens by reducing insulin levels, which in turn reduces the ovarian stimulation of androgen production.

Overweight and obesity in children are markers for, rather than the direct cause of, poor academic performance, which is more strongly linked to socioeconomic status and poor nutrition.

Educators and policymakers should not assume that overweight children are failing academically because of their weight. Instead, they should address underlying factors like poverty, nutrition, and social stigma, which are the true drivers of academic performance.

A lower omega-6 to omega-3 ratio (specifically 2.5:1) reduces rectal cell proliferation in patients with colorectal cancer, whereas a ratio of 4:1 with the same amount of omega-3s had no effect.

If managing colorectal cancer risk, aim for a very low omega-6 to omega-3 ratio (around 2.5:1). This requires significantly reducing seed oils (corn, soy, sunflower) while increasing omega-3 sources. Simply taking fish oil pills without changing your background fat intake may not provide the same anti-proliferative benefits.

Purely restrictive bariatric procedures (e.g., adjustable gastric banding) are more commonly associated with weight regain and weight loss failure compared to malabsorptive procedures (e.g., Roux-en-Y bypass).

If you are considering bariatric surgery, understand that the type of surgery matters. Malabsorptive procedures like Roux-en-Y bypass tend to result in better long-term weight loss than purely restrictive procedures like gastric banding. Gastric banding has a higher risk of weight regain.

Estrogen rapidly activates AMP-activated protein kinase (AMPK) in skeletal muscle via non-genomic mechanisms, promoting fat oxidation and down-regulating lipogenesis.

Estrogen helps your muscles burn fat quickly by turning on an energy sensor called AMPK. This happens fast, suggesting estrogen has immediate metabolic benefits beyond long-term structural changes.

Estrogen increases perilipin protein levels in adipocytes, which suppresses basal lipolysis but significantly enhances catecholamine-stimulated lipolysis.

Estrogen helps your fat cells release stored fat more efficiently when stimulated by stress or exercise (catecholamines) by increasing a protective protein called perilipin. This makes your fat cells more responsive to signals that tell them to burn fat.

Consumer wearable sleep trackers generally overestimate total sleep time and sleep efficiency while underestimating wake after sleep onset compared to polysomnography, with high sensitivity but low specificity for wake detection.

Use wearable sleep trackers to observe long-term trends in your sleep habits, not to diagnose sleep disorders. Expect them to overestimate how much you slept and underestimate how much you were awake. For clinical concerns, rely on professional sleep studies (PSG).

Rotating night shift work (defined as ≥3 night shifts per month) is associated with a statistically significant but small absolute increase in coronary heart disease (CHD) risk in women, with risk increasing in a duration-dependent manner (≥5 years exposure).

For women in rotating night shift roles (≥3 nights/month), long-term exposure (≥5 years) is linked to a modestly higher risk of heart disease. The risk appears to be most relevant during active exposure and decreases after stopping shift work. Regular cardiovascular monitoring is advisable for those with this work history, particularly if they have other risk factors like obesity.

The increased CHD risk associated with rotating night shift work wanes over time after cessation of the shift work.

If you have worked rotating night shifts, your heart disease risk decreases the longer you have been off those shifts. Stopping rotating night work is a beneficial health decision.

The gut microbiome of healthy Japanese individuals exhibits a distinct functional profile characterized by high abundance of Actinobacteria (specifically Bifidobacterium) and a unique hydrogen metabolism pathway that favors acetogenesis over methanogenesis, which cannot be fully explained by diet alone.

This research highlights that gut microbiomes are population-specific and influenced by factors beyond just what you eat today. For Japanese individuals, a high abundance of Bifidobacterium and a preference for acetogenesis (producing acetate) over methanogenesis (producing methane) are characteristic. These features may contribute to health benefits like lower inflammation and longer lifespan, but they are deeply rooted in population-level adaptations, not just short-term dietary changes.

Noninvasive steatosis biomarkers (FLI, NAFLD-LFS, HSI, VAI, TyG) accurately diagnose the presence of hepatic steatosis but fail to quantify its severity, rendering them unsuitable for monitoring treatment-induced changes in liver fat.

Use these biomarkers (FLI, HSI, VAI, TyG) as a screening tool to identify who likely has fatty liver, especially if ultrasound isn't available. Do not use them to track if your diet or medication is working, as they cannot accurately measure how much fat is actually in the liver. They are good for 'rule-in' screening, not 'monitoring' treatment.