Browse the evidence

39.2% of participants screened positive for eating disorder signs and symptoms using the SCOFF questionnaire.

Practitioners should be aware that a significant portion of Brazilian adults may exhibit symptoms of eating disorders.

UPF consumption was higher in participants with binge eating and other eating disorders compared to those without ED symptoms.

Higher UPF consumption may be linked to specific eating disorder symptoms, indicating a need for dietary assessments in clinical settings.

There were no significant age-by-resilience interactions found.

Diet quality's impact on resilience appears consistent across different adult age groups.

The overall prevalence of sarcopenia in the studied population is 6.42%.

Practitioners should be aware of the prevalence of sarcopenia in older adults in urban-rural transition zones.

A long-term farming history is a strong, independent protective factor against sarcopenia.

Encouraging a farming lifestyle may help reduce sarcopenia risk in older adults.

The association between diabetes and sarcopenia was not statistically significant after adjusting for confounders.

Diabetes may not be a significant risk factor for sarcopenia when considering other factors.

The molecular clock component BMAL1 is required for satellite cell proliferation and the metabolic transition from oxidative to glycolytic energy sources during early muscle regeneration.

BMAL1 acts as a metabolic switch for muscle stem cells. When muscle is damaged, these cells must switch from resting energy (oxidative) to building energy (glycolytic) to multiply. BMAL1 regulates this switch. Disrupting your circadian rhythm (e.g., chronic shift work) might impair this metabolic flexibility, potentially slowing down the initial proliferation phase of muscle repair.

Social determinants of health, specifically poverty and food insecurity, are significant contributors to the high prevalence of obesity in communities of color.

For individuals in communities of color, obesity rates are heavily influenced by systemic factors like poverty and food insecurity. Addressing these social determinants is crucial for effective obesity management, alongside individual lifestyle changes.

Epigenetic priming via nutrient deprivation (caloric restriction) in the F0 generation increases the epigenetic plasticity of subsequent generations, allowing them to better adapt to varying diets and metabolic challenges.

Moderate caloric restriction (e.g., 50-70% of normal intake) during early development or pregnancy may 'prime' the epigenome, making offspring more metabolically resilient to future dietary challenges. However, extreme restriction should be avoided as it can lead to growth issues.

Ketogenic dietary therapies (KDTs) may improve cerebrovascular health and neuroprotection by shifting brain energy metabolism from glucose to ketone bodies (specifically β-hydroxybutyrate), reducing oxidative stress, and modulating inflammatory signaling, though current human evidence is limited and heterogeneous.

If you have cognitive concerns or are aging, a ketogenic diet might offer neuroprotective benefits by shifting your brain's fuel source to ketones, which may reduce inflammation and oxidative stress. However, current human evidence is not strong enough to recommend it broadly. If you try it, consider less restrictive versions like the Modified Atkins Diet for better long-term adherence, and be aware that benefits may take weeks to manifest as your body adapts (keto-adaptation).

Brown adipose tissue (BAT) activation and the 'browning' of white adipose tissue (WAT) represent a potential therapeutic avenue for increasing energy expenditure and reducing body weight, although its clinical relevance in humans remains debated.

You can potentially increase your energy expenditure by activating brown fat, but this is not a guaranteed or standalone solution for weight loss. Strategies like cold exposure and sustained physical activity may promote 'browning' of white fat, turning it into heat-producing tissue. However, since its clinical impact is still debated, focus on these as complementary tools to a balanced diet and regular exercise, not replacements.

Whey protein supplementation without resistance training significantly reduces daily protein intake in postmenopausal women, suggesting a compensatory eating mechanism.

If you take whey protein but do not exercise, you might actually end up eating less protein from your regular meals. This means your total protein intake may drop, which is why you won't see muscle benefits. To increase protein, focus on whole foods or ensure the supplement doesn't replace other protein sources.

Pharmacological inhibition of the postsynaptic scaffolding proteins PSD-95 (via UCCB01-147) and PICK1 (via mPD5) induces sustained weight loss in obese mice primarily through a non-aversive reduction in food intake, with effects persisting for days after treatment cessation.

This research identifies two specific brain proteins (PSD-95 and PICK1) that, when blocked by experimental drugs, cause obese mice to eat less without feeling sick, leading to significant fat loss that lasts for days after the drug is stopped. While not yet available for humans, this suggests a potential future treatment class that avoids the common side effects of current obesity drugs and offers sustained benefits.

Low glycaemic index (GI) or low glycaemic load (GL) diets do not result in greater weight loss or improved metabolic markers compared to higher GI/GL diets or other standard diets in people with overweight or obesity.

If you are trying to lose weight, switching to a low GI or GL diet is unlikely to give you better results than other diets. Focus on creating a sustainable energy deficit rather than prioritizing the glycaemic index of foods.

The 'Obesity Paradox'—where overweight or mildly obese patients have better prognosis in certain diseases—is likely an artifact of BMI's inability to distinguish between phenotypes and sampling errors, rather than a true protective effect of fat.

Do not rely on the 'obesity paradox' to excuse poor health. If you are overweight, focus on improving your metabolic health and body composition, as BMI alone is an imperfect predictor of risk.

In obese middle-aged and older adults, weight loss is associated with an increased risk of atherosclerosis (cIMT > 1.0 mm) compared to moderate weight stability.

If you are obese and older, be aware that losing weight in this observational study was linked to higher atherosclerosis risk. This may be due to unintentional loss from other health issues. Consult a doctor to ensure weight loss is intentional and healthy, rather than a sign of underlying disease.

Oriental Melon Stem Ethanol Extract (CMSE) reduces body weight and fat mass in high-fat diet-induced obese mice by increasing energy expenditure and enhancing brown adipose tissue thermogenesis, independent of calorie intake.

If you are looking for a supplement to support weight management, Oriental Melon Stem Extract (CMSE) shows promise in animal studies for boosting metabolism and burning fat without needing to eat less. The effective dose in mice translates to a high daily intake for humans (~2.3g), which falls within the range of dietary supplements. While not a magic bullet, it may support metabolic health and liver function when combined with a balanced diet.

Intensive lifestyle intervention (weight loss, reduced caloric intake, increased physical activity) does not significantly prevent diabetic peripheral neuropathy in patients with Type 2 Diabetes Mellitus (T2DM) and may have negative effects in some contexts.

While weight loss is generally good for health, aggressive lifestyle interventions alone may not prevent nerve damage in Type 2 Diabetes and should not replace standard glycemic management.

Time-restricted eating (TRE) does not significantly change systolic or diastolic blood pressure in adults.

Do not expect TRE to lower blood pressure significantly on its own. If you have hypertension, continue standard medical management.

Intermittent fasting (time-restricted feeding or alternate-day fasting) is not superior to continuous energy restriction for weight loss and may have limited long-term data.

Intermittent fasting (like time-restricted feeding) can help you lose weight, but it is not necessarily better than simply eating fewer calories every day. There is not enough long-term data to recommend it as a superior long-term strategy. Choose the method that fits your lifestyle best.

Activation of the AMPK signaling pathway ameliorates fatty liver disease (FLD) by inhibiting lipid synthesis and promoting fatty acid oxidation.

Supporting liver health involves maintaining cellular energy balance. While specific dietary interventions are not detailed in this mechanism review, the activation of AMPK (often associated with energy deficit or exercise) is a key biological mechanism for reducing liver fat. Focus on metabolic health markers rather than just fat intake.

AMPK activation reduces liver fat accumulation by downregulating lipid synthesis genes (FAS, SREBP-1c, ACC, HMGCR) and upregulating fatty acid oxidation genes (CPT1, PGC1, HSL, ATGL).

Understanding the specific genes involved (like CPT1 for burning fat and FAS for making fat) helps explain why metabolic health is complex. Interventions that activate AMPK can shift this balance.

Ethanol consumption inhibits AMPK activity and reduces CPT1 expression, leading to fatty liver disease.

Chronic alcohol consumption disrupts the liver's ability to regulate fat metabolism by inhibiting AMPK. Reducing alcohol intake may help restore this regulatory pathway.

Lipophagy, the selective autophagic degradation of lipid droplets, serves as a cytoprotective mechanism that prevents lipotoxicity and cell death (necrosis/apoptosis) by mobilizing fatty acids for energy production (ATP synthesis) and reducing toxic lipid accumulation.

Your body has a natural system (lipophagy) to break down stored fat for energy when needed. This process helps protect your cells from damage caused by excess fat. While you cannot directly 'dose' this molecular pathway, supporting metabolic health through regular physical activity and avoiding chronic overnutrition helps maintain the efficiency of your body's natural lipid management systems.