Browse the evidence

Administration of berberine or Rhizoma coptidis (RC) reduces body weight and visceral adipose tissue in high-fat diet-fed mice by inhibiting gut microbial degradation of dietary polysaccharides, which subsequently upregulates Fiaf protein expression and activates mitochondrial energy metabolism genes (AMPK, PGC1a, UCP2, CPT1a) in visceral adipose tissue.

In this mouse study, berberine (200 mg/kg) reduced obesity on a high-fat diet not by making you eat less or blocking fat absorption, but by changing gut bacteria to reduce carbohydrate breakdown. This shift triggered a signaling protein (Fiaf) that boosted energy burning in fat tissue. While promising, human dosing and bioavailability differ significantly from mice.

Chronic overnutrition triggers intracellular stress (oxidative, ER, and autophagy defects) in the hypothalamus, which activates proinflammatory pathways (IKKβ/NF-κB and JNK), leading to central neuroendocrine dysregulation and metabolic syndrome.

This research suggests that chronic overeating causes inflammation in the brain's hypothalamus, which disrupts the body's ability to regulate weight and blood sugar. Simply focusing on peripheral fat loss might not address the root cause if the brain's regulatory system remains inflamed. Strategies that reduce central inflammation or improve hypothalamic health may be critical for treating metabolic syndrome.

Activation of Toll-like receptor 4 (TLR4) in the hypothalamus by lipid excess is a key mechanism driving central metabolic inflammation, insulin resistance, and obesity.

Inflammation in the brain's lipid-sensing pathways (like TLR4) may drive insulin resistance and weight gain. Reducing central lipid exposure or inflammation might help restore metabolic balance, suggesting that brain health is as important as peripheral fat loss.

Autophagy defects in the hypothalamus contribute to the development of metabolic syndrome, including obesity and insulin resistance.

Maintaining healthy autophagy in the brain may be important for preventing obesity and insulin resistance. Lifestyle factors that promote autophagy, such as fasting or exercise, might support hypothalamic function and metabolic health.

Post-pyloric (small bowel) tube feeding in critically ill adults reduces the rate of pneumonia compared to gastric (stomach) tube feeding, likely by bypassing gastric motility issues and reducing gastroesophageal reflux.

For critically ill adults needing tube feeding, placing the tube into the small intestine (post-pyloric) rather than the stomach significantly lowers the risk of developing pneumonia. This benefit comes at the cost of a more difficult initial tube placement procedure. However, it does not appear to shorten ICU stays, reduce mortality, or decrease the time on mechanical ventilation compared to standard stomach feeding. Use post-pyloric feeding if your institution has the expertise and it is feasible, particularly for patients at high risk of aspiration.

Traditional Cognitive Behavioral Therapy (CBT) is the first-line psychological treatment for obesity but does not necessarily produce successful weight loss, primarily functioning to reduce binge eating episodes and psychopathology rather than directly reducing body weight.

If you are using CBT for obesity, manage your expectations: the primary goal is to fix the psychological relationship with food (like binge eating) and improve mood, not necessarily to drop pounds quickly. Weight loss is a secondary outcome that may not happen for everyone, and success is measured by behavioral changes and reduced psychopathology first.

Capsaicin, the active compound in hot chili peppers, enhances the intestinal absorption of micronutrients like calcium, iron, and zinc by increasing intestinal permeability and absorptive surface area.

Consuming spicy foods may help your body absorb more minerals from your food. This is due to capsaicin improving how your intestines work. However, this effect is subtle and should not replace eating nutrient-dense foods.

A high-fiber diet combined with advanced age (centenarian status) establishes a distinct gut microbiota architecture characterized by increased Roseburia and Ruminococcaceae, which is associated with health and longevity.

For older adults aiming to support longevity, incorporating a high-fiber diet rich in legumes, cereals, and vegetables may help cultivate a gut microbiota profile associated with centenarians. This involves increasing the intake of fiber-rich foods to potentially boost beneficial bacteria like Roseburia and Ruminococcaceae.

Nonalcoholic fatty pancreas disease (NAFPD) is strongly associated with obesity and metabolic syndrome, serving as an early marker for ectopic fat deposition and increasing the risk of type 2 diabetes, cardiovascular disease, and acute pancreatitis.

If you have obesity or metabolic syndrome, ask your doctor about pancreatic fat if you undergo abdominal imaging (CT/MRI). It is a strong indicator of your overall metabolic health and risk for diabetes and pancreatitis. Managing weight and insulin resistance is the primary way to reduce pancreatic fat.

Gut microbiota composition differs between lean and obese individuals, with obese phenotypes showing a higher Firmicutes-to-Bacteroidetes ratio, which may enhance energy harvest from the diet.

Obesity is associated with a gut microbiome that extracts more energy from food. While changing this ratio is challenging, a diet rich in fiber may support a healthier microbiome profile.

Surgical weight loss induces specific psychobiological changes, including altered eating patterns (decreased bingeing, increased satiety) and hormonal shifts (elevated enteroglucagon, decreased pancreatic polypeptide), which help regulate the body weight set point.

Surgery not only restricts food intake but also changes the body's hormonal signals for hunger and satiety, which may help maintain weight loss by altering the body's 'set point'.

Obese humans with Non-Alcoholic Steatohepatitis (NASH) exhibit decreased expression of cytochromes P450 involved in bioactive lipid synthesis, mirroring findings in MyD88-deficient mice.

In advanced liver disease (NASH), the liver's ability to produce protective fats (via CYP450 enzymes) is reduced. This suggests that liver health is a critical component of overall metabolic health, and protecting the liver from fat accumulation may preserve these protective pathways.

The age-related accumulation of oxidized proteins impairs cellular proteolytic systems (proteasomes and lysosomes), creating a feedback loop that accelerates aging and contributes to age-related diseases.

Aging involves the accumulation of damaged proteins that can clog cellular cleanup systems. While this paper focuses on the mechanism rather than a specific diet or exercise protocol, it suggests that maintaining protein homeostasis (through adequate repair mechanisms and potentially reducing oxidative stress) is key to slowing age-related decline. Focus on healthy lifestyle factors that reduce oxidative stress.

Caloric restriction (CR) extends lifespan in many species, but its benefits in humans are uncertain and potentially offset by increased mortality risk associated with low body weight.

While caloric restriction works in animals, extreme restriction in humans may increase mortality risk. Aim for moderate, sustainable eating habits that support metabolic health rather than striving for very low body weight.

Metformin, a common diabetes drug, inhibits mTORC1 and increases longevity in model organisms, with observational data suggesting it may decrease all-cause mortality in humans.

Metformin is a well-tolerated diabetes drug that may offer longevity benefits. While not currently approved for this use, it is a promising candidate for anti-aging therapy, and ongoing trials will clarify its efficacy in healthy individuals.

Mitochondrial DNA mutations and dysfunction contribute to aging, but the extent to which they drive normal aging versus progeroid syndromes is still debated.

Mitochondrial health is important for aging, but focusing solely on mtDNA mutations may be misleading. A holistic approach to health, including exercise and nutrition, supports mitochondrial function.

Dietary supplementation with krill oil or pine nut oil prevents or reverses hepatic steatosis by inhibiting hepatic de novo lipogenesis and enhancing fatty acid oxidation.

If you are at risk for fatty liver, incorporating sources of n-3 polyunsaturated fatty acids, such as krill oil or pine nut oil, may help reduce liver fat accumulation. These supplements work by slowing down the liver's production of new fat and increasing fat burning. However, current evidence is based on animal studies, so human dietary guidelines should prioritize overall healthy fat intake.

Dietary administration of Conjugated Linoleic Acids (CLA), specifically the trans-10,cis-12 isomer, induces hepatic steatosis by stimulating de novo lipogenesis and increasing plasma insulin.

Be cautious with CLA supplements. While they may help reduce body fat, they can also cause fatty liver and increase insulin levels in animal studies. The potential liver damage may outweigh the fat loss benefits.

Dietary supplementation with Allium cepa (onion) extracts, particularly those rich in quercetin and organosulfur compounds, inhibits adipogenesis and promotes browning of white adipose tissue, leading to reduced fat accumulation and improved lipid profiles in preclinical models.

Incorporating onion peel extracts or quercetin-rich onion preparations into your diet may support metabolic health by inhibiting the formation of new fat cells and promoting the browning of white fat. While not a magic bullet for weight loss, it serves as a supportive dietary strategy for managing lipid profiles and insulin sensitivity, particularly when combined with a balanced diet.

A ketogenic diet significantly reduces maximal work load and work load at lactate threshold compared to a mixed diet in off-road cyclists, indicating compromised high-intensity performance.

If you are an endurance cyclist, switching to a high-fat, low-carb diet for a month during your base training phase can significantly boost your aerobic capacity (VO2max) and lactate threshold, largely because you lose weight and your body becomes more efficient at burning fat. However, be prepared for a drop in your maximum sprint power and high-intensity efforts, as your body will have less glycogen for those explosive moves. This is a trade-off: better endurance efficiency for less top-end speed.

Calorie restriction (15-30% reduction) inhibits tumor growth and enhances antitumor immunity by reducing IGF-1 signaling, lowering glucose levels, and remodeling the tumor microenvironment to increase CD8+ T cells while decreasing immunosuppressive MDSCs and Tregs.

If you have cancer, discuss with your oncologist whether a supervised calorie restriction of 15-30% might be appropriate as an adjunct to standard therapy. It is not a cure, but it may help improve the effectiveness of your treatment by altering your body's metabolism and immune response.

Ketogenic diets and fasting-mimicking diets may enhance the efficacy of cancer treatments by altering tumor metabolism and immune response, though mechanisms remain largely unexplored.

Ask your oncologist if a ketogenic or fasting-mimicking diet could be a safe adjunct to your cancer treatment. These diets may help your body respond better to therapy, but they are not cures and require careful monitoring.

Sotagliflozin is a dual SGLT1/SGLT2 inhibitor that reduces postprandial glycemia by blocking intestinal glucose absorption and renal glucose reabsorption.

Sotagliflozin is a newer diabetes medication that works in two places: your intestines and your kidneys. It helps lower blood sugar spikes after meals by preventing sugar absorption in the gut and removing sugar through urine. It is still being studied for long-term safety.

There is insufficient evidence to evaluate the effects of sedentary behavior interventions on inflammation or vascular function biomarkers.

Current research does not provide enough data to determine if reducing sitting time affects inflammation (like CRP) or vascular health (like arterial stiffness). More high-quality studies measuring these specific outcomes are needed.