Browse the evidence

Consuming seaweed carries risks of heavy metal and iodine contamination, requiring regulated sourcing and processing to ensure safety.

Be cautious when consuming seaweed due to potential heavy metal and iodine contamination. Choose products from regulated sources that adhere to safety standards and labeling requirements to minimize health risks.

Green extraction technologies (microwave, ultrasound-assisted) are efficient for recovering antioxidants from fruit and vegetable waste streams, offering yields similar to conventional methods with milder operating conditions.

This information is primarily relevant for food scientists and manufacturers. For consumers, it implies that processed foods or supplements derived from 'green extraction' may retain high antioxidant levels, but direct consumption of fresh produce remains the primary source.

Frequent consumption of fungi and algae is associated with an increased prevalence of metabolic syndrome in Chinese men, whereas frequent consumption of nuts and pork is associated with a decreased prevalence in Chinese women.

For Chinese adults, dietary advice should be sex-specific. Men should monitor their intake of fungi and algae, as high frequency is linked to higher metabolic syndrome risk. Women may benefit from including nuts and pork in their diet, as high frequency is linked to lower risk. These findings highlight that 'healthy' foods may have different impacts based on sex.

Administration of specific probiotics, such as Lactobacillus johnsonii N6.2, can hinder the development of diabetes in susceptible models by regulating gut integrity and modulating tight junction proteins like claudin-1.

If you have a genetic predisposition to diabetes or gut issues, maintaining gut barrier integrity is crucial. While this paper highlights Lactobacillus johnsonii N6.2 as a potential helper in animal models, it emphasizes that personalized nutrition and microbiome manipulation are key. Focus on a diet that supports your specific microbiome rather than relying on a single supplement.

Fecal microbiota transplantation (FMT) from lean, insulin-sensitive donors can significantly improve insulin sensitivity in insulin-resistant obese men within 6 weeks.

FMT from lean donors shows promise for improving insulin sensitivity in obese men, but it is not a guaranteed fix for everyone. This is a complex medical intervention. Current evidence suggests that dietary changes and lifestyle modifications are more accessible and foundational steps to support a healthy microbiome.

Overweight and obese individuals exhibit a gut microbiota profile characterized by higher abundance of Collinsella aerofaciens, Dorea formicigenerans, and Dorea longicatena compared to lean individuals.

Your gut bacteria profile differs if you are overweight or obese compared to if you are lean. Specifically, higher levels of Collinsella aerofaciens, Dorea formicigenerans, and Dorea longicatena are associated with higher body weight. Understanding these differences may help tailor dietary strategies for weight management.

FGF21 analogs reduce hepatic steatosis and lipotoxicity in NASH by suppressing de novo lipogenesis and increasing mitochondrial fatty acid oxidation, independent of weight loss.

FGF21 analogs are emerging therapies that target the hormonal drivers of liver fat. They work by telling the liver to stop making new fat and burn existing fat, rather than just restricting calories. This addresses the root cause of NASH (steatosis) rather than just the scarring (fibrosis).

FGF21 analogs exert direct anti-inflammatory effects in NASH by suppressing pro-inflammatory cytokine expression (TNF-a, IL-6, IL-1b) and inhibiting immune cell infiltration into the liver.

FGF21 analogs help reduce liver inflammation by blocking the signals that recruit immune cells and produce damaging cytokines. This helps prevent the progression from fatty liver to scarring (fibrosis).

Endogenous FGF21 levels are elevated in NASH patients but are insufficient to ameliorate disease due to a 'FGF21-resistant state' caused by receptor downregulation and enzyme-mediated inactivation.

Your body naturally produces more FGF21 when you have fatty liver, but it doesn't work well enough to fix the problem. This is why specialized FGF21 analogs are being developed to bypass this resistance.

In elderly individuals, lower circulating levels of Insulin-like Growth Factor-1 (IGF-1) and Mechanical Growth Factor (MGF) are independently associated with reduced appendicular skeletal muscle mass (ASMI) and sarcopenia.

If you are over 60, your natural production of IGF-1 and MGF declines, which contributes to muscle loss. While you cannot easily change your age, you can support your hormonal health through adequate protein intake (at least 0.6 g/kg/day) and resistance training, which may help mitigate the decline in these growth factors.

Certain pharmaceutical drugs (ACE inhibitors, statins, mTOR inhibitors) and lifestyle interventions (exercise) can increase circulating Klotho levels, potentially offering therapeutic benefits for age-related diseases.

Regular physical activity and adherence to prescribed medications for blood pressure, cholesterol, or metabolic health may naturally support higher Klotho levels. This suggests that standard health maintenance practices contribute to longevity mechanisms.

Nicotinamide mononucleotide (NMN) supplementation increases NAD+ levels in aged organisms, which reverses age-related declines in mitochondrial function, insulin sensitivity, and cognitive performance.

Current evidence for NMN's anti-aging benefits comes from animal studies showing improved metabolic and cognitive health. Human clinical trials are ongoing, but no efficacy data is yet available. Do not expect proven anti-aging results in humans until more clinical data is published.

NMN supplementation improves specific age-related physiological declines, including insulin sensitivity, vascular function, and cognitive performance, in aged animal models.

Animal studies show NMN can improve insulin sensitivity, blood vessel health, and memory in old age. However, these results have not been confirmed in humans. Wait for clinical trial results before expecting these specific benefits.

Gender-affirming hormone therapy (GHT) with estrogen in transgender females (TGF) is associated with an increased risk of myocardial infarction and ischemic stroke compared to cisgender females, whereas testosterone therapy in transgender males (TGM) does not show consistent evidence of increased cardiovascular or cerebrovascular disease risk.

If you are a transgender woman taking estrogen, be aware that your risk of heart attack and stroke may be higher than that of cisgender women, so regular cardiovascular check-ups are important. If you are a transgender man taking testosterone, current evidence does not show a significantly increased risk of heart or brain vessel disease, though blood pressure and lipids should still be monitored.

Gender-affirming hormone therapy (GHT) is associated with alterations in blood pressure, with some studies showing increases in both transgender females and males, while others show decreases or no change depending on the formulation and duration of therapy.

Your blood pressure may change after starting hormones. It can go up or down depending on the type of hormone and how long you've been taking it. Regular monitoring is key to catching any changes early.

Gender-affirming hormone therapy (GHT) with estrogen in transgender females (TGF) is associated with an increased risk of venous thromboembolism (VTE), whereas no increased risk of VTE has been demonstrated in transgender males (TGM).

If you are a transgender woman taking estrogen, be aware that your risk of blood clots may be higher than that of cisgender women, especially with oral formulations. Transdermal estrogen may carry a lower risk. Discuss formulation options with your provider.

SIRT1 promotes lipid metabolism and mitochondrial biogenesis in adipocytes by regulating key enzymatic pathways including PPARα and SREBF1c.

SIRT1 activity is crucial for healthy fat cell function, promoting mitochondrial health and lipid metabolism. While boosting NAD+ precursors like NMN can support this pathway in cell models, human application requires understanding that SIRT1 is just one part of a complex metabolic system.

Plasma levels of NAD+ and NADP+ significantly decline with age, while levels of their reduced forms (NADH, NADPH) and catabolites (NAM, MeNAM, ADPR) increase, indicating a dysregulated NAD+ metabolome in normal aging.

This study confirms that NAD+ levels drop significantly as you age, which is linked to cellular energy and repair issues. While this paper doesn't prescribe a fix, it highlights that this decline is a key feature of aging and suggests that maintaining or boosting NAD+ levels (e.g., through precursors like NR or NMN, as mentioned in references) might be a viable strategy for healthspan.

Chronic undernutrition is associated with dysregulated PPARα and FXR signaling, leading to decreased bile acid levels, suppressed secretion of complement and coagulation factors, and increased autophagy.

In cases of severe chronic undernutrition, the body's metabolic sensors (PPARα and FXR) become dysregulated, leading to low bile acids and impaired immune/clotting functions. This suggests that nutritional rehabilitation should potentially target these specific pathways (e.g., bile acid replacement or receptor agonists) to restore normal metabolic function, rather than just providing calories.

Reduction in growth factor signaling, particularly the GH/IGF-1 pathway and cell cycle genes, is a transcriptional signature of aging in various tissues.

Aging is associated with reduced signaling from growth factors like IGF-1. Paradoxically, reducing this signaling (e.g., via genetic manipulation or drugs) can extend lifespan in many organisms, suggesting that lower growth factor signaling may be beneficial for longevity.

Reshaping the food environment requires simultaneous, diverse, and innovative strategies that prioritize long-term household financial management and socially-oriented healthy food practices.

For policymakers: Design interventions that combine financial support (e.g., subsidies for healthy food) with social and cultural support (e.g., community food programs). Avoid siloed approaches.

Fasting-induced changes in the gut microbiome (specifically enrichment of propionate production and depletion of Escherichia coli) and immune cells (MAIT cells) are associated with sustained blood pressure reduction, independent of weight loss.

The benefits of fasting on blood pressure appear linked to gut bacteria changes (increased propionate producers, decreased E. coli) and immune system modulation (reduced inflammatory MAIT cells). These changes occur independently of weight loss, suggesting a direct metabolic/immune mechanism.

In Type 2 Diabetes patients, increased plasma Interleukin-6 (IL-6) levels are significantly correlated with the abundance of Gram-negative gut bacteria, specifically Prevotella copri and Bacteroides vulgatus, suggesting these microbes drive systemic inflammation and insulin resistance.

This research highlights that in Type 2 Diabetes, high levels of specific gut bacteria (Prevotella and Bacteroides) are linked to higher inflammation (IL-6) and insulin resistance. While this paper does not prescribe a treatment, it suggests that managing gut health through diet may be a relevant factor in addressing the inflammatory component of diabetes, alongside standard medical care.

Targeted elimination of senescent cells (senolysis) using pharmacological agents reverses age-related pathological changes and improves organ function in animal models.

Research indicates that clearing out 'zombie' (senescent) cells can improve heart function and reduce arterial stiffness in aging models. While specific senolytic drugs are still in development, the mechanism suggests that future therapies could target these cells to delay age-related diseases.