Browse the evidence

Training variables such as program duration, frequency, and total number of sessions do not significantly predict the effects of plyometric jump training on most physical fitness attributes in basketball players, except for total sessions on squat jump height.

Do not stress over finding the 'perfect' plyometric program dose (exact weeks, sessions per week, or total sessions). The research shows these specific metrics do not strongly predict success for most fitness outcomes. Instead, focus on consistent implementation and movement quality. Note that more total sessions might slightly help squat jump height, but this is a minor effect.

Astaxanthin supplementation (0.02% in diet) ameliorates insulin resistance and stimulates mitochondrial biogenesis in skeletal muscle of high-fat-diet-induced obese mice by activating the AMPK pathway.

In obese mouse models, consuming 0.02% Astaxanthin in the diet for 24 weeks improved insulin sensitivity and increased mitochondrial density in muscle by activating the AMPK pathway. This effect was independent of antioxidant activity in the muscle itself. Human translation requires caution as this was a murine model with specific dietary conditions.

Obesogens can induce transgenerational obesity through epigenetic modifications (DNA methylation, histone retention, non-coding RNA) that persist in unexposed generations.

Since environmental exposures can affect future generations, minimizing chemical exposure (plastics, pesticides) is crucial for reproductive health and the long-term metabolic health of descendants.

IL-1β antagonists (e.g., anakinra, gevokizumab) improve glycemia and beta-cell function in type 2 diabetes, but their effect on cardiovascular events is still being determined in large trials.

Blocking specific inflammatory proteins like IL-1β can improve blood sugar control and protect beta-cells in type 2 diabetes. While promising, these treatments are currently biologics (injections) and are still being studied for their long-term impact on heart disease. They represent a targeted approach to the inflammatory component of diabetes.

Salsalate, a non-acetylated salicylate, lowers blood glucose and triglycerides in type 2 diabetes by activating AMPK and inhibiting NF-κB, but its effect on cardiovascular plaque progression is unclear.

Salsalate, a form of salicylate, can lower blood sugar and triglycerides in people with type 2 diabetes by activating AMPK, a key metabolic sensor. While it shows promise for glycemic control, its effect on preventing heart disease (plaque progression) is not yet clear. It is not a standard treatment but may be considered in specific cases.

Inhibition or genetic deletion of the enzyme Stearoyl-CoA Desaturase 1 (SCD1) confers resistance to diet-induced obesity and hepatic steatosis by increasing fatty acid oxidation and thermogenesis.

This paper highlights SCD1 as a key enzyme. While you cannot directly 'dose' SCD1 inhibition safely without medical supervision, consuming oleic acid (via olive oil) may naturally modulate this pathway. The research suggests that high SCD1 activity is linked to obesity, so maintaining healthy levels through diet (oleic acid) is preferable to high SCD1 activity driven by saturated fats.

Prolonged consumption of LCS beverages is advised against in children due to a lack of long-term safety data and potential adverse effects on taste preferences and metabolic health.

For children, water is the only recommended beverage. LCS beverages should not be a regular part of a child's diet because we don't know the long-term effects on their developing taste preferences and metabolism. The only exception is for children with diabetes who need to manage blood sugar spikes, and even then, it should be used sparingly and under medical guidance.

Observational studies linking LCS beverage consumption to increased risks of type 2 diabetes, stroke, and dementia are likely confounded by reverse causation and adiposity, rather than indicating a direct causal harm from LCS beverages.

Don't panic about the headlines linking diet soda to diabetes or stroke. The science suggests that people who are already overweight or unhealthy are more likely to drink diet soda, not that the soda causes the disease. However, since water is still the best choice, use LCS beverages as a tool to cut sugar, not as a health tonic.

Gut microbiome composition (specifically enterotype) mediates the relationship between dietary intake (fiber, artificial sweeteners) and circulating metabolites (bile acids), meaning the metabolic response to diet is dependent on an individual's microbial profile.

Your gut bacteria determine how your diet affects your blood chemistry. For example, eating fiber might increase beneficial bile acids in some people but not others, depending on their specific gut microbial type (enterotype). This suggests that personalized nutrition, based on microbiome profiling, may be necessary to optimize metabolic health, as standard dietary advice may not yield the same metabolic benefits for everyone.

Sarcopenia is associated with a gut microbiome profile characterized by reduced microbial diversity and a depletion of butyrate-producing genera (Lachnospira, Roseburia, Eubacterium), which correlates with reduced muscle mass and function.

If you are experiencing age-related muscle loss, consider that your gut health may be a contributing factor. The research shows that people with sarcopenia have less diverse gut bacteria and fewer beneficial, butyrate-producing species. While this does not replace resistance training and adequate protein intake, it suggests that supporting gut health (e.g., through diverse fiber intake or probiotics) might be a valuable adjunct strategy to preserve muscle mass in older adults.

Sarcopenia is associated with an overrepresentation of lipopolysaccharide (LPS) biosynthesis pathways in the gut microbiome, suggesting a pro-inflammatory state that may drive muscle catabolism.

The study suggests that sarcopenic individuals may have gut bacteria that produce more inflammatory endotoxins (LPS). This chronic low-grade inflammation may contribute to muscle breakdown. Managing gut inflammation through diet (e.g., reducing processed foods that feed pathogenic bacteria) might help mitigate this inflammatory drive on muscle tissue.

Extremely high HDL cholesterol levels (e.g., >116 mg/dL in men, >135 mg/dL in women) are associated with increased all-cause mortality.

While increasing HDL through exercise and diet is generally beneficial, aim for moderate levels. Extremely high HDL levels (above 116 mg/dL for men and 135 mg/dL for women) may not provide additional cardiovascular benefits and could be associated with higher mortality risk.

Mobile health wearable devices provide feasible but unreliable sleep monitoring compared to polysomnography (PSG), with significant limitations in detecting sleep stages and total sleep time accuracy.

Wearable sleep trackers are useful for observing general trends and improving sleep hygiene awareness, but they should not be used to diagnose sleep disorders or make medical decisions. For clinical accuracy, polysomnography remains the necessary standard.

Higher expression of the cardiolipin synthase gene CRLS1 in human subcutaneous adipose tissue is positively correlated with insulin sensitivity and negatively correlated with insulin resistance.

In humans, higher levels of the enzyme that makes cardiolipin (CRLS1) in belly fat are linked to better insulin sensitivity. This suggests that supporting the health of this enzyme might be beneficial for metabolic health, although the exact way to do this is not yet defined.

Elevated circulating asprosin levels are positively associated with insulin resistance, type 2 diabetes, and obesity in adult populations, suggesting asprosin acts as a biomarker for metabolic dysregulation.

If you have insulin resistance or type 2 diabetes, your body may be producing higher levels of the hormone asprosin, which is linked to your condition. While this doesn't change your immediate treatment, it highlights the importance of managing blood sugar and weight, as lower asprosin levels are associated with better metabolic health. Future treatments may target this hormone.

Genetic mutations or activation of the Wnt/β-catenin signaling pathway, specifically involving LGR4, RSPOs, and ZNRF3/RNF43, regulate adipose tissue development and obesity risk by controlling the balance between adipocyte proliferation (hyperplasia) and differentiation (hypertrophy) in a depot-specific manner.

This research suggests that obesity is not just about calories but involves complex genetic signaling (Wnt/β-catenin) that dictates how fat cells grow and store energy. While you cannot change your genetics, understanding this helps explain why fat storage differs by body area (visceral vs. subcutaneous) and why some people are more prone to obesity. Lifestyle interventions remain relevant as they interact with these signaling pathways.

Wnt/β-catenin signaling exerts depot-specific effects on white adipose tissue (WAT), where its activation in adipose precursor cells (APs) promotes proliferation (hyperplasia) in visceral WAT (vWAT) under high-fat diet conditions, while its role in subcutaneous WAT (sWAT) involves promoting differentiation and hypertrophy of mature adipocytes.

Fat storage is not uniform across the body. The Wnt/β-catenin signaling pathway regulates how fat cells grow differently in visceral (abdominal) versus subcutaneous (under skin) areas. High-fat diets trigger this pathway to increase the number of fat cells in the visceral area, which is more metabolically harmful. This explains why visceral fat accumulation is a key risk factor for metabolic diseases.

Mutations in the LGR4 gene, specifically the A750T variant, are associated with increased obesity risk, central obesity, and metabolic complications in humans, and ablation of Lgr4 in mice resists diet-induced obesity by promoting browning of visceral white adipose tissue.

Genetic variations in the LGR4 gene can predispose individuals to central obesity and metabolic issues. In mice, removing this gene prevents obesity by promoting the browning of fat, which burns energy. This suggests that targeting the LGR4 pathway could be a potential therapeutic strategy for treating obesity and its complications.

Government-imposed confinement and mobility restrictions during the COVID-19 pandemic caused a significant decrease in Health-Related Quality of Life (HRQoL) among pregnant women, primarily driven by increased anxiety, depression, and pain.

Confinement can significantly lower your quality of life during pregnancy, increasing anxiety and pain. To mitigate this, seek online support for childbirth preparation and maintain communication with healthcare providers to address fears of contagion.

Government-imposed confinement and mobility restrictions during the COVID-19 pandemic did NOT significantly alter the adherence to the Mediterranean Diet among pregnant women.

Contrary to fears, confinement did not necessarily ruin dietary habits for these pregnant women. If you already follow a healthy diet, you may be able to maintain it during restrictions.

Encapsulation techniques (e.g., spray drying, coacervation) protect probiotics from environmental stressors (heat, acid, oxidation) during production, storage, and gastrointestinal transit.

Look for probiotic products that mention 'encapsulation' or 'delayed release.' This technology helps the bacteria survive stomach acid so they can reach your intestines where they are needed.

Gut microbiota composition influences obesity risk through energy harvesting efficiency, specifically via the Firmicutes-to-Bacteroidetes ratio and short-chain fatty acid (SCFA) production.

Focus on dietary diversity and fiber intake to support a healthy gut microbiome. While not a magic bullet, a diet rich in prebiotics and probiotics may help regulate energy balance and reduce obesity risk by influencing gut bacteria composition.

Short-chain fatty acids (SCFAs) produced by gut microbiota influence host energy homeostasis and adipose storage through multiple mechanisms including GPCR signaling and histone deacetylase inhibition.

Increase your intake of fiber-rich foods (vegetables, fruits, whole grains) to boost SCFA production. This supports gut health and may help regulate energy balance and reduce inflammation.

Dysbiosis and increased gut permeability (leaky gut) contribute to obesity through metabolic endotoxemia and low-grade inflammation.

Focus on reducing inflammation through a balanced diet rich in anti-inflammatory foods. Addressing gut health may help manage obesity-related inflammation.