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.

Women with obstructive sleep apnea (OSA) experience similar or worse health consequences, including cardiovascular risk and cognitive impairment, compared to men despite having lower disease severity (lower AHI).

If you are a woman experiencing fatigue, insomnia, or mood disturbances, do not dismiss them just because your sleep study shows a 'mild' Apnea-Hypopnea Index (AHI). Women often suffer significant health consequences and cognitive impairment at lower AHI levels than men. Advocate for treatment based on your quality of life and symptom burden, not just the severity score.

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.

Enobosarm, a selective androgen receptor modulator (SARM), prevents and treats muscle wasting in cancer patients by increasing lean body mass and physical function without the androgenic side effects of traditional anabolic agents.

If you have advanced lung cancer and are starting chemotherapy, ask your doctor about Enobosarm. It is a drug designed to build muscle without the harsh side effects of older steroids. The standard dose is 3mg taken once a day for about 5 months. The goal is to keep your muscle mass from dropping and help you stay physically active.

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.

Globalization and economic policies favoring cheap fats, sugars, and fast food create an 'obesogenic environment' that drives obesity and diabetes rates, particularly among low-income populations.

Healthy food is often more expensive and less available than processed food due to global economic policies. Focus on community-level advocacy for better food access and policy changes, as individual choices are constrained by these systemic factors.

Higher total and free testosterone levels are associated with increased mortality from lung cancer in older men, potentially due to hormonal stimulation of tumor growth or residual confounding by smoking.

In older men, higher testosterone levels were linked to higher lung cancer death rates in this study. However, the authors suggest this might be due to smoking habits rather than testosterone itself. Do not assume high testosterone causes cancer, but be aware of the association in observational data.

Implementing excise taxes on sugar-sweetened beverages (SSBs) in middle-income countries reduces net energy intake and prevents further growth in obesity prevalence, though it does not permanently reduce population weight.

For policymakers in middle-income countries, implementing an excise tax on sugary drinks is an effective strategy to halt the rise in obesity rates. While it won't cure existing obesity, it reduces net calorie intake by making sugary drinks more expensive, leveraging consumer price sensitivity. The key is that the tax must be structured to pass through to consumer prices.

There is no definitive evidence that specific foods or drinks (e.g., fat, coffee, alcohol) consistently cause or prevent GERD symptoms across all populations.

Don't obsess over avoiding specific foods like coffee or fat unless you personally notice they trigger your symptoms. The evidence is mixed, and blanket restrictions are not supported by definitive data. Focus on weight loss first.

Sodium butyrate supplementation prevents high-fat diet-induced obesity and insulin resistance in mice by inducing epigenetic repositioning of the -1 nucleosome in nuclear-encoded mitochondrial genes, thereby restoring skeletal muscle mitochondrial adaptation and complete beta-oxidation.

In this mouse model, adding sodium butyrate to a high-fat diet prevented obesity and insulin resistance by changing how mitochondrial genes were expressed in muscle. This suggests that sodium butyrate might help mitigate the metabolic damage of a poor diet by improving muscle energy processing, independent of calorie counting.

Pharmacological inhibition or genetic deficiency of Stearoyl-CoA desaturase 1 (SCD1) reduces body adiposity and prevents diet-induced obesity by increasing energy expenditure and fatty acid oxidation.

Current research suggests that targeting the SCD1 enzyme could be a viable strategy for treating obesity. In animal models, reducing SCD1 activity leads to increased fat burning and resistance to weight gain, even with high food intake. While not yet a human treatment, this highlights the importance of lipid metabolism enzymes in body weight regulation.

Inhibition of Stearoyl-CoA desaturase 1 (SCD1) protects against hepatic steatosis (fatty liver) by decreasing de novo fatty acid synthesis and increasing fatty acid oxidation.

Fatty liver disease is closely linked to the activity of the SCD1 enzyme. Research in mice shows that inhibiting this enzyme reduces liver fat by shifting metabolism toward fat burning and away from fat storage. This suggests that therapies targeting SCD1 could help treat non-alcoholic fatty liver disease.

Deficiency in Stearoyl-CoA desaturase 1 (SCD1) improves insulin sensitivity and glucose tolerance in skeletal muscle.

Insulin resistance is linked to how fats are processed in the body. Studies in mice show that reducing SCD1 activity improves how muscles respond to insulin and handles glucose. This suggests that targeting SCD1 could be a strategy for managing type 2 diabetes and insulin resistance.

Activation of brown adipose tissue (BAT) via cold exposure or pharmacological agents increases energy expenditure and reduces body fat mass in animal models, suggesting a viable anti-obesity therapeutic strategy.

Your body has a hidden calorie-burning system called brown fat, which is more active in lean, younger people. You can activate it by exposing yourself to cold temperatures (like cool showers or wearing lighter clothing in winter), which triggers your nervous system to burn fat for heat. While this works well in mice, human results vary, and older or obese individuals may have less active brown fat. Pharmacological drugs targeting this system are in development but not yet available.

Pharmacological activation of brown adipose tissue using natriuretic peptides (NPs) or beta-3 adrenergic agonists can increase energy expenditure and recruit brown-like (beige) fat in white adipose tissue.

Scientists are developing drugs that mimic the effects of cold exposure by targeting specific hormones (like natriuretic peptides) or receptors (beta-3). These drugs aim to turn your white fat into energy-burning 'beige' fat. While promising in mice, these treatments are still in clinical trials for humans and are not yet available for general use.

Brown adipose tissue (BAT) contributes minimally (approx. 1%) to total cold-induced thermogenesis in humans, with deep cervico-thoracic skeletal muscles serving as the major contributor.

Exposing yourself to cold will not significantly boost your daily calorie burn through brown fat alone. While your brown fat does become more active in the cold, it only accounts for about 1% of the extra energy you burn. The real heat production comes from your deep neck and chest muscles, not just your fat. Don't rely on cold exposure as a primary weight loss strategy.

Brown adipose tissue oxygen consumption and energy expenditure are directly linked to its blood flow and the uptake of circulating non-esterified fatty acids (NEFA), both at rest and during cold exposure.

If you have active brown fat, its ability to burn calories is tightly coupled to how much blood flows to it and how many fatty acids are available in your blood. Cold exposure increases blood flow and fatty acid uptake, which drives this process. However, since the total energy burned is small, this mechanism does not translate to significant weight loss.

Shifting from red meat (cow/sheep) to white meat (pigs/poultry) without reducing total meat consumption yields minimal health benefits compared to reducing total meat and dairy.

Simply swapping beef for chicken or pork offers only modest health benefits. To make a significant difference in your heart health and cancer risk, you need to reduce your overall meat and dairy intake and replace it with more fruits, vegetables, and grains.

Therapeutic silencing of miR-33 using antisense oligonucleotides increases plasma HDL cholesterol levels by targeting cholesterol efflux transporters ABCA1 and ABCG1.

While direct 'miR-33 silencing' is not a current consumer supplement, this research highlights why some individuals struggle with HDL levels despite diet. Future therapies targeting this pathway may offer treatment for dyslipidemia, but current lifestyle interventions (diet/exercise) remain the primary method to influence these genetic pathways naturally.

Inhibition of miR-122 using antisense therapy significantly reduces circulating cholesterol and triglyceride levels in the liver.

Anti-miR-122 therapy is a potential future treatment for fatty liver and high cholesterol. It works by blocking a specific liver RNA (miR-122) that normally promotes cholesterol production. Current management relies on diet and exercise, but this pathway may soon be targetable by drugs.

Overexpression of miR-27a accelerates adipolysis (fat breakdown) by targeting RXRα and PPARγ, thereby reducing lipid storage in cells.

miR-27a promotes fat breakdown. While not a current supplement, understanding this pathway may lead to future treatments for obesity that target fat storage genes.

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.

Chronic low-grade inflammation in obesity serves a beneficial physiological function by increasing energy expenditure and promoting adipose tissue remodeling, thereby limiting adiposity and improving glucose homeostasis.

Do not assume that suppressing all inflammation is beneficial for weight management. In obesity, inflammatory processes help regulate energy expenditure and tissue health. Suppressing these signals (e.g., via certain anti-inflammatory drugs) may inadvertently reduce energy expenditure and promote weight gain, potentially worsening metabolic outcomes.