Browse the evidence

Green Tea Extract (GTE) supplementation increases 24-hour energy expenditure and fat utilization in active individuals, but does not consistently improve sprint performance or antioxidant enzyme levels in trained sprinters.

If you are trying to manage body fat, Green Tea Extract (specifically with EGCG and caffeine) may help slightly increase your daily energy expenditure and fat burning. However, do not expect it to improve your sprint performance or replace proper training and diet.

Endurance training (ET) improves mitochondrial biogenesis, density, and function in aged skeletal muscle, thereby attenuating age-associated declines in mitochondrial protein synthesis and energy production.

Incorporate regular aerobic exercise into your routine to support muscle health and energy levels. Aim for 150-300 minutes of moderate-intensity activity (like brisk walking) or 75-150 minutes of vigorous activity per week. Break this into sessions of at least 10 minutes. This helps improve your mitochondria, which are the energy powerhouses of your muscle cells, and supports overall muscle function.

Plant-based meat alternatives may have a lower environmental footprint than feedlot beef but a higher footprint than pasture-raised beef, and their nutritional complexity is underestimated by reductionist formulation.

If you are choosing plant-based meats for environmental reasons, know that they are generally better than feedlot beef but may not be as good as pasture-raised beef. Focus on a balanced diet that includes diverse plant sources to maximize health benefits, rather than relying solely on processed alternatives.

Baseline metabolite levels (BCAA, tyrosine, betaine, choline) do not predict the magnitude of weight loss achieved after bariatric surgery or lifestyle interventions.

Your baseline blood levels of BCAA, tyrosine, betaine, or choline will not tell you how much weight you will lose after surgery or a diet program. While these markers might predict whether your diabetes remits, they do not predict the magnitude of weight loss.

Obese gut microbial communities exhibit higher branched-chain amino acid (BCAA) catabolism and hexanoic acid production, which may negatively impact energy balance and metabolic health.

Obese gut bacteria may metabolize proteins differently, producing metabolites like hexanoic acid that could affect energy balance. This highlights why metabolic health in obesity is complex and not just about calorie intake.

Meal timing is not associated with body composition (fat mass, lean mass, or BMI) in young adults, regardless of sex.

Changing when you eat will not directly change your weight or body fat percentage. Focus on total calorie intake and exercise for body composition changes. However, timing may still be useful for metabolic health markers like insulin sensitivity.

Macrophage-specific lipoprotein lipase (LPL) promotes atherosclerosis by acting as a bridging molecule for remnant lipoprotein uptake, leading to foam cell formation and plaque progression.

LPL helps clear fat from blood, but in immune cells within artery walls, it helps build plaques. Therapies targeting LPL must distinguish between clearing blood fat (good) and feeding artery plaques (bad).

Triple agonists targeting GLP-1, GIP, and Glucagon receptors improve energy expenditure and restore body weight in diet-induced obesity models more effectively than dual or mono-agonists.

Triple hormone agonists (GLP-1/GIP/Glucagon) are in development and show promise in animal studies for boosting energy expenditure and weight loss beyond what dual agonists achieve. They are not yet standard clinical care.

Semaglutide therapy in older adults with type 2 diabetes accelerates muscle mass loss and functional decline, with higher doses and lower baseline muscle mass predicting greater loss.

If you are taking Semaglutide and are over 65 with diabetes, monitor your muscle strength. The medication can cause muscle loss, especially at higher doses. To counter this, focus on resistance training and adequate protein intake, and discuss dose adjustments with your doctor if you notice weakness.

Lower-body fat (LBF) is associated with more favorable left ventricular contractility, potentially acting as a metabolic sink that protects against ectopic fat deposition.

While reducing visceral fat is critical, having some lower-body fat may offer metabolic protection by storing excess lipids safely. However, this benefit is overshadowed by high visceral fat.

Sleeve Gastrectomy (SG) in adolescents results in a blunted reduction in Resting Energy Expenditure (REE) relative to total body weight loss compared to lifestyle-induced weight loss, potentially aiding long-term weight maintenance.

For adolescents with severe obesity, Sleeve Gastrectomy appears to preserve metabolic rate better than lifestyle-induced weight loss, which typically causes a sharp drop in energy expenditure. This 'blunting' of metabolic adaptation may help explain why surgery often leads to more sustained weight loss compared to diet and exercise alone.

Unintentional weight loss in type 2 diabetes is associated with a higher risk of all-cause mortality, whereas the association with intentional weight loss is unclear.

Unintentional weight loss in type 2 diabetes should be taken seriously as it may signal underlying health issues and is linked to higher mortality. The impact of intentional weight loss on mortality is less clear, so patients should focus on overall health management rather than just weight loss.

Brown adipose tissue (BAT) activation and 'browning' of white adipose tissue represent a potential therapeutic target for increasing energy expenditure and reducing body weight.

Activating brown fat through cold exposure or potentially future medications may help burn more calories. However, this is still an area of active research, and current approved treatments focus more on hormonal regulation.

Short-chain fatty acids (SCFAs) produced by gut microbiota from dietary fiber can influence satiety, energy expenditure, and glucose metabolism, but human trials on oral SCFA supplementation have shown mixed or null results for improving glucose metabolism or vagal tone.

Prioritize dietary fiber intake to naturally produce SCFAs in the gut, rather than relying on oral SCFA supplements, which have not consistently shown benefits in human trials.

In adults with type 2 diabetes, weight gain is associated with a significantly increased risk of cardiovascular disease events and all-cause mortality, whereas intentional behavioral weight loss interventions have not demonstrated a statistically significant reduction in CVD events.

For adults with type 2 diabetes, gaining weight is clearly linked to higher risks of heart disease and death. However, simply trying to lose weight through diet and exercise has not been proven to reduce the risk of cardiovascular events in this population, according to this review. Patients should focus on overall cardiovascular risk management rather than assuming weight loss alone protects the heart.

Increased oxidative stress (ROS) and mitochondrial dysfunction are early markers of weight gain, potentially preceding other metabolic changes.

Be aware that long-term weight gain, especially from high-fat/sucrose diets, may increase oxidative stress and mitochondrial dysfunction, which can further promote weight gain. Addressing these underlying metabolic issues may be key to breaking the cycle.

The MAPK signaling pathway (specifically ERK, JNK, and p38) plays a complex, context-dependent role in obesity, regulating appetite, adipogenesis, and insulin resistance, with effects varying between in vitro and in vivo models.

Obesity involves complex signaling networks like MAPK that regulate fat storage and insulin sensitivity. The fact that these pathways have conflicting effects in different contexts explains why single-target interventions often fail and why obesity is a heterogeneous disorder.

Ketogenic diets may have anti-cancer effects by exploiting the Warburg effect, starving cancer cells of glucose and making them more vulnerable to chemotherapy and radiation.

KD is being studied as an adjuvant therapy for cancer to starve cells of glucose. Consult your oncologist before trying this.

Increasing energy expenditure through mitochondrial uncoupling in specific organs (like the liver) is a promising therapeutic strategy for metabolic diseases, but previous attempts with non-specific uncouplers (like DNP) failed due to severe side effects.

Current non-specific energy expenditure boosters are unsafe. However, research is focusing on organ-specific strategies (like liver-targeted uncoupling) to treat metabolic diseases safely. This is not yet a available clinical option.

In rural South African adults (40-60 years), moderate-to-vigorous physical activity (MVPA) is not associated with Body Mass Index (BMI), contradicting the assumption that increased physical activity reduces obesity risk in this population.

For adults in this rural South African setting, increasing physical activity alone is unlikely to reduce BMI. Public health efforts should prioritize dietary interventions, specifically reducing sugar-sweetened beverage intake, rather than focusing solely on increasing physical activity for weight control.

Higher Socioeconomic Status (SES) is positively associated with higher BMI in both men and women in this rural South African population, acting as a proxy for access to calorie-dense foods like sugar-sweetened beverages.

In this community, having higher income is linked to higher BMI, likely due to increased consumption of sugar-sweetened beverages and processed foods. Weight management strategies should focus on identifying and reducing intake of these specific high-calorie, low-nutrient foods rather than just general 'eating less'.

Time-Restricted Feeding (16/8) does not significantly reduce body fat mass in healthy, normal-weight young men over 4 weeks, despite increasing fat-free mass.

If you are already at a healthy weight, TRF alone may not burn more fat than your normal eating pattern unless you naturally eat fewer calories during the restricted window. Focus on maintaining your training and protein intake; fat loss may not occur without a caloric deficit.

A ketogenic diet reduces oxidative stress and improves mitochondrial function by activating antioxidant pathways (Nrf2) and scavenging reactive oxygen species (ROS) via ketone bodies like beta-hydroxybutyrate.

Adopting a ketogenic diet may help reduce cellular damage associated with aging and chronic disease by shifting your body's energy source to ketones, which appear to protect mitochondria and reduce oxidative stress.

Improvement in glycemic control in T2D patients leads to energy conservation via reduced glucosuria and osmotic water weight loss, which mechanically impedes scale-based weight reduction.

When you start treating your diabetes effectively, your blood sugar drops. This means your body stops peeing out calories (glucosuria) and starts storing water and glycogen again. You might see the scale go up by a few pounds. This is not fat gain; it is your body recovering from dehydration and energy loss. Do not stop your diabetes treatment because of this scale increase.