Browse the evidence

No single vegetable oil crop is inherently 'good' or 'bad'; the environmental and social impact depends entirely on the production system, trade practices, and local context.

Don't just look for 'palm oil-free' labels. Focus on supporting sustainable certification and production practices. No oil crop is inherently evil; the impact depends on how and where it is grown. Consider the broader environmental trade-offs of different oils.

Increased food intake during lockdown was primarily driven by increased consumption of bread and confectionary, with confectionary consumption increasing in 64.4% of those who ate more.

When food intake increases during lockdown, it is often driven by bread and confectionary. Be aware that even if you cook at home, the quality of food may shift towards carbohydrates.

Subclinical diabetic cardiac myopathy, characterized by reduced systolic and diastolic reserve during exercise, contributes to reduced exercise tolerance in T2DM.

Your heart may not pump as efficiently during exercise as a non-diabetic's, even if it looks normal at rest. This 'subclinical' dysfunction limits how much oxygen your muscles can use. Exercise training may help improve this cardiac reserve over time.

Skeletal muscle mitochondrial dysfunction and reduced capillary density contribute to early fatigue and reduced peripheral oxygen extraction in T2DM.

Your muscles may have fewer capillaries and less efficient mitochondria, making it harder to use oxygen during exercise. This leads to early fatigue. Resistance and aerobic training can help improve muscle capillary density and mitochondrial function.

Endothelial dysfunction and impaired vasodilation during exercise reduce muscle blood flow and oxygen diffusion in T2DM.

Your blood vessels may not dilate properly during exercise, limiting blood flow to your muscles. This is partly due to endothelial dysfunction. Regular exercise can help improve endothelial function over time.

Cardiac autonomic neuropathy and altered autonomic tone contribute to impaired heart rate adjustment and reduced exercise tolerance in T2DM.

Your nervous system's control over your heart rate may be impaired, leading to slower heart rate adjustments during exercise. This is more common in those with longer disease duration or poor blood sugar control. Monitoring heart rate during exercise can be helpful.

In patients with type 2 diabetes, higher BMI (overweight/obese) is associated with lower all-cause mortality compared to normal weight, a phenomenon known as the 'obesity paradox'.

If you have type 2 diabetes, do not use the 'obesity paradox' as an excuse to maintain a high BMI. While some studies show obese diabetics live longer than lean ones, this is likely due to biases like muscle mass or fitness, not the fat itself. Standard medical advice remains to lose weight if overweight, as it improves metabolic markers and does not increase mortality risk.

Menstrual cycle phase and oral contraceptive use do not significantly influence exercise performance or muscular hypertrophy in response to resistance training.

Train consistently regardless of your cycle phase. There is no evidence that you will lose muscle gains or performance by training during your luteal phase or while on birth control. Focus on progressive overload and consistency rather than phase-specific modifications.

The presence of markets (grocery stores) in one's local food environment is negatively associated with obesity and abdominal obesity, although this association may not be significant when accounting for city-level clustering.

Having grocery stores nearby is associated with a lower risk of obesity, although this effect might be influenced by broader city-level factors. If you have access to markets, use them to stock up on healthy foods. However, be aware that your overall city environment also plays a role.

Among Indian women with PCOS, adherence to a vegetarian diet is associated with significantly higher pro-inflammatory markers (hs-CRP, resistin) and lower anti-inflammatory markers (adiponectin) compared to non-vegetarian counterparts.

If you have PCOS and follow an Indian vegetarian diet, your inflammatory markers (like hs-CRP) might be higher than if you ate a non-vegetarian diet with more fat and protein. This doesn't mean you should stop being vegetarian, but it suggests that the specific high-carbohydrate, low-fat composition of traditional Indian vegetarian diets might not be optimal for inflammation in this specific group. Consider discussing macronutrient balance with a dietitian.

Human milk consumption in infancy is associated with lower risk of obesity, type 2 diabetes, and cardiovascular disease in adulthood, mediated by improved glucose homeostasis, lipid metabolism, and gut microbiota modulation.

Breastfeeding offers long-term metabolic advantages, including lower risks of obesity and diabetes, likely due to unique components like oligosaccharides that shape gut health and energy regulation. If breastfeeding is not possible, focus on high-quality nutrition for the infant, as the metabolic programming benefits are significant but not exclusive to breast milk.

Weight loss interventions induce significant but small changes in DNA methylation (DNAm) across the genome, and baseline DNAm levels at specific loci (e.g., TNF-α, LEP, CLOCK, PER2) can predict the magnitude of weight loss response.

Your body's epigenetic markers (DNA methylation) change when you lose weight, and your starting levels might predict how much weight you'll lose. While these changes are small on a genome-wide scale, specific markers like TNF-α and LEP show promise as predictors. This suggests personalized medicine may eventually use these markers to tailor weight loss strategies, but for now, standard interventions (diet/exercise/surgery) remain the primary lever.

PP protects against beta-cell apoptosis and may improve insulin sensitivity by enhancing the availability of insulin receptors.

PP may protect beta-cells and improve insulin sensitivity, suggesting potential anti-diabetic benefits.

Weight loss in obese individuals fails to resolve visceral adipose tissue (VAT) inflammation because senescent CD153+ PD-1+ CD4+ T cells persist and continue to produce osteopontin, maintaining a chronic inflammatory loop despite fat mass reduction.

If you have been obese for a long time, simply losing weight may not fully restore your metabolic health because your body retains 'senescent' immune cells that keep you inflamed. To mitigate this, focus on strategies that reduce chronic inflammation (like exercise and anti-inflammatory diets) in addition to weight loss, as weight loss alone may not clear these persistent immune cells.

GLP-1 receptor agonists (specifically exenatide) reduce fat mass and energy intake in HO patients but do not significantly alter BMI compared to placebo in the short term, and may decrease total energy expenditure.

Exenatide may help reduce fat mass and waist size in HO, but it often fails to lower BMI significantly. It is not a magic bullet for HO and requires careful monitoring for side effects like nausea.

Setmelanotide (MC4R agonist) is effective in reducing hunger and BMI in patients with HO due to hypothalamic injury, particularly those with specific genetic defects or structural damage affecting the melanocortin pathway.

Setmelanotide is a promising new treatment for HO that targets the root cause (MC4R deficiency). It requires daily injections and may cause skin darkening, but it is one of the few treatments showing efficacy in reducing BMI in this specific population.

Post-liver transplant lifestyle interventions must prioritize psychological coping and emotional resilience before addressing physical diet and exercise prescriptions to ensure adherence and effectiveness.

If you have had a liver transplant, do not force yourself into a strict diet or exercise routine until you feel emotionally stable. Your medical team should address your anxiety and coping mechanisms first. Once you feel mentally ready, start with small, guided physical activities tailored to your specific recovery stage.

Exogenous administration of undercarboxylated osteocalcin (ucOC) improves whole-body and skeletal muscle glucose metabolism and insulin sensitivity in animal models, though human evidence remains discordant.

Current research suggests that bone-derived factors like osteocalcin may help regulate blood sugar, especially in muscle. However, because human studies are inconsistent, there is no specific protocol to manipulate osteocalcin levels for diabetes treatment yet. Focus on proven methods: exercise (which naturally increases ucOC) and maintaining healthy bone density.

Sclerostin levels are elevated in individuals with Type 2 Diabetes and insulin resistance, and blocking sclerostin signaling improves insulin sensitivity in animal models.

High levels of sclerostin are linked to insulin resistance. While drugs targeting sclerostin (like romosozumab) exist for osteoporosis, their metabolic benefits are still being studied. For now, exercise and weight management remain the best ways to improve insulin sensitivity.

GLP-1 receptor agonists (specifically exenatide) reduce body fat and waist circumference in patients with hypothalamic obesity, with greater adiposity reduction observed in those with more extensive hypothalamic damage.

For patients with hypothalamic obesity, weekly exenatide injections (2 mg) can significantly reduce body fat and waist circumference, even if BMI changes are modest. This treatment is particularly effective for those with severe hypothalamic damage, likely because it works through brain pathways outside the damaged area. Side effects are mostly gastrointestinal.

Setmelanotide, a melanocortin-4 receptor (MC4R) agonist, reduces hunger and BMI in patients with hypothalamic obesity caused by acquired hypothalamic injury, marking a potential breakthrough for this condition.

Setmelanotide is an MC4R agonist that reduces hunger and BMI in patients with hypothalamic obesity. It is FDA-approved for genetic obesity and is showing effectiveness for acquired hypothalamic injury. A large Phase 3 trial is currently underway.

A technology-based intervention combining weekly telephone counseling with WiFi scale monitoring is not effective in reducing excess gestational weight gain among women with overweight or obesity compared to treatment as usual.

For pregnant women with overweight or obesity, using a WiFi scale and weekly phone calls with a dietitian starting in the second trimester does not appear to be enough to prevent excessive weight gain compared to standard care. The intervention failed to show benefits, suggesting that more intensive or earlier-starting interventions may be required for this high-risk group.

Skeletal muscle regeneration efficiency is time-of-day dependent, with injury occurring during the active phase (when satellite cell BMAL1 expression peaks) resulting in enhanced repair compared to injury during the inactive phase.

If you sustain a muscle injury or undergo strenuous exercise that causes damage, your body repairs the tissue more effectively during your active phase (typically daytime for humans). This is driven by satellite cell clocks peaking in activity (BMAL1) during this time. While you cannot control the injury, scheduling intense training sessions during your active phase may theoretically support faster or more robust repair compared to late-night sessions, though human data is still emerging.

The molecular clock component BMAL1 is required for satellite cell proliferation and the metabolic transition from oxidative to glycolytic energy sources during early muscle regeneration.

BMAL1 acts as a metabolic switch for muscle stem cells. When muscle is damaged, these cells must switch from resting energy (oxidative) to building energy (glycolytic) to multiply. BMAL1 regulates this switch. Disrupting your circadian rhythm (e.g., chronic shift work) might impair this metabolic flexibility, potentially slowing down the initial proliferation phase of muscle repair.