Browse the evidence

Vegetarian and vegan diets are associated with a significantly higher risk of haemorrhagic and total stroke compared to meat-eating diets, an association that is not explained by standard cardiovascular risk factors.

While vegetarian diets lower heart disease risk, they are associated with a higher risk of stroke, particularly haemorrhagic stroke. This risk is not explained by standard factors like blood pressure or cholesterol. Vegetarians should ensure a balanced diet, potentially paying attention to nutrients like Vitamin K and B12, and consult healthcare providers for personalized advice.

Daily supplementation with 400 IU or less of vitamin D and 1000 mg or less of calcium provides no benefit for the primary prevention of fractures in community-dwelling, postmenopausal women.

If you are a postmenopausal woman living independently (not in a nursing home) and do not have diagnosed osteoporosis or vitamin D deficiency, you should not take daily supplements of 400 IU vitamin D and 1000 mg calcium specifically to prevent fractures. Current evidence shows this combination does not reduce fracture risk and may increase the risk of kidney stones. Focus on diet and exercise instead.

Supplementation with vitamin D and calcium increases the incidence of kidney stones in community-dwelling adults.

Be aware that taking combined vitamin D and calcium supplements increases your risk of developing kidney stones. While the absolute risk is small (about 1 extra case per 273 women over 7 years), it is a confirmed side effect. If you are not deficient, the risks may outweigh the unproven benefits.

Metabolomic age acceleration (mAA) and DNA methylation age acceleration (DNAmAA) capture distinct aspects of the aging process, as they are uncorrelated with each other despite both being associated with different risk factors.

Relying on just one 'biological age' test might give you an incomplete picture. This research suggests that metabolic health (blood/urine markers) and genetic expression (DNA methylation) track aging differently. To truly understand your aging trajectory, you might need to look at multiple health indicators rather than relying on a single metric.

Higher abundance of bacterial L-methionine biosynthesis pathways is associated with increased presence of carotid plaque and maximum stenosis (atherosclerosis) in obese individuals.

In obese individuals, specific gut bacteria that produce L-methionine are linked to higher atherosclerosis risk. While this study is observational, it suggests that managing gut microbiome composition (potentially through diet) may be relevant to cardiovascular health, particularly in those with obesity. Focus on fiber-rich diets that support diverse microbiota.

Higher abundance of Ruminococcus sp_5_1_39BFAA is positively associated with hepatic fat content (liver fat) in obese individuals.

In obese individuals, higher levels of a specific gut bacterium (Ruminococcus sp_5_1_39BFAA) are linked to more liver fat. This highlights the importance of gut health in metabolic management. Strategies to support a healthy microbiome (e.g., diverse plant fibers) may indirectly support liver health.

Genetic variants, particularly PNPLA3 (rs738409 C>G), are strongly associated with liver steatosis and progression of liver damage, independent of insulin sensitivity and BMI.

If you have a family history of fatty liver, you may have genetic risks. Regular monitoring and healthy lifestyle choices are still important to manage the risk.

Obesity causes a shift in HDL subclass distribution from large, protective HDL2 particles to small, dense HDL3 particles, and impairs HDL functionality, including reduced cholesterol efflux capacity and anti-inflammatory properties.

Obesity doesn't just lower your HDL cholesterol number; it makes the HDL you have less effective at protecting your heart. This happens because excess fat increases enzymes that break down HDL and reduces protective proteins like adiponectin. To counter this, focus on weight loss and reducing inflammation, as these changes can restore HDL function and shift the balance back to more protective HDL particles.

Long-term consumption of dietary gluten is not associated with an increased risk of coronary heart disease in adults without celiac disease.

If you do not have celiac disease, there is no evidence that eating gluten harms your heart. In fact, avoiding gluten might lead you to eat fewer whole grains, which are good for your heart. You do not need to follow a gluten-free diet for cardiovascular health.

Obesity creates a pro-inflammatory environment in white adipose tissue that impairs signaling of fibroblast growth factor 21 (FGF21) by downregulating its co-receptor β-Klotho, leading to FGF21 resistance.

In obesity, the body's natural fat-burning signals (like FGF21) get blocked by inflammation. This means that simply having high levels of these hormones doesn't work; the fat cells stop listening. Reducing inflammation may be necessary to restore these fat-burning pathways.

Central serotonergic signaling acts as an anorexigenic mechanism in the homeostatic circuitry by integrating metabolic signals to suppress food intake when energy needs are met, whereas peripheral serotonergic signaling promotes energy absorption and storage.

Your brain uses serotonin to decide when to stop eating. This process happens in specific brain areas that listen to your body's energy signals. If this system is disrupted, you might eat more than you need, contributing to weight gain. Understanding this helps explain why some medications affecting serotonin can impact weight.

Obesity is associated with disturbed serotonergic signaling, specifically decreased central serotonin release and altered receptor availability, which may contribute to the failure to suppress food intake.

In obesity, the brain's serotonin system often becomes less sensitive or releases less serotonin, making it harder to feel full. This biological change can drive overeating. Treatments that target this system (like certain drugs) may help restore this signaling.

Selective serotonin reuptake inhibitors (SSRIs) are associated with an increased risk of long-term weight gain, contrasting with their short-term anorexigenic effects.

If you take SSRIs, be aware they may contribute to weight gain over time. Talk to your doctor about monitoring your weight and discussing alternative treatments if this is a concern.

Quantitative molecular and phenotypic biomarkers (e.g., DNA methylation, telomere length, physical function) can accurately measure physiological age and predict healthspan and lifespan.

Use available biomarkers (like blood tests or physical function metrics) to track your biological age rather than just your calendar age. This helps you assess your 'healthy aging' status and potentially predict your healthspan, allowing for earlier interventions to prevent age-associated diseases.

Integrating multiple biomarkers (molecular and phenotypic) using statistical or machine learning algorithms provides a more powerful prediction of physiological age than single biomarkers.

For the most accurate assessment of your biological age, use integrated panels that combine multiple blood tests and physical metrics, analyzed by advanced algorithms, rather than relying on a single test.

Elevated plasma acylcarnitine levels, particularly long-chain species, are biomarkers of insulin resistance and incomplete fatty acid oxidation in Type 2 Diabetes, reflecting mitochondrial stress rather than directly causing insulin resistance.

High levels of acylcarnitines in the blood are a sign of how your body is processing fats and sugars, indicating mitochondrial stress in T2D. This helps doctors understand the severity of metabolic dysfunction.

Shorter leukocyte telomere length (LTL) is associated with a significantly higher risk of all-cause mortality and cardiovascular disease (CVD).

Your blood test's telomere length isn't a destiny, but a status report. Shorter telomeres correlate with higher heart disease and mortality risk. You can influence this trajectory by managing stress, exercising regularly, maintaining a healthy weight, and avoiding smoking, as these factors are linked to slower telomere shortening.

Metabolic syndrome prevalence in Indian adults is 30%, with significantly higher rates in females (35%) compared to males (26%), and in urban residents (32%) compared to rural (22%) and tribal (28%) populations.

If you are an adult in India, your risk of metabolic syndrome is about 1 in 3. Women and city dwellers face a higher risk. Regular screening for blood pressure, blood sugar, and cholesterol is crucial, especially if you live in an urban area or are female.

Historical weight-loss drugs (Thyroid hormones, DNP, Amphetamines) failed due to narrow therapeutic windows and severe adverse effects, despite some efficacy.

Historical weight-loss drugs like DNP, thyroid extracts, and amphetamines were largely withdrawn or restricted due to severe side effects (cataracts, heart issues, addiction) and limited efficacy (<10% weight loss). Their failure highlights the need for safer, more effective modern therapies like polyagonists.

Non-nutritive sweeteners are less acidogenic than sugar and may increase oral pH, potentially reducing the risk of dental caries.

If you are concerned about tooth decay, switching from sugar-sweetened drinks to those with non-nutritive sweeteners is a beneficial change. The research indicates that NNSs produce less acid in the mouth than sugar, leading to a higher oral pH which is protective against cavities.

Flavin Monooxygenase 3 (FMO3) activity promotes dyslipidemia and atherosclerosis by regulating hepatic lipogenesis, gluconeogenesis, and impairing transintestinal cholesterol export (TICE).

FMO3 is an enzyme that not only processes nutrients into TMAO but also directly regulates how your liver handles fats and sugars. High FMO3 activity is linked to worse lipid profiles and increased atherosclerosis risk. This regulation happens through complex gene signaling (FXR, LXR, PPARa) that controls cholesterol export and fat storage.

Indian diets exhibit a significant caloric deficit in protein sources (6-8% of total calories) compared to the EAT-Lancet reference diet (29%), driven by low consumption of legumes, animal proteins, and tree nuts across all income and geographic groups.

Current Indian dietary patterns, even among the wealthy, fail to provide adequate protein, contributing to health issues. To align with healthy standards, individuals must significantly increase intake of protein-rich foods like legumes, nuts, dairy, and potentially animal proteins, while reducing the disproportionate share of calories derived from cereals.

Low serum levels of IGF-I are associated with the severity of NAFLD, including inflammation, hepatocyte ballooning, and fibrosis, even in non-GHD patients.

If you have NAFLD, your IGF-I levels might be low, which correlates with more severe liver damage. While this doesn't mean you should take IGF-I supplements (which are not standard), it highlights the importance of the GH-IGF-I axis in liver health.

Obesity is associated with a specific gut microbiota composition characterized by a higher Firmicutes-to-Bacteroidetes ratio, lower bacterial gene richness, and increased gut permeability leading to metabolic endotoxemia.

Obesity is linked to a less diverse gut microbiome with specific bacterial imbalances. While you cannot directly 'buy' a healthy microbiome, eating a diverse, fiber-rich diet supports the bacteria that help regulate energy and inflammation.