Browse the evidence

Adherence to a Western diet for two weeks significantly increases plasma levels of specific fatty acids (myristic, linoelaidic, linoleic, alpha-linoleic, pentadecanoic acid) and urinary acesulfame K, serving as biomarkers for unhealthy eating patterns.

If you consume a Western diet high in processed foods, red meat, and artificial sweeteners, your body reflects this quickly. Within two weeks, levels of specific fatty acids (like myristic and linoelaidic acid) and acesulfame K rise in your blood and urine. This objective change signals that your diet is shifting towards an unhealthy pattern, highlighting the importance of reducing processed foods and artificial sweeteners.

Higher long-term circulating levels of de novo lipogenesis-related fatty acids (palmitic acid 16:0, palmitoleic acid 16:1n-7, and oleic acid 18:1n-9) are associated with increased all-cause, cardiovascular, and non-cardiovascular mortality in older adults, whereas higher levels of stearic acid (18:0) are associated with lower mortality risk.

For older adults, high levels of certain fatty acids in the blood (palmitic, palmitoleic, and oleic acids) signal higher long-term mortality risk, while stearic acid signals lower risk. These levels reflect metabolic processes like de novo lipogenesis, often driven by excess carbohydrate and alcohol intake. Focus on metabolic health markers rather than just total fat intake.

GLP-1 receptor agonists (semaglutide, liraglutide, dulaglutide, exenatide) produce a statistically significant but clinically modest reduction in systolic blood pressure (SBP) compared to placebo, with effects ranging from -1.46 to -3.40 mmHg.

GLP-1 medications (like Ozempic or Wegovy) consistently lower systolic blood pressure by a small but measurable amount (1-3 mmHg). This benefit occurs regardless of whether you have diabetes. It is not a substitute for blood pressure medication, but it is a favorable side effect that supports heart health.

GLP-1 receptor agonists generally do not significantly reduce diastolic blood pressure (DBP), with the exception of exenatide.

Do not expect GLP-1 medications to significantly lower your diastolic (bottom number) blood pressure, unless you are taking exenatide. Most GLP-1s primarily affect systolic pressure.

Selective, long-acting NK2R agonists (e.g., EB1002) reduce body weight and improve insulin sensitivity in obese mice and diabetic macaques by simultaneously increasing energy expenditure and suppressing appetite without causing aversive side effects.

This research identifies a new drug target (NK2R) that could lead to medications for obesity and type 2 diabetes. These drugs work by making your body burn more energy and reducing your appetite, without causing the unpleasant side effects often associated with other weight loss treatments. While promising in animals, this is not yet a human treatment.

Salivary testosterone and cortisol ratios are inconsistent predictors of strength performance and are not practical for regular training regulation due to high variability between individuals and lack of immediate utility.

Do not rely on blood or saliva tests for daily training decisions. They are expensive, invasive, and inconsistent. Instead, use performance metrics like barbell speed or how hard the set felt (RPE) to guide your training.

Increases in multimorbidity and frailty indices over an 8-year period are associated with subsequent poorer cognitive function, reduced physical function (gait speed), and increased mortality risk in adults with type 2 diabetes.

For adults with type 2 diabetes, keeping track of the number of chronic diseases and physical deficits (frailty) is a strong predictor of future cognitive decline, mobility issues, and death. However, simply improving these specific counts through lifestyle changes may not be enough to guarantee better long-term cognitive or survival outcomes, suggesting a need for a broader approach to healthspan.

Higher habitual levels and increases in plasma phospholipid palmitic acid (16:0), 7-hexadecenoic acid (16:1n-9), and vaccenic acid (18:1n-7) are positively associated with an increased risk of incident heart failure in older adults.

For older adults, maintaining healthy metabolic function is crucial for heart health. While this study doesn't prescribe a specific diet, it highlights that high levels of certain fatty acids (16:0, 16:1n-9, 18:1n-7) in the blood are linked to heart failure risk. These fatty acids are produced by the body (de novo lipogenesis) from excess carbohydrates, sugars, and alcohol, rather than just from eating fat. Therefore, managing carbohydrate and sugar intake may help regulate these fatty acid levels and potentially reduce heart failure risk.

In type 2 diabetes patients, maintaining a lower body mass index (BMI) does not provide greater protection against vascular complications and may increase the risk of specific complications like peripheral neuropathy and peripheral arterial disease.

If you have Type 2 Diabetes, do not assume that losing as much weight as possible is the best strategy for your health. This study shows that being too thin (BMI < 21.6) increases your risk of nerve damage (neuropathy) and circulation problems (PAD) just as much as being overweight. Aim for a moderate BMI range (around 23.5–25.2 kg/m2) to minimize vascular risks, rather than pursuing extreme weight loss.

Epicardial adipose tissue volume is a stronger predictor of atrial fibrillation risk than general anthropometric indices like BMI or waist circumference.

Fat stored directly around the heart (epicardial fat) is a major driver of atrial fibrillation in obese people. This risk is higher than what BMI alone suggests. Weight loss reduces this fat and improves heart rhythm.

Bariatric surgery reduces all-cause and cardiovascular mortality and heart failure incidence, but its effect on reducing *incident* atrial fibrillation is not statistically significant.

Bariatric surgery significantly reduces death and heart failure in obese patients, but it does not significantly reduce the risk of *developing* new atrial fibrillation. It is still beneficial for overall heart health.

Bariatric surgery (specifically Roux-en-Y gastric bypass and sleeve gastrectomy) is superior to behavioral and pharmacological interventions for long-term weight loss maintenance because it alters gut hormones and brain reward circuits, reducing compensatory hunger and metabolic adaptation.

Bariatric surgery is currently the most effective long-term intervention for obesity, largely because it biologically reduces hunger and alters food reward. However, it is not a permanent cure; significant weight regain can still occur. It should be viewed as a tool that facilitates weight loss, but long-term success still requires ongoing behavioral and nutritional support.

Obesity is a chronic, relapsing disease driven by a syndemic interaction of macro-systems (climate, globalization, policy) and micro-systems (behavior, environment), rather than solely individual choice.

Stop blaming yourself or others for obesity. Recognize it as a chronic disease shaped by your environment, food systems, and socioeconomic status. Seek medical help and policy changes rather than relying solely on willpower.

Body Mass Index (BMI) is an insufficient and potentially misleading sole diagnostic measure for obesity due to its inability to capture phenotypic heterogeneity and visceral adiposity.

Do not rely on BMI alone to assess your health. Ask your doctor for additional metrics like waist circumference, blood pressure, and blood sugar levels to get a complete picture of your metabolic health.

SGLT2 inhibitors and GLP-1 receptor agonists reduce major cardiovascular events and improve cardiac structure/function through anti-inflammatory, anti-oxidative, and metabolic mechanisms, independent of glucose lowering.

If you have T2DM and heart disease or risk factors, ask your doctor about SGLT2 inhibitors or GLP-1 RAs. These drugs do more than lower blood sugar; they actively protect your heart, reduce inflammation, and lower the risk of heart failure and death, regardless of your glucose levels.

SGLT2 inhibitors reduce oxidative stress and inflammation in cardiac tissue by improving nitric oxide bioavailability, stimulating Nrf2/ARE signaling, and suppressing NADPH oxidase.

SGLT2 inhibitors help protect heart cells from damage caused by oxidative stress and inflammation, which contributes to their ability to prevent heart failure.

SGLT2 inhibitors reduce the incidence of atrial fibrillation (AF) and atrial flutter (AFL) by reducing atrial dilation, intracellular sodium/calcium levels, and epicardial adipose tissue.

Taking SGLT2 inhibitors may lower your risk of developing irregular heartbeats like atrial fibrillation, which is a common complication in diabetes and heart failure.

GLP-1 receptor agonists reduce stroke risk but do not significantly prevent the onset of atrial fibrillation or atrial flutter, and may increase heart rate.

GLP-1 RAs are effective at reducing stroke risk, but unlike SGLT2 inhibitors, they do not appear to prevent atrial fibrillation and may slightly increase heart rate.

Fibroblast growth factor 21 (FGF21) acts as a specific negative feedback signal that reduces carbohydrate (sweet) preference in response to high sugar intake.

High sugar intake triggers the release of FGF21, a hormone that naturally reduces your desire for sweets. Consistently high sugar intake may blunt this system or require higher thresholds to trigger it. Reducing initial sugar loads may help restore this natural regulatory feedback loop.

GLP-1 receptor agonists (GLP-1 RAs) induce significant gastrointestinal adverse events (nausea, vomiting, diarrhea, constipation) by slowing gastric emptying and increasing gastric accommodation, with incidence rates ranging from 18% to 52% depending on the specific agent and dose.

If you are prescribed a GLP-1 drug like semaglutide or liraglutide, expect a high chance of nausea or vomiting, especially when starting. The paper advises starting at the lowest dose and increasing slowly. Crucially, you must adjust your diet: eat smaller meals, reduce fat, and avoid raw fiber. If you continue to have side effects, ask your doctor about dose de-escalation. Do not assume the sickness is what causes the weight loss; the drug works directly, but the side effects are a common hurdle to manage.

GLP-1 receptor agonists delay gastric emptying and increase gastric accommodation, which contributes to satiety but poses a significant risk of aspiration during perioperative procedures, necessitating specific preoperative management guidelines.

If you are having surgery and take a weekly GLP-1 shot (like Ozempic or Wegovy), tell your surgeon and anesthesiologist. For elective surgery, you may need to stop the drug 4 weeks beforehand. If it's an emergency, they will check your stomach with an ultrasound and may give you a drug (erythromycin) to empty it. This is a new standard of care to prevent choking on stomach contents during anesthesia.

Some GLP-1RAs (e.g., Lixisenatide, Exenatide, oral Semaglutide) show neutral cardiovascular outcomes in patients with Type 2 Diabetes, suggesting that not all GLP-1RAs provide cardiovascular protection.

Not all GLP-1 medications protect the heart. Drugs like Lixisenatide, Exenatide, and oral Semaglutide have shown neutral effects on major cardiovascular events in large studies. If you have heart disease, ask your doctor if your specific GLP-1 medication has proven cardiovascular benefits.

In overweight or obese adults with diabetes, unintentional or general weight loss is associated with a statistically significant increase in all-cause and cardiovascular disease mortality compared to weight stability.

If you have diabetes and are overweight or obese, do not pursue weight loss unless it is explicitly intentional and monitored, as general weight loss is linked to higher mortality in this group. Focus instead on glycemic control and avoiding muscle loss. Consult your endocrinologist before attempting any weight reduction strategy.

In patients with established incident cardiovascular disease, higher body mass index (overweight and obesity) is associated with a more favorable prognosis for subsequent stroke, peripheral vascular disease, and mortality (CVD-related and all-cause) compared to normal BMI, regardless of metabolic health status.

If you have had a heart attack, stroke, or peripheral vascular disease, being overweight or obese is not necessarily a bad thing for your survival. In fact, this large study shows that having extra weight is linked to a lower risk of dying from heart issues or other causes compared to being normal weight. Do not aggressively try to lose weight without consulting your doctor, as maintaining energy reserves might be protective. Instead, focus on controlling blood pressure, cholesterol, and diabetes.