Browse the evidence

Initiation of modern antiretroviral therapy (ART), specifically integrase strand transfer inhibitors (INSTIs) like dolutegravir and bictegravir combined with tenofovir alafenamide (TAF), causes significant, sustained weight gain in people living with HIV, disproportionately affecting women and Black patients.

If you are living with HIV and starting or taking modern medication (specifically drugs ending in '-gravir' like dolutegravir or bictegravir, and TAF), expect significant weight gain, especially if you are a woman or Black. This is not just 'getting older' or 'eating too much'; it is a known side effect of the medication's interaction with your metabolism. Talk to your doctor about your risk factors. They may consider regimens with TDF (which mitigates weight gain) or other alternatives, though these may have other side effects. Be aware that standard diet and exercise might be less effective for this specific type of gain, and emerging weight-loss medications might be considered in the future.

Integrase strand transfer inhibitors (INSTIs), particularly dolutegravir and bictegravir, are the primary drivers of weight gain in modern ART regimens, with effects observed as early as 4 weeks post-initiation.

If you are taking an INSTI (like dolutegravir or bictegravir), be aware that these drugs are strongly linked to weight gain, often starting within weeks of taking them. This is a known side effect of the drug class, not just your lifestyle. If you are at high risk (e.g., woman, Black patient), discuss your concerns with your doctor. They might consider alternative regimens, though these may have other trade-offs.

When subcutaneous white adipose tissue (scWAT) reaches its maximal storage capacity, it becomes dysfunctional and fails to store lipids appropriately, leading to ectopic fat accumulation in the liver and visceral depots, thereby causing non-alcoholic fatty liver disease (NAFLD).

If you are obese, your body's ability to store fat safely in your subcutaneous areas (like thighs and arms) may be maxed out. Once this 'buffer' is full, excess fat spills over into your liver and visceral organs, causing disease. Strategies to improve metabolic health should focus on preventing this overflow, potentially through interventions that support adipose tissue health or reduce caloric intake to match storage capacity.

Biomarker-based personalized nutrition plans do not result in greater weight loss or improvements in cardiometabolic health compared to a generic, generally healthy diet in individuals with overweight or obesity.

If you have overweight or obesity, following a generally healthy, balanced diet that provides enough food to satisfy you will result in similar weight loss and health improvements as following a highly personalized, biomarker-driven diet plan. You do not need to undergo expensive metabolic testing or follow complex personalized rules to achieve significant health benefits; consistency with a healthy, isocaloric diet is sufficient.

GLP-1 monotherapy (liraglutide, semaglutide) is associated with high discontinuation rates due to gastrointestinal side effects, limiting long-term adherence.

Be aware that GLP-1 monotherapy can cause significant gastrointestinal side effects, leading to high discontinuation rates. Discuss titration strategies with your provider to minimize these effects.

GLP-1 receptor agonists directly modulate immune cell function, specifically suppressing T-cell activity and pro-inflammatory cytokine release, independent of metabolic changes.

GLP-1 medicines interact directly with your immune system. They can dampen the activity of T cells, which are key drivers of inflammation. This direct interaction helps reduce the production of inflammatory markers like TNF-α and IL-2, contributing to overall health benefits beyond blood sugar control.

GLP-1 receptor agonists reduce cardiovascular events and atherosclerosis progression through weight-loss-independent anti-inflammatory mechanisms involving endothelial and immune cell modulation.

GLP-1 medications like semaglutide and liraglutide are proven to reduce the risk of heart attacks, strokes, and cardiovascular death in people with type 2 diabetes and obesity. This protection is partly due to direct anti-inflammatory effects on blood vessels, independent of weight loss. These benefits are significant enough to be a primary reason for prescribing these drugs in high-risk patients.

Chronic inflammation, oxidative stress, and gut dysbiosis form a reciprocal triad that perpetuates the pathophysiology of obesity.

Focus on reducing inflammation through diet (anti-inflammatory foods, fiber) and managing stress, as these factors directly impact gut health and oxidative stress, which in turn affect weight regulation.

Reduction of adipocyte-derived SPARC protects against high-fat diet-induced obesity and metabolic dysfunction in female mice by enhancing energy expenditure and lipolysis.

This research identifies SPARC, a protein elevated in obesity, as a key regulator of fat storage. Reducing SPARC (naturally via caloric restriction or potentially via future therapies) may help manage weight by increasing energy expenditure and breaking down fat, particularly in women. While not a direct diet advice, it highlights that lowering this specific protein is linked to improved metabolic health.

SPARC acts as a priming signal for the NLRP3 inflammasome in macrophages, driving chronic inflammation associated with obesity.

Chronic inflammation in obesity is driven by SPARC activating immune cells. Reducing SPARC levels, as seen with weight loss, reduces this inflammation.

GLP1R agonism reduces coronary artery disease (CAD) risk primarily through body weight lowering (BMI) rather than through the reduction of type 2 diabetes (T2D) liability.

If you are using a GLP-1 agonist (like semaglutide or tirzepatide) for heart health, the primary benefit comes from the weight loss it induces, not just from lowering blood sugar. Even if your blood sugar is already well-controlled, the drug's effect on reducing body weight is what significantly lowers your risk of coronary artery disease. This supports using these medications for cardiovascular prevention in obese individuals, regardless of diabetic status.

An intensive, early post-bariatric lifestyle intervention combining nutritional-behavioral tele-counseling and supervised exercise does not improve weight loss or secondary health outcomes compared to standard care alone.

If you have had bariatric surgery, standard post-operative care is likely sufficient for optimal weight loss. Adding an intensive, early lifestyle program with frequent counseling and exercise sessions does not improve results and may be unnecessarily burdensome. Focus on sustainable habits rather than intensive early intervention.

Stimulating the release of endogenous intestinal GIP via K-cell activation reduces food intake and body weight in mice through a central nervous system mechanism.

This research suggests that the hormone GIP, released from the gut after eating, plays a direct role in signaling satiety to the brain. While this is currently demonstrated via genetic manipulation in mice, it implies that therapies enhancing natural GIP release or mimicking its action could help reduce food intake and body weight, potentially offering an alternative or complement to GLP-1 based treatments.

Expert consensus identifies 14 biomarkers of aging suitable for use as outcome measures in human intervention studies, spanning physiological, inflammatory, functional, and epigenetic domains.

When designing an aging intervention study, use one or more of the 14 consensus biomarkers (IGF-1, GDF15, hsCRP, IL-6, muscle mass/strength, grip strength, TUG, gait speed, balance, frailty index, cognitive health, blood pressure, or DNA methylation/epigenetic clocks) as your primary outcome measures. These are validated by expert consensus for detecting changes in biological age.

Blood-based inflammatory biomarkers (IL-6, TNF-α) are suitable for field testing using dry blood spot sampling, unlike DNA methylation-based biomarkers which require advanced laboratory processes.

For field studies, consider using dry blood spot sampling to measure IL-6 and TNF-α, as these can be collected remotely and analyzed, unlike DNA methylation which requires advanced lab processing.

In Type 1 Diabetes, fracture incidence rates have remained stable or increased in women, despite overall improvements in diabetes management and the adoption of newer technologies.

If you have Type 1 Diabetes, especially if you are a woman, be aware that your fracture risk may not be decreasing as much as it is for Type 2 Diabetes patients. Focus on preventing hypoglycemia, as low blood sugar events are linked to higher fracture risk. Discuss bone health specifically with your endocrinologist.

Compared with animal protein, plant protein results in lower muscle mass, with a stronger negative effect observed in younger adults (<60 years) than in older adults (≥60 years).

If your goal is maximizing muscle mass, animal protein may offer a slight advantage over plant protein, particularly in younger adults. However, the difference is small, and plant protein is still effective. Focus on getting enough total protein and combining plant sources if possible.

There is no significant difference between plant and animal protein for muscle strength or physical performance.

You do not need animal protein to build strength or improve physical performance. Plant protein is equally effective for these outcomes. Focus on consistent training and adequate protein intake.

Post-exercise supplementation with 40g of whey protein provides no additional benefit to cardiorespiratory fitness or cardiometabolic health adaptations compared to an isocaloric placebo when combined with low-volume high-intensity interval training (LOW-HIIT) in sedentary, healthy adults.

If you are sedentary and start doing low-volume high-intensity interval training (HIIT), you do not need to rush to consume 40g of protein immediately after your workout to get the best heart and metabolic health benefits. Consuming an equivalent amount of calories from carbohydrates (like maltodextrin or even just eating a normal meal) provides the same improvements in fitness and blood pressure. Focus on consistency with the training rather than expensive post-workout supplements.

High post-diagnostic consumption of ultra-processed foods (UPFs) is associated with a significantly increased risk of cardiovascular disease (CVD) mortality in patients with stages I–III colorectal cancer (CRC), but not with CRC-specific or all-cause mortality.

For colorectal cancer survivors, reducing ultra-processed food intake (aiming for <3.6 servings/day) is strongly linked to a lower risk of cardiovascular death, which is a major cause of mortality in this group. While this reduction did not show a direct link to preventing cancer recurrence in this study, prioritizing whole foods over processed options supports heart health, a critical component of long-term survivorship.

PPAR agonists (specifically pioglitazone) improve individual histological features of NASH (steatosis, ballooning, inflammation) and can improve fibrosis.

Pioglitazone, a PPAR agonist, improves liver inflammation and fat in NASH patients. It is taken orally (30-45 mg daily). A significant side effect is weight gain (~2.5 kg), which might be undesirable for obese patients. It can also improve fibrosis.

Targeting the melanocortin-4 receptor (MC4R) with biased agonists that favor Gq/11 signaling over Gs signaling reduces food intake and adiposity without causing adverse cardiovascular effects like hypertension and tachycardia.

If you have a specific genetic form of obesity linked to MC4R, a drug called setmelanotide may help you lose weight and improve glucose tolerance without raising your blood pressure, unlike some older treatments. This is because it targets the specific receptor pathway that controls appetite without triggering the heart-related side effects.

GLP-1RAs exhibit neuroprotective effects and may improve symptoms in patients with obesity-related heart failure with preserved ejection fraction (HFpEF) and cognitive dysfunction associated with type 2 diabetes.

For patients with obesity-related heart failure with preserved ejection fraction (HFpEF) and type 2 diabetes, GLP-1 receptor agonists like semaglutide can significantly reduce heart failure symptoms and improve physical limitations. Additionally, there is emerging evidence that these medications may offer neuroprotective benefits, potentially slowing cognitive decline in patients with T2DM.

Adipose tissue dysfunction, specifically the release of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and free fatty acids from visceral fat, drives insulin resistance and beta-cell dysfunction in obesity.

Fat is not just stored energy; it actively sends inflammatory signals that block your body's ability to use insulin. Reducing visceral fat reduces this inflammation, thereby improving insulin sensitivity.