Browse the evidence

Acute ingestion of 10g inulin-propionate ester increases postprandial PYY and GLP-1 levels and reduces energy intake by approximately 14% in healthy adults.

Taking 10g of this specific propionate ester with a meal can help you eat less during that meal by triggering fullness hormones. This effect happens about 4 hours after ingestion when the propionate reaches the colon.

Supplementation with EPA and DHA (2.7 g/day EPA) reduces the production of pro-inflammatory eicosanoids (like PGE2) and cytokines (TNF-alpha, IL-1beta) by altering cell membrane phospholipid composition and inhibiting NF-kB activation.

To reduce inflammation, standard fish oil doses may be insufficient. Research suggests a threshold of approximately 2.7 grams of EPA per day is needed to significantly lower inflammatory markers like PGE2. This is higher than typical dietary intake. For conditions like RA, this dosage has shown clinical benefits like reduced stiffness and pain.

Adipose tissue expression of tumor necrosis factor (TNF) increases with obesity and decreases significantly with weight loss, correlating inversely with lipoprotein lipase (LPL) activity.

Weight loss reduces the production of TNF, a hormone-like substance in fat tissue that promotes fat storage by inhibiting LPL. This suggests that as you lose weight, your body's biological resistance to storing fat decreases, potentially making further weight loss easier, although other factors also regulate fat storage.

High-volume, intense exercise training and competition are associated with transient immune dysfunction and an increased risk of upper respiratory tract infections (URTI).

If you are training for a marathon or competing in endurance events, be aware that your risk of getting sick spikes in the days following the event. Prioritize recovery, sleep, and nutrition immediately after heavy exertion to mitigate this risk.

A modest reduction of 1 g of salt per day, achieved gradually, is still cost-saving and reduces cardiovascular events, making it a viable long-term public health target.

You don't need to eliminate salt to see benefits. A modest reduction of 1 gram per day, achieved gradually over time, is still cost-saving for the healthcare system and reduces heart disease and stroke risk. Focus on small, sustainable changes to your diet, particularly reducing processed foods.

SGLT2 inhibitors (e.g., Dapagliflozin) lower blood glucose by preventing renal glucose reabsorption, resulting in reduced HbA1c, fasting plasma glucose, blood pressure, and body weight.

SGLT2 inhibitors like Dapagliflozin are a newer class of diabetes medication that work by removing excess sugar through urine. This process helps lower blood sugar, blood pressure, and body weight. While effective, they carry a risk of genital infections and potentially breast or bladder cancer, requiring monitoring.

GLP-1 receptor agonists (e.g., Exenatide, Liraglutide, Lixisenatide) lower HbA1c, promote weight loss, and reduce hypoglycemia risk by stimulating insulin secretion and increasing satiety.

GLP-1 receptor agonists are injectable medications that help lower blood sugar, promote weight loss, and reduce the risk of hypoglycemia. They work by mimicking a hormone that increases insulin, decreases glucagon, and makes you feel full. They are effective for both weight loss and glycemic control, with similar safety profiles in elderly and younger patients.

Acute administration of glucose (oral or intravenous) and food intake causes a significant decrease in plasma ghrelin concentrations, reaching a nadir of approximately 66-69% of basal levels, indicating ghrelin reflects acute feeding state.

Eating food, particularly carbohydrates, triggers a rapid drop in ghrelin (the hunger hormone). This is a metabolic signal, not just a result of your stomach being physically full. Water alone does not trigger this hormonal drop, suggesting that nutrient content is key to hormonal satiety.

Habitually sleeping 5 hours or less per night significantly increases the risk of developing hypertension in adults aged 32-59, independent of obesity and diabetes.

If you are between 32 and 59 years old, consistently sleeping 5 hours or less a night puts you at double the risk of developing high blood pressure compared to sleeping 7-8 hours. This risk exists even if you are not overweight or diabetic. Prioritize getting 7-8 hours of sleep to protect your cardiovascular health.

Short sleep duration increases hypertension risk through mechanisms including elevated 24-hour blood pressure, increased sympathetic nervous system activity, and structural cardiovascular adaptations.

Sleeping less than 5 hours doesn't just make you tired; it keeps your blood pressure high all day and night, stresses your nervous system, and can physically change your heart and arteries over time. Consistent sleep is a structural necessity for blood pressure regulation.

Leptin-replacement therapy significantly improves glycemic control, reduces triglyceride levels, and decreases liver volume in patients with lipodystrophy and leptin deficiency.

If you have a rare condition called lipodystrophy that causes a severe lack of body fat and leptin, leptin replacement therapy can dramatically improve your blood sugar, lower dangerous triglyceride levels, and shrink your liver. This treatment is not for general obesity but is a critical therapy for this specific hormonal deficiency.

In patients at high cardiovascular risk who have achieved LDL-C goals, elevated triglycerides (≥1.7 mmol/L) and/or low HDL-C (<1.0 mmol/L) remain independent predictors of cardiovascular events, and therapeutic targeting of these markers provides incremental risk reduction.

If you are at high risk for heart disease and your LDL cholesterol is already at the target level, do not stop monitoring your lipids. Check your triglycerides and HDL levels. If triglycerides are high (≥150 mg/dL) or HDL is low (<40 mg/dL), discuss with your doctor. The first step is lifestyle changes (diet, exercise), but if these don't correct the levels, adding medications like niacin or fibrates, or intensifying your current therapy, may be necessary to further reduce your risk.

Adipocyte hypertrophy (enlargement) in white adipose tissue drives insulin resistance and metabolic disorders through inflammation, hypoxia, and lipotoxicity, whereas hyperplasia (increased adipocyte number) is associated with improved insulin sensitivity and metabolic health.

If you are gaining weight, understand that your body's response matters. If your fat cells are getting huge (hypertrophy), you are at higher risk for insulin resistance. If your body creates new, smaller fat cells (hyperplasia), it may be protecting your metabolic health. Strategies that promote adipogenesis (like certain medications or lifestyle changes that avoid extreme caloric surges) might be metabolically superior to those that just cause massive cell enlargement.

Ghrelin is the only known hormone that powerfully increases food intake, with levels surging before meals and suppressing after eating, playing a key role in meal initiation and hunger.

Ghrelin is your body's 'hunger hormone.' It rises before meals to prepare you for eating and falls after. Understanding this can help normalize the experience of hunger as a natural biological signal rather than a personal failing.

Faecalibacterium prausnitzii levels are significantly lower in obese individuals with Type 2 Diabetes and are negatively correlated with inflammatory markers (hs-CRP, IL-6), suggesting its role in reducing low-grade inflammation independently of calorie intake.

Low levels of Faecalibacterium prausnitzii are linked to higher inflammation in obese people with diabetes. Surgery helps restore this bacteria, which may help lower inflammation. This benefit appears to happen regardless of how much the patient eats, suggesting the surgery itself creates a gut environment that supports this beneficial bacteria.

Body weight reduction significantly increases plasma levels of the anti-inflammatory protein adiponectin, with the magnitude of increase correlating with reductions in BMI and hip circumference.

For severely obese individuals, significant weight loss (whether through surgery or other means) triggers a beneficial hormonal response by increasing adiponectin, an anti-inflammatory protein. This suggests that reducing fat mass actively improves metabolic health by removing the 'brakes' on this protective hormone, potentially lowering cardiovascular risk.

A single bout of resistance exercise increases mixed muscle protein synthesis (MPS) and breakdown (MPB) rates, with MPS elevation persisting for at least 48 hours, but net protein balance remains negative in the fasted state because MPB also increases.

If you want to build muscle, do not train in a fasted state. This study shows that while exercise boosts protein synthesis for 48 hours, it also boosts breakdown. In a fasted state, your body breaks down more protein than it builds, resulting in a net loss. To turn this exercise stimulus into muscle growth, you must consume protein to shift the balance from negative to positive.

Sensible sun exposure produces vitamin D3 in the skin, which is metabolized into 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, regulating calcium/phosphate metabolism and influencing chronic disease risk (autoimmune, cancer, cardiovascular, infectious, schizophrenia, type 2 diabetes).

Get sensible sun exposure to support your vitamin D levels, especially if you live at higher latitudes, have darker skin, or are older. The body regulates production to prevent toxicity, so you don't need to worry about overdose from the sun. If you cannot get enough sun, consider food fortification or supplements as part of a three-part strategy.

Aging significantly decreases the skin's capacity to produce vitamin D3, requiring older adults to have greater sun exposure or supplementation to maintain healthy vitamin D levels.

As you age, your skin becomes less efficient at producing vitamin D from sunlight. You may need more sun exposure or consider supplementation to maintain healthy levels.

Sleep, particularly slow-wave sleep, enhances the formation of immunological memory by facilitating the redistribution of naïve T cells to lymph nodes and promoting pro-inflammatory cytokine production (e.g., IL-12, IL-1, TNF-alpha).

Prioritize 7-9 hours of quality sleep, especially after vaccination or during illness. Slow-wave sleep is critical for your immune system to 'save' the memory of pathogens. Sacrificing sleep for activity directly impairs your immune defense and vaccine efficacy.

Prolonged sleep loss or wakefulness acts as a stressor that suppresses immune function, increasing susceptibility to infection and inflammation.

Chronic sleep loss is not just fatigue; it is a state of physiological stress that suppresses your immune system. Consistently getting less than 7 hours of sleep increases your risk of infection and inflammation.

Increasing dietary intake of long-chain omega-3 fatty acids (EPA and DHA) through fish consumption or supplementation reduces the incidence and severity of chronic inflammatory diseases by shifting eicosanoid production from pro-inflammatory to anti-inflammatory mediators.

To reduce chronic inflammation, aim for 0.5–1.8 grams of EPA/DHA daily. The easiest way is eating two servings of oily fish (like salmon or mackerel) per week. If you don't eat fish, take a standard fish oil supplement providing roughly 300-1000mg of combined EPA/DHA daily. This shifts your body's chemical messengers from pro-inflammatory to anti-inflammatory, lowering risks for heart disease and arthritis.

EPA and DHA suppress inflammatory gene expression by inhibiting the transcription factor NF-kB and activating PPARs, thereby reducing the production of pro-inflammatory cytokines like IL-6 and TNF-alpha.

This mechanism explains why fish oil works: it turns down the 'volume' of inflammatory signals in your cells by blocking specific genetic switches (NF-kB). This is why consistent intake matters more than a single dose.

Daily supplementation of 400 IU of vitamin D prevents nutritional rickets in children, whereas 800 IU of vitamin D combined with appropriate calcium intake reduces osteoporotic fracture risk in vitamin D-deficient or institutionalized elderly subjects.

If you are an older adult living in care or have low vitamin D levels, take 800 IU of Vitamin D3 daily along with adequate calcium to help protect your bones from fractures. For children, 400 IU daily is the standard to prevent rickets. Do not assume mega-doses work better; very high single doses may actually increase fracture risk.