Browse the evidence

DNA methylation at the PHGDH locus is associated with BMI, potentially linking serine biosynthesis pathways to obesity.

This research identifies a link between the serine biosynthesis pathway (PHGDH) and body weight. While not yet a target for intervention, it highlights the importance of balanced nutrition in supporting metabolic enzyme function.

Genetic enhancement of hepatic mitochondrial fatty acid oxidation (FAO) via CPT1A overexpression rescues insulin resistance and reduces steatosis in obesity models without increasing oxidative stress.

This paper highlights that simply increasing fat oxidation in the liver is beneficial for insulin resistance, but current pharmacological inhibitors fail due to side effects. Future therapies might target the CPT1 enzyme directly to boost oxidation without causing liver damage, potentially treating fatty liver and insulin resistance simultaneously.

Increased mitochondrial fatty acid oxidation in skeletal muscle during obesity may contribute to insulin resistance through the accumulation of incomplete oxidation intermediates (acylcarnitines) and oxidative stress.

For obese individuals, simply increasing fat oxidation in muscles (e.g., via high-fat diets) can worsen insulin resistance if the mitochondria cannot process the fat completely. Exercise remains beneficial as it likely coordinates FAO with TCA cycle capacity, whereas uncoordinated high fat oxidation can be harmful.

Long-term cross-sex hormone therapy does not increase the occurrence of cardiovascular events (myocardial infarction, DVT, cerebrovascular events) in transgender men, despite some negative changes in metabolic risk factors.

Trans men on testosterone therapy should have their metabolic health (lipids, blood pressure) monitored regularly. However, current studies do not show an increased risk of actual cardiovascular events like heart attacks or strokes, though long-term data is still being gathered.

Dietary intake of medium-chain fatty acids (MCFAs) from sources like virgin coconut oil can increase the Bacteroidetes/Firmicutes ratio and reduce obesity and inflammatory bowel disease (IBD) in animal models, although high-concentration coconut oil diets may have the opposite effect.

Focus on the quality of fats rather than just avoiding fat. Moderate intake of medium-chain fatty acids (found in coconut oil) may support a healthy gut microbiome and reduce inflammation in animal studies, but very high intake of coconut oil might have negative effects. Balance is key.

High intake of long-chain fatty acids (LCFAs), particularly from saturated sources like palm oil and lard, increases the Firmicutes to Bacteroidetes ratio, leading to obesity, insulin resistance, and inflammatory bowel disease in animal models.

Limit high intake of saturated long-chain fatty acids (found in palm oil, lard, and large amounts of butter). These are linked to negative gut microbiota changes and metabolic issues in animal studies. Opt for unsaturated fats like olive oil (MUFAs) or fish oil (PUFAs) for better metabolic health.

Targeted food taxes on high-saturated-fat items fail to reduce cardiovascular disease mortality because the reduction in saturated fat is offset by a rise in salt consumption due to cross-elasticity of demand.

Simply taxing fat does not guarantee heart health because people switch to other unhealthy options like salty snacks. To be effective, taxes must target specific nutrient combinations (like salt) or use a scoring system (SSCg3d) rather than just fat content, and even then, the impact is modest without broader industry reformulation.

Targeted food taxes based on a nutrient scoring system (SSCg3d) or optimized for best health outcomes can avert 2300-3200 cardiovascular deaths per year in the UK primarily by reducing salt intake.

If governments implement food taxes, they must target specific nutrient profiles (like salt) rather than just fat. A well-designed tax can save thousands of lives by reducing salt intake, even if the percentage change in diet is small.

Consumption of Daucus carota (carrots) provides bioactive phytochemicals (phenolics, carotenoids, polyacetylenes, and ascorbic acid) that reduce the risk of cardiovascular disease and cancer through antioxidant, anti-inflammatory, and lipid-modifying mechanisms.

Eat carrots regularly. Different colors offer different benefits: orange for eye/immune health (beta-carotene), purple/black for heart health and cancer risk reduction (anthocyanins/phenolics), and yellow for eye health (lutein). You don't need to buy expensive specialty varieties; standard orange carrots provide significant provitamin A. Processing (like blanching) can increase some phenolics, but cooking methods vary in their effect on other nutrients.

Breastfeeding is associated with a lower incidence of obesity and better long-term metabolic profiles (e.g., lipid levels, blood pressure) compared to formula feeding.

Breastfeeding is associated with a lower risk of childhood obesity and better metabolic health. If you are able to breastfeed, it provides benefits that extend beyond nutrition, including behavioral feeding patterns that help regulate intake.

Combined oral administration of Scutellariae Radix and Coptidis Rhizoma extracts improves glucose and lipid metabolism in Type 2 Diabetes Mellitus (T2DM) models by downregulating the MAPK inflammatory pathway and upregulating the PI3K/Akt insulin signaling pathway.

This research suggests that a specific combination of Scutellariae Radix and Coptidis Rhizoma extracts may help regulate blood sugar and lipids in T2DM by reducing inflammation and improving insulin signaling. However, this is an animal study; human dosing, safety, and efficacy are not established here. Do not self-medicate with these herbs based on this paper alone.

Living in neighborhoods with better physical environments (defined by better walking environments and greater availability of healthy foods) is associated with lower body mass index, independent of individual-level socioeconomic factors.

If you live in an area with poor walkability or limited access to healthy food, your BMI may be higher regardless of your personal efforts. To counteract this, you may need to be more intentional about creating your own 'healthy environment' (e.g., planning grocery trips to distant healthy stores, finding alternative exercise spaces) or advocate for local policy changes that improve walkability and food access.

Saturated fatty acids (e.g., palmitate) induce skeletal muscle atrophy and insulin resistance by promoting the accumulation of toxic lipid intermediates like ceramide and diacylglycerol (DAG), which inhibit insulin signaling and activate catabolic pathways.

If you are concerned about muscle loss, especially with age or obesity, reducing saturated fat intake (like palmitate) may help preserve muscle mass by improving insulin sensitivity and reducing inflammatory lipid intermediates. Prioritize unsaturated fats which appear to protect against muscle wasting.

Higher socioeconomic status (SES) is significantly associated with increased odds of overall obesity in urban adults, while longer urban residence is associated with higher odds of hypertension.

In rapidly urbanizing areas, obesity risk is not just a 'poor person's problem' but is strongly linked to higher socioeconomic status and urban lifestyle. Public health interventions should target affluent urban populations for obesity prevention and those with long urban residence for hypertension management, focusing on physical activity and diet quality rather than just food access.

Foreign direct investment (FDI) by transnational food companies into developing countries drives the nutrition transition by increasing the availability, lowering the prices, and expanding the marketing of highly processed foods, thereby increasing their consumption.

Public health policy should target foreign direct investment in the food sector as a primary lever for improving population health. Governments in developing countries should implement regulatory conditionalities on foreign food companies, such as restrictions on marketing to children and requirements for nutritional standards, to 'redirect' the nutrition transition towards healthier outcomes.

High-fructose intake contributes to NAFLD pathogenesis by promoting de novo lipogenesis, hepatic insulin resistance, and leptin resistance.

Limit high-fructose corn syrup and added sugars. High fructose intake drives liver fat production and insulin resistance independently of weight gain. Focus on reducing processed foods and sugary drinks rather than eliminating all natural fruit sources.

Resveratrol protects human endothelial cells from oxidative stress-induced senescence by activating SirT1 expression and activity.

To potentially protect your blood vessel lining from age-related damage, focus on sources of Resveratrol like red grapes or supplements, as it appears to activate SirT1, a protein that helps cells resist stress and aging. The study suggests a specific activation threshold, implying that adequate dosing is critical for this benefit.

Higher gut microbial alpha diversity is associated with lower arterial stiffness (measured by carotid-femoral pulse wave velocity) in middle-aged women, independent of traditional cardiovascular risk factors.

For women, maintaining a diverse gut microbiome through a fiber-rich diet may support arterial health. While this study does not prove that changing your diet will directly lower blood pressure or stiffness, it highlights that the microbes in your gut are linked to how stiff your arteries are, a key marker of cardiovascular aging. Focus on dietary diversity to support microbial richness.

The addition of medroxyprogesterone acetate (MPA) to estrogen therapy may abrogate the cardiovascular protective effects of estrogen, potentially explaining the negative results in combined HRT trials like HERS and WHI.

For women requiring uterine protection, the choice of progestin matters. MPA, commonly used in HRT, may negate the heart-healthy lipid changes caused by estrogen. Women concerned about cardiovascular risk should discuss whether alternative progestins or estrogen-only therapy (if no uterus) are appropriate options.

Administration of ursodeoxycholic acid (UDCA) attenuates high-fat diet-induced obesity in mice by increasing hepatic levels of non-12-hydroxylated bile acids (non-12-OH BAs), which enhances GLP-1 secretion and upregulates UCP1 and PGC1a in brown adipose tissue.

This research suggests that ursodeoxycholic acid (UDCA) may help prevent obesity in the context of a high-fat diet by boosting beneficial bile acids (non-12-OH BAs). These bile acids signal the body to burn more energy (via UCP1 in fat tissue) and release satiety hormones (GLP-1). While this is a promising therapeutic avenue, it is currently based on animal models. For humans, maintaining a healthy weight through diet and exercise remains the primary strategy, but this mechanism highlights why bile acid health is important for metabolic function.

Exercise provides an anti-ageing effect by preventing telomere shortening and modifying DNA methylation patterns, which may mitigate age-related bone loss and osteoporosis.

Engage in regular exercise, especially after age 40, not just for muscle or weight, but for cellular health. This helps protect your telomeres and DNA methylation patterns, which are linked to how fast your body ages and your risk of bone diseases.

Aging causes preadipocytes to lose the capacity for proliferation and differentiation, leading to impaired lipid storage, increased susceptibility to lipotoxicity, and fat redistribution from subcutaneous to visceral/ectopic depots.

As you age, your body's ability to store fat safely in subcutaneous tissue declines, pushing it into dangerous visceral and organ areas. This is driven by cellular changes in fat progenitors, not just calories. Understanding this highlights the importance of maintaining metabolic health and potentially targeting inflammation, rather than just focusing on weight loss.

Saturated fatty acids (specifically palmitate) induce lipotoxicity and inflammation in preadipocytes, creating a self-perpetuating cycle of cellular stress and metabolic dysfunction.

The type of fat you eat matters. Saturated fats can trigger inflammation and stress in fat cells, especially as you age. Choosing unsaturated fats may help protect fat cell function and reduce inflammation.

Fat depot origin (subcutaneous vs. visceral/omental) determines inherent differences in preadipocyte function, with subcutaneous preadipocytes generally having a higher capacity for differentiation and lipid accumulation than omental preadipocytes.

Where fat is stored matters. Subcutaneous fat (under the skin) tends to be healthier and more functional than visceral fat (around organs), which is more prone to dysfunction and inflammation, especially with age.