The 5 Most Inflammatory Foods to Ditch For Good (feel it immediately)

DeLauer presents two studies. The first, in type 2 diabetics, found that drinking 1 liter of sugary soda daily for six months raised uric acid by 15%, while diet soda, milk, and water did not. Uric acid is a precursor to inflammatory responses. The second, a mice study, compared high glucose, high fructose, and control diets. Fructose and sucrose (glucose+fructose) groups showed hyperinsulinemia, increased adipokines (inflammatory cytokines from fat cells), fatty liver deposits, and necroinflammation—a progression from fatty liver to steatohepatitis. Fructose was slightly more potent, likely because humans are not designed to handle large fructose loads without fiber. He emphasizes that the problem is refined sugars devoid of fiber, not whole fruits.

DeLauer explains that trans fats are created by adding hydrogen to unsaturated fats to make them solid at room temperature. A study in Nutrition on 730 women found a linear relationship: those with the highest trans fat intake had CRP levels 73% higher and IL-6 levels 17% higher than those with low intake. He notes that CRP and IL-6 are powerful predictors of cardiovascular disease, with CRP influencing atherogenesis (plaque formation) and IL-6 and TNF-α being indicators of coronary heart disease. Additionally, trans fats are associated with increased visceral adipose tissue, which itself leaks inflammatory cytokines, creating a vicious cycle.

DeLauer details two pathways. First, an observational study found sex-specific biomarkers: women had higher uric acid, men higher CRP. Both lead to increased IL-6 and systemic inflammation. Second, alcohol directly damages intestinal epithelial cells, compromising tight junctions. This allows lipopolysaccharides (LPS) from gut bacteria to enter the bloodstream, where the immune system attacks them, causing widespread inflammation. He calls alcohol a poison that is very difficult for the liver to process, and the gut damage is a 'very real thing' despite the overhyped term 'leaky gut.'

DeLauer cites a Circulation meta-analysis of over 1 million people showing no significant association between unprocessed red meat and cardiovascular disease or diabetes. However, processed meat consumption significantly increased risks. The proposed mechanism is AGEs—compounds formed when reducing sugars react with proteins during processing, akin to caramelizing onions. AGEs accumulate in arteries, trap plasma proteins, reduce nitric oxide synthesis, and stiffen vessel walls, promoting plaque and inflammation. He also acknowledges a possible confounder: processed meat eaters may also consume more refined carbs, but the independent effect of processing remains strong.

DeLauer presents two rodent studies. The first found that sodium benzoate at 200, 400, and 700 mg/kg body weight increased TNF-α, IL-6, and IL-1β, while 70 mg/kg did not, indicating a dose-dependent inflammatory effect. The second study gave 200 mg/kg and observed impaired maze performance, suggesting neuroinflammation or anxiety. He notes that while these are animal studies, the combination of sodium benzoate with sugar in sodas creates a 'double whammy' of inflammatory triggers. He advises caution, especially with high consumption.

DeLauer explains that gut health plays a huge role in insulin resistance. A healthy microbiome produces short-chain fatty acids (SCFAs) like butyrate, which support glucose metabolism at the cellular level. Conversely, an imbalanced gut can lead to LPS leakage when the intestinal barrier is compromised, triggering inflammation. He personally takes Seed Daily Synbiotic and calls it the only probiotic he'd recommend, noting its ability to survive digestion and colonize the gut. He offers a 25% discount link in the description.

After detailing sugar's inflammatory effects, DeLauer suggests switching to erythritol, stevia, or monk fruit. He notes that in the soda study, diet soda did not increase uric acid, but he remains cautious about artificial sweeteners. He doesn't elaborate on mechanisms for these alternatives, simply positioning them as a way to 'lessen that impact' of sugar.

DeLauer discusses a study published in Circulation that pooled data from over 1 million people across 20 studies. The findings showed no significant link between unprocessed red meat and cardiovascular disease or type 2 diabetes. However, processed meat consumption was associated with a 42% higher risk of cardiovascular disease and a 19% increased risk of type 2 diabetes. He explains that the likely mechanism is the formation of advanced glycation end products (AGEs) during processing. These AGEs form when reducing sugars react with proteins, similar to caramelizing onions. They can accumulate in arteries, trap plasma proteins, reduce nitric oxide synthesis, and make vessel walls less flexible, promoting plaque formation and inflammation. He also notes a possible confounding factor: people who eat processed meats may also consume more refined carbs, but the data still points to a direct effect of processing. He advises choosing fresh, unadulterated lean cuts over processed options like bologna.

DeLauer cites a study in Food and Function where mice were divided into high-glucose, high-fructose, and control groups. Both fructose and sucrose groups showed hyperinsulinemia and increased adipokines (inflammatory cytokines from fat cells), fatty liver deposits, and necroinflammation—a progression from simple fatty liver to steatohepatitis. Fructose was slightly more potent, which he attributes to our evolutionary design: we are not meant to consume large amounts of fructose without the fiber matrix of whole fruit that slows absorption. He emphasizes that the real problem is refined sugars stripped of fiber, not whole fruits.

DeLauer presents two rodent studies. The first, in Drug and Chemical Toxicology, tested doses of 70, 200, 400, and 700 mg/kg body weight. Only the 70 mg/kg dose did not increase inflammation; higher doses raised TNF-α, IL-6, and IL-1β. The second, in Neuroscience, gave 200 mg/kg and found mice had difficulty completing a maze, suggesting increased anxiety or cognitive impairment. Researchers speculate this could be due to brain inflammation. He notes that while these are rodent models and causation isn't proven, the dose-dependent response is concerning, especially when sodium benzoate is consumed alongside sugar in soft drinks—a 'double whammy.'

DeLauer references a study in the journal Alcohol with 840 women and 490 men. In women, alcohol intake correlated with elevated uric acid, a precursor to CRP and IL-6. In men, it directly correlated with higher CRP. He also details the leaky gut mechanism: alcohol damages intestinal epithelial cells, loosening tight junctions. This allows lipopolysaccharides (LPS) from gut bacteria to enter the bloodstream, triggering an inflammatory cascade. He calls alcohol 'literally a poison' and emphasizes that both pathways converge on systemic inflammation, increasing cardiovascular risk.