The idea that “dietary fat definitively increases LDL” is already oversimplified. Not all LDL is the same, and context matters. Saturated fat may raise LDL-C in some individuals, but it also raises HDL and shifts LDL particle size toward larger, less atherogenic forms. More importantly, saturated fat has been shown to lower lipoprotein(a), which is a far stronger and more independent predictor of cardiovascular risk than LDL-C. The simplistic “saturated fat → higher LDL → higher risk” chain ignores the fact that cardiovascular risk is driven primarily by insulin resistance, chronic inflammation, and oxidized lipoproteins, not LDL-C alone. Furthermore, blaming VLDL without addressing the fact that excess carbohydrate, especially refined sugar, is the main driver of elevated VLDL, is misleading. LDL-C remains the weakest predictor of outcomes compared to insulin resistance, triglyceride-to-HDL ratio, and lipoprotein(a).
As for the Seven Countries Study, Gil tries to nitpicks a single page to prove Lustig “missed a sentence.” But Lustig’s broader critique still stands. Keys cherry-picked countries, excluded France and Germany, and produced ecological correlations, not causal evidence. That weak foundation still ended up shaping over 30 years of dietary policy demonizing fat while ignoring sugar. Lustig was highlighting how sugar got sidelined in the debate,
Gil on omega-6 fatty acids also ignores a crucial fact, but here he hides behind RCTs showing no short-term rise in CRP or IL-6. In reality, chronic high omega-6 intake shifts the eicosanoid balance toward pro-inflammatory signaling, especially in the absence of adequate omega-3s. Mechanistic data and population studies suggest that an excessively high omega-6 to omega-3 ratio worsens systemic inflammation and metabolic dysfunction. Lustig’s concern was directionally correct, excess seed oils in the modern food system displace more protective fats.
Lustig’s central thesis, that processed sugar and fiberless ultraprocessed food drive obesity, diabetes, and metabolic syndrome, has aged remarkably well. His emphasis on sugar-sweetened beverages, loss of dietary fiber, and the metabolic chaos of fructose without fiber has only been reinforced by newer data. Gil nitpicks details to look authoritative, but he avoids addressing that Lustig’s big picture was prescient. The explosion of NAFLD, diabetes, and obesity tracks precisely with the shifts Lustig described.
Dr. Gil Carvalho, in particular, has made a name for himself by defending outdated, reductionist models of nutrition. His tendency to cherry-pick data that fits a pro-seed oil, pro-pharmaceutical narrative while dismissing evidence on insulin resistance, omega-6 imbalance, and the benefits of saturated fat lowering Lp(a) does a disservice to the public. By framing complex metabolic issues as simplistic “LDL up, risk up,” he perpetuates the very misconceptions that keep people sick and reliant on medications rather than addressing root causes through diet and lifestyle.
The reality is that Lustig anticipated where nutrition science would eventually land. It is not simply about LDL-C, it is about metabolic dysfunction, ultraprocessed food, sugar without fiber, and the quality rather than the quantity of fat. Instead of debunking him, Gil ends up reinforcing the core of Lustig’s message.
If anything, history has validated Lustig while exposing the fragility of the simplistic fat and LDL narrative.
