Skool Member Question: When lower carbs are eaten, my cholesterol goes up. Even if I stay lower saturated fat, lower carb makes it shoot up. Everyone freaks out, and I’m never certain if I should also freak out. What becomes very clear, once you step back and look at cholesterol through a true systems biology lens, is that not all elevations are created equal; what we casually call “high cholesterol” is not a single condition, but a collection of distinct physiological states, each driven by a different mechanism, each requiring a different intervention, and each easily misinterpreted if we rely on a single marker like low-density lipoprotein cholesterol (LDL-C) and total cholesterol (TC). At the highest level, these states fall into four primary buckets: mobilization (cholesterol is being moved), clearance defects (cholesterol cannot be removed efficiently), overproduction (cholesterol particles are being produced in excess), and genetic risk amplification (cholesterol becomes more dangerous independent of its quantity); layered across all of this, in certain individuals, is a fifth modifier, Saturated Fatty Acid Hyper-Reactivity Disorder (SFAHD), where dietary saturated fat disproportionately amplifies lipid and inflammatory signaling. If you do not identify which of these you are dealing with, you are not treating physiology; you are reacting to numbers. The first category, and the one most relevant during active weight loss, is mobilization; this is where lipolysis is increased, often in the setting of carbohydrate reduction across a spectrum of dietary patterns (Mediterranean, Paleo, Atkins, Keto, Carnivore, whether <150g, <100g, <50g, or <20g), where the body shifts from reliance on incoming glucose to stored energy. As adipocytes release triglycerides, they also release cholesterol; the largest storage depot of cholesterol in the body is not the liver, but the fat cell itself. So when you begin “emptying the warehouse,” you are not just moving out fuel—you are moving out packaging material as well; blood cholesterol rises not because something is broken, but because something is finally moving. This is the “cleaning out the storage unit” analogy, where everything that was hidden is now in the parking lot, and it looks worse before it looks better. A more extreme expression of this exists in the Lean Mass Hyper-Responder (LMHR) phenotype, where lean, insulin-sensitive individuals exhibit very high LDL-C alongside low triglycerides and high HDL; here, the system is not congested—it is operating at high speed, with lipid particles constantly trafficking energy, unloading triglycerides, and returning cholesterol-enriched. This is not a traffic jam; it is a high-speed logistics network. Clinically, the question is not panic, but context; ApoB, LDL-P, and longitudinal markers (like CAC) determine whether this is benign adaptation or emerging risk.

Whether you are leaning back into nutrition changes or are just getting started with functional nutrition, where to start is the same...so let's briefly touch on the 3 worst culprits in the modern diet... Comments are questions are welcome!

When someone asks whether snacks can be incorporated during weight loss, what they are really asking—whether they realize it or not—is a far deeper question about control of physiology, not control of calories. In a properly constructed nutrition system, weight loss is not something you force through restriction (avoiding snacks); it is something that emerges as a byproduct of restored metabolic signaling. This is really the distinction between top-down control and bottom-up regulation, where intake is managed consciously in the prefrontal cortex (counting calories, restricting, constantly negotiating with yourself about the bag of chips on the kitchen counter) versus allowing intake to be governed subconsciously through hypothalamic integration of peripheral signals—gastric stretch, hormonal feedback like GLP-1, PYY, CCK, and real-time nutrient sensing—that come from eating a whole food diet. One is effortful and finite; the other is automatic and durable. So the real question is not, can I eat snacks? Rather, it is: who is driving the system? Is it the part of your brain that has to think, track, and override impulses all day, or the biology that is designed to regulate hunger, fullness, and energy balance without you having to think about it at all? A “snack,” in this context, is not defined by its size or even its food composition, but by its timing relative to a completed metabolic cycle. Every time we eat, we initiate a highly coordinated and predictable cascade that is designed to start, run, and finish. Food enters the stomach, gastric distension activates the vagus nerve (a mechanical stretch signal, which I often describe as mimicking—without metabolic surgery—the restrictive signaling of a Roux-en-Y pouch), sending information to the hindbrain and hypothalamus that food has arrived. This is soon followed by the release of key satiety hormones: CCK (slows gastric emptying, signals fullness), GLP-1 (enhances insulin response, delays emptying, promotes satiety), PYY (reduces appetite), and, over time, improvements in leptin sensitivity (long-term energy balance signaling).