Control Hunger and Blood Sugar Using Satiety Signals

Why am I hungry again, even after I ate?

If hunger were only about calories, you would not feel your appetite surge just because it is “your usual lunchtime.”

This framework treats hunger and satiety as a coordinated system. Hormones matter, but they do not act alone. The nervous system, the gut, and even the physical sensation of eating (chewing, texture, mouth feel) combine to determine whether you keep eating, stop eating, or start thinking about food long before you actually need energy.

A common misconception is that appetite is purely psychological or purely metabolic. The perspective here is that it is both, and it is measurable. Specific brain regions integrate signals from the bloodstream and the gut, and those signals are heavily shaped by modern food environments.

Another misconception is that you can “hack” hunger with one supplement or one trick. The discussion highlights something more practical, hunger tends to be predictable once you understand the levers, meal timing consistency, food processing, macronutrient order, and movement.

Pro Tip: If your hunger shows up like clockwork, treat it as a trainable signal. Keeping meal times consistent for a couple of weeks can make hunger more predictable, and shifting meal times will often feel uncomfortable at first because the hormonal signals lag behind your new schedule.

The brain’s control centers, hypothalamus and insular cortex

The brain is not passively receiving hunger signals. It is actively deciding what those signals mean.

One major hub is the hypothalamus, a deep brain structure involved in homeostasis. Within it, a region called the ventromedial hypothalamus has long been tied to feeding. What makes it famous is a paradox: disrupting this area can produce opposite outcomes. In some cases, damage leads to hyperphagia (excessive eating). In other cases, damage makes animals eat less or even find food aversive.

That paradox is the point. It suggests there is not one “eat” center and one “stop eating” center. There are multiple neuron populations intermingled, some pushing feeding, others pushing satiety.

Why mouth feel is not a trivial detail

Another key node is the insular cortex, a cortical area heavily involved in interoception (the sense of what is happening inside your body). The insular cortex receives input from the mouth, including touch receptors, not just taste receptors.

This is easy to overlook. Many people think appetite is about taste, sweet, salty, bitter. The framing here emphasizes tactile sensation, chewing, texture, and consistency, as a genuine control signal for enjoyment and stopping. In practical terms, foods that are easy to consume quickly can reduce the time and sensory feedback that normally helps satiety build.

Did you know? The brain region most associated with “how food feels in your mouth” is also deeply involved in internal body awareness, including signals from the gut and cardiovascular system. This is one reason appetite can shift with stress, sleep loss, or illness.

A surprising clue from a classic rat experiment

A particularly vivid experiment helps explain why appetite cannot be understood by brain circuitry alone.

Researchers used a procedure called parabiosis, surgically linking two rats so they shared a blood supply while keeping separate brains and mouths. When the ventromedial hypothalamus was lesioned in one rat, that rat became very obese. The other rat, sharing the blood factors, became very thin.

That result strongly implies that something circulating in the blood, in other words, endocrine or hormonal signals, was driving part of the feeding and weight change.

This is the pivot point of the video’s perspective: hunger is not only a “brain decision,” it is also a “blood and gut chemistry” story. And because meal timing and food type change what circulates in blood, appetite can become trainable and, to a degree, predictable.

Important: If you have diabetes, frequent hypoglycemia, a history of eating disorders, are pregnant, or take glucose lowering medications, changes in meal timing or exercise routines should be discussed with a clinician. What feels like a simple “hunger protocol” can meaningfully change blood sugar.

The hunger and satiety hormones to know, MSH, AgRP, ghrelin, CCK

The core hormones discussed function like accelerators and brakes.

Some of these signals originate in the brain, and others originate in the gut. The key is that they converge on brain circuits that influence motivation, cravings, and the felt sense of hunger.

MSH and AgRP, the brain’s internal brake and accelerator

Within a hypothalamic area called the arcuate nucleus, there are neuron populations with opposing roles.

The practical implication is not that you can consciously control these neurons, but that your meal timing and food choices influence the signals that push these neurons.

Ghrelin as a meal timing clock

Ghrelin is presented as especially important because it relates to when you get hungry, not only whether you get hungry.

Ghrelin is released from the gastrointestinal tract and increases the desire to eat. It also creates anticipatory signals, you start thinking about foods you typically eat at that time of day. A central idea is that ghrelin becomes pavlovian, it can align with habitual meal times. If you regularly eat breakfast at 8 a.m., ghrelin secretion can rise shortly before 8 a.m., nudging hunger even if blood glucose has not dropped dramatically.

What makes this unique is the claim that ghrelin is shaped by clocks in the body. The discussion notes a “clock in the liver” linked to a clock in the hypothalamus, helping align hunger rhythms to routine.

So when you suddenly skip a meal or shift meal timing, ghrelin can still surge at the old time. You feel hungry because the signal is there, not necessarily because you are in immediate danger of running out of fuel.

What the research shows: Ghrelin is widely recognized as an orexigenic (appetite stimulating) hormone, and it rises before meals and falls after eating in many contexts, although individual patterns vary. Reviews describe ghrelin’s role in meal initiation and reward-related eating behavior, including food cue responsiveness National Center for Biotechnology Information overviewTrusted Source.

CCK as a satiety signal tied to fats and amino acids

Cholecystokinin (CCK) is described as a potent hunger reducing signal released from the GI tract.

The key detail in this video’s viewpoint is what triggers CCK release: gut sensing of fatty acids, amino acids, and also sugar. The gut’s ability to detect these nutrients depends on specialized neurons and the integrity of the gut mucosal lining and microbiome.

Two specific nutrient categories are emphasized as CCK stimulators:

The discussion also emphasizes amino acids. The argument is that humans are not only “calorie foraging,” we are unconsciously fat foraging and amino acid foraging, eating until satiety signals reflect that enough key nutrients have arrived.

This is a different framing than “just eat less.” It suggests that meals lacking adequate protein or healthy fats may leave satiety signaling underpowered, which can make overeating more likely later.

Processed foods, emulsifiers, and why fullness signals fail

Ultra-processed foods do not only make it easier to overeat because they are tasty.

The unique mechanism highlighted here is emulsifiers.

Emulsifiers are common in processed foods because they help fats mix with water and improve texture and shelf life. The discussion compares them to detergents, substances that help dissolve and mix compounds that normally separate.

The claim is that emulsifiers can disrupt the mucosal lining of the gut. In this framing, the damage is not just “inflammation” in the abstract. It is structural and functional: neurons that innervate the gut may retract deeper, reducing the gut’s ability to sense what is in the food. If the gut cannot accurately detect fatty acids and amino acids, then satiety signals like CCK may not deploy properly.

That leads to a specific pattern many people recognize: you can eat a lot of highly processed food and still not feel satisfied.

At the same time, the discussion points to a parallel sugar sensing pathway in the gut that sends subconscious signals to the brain via the vagus nerve, triggering dopamine release and craving for more of that food. The combination is powerful: weaker satiety brakes and stronger craving accelerators.

This is one reason the argument against ultra-processed foods is not moralistic. It is mechanistic. The food is engineered in a way that can distort the normal gut-brain accounting of what you have eaten.

»MORE: If you want a practical label-reading checklist, create a simple “processed food audit” for your pantry. List foods that contain emulsifiers (often words like polysorbate, carboxymethylcellulose, lecithins, mono- and diglycerides). Then experiment with swapping just one daily item for a minimally processed alternative for 2 weeks.

Research outside the video supports concern that some emulsifiers may negatively affect gut barrier function and microbiota composition in ways that could influence metabolic health, although exact effects can depend on the specific additive and dose. Reviews summarize these mechanisms and uncertainties in human translation Frontiers in Nutrition reviewTrusted Source.

Blood sugar basics, insulin, glucagon, and why spikes matter

Appetite control and blood sugar control overlap.

They overlap because blood glucose shifts influence hunger hormones, and because insulin and related signals influence how quickly you feel satisfied and how soon you feel hungry again.

Insulin, the glucose manager

Insulin helps shuttle glucose into tissues and keeps blood glucose within a healthy range. The discussion gives a typical euglycemic fasting range as about 70 to 100 mg/dL (commonly reported in mg/dL in clinical settings, sometimes written differently in transcripts).

Why does the body care so much about keeping glucose in range? The discussion emphasizes that chronically high glucose can damage neurons and contribute to complications like peripheral neuropathy and diabetic retinopathy.

For context, major medical organizations describe diabetes as a condition of chronic hyperglycemia due to defects in insulin secretion, insulin action, or both, and they outline complications affecting nerves, kidneys, and eyes American Diabetes Association Standards of CareTrusted Source.

Type 1 vs type 2 diabetes, briefly

The video distinguishes:

The discussion notes that type 2 diabetes is often, though not always, associated with overweight or obesity, and that weight management can be part of management for many people.

Glucagon, the counterbalance

When you are hungry, glucagon helps mobilize stored energy, pulling from liver and muscle glycogen. When those stores are depleted, the body can increasingly rely on fat stores.

This insulin-glucagon push-pull is one reason meal composition and timing can change how you feel between meals. Steep rises and falls in glucose can drive stronger hunger signals in some people, while steadier glucose curves can feel calmer.

Practical tools to blunt glucose spikes and feel full sooner

The discussion highlights a set of behavioral “entry points” that do not require extreme diets.

These are not presented as cures. They are presented as ways to shape the slope of your glucose curve and the strength of satiety signaling.

Food order matters more than most people realize

A key practical insight is that the order you eat macronutrients can change how quickly glucose rises.

If you eat a mixed meal containing a carbohydrate (like rice), a protein (like salmon), and a fibrous vegetable (like asparagus or cabbage), glucose will rise. But if you begin with the fibrous component, the rise in glucose may be blunted and spread out.

The framing is simple: fiber first can slow the glucose climb, which can help you reach satiety earlier in the meal.

This aligns with research on “carbohydrate last” meal patterns. Controlled studies have found that consuming protein and vegetables before carbohydrates can reduce post-meal glucose excursions in people with type 2 diabetes BMJ Open Diabetes Research and CareTrusted Source.

A simple, non-neurotic meal sequence

You do not need to eat each component in isolation. The idea is to bias the first 5 to 10 minutes of the meal.

A short closing thought matters here: the goal is not perfection. The goal is to shape the curve most days.

Pro Tip: If you love dessert, try moving it to the end of a meal that started with fiber and included protein. Many people find the same dessert feels less “activating,” and they want less of it.

Why “stable blood sugar” feels like emotional stability

The discussion describes two broad patterns:

Some people have relatively stable blood sugar and can go long periods without eating. Others feel shaky, jittery, sweaty, or overly keyed up when glucose swings.

That experience is not just in your head. Rapid glucose changes can activate stress-like sensations in the body, and in people taking glucose-lowering medications, hypoglycemia can be dangerous.

If you suspect significant glucose variability, consider discussing monitoring options with a clinician. Continuous glucose monitors can be medically indicated for diabetes and sometimes used in research or wellness settings, but interpretation still benefits from medical context.

Exercise as a glucose and appetite regulator

Movement is not only about burning calories.

In this framework, movement changes where glucose goes and how your tissues respond to insulin.

Two time windows are emphasized:

This aligns with clinical guidance that post-meal physical activity can help reduce postprandial glucose, particularly in people with insulin resistance or type 2 diabetes American Diabetes Association physical activity guidanceTrusted Source.

Zone 2 cardio vs high-intensity work, different benefits

The discussion draws a useful distinction.

Zone 2 cardio (steady state work where nasal breathing is possible and conversation is still feasible) done for 30 to 60 minutes, 3 to 4 times per week is described as supporting blood sugar stability and insulin sensitivity. In plain language, it can make glucose management more resilient, so higher-sugar meals produce less dramatic swings.

By contrast, high-intensity interval training (HIIT) and resistance training are described as particularly good at driving glucose back into glycogen stores in muscle and liver. These training styles also can increase basal metabolic rate for some period after training.

A practical way to combine these ideas:

Expert Q&A

Q: If I walk after meals, does it replace exercise?

A: Post-meal walking is best viewed as a glucose management tool, not a complete fitness plan. It can reduce the size of post-meal glucose spikes for many people, but it does not fully replace the cardiovascular and strength adaptations you get from dedicated training.

If you are new to exercise, post-meal walks are a gentle entry point. If you already train, they can complement your program without adding much recovery cost.

Andrew Huberman, PhD (as presented in the Huberman Lab Essentials discussion)

Medications and diets mentioned, metformin and ketogenic diets

This section is not about self-prescribing. It is about understanding what was mentioned and what questions it raises.

Metformin

Metformin is described as a prescription drug developed for diabetes that can lower blood glucose and increase insulin sensitivity. The discussion notes that it acts strongly on liver metabolism and involves mitochondrial mechanisms, including the AMPK pathway.

Metformin is widely used, and professional guidelines discuss its role in type 2 diabetes management, often as first-line pharmacotherapy alongside lifestyle interventions, depending on the individual American Diabetes Association Standards of CareTrusted Source.

If you are not diabetic but are considering metformin for longevity or weight, that is a clinician conversation. Benefits, side effects (including gastrointestinal effects and rare lactic acidosis risk in specific settings), and contraindications depend on kidney function and other factors.

Ketogenic diets and glucose

The ketogenic diet is described as having strong support for lowering blood glucose, which is expected given the low carbohydrate intake.

The discussion references “22 studies” showing notable decreases in blood glucose, and it flags an additional nuance: long periods in ketosis may alter thyroid hormone levels, and returning to higher carbohydrate intake afterward may feel different in terms of carbohydrate handling.

Research reviews generally support that very low carbohydrate diets can reduce HbA1c and body weight in many people with type 2 diabetes, at least in the short to medium term, though adherence, lipid changes, medication adjustments, and long-term outcomes vary Cochrane review on low-carbohydrate dietsTrusted Source.

Important: If you have diabetes and are considering a ketogenic or very low carbohydrate diet, do not do it without medical supervision. Medication doses, especially insulin and sulfonylureas, often need adjustment to reduce hypoglycemia risk.

Key Takeaways