The Metabolic Classroom with Dr. Ben Bikman
Episode: Ketogenesis & Stress: Can Stress Hormones Actually Be Good For You?
Date: October 15, 2025
Host: Dr. Ben Bikman (Insulin IQ)
Episode Overview
In this episode, Dr. Ben Bikman explores the intriguing relationship between stress and the metabolic process of ketogenesis. He challenges the common perception that stress hormones are inherently harmful, positing instead that they play an essential adaptive role in energy metabolism—especially in conditions like fasting or a low-carbohydrate diet. The episode provides a mini-lecture that blends physiology, biochemistry, and practical insights about how our bodies respond to both metabolic and non-metabolic stress, with a particular focus on ketone production.
Key Discussion Points & Insights
1. Understanding Stress from a Biological Perspective
[03:00 - 05:30]
- Stress, in the body, is a coordinated response to threats—physical, emotional, or metabolic (like fasting).
- Contrary to its bad reputation, stress is crucial for survival, mobilizing the body’s energy resources.
- This response is orchestrated via two main systems:
- Sympathetic Nervous System (SNS): Acts as the body’s “rapid response team.”
- Hypothalamic-Pituitary-Adrenal (HPA) Axis: Provides a slightly slower, sustained adaptation to stress.
“We often think of stress as something that harms us… But stress also initiates some incredible adaptations in the body, particularly when it comes to how we produce and use energy.”
— Dr. Ben Bikman [02:10]
2. The Physiology of Stress: Hormonal Redundancy
[05:30 - 11:30]
- Sympathetic Nervous System:
- Within seconds, the brain signals the adrenal medulla to release epinephrine (adrenaline) and some norepinephrine.
- These catecholamines raise heart rate, BP, dilate pupils, and—importantly—mobilize fat for energy.
- HPA Axis:
- Hypothalamus releases CRH → Pituitary releases ACTH → Adrenal cortex releases cortisol.
- Cortisol: Not just a stress hormone, but better termed an “adaptation hormone.” Raises blood sugar, promotes fat breakdown, and makes cells less sensitive to insulin.
- Other hormones upregulated during stress:
- Glucagon: Raises blood glucose.
- Growth hormone: Promotes fat breakdown, impairs insulin effects in certain cells.
- Even prolactin and antidiuretic hormone (ADH) rise, but play smaller roles in metabolism.
“Perhaps calling these guys stress hormones, while not wrong, perhaps gives rise to some incorrect thinking.”
— Dr. Ben Bikman [11:00]
3. Acute vs. Chronic Stress
[12:00 - 14:40]
- Acute stress (short-lived): Mobilizes energy quickly for immediate use (e.g., fight-or-flight, exercise).
- Chronic stress (persistent): Prolonged hormone exposure can be harmful—promoting insulin resistance, muscle breakdown, and metabolic dysfunction.
4. The Link Between Stress Hormones and Ketogenesis
[14:40 - 23:50]
- The same hormones upregulated in response to external stress (e.g., epinephrine, cortisol) are also elevated during fasting or low-carb eating.
- The body interprets fasting or carbohydrate scarcity as metabolic stress, leading to similar hormonal adaptations.
- Stress hormones support the shift from glucose-based to fat-based fuel (i.e., transition to ketone production).
"Rather than thinking of them strictly as stress hormones, we might more accurately think of them as metabolic adaptation hormones—signals that help the body adapt, switch fuel sources, and just maintain balance in the face of changing energy availability."
— Dr. Ben Bikman [16:20]
5. The Biochemistry of Ketogenesis
[18:00 - 23:50]
- Fat Mobilization: Stress hormones signal fat cells to break down triglycerides into free fatty acids and glycerol.
- Liver Processing:
- Free fatty acids enter the liver, undergo beta-oxidation → lots of acetyl-CoA.
- Acetyl-CoA usually enters the citrate cycle, but in low-carb/fasted states, oxaloacetate is diverted for gluconeogenesis (glucose creation).
- When citrate cycle is bottlenecked, acetyl-CoA is shunted into ketogenesis—production of ketone bodies.
- Ketones are an efficient, preferred fuel for the brain and muscles when carbs are scarce.
“Ketogenesis is the body's elegant solution to a shortage of carbohydrates.”
— Dr. Ben Bikman [18:10]
6. How Each Stress-Related Hormone Drives Ketogenesis
[24:00 - 32:00]
- Epinephrine:
- Rapidly activates hormone-sensitive lipase in fat cells, increasing free fatty acids by >50% and quickly doubling ketone production.
- Promotes glucagon release, inhibits insulin, further stimulating the liver’s ketogenic machinery.
- Norepinephrine:
- Direct nerve-to-fat cell signaling (not just hormonal), amplifies fat breakdown locally.
- Cortisol:
- Doesn’t initiate but sustains ketogenesis—maintains gluconeogenesis, keeps oxaloacetate scarce and acetyl-CoA available for ketogenesis.
- Selectively burns peripheral fat.
- Growth Hormone:
- Increases during fasting/stress, makes fat cells insulin-resistant, boosting fat mobilization.
- Glucagon:
- Increases ketogenesis by upregulating necessary enzymes.
- ADH (Antidiuretic Hormone):
- Modestly enhances fat breakdown.
"Many of these so-called stress hormones are maybe…mislabeled and we ought to call them metabolic adaptation hormones."
— Dr. Ben Bikman [31:10]
7. The Sympathetic Nervous System’s Direct Role
[32:00 - 34:10]
- Rapid, direct stimulation of fat and liver tissues—nerves release norepinephrine before hormone levels even change.
- Enables almost immediate metabolic adaptation, preceding even the hormonal cascade.
8. Adaptation Versus Dysfunction: Context is Key
[34:10 - 38:00]
- Stress hormones are critical for adaptation—facilitating fuel switching and fat loss when energy is scarce.
- Chronically elevated stress hormones (due to poor sleep, anxiety, processed foods, persistent psychological stress) can disrupt this balance, leading to negative metabolic outcomes.
- The hormones themselves are not “bad”—it's the context and chronicity of their activation that matter.
“These hormones often get painted in a negative light, but the truth is they are critical metabolic tools, especially in the context of fasting and carbohydrate restriction, even exercise…Context matters.”
— Dr. Ben Bikman [35:50]
Notable Quotes & Memorable Moments
-
On the purpose of metabolic stress:
“What we often interpret as a stress response is simply in reality the body executing a pretty brilliant metabolic pivot.”
— Dr. Ben Bikman [21:50] -
Reframing stress hormones:
“Perhaps we should stop thinking of these as mere stress hormones and instead recognize them as adaptive metabolic signals…that help us become metabolically resilient.”
— Dr. Ben Bikman [38:00]
Key Takeaways
- Stress hormones (epinephrine, norepinephrine, cortisol, glucagon, growth hormone, ADH) play a vital role in adaptive metabolism, not just ‘stress.’
- Ketogenesis is a highly coordinated metabolic response to energy scarcity, orchestrated by hormonal and nervous signals.
- Both acute stress (like fasting or exercise) and metabolic stress (like low-carb diets) trigger these pathways to maintain homeostasis.
- Chronic over-activation of stress pathways is harmful, but intermittent or targeted activation builds metabolic resilience.
- Language matters—calling these “adaptation hormones” instead of solely “stress hormones” shifts how we understand their role.
Important Timestamps
| Segment | Topic | Timestamp | |--------------|---------------------------------------------------------------------------------------------------------------------------------------------|------------| | Opening | Intro to topic, overview of stress and energy metabolism | 02:10 | | Stress Setup | Physiology and two main stress response systems: SNS & HPA axis | 03:00–11:30| | Hormones | Redefining stress hormones, including glucagon and growth hormone | 11:30–14:40| | Ketogenesis | Biochemistry behind fat breakdown and ketone creation | 18:00–23:50| | Hormonal Drive| How each hormone accelerates ketogenesis | 24:00–31:10| | Neural Angle | Direct nerve influence on fat and liver | 32:00–34:10| | Conclusion | Recap on adaptive vs. chronic stress, metabolic resilience | 35:50–38:00|
Closing Note
Dr. Bikman encourages listeners to look at stress responses as adaptive tools for metabolic flexibility and health, rather than something to be universally avoided. By intentionally and periodically activating these adaptive metabolic signals—through fasting, carb restriction, or exercise—we can enhance our metabolic health and resilience.
For more knowledge and better health, stay tuned to The Metabolic Classroom.
