Transcripts & Slides
Lesson 1 Takeaways
- Insulin and glucagon work together like a seesaw – when one is up, the other is down.
- Glucagon has more direct control over glucose production than insulin. Insulin modulates glucagon production.
- Hyperglycemia is due to glucagon releasing excess glucose production from the liver.
- Exercise increases insulin sensitivity and glucose uptake into cells via contraction-stimulated GLUT4 transport.
- A low carb diet can help create a healing environment and improve insulin sensitivity.
- Infections and inflammation hinder mitochondrial function and glucose utilization.
- GLP-1 stimulation (via exercise, bitters, supplements) increases insulin secretion and lowers glucagon.
- GABA taken with meals suppresses glucagon production.
- Bile optimization helps regulate glucose levels.
- Key markers: glucose, A1C, Glycomark, C-peptide. Patterns indicate issues like insufficient insulin or excess glucagon.
- Movement and mitochondrial support are key interventions based on glucose patterns.
- Don’t just treat symptoms – understand what’s driving glucose/insulin issues.
- Use glucometer to track glucose response to meals and determine insulin sensitivity.
- The goal is to bring balance and help the body regulate itself, not just lower glucose.
- High glucometer readings show the body’s stress response, not “bad” food choices.
Lesson 2 Takeaways
- Glucometer readings show the body’s real-time glucose response to diet, sleep, stress, infection, etc.
- Fasting glucose reflects overnight hormone response; post-meal response shows insulin sensitivity.
- Glucose should rise 30 points after eating then return to baseline in 2 hours.
- Tracking glucose response without timing or food details has limited benefits.
- The goal is to understand client’s unique patterns, not follow rigid protocols.
Lesson 3 Takeaways
- Viewing stress as just an adrenal issue prevents lifestyle modifications for root causes.
- The brain graph shows modifiable HPA stress stimuli like blood sugar, inflammation, etc.
- Sleep, relationships, infections, inflammation drive HPA axis – not adrenal gland weakness.
- Client symptoms may improve before labs change – lifestyle changes drive lab improvements.
- Cortisol tests only show a snapshot – symptoms give clinical context.
- Adrenal gland supplements don’t address why cortisol is dysregulated.
Lesson 4 Takeaways
- The HPA axis controls cortisol release, not just the adrenal glands.
- Hyperfocus on “adrenal fatigue” is misleading – the issue is in the brain.
- Stress begins in the hypothalamus, not the adrenals. The adrenals just respond.
- Hans Selye’s “General Adaptation Syndrome” model was flawed and drove adrenal fatigue belief.
- The HPA axis anticipates metabolic needs and directs resources accordingly via cortisol.
- Thomas Guilliams gave a new scientific model of HPA function in 2014.
- Clinicians should focus on modulating client stressors, not just giving adrenal support.
- Improving diet, lifestyle, environment impacts the brain signals that direct cortisol release.
- The HPA axis maintains circadian cortisol rhythms to direct gene expression and metabolism.
- Stress disrupts the ability of the HPA axis to maintain a healthy cortisol rhythm.
- Symptom relief from adrenal supplements doesn’t equal improved HPA axis function.
- Unless stress stimuli change, cortisol levels won’t change long-term.
- Improving diet, lifestyle, and environment relieves root cause stressors on the HPA axis over time.
- The HPA axis communicates the body’s stresses – we must listen and modify stress stimuli.
[progressally_complete_button text="MODULE COMPLETED" objective_id="all"]