Metabolic Health

Modern chronic diseases—from type 2 diabetes to cardiovascular decline—are symptoms of deeper, interconnected dysfunction. At the root is a vicious synergy between three forces: insulin resistance, chronic inflammation, and mitochondrial breakdown. This "Metabolic Trifecta" creates a feedback loop that drives fatigue, brain fog, and systemic breakdown.

Understanding and reversing this root system is essential for sustainable, full-spectrum health.

1. Insulin Resistance: The Gateway to Metabolic Collapse

Insulin resistance impairs the body’s ability to move glucose into cells, elevating both blood sugar and insulin levels. Over time, this leads to:

• Increased fat storage (especially visceral fat)

• Hormonal disruption and inflammation

• Reduced metabolic flexibility

Jayedi et al. (2022) found that carbohydrate restriction significantly improved insulin sensitivity, HbA1c, and triglyceride levels in individuals with type 2 diabetes—with greater effects seen at higher levels of carb reduction.

Early markers like a high triglyceride-to-HDL ratio (TG/HDL) can flag systemic insulin resistance well before overt disease appears (Chauhan et al., 2021).

2. Chronic Inflammation: The Hidden Accelerator

Visceral fat releases cytokines like TNF-α and IL-6, fueling low-grade inflammation—a condition now known as "metaflammation."

This inflammatory state:

• Worsens insulin resistance

• Damages blood vessels

• Disrupts hormone signaling

Hotamisligil (2006) was among the first to define inflammation as the core mechanism linking obesity and metabolic disease.

Aramburu et al. (2024) identified ultra-processed food (UPF) intake as a key trigger for metaflammation. Participants with the highest UPF consumption had elevated C-reactive protein (CRP) levels and significantly higher rates of metabolic syndrome.

3. Mitochondrial Dysfunction: The Energy Crisis Within

Mitochondria are the engines of the cell, generating ATP via oxidative phosphorylation. Under metabolic stress, they become damaged, leaky, and inefficient—leading to:

• Decreased cellular energy

• Elevated reactive oxygen species (ROS)

• Impaired insulin signaling

Zhu et al. (2022) showed that ketogenic diets enhance mitochondrial biogenesis and reduce oxidative stress biomarkers—restoring metabolic flexibility.

Shumazu et al. (2013) found that β-hydroxybutyrate (BHB) acts as an epigenetic signal, inhibiting histone deacetylases (HDACs) and reducing oxidative damage in key metabolic tissues.

4. The Vicious Cycle: How the Trifecta Feeds Itself

Each element of the trifecta worsens the others:

• Insulin resistance elevates visceral fat → triggers more inflammation

• Inflammation damages mitochondria → increases ROS and metabolic dysfunction

• Mitochondrial dysfunction impairs glucose metabolism → worsens insulin resistance

Mattson et al. (2017) describe this loop as a self-reinforcing metabolic spiral—one that underpins most chronic diseases.

5. Breaking the Cycle: A Systems-Based Approach

The only way out is through a multi-layered, root-focused strategy:

• Low-carb or ketogenic nutrition: Improves insulin sensitivity and mitochondrial health (Jayedi et al., 2022; Zhu et al., 2022)

• Intermittent fasting: Stimulates autophagy and mitochondrial repair (Mattson et al., 2017)

• Anti-inflammatory lifestyle: Minimizing UPFs and increasing polyphenol-rich whole foods reduces metaflammation (Aramburu et al., 2024)

Sustainable metabolic health isn’t about fixing one problem. It’s about treating the system that fuels them all.

Integration with the Axis + Alchemy Framework

• Enhances HRV and breathwork outcomes by reducing systemic inflammation and sympathetic overdrive

• Supports emotional coaching by improving blood sugar regulation and brain energy

• Anchors identity work in restored vitality, resilience, and cellular energy

• Builds deep metabolic resilience from the inside out

Client Insight

You’re not broken. You’re inflamed, insulin-resistant, and running on depleted mitochondria.

Healing isn’t about cutting calories—it’s about restoring communication between your cells, your hormones, and your energy systems.

Once you break the trifecta, vitality returns. And with it, the ability to build a new future.

References

Jayedi, A., et al. (2022). Dose-dependent effect of carbohydrate restriction on type 2 diabetes. Nutrition Reviews. https://doi.org/10.1093/nutrit/nuac029

Chauhan, A., et al. (2021). TG/HDL ratio as a marker of insulin resistance and cardiovascular risk. Journal of Lipid Research, 62, 100035. https://doi.org/10.1016/j.jlr.2021.100035

Hotamisligil, G. S. (2006). Inflammation and metabolic disorders. Nature, 444(7121), 860–867. https://doi.org/10.1038/nature05485

Aramburu, J., et al. (2024). Ultra-processed foods and metabolic outcomes. Nutrition & Metabolism, 21(1), 23. https://doi.org/10.1186/s12986-024-00894-5

Zhu, H., et al. (2022). Ketogenic diet and mitochondrial health. Frontiers in Nutrition, 9, 937211. https://doi.org/10.3389/fnut.2022.937211

Shumazu, T., et al. (2013). BHB inhibits HDACs and reduces oxidative stress. Science, 339(6116), 211–214. https://doi.org/10.1126/science.1227166

Mattson, M. P., et al. (2017). Fasting and mitochondrial resilience. Cell Metabolism, 26(4), 801–812. https://doi.org/10.1016/j.cmet.2017.08.004

One of the most overlooked drivers of metabolic dysfunction is not sugar—but oil. Specifically, the modern overconsumption of omega-6 fats has tipped a delicate evolutionary balance, pushing the body into a chronic inflammatory state.

This article explores the omega-6/omega-3 ratio, its impact on cellular signaling and insulin resistance, and how restoring fat quality is critical for calming inflammation and reviving metabolic resilience.

1. Omega-6 vs. Omega-3: Evolution Outpaced

For most of human history, diets maintained a roughly 1:1 to 4:1 balance between omega-6 and omega-3 fats—both essential, but with different roles.

Today’s Western diet often exceeds a ratio of 15:1 to 20:1 due to widespread use of:

• Seed oils (soybean, corn, sunflower, safflower)

• Ultra-processed snack foods

• Grain-fed meat and dairy

DiNicolantonio & O’Keefe (2018) report that this imbalance skews cellular signaling toward inflammation, increasing the risk of metabolic syndrome, cardiovascular disease, and mood disorders.

2. Mechanisms: How Omega-6 Fuels Inflammation

Omega-6 fats (particularly linoleic acid) are converted into arachidonic acid—a precursor to inflammatory eicosanoids such as prostaglandins and leukotrienes.

This cascade promotes:

• Insulin resistance via inflammatory signaling in adipose tissue

• Endothelial dysfunction and increased cardiovascular risk

• Suppression of mitochondrial function and energy metabolism

3. Omega-3: The Anti-Inflammatory Counterbalance

Omega-3 fatty acids (EPA and DHA) serve as raw materials for anti-inflammatory and pro-resolving molecules:

• Enhance insulin sensitivity by modulating membrane fluidity and signaling

• Lower triglycerides and improve HDL cholesterol levels

• Produce Specialized Pro-Resolving Mediators (SPMs) that actively resolve inflammation rather than just suppress it

In clinical studies, EPA/DHA supplementation has consistently improved markers of metabolic health—including HOMA-IR, triglyceride levels, and CRP.

4. The Omega Ratio and Metabolic Outcomes

Wu et al. (2011) found that fatty acids generated via de novo lipogenesis (DNL)—a process upregulated by excessive omega-6—were significantly associated with coronary heart disease in older adults.

DiNicolantonio & O’Keefe (2018) emphasized that reducing the omega-6/omega-3 ratio from 20:1 toward 4:1 led to reduced inflammatory markers and improved mitochondrial efficiency.

More recently, Bhardwaj et al. (2024) warned that the nutrient quality decline—including distorted fatty acid profiles—is contributing to a silent epidemic of metabolic dysfunction across generations.

5. Rebalancing the Modern Fat Profile

Key shifts to restore omega balance include:

• Prioritize cold-water fatty fish (salmon, sardines, mackerel) and grass-fed meats

• Reduce seed oils and foods fried in industrial vegetable oils

• Increase flax, chia, and walnuts for plant-based omega-3s

A real-food, nutrient-dense approach helps repair inflammatory tone and support cellular resilience.

Integration with the Axis + Alchemy Framework

• Reduces systemic inflammation, supporting HRV optimization and autonomic regulation

• Enhances metabolic and mitochondrial resilience by improving cell membrane function and fat oxidation

• Supports nervous system repair through improved neuroinflammatory balance

• Aligns with nutrition re-patterning as a gateway to long-term metabolic and emotional stability

Client Insight

You don’t have to fear fat. You just have to choose the right ones.

When your cells stop swimming in inflammatory oils and start thriving on clean, omega-rich fats, the fire quiets—and your energy returns.

Inflammation isn’t just a response. It’s a signal. And your plate is where it begins to shift.

References

DiNicolantonio, J. J., & O’Keefe, J. H. (2018). Importance of maintaining a low omega-6/omega-3 ratio for reducing inflammation. Open Heart, 5(2), e000946. https://doi.org/10.1136/openhrt-2018-000946

Wu, J. H. Y., et al. (2011). Fatty acids in the de novo lipogenesis pathway and risk of coronary heart disease: The Cardiovascular Health Study. Circulation, 123(20), 2491–2499. https://doi.org/10.1161/CIRCULATIONAHA.110.977935

Bhardwaj, R., et al. (2024). An alarming decline in the nutritional quality of foods: The biggest challenge for future generations’ health. Nutrients, 16(2), 341. https://doi.org/10.3390/nu16020341

Breaking the Cycle: How Lifestyle Stressors Disrupt Metabolic Health

Modern life doesn’t just burn people out mentally—it wears them down metabolically. Chronic stress, disrupted sleep, irregular circadian rhythms, and low movement levels form a web of lifestyle stressors that compound to impair hormonal signaling, blood sugar regulation, and inflammation control.

This article unpacks how each of these stressors sabotages metabolism—and how restoring rhythm, rest, and resilience can reset the system.

1. Stress and Cortisol Dysregulation

Cortisol is a survival hormone. In small doses, it’s adaptive. But chronic elevation leads to:

• Increased visceral fat storage

• Reduced insulin sensitivity

• Disrupted hunger and satiety hormones

Caplin et al. (2021) found that individuals with regular high-intensity exercise exhibited a blunted cortisol response to acute psychosocial stress. This suggests that movement can recondition the stress axis and protect against metabolic fallout.

2. Circadian Disruption and Evening Hunger

The circadian system regulates metabolism—and when it’s out of sync, so is the body.

Scheer et al. (2013) demonstrated that the circadian clock itself drives increased hunger and cravings in the evening, independent of food intake or physical activity. Eating late:

• Increases insulin resistance

• Impairs glucose tolerance

• Reinforces fat storage over oxidation

Chronically late eating trains the body to operate out of sync with natural metabolic rhythms.

3. Sleep Deprivation and Hormonal Chaos

Poor sleep drives hormonal shifts that increase food intake and reduce energy output:

• Elevated ghrelin (hunger hormone)

• Suppressed leptin (satiety hormone)

• Reduced insulin sensitivity

Sleep-deprived individuals consistently choose higher-calorie, higher-carbohydrate foods—especially in the evening—worsening blood sugar swings and energy crashes.

4. Sedentary Behavior and NEAT

While structured exercise is beneficial, daily movement outside of workouts—Non-Exercise Activity Thermogenesis (NEAT)—is a major factor in energy balance.

Levine (2007) highlighted that individuals with high NEAT levels burned up to 2,000 more calories per day compared to sedentary counterparts, independent of exercise routines.

Low NEAT levels:

• Decrease insulin sensitivity

• Impair lipid metabolism

• Contribute to weight gain and metabolic inflexibility

5. A Systems View: Metabolism Responds to Rhythm

These lifestyle stressors don’t act in isolation—they layer:

• Stress disrupts sleep

• Sleep disruption increases hunger

• Evening cravings collide with circadian misalignment

Addressing the root system requires rhythm restoration:

• Move often: Break up sedentary time with micro-movement

• Sleep early: Aim for consistent sleep-wake cycles

• Eat with light: Align meals with circadian rhythm

• Downshift stress: Use breathwork, nature, and boundaries to restore recovery mode

Integration with the Axis + Alchemy Framework

• Supports HRV and nervous system retraining by restoring parasympathetic balance

• Enhances metabolic healing by improving hormonal rhythms and insulin sensitivity

• Grounds behavioral coaching in nervous system and circadian science

• Builds long-term resilience by rewiring recovery patterns and energy systems

Client Insight

You can’t out-diet a life lived against your biology.

Metabolic health isn’t just about food. It’s about rhythm, rest, movement, and emotional recovery.

When your life starts to work with your body—not against it—healing stops being a battle. It becomes a homecoming.

References

Caplin, J., et al. (2021). Exercise intensity and cortisol response to psychosocial stress. Journal of Applied Physiology, 131(3), 955–962. https://doi.org/10.1152/japplphysiol.00245.2021

Scheer, F. A. J. L., et al. (2013). The internal circadian clock increases hunger and appetite in the evening independent of food intake and other behaviors. Obesity, 21(3), 421–423. https://doi.org/10.1002/oby.20351

Levine, J. A. (2007). Non-exercise activity thermogenesis (NEAT): Environment and biology. American Journal of Physiology-Endocrinology and Metabolism, 292(3), E675–E699. https://doi.org/10.1152/ajpendo.00562.2006

In an era shaped by processed food, chronic stress, and physical inactivity, many have lost a key evolutionary advantage: the ability to switch efficiently between fuel sources. This capacity—known as metabolic flexibility—is critical for blood sugar control, energy stability, disease prevention, and healthy aging.

This article explores how impaired flexibility sets the stage for chronic disease—and how restoring it can unlock long-term resilience.

1. What Is Metabolic Flexibility?

Metabolic flexibility is the body’s ability to switch between burning glucose and fatty acids depending on nutrient availability and energy demand. In a healthy state:

• You burn fat during fasting, low-intensity activity, or sleep

• You burn glucose after meals or during intense activity

However, in insulin resistance, this switching becomes impaired. The body stays locked in glucose dependence—even during fasting—leading to energy crashes, inflammation, and fat storage.

2. The Cost of Inflexibility

Metabolic inflexibility is an early signal of dysfunction. It leads to:

• Impaired fat oxidation

• Excessive glucose reliance

• Mitochondrial inefficiency and oxidative stress

Kelly et al. (2020) found that reduced metabolic flexibility was a strong predictor of insulin resistance and progression to type 2 diabetes—even in individuals with normal body weight. These findings suggest that metabolic inflexibility is a root cause, not just a symptom.

3. Rebuilding Flexibility with Nutrition

Low-carbohydrate and ketogenic diets reduce insulin levels and shift the body toward fat oxidation. Over time, this enhances:

• Mitochondrial biogenesis

• Ketone production (BHB, acetoacetate)

• Energy stability

In a landmark study, Volek et al. (2016) showed that keto-adapted endurance athletes burned up to 1.5g of fat per minute during exercise—nearly double the rate of carb-adapted peers—without compromising performance. This is a hallmark of superior metabolic flexibility.

4. Fasting: A Flexibility Amplifier

Fasting trains the body to switch fuel sources, especially from glucose to ketones. This metabolic switch:

• Increases fat oxidation

• Triggers autophagy and mitochondrial repair

• Reduces oxidative stress and insulin demand

Mattson et al. (2017) found that intermittent fasting improved metabolic flexibility, increased insulin sensitivity, and enhanced cellular resilience across multiple systems, including the brain and liver.

5. Metabolic Flexibility and Longevity

Long-term flexibility reduces metabolic wear and tear. It improves:

• Blood sugar variability

• Lipid profiles (lower triglycerides, improved HDL)

• Mitochondrial function

These benefits are associated with reduced risk of:

• Type 2 diabetes

• Cardiovascular disease

• Alzheimer’s and Parkinson’s disease

Metabolic flexibility is not just about energy—it’s about adaptability and survival.

Integration with the Axis + Alchemy™ Framework

• Enhances HRV recovery and glycemic stability, reducing reactive loops

• Anchors nutritional coaching in metabolic science, not calorie control

• Supports energy and cognition through steady ATP production

• Enables longevity-focused transformation by restoring the body’s natural adaptability

Client Insight

If you feel like your energy is unstable, your cravings unpredictable, or your performance inconsistent—it may not be your willpower. It may be your metabolic machinery.

Restoring flexibility means your body starts responding again—not just reacting. Energy steadies. Resilience returns.

You stop burning out, and start burning fuel—efficiently.

References

Volek, J. S., et al. (2016). Metabolic characteristics of keto-adapted ultra-endurance runners. Metabolism, 65(3), 100–110. https://doi.org/10.1016/j.metabol.2015.10.028

Mattson, M. P., et al. (2017). Impact of intermittent fasting on health and disease processes. Cell Metabolism, 26(6), 102–114. https://doi.org/10.1016/j.cmet.2017.10.006

Kelly, C. T., et al. (2020). Metabolic flexibility as a predictor of cardiometabolic health. The Journal of Physiology, 598(7), 1253–1265. https://doi.org/10.1113/JP278691

While average blood glucose and HbA1c are commonly used markers of metabolic health, they don’t tell the full story. One of the most damaging—but often overlooked—factors is blood sugar variability (BSV): the swings in glucose levels that occur throughout the day.

Even in people without diabetes, these fluctuations drive inflammation, oxidative stress, and long-term cardiometabolic risk.

1. What Is Blood Sugar Variability?

BSV refers to the amplitude and frequency of glucose spikes and dips:

• After meals

• In response to stress

• Due to circadian misalignment

Unlike chronic hyperglycemia, BSV focuses on the swings—especially post-meal spikes—which place significant stress on the body’s metabolic and vascular systems.

Lin et al. (2023) showed that women experience significantly greater glucose variability during the luteal phase of the menstrual cycle, linking hormonal fluctuations to impaired glucose regulation.

2. Why Glucose Swings Matter

Spikes in blood sugar—especially after high-glycemic meals—trigger:

• Oxidative stress via reactive oxygen species (ROS)

• Activation of NF-κB, a transcription factor that drives inflammatory cytokines

• Endothelial dysfunction, increasing arterial stiffness and cardiovascular risk

In fact, glucose variability has been shown to produce more oxidative stress than sustained high glucose levels.

Scheer et al. (2013) found that late-day eating led to larger glucose excursions and worsened insulin responses, independent of total food intake—emphasizing the role of circadian timing.

3. Hidden Triggers of Variability

Many people unknowingly experience high BSV from common daily habits:

• Late-night meals or irregular meal timing

• Sleep deprivation, which reduces glucose tolerance

• Ultra-processed foods, high in refined carbs and low in fiber

• Food combinations, such as pairing high-fat and high-carb foods

Gannon et al. (1993) found that mixed macronutrient meals (e.g., fat + refined carbs) produced exaggerated glucose and insulin responses compared to meals with fiber or protein first.

4. Managing Variability with Smart Strategies

Blood sugar variability can be reduced through:

• Meal sequencing: Eat fiber and protein before carbohydrates (Shukla et al., 2015)

• Circadian alignment: Prioritize earlier meals

• Whole-food swaps: Replace UPFs with fiber-rich plants and healthy fats

• Continuous glucose monitoring (CGM) to identify hidden triggers

Jospe et al. (2024) found that CGM use significantly improved dietary self-awareness and led to sustainable behavior change in real-world users—even those without diabetes.

Integration with the Axis + Alchemy™ Framework

• Improves HRV and nervous system regulation by stabilizing glycemic stress

• Anchors nutrition coaching in real-time biofeedback and personalized tracking

• Reduces inflammation and reactivity, supporting energy and mood regulation

• Enables resilience-based change by calming the metabolic-nervous system interface

Client Insight

You don’t need to have diabetes to be harmed by sugar swings.

Spikes and crashes wear down your body’s energy systems, mood stability, and hormonal balance. When you smooth your glucose curve, everything else gets easier—focus, energy, sleep, and resilience.

Small changes in food timing and composition can make a profound impact.

References

Lin, Y., et al. (2023). Blood glucose variance measured by continuous glucose monitors across the menstrual cycle. Journal of Clinical Endocrinology & Metabolism, 108(1), 23–32. https://doi.org/10.1210/clinem/dgac456

Scheer, F. A. J. L., et al. (2013). The circadian clock increases hunger and appetite in the evening independent of food intake. Obesity (Silver Spring), 21(3), 421–423. https://doi.org/10.1002/oby.20351

Gannon, M. C., et al. (1993). Effect of added fat on glucose and insulin responses in type 2 diabetes. Diabetes Care, 16(12), 1655–1660. https://doi.org/10.2337/diacare.16.12.1655

Jospe, M. R., et al. (2024). Leveraging continuous glucose monitoring as a catalyst for behaviour change. BMC Public Health, 24, 113. https://doi.org/10.1186/s12889-024-17535-0

Shukla, A. P., et al. (2015). Food order has a significant impact on postprandial glucose and insulin levels. Diabetes Care, 38(7), e98–e99. https://doi.org/10.2337/dc15-0429

nsulin resistance often hides in plain sight. Long before it becomes type 2 diabetes or cardiovascular disease, it quietly drives inflammation, metabolic dysfunction, and hormonal disruption. This "quiet epidemic" underlies a wide range of chronic conditions—and yet it remains poorly understood and vastly underdiagnosed.

This article explores the continuum of insulin resistance, how it disrupts metabolism system-wide, and why early recognition is essential for prevention and recovery.

1. The Insulin Resistance Continuum

Insulin resistance is not a switch—it’s a spectrum:

• Early stage: Slight elevations in fasting insulin, glucose, or HOMA-IR (homeostatic model assessment)

• Mid-stage: Elevated triglycerides, increased visceral fat, post-meal glucose spikes

• Late stage: Full-blown metabolic syndrome, type 2 diabetes, NAFLD (non-alcoholic fatty liver disease)

Chauhan et al. (2021) found that the triglyceride-to-HDL ratio (TG/HDL) is a reliable and simple marker of insulin resistance and correlates with cardiovascular risk even in non-diabetic populations.

2. How Insulin Resistance Fuels Disease

Chronically elevated insulin and glucose levels wreak metabolic havoc:

• Promote fat storage (especially visceral fat)

• Drive systemic inflammation via adipose tissue cytokines (e.g., TNF-α, IL-6)

• Disrupt endothelial function and raise blood pressure

• Alter lipid metabolism, increasing triglycerides and lowering HDL

In a 2-year RCT, Foster et al. (2010) found that participants on low-carb diets had greater reductions in fasting insulin, triglycerides, and body weight—along with significantly higher HDL cholesterol—compared to those on low-fat diets.

3. Women and Glucose Variability

Insulin resistance and glucose fluctuations often affect women differently.

Lin et al. (2023) showed that glucose variability increases during the luteal phase of the menstrual cycle. These fluctuations:

• Worsen insulin sensitivity

• May explain PMS-related cravings and fatigue

• Highlight the need for cycle-aware nutrition and stress regulation

4. Hidden Dangers: Beyond Diabetes

Insulin resistance is increasingly linked to diseases beyond blood sugar:

• Alzheimer’s disease ("type 3 diabetes") via insulin signaling disruption in the brain

• PCOS through insulin-driven androgen elevation

• Certain cancers (e.g., breast, colorectal) due to mitogenic insulin pathways

Kakehi et al. (2017) found that even modest elevations in blood glucose—below diabetic thresholds—were associated with significantly higher cancer mortality in large population cohorts.

5. Restoring Insulin Sensitivity: Where Change Begins

Insulin resistance is modifiable—even reversible—with lifestyle:

• Low-carb or ketogenic diets reduce insulin demand and improve glycemic control

• Intermittent fasting enhances insulin sensitivity and fat oxidation

• Movement and strength training increase GLUT-4 transporters and improve glucose uptake

Addressing insulin resistance early may be one of the most powerful interventions for preventing disease and restoring long-term metabolic health.

Integration with the Axis + Alchemy™ Framework

• Anchors nutrition and metabolic coaching in early-stage dysfunction, not late-stage symptoms

• Enhances HRV and blood sugar stability, supporting autonomic regulation

• Supports female-specific metabolic patterns, including cycle-aware coaching

• Reinforces longevity strategies by addressing the root of metabolic wear and tear

Client Insight

If your energy feels inconsistent, your cravings uncontrollable, or your bloodwork "normal but not optimal"—insulin resistance may be the missing piece.

This isn’t about sugar alone. It’s about restoring how your cells listen, respond, and heal.

When you bring insulin back into balance, your body begins to remember what health feels like.

References

Chauhan, A., et al. (2021). TG/HDL ratio as a marker for insulin resistance and atherosclerosis. Journal of Lipid Research, 62, 100035. https://doi.org/10.1016/j.jlr.2021.100035

Foster, G. D., et al. (2010). Weight and metabolic outcomes after 2 years on low-carb vs. low-fat diets. Annals of Internal Medicine, 153(3), 147–157. https://doi.org/10.7326/0003-4819-153-3-201008030-00005

Lin, Y., et al. (2023). Blood glucose variance measured by CGMs across the menstrual cycle. Journal of Clinical Endocrinology & Metabolism, 108(1), 23–32. https://doi.org/10.1210/clinem/dgac456

Kakehi, E., et al. (2017). Non-diabetic glucose levels and cancer mortality. Diabetology International, 8(4), 234–240. https://doi.org/10.1007/s13340-017-0316-7

Ultra-processed foods (UPFs) have infiltrated modern diets, now making up more than half of daily caloric intake in many industrialized nations. But their impact extends far beyond excess calories—they hijack satiety, drive inflammation, and erode metabolic health from the inside out.

This article breaks down how UPFs alter appetite, hormonal balance, and chronic disease risk—and why cutting them out may be one of the most powerful interventions for restoring metabolic function.

1. What Defines Ultra-Processed Foods?

UPFs are industrially formulated products made largely from isolated substances:

• Refined oils, sugars, starches, protein isolates

• Artificial flavors, preservatives, emulsifiers, colorings

Common examples:

• Sugary beverages

• Packaged snacks and pastries

• Instant noodles and ready-made meals

• Processed meats and meat substitutes

These foods are engineered for taste, shelf life, and consumption speed—not for nourishment. They are typically high in refined carbs, trans fats, sodium, and low in fiber, protein, and micronutrients.

2. Metabolic Impacts: Beyond the Calories

The damage caused by UPFs isn’t just about overeating—it’s about how they bypass natural satiety mechanisms and disrupt metabolic signals.

Hall et al. (2019) conducted a landmark randomized controlled trial in a metabolic ward. Participants consuming a UPF diet spontaneously ate ~500 extra calories per day and gained weight—despite having matched macronutrient and energy density to a whole-food control diet.

Hamano et al. (2024) found that UPFs reduce chewing time, speed up ingestion, and blunt satiety signaling—amplifying calorie intake without conscious awareness.

3. Inflammation, Insulin Resistance, and Hormonal Disruption

UPFs promote systemic inflammation through:

• Excess refined carbs and seed oils

• Low fiber content

• Additives that impair gut and immune function

Aramburu et al. (2024) reported that higher UPF intake was associated with elevated fasting glucose, triglycerides, hsCRP (a marker of inflammation), and insulin resistance—even after adjusting for BMI.

4. The Neurological Hijack: Reward, Addiction, and Overeating

UPFs are designed to light up the brain’s reward system:

• Hyper-palatable combinations (fat + sugar + salt)

• Additives that stimulate dopamine release

• Textures that require minimal chewing and bypass satiety cues

LaFata et al. (2024) reviewed evidence indicating that approximately 14% of adults exhibit symptoms consistent with ultra-processed food addiction—including loss of control, cravings, and continued use despite harm.

5. A Nutritional Pivot Point

Reducing UPF consumption is a keystone intervention:

• Restores hormonal balance (GLP-1, leptin, ghrelin)

• Improves insulin sensitivity and blood sugar regulation

• Reduces inflammation at the root of chronic disease

• Rebuilds satiety and intuitive eating through whole-food patterns

UPFs are not just food—they are a modern environmental toxin.

Integration with the Axis + Alchemy™ Framework

• Supports metabolic recalibration by removing inflammatory and dysregulating inputs

• Enhances HRV, energy stability, and emotional resilience by restoring glycemic control

• Aligns with behavioral coaching to support identity shifts and food re-patterning

• Reinforces long-term transformation by targeting a core disruptor of metabolic regulation

Client Insight

It’s not your fault if you feel out of control around certain foods—they were designed to override your biology.

But the solution isn’t shame. It’s strategy. When you stop feeding the system that’s hijacking your hunger, you regain the clarity and energy to build something better.

Remove the UPFs, and your real metabolism returns.

References

Hall, K. D., et al. (2019). Ultra-processed diets cause excess calorie intake and weight gain: An inpatient randomized controlled trial. Cell Metabolism, 30(1), 67–77.e3. https://doi.org/10.1016/j.cmet.2019.05.008

Hamano, M., et al. (2024). Reduced chewing and energy intake with UPFs: A behavioral mechanism of overconsumption. Nutrition Journal, 23(1), 42. https://doi.org/10.1186/s12937-024-00912-z

Aramburu, J., et al. (2024). Ultra-processed food consumption and cardiometabolic outcomes in adults: A cross-sectional analysis. Nutrition & Metabolism, 21(1), 12. https://doi.org/10.1186/s12986-024-00884-7

LaFata, E., et al. (2024). Ultra-processed food addiction: A research update. Current Obesity Reports, 13(2), 101–112. https://doi.org/10.1007/s13679-024-00523-x

For decades, obesity has been viewed through the lens of energy balance: calories in vs. calories out. But this model fails to explain why so many struggle with weight despite following caloric guidelines. A deeper look reveals that hormonal regulation—not just caloric intake—is central to fat storage, energy metabolism, and hunger.

The Carbohydrate-Insulin Model (CIM) offers a compelling framework that connects high-carbohydrate diets to hormonal shifts that drive obesity from within.

1. The Carbohydrate-Insulin Model: A Paradigm Shift

CIM posits that refined carbohydrates elevate insulin, which drives fat storage, reduces fat oxidation, and triggers a hunger-fatigue cycle. This model reframes obesity as a hormonal disorder of energy partitioning.

Ludwig et al. (2022) demonstrated that postprandial insulin responses were more predictive of future weight gain than caloric intake alone—suggesting that food quality, not just quantity, determines long-term weight outcomes.

Friedman et al. (2024) added to this paradigm by describing obesity as a "trapped fuel" disorder, where energy becomes sequestered in fat cells due to insulin-driven metabolic signaling.

2. Insulin: The Master Fat-Storage Hormone

Insulin plays a central role in energy partitioning:

• Promotes lipogenesis (fat creation)

• Inhibits lipolysis (fat breakdown)

• Encourages nutrient storage in adipose tissue

Chronically elevated insulin lowers metabolic rate by reducing sympathetic tone and nutrient availability.

Ebbeling et al. (2012) found that participants on a very low-carbohydrate diet expended ~300 more kcal/day compared to those on a low-fat diet during weight maintenance, reinforcing insulin’s influence on resting energy expenditure.

3. Metabolic Rate: Preserving Energy Output During Weight Loss

One major challenge with traditional weight loss is the body's compensatory reduction in resting energy expenditure (REE). However, CIM-aligned diets appear to protect against this adaptation.

In Ebbeling et al.’s study, the low-carb group maintained higher REE, while the low-fat group showed significant metabolic slowdown—even though both groups consumed the same total calories.

This supports the idea that macronutrient quality—not just quantity—determines metabolic output.

4. Appetite and Satiety: Hormonal Stability Over Willpower

Refined carbohydrates cause blood sugar spikes and crashes, which:

• Trigger hunger and irritability

• Increase ghrelin (hunger hormone)

• Suppress GLP-1 and leptin (satiety hormones)

Low-carb diets help stabilize these responses:

• Improve glycemic control

• Increase fullness and reduce cravings

Hall et al. (2019) found that participants eating ultra-processed diets consumed ~500 more kcal/day—driven not by hunger, but by disrupted satiety signaling and reward-based eating.

5. Is CIM the Whole Picture?

While critics argue that energy balance still matters, the CIM doesn’t deny this—it reframes what drives energy imbalance. Hormones affect both calorie intake and expenditure.

A hybrid model suggests:

• Hormones regulate appetite and fat storage

• Caloric excess still contributes, but is downstream of hormonal shifts

• Sustainable weight loss must address insulin and metabolic health

Integration with the Axis + Alchemy™ Framework

• Anchors nutritional coaching in hormonal regulation, not caloric punishment

• Enhances appetite and energy regulation through glycemic control

• Supports HRV and nervous system resilience by reducing glycemic stress

• Reframes weight challenges as biological, not moral, reducing shame and increasing agency

Client Insight

You’re not overeating because you lack willpower. Your body is following hormonal cues designed to protect you from starvation.

When you shift from fighting your biology to feeding it wisely, fat loss becomes sustainable, not punishing.

Obesity isn’t just about calories. It’s about communication—between food, hormones, and cells. And it can be healed.

References

Ludwig, D. S., et al. (2022). Competing paradigms of obesity pathogenesis: Energy balance vs. carbohydrate-insulin models. American Journal of Clinical Nutrition, 116(5), 1241–1254. https://doi.org/10.1093/ajcn/nqac147

Friedman, J. M., et al. (2024). Obesity as a disorder of fuel partitioning: A hormonal perspective. Obesity Reviews, 25(1), e13502. https://doi.org/10.1111/obr.13502

Ebbeling, C. B., et al. (2012). Effects of dietary composition on energy expenditure during weight-loss maintenance. JAMA, 307(24), 2627–2634. https://doi.org/10.1001/jama.2012.6607

Hall, K. D., et al. (2019). Ultra-processed diets cause excess calorie intake and weight gain: An inpatient randomized controlled trial. Cell Metabolism, 30(1), 67–77.e3. https://doi.org/10.1016/j.cmet.2019.05.008

Modern eating patterns—frequent meals, snacks, and late-night eating—have created a metabolic environment of near-constant insulin elevation. This chronic hyperinsulinemia is a silent driver of inflammation, fat storage, and metabolic breakdown.

Strategic fasting reintroduces what our biology evolved with: metabolic downtime. It restores insulin sensitivity, reduces inflammatory signaling, and activates cellular repair systems.

1. Hyperinsulinemia and Inflammation

Persistently elevated insulin levels:

• Promote visceral fat accumulation

• Suppress lipolysis (fat burning)

• Increase oxidative stress and cytokine production (e.g., IL-6, TNF-α)

Jayedi et al. (2022) found that carbohydrate restriction—which lowers insulin—significantly reduced inflammation markers (CRP, IL-6) and improved glycemic control in individuals with type 2 diabetes.

2. Fasting as a Hormonal Reset

Fasting introduces periods of low insulin, allowing for:

• Improved insulin sensitivity

• Activation of AMPK, a metabolic master switch

• Increased ketone production (e.g., BHB), which has anti-inflammatory effects

Mattson et al. (2017) demonstrated that intermittent fasting (IF) improved metabolic parameters, reduced oxidative stress, and enhanced cognitive resilience in both animal and human studies.

3. Autophagy: Cellular Clean-Up and Immune Balance

One of fasting’s most profound effects is the activation of autophagy:

• Removes damaged mitochondria, proteins, and organelles

• Enhances immune regulation

• Prevents buildup of inflammatory debris

Shao et al. (2016) reported that fasting-induced autophagy promoted plaque stability in atherosclerosis and reduced inflammatory cell death, highlighting its systemic anti-inflammatory potential.

4. Insulin and Inflammatory Pathways

Insulin isn’t just a metabolic hormone—it activates immune responses:

• Upregulates NF-κB and other inflammatory mediators

• Stimulates hepatic lipogenesis and fat accumulation

• Increases endothelial dysfunction and vascular inflammation

Fasting blunts these effects by reducing basal insulin levels, especially when combined with carbohydrate restriction.

5. A Metabolic Recalibration Strategy

Integrating fasting strategically can:

• Improve metabolic flexibility

• Reduce postprandial inflammation

• Enhance cellular repair and resilience

Options include:

• Time-restricted eating (e.g., 8–10 hour feeding windows)

• Intermittent fasting (e.g., 16:8, 5:2)

• Periodic 24-hour fasts under guidance

Integration with the Axis + Alchemy™ Framework

• Supports HRV and autonomic recovery by lowering inflammatory load

• Enhances insulin sensitivity and metabolic stability, amplifying dietary strategies

• Reinforces cellular and cognitive resilience through autophagy and ketone metabolism

• Anchors identity transformation by linking discipline to physiological empowerment

Client Insight

You don’t need to fight your metabolism—you need to give it a break.

Fasting isn’t deprivation. It’s restoration.

When you stop eating all the time, your body starts healing all the time. And in that space, real resilience is rebuilt.

References

Jayedi, A., et al. (2022). Dose-dependent effect of carbohydrate restriction for type 2 diabetes management. Clinical Nutrition, 41(3), 627–636. https://doi.org/10.1016/j.clnu.2021.11.011

Mattson, M. P., et al. (2017). Impact of intermittent fasting on health and disease processes. New England Journal of Medicine, 381(26), 2541–2551. https://doi.org/10.1056/NEJMra1905136

Shao, B., et al. (2016). The roles of macrophage autophagy in atherosclerosis. Acta Pharmacologica Sinica, 37(2), 150–156. https://doi.org/10.1038/aps.2015.146