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- The Hidden Blood Sugar Link Behind Fibromyalgia, ME & EDS
The Hidden Blood Sugar Link Behind Fibromyalgia, ME & EDS
New evidence shows insulin spikes can worsen pain, fatigue, and brain fog — here’s how to stabilise your energy naturally
Hi Friend
Today I want to share something that many people with chronic illness seldom talk about — insulin spikes / insulin resistance — and how fluctuations in blood sugar and insulin can worsen symptoms in fibromyalgia, ME/CFS, and Ehlers-Danlos / hypermobility. Understanding this link gives us another lever to pull toward stabilization and reduction of symptom burden.
Let's dive into the science — and practical tips you can begin applying. PS if you havn’t already you can join the waitlist of my online platform which will really help your diet, we will have a weekly live chef and nutrition modules from university professors included. Waitlist HERE.
🧬 What is an “insulin spike” / insulin resistance?
When we eat carbohydrates, blood glucose rises. The pancreas responds by releasing insulin, a hormone whose job is to help cells (muscle, fat, liver) take up glucose from the bloodstream.
If cells are sensitive to insulin, glucose is readily taken up and levels normalize.
But with repeated spikes, chronic stress, inflammation, or metabolic dysfunction, cells can become less responsive to insulin. This is called insulin resistance (IR).
The pancreas compensates by producing more insulin (hyperinsulinemia) to push glucose into cells. Over time, this system becomes strained, and blood sugar control breaks down further.
Insulin isn’t just a “blood sugar hormone.” It also influences:
Inflammatory pathways
Growth factor signalling
Vascular tone and microcirculation
Neuronal metabolism
So dysregulation here can ripple into many systems.
🔍 What does the research show — links to chronic pain & fatigue
Here’s what current studies suggest about insulin dysregulation and its relevance to fibromyalgia, ME/CFS, and connective tissue disorders:
Fibromyalgia & insulin resistance
A 2025 case-control study in non-diabetic women with fibromyalgia found significantly higher HOMA-IR scores (a proxy for insulin resistance) compared to matched controls.
In that same study, patients with a particular COMT gene variant (A/A) had higher pain sensitivity and more severe fibromyalgia symptoms, and this correlated with greater IR.
Earlier observational work (e.g. the Pappolla group) showed that HbA1c — often used to monitor average blood sugar — was modestly higher in fibromyalgia patients versus controls, even when still in the “normal” range by current standards.
The hypothesis is that IR can impair cerebral microvascular perfusion (reduced blood flow in small vessels in the brain), contributing to central sensitization of pain, and worsening fatigue / brain fog.
While causality is not yet proven, the association is strong enough that researchers are calling for controlled trials of insulin-sensitising drugs (e.g. metformin) or lifestyle interventions in fibromyalgia.
Metabolic dysregulation in ME/CFS & overlap with metabolic syndrome
People with ME/CFS, fibromyalgia, and Long COVID show increased prevalence of metabolic syndrome features (abdominal fat, insulin resistance, dyslipidaemia, hypertension) compared to matched controls.
Because many with ME/CFS or fibro are relatively sedentary (due to post-exertional malaise, pain, fatigue), their metabolic flexibility (ability to switch between fat and glucose metabolism) is often impaired, making them more vulnerable to insulin dysregulation.
Hyperinsulinemia (excess insulin) is sometimes called the “foundation” upon which many chronic disorders build (cardiovascular disease, non-alcoholic fatty liver, inflammation). Insulin dysregulation also impairs AMPK signaling (a key intracellular energy sensor) and mitochondrial function, both of which are already thought to be compromised in ME/CFS.
Ehlers-Danlos / connective tissue + metabolic cross-talk
While direct research connecting insulin resistance to Ehlers-Danlos is limited, there are plausible mechanistic bridges:
People with EDS / hypermobility often deal with pain, micro-injuries, inflammation, and oxidative stress. These stresses can promote metabolic dysfunction and insulin resistance via chronic inflammatory pathways.
Dysregulated microcirculation is common in EDS (capillary fragility, vascular features). Impaired glucose/insulin signalling in the microvasculature could further degrade perfusion and healing.
Because hypermobile individuals tend to have less mechanical load (i.e. avoid heavy exercise to avoid joint injury), they may inadvertently reduce insulin sensitivity over time unless counteracted.
In short: insulin dysregulation may amplify all of the biologic stressors already present in fibro, ME, and hypermobility states.
⚠️ How insulin spikes may worsen symptoms in YOU
Here’s how unstable blood sugar / insulin surges might worsen the specific symptoms your audience already faces:
Symptom | Possible Mechanism via Insulin / Glucose Instability |
---|---|
Worsening pain / central sensitisation | IR → microvascular dysfunction (brain, spinal cord) → impaired nutrient & oxygen delivery → more sensitization |
Fatigue / post-exertional malaise | Impaired glucose uptake in muscle → poor ATP generation → metabolic “crash” after small effort |
Brain fog / cognitive issues | Dysglycemia + reduced cerebral perfusion → neuronal energy deficits, oxidative stress |
Inflammation / immune activation | Insulin is a growth/mitogenic factor; hyperinsulinemia can amplify pro-inflammatory signalling |
Poor healing / micro-injury repair | Insulin and glucose are important for wound healing; instability impairs collagen turnover and repair |
Mood imbalances / dysautonomia | Fluctuations in blood sugar influence cortisol and sympathetic responses, exacerbating autonomic dysregulation |
These aren’t hypothetical — they align well with the overlapping biology patients with fibro, ME/CFS, and EDS often report.
🛠 Practical Strategies: What You Can Do (Even Now)
Below are evidence-informed, practical steps you (or your readers) can try to stabilise insulin and buffer the harmful ripple effects. Always coordinate with your physician before making major changes, especially if you take medications.
Lower glycemic load & refine carbohydrate quality
Favour slow-digesting carbs (e.g. lentils, whole grains, vegetables) rather than refined sugars.
Pair carbs with protein + healthy fats or fiber to slow absorption.
Use small, frequent meals or “protein-first” strategy
Especially in those with blood sugar instability, starting a meal with protein/fat can blunt the insulin surge.
Avoid large glucose “spikes” by moderating portion size.
Time nutrient intake around tolerable movement
If you can tolerate gentle activity (e.g. walking, stretching), try consuming some carbs before or after that window to improve uptake.
But avoid overexertion — only use this if your energy envelope allows.
Strength or resistance work, within tolerance
Resistance training (even very gentle) tends to improve insulin sensitivity in muscle.
For hypermobile folks, low-impact resistance (e.g. resistance bands, aquatic therapy) may help.
Manage stress, sleep, circadian rhythm
Chronic stress (elevated cortisol/adrenal axis) antagonizes insulin sensitivity.
Prioritise sleep hygiene, consistent sleep-wake cycles, and techniques to support vagal tone (like deep breathing).
Nutrient & supplement support (under medical supervision)
Magnesium, chromium, alpha-lipoic acid, berberine — known insulin-sensitising supplements (evidence varies).
Omega-3 fatty acids (anti-inflammatory).
Watch for interactions if you’re on medications (e.g. hypoglycemics).
Regular monitoring
Ask your doctor for fasting insulin + glucose + HbA1c + HOMA-IR if possible.
If you use continuous glucose monitors (CGMs), observe how your glucose responds to specific meals, especially if symptoms flare after particular foods.
Personalise & iterate
Each body is different; keep a log of meals, symptoms, energy, and see your personal triggers.
Gradual changes are safer and more sustainable.
✅ How this ties back to The Mend Collective's mission
At The Mend Collective, our objective is to retrain internal regulation, not chase “quick fixes.” Stabilising metabolic signals — including insulin and glucose dynamics — is a powerful under-recognised lever of regulation.
By adding metabolic stabilisation to the focus on nervous system, immune, and tissue systems, we give the body a more stable foundation on which it can begin to regulate, recover, and withstand stress. This will all be helped with our live weekly chef and self paced nutrition modules to ensure you have everything you need to have your diet covered
If you’re on my waitlist, you’ll soon get modules covering metabolic regulation (nutrition, movement, glucose balance) integrated with pacing and nervous-system therapies. If not join HERE
Stay Well
Dr Ahmed
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