2.2.6 Cortisol, limbic system, glycogen and IFN-γ
Cortisol is the “master” negative regulator for IFN-γ related immune activity and promotes catabolic energy availability via epinephrine (adrenaline).
Elevated cortisol doesn't just suppress immune function; it also alters neurotransmitter balance, which can influence mood, cognition, and energy levels.
What this means is that any/all influences which promote cortisol also decrease IFN-γ activity and provide some “relief” for many of the symptoms observed in ME/CFS.. while potentially creating others. This allows periods of increased functionality, while simultaneously inhibiting the necessary suppression of the pathogens that are triggering the innate immune response pathways.
In the disease model, we have described how cortisol acts as a “sensor” and signalling relay for insufficiencies of NAD+, P5P and glucose / glycogen, via phosphatidylserine and 11HSDβ1/2 flux (see figure 4). The metabolism for NAD+ and P5P is altered by IFN-γ and they act as upstream sensors for specific IFN-γ activities which can upset the metabolism or cause excessive tissue damage via oxidative stress. An inverted diurnal cortisol release pattern is expected.
When any of the sensed metabolites are insufficient, cortisol increases, signalling for an increase of epinephrine. This promotes energy "scavenging" or "catabolism", while inhibiting IFN-γ immune activity. This allows some of the cofactors and metabolites to replenish and by doing so, it helps restore normal metabolism. However, the same cortisol -> epinephrine elevation also signals for your cells to stop storing glycogen and instead use the existing glycogen pools for energy (see figure 1, upper right). Glycogen storage can therefore become problematic when cortisol -> epinephrine is dysregulated and chronically elevated.
As the metabolites reach sufficiency, cortisol levels normalise. If any triggers for IFN-γ are still present, then IFN-γ activity will resume and the cycle will repeat, as necessary.
Exercise, sex hormones and heat can increase IFN-γ. Dietary supplements can support IFN-γ activity. Cortisone medications are potent immunosuppressants and will inhibit IFN-γ.
Appropriate carbohydrate and protein intake (with uninhibited metabolism) supports optimal glycogen homeostasis. Sublingual and liposomal NMN can efficiently support NAD+ biosynthesis. Creatine can reduce the methylation “costs” associated with use of this pathway and also increase glucose transport. Magnesium and zinc can support B6 -> P5P metabolism. Manganese sufficiency is required for conversion of other substrates (protein -> amino acids, fats -> fatty acids) into glycogen, usually via the TCA cycle to the glycolysis pathway, however flowing in reverse.
Hypothyroidism affects both glucose metabolism and “B6 toxicity” / P5P insufficiency. The thyroid hormone, T3 (tyrosine, heme iron, iodide, selenium, calcium) is required to maintain FMN levels, needed for P5P recycling and to induce pyruvate flux into the TCA cycle.
Chronic hypoxia can be a significant contributor to this cascade.
The primary sex hormones (testosterone / DHT in males, estradiol in females) sense the elevation of NADPH (created during physical / metabolic activity), with sufficiency of NAD+, magnesium, boron and zinc. These primary sex hormones then promote creatine synthesis and glucose uptake. They inhibit cortisol levels, promote nitrogen metabolite recycling and glycogen synthesis. This also allows IFN-γ activity to increase, which is also needed for tissue adaptations to exercise. Non-optimal sex hormones can cause chronic cortisol increase.
In a normal, healthy state, the overnight rise in cortisol guides the liver to replenish glycogen and ensures a steady trickle of glucose when we first stand up.
In severe ME/CFS this diurnal rhythm is delayed, blunted at night and erratic by day. With hepatic glycogen never fully restored, even small physical or emotional stresses deplete the reserve. The body responds with abrupt pulses of cortisol and epinephrine to keep blood glucose within safe limits, but these surges have costs and the repetitive signalling can contribute to nervous system adaptations / programming towards hyper-arousal and sympathetic overdrive.
Some of these costs can influence further self-sustaining cycles, eg.
Increased protein catabolism - cortisol mobilises amino-acids for gluconeogenesis, gradually lowering the circulating pools of tyrosine, histidine, asparagine and aspartate that are needed for neurotransmitter and enzyme synthesis, affecting energy metabolism, causing additional epinephrine spikes / sympathetic bias.
Dysregulated metabolic feedback - frequent intermittent epinephrine bursts further inhibit glycogen synthase, perpetuating the under-filled liver glycogen tank, causing additional epinephrine spikes / sympathetic bias.
Sympathetic overdrive
There are also many influences observed in ME/CFS which can contribute to sympathetic overdrive and chronic flight/flight. Overall, the balance is normally biased heavily against being able to maintain parasympathetic sufficiency and (liver) glycogen stores.
This bias NEEDS to be shifted towards a neutral balance to restore normal energy metabolism and help remove glycogen deficiency as an influence in debilitating symptoms like POTS, PEM and sleep disorders. This means removing as many unnecessary sources / triggers of epinephrine spikes. Some of these influences also can induce a long-term shift / up-regulation of epinephrine synthesis / release.
Separately, the catecholamine degradation pathways needs to be restored and adrenergic receptor expression / sensitivity restored, to remove unhelpful "hair-trigger" response to stimuli.
The clinical picture may include fasting intolerance, exaggerated post-exertional malaise, morning hypoglycaemia and wide swings in lactate that resemble certain glycogen-storage disorders, albeit driven by signalling rather than an inborn enzyme defect.
Therapeutic priorities are (i) frequent balanced meals that combine low-glycaemic carbohydrate with medium-chain triglycerides (or large doses of L-carnitine / acetyl L-carnitine used in the protocol), (ii) consider nocturnal adrenergic dampening (for example low-dose clonidine / ivabradine) to allow normal cortisol timing, and (iii) graded re-entrainment of sleep-wake cues so that the liver again “expects” to store glycogen after dusk.
Overall, multiple biochemical bottlenecks converge in ME/CFS to disturb catecholamine balance:
eg.
1. Queuine deficiency (secondary to microbiome dysbiosis) and tetrahydrobiopterin (BH₄) depletion slow translation and activity of tyrosine hydroxylase, the rate-limiting step in dopamine production, causing reduced dopamine synthesis.
2. Acetaldehyde directly inhibits aldehyde dehydrogenase (ALDH), depletes zinc and inhibits thiamine pyrophosphate (active Vitamin B1) synthesis. The zinc deficiency leads to further deficiencies of active B vitamins. Low FAD (active Vitamin B2) and zinc limit monoamine oxidase (MAO) and catechol-O-methyl-transferase (COMT) activity. Released dopamine, norepinephrine and epinephrine may therefore persist longer.
3. Acetaldehyde depleting zinc also affects P5P metabolism and dopamine synthesis by inhibiting aromatic L-amino decarboxylase (AADC) activity.
4. Acetaldehyde triggering mast cell activation and histamine release affects tyrosine hydroxylase activity.
5. Low iron and/or neural hypoxia, affecting phenylalanine and tyrosine hydroxylase.
6. P-cresol from dysbiosis, affecting dopamine beta hydroxylase.
7. Oxidative stress affecting phenylalanine, tyrosine and dopamine beta hydroxylase.
8. Electrolyte deficiencies affecting tyrosine hydroxylase, VMAT2, DAT and NET transporters.
9. cAMP-PKA dysregulation from chronic endogenous opioid synthesis pathway being activated by ALDH inhibition, if MAO is still functioning.
..This is not an exhaustive list.
Chronic sympathetic over-activity down-regulates vascular β₂- and presynaptic α₂-adrenoceptors. The system compensates with larger and less predictable bursts of catecholamines to achieve ordinary physiological tasks (for example standing or minimal exertion). This can also be exacerbated by (presumed regulatory, as a compensation) "autoimmune" antibodies for adrenergic receptors.
These receptor alterations also mean that any shift towards parasympathetic sufficiency can induce a level of temporary hypometabolism until the homeostasis resets, over a few weeks. The level of hypometabolism may also be enough to force a reflex into sympathetic spikes, exacerbating efforts towards normal homeostasis.
When catecholamine levels normalise, but receptors remain desensitised due to the previous sympathetic overdrive, chronic PTSD or stress, symptoms like fatigue, cognitive dullness, low BP, and orthostatic intolerance can appear. This results from a “relative catecholamine deficiency.” Even with normalised levels, desensitised receptors (like alpha2 and beta2) mean there's a decreased adrenergic tone and paradoxical crashes. Surges of epinephrine may occur after episodes of low energy, causing hypoglycemia-related adrenal bursts and crashes, leading to unexpected symptoms like anhedonia and fatigue.
Clinical tell-tales of an epinephrine surge while receptors are still half-asleep:
0–5 min - Sudden heart-in-throat palpitation, cold sweat, tremor, pilo-erection, brief spike in systolic BP. EPI acts on the fraction of β₁/β₂ receptors that are not desensitised; α₁ vasoconstriction is relatively spared.
5–30 min - Shaky hunger, light-headedness, hyper-alert or “wired” feeling. Hepatic glucose release overshoots; brain re-gains perfusion but over-reacts
30–120 min - Crash: profound fatigue, yawning, headache, sometimes nausea. As EPI is metabolised the receptor deficit is unmasked again; glycogen is partly spent, leaving a transient energy hole
Exercise intolerance and easy fatigability will occur. β₂-adrenergic drive to skeletal muscle and myocardium is blunted, so peak cardiac output and mitochondrial substrate flux lag behind demand. This mirrors the desensitisation seen in chronic muscle-pain cohorts.
Impaired β-oxidation impairs catabolic energy metabolism and means small drops in glucose activate hypothalamic “fuel alarm” pathways, causing adrenaline surges that can feel indistinguishable from panic. Sleep will temporarily become broken and difficult, relative to glycogen stores and norepinephrine "long" pulses.
The brain has a hard-wired crisis response for cellular energy deficit -
1. The ventromedial hypothalamus senses falling intracellular ATP or glucose.
2. It fires the sympatho-adrenal axis, causing the adrenal medulla releases epinephrine.
3. Epinephrine burns glycogen stores, elevates hormone‑sensitive lipase in adipose tissue, and raises cardiac output.
This
counter-regulation is best documented in insulin-induced hypoglycaemia:
even modest falls in plasma glucose produce a several-fold surge in epinephrine
that is not fully replaceable by glucagon alone.
These changes can reinforce an anxiety-phobia cycle. Each adrenergic spike produces tachycardia, dizziness and a sense of impending collapse; the cortex learns to associate ordinary movement with danger, encouraging further inactivity and social withdrawal. Poor sleep prevents overnight receptor resensitisation, and the cycle repeats. A large part of overcoming this vicious trap is awareness of the issue and then learning to consciously override the signals being fed to the nervous system while the transition is underway.
Will the receptors wake up? Yes, but slowly:
β-receptor resensitisation needs days-to-weeks of lower catecholamine tone and adequate omega-3 intake (membrane fluidity matters).
The α₂ presynaptic brake tends to reset faster (days), which is why clonidine/guanfacine at night could smooth the ride during taper.
Adequate sleep and micronutrients (esp. Mg²⁺, Zn²⁺ and B-vitamins) can also hasten the up-regulation of G-protein coupling units.
Ketotifen can also be particularly helpful. Histamine released from mast cells can stimulate sympathetic outflow and locally augment norepinephrine release. Blocking H1 and stabilising mast cells removes that extra push on the accelerator. Long-term oral ketotifen has been shown to increase β2-adrenergic receptor density. Central H1 blockade and mild anticholinergic tone tilt the ANS parasympathetic, lowering baseline sympathetic tone and improving slow-wave sleep - both conditions that favour receptor resensitisation. Net effect: fewer histamine-triggered norepinephrine releases, shallower epinephrine spikes, and a slow rise in β-receptor responsiveness.
(Practical caveats: drowsiness - take at night, anticholinergic dry-mouth, and mild orthostatic drops; dose-titrate over a week from 100 mcg to avoid a “hung-over” feel.)
Until then, oscillating between “underpowered” and “epinephrine dump” is common. Forewarned is forearmed: frequent small meals with complex carbs and fat, gentle aerobic work (appropriate levels of walking, etc.) to retrain β-oxidation, and cautious use of α₂ agonists or low-dose β-blockers can soften the swings while the receptors crawl back to baseline.
This area of homeostasis reset can be challenging and without awareness, it can easily create another loop / trap. Don't be fall into it.
In this protocol, restoring homeostasis starts with biochemical housekeeping. Replenishing the minerals, reducing acetaldehyde through targeted antimicrobial therapy and binders, and rebuilding queuine-producing microbial colonies can give the enzymatic machinery a chance to recover and reduce influences promoting sympathetic overdrive.
Frequent meals that pair low-glycaemic carbohydrates with medium-chain triglycerides (and/or the protocol dosing acetyl L-carnitine) helps protect the liver’s limited glycogen and spare amino-acids, while spirulina and other metabolic supports help realign cortisol timing.
As adrenergic spikes quieten, short recumbent muscle contractions or very gentle cycling become tolerable, promoting vascular conditioning without provoking post-exertional malaise. This can open up to walking and other activities as they become appropriate. A brief daily video call or other similarly "low-demand" social contact can then begin to reactivate normal reward pathways and help shift the balance towards a more parasympathetic state. Within this framework, behavioural strategies such as paced breathing or graded exposure need no longer fight against biochemical headwinds and instead build on a slowly stabilising neuroendocrine landscape.
As described above, chronic disease-related lifestyle factors and trauma imprinting / learned responses to stimuli - namely stress / fear / anxiety - cause the limbic system to promote cortisol levels and inhibit the IFN-γ pathway / immune response, while decreasing glycogen stores. As this also temporarily decreases some “ME/CFS” symptoms, before rebounding, a persistent cycle of fear / anxiety, and immune dysregulation can also be learned / imprinted.
Has your life been entirely devastating for many months or years?
Have you lost nearly everything?
(Are you lonely?)
..Have you been medically gaslit (or abandoned) during this time and have therefore spent many of your days isolated from your friends, loved ones and former life, while possibly laying for long periods in your own filth and often a mouldy bedroom?
These circumstances can reliably create trauma.. and guess what? No one - literally, no one - can deal with their trauma, alone!
What you’re experiencing is what NORMALLY HAPPENS when a sensitive, intelligent system is asked to survive without the right support. Trauma isn’t imagined. It’s imprinted in cells. It alters your hormones, neurotransmitters, immune function, and even nutrient handling. That’s intrinsic biology, not something to blame.
If your nervous system feels like it’s running the show lately - prioritising short-term survival over long-term repair, THAT'S NOT YOUR FAULT. It’s the body’s normal way of surviving / coping. However, over time and repeat exposure to stressors or trauma, your nervous system adapts to existing in this harsh environment and is often reluctant to reset the alarm system, especially if it thinks you might still be unsafe. When this happens, it needs gentle reminders to hand control back to the repair systems.
The nervous system is NOT malfunctioning - it's adapting to chronic stressors and trying its best to keep you safe.
By understanding these adaptations, we can work WITH the body to restore balance.
If you find yourself in this situation - which is entirely expected after "living" with ME/CFS or any other named entry-point to the disease model) - then getting help is essential to your recovery.
Trauma counselling / therapy and brain retraining programs like DNRS can be game-changing for people who are suffering from chronic "fight or flight" programming. However, this protocol also describes an anxiety -> phobic response trap that can cage people and ways to navigate this successfully. From my observations, this affects a significant number of people.
Stellate Ganglion Blocks (SGB) can be another helpful intervention, by resetting and controlling this state, however they are not a long-term solution, unless you use them as a helpful educational tool, to experience a period of remission from the crisis state, which helps you learn to rebuild trust in your body. NB. SGBs should not be used until the underlying issues causing hypometabolism are resolved, otherwise you'll feel like you've taken a backwards step in functionality. The crisis state is providing a level of energy to sustain you, even if that's dysregulated.
If you are affected by this subconscious programming, you will struggle to make forward progress while still in a chronic "fight or flight" state, due to the downstream metabolic consequences:
The "fight or flight" and/or "crashed" state may also lead to significant amounts of lactic acid and oxalates being generated. If the lactic acid can't be metabolised efficiently to usable energy, this can cause swollen / inflamed / numb / tingling body parts, especially in areas with smaller blood vessels, such as hands, feet, face and lungs.
Lactic acidemia can also make it very difficult to restore missing bacteria which are pH sensitive, eg. bifidobacterium, as excess lactic acid is secreted into the GI tract and also excreted via your kidneys, leading to frequent urination, "sandy urine", kidney stones, etc.
If you are feeling lost or in a crisis, THRIVE Lifeline offers 24/7 international text-based crisis support to anyone aged 18+, with a specific focus on multiple marginalized communities. They do not engage in non-consensual "active rescue" and they prioritise the texter's consent + autonomy.
For urgent help
SMS: +1.313.662.8209
General enquiries
Website: https://thrivelifeline.org/
Email: info@thrivelifeline.org
Anxiety, isolation, and phobia
Before continuing, for clarity, I'll restate my previously published, long-standing position against using CBT and GET as a primary therapy for ME/CFS and similar diseases:
I anticipate that there is a special place in hell reserved for clinicians who negligently misdiagnose ME/CFS patients with a purely psychological disease or "anxiety", or force patients with measurable mitochondrial dysfunction from chronic infections / dysbiosis / induced malnutrition to perform "graded exercise".
You wouldn't initially prescribe a diagnosed septicaemia patient CBT and GET as their primary therapy, so it's appalling that this continues to be the "gold standard approach" taken by numerous clinicians for ME/CFS patients. There are decades of evidence against this.
Yes, once the infections and malnutrition are sufficiently resolved and mitochondrial metabolism allows for it, physical rehabilitation is absolutely encouraged as part of the recovery process.
Yes, there are neurological and psychological issues created in this disease model - biochemically and from trauma, isolation, coping mechanisms and learned fear responses. These each require different interventions.
[/RANT]
This section explores the connections between anxiety, isolation, and phobic responses to symptoms in individuals with ME/CFS or similar chronic diseases. Drawing on parallels between chronic pain, fibromyalgia and ME/CFS, it aims to provide a clearer understanding of these challenges and how to exit another closed-loop / cycle which can be present in some patients.
Understanding the fear-avoidance cycle
A fear-avoidance model, initially developed in the context of chronic back pain by Dr Sarno as "Tension Myositis Syndrome (TMS)" and later extended by Dan Buglio as "Perceived Danger Pain (PDP)", also provides a working description for an observed pattern of daily experiences, physiological responses and behaviour that may create a further trap for some people already suffering from ME/CFS.
A popular example of perceived danger pain is the "Rubber Hand
Illusion" - a psychological experiment that demonstrates how the brain
can be tricked into perceiving a fake hand as part of one's own body. In
this setup, a participant's real hand is hidden from view, and a rubber
hand is placed in front of them. Both the hidden real hand and the
visible rubber hand are simultaneously stroked with brushes. Over time,
many participants begin to feel as though the rubber hand is their own.
This illusion highlights the brain's ability to integrate visual and
tactile information to create a sense of body ownership. https://youtu.be/sxwn1w7MJvk
In chronic pain, the fear of pain or "perceived danger pain" can lead to avoidance behaviors, which ultimately reinforce fear and reduce / prevent pain-free movement. The brain creates a genuine sensation of pain and measurable metabolic alterations to a perceived danger, to try and keep you safe. This is described as a learned phobic response that happens even when the original danger has been removed.
https://journals.lww.com/pain/fulltext/2022/08000/impaired_pain_related_threat_and_safety_learning.18.aspx
Similarly, some people with ME/CFS may fear pain from triggering or exacerbating existing metabolic symptoms such as mast cell activation syndrome (MCAS), post-exertional malaise (PEM), inflammation, sleep deprivation, etc, leading them to increasingly avoid foods, supplements and people, along with physical and mental activities. This avoidance can result in severe deconditioning, increased isolation, and a greater severity of symptoms, perpetuating a closed-loop / cycle of fear and avoidance.
Notably, even the possibility of avoiding discomfort can paradoxically increase fear over time. Studies show that individuals who are given the option to avoid pain experience increased fear when that option is removed, highlighting how avoidance can amplify anxiety rather than reduce it.
https://academic.oup.com/abm/article-abstract/55/3/216/5876277
Anxiety, isolation, and heightened threat response
Anxiety is a significant factor for individuals living with ME/CFS, similar to its role in chronic pain. People with ME/CFS often experience heightened anxiety - created by the mitochondrial dysfunction and downstream energy crisis. Neural hypoxia is one of the more common influences, downstream of immune activity, impaired iron homeostasis, oxidative stress, blood-flow and structural issues.
Additional anxiety can also sometimes be driven by feelings of inadequacy and/or fear from not being able to participate in life and fulfil roles as parents, lovers, workers, or friends. This anxiety is often compounded by fear of the unknown, thanks to inadequate medical care and also anticipatory fear - worrying about potential symptoms exacerbation by taking even small actions. This leads to heightened stress and worsened symptoms.
Isolation and unrefreshing sleep further intensifies this anxiety. For those with ME/CFS, reduced social contact can enhance the brain’s threat-detection systems, making individuals more likely to interpret normal bodily sensations as signs of danger. Studies indicate that even brief periods of social isolation can increase vigilance to perceived threats, which contributes to the cycle of fear and avoidance.
https://royalsocietypublishing.org/doi/10.1098/rsos.240101
Moreover, as a "perceived danger syndrome", symptoms related to immune activity and die-off, such as inflammation, pain, elevated histamine, rashes, nausea, diarrhoea or flu-like sensations, can be misinterpreted by the brain as a danger signal.
This heightened threat perception can create a feedback loop where normal immune responses are seen as threatening, further amplifying anxiety, acting as a "fight-or-flight" trigger, chronically depleting glycogen stores, altering blood-flow and leading to more avoidance behaviors.
This misinterpretation by your subconscious brain reinforces the fear-avoidance cycle, making it more difficult for people to break free from the loop of symptom exacerbation and fear. The brain can even create real, measurable symptoms of physical pain and emotional fatigue in the process of keeping you safe.
The phobic response to symptoms
"Do not be bluffed by a symptom.
Accept it. Float through it.
Let time pass." - Claire Weekes, MD
The pattern I call the "phobic loop" has deep roots in biology -
trauma, metabolism, inflammation, sensory gating. However, the
experience of being trapped in that loop isn't new. Decades ago, a
brilliant Australian physician named Dr. Claire Weekes described a nearly identical cycle,
using language like “first fear, second fear,” and explaining how a
sensitised nervous system can become stuck in protective sympathetic overdrive. She
wasn’t dismissing symptoms - she was validating them. Her key insight was that the fear of the symptom was more disabling than the symptom itself.
What
she offered patients was a way to float through the storm - not by
ignoring it, but by removing the "fuel": the resistance, the bracing,
the fear of fear. There are similarities to key elements in this section
- restoring safety to the system, not by silencing it, but by helping
it stand down.
Repeated experiences of PEM, MCAS, etc., can result in a conditioned, phobic response to certain triggers. This means that the brain starts to associate specific activities—such as physical exertion or even mental tasks—with symptom exacerbation, leading to an increased fear response. The brain, in a state of chronic stress or "under siege", may misinterpret normal sensations as threats, reinforcing feelings of vulnerability and the development of phobic responses to a wide range of stimuli.
People with ADHD and/or OCD-like traits are expected to have a
more difficult time with this, as the subconscious hyper-focus and
pattern-recognition traits can easily be fixated on the symptoms,
instead of the recovery progress. As an analogy, I'm reminded of a lesson once given by my motorcycle riding instructor:
When
riding a motorcycle, you seamlessly "merge" with the bike, to the point
that wherever you're looking is where the bike will travel towards.
Imagine a scenario where you're riding a motorbike around a large
paddock that has a single tree in the middle of it. The paddock is so
large that there is absolutely no reason that the tree should present a
significant risk of collision - you have a lot of wide open space to
enjoy. However, if you're consciously or subconsciously afraid of
hitting the tree, you'll keep glancing or looking over at it to make
sure you're safe. Consequently, by these actions, you'll increase the
risk of actually hitting the tree, or perhaps succeed in doing so. By
simply focusing on the wide open space where you want to actually be
riding, you will be significantly safer and enjoy your ride more.
This lesson applies to ME/CFS in the same way: don't focus on the symptoms - focus on the destination. Trust your body. The symptoms that we worry about the most may persist the longest. We give energy and life to things by paying attention to them.
It's important to understand that your symptoms are NOT imagined - they’re real, measurable, and rooted in biology. Whereas, HOW your nervous system INTERPRETS and AMPLIFIES those symptoms can change the entire trajectory of the illness.
In other words, it's NOT "in your head", it's "through your head" ...and that gives us tools to work with.
The loop is debilitating, but not irreversible. Every loop has a way out - and that’s what this section is about.
Steps towards recovery
Several strategies can help people with ME/CFS, etc., navigate the complex interplay of physical and psychological symptoms:
Recognizing the Role of the Mind: Understanding the powerful connection between the mind and body is crucial. Anxiety and fear can perpetuate symptoms, so addressing these emotions is an essential part of recovery.
Daily Mantras / Replacing Unhelpful Thoughts: This can help re-frame negative thoughts and beliefs about symptoms, thereby removing unnecessary obstacles, fears and anxiety, eg.
1. "This is a chapter in my life, not the whole story."
This
mantra puts the illness experience into perspective, reminding people
that their lives are not defined by their symptoms. It encourages them
to look beyond the present moment and envision a future filled with
possibility. It helps to counteract the sense of hopelessness that can
accompany chronic illness. It reminds people that their lives are still
unfolding and that their illness, while a significant challenge, does
not have to define their identity or their future.
2. "I choose to focus on what I can do, not what I can't."
This
mantra promotes a positive outlook and encourages individuals to find
joy and fulfillment in the present moment, even within the constraints
of their illness. This affirmation helps to shift attention away from
limitations and towards possibilities. It encourages people to explore
activities that bring them joy and a sense of accomplishment, however
small, to counteract the sense of loss and frustration that can
accompany chronic illness.
3. "Every step I take, no matter how small, is a victory."
This
mantra celebrates small wins and acknowledges the courage it takes to
move forward even when faced with fear and uncertainty. It encourages
people to appreciate their efforts, no matter how seemingly
insignificant. It emphasizes that progress is not always linear and
that even small steps forward contribute to overall healing.
4. "I am not alone in this journey."
This
mantra reminds people that they are part of a larger community of people
who understand their struggles. It helps to combat feelings of
isolation and foster a sense of belonging. It underscores the importance
of connecting with others who have experienced the challenges of living
with ME/CFS. Sharing experiences, offering support, and learning from
one another can be a powerful source of healing and hope.
5. "I am learning to listen to my body with kindness and curiosity."
This
mantra encourages a compassionate and non-judgmental approach to
symptom management. It fosters a sense of collaboration with the body
rather than seeing it as an adversary. This affirmation helps to shift
the internal dialogue from one of self-criticism and blame to one of
understanding and acceptance. It encourages people to pay attention to
their body's signals and respond with care and compassion.
6. "My body is healing, even when I can't see it."
This
mantra fosters patience and hope, reminding people that recovery is a
process that may not always be visible. It encourages trust in the
body's innate capacity to heal. It helps to counteract the
discouragement that can arise when progress feels slow or setbacks
occur. It reminds people that healing is happening on multiple levels,
even when it's not immediately apparent.
7. "My symptoms are a signal, not a sentence."
This mantra helps to re-frame symptoms as messengers rather than threats. It acknowledges that symptoms are trying to communicate something, but they don't dictate the future or define one's limitations. It draws on the idea that pain, fatigue, and other symptoms in ME/CFS are often amplified by fear and anxiety. It encourages a shift in perspective from viewing symptoms as inherently dangerous to seeing them as signals that need to be understood and addressed.
8. "I am safe, even when I experience symptoms."
This mantra directly addresses the fear response, offering a powerful message of reassurance. It emphasizes the distinction between experiencing a sensation and being in actual danger. It is particularly helpful in breaking the cycle of fear and avoidance. By repeating this affirmation, people can begin to retrain their nervous systems to associate symptoms with safety rather than threat.
9. "I am stronger than my fear."
This mantra
empowers people to face their fears and challenge the limitations they
have imposed on themselves. It emphasizes that fear does not have to
control their lives. This affirmation promotes self-efficacy and
encourages individuals to take an active role in their recovery. It
reminds them that they have the inner strength to overcome their fears
and gradually expand their boundaries.
These mantras, when repeated regularly and with intention, can help to rewire the brain's threat response, reduce anxiety, and foster a sense of safety and empowerment in the face of challenging symptoms. With practice and persistence, belief in these mantras strengthen. It only takes a few wins or reductions of something to see this approach is helping.
Gradual Exposure and Pacing: Gradually increasing exposure to normal activities and day-to-day life, along with appropriate pacing, can help desensitize the nervous system and break the fear-avoidance cycle.
Emotional Processing: Techniques such as journalling, therapy, or other methods for exploring and expressing emotions can be key in addressing underlying emotional issues that may contribute to symptom persistence. Recovery is not linear. Record your wins as a list. On bad days go back to the listed wins list and focus on the positive.
Somatic Practices: Practices like mindfulness, gentle movement, and breath-work can help people with ME/CFS develop a greater sense of safety and connection with their bodies, shifting the nervous system from sympathetic to parasympathetic mode.
Try this:
Place your hand over your chest and breathe slowly into your ribs for 10 seconds.
As you exhale, say (in your head, or aloud): "I’m safe. I’m adaptive."
This isn't about "magic thinking" - it's reprogramming the body's fear interpretation loop through safe, predictable signals.
Self-Compassion: Cultivating patience and kindness towards oneself during the recovery journey is crucial, as ME/CFS recovery can be a slow, non-linear and challenging process.
Building Social Support: Connecting with others who understand the experience of ME/CFS and critically, are supportive of the process you are undertaking and / or are ideally further along the same recovery process than you, can reduce feelings of isolation, provide validation, and offer emotional peace.
Recovery from ME/CFS is a deeply personal journey of "putting Humpty Dumpty back together again". Everyone has slightly different shaped pieces to reassemble.