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Case Study: Julie

Insomnia, paradoxical responses, Crohns, mast cells, ‘everything’


Background / Details

Case History

Julie had experience regular illness as a child, and recalled being given multiple antibiotic prescriptions (as well as having her tonsils removed). She recalled being unhappy at both home and school. She experienced slow digestion for as long as she could remember, to the point that she assumed that 1-2x stools per week was normal (only coming to the conclusion that this was not after consulting her first practitioner in her 30s). She suffered from anaemia from her teenage years onwards, which was partially managed with large doses of iron supplements. She maintained a ‘normal’ life during her 20s, but was aware that she could not tolerate late nights, would come down with colds very frequently and was particularly prone to UTIs. However, as long as she nine hours of sleep each night, she was ‘OK-ish’. Her health began to fail after giving birth; her problems did not come during the pregnancy but in the months following (this is actually quite common and calls for us to consider the role of immune activity, which can spike after being suppressed by high levels of immunosuppressive progesterone that is part-and-parcel of a normal pregnancy). She developed major digestive symptoms and, after over a year of struggling with this, she was diagnosed with Crohns disease and prescribed a course of steroids and then sulfasalazine. This kept the symptoms ‘mainly’ under control but would flare whenever under high stress.


This was the case for the next few years, at which point she returned to work in the September, then moved house in November (as well as undergoing a six-month renovation project that started shortly after). After a particularly stressful day, she experienced anxiety for the first time and had an entirely sleepless night. She experienced sleepless nights from this point on, taking a long time to sleep and waking several times during the night. Anxiety also remained from this point on. After almost a year of struggling and after trialling various steps with different practitioners, Julie was no better. She resigned from her job to focus on rest and recovery. However, her condition declined further from this point.

She said a number of practitioners and doctors, trialling a variety of approaches that included the unusual nutritional approaches (both those advised by practitioners and also those recommended online), but also acupuncture, bioidentical hormones, a raw food diet and ozone therapy. She found that most nutritional approaches that focused on digestion did little but anything that focused on energy production or relaxation both resulted in bad reactions. She had taken both Iron and Vitamin D for many years but when she had trialled Carnitine, a B complex, Alpha Lipoic Acid, Ashwaganda, Valerian, Lemon Balm, 5-HTP and Magnesium, all saw her anxiety rocket in an identical fashion. The other approaches had little effect apart from the ozone, which saw her bed-bound for two days following each treatment (she was initially advised that this was a ‘good sign’ but, after a progressive decline in her wellbeing over the months she proceeded with this, it became clear that this was simply an insult to her system). Since this failure, she had been largely housebound, where she had seen a further worsening of symptoms and had hardly ventured outside in several years.


When I first met with Julie, she was experiencing a wide range of mast cell symptoms (sneezing after meals, bloating from all foods and liquids (including water), generally feeling better for ‘biege’ foods and itchiness) as well as severe adrenal-associated symptoms (anxiety, feeling tired-but-wired, low appetite, awful sleep no matter what, lots of symptoms that occurred at specific times of day, increased startle reflex, sensitivity to bright lights/loud noises, easy bruising, dizziness upon standing, low blood pressure, etc) and digestive symptoms (bloating from everything, nausea, low appetite, intestinal gas with a rotten egg odour, constipation with occasional swings to diarrhoea, with specific problems with cruciferous vegetables).

Initial Data

Julie had already seen a wide range of practitioners and had ended up with a number of test results.

Thyroid panel showed TSH in the range (but higher than ideal) and T3 at only 3.1 (which is technically inside the reference range, but right at the bottom and correlates with ‘Low T3 Syndrome’). She had undertaken a SIBO breath test, which came back negative, and serum iron and transferrin that were borderline/low (despite taking iron supplements), without any measurement of ferritin. She had low Vitamin D (despite taking large doses for several years), although only the standard test for the storage form had been taken.

Her Organic Acids test showed:

  • Markers for low Vitamin B1, B3, Biotin and especially Vitamin B2 and B6
  • Markers for dysbiosis
  • Raised ketones (while not on a ketogenic diet, indicative of ‘low carb limbo’) and raised Succinic Acid (consistent with adrenaline resistance)
  • Raised orotic acid (indicative of ammonia excess)
  • Low aconitic acid (a sign of mitochondrial hypoxia) with low pyruvic/lactic acid (indicating a poor hypoxia response)
  • Low manganese availability (not normally related to dietary intake, instead to bile release as this is needed to redistribute manganese)
  • Raised lipid peroxides (excess oxidative stress at cell membranes)

Points for Consideration

As with all cases of paradoxical reactions, the priority here was to consider why Julie was reacting badly to items that should be supporting her energy (and therefore brain activity) and calming her physical stress response. In these scenarios, we must consider how the mammalian brain has evolved to treat novel environments as suspicious (‘dangerous until proven otherwise’) and is therefore prone to feeling temporary unease when the inner environment is subject to such major change; restoring activity in networks that had previously been under-firing or reducing adrenaline (and its numbing effects) result in a novel inner environment and increased sensory signalling that the brain must ‘make sense’ of (something that links to neuroplasticity and represents a major tax on energy resources).

The intestinal gas (with a rotten egg odour) and the reactions to cruciferous vegetables stood out, as this flags the need to consider sulphate-reducing bacteria that convert dietary sulphur into hydrogen sulphide (a gas that can serve beneficial effects at low levels but causes bloating and, crucially, acts as a mitochondrial poison at high levels). The fact that her stool test had shown high levels of desulfovibrio confirmed this as a priority issue (sadly, she had previously been advised to take anti-microbial herbs that aren’t well suited to kill this species). It is relevant that hydrogen sulphide-dominant SIBO does not show up on the standard SIBO tests.

It also felt relevant to consider her iron and Vitamin D status. There are three reasons why someone would show low serum iron/transferrin; one is because there iron intake is exceptionally low (something that generally not been seen in developed nations, outside of vegan diets), the second is due to poor absorption and the third is due to poor iron recycling. This latter cause is most common, and it is easily identified by having high ferritin stores (showing that there is plenty of iron, it is simply not be recycled well). In these instances, the worst thing that a practitioner can do is add more iron into the system; doing so creates more hydroxyl radicals (‘rust’) which not only causes substantial oxidative stress, but the ‘rust’ convinces the body’s oxygen sensors that there must be plenty of oxygen. As a result, the response to hypoxia is blunted and a) energy production suffers in a big way, and b) there is a lack of uptake of copper, together with the manufacture of ceruloplasmin, the protein that works with copper around the body. This is important as copper is necessary to recycle iron, which leads to a self-perpetuating cycle.

Meanwhile, it is common to see Vitamin D levels stay low despite supplementation. This reliably occurs in inflammatory states, as activated immune cells themselves release enzymes that convert the storage form into the active form. This sees individuals pour huge amounts of Vitamin D into the system without making a dent on these levels. It makes calcidiol – the storage form and the version assess in standard tests – unreliable for this population.

One final thing that stood out was the possibility of mould. This is my first question whenever I see someone become worse after spending more time at home (and Julie had done just that, resigning from her job to permit more rest), and is often a contributing factor whenever we see a range of mast cell issues. The two together were impossible to ignore.

Initial Recommendations / Removing Obstacles

Primary Aims

On paper, our initial aims were quite clear. It was vital to tend to the mitochondrial hypoxia, as well as the variety of B vitamins that were short, tend to stress levels and support healthy digestion. But Julie was in an especially vigilant state and experienced insomnia/anxiety whenever steps were taken to improve energy availability. It is common to see CFS individuals struggle to tolerate any change in conditions in their inner environment, and somatic (“bodymind”) approaches are reliable in allowing the release of stored tension/trauma from the body, and a change in the way that sensory signals are processed (permitting a balanced response, in areas like the corticothalamic loops instead of just the hyper-reactive limbic system). However, Julie was mainly bedbound at this point and this meant that attending such sessions was not yet an option.

  • Extremely high ferritin (568 ug/L), with low copper and ceruloplasmin (both just within range even though both are ‘acute phase reactants’, meaning that they should rise whenever someone is subject to inflammation).
  • She also had low Vitamin A. This helped confirm my initial suspicion of poor recycling of iron (medically described as ‘anaemia of chronic disease’ or ‘anaemia of inflammation’)
  • A mould inspection, which showed extremely high levels of aspergillus and stachybotrys in her home

Dealing with mould is generally simple but expensive, as it typically involves paying specialists to resolve the problem. In Julie’s case, there were two issues, one involving the brickwork on wall that encased her bedroom and an ongoing leak beneath her bath. Both resulted in large colonies of black mould, a crucial problem due to the way that mould both drives inflammation, but does so in a way that inhibits the branch of the immune system that deals with bacteria/yeast/viruses and drives inflammatory pathways that can exaggerate the hypoxia seen in the cells. As with most mould-exposed individuals, it was not realistic to expect any meaningful change without taking action here.

I made recommendations to have specialists resolve the environment and, once we were content that these issues were tended to, to introduce mould binders (Chitosan).

Meanwhile, I stressed to Julie the importance of eating liver (something that I had previously recommended, but had not been integrated with enthusiasm) as this is the only food with especially generous levels of both copper and Vitamin A.

It took a lot longer than expected to undertake the work required in her home and, while waiting for this, Julie recorded very little improvement. This was frustrating for her and saw her trial Magnesium to see if this was now well-tolerated (it was not), and it meant that the recommendations I could make were also limited. For several months, my input was less on the usual sculpture of a plan and more with reassuring that the lack of progress was entirely what we’d expect if someone with energy issues is still subject to mould exposure.

Secondary Steps / Further Customization


Under normal circumstances, it takes several weeks to remove the ‘obvious’ obstacles so that we can make an assessment of where someone is really at and what areas will need more targeted intervention to reach the finish line. However, reaching this point is always delayed when mould exposure is holding things up, as the individual not only needs to arrange for remediation but also we need to bring in the mould binders and wait a couple of months to gauge a trajectory (note: when using natural binders, I expect an average of six months to remove accumulated mould toxins, but we should be able to see signs of the response after only two). Julie did not show much change, something that I see in almost half of those going through mould remediation process (and something that normally calls for support of the NRF2/antioxidant response). However, I was also weary of the ongoing activation of the stress response that may both limit the improvements we would otherwise see and leave her less able to respond to interventions that had impacts on the conditions in the central nervous system or energy availability here. Julie’s HRV scores were averaging just 21 rMSSD, a sign of major overactivation of the stress response.

Despite the above, there were some creeping signs of progress. While she did not feel much a difference, Julie was much more able to plan her meals for the week and was now getting outside on a near-daily basis (previously out of the question).

Further Recommendations

At this point, the rate-limiting factor was the stress response, something that meant any resources we had freed up would be instantly ‘stolen’ to get ready for a physical challenge. It also meant there would be very little resources to handle any switching on of the antioxidant response and that we can expect hypervigilance in the limbic system (and thus, any necessary support for the CNS/energy production were likely to trigger a return of anxiety).

Further Responses

Julie took the plunge and engaged in somatic work with a practitioner that primarily used Somatic Experiencing, but also employed transformational breathwork and EMDR. She felt particularly exhausted after her first two sessions but, following a major physical release in her third session, she found herself sobbing for the first time in decades. What followed was her first night of good sleep in years. What followed was a further trial of Magnesium. This time Julie slept better for it. She noted that Magnesium allowed her to come out of fight-or-flight long enough to feel the same sadness but, after physical expressing the impulse that came with this (crying), her sleep was not affected. Ever the days and weeks that followed, sadness faded from the dominant emotion to one of several that emerged each time we took steps that drove improvements in her neural function.

Julie continued to process a lot of stored tension (and the emotions that came out with it) over the coming months, but we were now able to introduce DIM to support her NRF2/antioxidant function, support for her energy production (with B2 a particularly powerful intervention) and Licorice to support her cortisol signalling. We were able to introduce Vitamin E also. At the third attempt, we were able to remove the yucca without a negative impact on anxiety. We were able to introduce Lemongrass without it flooring her (this still causes some major intestinal disturbance, but Julie was able to ride this out and now saw a drop in both bloating and brain fog). We saw a saw-toothed upward trend, with slow but ongoing changes in physical tension, improvements in sleep, daytime energy and HRV readings.

Final Steps / Getting to the Finish Line

Further Reassessment

After six months of ongoing progress, Julie reached a milestone and slept eight hours straight. This was not something she’d done since she was a child. Her rMSSD scores now averaged in the low 40s (indicating that, while she was still very much under excess stress, she was no longer in the ‘fight or flight’ state at all times). She still noticed some nausea from her first meal/drink of the day, general puffiness and a tendency towards higher heart rate/lower blood pressure but, all in all, the mast cell symptoms were much better. She was starting to see a number of changes in patterns, although one included an increase in intestinal pain.

It had now been 14 months since we started working together and so I suggested retaking the Organic Acids test and Iron/Copper panel, with a view to tending to the updated patterns and then looking into a stool test (although the bloating had reduced substantially since introducing the Lemongrass, bloating was still a fairly regular occurrence and this was especially the case after larger servings of carbohydrates).

Her repeat Organic Acids tests showed a marked improvement in a number of markers, notably the B vitamin status, bile movement and (as expected) ammonia status, although the hypoxia marker and the oxidative stress marker still remained (despite the ongoing supply of Vitamin E). The iron panel showed that ferritin had dropped but not by enough (now measuring 455 ug/L).

Getting It Over The Line

Our focus now turned to the iron issue, and employing the options that we now had; while there are many strategies that exist to help get iron out of tissues, Julie had not previously had the resilience to tolerate them. Specifically, our focus was split between a) controlling iron absorption and encouraging iron movement out of cells, b) supporting copper uptake and ceruloplasmin manufacture and c) supporting the hypoxia response (which not only enhances oxygen delivery to the central nervous system but, crucially, supports the first two areas of focus). This saw us employ polyphenols like Curcumin and Green Tea alongside thiol compounds like Alpha Lipoic Acid, while providing regular intake of liver (for both copper and Vitamin A) alongside Shilajit (which aids in absorption and delivery of copper to the deeper tissues). At the same time, we focused on the hypoxia response (specifically, enhancing levels of HIF-1a), which involved maintaining specific pathways of oxidative stress signalling (H202, which enhances HIF-1a) while limiting formation of other compounds (hydroxyl radicals, which reduce HIF-1a); the latter are generally driven by dysfunction of the electron transport chain in the mitochondria, and so we added Co-Q10, Lycopene and red light. Julie also donated blood several times.

The combined effect of the above (which proceeded alongside the ‘base’ support and ongoing somatic release) was gradual but powerful improvement in wellbeing, which tracked with a reduction in ferritin (down to 202 ug/L) over the course of the next eight months) and a disappearance of remaining mast cell symptoms. The improvement was so significant that Julie returned to work, taking a part-time job. This was a big deal for her, given that this was beyond any of her initial aims. She also re-engaged with ozone therapy, something that had previously had such a detrimental effect, but was now had the desired effects; this saw her feel particularly tired during the ‘start up’ (which lasted around eight weeks) but saw further improvements in wellbeing, energy/resilience, HRV and ferritin. This saw Julie cross a further milestone, to the point that she no longer felt that she was managing her energy budget each day and now, for the first time in decades, actually felt healthier than those around her. At this point, Julie was no longer noticing any Crohns symptoms and hadn’t for some time. She now wanted to speak to her doctor about trialling a removal of the Sulfasalazine medication.

Before making an appointment with her doctor, we undertook a further stool test. We saw that the Calprotectin marker (which is linked to Crohns) had plummeted in line with what Julie had noticed, which was very encouraging. There was also a number of imbalances still present (which we would still expect, having not taken acute measures here). We tended to the result, providing both herbal anti-microbials and targeted probiotic support. Julie felt subtle but noticeable benefits, mainly in that physical tasks seemed now to be ‘effort-free’, and she went on to remove her medication with zero negatives for doing so… this was a massive result!

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