Case Study: Caroline
Hormones & Weight Loss
Background / Details
Caroline’s childhood was spent in a stressful household and she experienced anxiety and eczema throughout her childhood and teenage years. Her periods were initially regular, but painful from the very beginning (and tended to come alongside oedema). However, in her 20s, she began to gain weight, she introduced a low-calorie diet (1,200kcals per day) with particularly low protein/fat intake, while undertaking regular exercise sessions (around 6x per week, normally running). This saw her drop weight and her oedema reduced with this, but she would never be able to shift any weight around the hips and buttocks and that she would see quick weight gain if she were to increase her calories above 1400kcals per day. She also found that her periods became irregular (getting only 3-4x per year) and remained that way from this point on.
In her 30s, Caroline consulted the doctor after struggling to conceive. She gave birth to two children in her 30s, with both pregnancies progressing without complications, and she was subject to a major lack of sleep in the aftermath (neither child slept well). Throughout this time, Caroline actually felt good apart from feeling uncomfortable with weight gain from both pregnancies. However, once her children began to sleep through, she found that she was unable to follow suit. She began to notice more digestive issues in the years that followed, now began to experience migraines ahead of her period and, when she attempted to revert to her ‘old’ schedule, found that she no longer saw any weight gain in response (finding that the only noticeable change was that her periods disappeared). She had spoken with her doctor, who suggested that she was peri-menopausal on account of her age (this felt like a bit of a stretch, as she was in her early 40s at the time).
Alongside the above, Caroline was experiencing major sugar cravings, a number of food sensitivities (feeling sluggish from heavier foods, like oils and meats, but feeling bloated from vegetables). This saw her tend to delay eating until the afternoon to avoid such symptoms. She also experienced a number of the common ‘adrenal’ patterns we find following sustained stress on the system, notably cold hands/feet, slow to get going in the morning/switching off at night, an afternoon slump followed by a second wind, feeling ‘tired but wired’, low blood pressure, dizziness upon standing, frequent urination and worsened sleep after exercise.
Caroline had already had a steroid hormone panel and a general blood test before coming to see me. The steroid hormone panel had been done in the follicular phase and showed low progesterone with particularly low estrogen. The FSH and LH markers were not out of range, showing clearly that this set-up was because the central nervous system was not asking for ovarian activity, which occurs in high-stress/low-energy states (this is very different from the results we would see in perimenopause, where the FSH and LH would be very high as the pituitary sends more and more signals to try to get some reaction from unresponsive ovaries). The blood levels showed normal lipids, biochemistry and blood counts, but had low ALP (which can indicate poor bile flow or be due to malnutrition or zinc deficiency).
Diet – Caroline was not eating enough. Her food quality was pleasing, but the total calorific intake was low and this was confounded by low intake of fats. Caroline had tried intermittent fasting several years previously and, while she did see the intended benefits on weight loss, it meant that she experienced no bloating during the morning and so stuck with this intake. I asked Caroline to measure her intake using one of the usual apps; this showed that, on a typical day, she was getting just over 1,000 calories per day (made up of 45g protein, 130g carbohydrates and 40g fats). This was doubly worried as she was doing fasted cardiovascular workouts three times per week.
Her Organic Acids test showed:
- Markers for low zinc and magnesium
- Raised lactic acid (indicative of slow mitochondrial activity and compensation through glycolysis, aka the ‘backup’ energy pathway) with low citric acid (consistent with blockage in the activity of the PDH enzyme, which allows carbohydrates to enter the mitochondria)
- Raised succinic acid (showing slow activity of PDH, which needs Co-Q10 and B2 but is also stimulated by adrenaline)
- Raised oxalates
- Production of ketones (while not on a ketogenic diet)
Points for Consideration
All in all, the results pointed to mitochondrial performance as a central feature. The raised lactic acid showed that her mitochondria were not meeting her baseline energy requirements; this pathway is designed for use when running for a bus but not while lying in bed. The low citric acid can be caused by a lack of B1/Alpha Lipoic Acid or due to inflammation; the test showed no issues with B1 and antioxidant status looked OK, which firmly pointed to inflammatory issues as a driver. Her Succinic acid marker could relate to a number of factors but, because her B2 and Co-Q10 markers looked good, this implicated adrenaline resistance as a problem (another common finding after long-term energy stress). Adding to these findings were markers for dysbiosis (especially yeast) and raised oxalates, this provided a framework that indicated connections between digestive conditions, inflammatory triggers and mitochondrial blockages. Another marker that stood out was the production of ketones, which indicated insufficient availability of carbohydrates (highly relevant as she was not consuming a ketogenic diet at the time). Insufficient energy is one of the most reliable drivers of adrenaline production, yet adrenaline has a potent effect on reducing appetite (which contributes to a further self-perpetuating cycle).
The over-arching narrative that connected the patterns we saw in Caroline’s case was a lack of resources and a lack of subsequent investment (most notably in the digestive tract). Digestion accounts for around 30% of all our energy requirements each day, yet does not actually help keep us alive today (and thus is ripe for ‘disinvestment’ when energy resources are limited and survival tasks need be prioritized). One of the major problems we had here was that the disinvestment in digestion was resulting in an inability to digest foods, but also permitting dysbiosis and oxalate issues (the latter can be driven by a lack of bile availability as well as increased yeast activity), and these inflammatory triggers appeared to be affecting mitochondrial performance and therefore forming a self-perpetuating cycle. This cycle appeared to be further magnified by a lack of adrenal activity (which means less control of inflammation, placing further energy burdens on a system in the midst of an energy crisis, and less control and the stress response, leading to further redistribution of available resources and further production of adrenaline).
Initial Recommendations / Removing Obstacles
It was clear that support should focus on breaking these cycles, both in reducing the activation of the stress response (adrenal support), supporting digestion (both to help regulate yeast populations and subsequent inflammatory burden/contribution to oxalate formation, but also to support appetite) and eliminating the obstacles that limit mitochondrial performance (limiting inflammation, providing necessary nutrients and ensuring that there were sufficient calories/carbohydrates). This would allow a more ‘fair’ assessment on where Caroline was actually at, although we also need to be on guard for two legacy events: feeling like a zombie when her adrenaline levels finally dropped (nearly certain when we see signs of adrenaline resistance) and the emergence of ‘new’ hormonal imbalances once we reached the threshold needed to restart investment in the ovarian activity (this reliably sees estrogen levels rise but we can never determine what sort of patterns we will encounter, and whether progesterone will rise with it, until we cross this bridge).
Carnitine – permits effective use of fats in the mitochondria. Vital to ensure optimal energy production but especially so whenever there are blockages in using carbohydrates.
Magnesium – involved in 600 different reactions around the body, but especially important in muscular relaxation, hydration, energy production and regulation of the stress response.
Zinc – key in hormonal balance, immune function, healing and neurotransmitter balance. Providing in a balanced formula (that includes copper) to avoid accidental copper deficiency (which would be doubly costly whenever there are mitochondrial problems).
Increased-calorie, low-oxalate diet – although other steps were vital to support a number of key pathways, we could not expect much improvement until we had achieved ‘energy security’. If signals of insufficient energy remain, this obligates further stress responses in an attempt to increase energy availability in the bloodstream. I also recommended that the vegetables Caroline include focus on low-oxalate vegetables to avoid further accumulation of oxalates and the inflammatory problems they can drive.
Digestive Enzymes and Swedish Bitters – although the management of the stress response is always key in permitting investment in the digestive response, this can be further supported with Swedish Bitters. Digestive Enzymes provide all-round support for each step of the process.
Calmer, sleeping better but feeling uncomfortably tired and moody – eating more and mitochondrial support (Carnitine and Magnesium) reduced the need for the stress response, while adrenal and neurotransmitter support (Licorice and Magnesium) helped calm this stress response further. This is pleasing from a therapeutic perspective, but can often see individuals feel entirely different to what they have become accustomed too.
Weight gain – another common feature following years whereby adrenaline has been played a crucial role in a) maintaining energy usage at the mitochondria and b) in liberating energy from fat cells. It is vital to reduce activation of the stress response (so that we can engineer a more balanced investment of available resources) but doing so guarantees a reduction in adrenaline, at a time when adrenaline sensitivity has already been reduced. It often takes 8-12 weeks of adequate feeding/low stress schedule until adrenaline sensitivity returns to a healthy baseline.
Hormonal symptoms – we were expecting the appearance of hormonal symptoms once activity in the ovarian axis was once again permitted. These duly arrived after a couple of months, manifesting as painful periods, intestinal bloating, a return of oedema (not experienced since she was regularly menstruating in her early 20s) and headaches pre-menstrually.
Overall, Caroline showed classic ‘start-up’ responses, which are particularly likely following a long period of low energy availability (and the adrenaline that comes with this). Many metrics were improved (HRV had leaped from being consistently in the low 20s to now bouncing around between 30 and 40 rMSSD), we saw a pleasing reduction in adrenaline-associated patterns, but the transition was tough. This was the case even before estrogen production kicked in (feeling like a zombie, much more emotional fluctuations now that adrenaline was not there to have a numbing effect) and even more so when hormonal activity returned.
Secondary Steps / Further Customization
We ran a hormonal panel, which showed that estrogen had gone from being particularly low to now being high. Progesterone levels were still low. It is common to see high estrogen levels whenever there is low activity at one particular estrogen receptor (the alpha receptor), which is necessary to register estrogen status at the brain; if this feedback is inhibited, then the brain requests more estrogen than is needed. This results in high estrogen levels in the circulation, which can now cause mischief at the beta receptors, which are found at the endometrial lining (heavy periods), neurotransmitter receptors (low mood/agitation) and fat cells (increased fat storage). Cortisol levels, insulin signalling and endotoxemia can downregulate the alpha receptor; it generally the case that such a set-up was already in place but was ‘masked’ until stress levels were sufficiently controlled and investment in ovarian activity was once again permitted. Restoring sensitivity at the alpha receptor was therefore a priority, which meant focus on the cortisol, insulin, inflammation and endotoxemia picture was warranted, together with direct modulation of the receptors themselves.
However, we needed to temper some of our expectations as it can take six months for stored oxalates to leave the body (and thus, six months until their inflammatory effect has been eliminated). Equally, it is commonly the case that periods can take several months to stabilize; this means that it is a rational choice to refer out to the doctor to discuss hormonal (progesterone) support, but it is also rational to give the body time to adjust (which tends to mean compensating for undue symptoms). Caroline wanted to see how her body adjusted, and therefore we discussed options to provide temporary support to help handle the headaches.
The role of stress still stood out as central in the picture (stress remains the most powerful driver of endotoxemia). All the signs of high adrenaline had now abated, although this had unmasked issues that were previous hidden, with its numbing effect now missing (leading to increased emotionality, especially anger, and conflict over maintaining her calorific intake) and its fat-burning effect also measurably absent (contributing to weight gain). It was also evident, from the patterns Caroline was noticing and from her HRV measurements, that she was in a ‘halfway house’ and that there were still further steps called for to fully transition into a state that was nor compromised by excessive activation of the stress response; energy stress was no longer a problem, but she was now increasingly stirred by emotions (that was not the case when adrenaline was high). I suggested that Caroline work with a somatic practitioner to aid in the transition to this ‘novel’ inner state and, meanwhile, provided herbal support to partially compensate for the reduced breakdown at fat cells as well as a change of diet, with the aim to reset insulin sensitivity.
We also considered the role of the gut lining and how increased permeability here may further contribute to the endotoxemia (and, as a result, the imbalance at estrogen receptors).
Ginkgo Biloba and Damiana – both particularly helpful to support blood flow during inflammatory states. Caroline felt an improvement in mood at baseline and no longer got any headaches pre-menstrually.
Ketogenic diet, Gynostemma, Xanthohumol – introduced to support insulin sensitivity and responsiveness at fat cells. Caroline was not exactly a fan of the ketogenic diet but neither did she feel uncomfortable on it. She initially struggled to get into ketosis, and dietary analysis showed she needed a minor adjustment (a reduction in protein intake). While this helped, it did not yield sufficient ketones. Further discussion revealed that she had noticed some loose stools, to which we ran a repeat blood test for ALP (which still read low, highlighting the likelihood of poor bile flow). We responded with Gentian Root and Taurine. She quickly saw an improvement in both comfort and in ketone readings, and her weight stabilized (although did not drop) after four weeks on this protocol.
Charcoal, Aloe Vera and Marshmallow/Gamma-Oryzanol – brough in to support integrity of the gut lining. We trialled several different items with different mechanisms but these were the ones that all impacted on Caroline’s sleep scores (which we tracked with an Oura ring).
Further Responses & Finishing the Job
Once we had applied the above, we saw a pleasing improvement in many areas. Caroline now digested foods well, had ‘decent’ energy across the day, no longer had slumps in the afternoon and had more resilience generally. She chose to use a cyclical ketogenic diet (typically four days of ketogenic eating, following by three of carbohydrate-based) and maintained progress. However, there was clearly some way to go: she still experienced hormonal symptoms (intestinal bloating was now gone and pre-menstrual headaches were handled, but the oedema and painful periods had dropped in intensity but were still present), was yet to lose any weight and her HRV readings were refusing to budge (consistently lingering in between 30-40). The connections between these factors made sense, and I had already explained to Caroline that, in years of tracking this, I am yet to see anyone struggling with their weight achieve their goals until their HRV settles into the 60-80 zone. As long as there is ongoing activation of the stress response, their will be the opening of the gut lining and therefore the endotoxemia that not only ruins energy signalling (tricking the hypothalamus into thinking that the individual is at risk of starvation, and must therefore restrict energy usage and encourage fat storage whenever possible) but also impacts on the activity of the estrogen receptor alpha (which then sees increased stimulation of the ovaries, more estrogen in circulation and more estrogen-related issues).
Caroline felt the effect of this support straight away (this is common when I do follow-up Organic Acids test, as we would expect when we’ve removed metabolic obstacles that would previously have limited response). She then began to lose weight; once this began, it was an almost linear journey of around 3kg weight loss a month for the next four months, before stabilizing at around 65kg. This was while following an identical protocol to that used in the months leading up to this change, speaking to the importance of the internal signals in retaining/releasing energy.
It was clear that something had to budge. We undertook a stool test to rule out anything that was blocking Caroline’s progress and attempted to remediate the imbalances shown (without seeing much improvement, as is almost always the case when an individual has low resources). We trialled neurotransmitter support (to support calm, focusing on GABA, serotonin and choline pathways) but again without success (although Lithium did a good job of further improving sleep, so this was kept).
A combination of hormonal support and somatic work achieved the breakthough: Caroline engaged in somatic experiencing, a ‘body-mind’ approach that uses the body to both generate key sensations and compel rewiring in areas of the brain that reflexively activate the system in response, and found that this was helpful. We saw movement on the HRV scores (with much more fluctuation than before) and changes on the frontline too. However, we also then added a specific hop extract to enhance alpha receptor activity and Resveratrol to enhance upstream signals that would play a role here. This had the desired effects on hormonal patterns but perhaps its biggest contribution was in allowing Caroline to get better results from her somatic work; she relayed how, from the first session she had since adding these items, she was able to ‘stay with’ many of the exercises, felt more joy/anger/etc and had wilder dreams in the nights following each session and, very importantly, her HRV measurements finally broke through their previous ceiling. She saw some weight loss for the first time, noting a drop of around 2kg.
Over the coming months, Caroline felt better and better. Her HRV measurements now averaged in the high 60s, with some days peaking even in the 90s. We ran further anti-microbial steps and, despite this approach following a similar path to previously, this time there was a stronger response to the introduction of anti-microbial herbs and a measurable reward on the other side of this. She saw improvements in her stool quality. On the other side of this successful intervention, we then repeated the Organic Acids test. This showed her to be a very different place than before, with a couple of new shortages now apparent: Carnitine and B6. We duly supplied both.