The ‘Everest Effect’ and Why No Protocols Work for You

The mitochondrial hypoxia I find in 80% of cases—and the simple test that reveals it

Like many, I’ve always maintained a healthy scepticism when I encounter any article that runs with the classic ‘everyone is doing it wrong and here is the solution’ format. However, while there is a flavour of this in this article, I think it’s helpful to point out three key differences between these ‘one simple solution’ tropes and what I’m sharing below, which are:

• The perspective I share below is not based on dogma or what feels right, or from an assessment of the research (and basing a verdict on which hypothesis has the best support in the available scientific literature). It is based on all the available evidence, including years of studying the entire evidence base, continuous digestion of the principles handed down to us by traditional healing systems and, most of all, from the frontline results I’ve recorded over 20 years (including the analysis of 13,500 functional test results)

• The patterns I speak of can be easily measured in an Organic Acids Test, a test that anyone can access

• the principles I speak of here are not revolutionary, and align with those used successfully for thousands of years and the fundamentals of human physiology

But first, some background. In my clinical practice, beyond the athletic population, I primarily serve two groups: people working toward sustainable weight optimization and those managing chronic, interconnected health challenges. These seemingly different populations share a remarkably similar set of experiences:

• The nutrient protocols that gave their social circle dramatic improvements produced minimal or negative effects

• Stress-reducing supplements either don't register or create unwanted activation

• The paleo diet that influencers rave about left them foggy, irritable and caused digestive chaos

• Their new-year-new-me workouts led nowhere but a state of exhaustion in the days afterwards

• Somatic work and meditation don’t work and just seem to cause agitation

Does this pattern resonate?

If so, it’s vital to stress that these interventions don't fail because you're ‘treatment-resistant’ or have ‘bad genes’ (although it is inevitable that you may feel this way). They fail because your body is functioning exactly as evolution designed it to, given the resources available.

And this speaks to the crux of the matter. When cellular energy reserves are insufficient, your metabolism activates ancient survival programming that blocks investment in any biological process that's resource-intensive but doesn't directly impact immediate survival. Your body isn't malfunctioning; it's executing millions of years of evolutionary wisdom that prioritizes staying alive today over feeling optimal tomorrow. Evolution has rewarded metabolic responses that ensure survival, even when those responses create fatigue, brain fog, and malaise (and block any response to intervention).

Put another way, I invite you to imagine you are in the middle of an assault on Mount Everest. You’ve woken at 5,500m and, as you boil up water from the stove, you notice your lungs working overtime. Your heart pounds as you stuff away the sleeping bag. As you pack away the tent and take your first steps outside, each movement feels weighted and you try your best to override the bone-deep fatigue that grips you… does this feel like a good time to do a ‘gut cleanse’? Does this feel like a suitable moment to start a new medication? Does this strike you as a fair environment to assess the effects of a new protocol?

This is the Everest Effect. And the key thing here is that a huge swathe of individuals are going about life with the exact same physiological deficits, wondering why they never respond to protocols the way they should. The only difference is that they are subject to the same cellular conditions regardless of their altitude.

The Real Bottleneck: Mitochondrial Oxygen Starvation

The fuel in question isn't glucose, fat, or even ATP directly. In most cases, it's oxygen availability at the mitochondrial level. Specifically, oxygen getting to where it's actually needed: inside your mitochondria, where it serves as the final electron acceptor in energy production.

For around 80% of those who cannot lose weight and individuals with complex/chronic illness, this oxygen delivery system has broken down in a very specific and predictable way. This mitochondrial hypoxia (often referred to as ‘pseudohypoxia’) is the key to understanding why you feel like your body is fighting against every attempt to help it, and why the path forward requires a break from the ‘Evidence-Based’ protocols. While it’s theoretically correct to say that studies do indeed show a benefit for a whole multitude of different approaches, the key issue is that these studies were almost certainly undertaken on a population without such challenges. As a result, any conclusions simply do not apply to you.

This speaks to a cornerstone of personalised medicine, which centres on the key question: what do you need to have a fair chance of responding the way you should? While there is never just one thing that people need to address, it comes down to this: I run an Organic Acids Test on every single individual who comes to see me and, in these circumstances, a full four-fifths of people show this pattern on their Organic Acids Test; low aconitic acid, without any rise in lactic/pyruvic acid.

Low aconitic acid is the hallmark sign of mitochondrial hypoxia, while lactic/pyruvic acid rise whenever the hypoxia response is deployed (thus, the lower levels of these metabolites shows us that no such response is occurring). 20 years of doing this shows me very clearly that people with this issue will never ever get the responses they should until they deal with it.

But first, let’s understand it. What follows is the step-by-step cascade that traps millions of people in a state where healing becomes nearly impossible—and more importantly, what can actually be done about it.

The Cascade of Mitochondrial Hypoxia

Step 1: Initial Electron Transport Chain Disruption

The crisis begins at your cellular power plants—the mitochondria. If the mitochondria is the furnace, then the electron transport chain (ETC) is the ‘conveyor belt’ that passes food energy (in the form of electrons) to the furnace so that they can react with oxygen, doing so to generate ATP (cellular energy). When this system runs smoothly, electrons flow orderly from Complex I through IV, with oxygen waiting at the end to react with them.

But various stressors—infections, toxins, nutrient deficiencies, chronic stress—can cause electron leakage at Complexes I and III. Instead of flowing neatly to oxygen, electrons escape prematurely and react with whatever molecules they encounter, creating reactive oxygen species (ROS). This is a known feature of the condition often labelled as chronic fatigue syndrome (although is not exclusive to this condition).

This is a twofold problem. Not only are you producing less energy (ATP) for the cell, there is the generation of these cellular insults.

Step 2: Copper Uptake Failure (The First Vicious Cycle)

As one of the triumphs of 2.7 billion years of mammalian evolution, the biochemistry of the body and the mitochondria is as elegant as you might imagine. As such, the electron transport chain doesn't just produce energy—it communicates what is happening at this critical junction, and send signals back to other areas of the cell to co-ordinate the delivery of resources needed to continue performing this function. One such message involves retrograde signals to increase uptake of copper (a nutrient that is key in using oxygen). In essence, these signals say “energy production is running smoothly, upload more resources."

When electron flow becomes disrupted, this signalling breaks down. Specifically, copper uptake becomes impaired—both from the gut and into cells. This creates an immediate vicious cycle:

• Less cellular copper means less efficient oxygen utilization in mitochondria (copper is essential for Complex IV on this electron transport chain)

• Poor oxygen utilization means less efficient electron flow

• Reduced electron flow means even less copper uptake signalling

• The cycle perpetuates and worsens

[note: this is why many individuals start eating copper-rich foods – like liver - yet, despite the amazing results reported by other citizens of the internet, they don’t see it and their serum copper levels don’t budge on testing. Providing copper is essential but we need to ensure there is a fair chance to make use of it].

Step 3: Oxygen Rerouting and False Sensing

With mitochondrial oxygen utilization compromised, something predictable happens: oxygen that should be consumed by mitochondria accumulates in the cytoplasm (the main cellular space). This is the opposite of what should happen—cytoplasmic oxygen levels should be very low.

Why is this ‘rerouting’ of oxygen so important? Because your cells have ‘oxygen sensors’ (PHD, or prolyl hydroxylase domain enzymes) but they are located in the cytoplasm. If there is a lack of oxygen at the mitochondria and only a small amount of this leaks out, the cytoplasmic concentration indicates that all is good. The oxygen sensors conclude that plenty of oxygen is available and limit further entry. They fail to trigger the hypoxia-inducible factor (HIF-1α) response—your body's primary mechanism for increasing oxygen delivery to tissues.

Step 4: Iron Mismanagement Amplifies the Problem

Remember that copper deficiency from Step 2? Copper is not just essential for proper oxygen utilization, it’s also crucial for proper iron management. Without adequate copper, the copper-dependent enzyme ceruloplasmin cannot adequately convert iron from its highly reactive ferrous (Fe2+) form into the ‘safer’ ferric (Fe3+) form.

This excess ferrous iron makes the PHD enzymes even more reactive, as it has evolved to limit oxygen uptake when there is excess iron (oxygen + iron = rust… your cells do not want to be rusted). This is a sensible and clever step, except we see big problems when these oxygen sensors are already running on an inaccurate signal (due to the ‘leak’ of oxygen into the cytoplasm).

The result? Further limitation on oxygen uptake and a deepening of the oxygen crisis.

Step 5: The Nitric Oxide Depletion Trap

Under normal circumstances, your cells have an elegant fail-safe system. When nitric oxide is produced in mitochondria (which competes with oxygen and reduces energy production), an equal amount of nitric oxide should be present in the cytoplasm. This cytoplasmic nitric oxide competes with oxygen for binding to the PHD enzymes, essentially "blinding" them so they can't detect the false oxygen abundance signal.

This triggers the appropriate hypoxia response, increasing oxygen delivery and correcting the problem.

But in the ROS-rich environment created by electron transport chain dysfunction, cytoplasmic nitric oxide gets rapidly converted to superoxide. The fail-safe system breaks down. There's no longer much nitric oxide to compete with oxygen at the PHD enzymes (the ‘oxygen sensors’), which are already receiving more oxygen than should be the case and already boosted into over-regulation by iron mismanagement.

Even less of the HIF-1a signal (the hypoxia response) is permitted, even less oxygen enters the cell, and the cycle escalates further.

Although the mechanics driving this are obvious very different, the lack of oxygen availability at the mitochondrial electron transport chain – the area where the body uses oxygen to form energy – now perfectly replicates the same limitations and cellular consequences found at altitude.

The Perfect Storm: Why This System Collapses

This oxygen crisis doesn't happen in isolation. Put the system under stress and it will normally handle it. Push it under sustained stress and then gradually hobble the very structures it leans on in these times, and we see the problems I describe here. They are triggered and perpetuated by specific, identifiable causes:

Stress and Endotoxin Translocation

Chronic stress triggers a fascinating survival mechanism: it opens tight junctions in the gut lining to increase absorption of sugars and salts, providing quick energy for fight-or-flight responses. Unfortunately, this same mechanism allows endotoxins (LPS) from gut bacteria to enter circulation.

These endotoxins trigger massive inflammatory responses and promote inappropriate nitric oxide production in mitochondria. This nitric oxide directly competes with oxygen here, impacting on oxygen usage and, thus, on energy production. This is one of the costs of the stress response, and doesn’t tend to cause any major issues if it is used occasionally. However, over-usage of the stress response – extremely common in the productivity cult we call modern society – means that there can be an ongoing stream of endotoxins and an ongoing limitation on oxygen availability. Many people can keep some sort of balance on this, providing that they have sufficient cortisol activity to regulate this nitric oxide release and to turn off the stress responses as soon as they are no longer required… but…

Impaired Cortisol Activity

Your adrenal system evolved to handle acute stressors with cortisol spikes followed by recovery periods. But chronic endotoxin exposure creates a different problem: excessive/sustained activation of the stress response results in excessive influx of endotoxins. As well as driving inflammatory activity, these endotoxins downregulate cortisol receptor activity.

This is big. Why? Because, with less cortisol activity, you cannot turn off stress responses effectively. You cannot control inflammation, including the nitric oxide that is being formed by these very stress responses (this contributes to why a decent proportion of individuals, most notably those with a ‘ME/CFS’ label (or indeed ‘adrenal fatigue) see my article here) a steep drop in cortisol production, as cortisol is formed in the mitochondria of the adrenal cortex so is just as sensitive to limitations as energy production is).

We again find ourselves focusing on the role of chronic stress – regardless of the cause of such stress – in that, if we cannot break this cycle, we will see increased metabolic costs for each episode of stress, with such costs leaving us less able to regulate inflammation and effectively (both factors that are extremely stressful for the body… cue further stress response… and repeat).

Mitochondrial Nutrient Blockages

Even without the oxygen delivery crisis, mitochondria require specific nutrients to function. Common deficiencies that directly impair energy production include:

• B1 (thiamine): Often depleted by mold exposure or high-carbohydrate diets

• B2 (riboflavin): Commonly deficient due to gut microbiome imbalances

• Magnesium: Universally deficient due to soil depletion and stress-induced losses

• Copper: Requires adequate liver consumption (which is rare in modern diets)

• Carnitine – commonly low on low-meat diets and production disturbed when methylation is affected, also in liver/kidney issues

• NAD+ - depleted in inflammation or via excess sugar intake (or sugar spikes due to adrenaline)

I’ve noted the above because they are so common, these are not the only issues we run into. In any case, testing is important; while I can easily see the expected patterns in anyone who is experiencing mitochondrial issues, I can’t know exactly which step of energy production is affected (and thus, which specific agent is called for). We always want to address both oxygen issues and any adjacent blockages; this is because anything that limits energy forces the body into more of a stress response in an attempt to get enough energy into circulation (and, as I hope I have made clear above, limiting this stress response is essential).

The Self-Perpetuating Trap

The cruel irony is that low energy drives the system deeper into stress responses, creating more opening of the gut lining and more endotoxin translocation precisely when the person has the least capacity to handle it. Amazingly, a decent number of people will feel ‘kinda sorta’ OK despite these challenges. However, they will need especially high cortisol output just to maintain basic function—they're running their stress response system "overtime" to stay afloat (recall that lower receptor response calls for extra high output to compensate).

What’s key here is that these individuals cannot afford any reduction in cortisol or any additional stressor. They're living on the edge of their compensatory capacity, which explains why seemingly minor triggers—a virus, a stressful event, exposure to mould—can cause complete systemic collapse.

Why Treatments Fail: The Resource Problem

Now you can understand why, regardless of how well-sourced the anti-fungal herbs were and no matter how many billions of viable the probiotic mixture, that anti-candida cleanse was never going to work. Even if the herbs were picked and blessed by Himalayan virgins and you got hold of a super-mega-potent source of a clinically-proven probiotic, your nervous system is obligated to reduce investment into the gut for as long as the energy emergency continues. This impacts on the conditions and makes it impossible to bring about the changes we want to see here.

It’s why SIBO (Small Intestinal Bacterial Overgrowth) is often considered ‘hard-to-treat’ and why so many feel hopeless that they will ever get bloating under control. Same goes for detoxification; it’s a very energy-intensive process and one that can go highly off-track if phase 3 detox is shut down (spoiler alert: it’s always shut down during energy emergencies).

Hormonal interventions often generate some initial response but, aside from post-menopausal interventions (different discussion), what we’re talking about here is altering signals in how the body uses its resources. There are corners of the internet that pin their mast to the idea that ‘its all thyroid’; this often initiates a long-and-winding journey towards the promised land of an appointment with a doctor who will prescribe T3. I’ve seen a several cases where this was indeed a missing link but, for many more, this is forcing the body to spend the one resource it is running dangerously low of. It doesn’t end well.

“Eating clean” is fine. But this often means removing junk and not replacing it. Which means eating less. Which means big problems and more adrenaline release.

In general, therapeutic interventions require cellular resources to implement. They work by changing how your metabolic pathways and organ systems use their energy. But the human body is exquisite in prioritizing tasks and always prioritizes survival (and if these means blocking activity in the pre-frontal cortex or limiting the metabolic rate to achieve this goal, then it will do just that).

It’s not that the ‘usual’ advice is wrong. There’s often sound logic and solid research behind it. But it forgets one crucial factor: your body has evolved to prioritize survival and it is categorically engineered to block investment in any pathway while dealing with energy emergency.

Here's why these specific issues stand out as particularly incompatible with generic protocols (“you add this amount of the supplement for the first week, then move onto the next stage on week 2” etc) or trial-and-error supplementation (“low on energy? Green Tea Catechins have been shown to increase ATP production by 35% and we’ve got the best one”, etc).

The Route Back to Base Camp: Giving Your System a Fair Chance

Step 1: Support adrenals

The adrenal system is there to help our system maintain resilience during stress. Its purpose is to help maintain allostasis in the face of these insults and is therefore not coincidental that we drop further and further into this cycle in line with reduced cortisol activity.

Adrenal support therefore stands out as a priority in helping to restore regulation to the metabolism. Licorice Root helps boost cortisol availability, while adaptogenic herbs (such as Rhodiola Rosea, Ashwagandha and Korean Ginseng) help restore cortisol sensitivity at receptors.

It’s important to note that Korean Ginseng is, on paper, an ideal solution (as it also has impressive effects in regulating nitric oxide formation and supporting circulation in the central nervous system) but the combination of these effects can be highly activating. Also worthwhile noting that anything that supports cortisol will reliably lower activation of the stress response and, with it, lower adrenaline release. This is important because many of us will notice an ‘intolerance’ of the inner state that we encounter when adrenaline drops after it has been excessively high for long periods of time…

Step 2: Retrain (Detrain) Stress Response

… and this is where handling stored stress is vital. When I speak of stress (a term that comes with a lot of cultural baggage), I am referring to the gap between the resources you have and the resources we need. The bigger the gap, the bigger the stress response needed to bridge it.

We have two alarm centres in our nervous system, the amygdala and the brain stem, which help launch reflex responses to ensure we have access to enough resources to meet perceived demands. If a tiger jumps in through the window, these alarm centres wisely conclude that there is a need for a massive amount of resources (and thus, there is now a massive gap between what we have and what we need). The result is a massive stress response, and one that occurs reflexively.

The reflexive nature is key. These zones have been rewarded by for the speed of their response rather than the accuracy, and so these must occur via Pavlovian associations. However, the downside of this design is that, if we have any out-of-date associations still in play, then this can see these alarm centres react to sensory inputs that do not actually call for the need to flood our system with adrenaline and glucose. This is why it is so common to hear from individuals whose HRV scores stay in a deep sympathetic state (eg. 20-30 rMSSD) no matter what they do.

Somatic approaches, and conscious connected breathwork in particular, can be fantastic to avoid the usual physiological hijack that would occur when bringing our attention to the sensory signals in question (a hijack that is designed to thrust our attention outwards to better react to threats). This is important, as this outward focus physically disconnects us from our internal environment (meaning we cannot access or process the content). Staying ‘internal’ allows us to process the content in a way that sees it moved from the implicit memory network to the explicit memory network. This means that the alarm centres no longer have the opportunity to react to it in the same way (and no longer launch unnecessary, round-the-clock stress responses).

One note here: most people will find limited benefits from these approaches unless they have also provided basic metabolic/adrenal support (which helps lower output of adrenaline, another factor that forces our attention outward).

Step 3: Identify Specific Mitochondrial Blockages

An Organic Acids Test (OAT) reveals your individual pattern of metabolic dysfunction. It tells us, which specific nutrients are limiting energy production, whether oxidative stress management systems are overwhelmed, if inflammatory triggers are creating ongoing cellular damage and whether neurotransmitter imbalances are impacting on mood and our ability to benefit from the somatic work described above.

Rather than generic protocols, this allows for precision interventions targeting your actual bottlenecks.

Additionally, it’s worth noting that it's good practice to run a full copper iron panel (available as a blood test) for all humans but especially crucial in these cases, given the interplay between copper, iron and oxygen.

Step 4: Eat Enough

I know, it sounds simple. Yet this is a stumbling block in more than half of all individuals that I work with. Adrenaline has a potent appetite-suppressing effect. Digestive disturbances also reliably curb hunger. This helps explain why so many individuals on long health journeys come in eating a surprisingly low amount each day (surprising for them, at least). Some individuals may also have complex dieting history and find themselves anxious about the idea of eating enough after becoming habituated to limiting calories for so long. This can make things more complex.

The above factors speak to how, as in every other area, we need to consider what obstacles may stand in the way of any given individual in getting enough food. However, as simple as it sounds, there is no possible way to generate a state of energy security if there isn’t enough energy coming in.

Step 5: Add tactical interventions specifically for mitochondrial hypoxia

There are a number of agents that can be helpful in these circumstances, although it is worthwhile sharing that these additional steps tend to help only after the first three steps have been actioned.

Including options that fall outside the scope of nutritional therapy, these approaches centre on:

• Improving oxygen usage at the electron transfer chain (red light, Co-Q10, copper, melatonin, methylene blue, avoidance of seed oils)

• Improved HIF-1a activation (cordyceps)

• Inhibit/neutralize nitric oxide (hydroxocobalamin form of B12 and, at a later date, various polyphenols (such as curcumin, those in green tea, etc) and alpha lipoic acid)

• Supporting endoplasmic reticulum activity (this plays a supporting role in mitochondrial bioenergetics, but a very important one)

• Supporting antioxidant status (Liposomal Glutathione, Vitamin C, E, and ‘true’ antioxidants like lycopene and astaxanthin)

Step 6: Rest (The Hardest Step)

The most important intervention is also the most difficult for most people to implement: genuine rest. Not productivity-focused "self-care" or scheduled relaxation, but actually reducing the energetic demand on your system.

This is challenging because almost everyone in the modern world carries unprocessed sensory signals and emotional material that only emerge to awareness when adrenaline drops. People often feel worse initially when they try to rest genuinely, which creates a compulsion to return to familiar busy-ness or stimulation.

But without this foundational step—allowing your system to shift from survival mode into recovery mode—no amount of supplements, therapies, or protocols will create lasting change.

Step 7: Deal With What’s Left

While I will see reliable changes from doing the above – yes, even in those that ‘never respond to anything – it is inevitable that there will be some legacy burdens that need attention. These vary from one person to the next, but the overbearing pattern here is that individuals can now deploy the very same steps that have previously failed and actually benefit from them.

Reminder: Energy Metabolism Governs Everything

One thing that I want to stress is that, while it is easy to consider the Everest Effect as a ‘just a mitochondrial thing’ – something that is relevant for fatigue and weight loss but not a big deal outside these areas – it is a big deal for pretty much any process in the body.

This is because the human body prioritizes energy management above all else. Anything that has such a profound effect on the energy status of cells will force a robust shift in function across a wide range of pathways and organ systems.

We see this play a central role in all manner off challenges, such as:

• Anxiety: low baseline energy forces the body into a pronounced stress response. The ‘fight-and-flight’ response involves a potent release of adrenaline, which both triggers the release of emergency energy from storage and makes us wired/over-activated.

• Cardiovascular Health: the raised adrenaline spikes our blood sugar levels (something that we ‘pay double’ for when there is impaired mitochondrial activity; this is a situation where there are particular high sugars in the bloodstream but reduced disposal in the mitochondria. This forces cells to limit their uptake to avoid the damage that occurs from attempting to hold too much energy, and they do so through downregulating the insulin receptor. This is insulin resistance. The excessive formation of ROS (reactive oxygen species) places all structures in the body under increased oxidative stress, which can have implications for the health of artery linings.

• Hair Loss: like all other cells in the body, hair follicles need energy. But its relevant that they are particularly sensitive to reduced availability of thyroid hormones and iron. Our systems naturally downregulate the formation of T3, the active thyroid hormone, when sensors pick up on low energy availability (a situation that can be described as running an ‘economy mode’. Iron dysregulation is particularly common in these scenarios, with our systems designed to limit iron availability to avoid excessive ‘rusting’ (with the cost being an iron starvation at sites that need it).

• Inflammation and Autoimmunity: the excessive formation of ROS promotes cellular injury; while such insults are part and parcel of human existence, the increased rate of insults forces an ongoing inflammatory response (in a bid to repair any damage). Equally, the forced stress response dictates the withdrawal of vagal tone, important because the activity of the vagus nerve plays an important role in dampening inflammatory responses. But the most important connection here is how any round-the-clock stress response drives the opening of the gut lining, which allows the flux of endotoxins from the gut into the bloodstream. These endotoxins drive a potent inflammatory response, regardless of the quality of the diet or other anti-inflammatory measures we deploy.

• Mast Cells: the stress response and mast cell overactivity go hand-in-hand. This is because, whenever our hypothalamus detects any gap between the resources we have and the resources we need, it launches the stress response to bridge it. This starts with the release of CRH, which initiates a cascade of events that we collectively term the stress response. However, mast cells also have receptors for CRH and launch a defensive response whenever it rises (with MCAS diagnoses now inevitable).

• Focus, Mood and Concentration: there are many factors that influence our ability to concentrate and think clearly. Dopamine is one of the primary influences here. However, energy status and dopamine formation are intertwined (which makes sense, when we consider that dopamine’s evolutionary purpose is to generate motivate to take action on things that are good for our future status but call for usage of our current energy resources). In short, our system wisely downregulates cognitive performance to increase survival odds. Add to the disproportionate effects on cognitive activity – brain cells require 16x more energy than an average human cell – and the effects that adrenaline has on reducing activity in ‘non-emergency zones’ (think reasoning and language), and we have a situation that is guaranteed to leave someone feeling foggy and unable to benefit from the usual dopamine support (and other ‘cognitive enhancing’ supplements).

• Hormonal imbalances: the investment into the hormonal axis is tightly linked to both energy status and the stress response. When our systems invoke a stress response, there is automatic downregulation in the HPGA (Hypothalamic-Pituitary-Gonadal Axis). In men, this plays out fairly reliably in the form of low testosterone. In women, we see the same reduced investment but can see this manifest in a number of ways. In many cases (in pre-menopausal women), this will see insufficient stimulation to ovulate effectively; this means no fair chance for the rise in progesterone (and therefore the infamous ‘estrogen dominance’ pattern). A more complete disinvestment results in estrogen falling too (and, with it, a disappearance of periods). It’s also relevant that the stress-induced flux in endotoxins reliably messes with the sensitivity of certain estrogen receptors while sparing other types (resulting in excess estrogen activity at some parts of the brain and body, with the consequence being mood disturbances and a characteristic ‘estrogen-type’ fat storage).

The effects of mitochondrial hypoxia do not stop here but I hope the take-home message is clear: there is no aspect of human metabolism that is spared in these circumstances.

"But I've Already Tried Functional Medicine / Naturopaths / Specialists..."

If you've worked with practitioners before without success, it's likely because they were trying to ‘boost’ a system that was stuck in survival mode. Some of these will do nothing (think mitochondrial boosters that do not influence the rate-limiting step), some are destined to make things worse (think energy-intensive procedures, like detox procedures and gut cleanses) and some are a crap shoot that do actually help some of the time and cause chaos at others (think low-carb, vegan, paleo-type diets).

When I last counted, the average number of practitioners my clients had seen before me was 7.5. I’ve seen a lot of chronic/complex cases.

It has become clear that most functional medicine approaches have been corrupted by the allure of Evidence-Based Medicine™, a set of paradigms that assume that there is a ‘best’ treatment for any given label, ignoring the interplay of various mechanisms that can produce the same set of symptoms in different people, and concluding what makes up these ‘best’ treatments on the basis of the average responses generated from isolated interventions (measured in trials on participants whose metabolic burdens vary greatly from yours). One of the primary paradigms of this approach is to explicitly ignore any sources of evidence that are not Randomized Controlled Trials. Expertise and basic scientific principles are deliberately excluded from any analysis.

The testing I use and the sequence of interventions follows the actual physiology of how these systems recover, employing functional tests but using them within the framework of principles that are universal across all healing systems that have survived the test of time and while respecting the elegance of human metabolism.

In short, we systematically assess what your system needs to have a ‘fair chance’ and then build a realistic map of what specific steps are needed to achieve this.

Next Steps:

If this resonates with your experience, the next step is determining exactly where your system is stuck and what sequence of interventions will work for YOUR specific challenges.

1. Get an Organic Acids Test and work on the results with your existing practitioner. My newly-launched Lucid Labs project offers a range of functional tests, including the Organic Acids Test discussed in this article, and includes a personalised interpretation in the list price. This is a urinary test that you take at home and measures over 50 markers across different zones of the metabolism, which include the mitochondrial energy pathways. Find it for the US here and the UK here.

2. Work with me. I work with a limited number of clients one-on-one to:

• Identify your what is limiting your metabolic resources (we will see the pattern discussed above in around 80% of cases, but testing will determine exactly where the rate-limiting factor is)

• Determine whether you're in sympathetic or parasympathetic stress (using this to both identify suitable milestones and to know ahead of time what challenges you may face when the nervous system switches on energy investment in various systems)

• Create a personalized protocol that enhances your current resources rather than testing them

• Guide you through the recovery process so you know when you are on track (or not) and don't waste months on the wrong approaches

If you're ready to stop guessing and start with a clear roadmap based on your actual physiology, book a 15-minute call here to see if this approach is right for you.