The Science of Mitochondria & Benzo Withdrawal
Mitochondria & Benzo Withdrawal
Understanding Cause, Effect, and the Nervous System
By Coach Powes, Ph.D
Abstract
In recent discussions surrounding benzodiazepine withdrawal and protracted symptoms (often referred to as BIND), mitochondrial dysfunction has emerged as a proposed primary driver of symptomatology. While mitochondria play a critical role in cellular energy production and are responsive to physiological stress, this paper argues that mitochondrial changes observed in withdrawal states are more accurately understood as secondary, state-dependent effects of nervous system dysregulation rather than primary pathological drivers.
Introduction: Why This Conversation Is Happening Now
In recent months, increased attention has been placed on mitochondrial dysfunction as a potential explanation for the wide array of symptoms experienced during and after benzodiazepine withdrawal. Public discussions surrounding cases such as Jordan Peterson have amplified interest in biological explanations that extend beyond traditional models of neuroadaptation. For many individuals struggling with persistent symptoms, the idea that something measurable and cellular may be “wrong” offers both validation and a sense of direction.
However, as often happens in health discourse, a real and meaningful biological observation can become simplified into a totalizing explanation. The presence of metabolic or mitochondrial changes during periods of severe physiological stress does not necessarily imply causation. Rather, it raises a more important question: where do mitochondria sit within the broader hierarchy of nervous system function and stress response?
Understanding this distinction is essential, not only for scientific clarity but for guiding recovery in a way that preserves both accuracy and hope.
What Mitochondria Do: Clarifying the Biology
Mitochondria are intracellular organelles responsible for producing adenosine triphosphate (ATP), the primary energy currency of the cell. Beyond energy production, they are involved in calcium regulation, apoptosis, and the management of oxidative stress. Their function is highly dynamic and responsive to environmental input, including nutrient availability, hormonal signaling, and levels of physiological stress.
Importantly, mitochondria do not operate independently of the systems that regulate the body. They are deeply influenced by upstream signals, particularly those originating from the nervous system.
Changes in autonomic tone, stress hormone levels, and inflammatory signaling can all alter mitochondrial efficiency and output. In this sense, mitochondria are not static structures that become “damaged” in isolation, but adaptive components of a broader physiological network that continuously adjusts to internal and external demands.
The Benzo Concern
It is also worth briefly addressing why mitochondria have entered the benzodiazepine conversation in the first place. Some benzodiazepines have been shown to interact with a protein known as TSPO (the translocator protein), which resides on the outer mitochondrial membrane.
TSPO is involved in cellular stress signaling, inflammation, and steroid synthesis.
However, TSPO is not specific to benzodiazepines and is influenced by a wide range of physiological conditions, including chronic stress, immune activation, injury, and metabolic strain.
In fact, TSPO is commonly used in research as a general marker of neuroinflammation, not as evidence of a singular causal pathway.
As such, the presence of TSPO or mitochondrial involvement does not establish that benzodiazepines are causing primary mitochondrial dysfunction, nor does it explain the complexity of withdrawal states. Rather, it reflects the broader reality that the body is operating under stress, and that mitochondria, like many systems, are responding accordingly.
Moreover, the impact is downstream from benzo-induced neuroadaptation.
A cleaner mode is:
Benzo drug → GABA-A receptor effect → neuroadaptation/tolerance → withdrawal hyperexcitability/stress physiology → oxidative/metabolic/mitochondrial strain.
Much of this recent news about mitochondria and withdrawal stems from a social media buzz around Jordan Peterson's recent illness, and much speculation regarding the role his past psych med withdrawal may have played.
His daughter, Mikhalia Peterson, made waves with her questioning the impact mitochondrial damage may have had and its relationship with benzodiazepines. She interviewed a nutritionist who made some rather strong claims that are a bit overreaching and draw some powerful conclusions not supported by the science.
This created a flood of emotional reaction from much of the benzo community, as many saw it not only as another signal of the incredible impact these medications can have, but also as a way to further spread awareness about psych-med harm.
While I am deeply empathetic to this cause and would very much like to see more awareness in this area, I am cautious about jumping to conclusions with the science, overreaching, or spreading misleading science. I don't want people to get the idea that they are damaged beyond repair. Hence, my attempts to calm some fears with this article.
Let's continue.
The Hierarchy of Dysfunction: A Systems-Based Model
To understand the role of mitochondria in benzodiazepine withdrawal, it is helpful to establish a functional hierarchy of biological processes.
At the top of this hierarchy sits the brain’s interpretation of internal and external stimuli, particularly the limbic system, which governs threat detection and emotional salience. In states of withdrawal, this system often becomes sensitized, leading to persistent activation of the body’s stress response.
This heightened state of threat perception drives autonomic nervous system dysregulation, characterized by increased sympathetic (gas) activity and reduced parasympathetic (brake) tone. In turn, this shift influences hormonal output, including cortisol and adrenaline, and can promote low-grade inflammation.
These changes cascade downward into metabolic processes, including mitochondrial function and oxidative balance.
Within this framework, mitochondrial inefficiency is not the initiating event but rather a downstream effect of sustained dysregulation.
The system is, in essence, operating under conditions of chronic stress, and cellular energy production adjusts accordingly. This model aligns more closely with observed symptom patterns, particularly the fluctuating nature of withdrawal experiences, which are better explained by state-dependent nervous system changes than by fixed cellular damage.
Simply put, benzo withdrawal or BIND is not a result of mitochondrial dysfunction or depletion.
To claim mitochondria is responsible for a limbic brain through trauma response, sensitization, and dysregulation, is to nearly completely miss the actual science of benzodiazepines and their relationship to our neurology, emotional states, chemistry, and survival instincts.
Oxidative Stress: A System State, Not a Single Source
Oxidative stress is frequently cited in discussions of mitochondrial dysfunction, often as evidence of a primary metabolic disorder. While mitochondria do contribute to the production of reactive oxygen species (ROS), they are only one of several sources.
Immune activation, neuroinflammation, and chronic stress signaling all play significant roles in shaping oxidative balance.
In the context of benzodiazepine withdrawal, increased oxidative stress is more accurately understood as a reflection of systemic strain rather than isolated mitochondrial failure.
Elevated stress hormones, disrupted sleep, and heightened inflammatory signaling can all increase ROS production while simultaneously reducing the efficiency of antioxidant systems such as glutathione. This creates a temporary imbalance, one that is dynamic and reversible as the system stabilizes.
Framing oxidative stress as a system-wide phenomenon reinforces the importance of addressing upstream drivers rather than focusing exclusively on downstream effects. It shifts the focus from “repairing damage” to restoring balance.
Which is precisely the work we are doing in the benzo recovery school.
A systemic problem requires a systemic solution.
Why the Mitochondrial Model Is Appealing
The growing emphasis on mitochondrial dysfunction is not without psychological and cultural context. For many individuals, especially those who have been dismissed or misunderstood, a biological explanation offers validation. It affirms that their symptoms are real and rooted in the body, not imagined or purely psychological.
Additionally, mitochondrial models often come with actionable protocols, supplements, diets, and targeted interventions that provide a sense of control. In a landscape where recovery can feel uncertain, this sense of agency is understandably attractive. However, there is a subtle risk embedded in this model: the implication that the body is fundamentally damaged and must be repaired at a cellular level before recovery can occur.
This belief can inadvertently reinforce a sense of fragility and prolong a focus on internal dysfunction. It may also lead individuals away from the very mechanisms that most reliably support recovery, namely, nervous system regulation, behavioral engagement, and neuroplastic change.
Clinical Reality and Recovery Trajectories
Perhaps the most compelling argument against a primary mitochondrial model lies in clinical observation. Individuals recovering from benzodiazepine withdrawal frequently experience non-linear patterns of improvement, commonly described as “windows and waves.” These fluctuations can occur over short periods of time, often without any corresponding change in supplementation or metabolic intervention.
Such variability is difficult to reconcile with a model based on structural cellular damage, which would be expected to produce more consistent and predictable impairment. Instead, it aligns with a nervous system that is gradually recalibrating, sometimes stabilizing, sometimes reverting, but ultimately trending toward balance.
Moreover, many individuals achieve full recovery without engaging in targeted mitochondrial therapies. Their improvement is driven by changes in perception, behavior, and physiological regulation, further supporting the idea that the core issue is functional and adaptive rather than structural and degenerative.
Conclusion: Reframing Cause and Preserving Agency
Mitochondria play an essential role in human physiology, and their function can certainly be influenced during periods of stress, illness, and withdrawal. However, the evidence suggests that in the context of benzodiazepine withdrawal, mitochondrial changes are best understood as secondary responses to nervous system dysregulation rather than primary causes of symptoms.
This distinction is not merely academic. It has profound implications for how individuals understand their condition and approach recovery. A model that emphasizes system-level dysregulation preserves the possibility of change. It recognizes the body’s capacity to adapt, recalibrate, and heal.
Ultimately, the goal is not to dismiss biology but to place it in its proper context.
The nervous system, not the mitochondria, appears to be the primary driver of the withdrawal experience. And it is through the gradual retraining and stabilization of that system that recovery most reliably unfolds.
This is in no way meant to deny the role of benzo withdrawal and use in affecting things like mitochondria, TSPO, oxidative stress, neuroinflammation, etc., but to provide a rational lens through which we can understand the interrelationships.
The good news is that through steady tapering, navigating withdrawal, proper nutrition, exercise, conditioning, healing, and neuroplastic work, we can help the body naturally repair these factors. And perhaps most importantly, we need not be terrified of permanent damage or that these elements are holding us back from healing.
Works Cited
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McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation: Central role of the brain. Physiological Reviews, 87(3), 873–904.
Picard, M., & McEwen, B. S. (2018). Psychological stress and mitochondria: A systematic review. Psychosomatic Medicine, 80(2), 141–153.
Wallace, D. C. (2012). Mitochondria and cancer. Nature Reviews Cancer, 12(10), 685–698.
Salim, S. (2017). Oxidative stress and psychological disorders. Current Neuropharmacology, 15(7), 944–954.