Mental Health Plartform.

Obsessive-Compulsive Disorder (OCD)

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How can a ketogenic diet help treat the symptoms of Obsessive-Compulsive Disorder (OCD)?

Ketogenic diets are able to modify at least four of the pathologies we see in people with obsessive-compulsive disorder (OCD). These pathologies include glucose hypometabolism, neurotransmitter imbalances, inflammation, and oxidative stress. A ketogenic diet is a powerful dietary therapy that has been shown to directly impact these four underlying mechanisms that have been identified to be involved with obsessive-compulsive disorder (OCD) symptoms.

Introduction

In this blog post, I am not going to outline the symptoms or prevalence rates of OCD. This post is not designed to be diagnostic or educational in that way. Other than to say that OCD is highly related to other disorders such as Body Dysmorphic Disorder, Trichotillomania, Hoarding, and Excoriation Disorder (aka skin picking). If you suffer from any of those with or without a formal OCD diagnosis, you may also benefit from reading this blog post. If you have found this blog post, you know what OCD is and likely you or someone you love may already be suffering from it.

If you have found this blog post, you are looking for treatment options. You are trying to find ways to feel better and heal.

By the end of this blog post, you will be able to understand some of the underlying mechanisms going wrong in the brains of people suffering from OCD and how a ketogenic diet can therapeutically treat each of them.

You will come away seeing a ketogenic diet as a possible treatment for your OCD symptoms or as a complementary modality to use with psychotherapy and/or in place of medications.

Current psychopharmacology uses selective reuptake serotonin inhibitors (SSRIs), often (and hopefully) with cognitive-behavioral therapy (CBT) to treat OCD.

Katzman, M. A., Bleau, P., Blier, P., Chokka, P., Kjernisted, K., & Van Ameringen, M. (2014). https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4120194/

We can easily look up the side effects of any of these medications. The symptoms of OCD with and without psychotherapy can be so debilitating and chronic for some people, that enduring side-effects may seem a small price to pay for improved functioning. As a mental health counselor, I am quite biased toward the use of cognitive-behavioral therapy (CBT) and mindfulness skills as a treatment for OCD, seeing improvements in patients who do protocols with or without medication. But for some patients, medication and psychotherapy are not sufficient to improve symptoms. And some of my patients simply do not improve on current medications or do not tolerate the side effects of medications. And they are not alone.

Nonetheless, as many as half of all patients with OCD do not attain remission with current treatments, suggesting the considerable potential for further innovations in psychopharmacology for the disorder. 

Szechtman, H., Harvey, B. H., Woody, E. Z., & Hoffman, K. L. (2020).  https://doi.org/10.1124/pr.119.017772

Because over half of the people we attempt to treat with medication do not improve, it is our right and our responsibility to look outside of the standard of care for those suffering from OCD. To ask people suffering to wait until psychopharmacology catches up and provides effective treatment is inhumane. Especially when there are other interventions that could prove beneficial for this mental disorder.

So we are going to look at the literature to learn of some of the mechanisms of pathology we have seen in people who suffer from obsessive-compulsive disorder (OCD). We will discuss how the ketogenic diet can be a treatment for the underlying mechanisms found in symptom presentation with OCD.

What are the neurobiological changes seen in people suffering from OCD?

A previous post went into detail about how a ketogenic diet can modify symptoms of anxiety by affecting four areas of pathology seen in these disorders.

  • Glucose Hypometabolism
  • Neurotransmitter Imbalances
  • Inflammation
  • Oxidative stress.

In OCD we see these same pathologies occurring. There are areas of the brain with hypometabolism (not using energy properly), distinct neurotransmitter imbalances affecting mood and cognition, and inflammation. There is even a component of oxidative stress present in the obsessive-compulsive disorder (OCD) brain, exacerbating symptoms. Let’s review each of these. And consider how the ketogenic diet modulates all of these and may favorably improve symptoms.

OCD and Brain Hypometabolism

Changes in glucose activity have been documented in the orbitofrontal cortex (OFC) and the caudate nucleus and could correlate the presence and lack of obsessive-compulsive disorder (OCD) symptoms based on these findings. Neuroimaging studies using PET, SPECT, and fMRI have found that abnormally high activity occurs throughout the frontal cortex and connected subcortical structures. But that with successful treatment using SSRIs or behavior therapy this high activity returns to normal levels.  

Generally, we see hypermetabolism in obsessive-compulsive disorder (OCD). An increased metabolic rate in the left orbital gyrus and bilaterally in the caudate nuclei. But that is not to say that there is no hypometabolism component in OCD. It just may be more dependent on the course of illness and the activity being attempted.

Glucose hypermetabolism is later replaced by hypometabolism in the anterior cingulate cortex (ACC). This is thought to occur because the ACC eventually stops performing normal functions in this part of the brain. Why would the ACC do this? Because it redistributes functions to other brain structures because of abnormal circuitry that develops over the course of the illness. Brain structures will wire harder and stronger where there is increased activity. Brains are quite plastic, meaning if there is an area of overexcitability it will modify what brain structures are connected and to what degree.

Evidence from neuroimaging studies indicates that while there is one loop of hyperactivity, there is a second loop of hypoactivity between the dorsolateral prefrontal cortex (dlPFC) and dorsolateral caudate in patients with OCD. This hypoactivity is thought to underlie the cognitive inflexibility and deficits in executive function seen on neuropsychological assessments in OCD patients.

Thus, the prevailing hypothesis asserts that an imbalance between these 2 circuits is the underlying basis for OCD, as a hyperactive OFC generates obsessions and their associated ritualistic compulsions, while a hypoactive executive network prevents the individual from being able to switch to a new behavior.

McGovern, R. A., & Sheth, S. A. (2017). https://doi.org/10.3171/2016.1.JNS15601

We also see that OCD patients demonstrate working memory impairments that may be associated with glucose hypometabolism in the prefrontal cortex. These working memory impairments include not only simply trying to remember things for short periods, but also include problems with visual-spatial and executive functioning. These deficits in executive functioning, which are associated with brain hypometabolism, are part of symptom presentation. In order to have some control of our thoughts, or to move our thoughts away from more base thoughts devoted to fear and safety, we must have good executive functioning in the brain. For this reason, I would argue that hypometabolism is a relevant target of neurobiological intervention in those with OCD.

Also, I do not see many patients who do not have comorbidity with other disorders. Meaning, many of my patients have what is called dual diagnoses. Meaning they don’t just have OCD, but they have over mental illnesses that go along with it. And one comorbidity that I see quite often with OCD is depression. Depression is consistently seen to show a great deal of dysfunctional brain hypometabolism. This prominent hypometabolism component is correlated strongly and possibly causative of symptom presentation in depression in general, and is found present in those with comorbid OCD.

How a ketogenic diet treats hypometabolism in the OCD brain

Ketogenic diets are metabolic therapy for the brain. Ketogenic diets produce ketones. And ketones are used as an alternative fuel for the brain. Ketones can bypass broken metabolic machinery normally used to utilize glucose for fuel. Not only do brains love ketones, but a ketogenic diet helps neurons make more powerhouses for cells (mitochondria), increasing metabolism (energy expenditure) in important brain structures and connections seen in obsessive-compulsive disorder (OCD).

But wait, you may say. What about those other areas of hyperexcitability? Won’t a ketogenic diet rev all those up and make that loop (circuit) of the brain worse?

Absolutely not. Why?

our results suggest that brain network destabilization may reflect early signs of hypometabolism

Mujica-Parodi, L. R., et al., (2020). Diet modulates brain network stability, a biomarker for brain aging, in young adults. https://pubmed.ncbi.nlm.nih.gov/32127481/

Because the pathology of brain hypometabolism does not mean that the excitability is necessarily happening for the same reason. Ketogenic diets help to actually stabilize brain function by bypassing broken cell machinery that has resulted in the cell developing glucose hypometabolism. Also, supportive neuronal structures like astrocytes can upregulate their own ketone production, creating more energy overall in the brain. We will learn more about astrocytes later.

Hyperexcitability in some structures of the brain is much more likely due to neurotransmitter imbalance than glucose hypometabolism. Was I able to figure out exactly what causes the hyperexcitability? I don’t think the literature knows for sure. But we do see neurotransmitter imbalances that cause hyperexcitability and we know that unchecked inflammation can damage cell energy and cause areas of hypometabolism.

But because the ketogenic diet is not an intervention on a single component of mental illness, the way so many psychopharmacology treatments are, improving energy consumption in one hypometabolic structure is not going to cause another to rev up in a scary way.

recent evidence suggests that altering metabolism with a ketogenic diet enables a homeostatic state in the brain that is less excitable

Masino, S. A., & Rho, J. M. (2019). https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC6281876/

Remember? This intervention works on at least four factors going wrong (with a few more thrown in we may discuss at the end), and the improvements on one system do not seem to imbalance or cause side effects with the others. The ketogenic diet appears to work holistically with all involved mechanisms of intervention.

OCD and Neurotransmitter Imbalances

Neurotransmitter imbalances we see in OCD include neurotransmitters, including serotonin, dopamine, glutamate, and GABA.

Serotonin imbalance plays an active role in OCD. So much so that at least half with OCD improve on medications that leave more serotonin available in the synapses (SSRIs) to be used by neurons. There are a lot of reasons why a brain may not be making enough serotonin. Some could be not enough cofactors like iron, vitamin D, or B6, and possibly not enough amino acid precursors (Vegans and those eating too many highly processed foods, I am talking to you). But in OCD the lack of serotonin is thought to create problems with obsessions. And when we treat some people with SSRIs their obsessions decrease in intensity and frequency. But it doesn’t work for everybody.

The clinical benefits of selective serotonin-reuptake inhibitors (SSRIs) have implicated serotonin, but a clear understanding of its role in symptom onset, aggravation, and resolution remains elusive.

Lissemore, J. I., et al. (2021). https://doi.org/10.1007/978-3-030-57231-0_13

While we don’t understand why this occurs in OCD, the consensus seems to be that low serotonergic activity alters the orbitofrontal cortex response and that people with OCD must be treated with a serotonin agonist. What if there was a way to produce a physiological reaction in favor of serotonin balance that was not a serotonin agonist in the form of medication?

When we evaluate neurotransmitter systems of dopamine in patients with OCD we tend to see problems with dopamine receptors (D2). But we do not see a significant correlation between the faulty D2 receptor function and disease severity. At least not consistently in the literature. But we do know dopamine is involved because, in a pharmacological fMRI study of reinforcement learning, the use of dopamine receptor antagonists with obsessive-compulsive disorder (OCD) saw an unexpected therapeutic benefit.

One neurotransmitter system that appears to be important for OCD is that between glutamate and GABA. Glutamate is an excitatory neurotransmitter that is important to normal brain function, but when out of balance can be neurotoxic. It is best described as a gas pedal. GABA is an inhibitory neurotransmitter and we generally think of GABA as a chill, feel-good, not overwhelmed sort of neurotransmitter when it is in balance. GABA can be thought of like the brakes. The two need to be in balance in a well-functioning brain. But we do not see these two balanced in OCD.

Imbalances between the glutamate and GABA neurotransmitter systems in certain structures of the brain are thought to create the repetitive behavioral nature of some obsessive-compulsive disorder (OCD) symptoms. Some researchers posit that glutamatergic hyperactivity (making too much glutamate) associated with over-activity of certain pathways may underlie the development of OCD. We have a ton of animal studies with mice showing this and even two human studies. Elevated levels of glutamate were found in both studies of those who were unmedicated suffering from obsessive-compulsive disorder (OCD).

There is a growing body of evidence from neuroimaging studies, which implicate glutamatergic dysfunction in OCD. However, the evidence is divided regarding the exact nature of dysfunction.

Karthik, S., Sharma, L. P., & Narayanaswamy, J. C. (2020). Investigating the role of glutamate in obsessive-compulsive disorder: current perspectives. 
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7173854/

It is not as simple that there is just simply “too much glutamate” although that could be the case in some brain structures. It is an issue of imbalance of glutamate. Because we have also seen evidence of too little glutamate in the thalamus in those with OCD. Again, the brain is a complicated system. That we are attempting to treat with single mechanisms interventions in order to attain that balance. And for a lot of people with OCD, this is not working.

Lower levels of the neurotransmitter GABA are seen to correlate with high symptom severity in those with obsessive-compulsive disorder (OCD). Lower GABA appears to exist in the rostral anterior cingulate cortex, which is thought to have a role in deficits in cognitive control we see with OCD (e.g., ruminating thoughts).

In a meta-analysis of neuroimaging studies conducted in 2021, it was found that there were reductions in D2 receptors (dopamine), GABA receptors, and cingulate 5-HT receptors (serotonin). These types of findings regarding neurotransmitter systems in OCD provide ample evidence there is dysfunction in neurotransmitter balancing. Would not an intervention that has been shown to improve neurotransmitter balancing, of several neurotransmitter systems, as opposed to just one or two, not be worthy of discussion in the treatment of obsessive-compulsive disorder (OCD)?

I would say yes. The discussion of the ketogenic diet as a way to balance neurotransmitters (and not just one of them willy nilly) is most definitely warranted.

How a ketogenic diet treats neurotranmitter imbalances in the OCD brain

Ketone bodies are signaling bodies. Meaning they turn genes on and off and help determine a lot of processes. One of those is neurotransmitter balance. For example, acetoacetate, one type of ketone body is able to inhibit glutamate release from neurons in some parts of the brain but will enhance its transmission in other parts that need and want it. Can you imagine a psychopharmacological treatment doing that? Being able to help your brain use it exactly when and where it is needed? Without somehow messing up all the ratios by trying to control how much is made, or how often it hangs out in synapses? I think not. But ketones can do that.

Ketones also exert influences that are considered indirect. As ketones break down, their byproducts are used in systems that regulate neurotransmitter synthesis. These downstream effects influence and regulate the neurotransmitters glutamate and GABA. There is less production overall of glutamate in those on a ketogenic diet, and we see more GABA. For example, children on a ketogenic diet for epilepsy have higher cerebrospinal fluid GABA levels than control groups. We also see this favorable increase in GABA when using magnetic resonance spectroscopy in human studies.

But what about glutamate? Well, we know that the decreases in neuroinflammation that happen with a ketogenic diet improve the environment in which the brain makes neurotransmitters. While we will learn more about inflammation later in this blog post, it is relevant here to note that when a brain is inflamed it can disrupt normal neurotransmitter production. And this has been seen in the production of glutamate, reaching up to 100x more production of glutamate than normal in the brain. Obviously, this has neurotoxic effects. So wouldn’t it be great if there were a way to balance this neurotransmitter system?

Ketones just happen to enhance the conversion of glutamate to GABA, which likely is a significant part of the balancing effects we see when people adopt a ketogenic diet. As for serotonin and dopamine, we see balancing effects of those neurotransmitters also with the ketogenic diet. We see an upregulation of serotonin and balancing of dopamine. We also see much-improved cell membrane function, which is going to improve how well those neurons communicate and use the neurotransmitters made. You can learn a little more about this here.

Ketogenic diets supply neuronal membrane stabilization. Ketogenic diets increase the amounts and actions of ATP and adenosine. ATP (needed for energy) and adenosine are critical for metabolic stability. Adenosine, in particular, is well known to be neuroprotective and promote homeostasis (balance), stabilizing cellular membrane potential, which you need in order to make the right amount of neurotransmitters, allow them to stay the right amount of time, and allow them to be broken down when they are supposed to. There is no successful balancing of neurotransmitters without healthy cell membrane function.

I could go on about how we do not have psychotropic medications for OCD, or other disorders, that provide this for people in a balanced way. But I won’t because that would be slightly off-topic and is better for a future blog post.

My very important point that is relevant to the reader of this blog, is that a ketogenic diet improves neuronal membrane function and allows your receptors to work better. It also helps you store cofactors, improves membrane potential, and a host of other positive brain benefits that I just have not seen advertised as being possible with psychopharmacology.

OCD and neuroinflammation

Inflammation is a process in which you are hurt or under attack in some way, and your body tries to make it right. It also does this in the brain. In the brain, neuroinflammation can occur because of things crossing a leaky blood-brain barrier, neuronal bodies not having adequate energy dynamics to maintain themselves, or microglial attempting to come to your rescue as a form of immune system activation. Chronic inflammation and neuroinflammation, in particular, are seen in psychiatric diagnoses including depression and anxiety, and neurological issues as in dementia. So it should be no surprise for us to learn that OCD has a significant inflammatory component.

OCD is associated with low-grade inflammation, neural antibodies, and neuro-inflammatory and auto-immune disorders

Gerentes, M., Pelissolo, A., Rajagopal, K., Tamouza, R., & Hamdani, N. (2019). Obsessive-compulsive disorder: autoimmunity and neuroinflammation. https://doi.org/10.1007/s11920-019-1062-8

Although many of the studies finding higher inflammation in those with obsessive-compulsive disorder (OCD) are considered associational (there is a relationship with one being with the other more often), there is enough evidence to suggest that there is a role in the pathogenesis (how the disease begins) of OCD. There is enough evidence of inflammation having a causative role that there is discussion in the literature suggesting anti-inflammatory drugs be developed and repurposing of immunomodulatory therapies to treat OCD.

And that is good enough for me. If inflammation is a component of OCD then we need to treat it. So let me tell you about the highly anti-inflammatory effects of the ketogenic diet.

How a ketogenic diet treats inflammation in people with OCD

Ketogenic diets reduce neuroinflammation in a variety of ways

  • reduces oxidative damage (we will learn more about this soon)
  • improved neural energy metabolism (remember hypometabolism above?)
  • epigenetic effects as signaling bodies that modulate or turn off inflammatory pathways (turn genes on and off!)
  • positive effects on gut microbiome that reduces inflammation

Ketogenic diets reduce inflammation in all of those ways. Ketones, which are produced in the body during a ketogenic diet, are what we call signaling molecules. And a signaling molecule can turn some genes off and some genes on, and in the case of inflammation, this action is quite favorable towards LESS inflammation. A ketogenic diet provides the conditions in which this favorable signaling can occur. But it is also a dietary strategy that reduces or eliminates problems with hyperglycemia.

You can have episodes of hyperglycemia even if you are not diabetic. And when you have hyperglycemia it affects immune cells in a way that causes more inflammation. You do not make ketones if you are eating a lot of carbohydrates that are causing hyperglycemia, because hyperglycemia means you have spiked insulin quite high, and ketones are not made in those conditions.

So eating a ketogenic diet in order to treat your OCD will take away the inflammation that would occur when eating a standard American diet higher in carbohydrates and processed foods. It would also reduce inflammation using the ketones you generate and the improved micronutrient availability in your food choices by eating a well-formulated ketogenic diet.

Because we are discussing how one thing influences the other, it is a good time to include the below quote. It does such a good job illustrating how a single approach to mental health that is not systemic in nature is just never going to be sufficient for wellness.

Recent studies display that inflammation processes and the dysfunction of the immune system are likely to play a role in the pathophysiology of OCD, indicating that the disturbances in neurotransmitters such as serotonin and dopamine cannot be alone involved in the development of OCD.

Ghasemi, H., Nomani, H., Sahebkar, A., & Mohammadpour, A. H. (2020). https://doi.org/10.2174/1570180817999200520122910

Obsessive-compulsive disorder (OCD) treatment using a ketogenic diet also improves the functioning of the immune system. As we see in the above quote, the inflammatory process is driven in part by immune system dysfunction. Research has suggested quite strongly that immune system function improves significantly on a ketogenic diet. The effects of the ketogenic diet on immune function are so positive that in a recent article it was proposed for use in COVID-19 as a preventative treatment. It is quite likely that improvements in immune system functioning could be instrumental in reducing the inflammation that exists in the brains of those who suffer from obsessive-compulsive disorder (OCD). Someone with OCD may wish to use the ketogenic diet for this purpose in place of medication.

OCD and Oxidative Stress

Oxidative stress occurs when the brain’s ability to upkeep itself or fend off assaults is no longer sufficient. This can happen from inadequate micronutrient stores, immune system responses, or toxins that make it through a leaky blood-brain barrier. Countless reasons really. Just being alive creates oxidative stress. There is an excellent diagram showing different factors related to oxidative stress here (seriously it is really good, check it out).

But a healthy brain and body are able to fight off these assaults using our own antioxidant production. But in people with obsessive-compulsive disorder, this is clearly not happening to a sufficient degree.

Recent studies have shown more activity of free radical metabolism and the weakness of antioxidant defense system in OCD.

Baratzadeh, F., Elyasi, S., Mohammadpour, A. H., Salari, S., & Sahebkar, A. (2021). The Role of Antioxidants in the Management of Obsessive-Compulsive Disorder. https://doi.org/10.1155/2021/6661514

Oxidative stress has such a strong role in OCD, that discussion is made of the use of antioxidant therapies in its treatment. But what a lot of people do not consider is the role of ketones in helping people be able to use their own antioxidant systems in the body. So let’s discuss that next.

How does a ketogenic diet treat oxidative stress in those with OCD?

Ok, let’s take a look at the figure I recommended you look at prior. It is just too good to not use in our explanation.

Baratzadeh, F., Elyasi, S., Mohammadpour, A. H., Salari, S., & Sahebkar, A. (2021). https://www.hindawi.com/journals/omcl/2021/6661514/

We already know from our studies that ketogenic diets upregulate mitochondria and mitochondrial function. So we know a ketogenic diet would inhibit the mitochondrial dysfunction we see in this figure that is a factor in causing oxidative stress.

We have also learned how a ketogenic diet improves neuronal membrane function. We see in this figure how impaired neuronal membrane functioning contributes to oxidative stress. So a ketogenic diet could very much keep this factor contributing to oxidative stress from happening in the first place.

We have discussed how ketones are signaling bodies, that are able to turn down inflammation by having a highly beneficial effect on inflammation pathways. This is not an assumption on my part. It is in the literature and provided to some degree in the reference list below. Ketogenic diets are powerful interventions for inflammation. And if we can keep inflammation down, we keep the oxidative stress down we see in OCD brains.

These are all very exciting aspects and show that ketogenic diets are a very powerful, multi-functioning holistic intervention. But the part of the figure that I like to focus on when teaching people about oxidative stress and its influence on psychiatric disorders pertains to this box here:

https://www.hindawi.com/journals/omcl/2021/6661514/fig2/ (I modified this figure with red circle)

I am a firm believer in the power of endogenous (your body makes it, you don’t eat it or swallow it as a supplement) antioxidants. And the most powerful one you make, under the right conditions, is glutathione. Glutathione is a very powerful antioxidant and ketones play a role in your body’s ability to make it and use it well.

Ketones have neuroprotective qualities that interfere with the formation of reactive oxidant species that create oxidative stress and they are also instrumental in tipping the balance of energy metabolism in such a way that it favors the destruction of oxidative products through the use of glutathione.

A well-formulated ketogenic diet also is nutrient-dense and will allow you to both increase and store (due to improved membrane function) those micronutrients that are needed to make glutathione in the first place.

Do you get it?

You don’t have to eat rainbow-colored vegetables and fruits or take a lot of vitamin C or E. You can have a nutrient-rich diet that provides the building blocks to create the most powerful antioxidant we know of, in your own body, and then use ketones to unlock their power.

And this can help you combat and/or completely eliminate the oxidative stress that is currently exacerbating your symptoms of obsessive-compulsive disorder.

What other ways do ketogenic diets help OCD?

Ketogenic diets do so many great things to a brain in distress, and to the OCD brain in particular. But there is another factor that really deserves mention.

Ketones upregulate brain-derived neurotrophic factor (BDNF). Why would this be important to a person suffering from OCD? Well, there are a lot of reasons. But first, let’s start by saying that part of the therapeutic effect that some people see from using SSRIs for OCD is that these drugs somewhat increase BDNF. We use them for traumatic brain injuries for this reason. Will they upregulate it as much as a ketogenic diet? I don’t think so but I have no data to support or refute that assumption. I mention it here because I want you to understand that BDNF is instrumental in your recovery from obsessive-compulsive disorder (OCD).

BDNF is what will help you rewire those brain structures together in new and healthy ways. BDNF is what is going to help you get the most out of that exposure-response prevention (ERP) work you are doing with your therapist. Need to learn new ways of thinking and being while doing cognitive-behavior therapy for your OCD? BDNF is needed. And ketones are excellent at increasing the amount of BDNF in your brain, which can only help and is yet another way that ketogenic diets can be a complement to psychotherapy work. So while BDNF is not one of the four factors I normally write about when discussing ketogenic diets as a treatment for mental illness, it deserves a strong and honorable mention.

Conclusion

It is my sincere hope that you are beginning to see how all the components of action in a ketogenic diet work together. That you have acquired an understanding that improved neuroinflammation reduces oxidative stress. That less oxidative stress improves the environment in which the brain is making and balancing transmitters and improves important membrane functions. That you now understand that reduced neuroinflammation and oxidative stress mean there are fewer nutrients being depleted, and more available precursors available to do important things, like making enzymes and neurotransmitters. I hope it is clear that the improved energy neurons get on a ketogenic diet allows them to function better overall. And that the improved energy of these cells along with an upregulation of BDNF allows those same neurons to do the basic housekeeping they need to stay in good repair and make new learning connections.

Again, there are no randomized clinical trials yet using a ketogenic diet specifically to treat obsessive-compulsive disorder (OCD). We can only extrapolate possible benefits to this population, based upon the results seen in other neuropsychiatric and neurological disorders. We can be open to the idea that an intervention seen to reduce oxidative stress in one or many different populations, both in animal models and with humans, may very well successfully do so in OCD. We should at least discuss the possibility, and more importantly, inform you of that possibility. So you can make the very best treatment decisions that make sense for you!

I want to encourage you to learn more about your treatment options from any of the following blog posts. I write about different mechanisms in varying degrees of detail that you may find helpful to learn on your wellness journey. You may enjoy the Ketogenic Case Studies page to learn how others have used the ketogenic diet to treat mental illness in my practice. And you may benefit from understanding how working with a mental health counselor while transitioning to a ketogenic diet can be helpful here.

Share this blog post or others with friends and family suffering from mental illness. Let people know there is hope.

You can learn more about me here. If you would like to contact me you may do so here. If you just have a simple question please do not hesitate to reach out. Or let me know in a comment if you have found this blog post to be helpful on your wellness journey.

I truly believe you have the right to know all of the ways you can feel better.

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References

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Asl, M. A., Asgari, P., & Bakhti, Z. (2021). Treatment Approaches Based on Neuroscientific Data in Patients With Obsessive-Compulsive Disorder. International Clinical Neuroscience Journal, 8(3), 107–117.

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Batistuzzo, M. C., Sottili, B. A., Shavitt, R. G., Lopes, A. C., Cappi, C., Mathis, M. A. de, Pastorello, B., Diniz, J. B., Silva, R. M. F., Miguel, E. C., Hoexter, M. Q., & Otaduy, M. C. (2021). Lower Ventromedial Prefrontal Cortex Glutamate Levels in Patients With Obsessive–Compulsive Disorder. Frontiers in Psychiatry, 12. https://doi.org/10.3389/fpsyt.2021.668304

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Baxter, L. R., Phelps, M. E., Mazziotta, J. C., Guze, B. H., Schwartz, J. M., & Selin, C. E. (1987). Local cerebral glucose metabolic rates in obsessive-compulsive disorder. A comparison with rates in unipolar depression and in normal controls. Archives of General Psychiatry, 44(3), 211–218. https://doi.org/10.1001/archpsyc.1987.01800150017003

Baxter, L. R., Schwartz, J. M., Phelps, M. E., Mazziotta, J. C., Guze, B. H., Selin, C. E., Gerner, R. H., & Sumida, R. M. (1989). Reduction of prefrontal cortex glucose metabolism common to three types of depression. Archives of General Psychiatry, 46(3), 243–250. https://doi.org/10.1001/archpsyc.1989.01810030049007

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