Mental Health Plartform.

Social Anxiety Disorder (SAD)


How could a ketogenic diet help treat the symptoms of Social Anxiety Disorder (SAD)?

Ketogenic diets are able to modify at least four of the pathologies we see in people suffering from Social Anxiety Disorder. These 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 the symptomatology of Social Anxiety Disorder.


In this blog post, I will not be listing the symptoms or prevalence rates of Social Anxiety Disorder (SAD). This post is not designed to be diagnostic or educational in that way. If you have found this blog post, you probably know what Social Anxiety Disorder is and it is possible or likely that 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 reduce symptoms and increase your functioning in social situations.

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 social anxiety 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 social anxiety or as a complementary modality to use with psychotherapy and/or in place of medications.

Clinical experience and limited systematic data suggest that augmentation with benzodiazepines or gabapentin, or switching to monoamine oxidase inhibitors, benzodiazepines or gabapentin can be useful in treatment-resistant cases. Cognitive-behavioral treatment can also be a helpful adjunct or alternative in non-responders to pharmacological treatment of SAD.

The current standard of treatment for Social Anxiety Disorder is the use of pharmacology and/or psychotherapy in the form of Cognitive-Behavioral Therapy (CBT). CBT helps clients look at their thoughts and beliefs around social situations which can be quite helpful There is also a significant behavioral component of exposure therapy, in which clients would create a list of social anxiety-provoking situations and rate the subjective level of anxiety they felt at the idea of doing those activities. They would then actually do the things on the list, exposing themselves to the behaviors until they felt zero anxiety doing so.

But when you look at the list of medication types above, that are considered standard of care psychopharmacology, you have some real potential problems.

  1. These medications often have side-effects that are really unpleasant. Some can even create physical dependance.
  2. Use of fast acting medications can create a psychological dependance on their use in stressful situations.
  3. Access to faster acting anxiety medications can become a barrier for people to learn to reach for other tools of coping (e.g., mindfulness or CBT techniques).
  4. These medications all potentially get in the way of effective behavioral therapy for social anxiety. If you are medicated while doing behavior therapy you cannot habituate and expose effectively. The anxiety will come back when you stop your medication.

What are the neurobiological changes seen in Social Anxiety Disorder? Where are possible pathways of intervention?

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 types of disorders.

  • Glucose Hypometabolism
  • Neurotransmitter Imbalances
  • Inflammation
  • Oxidative stress

In Social Anxiety Disorder (SAD) we see these same underlying mechanisms. There are areas of the brain with hypometabolism (not using energy properly) and we see overexcitability in others. Also seen in Social Anxiety Disorder (SAD) are neurotransmitter imbalances, neuroinflammation, and oxidative stress as part of the underlying disease process. Let’s review each of these as they are seen in the development and/or perpetuation of Social Anxiety Disorder (SAD).

Social Anxiety and Hypometabolism



  1. The physiological state of having an decreased rate of metabolic activity

When we compare whole-brain analysis using functional MRI (fMRI) of people with Social Anxiety Disorder there is significantly lower activation (hypometabolism) in the left anterior cingulate gyrus. This part of the brain is responsible for attention control.

Hypometabolism of the cingulate gyrus has a strong role in the creation of anxiety in social situations. Those with Social Anxiety Disorder show lower activation in the cingulate gyrus, which is responsible for the process of attention control.

What does this mean for those experiencing symptoms?

Anyone who has ever experienced social anxiety knows what this feels like. When you are socially anxious, you cannot be fully present with whomever you are talking to or even enjoy the environment you are in. Why? You cannot focus your attention exclusively on the interaction. And as a result, a huge part of your attention is being used to fuel your anxiety.

Instead of being able to have a simple conversation, your attention is focused on what to say next so you don’t feel stupid, evaluating what you think the other person thinks of you and possibly imagining worst-case social scenarios that are not even happening.

Successful treatment of Social Anxiety Disorder using behavioral exposure therapy will show positive changes in activation of the cingulate gyrus. Reflecting the person’s improving ability to utilize this part of the brain better and thereby holding attention on primarily the conversation they are having. This better brain activation results in more positive thoughts regarding the self in social situations and less tendency to ruminate on actual or perceived negative social moments.

How does a ketogenic diet treat hypometabolism in Social Anxiety Disorder (SAD)?

We know from past posts discussing ketogenic diets for mental illness (here, here, and here) that it is a powerful metabolic therapy for the brain. Sometimes brains stop using glucose effectively as a form of fuel in many structures. There are many theories about why this happens. It can develop in response to high carbohydrate diets. We can begin to to see impaired utilization of glucose as fuel in our 30s, and possibly sooner. The brain’s ability to take in and use glucose depends on insulin sensitivity. The higher carbohydrate laden our diets, the more insulin our body must produce. And over time that increase in insulin actually reduces the ability of our cells use glucose as fuel. While I could not find any specific studies suggesting insulin resistance was directly responsible for areas of brain hypometabolism seen in those with Social Anxiety Disorder, it does not seem an unlikely culpruit. Regardless of the causation, if a brain cannot utilize glucose as well, it needs an alternate fuel. Implementing a low carbohydrate dietary therapy can reduce levels of insulin and allow ketones to be generated by the body and used in the brain for energy.

Ketones themselves are an energy source for the brain that have powerful effects as signaling molecules. These signaling molecules help increase the number and health of important cellular energy structures known as mitochondria. These mitochondria are the power plants of your cells. Brains need and want a lot of them and they need and want them in good repair! Ketones provide this for the impaired brain. And they can most certainly theoretically provide it for the struggling cingulate gyrus we see prominent in Social Anxiety Disorder.

Social Anxiety and Neurotransmitter Imbalances

Treating Social Anxiety Disorder with psychopharmacology includes medications that act on GABA, glutamate, and other neurotransmitter systems.

We know from a past blog post (here) that a ketogenic diet improves the environment in which your brain makes neurotransmitters and it creates an environment in which they function better. Ketogenic diets increase the neurotransmitter GABA which has a natural soothing of anxiety. It is the neurotransmitter that makes you feel like you can handle life and that there is no reason to be overwhelmed. It is the neurotransmitter that psychopharmacology attempts to alter with benzodiazepines and gabapentin. Except when they do, it usually comes with side effects like being sleepy or feeling out of it. How nice would it be to increase your GABA without having to check out for the night? Ketogenic diets do that. They naturally increase your GABA in a balanced way that doesn’t cause these types of issues. You are just more chill. Not sleepy.

Brains that have stressful internal environments like inflammation and oxidative stress (spoiler alert: the Social Anxiety Disorder brain has this happening) influence the creation of different neurotransmitter ratios being made. A brain under the duress of trying to perform in a constantly hostile internal biological environment is not going to make more GABA. It is going to make the excitatory neurotransmitter Glutamate, and possibly 100x more than it would normally. The pathway in which this happens also depletes important resources needed to ensure balanced levels of other important neurotransmitters.

The neurotransmitter glutamate in too high of levels is neurotoxic and does a lot of damage. It also makes you feel terribly anxious and overwhelmed. Ketogenic diets keep the excitatory neurotransmitter Glutamate in check by improving the biological environment in which your brain is trying to function.

Additionally, recent research has shown that the interaction between dopamine and serotonin transport is a distinct type of neurotransmitter imbalance seen in Social Anxiety Disorder.

“We see that there is a different balance between serotonin and dopamine transport in people with social anxiety disorder compared with control subjects. The interaction between serotonin and dopamine transport explained more of the difference between the groups than each carrier individually. This suggests one should not focus exclusively on one signal substance at a time, the balance between different systems may be more important”

Olof Hjorth, Ph.D. student at the Department of Psychology at Uppsala University, Sweden. (

You just might not need a medication like an MAOI if your cell membranes were working in top form. Ketogenic diets greatly improve cell membrane function through any number of mechanisms, including reduced inflammation and oxidative stress (I promise we will get there), the signaling powers of the ketones themselves, or their use as an efficient and preferred fuel source. And because a well-functioning cell membrane directly enhances your brains’ ability to balance neurotransmitters, I include it here for your consideration.

How does the ketogenic diet help treat neurotransmitter imbalances seen in Social Anxiety Dsiorder?

SAD is associated with mainly increased expression in the transporters for serotonin and dopamine seen in fear and reward-related brain regions. It just so happens that ketogenic diets have been seen to increase serotonin and decrease excessive levels of dopamine.  It was already known that there are differences in serotonin reuptake (how long the neurotransmitter hangs out to be used) in those with Social Anxiety, but this understanding of dopamine’s role is new and exciting.

The rationale for the use of the ketogenic diet is based on the potential mood stabilizing effects through level modifications of metabolites such as dopamine and serotonin and the regulation of GABA/glutamatergic neurotransmission, mitochondrial function and oxidative stress.

It would not be thorough to leave this section just at neurotransmitter function. When they discuss psychopharmacology for Social Anxiety Disorder, and they discuss the role of monoamine oxidase inhibitors (MAOI), they are attempting to control an enzymatic reaction to modify levels of the neurotransmitters norepinephrine, serotonin, and dopamine in the brain. They block the removal of these neurotransmitters. They do not balance these neurotransmitters. They do not make these neurotransmitters work together in a beautifully balanced symphony in any way. Also, these drugs have side effects which I will not go into here, but you can easily Google.

So, we have to talk about how ketogenic diets improve cell membrane function. I wrote briefly about it here but let me get you up to speed. Ketogenic diets optimize your neuronal functioning. So this means that these neuronal membranes can better accomplish all of these VERY important tasks:

  • accumulate nutrients
  • reject harmful substances
  • catalyze enzymatic reactions
  • create electrical potential
  • conduct nerve impulses
  • remain sensitive to neurotransmitters and modulators
  • decreased hyperexcitability

The well-documented neurotransmitter balancing effects of ketogenic diets, in particular, seen with GABA, glutamate, serotonin, dopamine, and norepinephrine, clearly provide support as a potential treatment modality for those suffering from Social Anxiety Disorder.

Social Anxiety and Inflammation/Oxidative Stress

I have included oxidative stress and inflammation together under the same heading because one condition perpetuates the other and vice versa. One marker of inflammation that is often studied is an immune-mediated response known as inflammatory cytokines.

Studies conducted over the past few years suggest that anxiety disorders may be characterised by lowered antioxidant defences


The easiest way to talk about it these two mechanisms is to think that our environment and experiences increase inflammation, and when inflammation can no longer be controlled, it results in oxidative stress.

Inflammation can come from many things. Pollution, substances, diets higher in carbohydrates than our body can currently metabolize, traumatic events, terrible relationships, being sick with a virus, or other lifestyle factors like not getting enough movement.

Oxidative stress is well-established as having a role in anxiety disorders. When it comes to fear and anxiety, there is some debate going on around whether having fearful experiences increases inflammation and thereby oxidative stress, or whether unchecked inflammation increases oxidative stress and then creates symptoms of fear and anxiety. I believe the etiology (how it starts) could be either. Regardless of what comes first, we want to reduce inflammation and oxidative stress as much as possible, by whatever means we can.

Perhaps unsurprisingly, we see a reduction in oxidative stress when we use Cognitive-Behavioral Therapy for Social Anxiety Disorder (SAD). This makes sense because we have reduced the level of stress involved in social situations by changing how we think about them or habituating our nervous system to them. This reduction in both perceived and actual stress would of course reduce inflammation and the body’s response to what was once determined to be scary or dangerous.

Your brain is going to have some level of oxidative stress that naturally occurs. We already have a great antioxidant system in the body and brain, using the most powerful antioxidant there is called glutathione. But when we are exposed to particularly stressful situations (i.e., experiencing trauma, unhealthy relationships, etc) or doing things that add more stress (i.e., inflammatory diets with sugar and highly processed foods, insufficient physical activity, smoking, etc.) then our body cannot make enough glutathione. Your body becomes depleted of micronutrients dealing with those stressors and it needs them to make enough antioxidants to reduce inflammation and combat oxidative stress.

And it’s great if you take antioxidants. In fact, taking antioxidants can help modulate symptoms of anxiety and other psychiatric issues. But you cannot outrun poor lifestyle and behavioral choices or events by ingesting a lot of antioxidants. There are plenty of people trying this with a lot of expensive supplements and it is my understanding the results are equivocal.

Also, this ignores the fact that we are behaving in a way that causes damage to our body. It would be like putting a hole in your wall every day and just making sure that you have enough spackle, sand paper, paint and dry time before the next hole happens. How long do you think it will be before your house is in very bad shape? With some holes only partially repaired and some not at all. At what point or how long will it take for the structural integrity of the walls to really not work well anymore? Probably sooner than you imagine. This would be a silly way to handle damage. But this is what we do when we try to outrun inflammation, whether through diet or lifestyle, by only increasing our antioxidants and/or popping a multivitamin. Much better to stop the behavior that puts holes in the walls. Much better to stop the conditions that cause excess inflammation and metabolic stress.

But I digress.

Oxidative stress depletes your micronutrient stores and glutathione. It puts cells in a constant state of stress and inhibits the number and functioning of important cell structures, like mitochondria. Eat all the food you want, but if your mitochondria are impaired your energy is going to be low, both to enjoy life and to repair your body. Insufficient and poorly functioning cell mitochondria mean that there is less energy to maintain cell functioning and do all the things that need to happen to combat inflammation.

Oxidative stress also decreases Brain-Derived Neurotrophic Factor (BDNF), which you need to help heal your brain after the damage is done, or even just to learn new things. Is it any surprise that we cannot learn easily when we are stressed?

Depletion of the brains most important antioxidants, like glutathione, allow significant damage to occur in the form of neuroinflammation and a faster aging brain. Oxidative stress, which is basically the brain’s inability to deal with the level of neuroinflammation going on, will create an environment that will influence your neurotransmitter balance. A high-stress environment in the brain essentially leads to uncomfortable and unfavorable neurotransmitter imbalances. We just learned about this above when we mentioned glutamate in the neurotransmitter imbalance section. But because inflammation and the subsequent oxidative stress have direct effects on neurotransmitters let’s revisit by naming a pathway involved.

When your brain tries to make neurotransmitters in an environment of oxidative stress, the kynurenine pathway will sneak tryptophan away from the making of other neurotransmitters. It then takes that precious tryptophan and makes more glutamate, increasing your anxiety.

Tryptophan is a building block (precursor) for serotonin, and when there is less available this means you get to experience less serotonin, and all the anxiety-producing and behavioral effects involved in that.

Oxidative stress also gets in the way of you making and effectively using these and other neurotransmitters in the balanced and magical ratios you need to live your life with less social anxiety.

For all these reasons we need to find an effective way to reduce oxidative stress when we think about treating social anxiety.

You just might not need a medication like an MAOI if your cell membranes were working in top form. Ketogenic diets greatly improve cell membrane function through any number of mechanisms, including reduced inflammation and oxidative stress (I promise we will get there), the signaling powers of the ketones themselves, or their use as an efficient and preferred fuel source. And because a well-functioning cell membrane directly enhances your brains’ ability to balance neurotransmitters, I include it here for your consideration.

How does the ketogenic diet help treat inflammation and oxidative stress in those with Social Anxiety Dsiorder?

An inflamed brain is not one that can function properly. For example, inflammatory cytokines trigger the activation of an enzyme that degrades serotonin and the amino acid precursor tryptophan. It is believed this is one of the many mechanisms involved between inflammation and the neurotransmitter imbalances seen in anxiety disorders. Ketogenic diets are very effective at reducing inflammation.

Ketones, which are what we produce on a ketogenic diet, happen to influence all of these relevant mechanisms and pathways needed to reduce oxidative stress.


Ketogenic diets are metabolic therapies, that improve metabolism in the brain. Metabolism is just a word referring to how well your cells make and burn energy. This has the potential to directly treat areas of hypometabolism (hypo=low, metabolism=energy use) seen in the neuronal structures of people experiencing social anxiety.

A reduction in the excitatory neurotransmitter glutamate and an increase in GABA and serotonin can only help social anxiety. And it will do it in a way that does not cause problematic side-effects. Ketones also increase the number and health of mitochondria in cells while improving cellular functioning at the level of the cell membrane. They reduce inflammation as signaling molecules that are able to turn down the expression of inflammatory pathways and turn up other important antioxidant functions, like glutathione production.

Improved cell membrane function helps increase micronutrient stores, cell communication, and allows those neurotransmitters to hang out for just the right amount of time before your body makes more in just the right amounts. Thereby, potentially alleviating your anxiety symptoms in a multifunctional way I am not sure any developed current psychopharmacology can duplicate with the same absence of side-effects.

It is my hope that after reading this post you will have a better understanding of not only the biological mechanisms involved in the pathology and symptoms experienced by those suffering from Social Anxiety Disorder (SAD), but also the understanding of how the ketogenic diet has direct influences on the multiple factors associated with healing and symptom reduction.

So ask yourself why would you NOT consider a ketogenic diet for the treatment of Social Anxiety Disorder (SAD)?

It’s OK if you don’t want to use a ketogenic diet, or other nutritional therapies to treat Social Anxiety Disorder (SAD). Convincing you to use the ketogenic diet to treat mental illness is not the purpose of my blog. The purpose of this post, and all the others, is to communicate that it is a viable option.

Because you have the right to know all of the ways that you can feel better.

You can learn more about me here. And if I can be of help on your wellness journey, please do not hesitate to contact me.

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Fedoce, A., Ferreira, F., Bota, R. G., Bonet-Costa, V., Sun, P. Y., & Davies, K. (2018). The role of oxidative stress in anxiety disorder: cause or consequence?. Free radical research52(7), 737–750.

Bandelow B. (2020) Current and Novel Psychopharmacological Drugs for Anxiety Disorders. In: Kim YK. (eds) Anxiety Disorders. Advances in Experimental Medicine and Biology, vol 1191. Springer, Singapore.

Blanco, C., Bragdon, L., Schneier, F. R., & Liebowitz, M. R. (2014). Psychopharmacology for social anxiety disorder. In Social Anxiety (pp. 625-659). Academic Press.

Dąbek, A., Wojtala, M., Pirola, L., & Balcerczyk, A. (2020). Modulation of cellular biochemistry, epigenetics and metabolomics by ketone bodies. Implications of the ketogenic diet in the physiology of the organism and pathological states. Nutrients12(3), 788.

Gzieło, K., Janeczko, K., Węglarz, W. et al. MRI spectroscopic and tractography studies indicate consequences of long-term ketogenic diet. Brain Struct Funct 225, 2077–2089 (2020).

Hjorth, O.R., Frick, A., Gingnell, M. et al. Expression and co-expression of serotonin and dopamine transporters in social anxiety disorder: a multitracer positron emission tomography study. Mol Psychiatry 26, 3970–3979 (2021).

Hur J., et al. (2021). Virtual Reality–Based Psychotherapy in Social Anxiety Disorder: fMRI Study Using a Self-Referential Task. In JMIR Ment Health 2021;8(4):e25731. URL:
DOI: 10.2196/25731

Imbalance between serotonin and dopamine in social anxiety disorder. Neuroscience News (2021). URL:

Jensen, N. J., Wodschow, H. Z., Nilsson, M., & Rungby, J. (2020). Effects of Ketone Bodies on Brain Metabolism and Function in Neurodegenerative Diseases. International journal of molecular sciences21(22), 8767.

Kerahrodi, J. G., & Michal, M. (2020). The fear-defense system, emotions, and oxidative stress. Redox Biology, 101588.

Martin, E. I., Ressler, K. J., Binder, E., & Nemeroff, C. B. (2009). The neurobiology of anxiety disorders: brain imaging, genetics, and psychoneuroendocrinology. The Psychiatric clinics of North America32(3), 549–575.

Mental health medications. National Institute of Mental Health.

Miller, A. H., Haroon, E., Raison, C. L., & Felger, J. C. (2013). Cytokine targets in the brain: impact on neurotransmitters and neurocircuits. Depression and anxiety30(4), 297–306.

Miller, A. H., Haroon, E., Raison, C. L., & Felger, J. C. (2013). Cytokine targets in the brain: impact on neurotransmitters and neurocircuits. Depression and anxiety30(4), 297–306.

Nuss P. (2015). Anxiety disorders and GABA neurotransmission: a disturbance of modulation. Neuropsychiatric disease and treatment11, 165–175.

Operto, F. F., Matricardi, S., Pastorino, G. M. G., Verrotti, A., & Coppola, G. (2020). The ketogenic diet for the treatment of mood disorders in comorbidity with epilepsy in children and adolescents. Frontiers in Pharmacology11, 1847.

Rebelos, E., Bucci, M., Karjalainen, T., Oikonen, V., Bertoldo, A., Hannukainen, J. C., … & Nuutila, P. (2021). Insulin resistance is associated with enhanced brain glucose uptake during euglycemic hyperinsulinemia: A large-scale PET cohort. Diabetes care44(3), 788-794.

Santos, P., Herrmann, A. P., Elisabetsky, E., & Piato, A. (2018). Anxiolytic properties of compounds that counteract oxidative stress, neuroinflammation, and glutamatergic dysfunction: a review. Brazilian Journal of Psychiatry41, 168-178.

Yu X, Ruan Y, Zhang Y, Wang J, Liu Y, Zhang J, Zhang L. Cognitive Neural Mechanism of Social Anxiety Disorder: A Meta-Analysis Based on fMRI Studies. International Journal of Environmental Research and Public Health. 2021; 18(11):5556.

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