Mental Health Plartform.

Generalized Anxiety Disorder (GAD)


How could a ketogenic diet help treat the symptoms of Generalized Anxiety Disorder (GAD)?

Ketogenic diets are able to modify at least four of the pathologies we see underlying Generalized Anxiety Disorder (GAD). 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 Generalized Anxiety Disorder (GAD) symptoms.


In this blog post, I am not going to outline the symptoms or prevalence rates of Generalized Anxiety Disorder (GAD). This post is not designed to be diagnostic or educational in that way. If you have found this blog post, you know what GAD is and likely you or someone you love may already be suffering from the debilitating symptoms associated with 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 GAD 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 Generalized Anxiety Disorder (GAD) symptoms or as a complementary modality to use with psychotherapy and/or in place of medications.

Current psychopharmacology for Generalized Anxiety Disorder (GAD) includes selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs). These antidepressants are first-line medication options for all anxiety disorders. Additional medications can include calcium modulator pregabalin, tricyclic antidepressants, buspirone, moclobemide, anticonvulsants, and atypical antipsychotics.

Why are these drugs prescribed for Generalized Anxiety Disorder (GAD)?

These drugs attempt to modulate complicated neurotransmitter systems that include serotonin, norepinephrine, and GABA. These are the most common targets of psychopharmacological approaches to these disorders. These are some of the neurotransmitter imbalances we see in patients suffering from Generalized Anxiety Disorder (GAD). 

However, patient responses to these medications designed to affect these neurotransmitter systems can often fall short of symptom relief.

Despite the efficacy of available pharmacological approaches, many patients do not achieve full remission, and novel treatment approaches are warranted.

Melaragno A., Spera V., Bui E. (2020) –

So what kind of pathology in the brain do we see in Generalized Anxiety Disorder (GAD)?

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.

Let’s explore which of these may or may not be present in the pathology of Generalized Anxiety Disorder (GAD).

Glucose Hypometabolism in the brain of those with Generalized Anxiety Disorder (GAD)

Hypometabolism of the brain means that some brain structures are not utilizing energy properly. People with Generalized Anxiety Disorder are seen to suffer from hypometabolism in the basal ganglia and white matter. Hypometabolism of the basal ganglia can be seen in sleep disorders in which people struggle with their sleep-wake cycle. Could hypometabolism of this brain area contribute to the inability to fall asleep or stay asleep due to worry? Possibly. I was unable to find where this possible connection was explored in Generalized Anxiety Disorder populations.

Primarily the basal ganglia are involved in motor learning, sequencing, and movement behaviors, and memory. While movement or motor issues are not part of the diagnostic criteria for Generalized Anxiety Disorder (GAD), there are complaints about working memory as a cognitive symptom of the disorder. Research has found abnormalities in brain metabolism in those with GAD, who attempt to recall from working memory while under emotion-inducing distractors.

This is not surprising, as the basal ganglia are also used for attention and filtering out distractions. For people with generalized anxiety, the act of worrying becomes an automatic behavior. There is an inability to determine what concern deserves attention and to worry constantly, even about possibilities that are highly unlikely. Would improvement in brain metabolism in these areas help reduce some of these symptoms of Generalized Anxiety Disorder (GAD)?

Female Basal Ganglia Brain Anatomy

This could mean that people with the disorder have a harder time discerning truly worrisome situations from mild annoyances. At the same time, the amygdala was more connected to a cortical executive-control network previously found to exert cognitive control over emotion.

Interestingly, in the brains of people with Generalized Anxiety Disorder (GAD), we also see issues with interconnectivity between brain structures.

Problems with interconnectivity occur between the amygdala and other brain structures. In the brain suffering from GAD, it has less connectivity to targets generally seen in normal brains. And when the amygdala was “over-connected” to these other brain structures, it seemed to influence where and how they in turn connected to other parts of the brain. These other structures are seen to then atypically connect to areas of the brain not normally seen to be so connected. Meaning, more connectivity was seen between areas there should not be. At least not in healthy brains with normal connectivity.

Of important note was that the amygdala region had less connection to the part of the brain responsible for evaluating the importance of a stimulus. It is hypothesized that this may be what causes GAD people to not know what to place importance upon regarding their concerns. And so people with GAD tend to worry about everything, as opposed to an actual likely threat or concern.

How could a ketogenic diet assist with hypometabolism and possibly even problems with interconnectivity?

Hypometabolism and keto

Ketogenic diets are used to improve brain metabolism in Alzheimer’s Disease and other neurological disorders. It improves insulin sensitivity in the brain for cells that are still able to use glucose. For parts of the brain no longer utilizing glucose well as a primary fuel, it provides the alternative fuel of ketones. Ketones are able to increase the functioning of existing mitochondria. These mitochondria are the powerhouses of neuronal cells. Not only do ketones help your mitochondria work better but ketones help your cells make more mitochondria. Which makes more energy for the brain. Which increases metabolism in the brain in a beneficial way.

Brain-Derived Neurotrophic Factor (BDNF) and Keto

Another powerful benefit of ketogenic diets is their ability to upregulate (make more of) something called Brain-Derived Neurotrophic Factor (BDNF). BDNF allows the brain to repair and grow new connections. If there are problems with interconnectivity in the brain, is it not logical to assume that an intervention that upregulates this factor would be an important part of recovery? Would not a ketogenic diet used in conjunction with cognitive-behavioral therapy (CBT) designed to change thinking patterns not be a powerful combination? An ample supply of BDNF could only be a positive factor in the treatment of Generalized Anxiety Disorder (GAD).

Neurotransmitter Imbalances seen Generalized Anxiety Disorder (GAD)

Just as with other mental disorders, we do not see a disruption in just one neurotransmitter. We instead see a disruption in the delicate balance of the neurotransmitter system. These include decreased GABA, increased glutamate, and decreases in serotonin. There is also some dysfunction in the neurotransmitter dopamine.

Decreases in GABA with an increase in glutamate are seen in other anxiety disorders, as described in this blog post here.

This neurotransmitter imbalance often occurs due to the environment in which they are being made. A brain suffering from inflammation and oxidative stress, which we will discuss more later in this post, is not a brain optimized to make and use neurotransmitters effectively.

A brain high in inflammation, for whatever reason (but it could very likely be due to eating highly processed carbohydrates), will cause something called the Tryptophan steal. Tryptophan is an amino acid that is a precursor to other neurotransmitters. When the brain is suffering from inflammation it will create less of (downregulate) the neurotransmitter GABA. And instead, it will take tryptophan and make more of an excitatory neurotransmitter known as glutamate. Which by itself would not be bad, except we are supposed to have adequate levels of GABA with our glutamate to keep our neurotransmitters in balance. Also, too much glutamate is neurotoxic to the brain. It ages the brain and causes damage. The tryptophan steal that occurs when the brain is under distress can cause up to 100x more glutamate in the brain than normal levels.

Cellular membrane function is crucial to maintaining neurotransmitter balance. Cell membrane function in neuronal cells allows the creation of neurotransmitters, how fast they fire, and how long a neurotransmitter stays around to be used within the synaptic cleft. This is relevant for those with Generalized Anxiety Disorder (GAD) because the reuptake of Dopamine in certain brain structures (e.g., striatum) is seen to be significantly lower in GAD patients than in healthy controls.

How could a ketogenic diet assist with neurotransmitter imbalances?

Mostly a ketogenic helps with neurotransmitter imbalances by reducing inflammation, so that the environment in which they are being made is a healthy environment to do so. But ketogenic diets have also been seen to restore neurotransmitter and ion channel functioning, which have very strong effects on how well neurotransmitters can work. In this small post, we discussed the importance of improved cell membrane function.

What it means for your brain is that all the work of making the right neurotransmitter balance is not enough. Your brain still must be able to use those neurotransmitters in a functional way. That means the ability to store important nutrients (cofactors) so neurotransmitters can be made, being able to break some neurotransmitters down, and being able to allow neurotransmitters to hang out in the synapses for the right amounts of time. Ketogenic diets allow these functions to be restored and allow neurotransmitter balance to occur through improved neuronal functioning. And if improved neuronal functioning accomplishing all that doesn’t sound like an important therapeutic target in an anxiety disorder like GAD, I am not sure what would be!

Oxidative Stress is seen in Generalized Anxiety Disorder (GAD)

We have all heard the term Oxidative Stress but may be unsure what it is and what it means for our body, other than it is “bad” and we need to avoid it. Oxidative stress happens. If you are alive then oxidative stress will occur just because your body is doing a lot of different biological processes that create substances your body has to deal with. And that is just what is happening internally. That does not even consider the impact of our environmental exposure outside of our body (e.g., chemicals, pollution, lifestyle).

Having a healthy lifestyle allows you to manage the amount of oxidative stress your body has to go through and it will even do things that help improve your ability to deal with what does occur. Exercise is a good example of this. It upregulates our ability to make antioxidants from pathways that exist in our own bodies, such as glutathione.

When we look at those with Generalized Anxiety Disorder (GAD) we see that there is a great deal of oxidative stress in this population.

Generalized anxiety disorder patients have higher oxidative stress index levels.

Ercan, et al., (2017);

They are still trying to tease out if oxidative stress causes GAD, or if GAD, because of the stress that is caused on the body with excessive worry, causes oxidative stress. And I would argue that it doesn’t matter. Let’s figure that part out later and do what we can to decrease oxidative stress. Let’s have it be a target of biological intervention and let’s also do our best to reduce worry in our thoughts with Cognitive-Behavioral Therapy (CBT).

oxidative modifications to proteins have actually been proposed as a potential factor in the onset and progression of several psychiatric disorders, including anxiety and depressive disorders

Fedoce, et al., (2018),

The inability to deal with these levels of oxidative stress in the brain destroys neurons. In the literature, they actually call it “extreme neuronal trauma” and as you can imagine, these traumatized cells are broken and cannot do all the functions they need to do to keep your brain working. They are not going to make neurotransmitters well, they are not going to have good working neuronal membranes, and they are not going to be able to store the nutrients they need in order to do cell maintenance or make needed enzymes that manage those neurotransmitters. Why we would expect that we could throw a serotonin reuptake inhibitor (SSRI) into such a complex system as a treatment? Throw all the neurotransmitters you want in there but if the membranes and machinery are busted it’s not going to work. Neuronal cells are being severely damaged and annihilated by oxidative stress. Talk about a band-aid mentality to mental illness. Why wouldn’t we just help people fix the synapses?

How could a ketogenic diet decrease oxidative stress?

Ketogenic diets are excellent for oxidative stress. This is not a speculation on my part. And this is not an assertion made only due to animal studies. This is a real-life and powerful effect seen in humans, in studies with actual human beings.

Cerebral metabolism of ketones has been shown to improve cellular energetics, increase glutathione peroxidase activity,15 reduce cell death16 and possesses anti-inflammatory and antioxidant capabilities in both in vitro and in vivo models.1720

One of my favorite things to talk about is glutathione. And not the kind you take in a pill that is given to you by your naturopath or functional medicine doctor. Oral glutathione isn’t used by the body so well and it’s expensive. Sometimes they will give you precursors in the form of vitamins and minerals, hoping your body will make more of its own glutathione, which is better and of which I completely approve. But nothing is going to upregulate (make more of)the production of endogenous (made by your own body) glutathione like a well-formulated (meaning nutrient-dense) ketogenic diet.

So treating oxidative stress in the GAD brain with a ketogenic diet should not be such a revolutionary and controversial stance. And quite frankly it is not. As you can see, there are some already identified mechanisms and clear effects of its use for the very underlying pathological processes we have identified with scientific inquiry.

Inflammation is seen in Generalized Anxiety Disorder (GAD)

Let’s discuss neuroinflammation. Neuroinflammation occurs for a lot of different reasons. Cognitive influences, like our interpretations of a situation, can cause inflammation. What we eat can cause inflammation, whether because our blood sugar levels are too high or we are having an immune reaction to a particular food. Inflammation can occur because something has crossed the blood-brain barrier that should not have. These all trigger an immune system response. And our brains have their own immune response and they respond with something called microglia.

Microglia tries to fix what is going wrong by releasing inflammatory chemicals. One type of inflammatory chemical that microglia release is cytokines. There are different types of cytokines. And they can be measured with serum blood tests. Your doctor may have ordered a CRP or a high-sensitivity CRP test for you. This is a marker of inflammation. But it is important to understand that there are a lot of different types of cytokines that increase inflammation. This can make research difficult. Some types of cytokines may be studied over others. Some will be studied in some populations but not in others. We do not have a nice clear picture. Particularly for Generalized Anxiety Disorder (GAD) populations

Inflammation and its association with people suffering from GAD are a little all over the place in the literature. Some studies have found people with GAD to have higher markers of inflammation. This is not surprising given that they tend to have more oxidative stress. Some people with GAD and certain genetic markers were seen to have more inflammation than others. This is again, not surprising. How our body manifests disease under the right epigenetic conditions would of course have a genetic component.

But higher markers of inflammation are not always seen in the literature for people with GAD. In fact, some have shown that people with GAD do not have higher inflammatory markers. But some studies are teasing out differences in subpopulations of those with GAD. For example, women who developed GAD later in life have higher markers of inflammation than those who develop it earlier in life. And we cannot seem to figure out if inflammation has a causative role in the etiology (creation) of GAD.

So I would say this. If you have only Generalized Anxiety Disorder (GAD), and no comorbid depressive symptoms, or comorbid Panic Disorder (which DOES see higher inflammatory markers), the role of the ketogenic diet on inflammation may not be of interest to you in your recovery. As a mental health counselor, however, I do not see too many patients with just pure GAD without any comorbidities. So inflammation may not be an issue in GAD, or it could be that it is an issue and there are not enough studies that include GAD as part of research with other comorbidities and this topic.

But just in case you have GAD and are suffering from dual diagnoses with other mental illnesses, I will discuss the effect of the ketogenic diet on inflammation.

How do ketogenic diets fight inflammation?

Ketogenic diets are metabolic interventions. Brain metabolism has direct effects on immune function in the brain. And as we know already from reading this blog post, immune function in the brain has direct effects on inflammation. High-fat, low-carbohydrate ketogenic diets create ketones, which decrease microglial activation and pro-inflammatory cytokines. Ketones are actually a signaling body, influencing gene expression, that can exert positive influences on the pathways that modulate inflammation. If you are wanting to dive a little deeper into exactly how ketogenic diets fight inflammation there is a most excellent article here.

Other ways that a ketogenic diet may help with reducing inflammation include gut microbiota modifications. We are still learning about all the ways ketogenic diets help fight inflammation. But regardless of whether you choose a ketogenic diet to help treat Generalized Anxiety Disorder or some other mental illness or neurological disorder, it is important to understand that neuroinflammation is toxic to brains. It breaks down the blood-brain barrier your body has put in place to try and protect your brain. It damages neuronal membranes and makes it difficult for neuronal cells to communicate with one another and function on their own. And it ultimately leads to cell death. And ketogenic diets have shown direct ways that they provide neuroprotective and anti-inflammatory benefits in human beings (not just animal studies).

Being that you are a human being, I submit this for your consideration in evaluating all the different options you have for feeling better.


A ketogenic diet is a viable option for those with Generalized Anxiety Disorder (GAD) as a treatment modality of consideration. Its effects in improving or treating brain hypometabolism, balancing neurotransmitters and improving neuronal function, and protecting the brain from oxidative stress and neuroinflammation are all mechanisms based on the scientific literature. These are also factors seen in populations suffering from Generalized Anxiety Disorer (GAD). The ketogenic diet may be a good option as a primary or complementary therapy that includes psychotherapy and./or medications. It can also be considered as a treatment for those wanting to avoid medications, for those whose medications are no longer working well, or who would like to take less medication in an attempt to reduce side effects.

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

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