I spoke with Andrew Gray (TikTok's @thegoomanstem) earlier in the week. He had just published 2 new resources in his area of expertise, virology, mental health and autoimmunity.
The Illustrated Treatment Guide to EBV and Goo Man's Guide to Mental Health Disorders are a gold-mine of modern research, easily-digestible explanations and health connections you've never considered.
He spoke about Epstein-Barr virus (EBV) and its ability to hijack major neural communication pathways, how any one of the thousands of herpes simplex virus (HSV) can lay dormant in your system for generations at a time. He elaborated on how the immune system and viruses dance back and forth chasing each other into activation-latency-reactivation cycles, each time pulling the host (you and me) further into imbalanced inflammatory states.
There was a point in our conversation where I realized that about 75% of the subject matter he had discussed was something I had read about directly or indirectly in my own diabetes research. While he was enlightening me to an entirely new side of these subjects, there was something remarkably familiar. I knew about GAD+GABA balance. I knew about altered glucose metabolism. Liver health? Yeah, definitely.
The degree of crossover in our alternative health pursuits was uncanny. I had always lumped viruses into the "pathogenic" category of possible influences on T1D, but never gave it my full attention. I wanted to know more. And that's what brings us here.
I think we need to pay more attention to viruses and their role in autoimmunity.
The why, how and when of it all is still up in the air, but there's too much really good information here to ignore. To help me lay it all out, I'm going to pose some questions, remarks etc and see where it takes me.
Viruses are very good at replicating and transmitting from host to host.
Googles: Explain virus replication and host-host transmission like I'm 5 years old
Unwashed hands, runny noses, uncovered sneezes in stagnant air. Viruses float and crawl all over the world around us. We get sick, learn it's viral and wait for it to run its course. Our immune system flairs and we take a day off of work while our body repairs its tissues and neutralizes the threat. We feel better a few days later and we're back to normal. Right?
Mmmmmmm maybe. But probably not. At least not entirely normal. Viruses are tricky in that they are able to enmesh themselves within the cells of their host. After an initial infection, their physical presence is not enough to illicit an immune response. They cloak themselves in an inactive state called latency. They take our DNA material and build themselves a nest. They leave bits and pieces of themselves in our cells after they leave (thus never actually truly leaving). And they can remain latent for days, months, years on end, waiting for opportunistic times to reactivate and send their progeny to new hosts.
Opportunity for new hosts takes the form of new illnesses, malnutrition and stressful times. Yet, it's technically possible to have a virus and never experience the illness associated with it.
Viruses have a vested interested in the organ systems and immune pathways directly tied to T1D.
GAD + GABA
Glutamate is one of the most important neurotransmitters in the brain and central nervous system. It's primarily known as an excitatory neurotransmitter, meaning it plays a key role in promoting the activation of neurons. Here are some key points about glutamate:
Excitatory Function:
Glutamate is the main excitatory neurotransmitter, meaning it increases the likelihood that the neuron it binds to will fire an action potential. This makes it crucial for neuronal communication, learning, memory, and overall brain function.
Learning and Memory:
Due to its role in synaptic plasticity—the ability of synapses to strengthen or weaken over time—glutamate is vital for learning and memory processes. It is involved in mechanisms such as long-term potentiation (LTP), which is believed to be a cellular basis for memory formation.
Neurotransmitter Pathways:
Glutamate is widely distributed throughout the brain and engages in various pathways, influencing a range of neurophysiological processes. It works by binding to both ionotropic and metabotropic receptors, including NMDA, AMPA, and kainate receptors.
Precursor for GABA:
Glutamate also serves as the precursor for the synthesis of GABA (gamma-aminobutyric acid), the primary inhibitory neurotransmitter. This conversion is facilitated by the enzyme *glutamic acid decarboxylase (GAD).
Regulation and Toxicity:
Although critical for normal brain function, excessive glutamate activity can be toxic and lead to excitotoxicity, which can cause neuronal injury or death. This is implicated in various neurological conditions, such as stroke, epilepsy, and neurodegenerative diseases like Alzheimer's disease.
Role in Metabolism:
Beyond its role as a neurotransmitter, glutamate plays a part in cellular metabolism. It is involved in the Krebs cycle and serves as a key metabolite in cellular energy production.
*Most with T1D are familiar with glutamic acid decarboxylase (GAD) because of the use of the GAD autoantibody as a metric for early T1D detection. Did you know that GAD antibodies are also used to detect multiple neurological syndromes, including stiff-person syndrome, cerebellar ataxia, and limbic encephalitis? These conditions are all considered to result from reduced GABAergic transmission (more on this later).
Viruses elevate cortisol as part of an acute immune reaction. Cortisol can influence glutamate levels in the brain. During acute stress, the increase in cortisol can lead to increased release of glutamate. This is because cortisol can enhance the activity of neurons, and as glutamate is the primary excitatory neurotransmitter, its release is often modulated in response to stress. Therefore, excess cortisol can lead to glutamate toxicity.
Excitotoxicity: Chronically elevated cortisol can lead to excessive glutamate release, which may cause excitotoxicity—overstimulation of neurons that can result in damage or cell death. This is particularly of concern in brain regions like the hippocampus, which is critical for learning and memory.
Impaired Memory and Cognitive Function: Prolonged high cortisol levels can impair cognitive function and memory. The hippocampus, rich in glucocorticoid receptors, can be particularly vulnerable, potentially leading to atrophy and reduced neuronal connectivity, contributing to memory deficits.
Mood Disorders: Chronic stress and high cortisol are associated with the development of mood disorders such as anxiety and depression. Alterations in glutamate transmission play a role in these conditions by disrupting normal neural communication and plasticity.
Impact on Neurogenesis: High levels of cortisol can suppress neurogenesis—the growth of new neurons—particularly in the hippocampus, further contributing to the negative cognitive effects and potentially playing a role in mood disorders.
With all of this cortisol and glutamate in circulation, what about GABA? GABA is the brakes to glutamate's gas, the yang to glutamate's yin. The interplay between elevated cortisol, excessive glutamate activity, and the overall stress response can have significant effects on GABA production and release.
Here's how these factors might impact GABAergic function:
Imbalance Between Excitatory and Inhibitory Signals:
Reduced GABAergic Activity: Chronic stress and elevated cortisol levels can disrupt the balance between excitatory (glutamate) and inhibitory (GABA) neurotransmission. Under stress, the enhanced excitatory signaling may overwhelm GABAergic inhibitory control, leading to insufficient GABA activity to counterbalance excitatory signals.
Altered GABA Receptor Function: Prolonged exposure to high cortisol can affect GABA receptor expression and function. Studies suggest that chronic stress can lead to downregulation or desensitization of GABA receptors, reducing the effectiveness of GABAergic inhibition (Orchinik et al., 1995).
Impact on GABA Synthesis:
Enzyme Regulation: Chronic stress might influence the expression and activity of enzymes involved in GABA synthesis, such as glutamic acid decarboxylase (GAD). Changes in enzyme levels can impact the production of GABA from glutamate, potentially reducing its availability.
Neurogenesis and GABAergic Interneurons:
Effects on Interneuron Health: Elevated cortisol levels and stress can negatively impact neurogenesis and the health of GABAergic interneurons, especially in stress-sensitive areas like the hippocampus. This can lead to a reduction in the number or functionality of these inhibitory neurons, further impairing GABA release.
Mood and Anxiety Disorders:
The alterations in GABA production and release due to chronic stress are implicated in mood and anxiety disorders. Reduced GABA levels have been associated with anxiety, depression, and other affective disorders, likely due to an inability to adequately modulate stress-induced excitatory signaling.
Behavioral and Cognitive Implications:
A reduction in GABAergic activity can lead to heightened anxiety, mood swings, and impairments in cognitive processes such as attention, learning, and memory. Insufficient inhibition can contribute to conditions where the brain is prone to overactivity and less able to maintain emotional and cognitive stability.
With this nervous system component in mind, the nervous system blasting glutamate to escape the perceived threat, lets also incorporate alternative sources of inflammation.
Enter: gut health and nutritional deficits. In addition to all the down regulation directly tied to stress, GABA production is also compromised via indirect cell inflammation and gut microbiome shifts. GABA is made by specific strains of bacteria in a healthy gut as a result of the fermentation of certain dietary fibers. The food we eat serves as the foundation from which our gut health interacts with us.
Viral infections, as well as nutritional deficiencies like iron overload, have been shown to suppress the bacteria strains tied to GABA production.
Here are some consistent findings across those with T1D:
Reduced Diversity:
One of the most consistent findings is a decrease in microbial diversity. A more diverse microbiome is generally associated with better health outcomes, and reduced diversity can signify a less resilient microbial community.
Altered Composition:
Individuals with T1D often exhibit a different microbial composition compared to healthy individuals. There tends to be a lower abundance of beneficial bacteria, such as certain Bifidobacterium and Lactobacillus species.
Increased Pathobionts:
Some studies have observed an increase in potentially harmful bacteria, sometimes referred to as pathobionts. These include bacteria that might contribute to inflammation or other disruptions in gut homeostasis.
Potential Loss of Protective Species:
Certain bacterial species thought to have protective effects against autoimmune processes may be found in reduced numbers. For example, butyrate-producing bacteria, which play a role in maintaining gut barrier function and reducing inflammation, are often less abundant.
Immune System Interaction:
The altered microbiome profile is thought to influence the immune system, possibly contributing to the autoimmune attack on pancreatic beta cells that characterizes T1D. Dysbiosis may promote systemic inflammation or lead to a compromised gut barrier, enhancing immune dysregulation.
Functional Changes:
Beyond compositional changes, the functional capacity of the gut microbiome is also altered. This might involve changes in metabolic pathways, such as those involved in the production of short-chain fatty acids (SCFAs) or other metabolites that influence immune responses.
Not only is our glutamate supply running our GAD and GABA production capacity to the ground, what we're eating (and not eating) is adding gas to the fire.
Which came first, the virus or the compromised environment?
One of main thoughts as Andrew explained the viruses hold on our system was: Is this the chicken or the egg?
Have viruses been around long enough from generation to generation to produce humans born with these compromised states?
-Or-
Have we become so malnourished over the past few generations that we've become the perfect, fertile ground for viral takeover?
And let's not forget a third option: Is this a perfect co-evolution of viral pathology combined with progressive malnutrition?
Who is calling the shots? Have viruses robbed our body's of its gut flora and capacity for nutrient absorption? Or, through what we eat and how we manage our food supply, have we made perfect home for viruses to run the show?
I don't know right now. It first struck me as an important point but now I'm not so sure.
Let's look at how we would approach either scenario.
Virus first. Remember, with viruses it's a game of containment and neutralization, not elimination. So we're looking to both eliminate what the virus needs to replicate and activate, while simultaneously giving our body the resources necessary to combat the virus.
Viruses like simple sugars and carbohydrates. It a quick source of energy. High sugar, high carb environments let the virus know it's in a safe place to replicate. So imagine a virus's luck in finding someone with T1D! Unregulated blood sugars create a viral playground.
So fending off viral replication and keeping them in latency has to do with limiting their energy sources. This could be a low-carb effort, this could be an insulin sensitization effort to prevent any unnecessary spikes.
There's also the antioxidant component. A virus's ability to create inflammation in the body is a means for overwhelming the immune system. This creates open windows for infection and establishing itself in compromised cells. Antioxidants (either naturally created or supplemented) are there to neutralize any inflammatory ROS and limit the strain on our immunity.
You can also take a more targeted approach with medications. Acyclovir, valacyclovir and famciclovir are some common antivirals prescribed for infections like herpes and shingles. These drugs are able to disrupt the replication cycle.
Let's pause for a second. Notice the nutritional roots of both the blood sugar regulation and antioxidant components. Limiting blood sugar spikes and boosting antioxidants has to do with our food! Some common foods and plant compounds used for their antiviral abilities? Berries, leafy greens, cruciferous vegetables, garlic, onions, sweet potatoes and carrots, turmeric, citrus fruits and ginger.
Which brings us right into the malnourishment theory.
Malnourishment and nutrient imbalances create a pro-viral environment in the body.
Those with T1D are chronically deficient in Vitamin D, magnesium, vitamin B12, and zinc. They also experience significant imbalances in iron/copper, calcium/magnesium, sodium/potassium.
The industrialized world is rife with artificially enriched products, processed foods, herbicides and pesticides that strip nutrients away and skew our food's natural balance. I talk all about the nutrient origins of disease in my eBook An Ironclad Cause.
When it comes to addressing these deficits, we're looking for nutrient dense, high-antioxidant foods. So what might those be?
Berries, leafy greens, cruciferous vegetables, garlic, onions, sweet potatoes and carrots, turmeric, citrus fruits and ginger.
Does that list ring a bell? Its the EXACT SAME LIST for antiviral foods.
We're interested in liver cleansing compounds (like to cruciferous vegtables, garlic and citrus fruits). We want fat-soluble vitamins (like the vitamin A found in sweet potatoes and carrots). We want magnesium and calcium (like those found in leafy greens).
The crossover is uncanny.
So at the end of the day, whether you're attacking the virus in hopes of allowing your body to fully recover, or you're replenishing your body to bolster it's viral defenses, YOU EAT THE SAME THINGS.
And now I need a break. Chew on this for a bit and let me know what you think in the comments.
Bon appetit!
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