Dr. Roger Seheult: Health Impacts of Vaping & Long Covid

Feb 25, 2025

Effects of Vaping and Nicotine on Health

The conversation around vaping and nicotine use has become increasingly complex, yet the fundamental truth remains clear: our lungs were designed for air and properly prescribed medications—nothing else.

While vaping advocates often position their product as a safer alternative to traditional cigarettes, the evidence suggests otherwise. The emergence of “popcorn lung” and other severe respiratory conditions linked to vaping cannot be ignored. Before the COVID-19 pandemic, Seheult witnessed numerous young patients in intensive care units due to vaping-related complications, particularly from underground products containing vitamin E oil mixed with nicotine.

Even commercial vaping products pose significant risks. Though they may contain fewer toxins than traditional cigarettes, they often deliver higher concentrations of nicotine, making them potentially more addictive. Rather than serving as an effective cessation tool, vaping frequently perpetuates nicotine dependency.

The landscape of nicotine consumption has evolved beyond traditional delivery methods. Non-smoked alternatives like nicotine gum and pouches have gained popularity, particularly among those seeking cognitive enhancement. These forms, while safer for lung health, still carry risks. Nicotine remains a vasoconstrictor that raises blood pressure, and its habit-forming properties are well-documented.

Medical professionals like Seheult regularly prescribe nicotine replacement therapy to help patients quit smoking, considering it a safer alternative to combustible tobacco. However, nicotine’s effects extend beyond simple stimulation. It interacts with both nicotinic and muscarinic acetylcholine receptors, creating subtle but powerful dependency patterns. Users often report improved verbal fluency and easier breathing, though the vasoconstriction actually works against optimal performance.

Emerging research suggests potential cognitive benefits for adults over 60, though this area requires further investigation. The key is understanding that while nicotine itself may have specific applications, the method of delivery significantly impacts its risk-benefit profile.

For those interested in respiratory health, the message is unambiguous: clean air remains the gold standard. Any deviation from this simple truth introduces unnecessary risks to our physiological systems.

Understanding Long Covid and Treatment Options

Long Covid is not just real – it’s a complex constellation of symptoms that persist for more than 12 weeks after infection. The most common manifestations include fatigue, headaches, and loss of taste and smell, but the condition’s heterogeneous nature makes it challenging to fully understand and treat.

At the heart of many long Covid cases lies mitochondrial dysfunction. Research has revealed significant downregulation in beta oxidation among long Covid sufferers compared to those who recovered normally. This means their bodies struggle to properly metabolize fatty acids in the mitochondria, likely due to damage from oxidative stress during the initial infection.

When evaluating long Covid patients, Seheult emphasizes the importance of ruling out obvious medical conditions through comprehensive testing, including echocardiograms and pulmonary function tests. Some cases reveal underlying issues like blood clots that require specific treatment. However, many patients show no clear medical abnormalities despite persistent symptoms.

One particularly interesting case involved a patient with severe shortness of breath (8/10 intensity) that had persisted for over a year. After ruling out various conditions, Seheult implemented an unconventional but scientifically-grounded approach focused on mitochondrial regeneration through two key interventions:

1. Strict intermittent fasting (no eating after 5:30 PM)
2. Regular sun exposure

The theory behind this approach involves allowing the body’s innate immune system to identify and clear damaged cellular components while promoting the generation of new, healthy mitochondria. This process is facilitated by the metabolic switch that occurs during fasting periods.

The results were remarkable – the patient’s shortness of breath decreased dramatically from 8/10 to 3/10, and their acid reflux completely resolved. While this specific protocol doesn’t work uniformly for all long Covid patients, it highlights the potential of addressing the condition through metabolic intervention.

Recent studies have also shown that the spike protein triggers toll-like receptor 4 inflammation, which can be mitigated by infrared light exposure. This finding provides additional support for the therapeutic potential of light exposure in long Covid cases.

While long Covid manifests differently in different people, certain foundational approaches like time-restricted eating and light exposure appear promising. These interventions are particularly valuable because they carry minimal risk while potentially offering significant benefits. For many patients who tend to stay indoors while sick, simply getting outside into natural light could be an important step toward recovery.

Olfactory Neurons and Covid Recovery

The complexity of COVID-19’s impact on individuals can be traced to the distribution of ACE2 receptors throughout the body. These receptors serve as binding sites for the SARS-CoV-2 virus, and their presence in olfactory neurons—genuine brain cells capable of regeneration—helps explain the varied neurological symptoms many experience.

Huberman points out that the disparity in COVID-19 symptoms, particularly brain fog lasting months, likely correlates with the virus’s ability to bind to ACE2 receptors in different individuals’ brains. The blood-brain barrier’s effectiveness in preventing viral entry may also play a crucial role in symptom severity.

Seheult explains that supporting cells adjacent to olfactory neurons, rather than the neurons themselves, contain high concentrations of ACE2 receptors. When these supporting cells die off, smell perception changes because the regeneration pattern differs from the original organization. This understanding has led to therapeutic approaches using “smell training” protocols, supported by randomized controlled trials using specialized scent markers manufactured in Europe.

The regeneration of olfactory neurons occurs through activity-dependent processes, requiring electrical stimulation triggered by various odors. This explains why effective smell training protocols incorporate diverse scents rather than focusing on a single smell. Interestingly, neurons responsible for detecting noxious odors show greater resilience, likely due to their critical role in survival mechanisms.

These noxious odor detection pathways follow a direct route to the amygdala, bypassing the thalamus, as Seheult and Huberman note. While individual odor maps vary based on personal experience, the neural pathways for detecting dangerous smells—smoke, decay, and other hazardous substances—remain remarkably consistent across humans, highlighting their evolutionary importance.

Training these pathways through systematic exposure to various scents has emerged as a viable rehabilitation strategy for COVID-19 patients experiencing olfactory dysfunction. This approach leverages the brain’s natural plasticity and the activity-dependent nature of olfactory neuron regeneration.

Mold Toxicity and Lung Health

When it comes to mold toxicity and lung health, the reality is more nuanced than many people realize. Mold-related health issues exist on a spectrum, and their impact depends on both the pathogen and the person’s immune system.

Consider Aspergillus, a common fungus that can affect the human body in two distinct ways. The first manifestation occurs when the fungus establishes itself in the lungs without invasion, potentially triggering an allergic response known as allergic bronchopulmonary aspergillosis. This condition presents with asthma-like symptoms and breathing difficulties, typically treated with a combination of steroids to reduce inflammation and antifungals to eliminate the root cause.

The second, more severe form is invasive aspergillosis, where the fungus actively invades lung tissue, creating cavitary lesions with fungal balls. These cases can be so severe that surgical intervention becomes necessary when medication proves insufficient.

Seheult emphasizes that we’re constantly exposed to mold and fungal spores in our environment. The outcome of these exposures depends on the interplay between germ theory and terrain theory. Some pathogens, like Neisseria meningitidis, can overwhelm even the healthiest immune systems. However, many other organisms only cause problems when they encounter a compromised immune system.

The relationship between mold exposure and illness isn’t simply about presence or absence – it’s about the balance between exposure burden and immune system capacity. Think of it like a football game: the outcome isn’t solely determined by one team’s strength or weakness, but by the dynamic interaction between both sides.

For those concerned about mold exposure, diagnostic options include antibody testing, though these results aren’t definitive. When mold actively grows in the lungs, it should be visible on a CAT scan and confirmable through biopsy and culture, allowing for targeted antifungal treatment.

However, some individuals may experience persistent symptoms without clear diagnostic findings, similar to reactive airways disease (RADs). In these cases, a single significant exposure can trigger ongoing respiratory issues, even without continued exposure to the initial trigger.

The realm of mold toxicity reveals an important truth about health: it’s rarely a simple matter of identifying a single cause or solution. Instead, it’s about understanding the complex interaction between environmental factors and our body’s defense mechanisms.

Read Andrew Huberman

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